FELINE

ORTHOPEDICS
Harry W Scott BVSc, CertSAD, CBiol, MIBiol, DSAS(Orth), FRCVS
Royal College of Veterinary Surgeons Specialist in
Small Animal Surgery (Orthopaedics)
Private Orthopaedic Referral Practice
Hampshire, UK

Ronald McLaughlin DVM, DVSc, Diplomate ACVS

Professor and Chief, Small Animal Surgery
Department of Clinical Sciences
College of Veterinary Medicine
Mississippi State University
Mississippi, USA

MANSON PUBLISHING/THE VETERINARY PRESS

Copyright © 2007 Manson Publishing Ltd
ISBN: 978-1-84076-056-9

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Disclaimer
Medical knowledge and best practice are constantly evolving as new research
and experience contribute to our understanding. While the authors have taken
every effort to eliminate inaccuracies, readers are advised to consult the most
current information available on procedures, products, dosages, and formulae.
Drug licensing varies between countries; the information given in this book
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 CONTENTS

PREFACE 6 Postoperative care 38

Posttraumatic osteomyelitis 39
ABBREVIATIONS 7
4 FRACTURE CLASSIFICATION, DECISION
1 INTRODUCTION TO FELINE MAKING, AND BONE HEALING 43
ORTHOPEDIC SURGERY 9 Fracture classification 43
Comparative features 9 Fracture decision making 45
Specific anatomic features and their Fracture healing 47
significance 10
Blood supply to bone 14 5 INSTRUMENTS AND IMPLANTS 50
Bone growth 14 Instruments 50
Implants 51
2 EXAMINATION AND DIAGNOSTIC TOOLS 17
Introduction 17 6 FRACTURE FIXATION METHODS:
Signalment 18 PRINCIPLES AND TECHNIQUES 58
History 18 Preoperative considerations 58
Physical examination 18 Fracture reduction 58
Orthopedic examination 18 Fracture stabilization methods 59
Diagnostic tools 19 Cancellous and corticocancellous bone
grafting 80
3 MANAGEMENT OF THE ORTHOPEDIC Implant removal 82
TRAUMA PATIENT 25 Delayed and nonunion fractures 82
Introduction 25 Articular fractures 84
Physical examination 25
Diagnostic tests 26 7 ARTHROLOGY 87
Resuscitation and stabilization of the trauma Classification of joint disease 87
patient 26 Investigation of joint disease 88
Pre- and postoperative stabilization of Degenerative arthritides 90
fractures and luxations 29 Infective inflammatory arthritides 94
Initial treatment of fractures 33 Immune-mediated inflammatory arthritides 97
Pre- and perioperative analgesia 35 Miscellaneous disorders of joints 101
Pre- and perioperative sedation 38 Ligaments and tendons 104
4

8 FRACTURES AND DISORDERS OF Postoperative care of femoral fractures 215

THE FORELIMB 107 Complications of femoral fractures 215
Part 1: Scapula and shoulder joint 107 Patellar fractures 215
Scapular fractures 107
Dorsal displacement of the scapula 111 Part 4: Stifle disorders 218
Shoulder luxations 111 Patellar luxation 218
Excision arthroplasty 113 Cruciate ligament injuries 222
Shoulder arthrodesis 113 Collateral ligament injury 225
Stifle luxation 228
Part 2: Humerus and elbow joint 115 Stifle arthrodesis 231
Humeral fractures 115
Traumatic elbow luxation 130 Part 5: Tibial and fibular fractures 233
Elbow arthrodesis 134 Proximal tibial fractures 233
Diaphyseal tibial fractures 238
Part 3: Radius and ulna 136 Distal tibial and malleolar fractures 242
Hemimelia 136
Radial head luxation 136 Part 6: Tarsal, metatarsal, and
Fractures 137 phalangeal injuries 244
Fractures of the tarsus 245
Part 4: Carpal, metacarpal, and phalangeal Luxations of the tarsus 247
injuries 145 Shearing injuries of the tarsus 250
Carpal joint injuries 145 Calcanean tendon lacerations 252
Metacarpal and phalangeal injuries 154 Avulsion of the Achilles tendon 254
Onychectomy (declawing) 157 Luxation of the superficial digital
Forelimb amputation 165 flexor tendon 255
Tarsal arthrodesis 255
9 FRACTURES AND DISORDERS OF THE Metatarsal and phalangeal fractures and
HINDLIMB 167 luxations 259
Part 1: Pelvis 167 Hindlimb amputation 259
Pelvic fractures (general) 167
Sacroiliac fractures/dislocation 169 10 FRACTURES AND DISORDERS OF
Ilial fractures 173 THE SKULL AND MANDIBLE 261
Acetabular fractures 176 Mandibular fractures 261
Ischial fractures 180 Maxillofacial fractures 271
Pubic fractures 180 Temporomandibular joint injury 273
Pelvic malunion fractures 180 Fractures of the neurocranium 277

Part 2: Coxofemoral joint 184 11 FRACTURES AND DISORDERS OF

Coxofemoral luxation 184 THE SPINE 279
Hip dysplasia 191 Surgical anatomy 279
Investigation of spinal disease 281
Part 3: Femoral and patellar fractures 192 Treatment of spinal disorders 294
Proximal femoral fractures 192 Common disorders of the spine 296
Diaphyseal femoral fractures 198 Uncommon diseases of the spine 313
Distal femoral fractures 208
 5

12 NEUROMUSCULAR DISORDERS 321 Neoplastic disorders of bone 342

Introduction 321 Infections of bone 349
Classification of neuromuscular disorders 322 Congenital defects 349
Causes of neuromuscular disease 322
Neuropathies 322 REFERENCES 351
Myopathies 328
Junctionopathies 332 APPENDIX 390

13 MISCELLANEOUS ORTHOPEDIC INDEX 391

DISORDERS 335
Metabolic bone diseases and disorders of
calcium metabolism 335
6

PREFACE

The most notable change in the companion animal population over the last few decades has been the steady rise
in popularity of the cat. Cats now outnumber dogs as domestic pets in many developed countries; it is estimated
that there are now at least 70 million domestic cats in North America alone. As a consequence the small animal
practitioner is confronted with cats suffering from a variety of orthopedic disorders on a daily basis. Existing
orthopedic texts are heavily biased in favour of the dog with cats receiving little or no mention, yet there are
many minor and a few major differences between the musculoskeletal systems of dogs and cats.
The motivation for writing this book was a desire by the authors to bring together all of the salient facts
concerning feline musculoskeletal disease and present them in an organized and accessible format. As far as
possible the information presented is based on the results of studies involving cats rather than being extrapolated
from other species. When evidence from such studies is lacking or when the evidence is anecdotal, reliance has
been made on the personal experiences and opinions of the authors. It is hoped that this book will play a small
part in the development and continued advancement of feline orthopedics as a discipline in its own right. The
text is intended to be of interest both to students and to practitioners involved in the treatment of feline
musculoskeletal disorders.

Harry W Scott
Ronald McLaughlin
 7

ABBREVIATIONS

ACD acid citrate dextrose IM intramuscularly

ANA antinuclear antibody IVDD intervertebral disc disease
AO Arbeitsgemeinschaft für IV intravenously
Osteosynthesefragen KE Kirschner–Ehmer
ASIF Association for the Study of Internal L + number lumbar vertebra or spinal cord
Fixation segment
AWG American wire gauge LC-DCP limited contact dynamic compression
C + number cervical vertebra or spinal cord plate
segment MCE multiple cartilaginous exostoses
Cd + number caudal vertebra or spinal cord segment MPSS methylprednisolone sodium
CK creatine kinase succinate
COP cyclophosphamide, vincristine MRI magnetic resonance imaging
(oncovin), and prednisolone MTU muscle tendon unit
CPD citrate phosphate dextrose NSAID nonsteroidal anti-inflammatory
CrCL cranial cruciate ligament drug
CSF cerebrospinal fluid OCD osteochondritis dissecans
CT computed tomography OSA osteosarcoma
DCP dynamic compression plate PCV packed cell volume
DJD degenerative joint disease PMMA polymethylmethacrylate
EDTA ethylenediamine tetra-acetic acid PMS polyarthritis/meningitis syndrome
ELISA enzyme-linked immunosorbent assay PPP periosteal proliferative polyarthritis
EMG electromyogram or PTH parathyroid hormone
electromyography rpm revolutions per minute
FCE fibrocartilaginous embolism RSH renal secondary hyperparathyroidism
FeLV feline leukemia virus S + number sacral vertebra or spinal cord
FeSFV feline syncytia-forming virus segment
FeSV feline sarcoma virus SC subcutaneously
FIP feline infectious peritonitis SLE systemic lupus erythematosus
FIV feline immunodeficiency virus SWG (Imperial) standard wire gauge
HBOC hemoglobin-based oxygen carrying T + number thoracic vertebra or spinal cord
solution segment
Ig immunoglobulin TMJ temporomandibular joint
ILN interlocking nail VCP veterinary cuttable plate
8

Dedication
Dedicated to the many veterinary clinicians who use their knowledge,
skills, and talents to enrich the lives of our feline friends.

CHAPTER 1
INTRODUCTION TO
FELINE ORTHOPEDIC
SURGERY
Musculoskeletal disease is less common in the cat than
in the dog, with the exception of abscesses and
cellulitis caused by cat bites1,2. An increasing
population of cats, living longer than ever before, and
more enlightened clients seeking improved veterinary
care, however, have led to feline orthopedics becoming
an important discipline in its own right. Optimal
diagnosis and treatment of feline orthopedic disorders
requires a species-specific approach that is expressed in
the familiar aphorism ‘cats are not small dogs’.
It is often stated that cats make good orthopedic
patients because of their small size, undemanding
lifestyle, and their ability to redistribute weight
and protect an injured limb. There is a common
misconception that feline fracture repair is simple to
perform and healing is not prone to complications. It
has been said that two cat bone fragments will unite if
placed together in the same room. This casual attitude
is not borne out by clinical and experimental studies,
which show that the cat is subject to the same range of
complications of fracture repair as the dog3–8. The
notion that feline orthopedics is straightforward is a
testimony to the cat’s ability to compensate for
impaired function.
The obvious drawback of small size is the difficulty
that this creates for the surgeon in terms of visualization
and manipulation of small bones and bone fragments.
The small bones of the distal extremities, in particular,
are not easy to visualize accurately on radiographs
and are difficult to manipulate and repair surgically.
A bad workman may blame his tools but even the most
dexterous of surgeons will be frustrated without the
correct instruments and implants. Fortunately the
armamentarium of the modern feline orthopedic
surgeon comprises a range of equipment designed for
small bone fracture repair that is ideally suited for cats.
Historically, there has been a trend towards conservative
treatment of many feline orthopedic injuries, the canine
equivalent of which would be treated surgically. While
9
conservative treatment may be appropriate, treatment
should always be tailored to the individual case. The
goal of the feline orthopedic surgeon should be to
return the patient to optimum function as quickly as
possible using the simplest means available.
COMPARATIVE FEATURES
In comparison with the dog, developmental
orthopedic disease is rarely encountered. Many of the
conditions that are commonly seen in immature dogs,
such as elbow dysplasia or aseptic necrosis of the
femoral head, have not been reported in the cat. A
number of developmental disorders, such as hip
dysplasia and patellar luxation, are recognized,
although their clinical significance in the cat may
differ from that in the dog.
Traumatic injury is a common occurrence and
musculoskeletal trauma accounts for a large
proportion of the disorders seen in the cat.
Orthopedic disorders of the feline hindlimb are
much more prevalent than those of the forelimb with
73% of all fractures involving the hindlimb or
pelvis and sacrum in one survey of over 100 cats9.
Knowledge of the comparative surgical anatomy
and physiology of the feline musculoskeletal system
is clearly of importance for the feline orthopedic
surgeon. When performing an orthopedic
examination, the clinician should be cognizant of
aspects that are unique to the cat. There are many
minor and a few major differences between
the musculoskeletal system of the cat and the
dog. Feline musculoskeletal anatomy predominantly
reflects the size, mobility, and diet of the cat. For
example, the cat’s retractile claw mechanism is
ideally suited for catching and holding small prey,
and the feline locomotor system is adapted for agility
and for great bursts of speed over short distances. In
comparison with the dog, the feline musculoskeletal
system tends to be more flexible, skeletal muscles are
10
more strap-like, and intervening connective tissues
are looser. Cats are relatively small and lightly built
and have a higher body surface area to weight ratio
than dogs. The corollary of this is that the cat’s
skeleton is of a lightweight design. Long bones have
a large medullary cavity and thin cortices and flat
bones, such as the scapula and pelvis, are only a few
millimeters thick. Additionally, the long bones are
relatively straight and tubular in comparison with
those of the dog. Differences in skeletal morphology
between breeds are relatively minor10 and it is,
therefore, potentially easier to standardize surgical
techniques, instruments, and implants for the cat
than for the dog.
Other notable features are the greater range of
motion in the spine and the shoulder in comparison
with the dog and the different distribution of weight
bearing between the fore- and hindlimbs when walking.
A recent study of cats using pressure platform analysis
showed that, as in the dog, limb load forces when
walking are greater in the forelimbs than in the
hindlimbs. However, in comparison with the dog,
the distribution of load at a walk is different, with the
hindlimbs of the cat sharing more of the load11. The
differences in range of motion of the major joints of
the appendicular skeleton have been well
documented12 (Table 1).
Familiarity with normal feline osteology is
essential for the correct interpretation of
radiographs. It is often helpful to radiograph the
contralateral normal limb and to have feline bones
or a skeleton and a set of normal feline radiographs
for comparison. An awareness of the differences
between the dog and the cat in the arrangement of
muscles and nerves, especially around the hip and
TABLE 1 RANGE OF MOTION OF THE MAJOR JOINTS OF THE APPENDICULAR SKELETON.
Joint
Shoulder Flexion–extension
Adduction–abduction
Elbow Flexion–extension
Carpus Flexion–extension
Hip Flexion–extension
Adduction–abduction
Stifle Flexion–extension
Tarsus Flexion–extension
elbow, is of importance when making a surgical
approach to these joints. In addition to specific
anatomic differences between the dog and the cat,
the relative sizes and dimensions of bones and
muscles may differ. For example, the feline ulna
and fibula are more substantial than their canine
counterparts, the lumbar vertebrae, in particular,
are longer and more slender, and the scapula is
broader and shorter.
SPECIFIC ANATOMIC FEATURES
AND THEIR SIGNIFICANCE
SHOULDER/BRACHIUM
• The acromion has both hamate and suprahamate
processes. The hamate process projects from
the distal aspect of the acromion (1). The
suprahamate process (metacromion) is a flat
protuberance extending caudally from the distal
spine of the scapula 10–20 mm proximal to the
acromion. The surgeon should be aware of this
structure when elevating the infraspinatus
muscle from the spine of the scapula during
surgical approaches to the distal portion of the
bone13.
• There is a beak-like bony projection called the
coracoid process extending craniomedially from
the rim of the glenoid. The coracoid process is
sufficiently large to be at risk of fracture.
• A small ossicle representing the clavicle is
consistently present. It is seen radiographically
as a slender curved bone, approximately 20 mm
long, just cranial to the shoulder joint, and can
easily be misdiagnosed as a fracture of the
scapula. It is a vestigial structure with no bony
connections and has no clinical significance.
Range of motion Range of motion
cat (degrees) dog (degrees)
170–190 125–145
100–120 80–100
130–155 140–150
160–180 175–190
150–170 150–170
80–100 100–120
150–170 130–150
140–170 155–185
 Introduction to feline orthopedic surgery
11
1

Hamate
Metacromion process

Metacromion

Supraglenoid Hamate
tubercle Supraglenoid
process
Coracoid tubercle
process
Coracoid
process
Clavicle
A B

1 A Lateral view of the scapulohumeral joint showing the coracoid process, suprahamate process of the acromion
(metacromion), hamate process of the acromion, supraglenoid tubercle, and clavicle.
B Ventral view of the scapula.

• The humerus is penetrated by an oval does not provide sufficient fixation, in

supracondylar (epicondylar) foramen just approximately 50% of cats it may be possible to
proximal to the medial epicondyle (2). Elevation drive a much smaller pin (<1.6mm) into the medial
and retraction of soft tissues during the surgical aspect of the condyle and still avoid the foramen14.
approach to this area is complicated by the
passage of the median nerve and the brachial
artery through this foramen. Great care should be
taken not to damage these neurovascular 2 2 Craniocaudal
structures when retracting the soft tissues about radiograph of the
the elbow13. elbow joint
• Similarly, when there is a humeral supracondylar showing the
fracture there may be impingement of bone supracondylar
fragments on the median nerve and brachial foramen on the
artery. In this situation the medial wall of the medial aspect of the
foramen can be removed using rongeurs to distal humerus
allow the nerve to course in the adjacent soft (arrow).
tissues5.
• Intramedullary pin insertion for humeral fracture
repair is complicated by the presence of the
supracondylar foramen. Pins placed distally in the
humerus can enter the foramen, damaging the
median nerve and brachial artery and penetrating
the elbow joint. Intramedullary pins should
generally be positioned 7–9mm proximal to the
medial epicondyle5. If this short intramedullary pin
12

• The ulnar nerve lies under the short part of the
medial head of the triceps brachii muscle (3).
This muscle runs caudal to the medial aspect of
the humeral condyle where it inserts on the
medial side of the olecranon process. Care should
be taken to avoid injury to the nerve when the
muscle is elevated to expose a fracture line13.
ELBOW/ANTEBRACHIUM
• In contrast to the dog the olecranon fossa is not
perforated by a supratrochlear foramen. The distal
humeral epiphysis is less prone to fracture because
of the absence of this foramen. Consequently,
humeral intracondylar Y and T fractures, and
lateral and medial condylar fractures are rare in
the cat.
• The straighter conformation of the distal
humerus and the humeral condyle, and the
relatively wide and thick epicondylar crests, in
comparison with the dog, may also help protect
this region of the skeleton from fracture.
Furthermore, incomplete ossification of the
humeral condyle, which is a common
predisposing cause of fracture in some breeds of
dog, has not been reported in the cat.
• A sesamoid bone in the tendon of origin of the
supinator muscle is a normal anatomic variant
present in approximately 40% of cats. This may
be visible on mediolateral radiographs of the
elbow joint where it articulates with the
craniolateral aspect of the radial head. It should
not be confused with an osteophyte or chip
fracture15.
• The anatomy of the feline antebrachium allows
considerable pronation and supination (45–55°)
and it is, therefore, important to attempt to
preserve motion between the radius and ulna
when undertaking orthopedic procedures in this
area. There is greater mobility between the two
bones in comparison with the dog. This means
that treatment of fractures of the antebrachium
by fixation of the radius or ulna alone is less likely
to result in adequate stability of the adjacent
bone5. It may be necessary to repair both
fractured bones, especially if one or both are
comminuted.

3 3 Medial aspect of the elbow joint

Brachial artery showing the passage of the median nerve
and brachial artery through the
Median nerve
supracondylar foramen in a caudocranial
direction. Note the position of the ulnar
Supracondylar nerve deep to the short part of the medial
foramen head of the triceps brachii muscle.

Ulnar nerve

Triceps brachii
muscle, short
part of medial
head
 Introduction to feline orthopedic surgery
HIP/THIGH
• Unlike in the dog, the ligament of the head of
the femur, or round ligament, is purported to
provide a significant proportion of the blood
supply to the femoral capital epiphysis16. This
may explain why aseptic necrosis of the femoral
head (Legg–Calvé–Perthes disease), commonly
seen in small breed dogs, has not been reported
in the cat. The blood supply via the round
ligament will also help protect the epiphysis from
vascular compromise after capital physeal
separation. Although these fractures should be
treated promptly, the prognosis in cats is
generally good, even in cases in which repair is
delayed.
• The arrangement of the muscles around the hip
differs from that of the dog. The tensor fascia
lata and the vastus lateralis muscles are broader
in cats. The craniolateral approach to the feline
hip is most commonly used. When making this
approach a longer incision is necessary through
the insertion of the tensor fascia lata muscle
than in the dog. Similarly the vastus lateralis
muscle requires more subperiosteal elevation
to gain adequate exposure of the femoral
neck17.
• The sartorius muscle is undivided in the cat,
unlike in the dog where it has cranial and caudal
bellies. This muscle may be encountered when
making a lateral approach to the femoral shaft.
• The sacrotuberous ligament, which in the dog
extends between the caudolateral angle of the
sacrum and the lateral part of the tuber ischium,
is absent in the cat.
• A kinematic study has shown that the principal
load-bearing areas of the feline acetabulum are
the central and caudal thirds rather than
the cranial third. This is of relevance to the
treatment of acetabular fractures. The frequent
recommendation that simple caudal acetabular
fractures should be treated conservatively may
need to be reconsidered in the cat18.
STIFLE/CRUS
• There is variable mineralization of the medial
fabella and the popliteal sesamoid bone19,20.
Unmineralized sesamoid bones will not be
visualized on radiographs.
• In contrast to that in the dog, the cranial cruciate
ligament is larger than the caudal cruciate
ligament21. This may be one of the factors
contributing to the relative infrequency of cranial
cruciate ligament rupture in the cat.
13
TARSUS
• The medial and lateral collateral ligaments of the
talocrural joint are each comprised of two short
ligaments; there is no long component as seen
in dogs. This is of relevance when performing
prosthetic collateral ligament replacement for
the treatment of talocrural luxation or
subluxation.
SPINE
• The nuchal ligament, which in the dog extends
from the spinous process of the axis to the tip of
the first thoracic spinous process, is absent in the
cat. The surgeon should be aware of this when
making a dorsal approach to the cervical spine.
The lack of ligamentous support accounts for the
propensity for neck ventroflexion with
neuromuscular disorders in the cat.
• The spine of the cat is more supple than that of
the dog. Part of this increased flexibility can be
accounted for by the fact that the intervertebral
discs contribute a larger proportion to the total
length of the vertebral column (20% in the cat
and 15–17% in the dog). The intervertebral
discs of the cat are prone to degeneration in the
same way as in nonchondrodystrophoid breeds
of dog. Affected cats are frequently
asymptomatic; the reasons for this have not yet
been determined.
• The spinal cord is longer relative to the
vertebral canal in the cat than in the dog. In
the past there has been some uncertainty about
the exact termination of the spinal cord. Various
levels from the caudal border of the seventh
lumbar vertebra (L7) to the caudal border of
the sacrum have been given by different
authors. There may be some slight individual
and breed variation but it is likely that the
cranial limit is accurate for adults and the more
caudal one for young kittens22,23. In
comparison with the dog, there is reasonably
close correlation between spinal cord segments
and vertebrae, and a focal lesion will therefore
tend to affect a smaller number of cord
segments in the cat.
14

BLOOD SUPPLY TO BONE developing periosteal callus, bone fragments, and

Arterial blood supply to a typical long bone is
provided by an afferent vascular system, comprised
primarily of the nutrient artery and the proximal
and distal metaphyseal arteries 24–27(4). Small
periosteal arterioles also provide blood to the outer
cortical layer in the region of fascial attachments and
muscle insertions. The intermediate vascular system
of compact bone comprises Haversian canals,
Volkmann canals, and minute canaliculi creating a
vascular lattice to provide nutrients to the
osteocytes. Venous drainage occurs via the efferent
vascular system from the periosteal surface of the
bone. This centrifugal blood flow from the
medullary cavity to the periosteal surface is
disrupted to varying degrees when fractures occur.
The afferent blood vessels then hypertrophy and
increase in number to reestablish the medullary
blood supply quickly. Additionally, a new and
temporary extraosseous blood supply develops from
the surrounding soft tissues to vascularize the
cortex. Revascularization and bone healing are
delayed by severe trauma to the bone and soft
tissues, overzealous soft tissue dissection and
improper tissue handling during surgery, poor
reduction of bone fragments, and inadequate
stabilization of the fracture.
BONE GROWTH
The bones of the appendicular skeleton grow in
length by endochondral ossification, and in width by
intramembranous ossification. Endochondral
ossification is characterized by osteoblastic conversion
of a cartilaginous model to bone. Longitudinal bone
growth occurs at the physes, which remain open until
bone growth has ceased. Functional physeal closure
occurs when there is anatomic continuity of osseous
tissue between the epiphysis and the diaphysis.
Closure of the physis and cessation of bone growth
occurs before fusion can be documented radio-
graphically.

Fascial
Medullary attachment
Periosteal arterioles
arteries

Periosteal
Nutrient arterioles
artery
Anastomosis
Periosteal
arteries
Nutrient
artery

Metaphyseal Medullary Extraosseous

artery artery arteries

A B C

4 A Arterial blood supply to normal mature bone.

B Schematic diagram showing the arterial blood supply of a section of the diaphysis of normal mature bone.
C Arterial blood supply to fractured bone showing the development of an extraosseous blood supply.
 Introduction to feline orthopedic surgery
15

GROWTH PLATES times and there is no precise sequence of physeal closure.

In contrast to those in the dog, the growth plates of
kittens are simple and flat. Physeal closure times were
documented in entire cats based on the radiographic
examination of 37 kittens and anatomic dissection of
eight kittens28. There are individual differences in closure
However physes can be classified on the basis of closure
times into first, middle, and last groups (5, Table 2)28.
The physes that close last are most prone to
delayed closure and cartilage remnants persist beyond
2 years of age in some cases.

First

Middle

Last

5 Cat skeleton showing closure times of the growth plates of clinical significance. Physeal closure times classified as first,
middle, and last.

TABLE 2 PHYSEAL CLOSURE TIMES IN THE CAT.

First (4–8 months) Middle (8–14 months) Last (14–24 months)
Scapular tuberosity Proximal ulna Vertebrae
Distal humerus Metacarpals Proximal humerus
Proximal radius Proximal femur Distal radius
Accessory carpal bone Distal tibia Distal ulna
Phalanges I & II Distal fibula Distal femur
Fibular tarsal bone Proximal tibia
Metatarsals Proximal fibula
16
Growth plate disturbances
Traumatic injury may cause disturbance in the
growth of the physis leading to a reduction or
cessation of growth and bone shortening.
Disturbances of physeal growth may also be
associated with angular limb deformity if there is
asynchronous growth in paired bones, such as the
radius and ulna (6), or if the disturbance in a single
physis is asymmetrical. In comparison with the dog,
6 The effect of neutering on growth plates
A B
6 Craniocaudal radiographs of the antebrachium showing
angular limb deformity. (Radiographs courtesy of Malcolm
McKee.)
A Carpal varus associated with a disturbance in the growth
of the distal radial physis.
B Postoperative view following corrective ostectomy and
application of a type 2 acrylic external fixator.
angular limb deformity is uncommon in the cat,
largely because of the smaller stature and reduced
overall growth potential. An important additional
factor is the linear shape of the distal ulnar physis of
the cat in contrast to the conical ulnar physis of the
dog. The shape of the canine physis increases
its surface area, facilitating rapid growth, but also
predisposes the germinal cells to compression injury.
In young cats the physes represent significant
structural weak links in the skeleton and Salter–Harris
fractures are a common occurrence in this age group.
A number of studies have reported on the effect
of neutering on physeal closure times in cats29–31. The
relationship between castration at about the time of
puberty (28 weeks of age) and the timing of physeal
closure was studied in male cats29. The time of closure
has also been compared in neutered and entire male
and female cats30. In both of these studies, physeal
closure was found to be delayed in castrated male cats
with some individuals having open physes beyond
4 years of age. One study looked at the effect of
neutering male and female cats at 7 weeks and
7 months of age on the proximal (first group) and
distal (last group) radial physes and eventual radial
length31. This study found that castration had no
effect on the timing of proximal radial physeal closure.
Castrated cats, however, had delayed closure of the
distal radial growth plate irrespective of the age at
castration. In female cats closure of the proximal radial
physis was delayed in cats neutered at 7 weeks of age
but not at 7 months of age, whereas closure of the
distal radial physis was delayed in both groups of
ovariohysterectomized cats. Final radial length was
found to be significantly increased in both groups of
neutered male and female cats compared with entire
cats. Neutering of immature cats of both sexes may
predispose to Salter–Harris fractures and the last
group of physes will be most at risk of injury.
 17

CHAPTER 2
EXAMINATION AND
DIAGNOSTIC TOOLS

INTRODUCTION diagnoses are then investigated with the aim of

Lameness is the predominant clinical sign in cats
with orthopedic disorders, but because of the cat’s
independent lifestyle this is less readily observed in
comparison with the dog. Investigation of lameness in
the cat has much in common with the dog but there
are important differences. Many of the conditions
encountered are similar but their significance may
differ and there are also causes of lameness that are
rarely or never seen in dogs. The goal of the
examination should be to formulate and prioritize
a list of differential diagnoses; these differential
achieving a specific diagnosis.
Causes of feline lameness have been reviewed
recently1. The more common musculoskeletal causes
of lameness are listed in Table 3. Lameness or limb
weakness may also be caused by a variety of
conditions unrelated to the limb bones and joints.
These include conditions of the spine and peripheral
nerves, such as vertebral fracture and brachial plexus
avulsion. These conditions should be suspected if
evidence of neurologic dysfunction is detected on
examination.

TABLE 3 DIFFERENTIAL DIAGNOSIS OF LAMENESS.

Diagnosis Skeletally immature <2 years Skeletally mature >2 years
Cat bites ++ +
Fractures ++ (often physeal) +
Traumatic luxations + ++ (hip>hock>stifle>
elbow>carpus>shoulder)
Avulsion injuries (tibial tuberosity, etc.) ++ –
Septic arthritis ++ +
Calicivirus arthritis ++ –
Periosteal proliferative polyarthritis ++ ++
Other immune-mediated polyarthritides + ++
Neoplasia (bone, periarticular soft tissue) + ++
Osteoarthritis – ++ (elbow & shoulder
most common)
Hip dysplasia ++ +
Patellar luxation ++ +
Cranial cruciate ligament rupture – ++

– to ++ indicates an increasing relative frequency of occurrence

18
SIGNALMENT
The age, sex, breed, and weight of the cat may give
an indication of the type of conditions most likely to
be encountered. For example, male (entire and
neutered) cats less than 2 years of age are more
likely to suffer from fractures and luxations as a
result of traumatic incidents 2,3. Degenerative
conditions such as osteoarthritis or cruciate disease
are relatively less common and are typically seen in
older cats. Joint and bone neoplasia is also more
common in the older cat, although lymphoma is an
important exception. There are a few nontraumatic
conditions that have a sex predisposition, such as
periosteal proliferative polyarthritis, but gender is
generally not a major factor. Cat bites and traumatic
conditions are more common in young cats,
probably because of their territorial aggression and
lack of experience of natural and man-made hazards.
Breed predispositions are less important in the cat
than the dog. This may be because pedigree cats are
seen less frequently than their canine counterparts.
The morphology of pedigree cats also differs very
little from nonpedigree cats so, in contrast to dogs,
conformation rarely plays a significant role in
musculoskeletal disorders. With the exception of
certain inherited and congenital disorders, there are
few conditions that are regularly seen more
frequently in specific breeds. Body weight may
predispose cats to clinical signs of musculoskeletal
disease in general and osteoarthritis in particular.
One study found that overweight cats were
2.8 times more likely and obese cats were 5.4 times
more likely to suffer from lameness visible to
owners4.
HISTORY
History taking is the component of the investigation
that is most likely to be neglected in practice
because it is perceived as time-consuming. However,
the history often provides relevant information
concerning the cause of musculoskeletal disease and
should always precede physical examination of the
patient. The astute feline clinician should be wary of a
number of pitfalls. Cats are small and light and have
an independent lifestyle, so they are very good at
disguising mild to moderate musculoskeletal
impairment. It is not unusual for the duration
of clinical signs to be underestimated by the
client because early signs have been overlooked.
An apparently acute condition may, therefore,
already be chronic at the time of first presentation.
Another difficulty is determining whether conditions
that are identified during subsequent investigations
are incidental when there has been no history of
clinical signs, for example, an osteoarthritic joint
identified radiographically. Additional problems are
commonly encountered with cats that have suffered
unobserved traumatic incidents. Cats are frequently
presented, having been missing for several days, with
an apparent orthopedic disorder and no history to
guide the clinician as to the cause. It should be
noted that some nontraumatic conditions, such as
ischemic neuromyopathy, might mimic unobserved
traumatic injuries, such as pelvic fracture or spinal
fracture/luxation.
PHYSICAL EXAMINATION
A general physical examination should precede the
specific orthopedic component of the examination.
The examination may detect evidence of concurrent
or intercurrent disease. This may provide clues to the
orthopedic disorder; for example, cats with certain
types of immune-mediated polyarthritis may have
disease of other body systems. Intercurrent disease
may influence the prognosis and have a bearing on
the administration of anesthetics and intravenous
fluids; a degree of renal insufficiency is not
uncommon in geriatric cats, for example. Cats with
unobserved trauma that have been missing are
generally cachectic and the immediate concern is
fluid and caloric resuscitation. Cats with traumatic
orthopedic injuries frequently have concurrent
injuries involving other body systems. The
investigation and treatment of the trauma patient are
discussed more fully in Chapter 3.
ORTHOPEDIC EXAMINATION
The specific orthopedic examination is performed in
a standard fashion regardless of species. The main
difficulties are the lack of patient compliance for gait
analysis and potential difficulties with the restraint of
a fractious and painful cat. Observation of the gait
should be made by allowing the patient to walk
unrestrained around an examination room. This can
sometimes only be achieved by allowing the cat to
settle first in a quiet environment or by observation
through a window from outside the room. It is
sometimes helpful to ask the owner to video the cat at
home. The cat’s posture and stance should also be
noted at this stage of the examination.
An initial evaluation is generally performed
with the cat in a standing position and using
 Examination and diagnostic tools
minimal restraint. Careful and methodical palpation
of the muscles and joints of the limbs should be
performed first, usually starting proximally and
working distally. It is helpful to compare left and
right limbs for overall symmetry, evidence of pain or
tenderness, muscle atrophy, and joint thickening or
swelling. Muscle atrophy is most easily detected
where there are large muscle masses adjacent
to bony prominences, such as the blade of the
scapula and the greater trochanter. Joint thickening
and swelling cannot usually be appreciated in the
hip and shoulder because of overlying muscle
masses. Synovial effusion is easier to detect with
the joint bearing weight but, in general, palpable
joint effusion is less common in comparison with
the dog.
A more focused orthopedic evaluation is
generally performed with the cat gently restrained in
lateral recumbency by an assistant. It is preferable to
commence the examination with the healthy limbs,
in order to accustom the cat to being handled and to
minimize the chances of the patient becoming
fractious. Careful palpation and manipulation of the
joints of all of the limbs is begun distally starting
with the phalanges and working proximally. The
range of joint motion is assessed by putting the
joints through a full range of flexion/extension
and abduction/adduction, as appropriate, while
observing the cat for any evidence of discomfort.
Joint stability is assessed at this time in lateral to
medial and cranial to caudal planes. Any evidence of
joint effusion, periarticular thickening, and crepitus
is noted. Specific manipulations such as the cranial
draw sign and tibial compression tests are identical to
those performed in the dog and are applicable to the
cat. Others, such as the Ortolani sign, are less
frequently performed. These maneuvers are best
performed under sedation or general anesthesia and
are discussed more fully with the relevant disorders.
Long bones and the overlying soft tissue structures
are also palpated along their length for irregularity or
discomfort. A maneuver that provokes an apparent
pain response should be repeatable to ensure its
significance. A comprehensive examination should
be performed on all four limbs before focusing
attention on the affected limb.
DIAGNOSTIC TOOLS
Following the orthopedic examination a decision
is made about treatment or further investigation.
Further investigations should be performed to
19
confirm a tentative diagnosis or to differentiate
between the different conditions in a short list of
differential diagnoses. In many cases the diagnosis
may be obvious and is achieved without the need for
further work up; for example, cat bites and cellulitis.
In other cases, where the condition is mild or where
there are financial constraints, it may be preferable to
start a therapeutic trial and reassess in the light of the
response to treatment.
RADIOGRAPHY
Radiography is the most commonly used ancillary
diagnostic tool in the investigation of orthopedic
disease. The use of radiography as an aid in the
investigation of joint disease is discussed in
Chapter 7. Radiographs should be interpreted in the
light of the clinical findings and should not be
used as a substitute for a correctly performed clinical
examination. Radiography is often used to confirm a
suspected clinical diagnosis and occasionally to
differentiate between two or more diseases with
similar clinical signs. Radiography is used in traumatic
injuries to assess the location and extent of fractures
and to assist with the planning of surgical repair.
For diaphyseal fractures, especially if there is
comminution, radiographs of the contralateral bone
are obtained to assist further with fracture planning
and bone repair. Radiographs of the thorax and
abdomen are warranted for cats that have suffered
severe trauma, irrespective of whether there are
clinical signs of a respiratory or abdominal disorder.
Feline radiography is best performed with the patient
heavily sedated or under a general anesthetic to
eliminate movement and allow optimum positioning.
Changes are often subtle and the bones are small, so
high quality radiographs are essential. Fine detail
screens should be used and human mammography
film/screen combinations are preferred for the distal
extremities. Radiographs should be correctly
collimated to minimize scatter and should be
obtained in two orthogonal planes (i.e. at right angles
to each other). Radiographic interpretation is
best made with the aid of a bright light and
magnifying glass, in addition to a conventional
viewer. Radiographic interpretation should be
thorough and complete so that each structure is
assessed according to its roentgen signs (i.e. changes
in number, position, size, shape, margin, opacity,
internal architecture, and function). The pattern of
changes for individual conditions is discussed in the
relevant chapters.
20

SYNOVIOCENTESIS AND JOINT FLUID ANALYSIS
Synoviocentesis and analysis of synovial fluid is an
underutilized procedure in feline medicine. Analysis
is particularly useful for differentiating between
degenerative and inflammatory causes of arthritis and in
determining whether an inflammatory arthritis is
infective or immune mediated. General anesthesia or
heavy sedation is required for synoviocentesis in the cat.
It is usually convenient to perform radiography first and
then immediately tap affected joints in the light of the
radiographic interpretation. A small area should be
clipped and prepared at the site of the puncture (7) but
it is not necessary to use surgical drapes or gloves. A
3ml syringe and a 25 gauge hypodermic needle of
sufficient length to penetrate the soft tissues (usually up
to 25 mm) is used to aspirate fluid from the joint. The
volume of fluid obtained from normal joints is typically
less than 0.25ml for the shoulder, elbow, stifle and hip
joints and less than 0.1ml from the carpal and tarsal
joints5. Difficulty may be encountered introducing the
needle into the hip joint and multiple attempts are
sometimes necessary.

A B C

D E F

7 Six sites for synoviocentesis.

A Carpus. The antebrachiocarpal joint is located with thumbnail pressure with the joint flexed. The needle is introduced
slightly to one side of the median plane.
B Elbow. The joint is held in flexion and the needle is introduced from the caudolateral aspect between the lateral humeral
epicondyle and the olecranon.
C Shoulder. Gentle traction is placed on the limb to open up the joint space. The needle is introduced into the
scapulohumeral joint from the craniolateral aspect just distal to the acromion process.
D Hock. The joint is held in flexion and the needle is introduced into the tarsocrural joint from the caudolateral aspect
between the lateral malleolus and the lateral trochlear ridge of the talus.
E Stifle. The joint is held partially flexed and the needle is introduced just medial or lateral to the mid-portion of the
straight patellar ligament and directed proximally.
F Hip. The femur is held partially abducted and rotated outwards. The needle is introduced into the coxofemoral joint
just caudal to the greater trochanter and directed cranially at an angle of approximately 45°.
 Examination and diagnostic tools
21

Synovial fluid from cats with inflammatory arthritis
may clot on standing (a positive fibrinogen clot test).
Clotting is prevented by placing samples that are to be
submitted for cytologic examination in blood tubes
containing ethylenediamine tetra-acetic acid (EDTA)
as an anticoagulant. Cells in synovial fluid degenerate
rapidly and cytologic examination should preferably
be performed within 4 hours. For submission to an
external laboratory, cooling to 4°C (39°F) provides
preservation for up to 24 hours. Samples for bacterial
culture should not be placed in EDTA because it
inhibits bacterial growth. Since the volume of synovial
fluid samples obtained from cats is small, proper
sample handling and correct choice of tests are critical
(Table 4).
The features of synovial fluid that are most
frequently evaluated are:
• Physical characteristics (volume, color, turbidity,
and viscosity).
• Cytologic examination (total nucleated cell count
and differential cell count).
• Mucin clot test.
• Bacterial culture.
Physical characteristics
The physical characteristics of the fluid are noted at the
time of collection. Normal synovial fluid should be of
low volume, should appear clear and colorless or straw-
colored, and should have a high viscosity. Aspiration of
more than 0.25 ml of fluid, even from the larger
joints, is abnormal and indicates joint effusion.
Turbidity indicates increased white or red cell counts
and a yellow discoloration, or xanthochromia, is
almost always due to the presence of heme
pigments derived from previous hemorrhage. Red
discoloration may indicate recent hemorrhage but is
more likely due to contamination during sampling,
which can be seen as a swirl of blood entering
the syringe during the procedure. A subjective
assessment of viscosity is made by performing the
string test, whereby synovial fluid is allowed to drip
slowly from the syringe (onto a slide) or a drop is placed
between the finger and thumb, which are then slowly
drawn apart. Normal fluid will produce a string that is at
least 20–40 mm in length. Viscosity is a measure of the
hyaluronic acid content and is reduced in inflammatory
arthropathies. The viscosity will also be reduced owing
to a dilution effect if there is a substantial joint effusion,
irrespective of the etiology.
Cytologic examination
If sample size is limited, cytologic examination should
take priority. A hemocytometer is used because fluid
volume is generally insufficient for Coulter counter
evaluation. Cytology provides estimates of the total
nucleated and differential cell counts, thus allowing
the important distinction to be made between
inflammatory and noninflammatory disease. Normal
feline synovial fluid is less cellular than canine synovial
fluid5,6. If necessary, examination can be performed

TABLE 4 SYNOVIAL FLUID ANALYSIS.

Normal joint Osteoarthritis Immune-mediated Bacterial
arthritis infective
arthritis
Volume (ml) 0–0.25 0–0.50 0–2.0 0.25–1.0
Color Clear/pale yellow Yellow Yellow-white White
+/– blood tinged +/– blood tinged
Clarity Transparent Transparent Transparent or opaque Opaque
Viscosity Very high High Low/very low Very low
Mucin clot Good Good–fair Fair–poor Poor
Spontaneous clot None Sometimes Often Often
White cells (cells/μl) <1000 1000–5000 5000–9000 5000–100000
Neutrophils <5% <10% 10–95% >95%
Mononuclear cells >95% >90% 5–90% <5%
Protein (g/l [g/dl]) 20.0–25.0 [2.0–2.5] 20.0–30.0 [2.0–3.0] 25.0–50.0 [2.5–5.0] >40.0 [>4.0]
22
on a stained smear prepared from a single drop of
synovial fluid. A smear is made on a glass microscope
slide at the time of collection, air-dried, and then
stained with a Romanovsky’s stain, such as Wright’s,
before examination. Many commercial laboratories
request submission of a freshly prepared unstained
air-dried smear in addition to a sample of fluid
in EDTA.
Mucin clot test
Although viscosity provides a guide to the amount of
hyaluronic acid in synovial fluid, the mucin clot
test gives a much more accurate semi-quantitative
assessment of the quality and the concentration of
hyaluronic acid and is not influenced by the dilution
effect of an effusion. A few drops of synovial fluid are
added to about 10ml of 2% glacial acetic acid in a glass
test tube and allowed to stand. Synovial fluid that has
been collected in a plain tube or in heparin should be
used, since the test is inhibited by the presence of
EDTA. Acid precipitation of a normal concentration
of well polymerized hyaluronic acid produces a tight
clot with a clear surrounding solution. The presence
of increasingly severe inflammatory pathology is
inferred from the production of a soft clot, a friable
clot, or flocculent material in a cloudy surrounding
solution.
Bacterial culture
This is used to isolate the causative organism and
guide antibiotic therapy in suspected cases of septic
arthritis and should include both aerobic and
anaerobic culture. Isolation of bacteria from
synovial fluid is inconsistent and a negative culture
does not rule out septic arthritis. The likelihood of
a positive culture can be significantly increased
either by submission of a sample of synovial
membrane or by inoculation of the synovial fluid
into sterile blood culture medium before submission
to the laboratory7. Liquid blood culture medium
reduces the in vitro phagocytosis of bacteria by
leukocytes and has a dilution effect on bacterial
inhibitors.
Other tests
Numerous other tests have been used to analyze
synovial fluid in humans but their value has not been
demonstrated in cats. Common additional tests include
measurement of glucose, which is decreased in
inflammatory disease, and protein, which is elevated in
inflammatory disease. Both of these tests require
concurrent submission of serum so that the two levels
can be compared.
PRESSURE PLATFORM GAIT ANALYSIS
Pressure platform gait analysis offers an objective
noninvasive method for evaluating limb function
in cats. The technique has been described
experimentally in normal cats8. Pressure platform gait
analysis has been used to evaluate long-term limb
function after onychectomy9 and also for assessment
and comparison of the efficacy of analgesic drugs
after onychectomy10.
FLUOROSCOPY
Although not generally available, fluoroscopy has
been used to aid in the intraoperative placement of
implants, such as pins and screws, and to assess
fracture alignment. Other uses include contrast
studies (myelography, arthrography) and location of
radiopaque foreign bodies.
SCINTIGRAPHY
Scintigraphy involves the injection of a radioisotope
(technetium methylene diphosphonate), which emits
gamma radiation. The agent is injected intravenously
and an image is created using a gamma camera showing
areas of increased bone turnover. Scintigraphy is
rarely performed in cats because of concerns about
radiation safety, expense, and lack of availability. The
technique is a very sensitive indicator of bone lesions
but is nonspecific.
SONOGRAPHY
Sonography has limited application for the investigation
of orthopedic disease because of the inability of
ultrasound to penetrate osseous tissues. Sonography has
been used for the investigation of Achilles tendon
injuries in cats11, and in the investigation of joint
disease, which is discussed in Chapter 7. Sonographic
assessment of secondary fracture healing of the long
bones has been described12 and a preliminary report
described the use of ultrasound-guided needle biopsy
for the diagnosis of bone lesions13. Use of this
technique is likely to be restricted to specialized centers
because of the small size of the structures under
investigation and difficulties in the interpretation of the
images obtained.
ADVANCED IMAGING TECHNIQUES
The use of magnetic resonance imaging (MRI) and
computed tomography (CT) has been restricted in the
past by their expense and lack of availability. They are
being used increasingly in the investigation of spinal
and joint disorders in dogs but there are few reports
of their use in cats. The small size of cats means that
imaging of feline structures requires the use of
 Examination and diagnostic tools
23

equipment that is capable of obtaining very high
definition images. Magnetic resonance imaging is
most useful for lesions involving the spinal cord and
nerve roots and for soft tissue structures of joints,
whereas CT is most useful for osseous lesions.
BONE BIOPSY
Bone biopsy is indicated in the definitive diagnosis of
proliferative and lytic bone lesions. Different types of
bone tumors and osteomyelitis caused by bacteria or
fungi may have a similar radiographic appearance
and can only be differentiated on the basis of
histopathologic examination. Biopsy is performed less
frequently in the cat than the dog because of the
relative infrequency of osteosarcoma. The Jamshidi-
type bone marrow biopsy needle is suitable for
obtaining bone biopsies from cats (8). Use of the
needle only requires one small incision and the size of
the sample obtained is small, thus minimizing the risk
of iatrogenic fracture. Jamshidi needles are available in
single-use or reusable versions. The single-use needle
can be reused a number of times but requires ethylene
oxide sterilization, whereas the reusable needle can
be autoclaved. An accurate histopathologic diagnosis
can be obtained in approximately 90% of cases if an
experienced histopathologist examines the sample. The
technique has been described in detail14. Briefly, the
site is clipped and prepared and a small incision is made
in the skin over the center of the lesion. The biopsy
tract may be contaminated with tumor cells and should
be positioned so that it can be included in the excised
tissue if definitive surgical treatment is to be performed
subsequently. The needle is advanced through the soft
tissues, with the stylet in place, until bone cortex is
contacted. The stylet is removed and the needle is
advanced until it contacts the transcortex. The needle
is removed and the specimen is pushed out using a
probe, which is inserted into the opening at the tip of
the needle. The process is repeated through the same
incision, so that at least two samples are obtained, one
from the center and the other in the transition zone.
Diagnostic accuracy can be increased if the bone is
radiographed postoperatively to confirm correct
selection of the biopsy site.

i ii iii 8

A B

8 Jamshidi-type bone marrow biopsy needle.

A (i) Cannula and screw-on cap. The cannula has a tapered point to retain the specimen in
the needle. (ii) Pointed stylet for use when the needle is advanced through the soft tissues.
(iii) Probe used to expel the specimen from the base of the needle.
B After the stylet has been removed, the needle is advanced through the bone using a
twisting motion until the opposite cortex is reached. The needle is then withdrawn and
the specimen expelled. The procedure is repeated using the same skin incision, with the
cannula directed towards the periphery of the lesion.
24
MUSCLE AND NERVE BIOPSY
Definitive diagnosis of many neuromuscular disorders
requires histopathologic examination of muscle and
nerve tissue. The procedures for muscle and nerve
biopsy and the processing of specimens have recently
been reviewed15. Samples should be sent to
laboratories specializing in the evaluation of nerve
and muscle biopsies (1–3). The laboratory should be
consulted beforehand for advice about the correct
selection and processing of samples.
ADDITIONAL LABORATORY TESTS
The extent of routine preoperative blood testing is
controversial but a biochemistry panel, hematology,
electrolytes, and urinalysis are recommended for any
cat >5 years old undergoing a lengthy orthopedic
procedure (>60–90 minutes). Blood testing is
particularly indicated for geriatric cats, and for cats
that have a preexisting medical condition or evidence
of intercurrent disease on clinical examination. Young
cats (<5 years old) presented for elective orthopedic
procedures require only a packed cell volume (PCV),
total protein, and urine specific gravity. Feline
leukemia virus (FeLV) and feline immunodeficiency
virus (FIV) tests may also be performed routinely
or if they are specifically indicated. Other tests
performed on the basis of the clinical signs and other
findings include coronavirus, antinuclear antibody,
rheumatoid factor, creatine kinase, toxoplasma
serology, and measurement of acetylcholine
receptor antibody and molecular techniques16. The
significance of these tests and the indications for
them are discussed in the relevant chapters. Sampling
and examination of cerebrospinal fluid are discussed
in Chapter 11.
(1) Dr GD Shelton, Comparative Neuromuscular
Laboratory, Basic Science Building, Room 1107,
University of California, San Diego, La Jolla, CA
92093-0612, USA. Tel: (858) 534 1537.
(2) Dr KG Braund, Peripheral Nerve Laboratory,
1476 Lakeview Ridge, Dadeville, AL 36853,
USA. Tel: (256) 825 2624, Fax: (603) 676 2383.
(3) Dr C Hahn, Neuromuscular Disease Laboratory,
Royal (Dick) School of Veterinary Studies, The
University of Edinburgh, Easter Bush, Midlothian,
EH25, UK. Tel: (131) 650 6236, Fax: (131) 650
6588, Email: vetneurolab@ed.ac.uk.

CHAPTER 3
MANAGEMENT OF
THE ORTHOPEDIC
TRAUMA PATIENT
INTRODUCTION
A logical approach to the assessment and management
of the traumatized cat will help maximize survival and
increase the success rate of subsequent surgery.
The major cause of feline orthopedic injury is
vehicular trauma; other etiologies include falls from
heights, animal fights, and gunshots wounds. Multiple
orthopedic injuries are not uncommon and there are
frequently injuries to multiple body systems (Table 5).
Thoracic injuries, in particular, are often seen in cats
with fractures and represent a common cause of death
following trauma1. In one study of 93 cats with
traumatic fractures, 38.7% had radiographic evidence
of thoracic trauma, the most common injuries being
lung contusion and pneumothorax2. Traumatic rib
fractures in cats, although usually of little clinical
significance in their own right, should alert the
clinician to the likely presence of other more severe
intrathoracic and orthopedic injuries3.
It is essential that the patient is adequately
stabilized and properly evaluated for concurrent
injury before performing orthopedic surgical
intervention. With the exceptions of fractures
TABLE 5 COMMON THORACIC AND ABDOMINAL INJURIES SEEN IN CATS WITH TRAUMATIC FRACTURES.
Thoracic injuries
Diaphragmatic rupture
Pulmonary contusion
Pneumothorax
Pneumomediastinum
Hemothorax
Pericardial tamponade
Posttraumatic arrhythmia
Rib fractures
Thoracic wall injuries
25
involving the skull and spine and open fractures,
there are few instances where orthopedic injuries
constitute an emergency. Since many concurrent
injuries produce minimal clinical signs on first
presentation, they can easily be overlooked in favor of
the more obvious orthopedic injuries. Diagnosis and
treatment of thoracic injury is especially important
prior to anesthetic administration. In one study, 40%
of cats showed no clinical signs suggestive of thoracic
injury despite having abnormalities detected
radiographically2.
PHYSICAL EXAMINATION
Examination of the orthopedic trauma patient can be
divided into three phases. As with all trauma victims,
triage of all of the injuries is very important. At the
time of first presentation evaluation of the respiratory
and cardiovascular systems should receive priority, in
order to identify potentially life-threatening injuries.
Orthopedic injuries are not immediately life-
threatening, whereas mortality due to thoracic trauma
or peritoneal hemorrhage in traumatized cats is not
uncommon.
Abdominal injuries
Abdominal rupture
Bladder rupture or avulsion
Ureteral avulsion
Perforation/tear of colon or rectum
Hepatic laceration
Gall bladder rupture
Splenic laceration
Kidney laceration or avulsion
Penetrating abdominal wounds
26
An initial rapid evaluation of the trauma patient is
performed by checking respiratory rate and character,
mucous membrane color, capillary refill time, and
pulse rate and quality. Careful observation of the cat’s
breathing pattern can provide an indication of the
location of the problem without immediate resort to
stressful diagnostic procedures4. The lungs and
heart should be auscultated, checking for evidence
of pulmonary or pleural pathology and cardiac
murmurs or arrhythmias, respectively. During the
initial examination, attention should also be paid
to the cat’s level of consciousness and ability to
ambulate. The integrity of the urinary bladder can be
checked by gentle abdominal palpation, although this
does not rule out trauma to the ureters or urethra.
Following stabilization of the patient and treatment
of life threatening injuries, a more thorough physical
and orthopedic examination can be performed.
This should encompass all body systems and include
a cursory neurologic examination. In those patients
suspected of having injury to the nervous system,
a complete neurologic examination is then performed.
The third and final phase of the examination
involves ongoing assessment including re-evaluation
for progression of clinical signs and the response to
treatment.
DIAGNOSTIC TESTS
The most important part of the assessment of the
trauma patient is the physical examination; however,
some ancillary testing is frequently indicated. All cats
that have sustained major trauma should have thoracic
and abdominal radiographs once they are stable. If
urinary tract trauma is suspected, contrast studies are
required to determine the location and nature of the
lesion. Laboratory investigations, such as blood gas
analysis or a coagulation profile, may be indicated in
specific cases. Cats with arrhythmias or tachycardia
may have myocarditis secondary to myocardial trauma
and should have electrocardiographic evaluation,
especially if anesthetic administration is contemplated.
The onset of posttraumatic arrhythmia is delayed 1–5
days after the traumatic episode and is characterized
by ventricular premature contractions or, in severe
cases, ventricular tachycardia.
RESUSCITATION AND
STABILIZATION OF THE
TRAUMA PATIENT
OXYGEN THERAPY
Cats that appear to be in respiratory distress following
trauma should receive immediate oxygen therapy.
Supplementary oxygen can be given during the initial
examination using a facemask or flow-by. Struggling
and excessive manipulation at this stage may be life-
threatening and should be avoided. Following this
cursory examination, cats with dyspnea should be
placed in an oxygen tent or cage while being
stabilized. Longer-term administration of oxygen is
best performed via a nasal cannula or a hood. A mild
sedative, such as butorphanol at a dosage of
0.2–0.4 mg/kg, may be required when these methods
are employed.
FLUID THERAPY
Fluid therapy in cats has recently been reviewed5,6.
Cats that have suffered major trauma will have
hypovolemic shock, as evidenced by pallor of the
mucous membranes, delayed or absent capillary refill,
hypothermia, weak or nonpalpable peripheral pulses,
and mental depression. The tachycardia typically
displayed by dogs is not a typical feature in the cat and
the heart rate is most often normal or slow. In
addition, cats that have suffered unobserved trauma
and been missing for several days will be cachectic
and dehydrated. The priority in all cases is to
restore hemodynamic stability by restoration of the
circulating blood volume. External hemorrhage will
be readily apparent but internal hemorrhage is less
easy to detect. The fracture hematoma alone may
account for substantial blood loss, especially when the
femur or pelvis is involved or where there are fractures
of multiple bones. Unfortunately, measurement of the
packed cell volume (PCV) in acute trauma cases will
not reflect the severity of blood loss, since there is a
lag period of up to 24 hours while fluid moves into
the circulation. Although overinfusion of fluids must
be avoided, one of the greatest causes of mortality in
cats requiring intensive care is underestimation and
underinfusion of intravenous fluids.
Cats presenting with hypovolemic shock should
have their circulating plasma volume restored as quickly
as possible. Crystalloids should be given routinely at
shock rates, and body temperature, urine output,
peripheral perfusion, and blood pressure (if available)
should be monitored. The crystalloids of choice for
acute hypovolemia are normal (physiologic) 0.9% saline
or Hartmann’s (lactated Ringer’s) solution. Attempted
resuscitation with crystalloids alone carries a high risk of
significant pulmonary edema and accumulation of
pleural fluid. Cyrstalloids are therefore usually used in
combination with colloid solutions. Colloid solutions
contain large molecules (e.g. dextrans, starch, or
albumin), which exert an osmotic effect that holds water
within the plasma. Colloids therefore provide more
effective and prolonged expansion of the circulating
 Management of the orthopedic trauma patient
volume than a similar quantity of a crystalloid solution.
Rapid infusion rates of colloids are less well
tolerated in cats than in dogs, and excessive rates can
cause seizures and other adverse reactions. In severe
cases of hypovolemic shock, a loading dose of fluid can
be given over a period of 5–10 minutes (10–20 ml/kg
isotonic crystalloid and 5 ml/kg of colloid). Infusion
rates of crystalloid of 40–60ml/kg/hour are acceptable
for a short time to counter life-threatening hypo-
volemia. The same dose of colloid can be repeated as
necessary every 5–10 minutes if systemic arterial blood
pressure remains low, and then maintained at
10–40 ml/kg/day. Accurate administration of these
fluids requires the use of pediatric burettes or infusion
pumps. The cat should be monitored closely and
systemic arterial blood pressure, if available, should be
checked regularly to prevent volume overload. Should
pulmonary edema develop as a result of overinfusion,
the infusion of crystalloid should be reduced, the colloid
should be stopped, and furosemide should be given at
2– 4 mg/kg IV.
After the first 24 hours, hypovolemia and fluid
deficits should have been corrected. If the cat is
unwilling or unable to take oral fluids, then sufficient
fluid to fulfill normal maintenance requirements will
be needed, together with fluid to replace any ongoing
abnormal losses, for example, those incurred as a
result of fracture surgery. The maintenance fluid
requirement in a healthy cat is 40–60 ml/kg/day.
BLOOD TRANSFUSION
Blood transfusions in the cat and dog have been
reviewed7,8. Blood transfusion is indicated in the
management of acute trauma if the patient
has hypovolemic shock and cannot be stabilized by
administration of crystalloids and colloids alone. This
may occur if the blood loss has been severe or if there is
ongoing hemorrhage. In the latter case, blood
transfusion is performed in conjunction with surgical
intervention to identify the source of hemorrhage
and prevent further blood loss. The other common
indication for blood transfusion is in the stabilized
patient that requires surgery and is moderately anemic
(PCV of 15–20% or less) as a result of previous blood
loss. Although cats appear to be more tolerant of anemia
than dogs, transfusion is indicated, especially if further
blood loss is anticipated during surgery. Unfortunately
transfusion is rarely performed in practice, probably
because of the lack of a commercially available blood
collection system, concerns about transfusion reactions,
and a lack of suitable donors.
Three blood types or groups have been identified in
cats (A, B, and AB). The blood group is determined by
27
the nature of the blood group antigens on the
erythrocyte cell membranes. In worldwide studies type
A has consistently been found to be the most common
type, whereas type AB cats are consistently uncommon.
The proportion of type B cats shows considerable
geographical and breed variation. Unlike dogs, in
addition to blood group antigens, cats also have
naturally occurring serum antibodies to red cell antigens
known as alloantibodies9. These alloantibodies can
result in severe transfusion reactions in blood that has
not been cross-matched. Type A cats generally have low
anti-B antibody titers and, if given type B blood, may
develop mild clinically inapparent transfusion reaction
with reduced red cell lifespan. All type B cats have high
anti-A titers and, if given even a single transfusion of a
small volume of type A blood, develop a severe
transfusion reaction10. Type AB cats have no naturally
occurring anti-A or anti-B antibodies.
It is, therefore, vital that donor–recipient
compatibility is established prior to first transfusion of
all cats11. Ideally, compatibility should be ensured by
both blood typing and cross-matching. A desktop
blood typing kit has recently been developed, which
requires only 0.25 ml of blood in EDTA and is easy
to use (Rapid Vet-H Feline, DMS laboratories). The
kit provides an accurate method by which feline blood
can be routinely typed in house12. Cross-matching is
used to assess the effect that recipient serum
antibodies will have on donor cells (major cross-
match) and the effect that donor serum will have on
recipient cells (minor cross-match). Cross-matching is
available at commercial laboratories, although, in an
emergency situation, crude cross-matching can be
performed in house.
The ideal blood donor should be healthy, have a
lean body weight >5 kg, should be vaccinated, and
should be negative on testing for feline leukaemia virus
(FeLV), feline immunodeficiency virus (FIV), and
Haemobartonella felis. The donor should have a PCV
at the high end of normal, preferably >35% (normal
range 24–45%) and the blood group should be known.
A cat’s blood volume is estimated at 66 ml/kg.
Between 10% and 15% of a donor’s circulating blood
volume may be safely removed, i.e. approximately
35–50 ml for a 5 kg cat. If the volume exceeds 15%,
crystalloids should be given to the donor to prevent
hypovolemia.
The amount of blood required by the recipient can
be calculated from the formula:
Blood needed (ml) = weight of recipient (kg) ×
desired PCV – recipient’s PCV × 66
donor’s PCV
28
As a rough guide, for every 2.2 ml of blood/kg
body weight transfused, the PCV of the recipient will
increase by 1%.
Blood is collected from the jugular vein of the
donor using a 50 ml syringe with a butterfly extension
set. The inside of the extension set and syringe should
be coated with approximately 1.3 ml of acid citrate
dextrose (ACD) or citrate phosphate dextrose (CPD)
per 10 ml of blood to be collected (removed from
a human blood transfusion pack). Sedation of the
donor is routinely performed, for example, using
ketamine combined with midazolam or diazepam (see
Table 8). Hypotensive agents such as acepromazine
should be avoided. The blood can be given
immediately, via either the intravenous or intraosseous
routes, through a blood giving set or in-line filter to
remove small clots. A maximum flow rate of
20 ml/kg/hour is normally recommended for
hypovolemic patients, but much greater rates can be
used in certain circumstances, such as when there is
ongoing hemorrhage. Blood not required for
immediate use can be stored for up to 4 weeks
provided it is kept refrigerated.
The recipient should be monitored closely for
signs of an acute transfusion reaction, especially
during the first 15 minutes of administration. Severe
reactions are characterized by hemolysis and systemic
anaphylaxis (tachycardia, hypotension, bradycardia,
apnea, vomiting, and pyrexia).
Blood substitutes
Because of the difficulties associated with blood
transfusion in cats, the availability of a red blood cell
substitute would be invaluable. A hemoglobin-based
oxygen carrying (HBOC) solution is licensed for
use in dogs and has been used in cats both
experimentally and clinically13–15. Because cats are
more vulnerable than dogs to volume overload slow
infusion rates are advisable (0.5–2.0 ml/kg/hour),
with a total dose of approximately 30–40 ml/kg.
Administration of HBOC to clinical patients was
documented in a retrospective study involving 72
cats13. There was a high incidence of complications
ranging from those that were mild and clinically
insignificant through to severe cardiovascular and
respiratory effects. Higher infusion rates were
associated with an increased risk of complications.
NUTRITION
It is not uncommon for feline patients to show
reluctance to eat or drink during a stay in hospital or
following discharge after surgery. Many cats can be
coaxed to eat by hand feeding or offering different
types of food. Appetite stimulant drugs can be
helpful in some cases but are usually not effective in
cats that are completely anorexic. The most
commonly used appetite stimulants are diazepam
administered intravenously at a dose of 0.5 mg/cat
and cryptoheptadine administered orally at a dose of
2 mg/cat twice daily.
Provision of adequate nutrition is important,
because undernutrition or malnutrition have a
negative influence on morbidity and mortality in
critically injured patients16. Adverse consequences
for the orthopedic surgical patient include increased
susceptibility to infection, delayed wound and
fracture healing, muscle weakness, major organ
failure, and death17. Protein and energy under-
nutrition is a common problem in the traumatized
cat. The cat’s protein requirement is 50% higher for
growth and more than 100% higher for maintenance
compared with that in the dog. Unlike in the dog,
the urea cycle and hepatic transaminases have a fixed
high rate of activity and therefore the cat cannot
adapt to the amount of protein consumed.
Nutritional support is indicated when the intake of
calories is reduced because a cat is unable or unwilling
to eat and in situations where there is an excessive
demand for protein and calories. Common indications
for nutritional support in the feline orthopedic patient
include:
• Substantial hemorrhage (traumatic and/or
surgical).
• Large open wounds.
• Fractures of the mandible or maxilla.
• Multiple orthopedic injuries.
• Anorexia because of intercurrent medical
conditions.
• Cats that have been missing for several days.
• Anorexia because of concurrent injury to other
body systems.
Nutritional support can either be provided by the
parenteral route, using a central venous catheter
or peripheral vein18, or by the enteral route, by force-
feeding or insertion of a feeding tube17. The
parenteral route is rarely used since it is expensive and
has a high complication rate. Enteral feeding is more
physiologic, is inexpensive, and is easy to perform
with few complications. Additionally, owners can
perform feeding by this route at home. Methods for
delivery of enteral nutrients include placement
of nasogastric, pharyngostomy, esophagostomy,
gastrostomy, or jejunostomy feeding tubes19.
 Management of the orthopedic trauma patient
29

Nasogastric or esopahgostomy feeding tubes are used PRE- AND POSTOPERATIVE

most commonly for feline orthopedic patients
requiring nutritional support. Gastrostomy tube
feeding may be indicated where it is anticipated that
longer-term nutritional support will be required
(weeks to months) but are rarely used for orthopedic
patients. Methods of placement of these tubes have
been described20,21. Nasogastric tube feeding is well
tolerated by cats for short-term enteral feeding (up to
10 days). The main advantages of nasogastric tubes
are that they are simple to place and placement does
not require the administration of a general anesthetic.
The disadvantages are that feeding is restricted to
liquid diets because of the small bore of the tube and
an Elizabethan collar is almost always required to
prevent premature removal. Esophagostomy tubes
are generally preferred for longer-term use. Because
of the larger bore of an esophageal tube, blended
commercial canned food can be used in addition to
commercial liquid diets. Long-term nutritional
support using esophageal tube feeding is well
tolerated by cats and has been associated with
minimal complications22. The surgeon should not
hesitate to place a feeding tube at the time of surgery
if it is anticipated that there will not be a rapid return
to oral feeding postoperatively. Tube feeding is
started immediately after recovery from anesthesia
and continued until the patient is feeding voluntarily.
It is possible for a cat to eat and drink normally with
a feeding tube in place.
STABILIZATION OF FRACTURES
AND LUXATIONS
Bandages and splints (Tables 6 and 7 ) are frequently
used preoperatively to provide temporary immo-
bilization and reduce swelling for fractures at or distal
to the elbow and stifle. Bandages, splints, slings, and
casts are often used to provide adjunctive fixation
postoperatively for fractures or after reduction of joint
luxations. In some cases external coaptation may be
used as the sole method of fracture fixation (see
Chapter 6). The principles and techniques for
application are the same as those for the dog and have
been well described elsewhere23.
For fractures distal to the elbow and stifle
joints, a soft, padded bandage should be applied
postoperatively to the limb to limit swelling. In most
cases, this bandage is removed 1–2 days after surgery
to allow early joint mobility. This also allows careful
examination of the limb for signs of neurologic
dysfunction or vascular impairment, and the initiation
of physical rehabilitation techniques. If the bandage is
left in place for a longer period of time, or when
external coaptation is used for fracture fixation, the
cat’s toes are observed for signs that the bandage is
too tight.
In cats with external fixators, incorporating the
frame and limb in a bandage will help reduce swelling,
prevent the frame from catching on objects in the
environment, and pad the frame and sharp points of

TABLE 6 EFFECT OF BANDAGES, SLINGS, SPLINTS, AND CASTS ON JOINT MOTION AND WEIGHT BEARING.
Region Weight bearing, Weight bearing, Nonweight-bearing, Nonweight-bearing,
joint still mobile joint immobilized joint still mobile joint immobilized
Shoulder - Spica splint Velpeau sling
Elbow Robert Jones/ Spica splint, - Velpeau sling
soft-padded bandage cast/splinted bandage
Carpus Robert Jones/ Cast/metasplint - -
soft padded bandage
Hip - - Ehmer sling, -
90/90 sling
Stifle Robert Jones/ Cast/ - 90/90 sling
soft padded bandage splinted bandage
Hock Robert Jones/ Cast/ - -
soft padded bandage splinted bandage
Digits Robert Jones/ Cast/ - -
soft padded bandage metasplint
30

TABLE 7 BANDAGES, SPLINTS, SLINGS, AND CASTS.

Type Indications
Robert Jones bandage Pre- (and post-) operative for
fractures or luxations at or distal
to the elbow or stifle
Soft padded bandage Post- (and pre-) operative for
fractures or luxations at or distal
to the elbow or stifle
Cast Postoperative immobilization
distal to the elbow or stifle (and
primary treatment of selected fractures)
Spica splint Pre- and postoperative for scapular,
shoulder, and humeral fractures, lateral
shoulder luxation, elbow luxation
Velpeau sling Postoperative for surgery proximal
to the elbow, medial shoulder luxation
Ehmer sling Craniodorsal hip luxation
90/90 sling Postoperative for surgery proximal
to the stifle, femoral fractures to help
prevent quadriceps contracture
Mason metasplint Pre- and postoperative immobilization
of distal extremities
Complications/Comments
Circulatory impairment digits
Circulatory impairment digits
Circulatory impairment digits,
pressure sores
Circulatory impairment digits,
not tolerated by some cats
Not well tolerated by most cats
Circulatory impairment distal
to the sling, not well tolerated
by some cats
Circulatory impairment distal
to the sling, not well tolerated
by some cats
Circulatory impairment digits

the pins. In most cases, the pin–skin interface is left
exposed and monitored daily for drainage or signs of
inflammation. In general, no cleaning is necessary.
However, if drainage develops, cleaning the pin–skin
interface daily with a mild soap or chlorhexidine
solution may be beneficial. If the frame is bandaged,
the foam portion from surgical scrub brushes can be
dried and packed around the pins beneath the
bandage.
ROBERT JONES BANDAGE
A Robert Jones bandage is a heavily padded,
bulky bandage often used preoperatively to provide
temporary stability and reduce swelling in fractures at
or distal to the elbow and stifle joints (9). Tape
stirrups are placed on the limb to apply traction while
the bandage is placed and to prevent the bandage
from slipping. Roll cotton or orthopedic wadding is
applied to the limb, beginning distally and
progressing proximally. In cats orthopedic wadding is
often easier to apply than roll cotton. Each wrap
should overlap the previous one by approximately
50%. A large quantity of padding is used to provide
bulk and is wrapped tightly around the limb. The
bandage must extend beyond the joints proximally
and distally to the fracture, but the distal aspect of the
digits is left exposed to monitor swelling. Elastic
gauze is then tightly wrapped over the padding
(distally to proximally) to provide compression. The
tape stirrups are reflected proximally and stuck to the
outer layer of gauze. Tightly wrapped cohesive
bandaging tape is then applied to cover the bandage.
If additional support is desired, a metal rod or
thermomoldable splint material (X-Lite, AOA
Kirschner Medical Corp.) can be incorporated into
the bandage before the Vetrap is applied. The splint
material is generally placed on the lateral aspect of the
fore- and hindlimb or the plantar aspect of the
hindlimb.
SOFT PADDED BANDAGE
A soft padded bandage, or modified Robert Jones
bandage, is similar to a Robert Jones bandage but uses
less padding. Because it is less bulky than the Robert
Jones bandage it provides less immobilization of the
limb. It is used primarily for support and control of
 Management of the orthopedic trauma patient
9 10
B
C Thermoplastic (VTP), IMEX Veterinary Inc., or
9 Application of a Robert Jones bandage.
A Application of stirrups and cotton roll.
B Application of conforming bandage. The stirrups are
folded back before application of the final layer.
C Application of Vetrap bandage.
postoperative swelling at or distal to the elbow or stifle
joints. The procedure for application of the bandage is
the same as the Robert Jones bandage except that less
orthopedic wadding or roll cotton is used. Splint
materials can be added as described above.
SPICA SPLINT
A Spica splint can be applied if immobilization of the
scapula, shoulder, humerus, or elbow is desired,
incorporating the entire forelimb and torso23 (10).
31
10 A completed Spica splint.
Spica splints may be used to immobilize fractures prior
to definitive repair, as ancillary support after internal
fixation, or to stabilize luxations of the shoulder or
elbow. They are occasionally used as a primary means
of fracture fixation. Unfortunately, some cats become
agitated when a Spica splint is applied.
Stirrups are applied to the distal limb to provide
traction while the splint is applied. The elbow and
shoulder joints should be slightly flexed and the limb
placed in a normal standing angle. Several layers of
cast padding are applied to the limb from the digits to
the axillary region. Application is continued around
the torso, wrapping both cranially and caudally to the
opposite shoulder in a modified figure-of-eight
pattern. Thermomoldable splint material (X-Lite,
AOA Kirschner Medical Corp.; Veterinary
Orthoplast, Johnson & Johnson) is then placed on the
lateral aspect of the limb from just proximal to the
digits to the dorsal mid-line. Alternatively, fiberglass
casting material can be used. Elastic gauze is then
placed to anchor the splint and conform it to the limb
and torso as it hardens. Cohesive tape or elastic tape is
placed to cover the bandage.
SLINGS
Slings are rarely used for primary fracture fixation, but
they may be used to prevent weight bearing after
fracture repair and to stabilize joint luxations.
Velpeau sling
Velpeau slings are indicated as a primary or
adjunctive stabilization to maintain reduction of
medial shoulder luxations and to immobilize
32
11
11 Velpeau sling application. The forelimb is flexed and
adducted against the body wall. Cast padding material is
applied, followed by roll gauze and Vetrap or elastic
adhesive tape. The bandage encircles the torso and the
flexed forelimb, wrapping cranial and caudal to the
opposite forelimb to prevent slippage. The material
should not be placed too tightly.
fractures of the scapula (11). To apply the Velpeau
sling, the forelimb is flexed and adducted against the
thorax. The limb is incorporated into a bandage (cast
padding, roll gauze, cohesive tape) that encircles the
torso. The bandage is placed cranial and caudal to
the opposite limb to prevent slippage. The bandage
should allow the cat to breathe normally, but must
be snug to prevent movement of the affected limb.
Velpeau slings are not well tolerated by most cats.
Ehmer sling
Ehmer (figure-of-eight) slings are used primarily to
prevent weight bearing on the hindlimb and to
stabilize craniodorsal hip luxations after closed
reduction24 (12). A light bandage is placed on the paw
over the metatarsus and phalanges (to protect soft
tissues and reduce swelling of the toes). The hock and
stifle joints are then flexed and adhesive tape is applied
around the limb in a figure-of-eight pattern. The tape
is placed from the bandage on the paw, medial to the
stifle between the thigh and inguinal area, over the
cranial and lateral aspects of the thigh, and then medial
to the tarsus to the bandage on the paw. Several passes
are needed to maintain the limb in a flexed position.
Adhesive tape sticks to the cat’s hair and reduces
slippage of the sling. Gauze may be used instead and is
easier to remove, but is more likely to slip prematurely.
In addition to maintaining flexion of the hindlimb, an
Ehmer sling also rotates the femur internally to
12
12 Ehmer sling application. A small padded bandage is
applied to the metatarsus and phalanges. The hock and
stifle joints are flexed and adhesive tape is applied in a
figure-of-eight pattern (the adhesive tape must not encircle
either the thigh or the distal limb). The tape is applied
from the bandaged foot, medial to the stifle joint, and over
the cranial and lateral aspects of the thigh, medial to the
tarsus, back to the foot.
stabilize the hip joint. If greater abduction of the limb
is required to prevent reluxation of the hip, tape from
the sling can be extended over the dorsal mid-line to a
band of tape placed around the caudal abdomen. This
is not necessary when prevention of weight bearing is
the goal and is often poorly tolerated by cats.
The most common problem with the sling is that it
is prone to slip off the cranial aspect of the stifle because
of the mobility of the skin in this region. Other
complications are discomfort, soft tissue trauma to the
metatarsal or thigh region, and swelling of the toes. The
sling is not generally applied for longer than 10 days.
90/90 sling
The 90°/90° flexion sling is a variation on the Ehmer
sling. It prevents weight bearing on the hindlimb by
maintaining the stifle and hock flexed at right angles
(13). It is used primarily on cats at high risk
of quadriceps contracture after repair of femoral
fractures25. Application is similar to the Ehmer sling
except that the material is simply wrapped circumfer-
entially around the thigh and metatarsus rather than
being placed in a figure-of-eight fashion. To apply, cast
padding is first placed around the metatarsus to protect
the soft tissues and minimize swelling of the toes. The
hock and stifle joints are positioned in 90° of flexion.
Elastic adhesive tape is placed around the thigh and
metatarsus to maintain flexion. Slings should not
generally be maintained for longer than 10 days.
 Management of the orthopedic trauma patient
13
13 90/90 sling application. The hock and stifle joints are
placed in 90° of flexion. Cast padding material is placed
around the metatarsal region to help reduce swelling of
the toes. Adhesive tape is applied circumferentially around
the femur and metatarsus to maintain flexion.
METASPLINTS
Metasplints (Mason metasplints) are used to immobilize
the extremities distal to the mid-antebrachium in
the forelimb and distal to the hock in the hindlimb.
These splints are not suitable for immobilization of
the proximal radius and ulna, the elbow joint, or the
talocrural joint.
INITIAL TREATMENT OF
FRACTURES
CLOSED FRACTURES
Fractures proximal to the elbow and stifle joints are
typically not immobilized prior to definitive repair26.
Scapular, humeral, pelvic, and femoral fractures are
generally closed because of the greater soft tissue
coverage. The cat is simply confined (and sedated if
necessary) to limit activity, reduce pain, and prevent
closed fractures from becoming open. If preoperative
immobilization of a proximal forelimb fracture is
required, a Spica splint may be used. Closed fractures
distal to the elbow and stifle joints are placed in a
Robert Jones bandage to reduce swelling and pain,
minimize further soft tissue injury, and to prevent
penetration of the skin by bone fragments24,27. A
splint may be incorporated into the bandage for
additional support if required.
OPEN FRACTURES
For information on the classification of open fractures
see Chapter 4.
Early, aggressive treatment of open fractures
is begun immediately to prevent contamination of
the site becoming a deep infection of the bone
and soft tissues. Cleaning and bandaging also
33
prevents further contamination of the fracture from
the environment.
1. A sterile bandage or dressing is applied to protect
the wound from further contamination and
reduce the likelihood of nosocomial infections.
Sterile gloves should be worn at all times when
treating the wound.
2. The cat is examined thoroughly and treated
appropriately for shock and any concurrent injuries.
Particular attention should be paid to thoracic
trauma (pneumothorax, hemothorax, pulmonary
contusions), neurologic injuries (cranial trauma,
spinal fractures/luxations), abdominal injuries
(hemorrhage, bladder ruptures, hernias), and
concurrent orthopedic injures (fractures, luxations).
3. The fracture site is radiographed to document the
severity of the orthopedic injury and aid selection
of the appropriate fracture fixation method.
4. When the cat is stable, the initial evaluation of
the wound is begun. Sedation or short-acting
anesthesia may be required to allow proper
treatment. Under aseptic conditions, the
bandage is removed and a swab is taken from
the wound for bacterial identification and
sensitivity testing. Both aerobic and anaerobic
cultures are indicated28,29.
5. Broad-spectrum antimicrobial drugs are
administered intravenously30. It is important to
begin antimicrobial therapy soon after the injury to
reduce the likelihood of subsequent bone
infections31. Intravenous administration of
fluoroquinlones is contraindicated because they
may induce retinal degeneration and these drugs
should be used with caution in cats with impaired
renal function32. Several antibiotics are appropriate
for the initial treatment of open fractures, including
cephalosporins (cefazolin at 22 mg/kg IV every 8
hours) and clindamycin (11 mg/kg IV every 12
hours)33,34. A combination of a cephalosporin and
an aminoglycoside may also be used to increase
efficacy against Gram-negative organisms35. The
use of gentamicin (6.6 mg/kg IV or SC every
24 hours) has been recommended36, but
aminoglycoside therapy should be used with
caution in traumatized cats to avoid renal
complications. In grade IIIb and IIIc fractures,
penicillins or metronidazole may also be given to
improve efficacy against anaerobic organisms37.
Antibiotic therapy is continued for 3–5 days and
altered, based on the results of sensitivity
testing30,31,38. In many cases, bacteria isolated from
open fractures are strains from the hospital where
the limb is being treated.
34
6. The wound is filled with sterile lubricating jelly and
the surrounding hair is shaved. The wound is
lavaged copiously to remove hair and debris; 1–2l
of fluid are recommended for most wounds,
although more lavage may be necessary in severely
contaminated wounds. A pulse-jet lavage system
may be used if available. Alternatively, a lavage
system comprised of a 1l bag of fluid, a sterile
intravenous administration line, a sterile three-way
stopcock, and a 60 ml syringe attached to a
19 gauge needle can be used (14). By adjusting the
stopcock, the lavage solution is drawn into the
syringe from the fluid bag and then injected
through the needle to lavage the wound. This
allows the clinician to maintain sterility, lavage the
wound with adequate pressure, and avoid excessive
force that can drive debris deeper into the wound37.
Sterile saline or lactated Ringer’s are most
commonly used for wound lavage. The addition of
antibiotics to the lavage solution is controversial and
probably provides negligible benefit39. However,
the use of a 0.05% chlorhexidine solution has been
shown to reduce contamination and improve
wound healing40. It is prepared by adding 12ml of
chlorhexidine solution (2%) to 500ml of sterile
water, saline, or lactated Ringer’s37. A precipitate
will form when chlorhexidine is mixed with saline.
More concentrated lavage solutions are avoided
since they may damage tissues and inhibit
14
14 Lavage system used for treatment of open wounds. The
system consists of a 1 l bag of lactated Ringer’s solution, a
sterile IV administration line, a sterile three-way stopcock,
and a sterile 60 ml syringe attached to a 19 gauge needle.
A 0.05% chlorhexidine solution may be used to reduce
contamination and improve wound healing: 12 ml of
chlorhexidine solution (2%) is added to each 500 ml of
lactated Ringer’s solution.
granulation tissue. A 1% or 0.1% povidone–iodine
solution (10% solution diluted 1:10 or 1:100 in
saline) may also be used for wound lavage and has
broad-spectrum antimicrobial activity. Many cats
have contact hypersensitivity to povidone–iodine
and stronger solutions can interfere with wound
healing41. Tap water should not be used as a lavage
solution because its hypotonicity may cause
additional cellular trauma37.
7. All debris and devitalized tissues are removed from
the wound (taking care to avoid damaging vessels
and nerves) with forceps, scissors, and the
mechanical action of the lavage solution42. Little
debridement is usually necessary in grade I open
fractures; however, extensive debridement may be
necessary in grade III open fractures. Where
possible, tissues that are grossly contaminated,
discolored, fail to bleed when cut, or are obviously
dried or devitalized are removed. Fat and
subcutaneous tissues are excised with minimal
consequence in most wounds. Excessive use of
electrocautery is avoided to minimize the amount
of devitalized tissue in the wound. Muscle is
assessed by color, consistency, circulation, and
contractility to determine its viability43. If the
viability of a tissue is in question, it may be left in
situ and removed later if it becomes devitalized. In
severely traumatized or contaminated wounds,
progressive debridement over several days may be
required to achieve a clean wound. In gunshot
injuries, accessible bullet fragments are removed;
however, healthy tissue should not be traumatized
in an effort to remove deeper bullet fragments. The
decision to remove or leave cortical bone fragments
can be difficult. Fragments that are devoid of soft
tissue attachments and not essential to fixation of
the fracture are removed so that they do not
become sequestra. Articular fragments and those
essential to fracture stabilization may be left in
place and lavaged. The wound is lavaged again after
the debridement is completed.
8. The fracture is stabilized surgically as soon as
possible. Early stabilization preserves existing
blood supply, promotes ingrowth of new
vasculature, and helps prevent infection. In many
cases, the fracture is stabilized at the time of
initial debridement44. If the fracture cannot be
immediately stabilized, a dressing is applied to the
wound and a sterile bandage is placed over it
until fixation can be performed. A splint may be
incorporated into the bandage to provide support
and improve comfort. Wet-to-dry dressings
changed daily can be used to aid in debridement
of the wound during bandaging.
 Management of the orthopedic trauma patient
35

PRE- AND PERIOPERATIVE fractures47–51. The cat’s cardiovascular status should

ANALGESIA
The assessment of pain in cats is notoriously difficult
because overt signs may be subtle. In one survey, only
one of 15 cats was given any analgesia after surgery45.
Assessment of pain is best made subjectively, by a
trained observer, on the basis of observation and
interaction46. Cats that are in pain typically become
inactive, sit at the back of their cage, and avoid human
interaction. They tend to resent or avoid handling and
may show signs of aggression. Occasionally a cat will
thrash around the cage violently, a reaction that is seen
more commonly in young animals.
Analgesic drugs should be administered to
increase comfort and reduce stress in all cats with
be carefully monitored when analgesics are used.
Preemptive analgesia is preferred to control pain in
cats scheduled for surgery. It prevents so-called ‘wind-
up’, which is sensitization of the central nervous
system from afferent nociceptive stimuli. If possible,
balanced (multimodal) analgesia is used. This involves
the simultaneous administration of two or more
analgesic techniques to achieve a synergistic effect,
reduce drug dosages, and minimize complications49.
Many drugs can be administered systemically to
provide analgesia in cats, including opioid drugs,
α2-adrenergic agonist drugs, and nonsteroidal
antiinflammatory drugs (NSAIDs) (Table 8).
Multimodal analgesia is usually achieved by

TABLE 8 ANALGESICS.
Drug Dose (mg/kg) Routes Duration (hours) Comments
Buprenorphine 0.01–0.02 IV, IM, SC 4–8 For mild to moderate pain
Butorphanol 0.1–0.3 IV 0.5–1 For mild to moderate pain
0.1–0.6 IM, SC 2–3
Carprofen 2.0–4.0 IV, SC 24 Only one treatment,
for mild to moderate pain
Fentanyl 0.002–0.005 IV bolus <0.5 Short duration unless given as
constant infusion
0.002–0.004 kg/hour Constant rate During infusion For moderate to severe pain
infusion + 0.5
0.025 (25 µg) patch Transdermal 72 Not recommended for
cats <2.0 kg (<4.4 lb)
Hydromorphone 0.5–0.1 IV, IM, SC 2–4 For moderate to severe pain
Ketoprofen 1.0–2.0 IV, IM, SC 24 Maximum 3 days;
contraindicated with renal disease,
hypovolemia, coagulopathies.
For mild to moderate pain
1.0 PO once daily Maximum 5 days
Medetomidine 0.001–0.01 IV, IM, SC 0.5–2 Monitor for cardiac depression,
reversible
Meloxicam 0.3 SC 24 Only one treatment,
for mild to moderate pain
0.1 (1 drop/kg) for 5 days PO once daily 24 Liquid palatable
followed by 0.02–0.04
(1–2 drops/cat)
Morphine 0.1–0.3 IM, SC 3– 4 Moderate to severe pain
0.06–0.12 kg/hour Constant rate During
infusion infusion
Oxymorphone 0.02–0.05 IV 3– 4 For moderate to severe pain
0.05–0.1 IM, SC 2–6
Xylazine 0.1–1.0 IV, IM, SC 0.5–2 Monitor for cardiac depression,
reversible
36
the administration of an opioid and an NSAID,
although consideration should also be given to the use
of local and epidural analgesia.
Opioids are suitable for moderate to severe
pain control. They have a rapid onset of action
and block central sensitization and autonomic
responses to surgery, but are short acting with the
exception of buprenorphine. Fractious cats may be
given buprenorphine orally by squirting the injectable
solution into the mouth so that it is absorbed
through the oral mucosa. NSAIDs are suitable for
mild to moderate pain control. They have a slower
onset of action than opioids, are long acting, reduce
peripheral pain sensitization, and have long-lasting
antiinflammatory effects at the surgery site.
The drug gabapentin, originally licensed as an
anticonvulsant, is clinically effective as a neuropathic
analgesic in humans. Based on anecdotal reports, the
drug shows promise in cats. The suggested dose is
2.5–5.0 mg/kg twice daily.
REGIONAL ANALGESIA
Epidural and local administration of analgesic agents
can also be used to provide regional analgesia in cats.
Local infusion
Local infusion of bupivacaine (1–2 mg/kg) at the
surgery site can be used to provide 2– 4 hours of
analgesia. The total dose of bupivacaine for a healthy
cat should not exceed 2 mg/kg (1.6 ml of a 0.5%
solution for a 4 kg cat).
TABLE 9 DRUGS USED FOR EPIDURAL ANALGESIA.
Drug Dose (mg/kg)
Bupivacaine (0.5%)+ 0.5–0.75
Morphine (10 mg/ml)+ 0.1–0.3
Morphine (10 mg/ml)+ 0.1
+Bupivacaine (0.5%)+ 0.1–0.2
Oxymorphone (1 mg/ml) 0.05–0.1
Fentanyl (0.05 mg/ml) 0.004
Medetomidine (1 mg/ml) 0.01
* The drugs are diluted with normal saline to achieve a total volume of approximately 0.2ml/kg.
+ Preservative-free morphine and bupivacaine are preferred. For intrathecal injection it is essential to use
preservative-free bupivacaine without epinephrine.
Epidural analgesia
Epidural administration is usually reserved for cats
that are already anesthetized in preparation for an
orthopedic procedure. Epidural administration of
bupivacaine alone provides 4–6 hours of pain relief
(Table 9). A single epidural injection of preservative-
free morphine can provide effective analgesia for
procedures on the hindquarters for up to 24 hours.
Bupivacaine may also be combined with morphine
for epidural injections. A recent study compared
the analgesic effects of epidural morphine with a
combination of morphine and bupivacaine in cats
undergoing onychectomy52. The combination of
drugs allowed a significant reduction in the quantity
of inhalation agent required to maintain general
anesthesia compared with morphine alone and gave a
longer duration of analgesia. The authors concluded
that preemptive epidural administration of morphine
with or without bupivacaine provided better
control of postoperative pain than repeated
injections of oxymorphone and ketoprofen. The
analgesic effects of epidural fentanyl and medeto-
midine have also been described53. Oxymorphone is
an opioid drug with similar properties to morphine
when used for epidural analgesia but with a shorter
duration of action.
The analgesic effects of drugs administered
by epidural injection are both volume- and dose-
dependent. A volume of 1 ml/5kg calculated on the
basis of lean or ideal body weight will generally
provide analgesia to the level of the first lumbar
Dose (ml/kg)* Onset of analgesia Duration of
(minutes) analgesia (hours)
0.1–0.15 10–15 3–6
0.01–0.03 20–60 10–24
0.01 10–15 24
0.02–0.04 - -
0.05–0.1 20–40 7–10
0.08 5–30 2–5
0.01 5–10 1–8
 Management of the orthopedic trauma patient
vertebra. The analgesic agent is diluted with normal
saline to achieve the desired volume for injection.
Contraindications to epidural analgesia
include thoracolumbar and lumbosacral fractures and
luxations. The reported incidence of complications
after epidural administration of morphine in a series of
dogs and cats was 0.75%54.
For a more detailed description of the technique
of epidural analgesia the reader is referred
elsewhere53,55,56. Generally a single injection is made
with a 40 mm 22 gauge spinal needle between L7 and
S1 (15). The cat is placed in lateral recumbency and
the area is clipped and prepared. For unilateral
procedures the cat should be placed with the surgical
site nearest the table. The injection is made in the
mid-line at the center of the lumbosacral depression.
The dorsal spinal processes of L7 and S1 are palpated
and the injection is made between these two points.
The spine is flexed at the lumbosacral junction by
drawing the hindlimbs cranially. The needle is
advanced perpendicular to the skin through the
ligamentum flavum. If bone is encountered the needle
is withdrawn slightly and walked cranially or caudally
along the bone as appropriate to find the space. Slight
resistance is encountered as the ligamentum flavum is
penetrated and the needle is advanced a further
2 mm until there is loss of resistance. The stylet is
removed and the needle hub is observed for blood or
cerebrospinal fluid (CSF). If blood is encountered,
the needle is removed and the procedure is repeated.
It is not uncommon for the needle to enter the
subarachnoid space in the cat. If CSF flows from
L4 L5 L6
15 Diagram showing the site for epidural injection. The dorsal spinous process of
the first sacral vetebra (S1) is more prominent in the cat than the dog. Using L7
and S1 dorsal spinal processes as palpable landmarks the injection site is
approximately in the caudal third.
37
the needle the injection can be made intrathecally but
the calculated dose is reduced by 40–50%52. A
number of methods have been described for
confirming the location of the needle in the epidural
space. The simplest method involves the injection of
0.5 ml of air. If the needle is correctly located, the
injection will proceed with no resistance and no visible
leakage of air into the subcutaneous tissues.
Transdermal patches
Transdermal fentanyl patches are suitable for use in
cats over 2.0 kg body weight50,57–61. The application
of a 25 µg/hour patch provides relatively consistent
analgesia for up to 72 hours after application. Plasma
concentrations reach effective levels 7 hours after
application61. To apply the patch, the skin over the
dorsal or lateral thorax is clipped and gently cleaned.
Scrub solutions and alcohol are avoided. The patch is
handled by the edge or gloves are worn to avoid
contact with the membrane. The adhesive backing on
the patch is placed directly on the skin and held in
place for 1–2 minutes. A bandage may be placed to
cover the patch and prevent inadvertent removal;
however, this is not always required. Transdermal
fentanyl patches can provide a steady-state opioid
concentration within the therapeutic range without
the need for repeated injections or oral drug
administration. However, fentanyl concentrations
may vary significantly in individual patients and cats
should be monitored for signs of insufficient
analgesia or adverse reactions, such as respiratory
depression.
15
1/3
S2 S3
L7 S1
38

PRE- AND PERIOPERATIVE
SEDATION
Sedative drugs are usually administered as
premedication before general anesthesia (Table 10).
Sedative drugs may be administered to stable cats that
are refractory to handling or intolerant of confinement
or bandages47,62. Sedation is often required during
radiography and bandaging procedures. Acepromazine
alone is not very effective and combinations of drugs
are usually preferred. Acepromazine combined with an
opioid will provide mild to moderate sedation and this
combination is frequently used for premedication.
Alpha 2 agonists, such as medetomidine and xylazine,
used alone have adverse effects on cardiopulmonary
function and are only used for healthy patients. The
addition of an opioid agent to the alpha 2 agonist may
reduce some of these adverse effects. Benzodiazepines,
such as diazepam or midazolam, given alone can
provide satisfactory sedation in cats that are very
ill and these agents may also be used in combination
with opioids given at the same dosages that
are recommended for use with alpha 2 agonists.
Ketamine, in combination with acepromazine and
diazepam or midazolam, provides effective sedation
and low doses of this combination are suitable for very
ill cats. Inclusion of both the acepromazine and the
benzodiazepine components of the mixture
increases its efficacy with no increase in the adverse
effects. Atropine (0.04 mg/kg) or glycopyrrolate
(0.005–0.01mg/kg) may also be administered to
control bradycardia during sedation.
POSTOPERATIVE CARE
Postoperative management is an important
component of treatment of the orthopedic trauma
patient. Immediate concerns include monitoring and
supporting respiratory and cardiovascular systems
during the anesthetic recovery period. Fatal
pulmonary fat embolism has been reported as
a complication of fracture repair and may be a cause of

TABLE 10 SEDATIVES.
Drug Dose (mg/kg) Routes Duration (hours) Comments
Acepromazine 0.01–0.03 IV 1–2 Avoid if history of seizures
0.05–0.1 IM, SC 2–6
Acepromazine 0.05 Avoid if history of seizures
+Butorphanol or 0.1–0.3 IM 2–5
+Buprenorphine or 0.005–0.01 IM 4–8
+Morphine 0.1–0.2 IM, SC 2–6
Medetomidine 0.05–0.08 IV, IM, SC 0.5–2 Monitor for cardiac depression,
reversible with atipamezole
Medetomidine 0.025–0.05
+Butorphanol or 0.1–0.2 IV, IM 2–3
+Buprenorphine 0.005–0.02 IV, IM 2–4
Xylazine 0.1–1.0 IV, IM, SC 0.5–2
Xylazine 0.2
+Butorphanol or 0.1–0.2 IV, IM 1–3
+Buprenorphine 0.005–0.02 IV, IM
Ketamine 2.5 Profound sedation for 12–20
minutes
+Diazepam or midazolam 0.25 IV
Ketamine 2.5–7.5 Lower doses of acepromazine and
ketamine are used in ill cats
+Midazolam and 0.25
+Acepromazine 0.05–0.1 IM
Diazepam 0.1–0.5 IV 0.5–1
 Management of the orthopedic trauma patient
unexplained chronic progressive postoperative
respiratory failure63. Cats lose body heat rapidly in
comparison with dogs because of their high surface
area to volume ratio. Attention must be paid to
thermoregulation, especially in cats that have received
sedative or anesthetic drugs. Analgesia is routinely
continued into the postoperative period to alleviate
pain and reduce stress. Other aspects of postoperative
management include radiography, antibiotic
theapy, bandaging, nutritional support, and physical
therapy64. The importance of good nursing care
should not be underestimated.
RADIOGRAPHY
Radiographs are obtained immediately after surgery
to confirm reduction and implant positioning.
Complications, such as the placement of implants
in joints, severe malalignment, or evidence
of inadequate stabilization may necessitate an
immediate return to the operating theater to correct
the problem. If available, intraoperative radiographs
are extremely helpful to monitor implant placement
during the procedure. Follow-up radiographs are
obtained every 3–4 weeks until the fracture is healed,
to monitor healing, check for signs of infection, and
observe for implant complications. Radiographs can
be obtained more frequently if complications
develop and additional monitoring is indicated.
ANALGESIA
Analgesic drugs are administered during recovery
from anesthesia and the cat is carefully observed for
signs of pain (see Table 8). Long-acting agents are
preferred for postoperative analgesia. For moderate to
severe pain control in the immediate postoperative
period a continuous intravenous infusion of an opioid
or a transdermal fentanyl patch can be used.
Analgesics are continued as necessary during fracture
healing, although many cats are quite comfortable
after a few days and medications can be reduced or
discontinued. NSAIDs should be used with caution in
cats. Carprofen, ketoprofen, meloxicam, and
tolfenamic acid have been shown to provide
effective short-term analgesia when administered
perioperatively to cats65.
ANTIBIOTICS
Antibiotics are not administered routinely after closed
fracture repair or after open stabilization under aseptic
conditions for procedures lasting less than 2 hours
(unless other factors dictate their use). The
prophylactic antibiotics administered during surgery
39
are usually adequate. However, for longer procedures,
or if contamination is present (or occurs during
surgery), therapeutic administration of antibiotics may
be necessary after surgery. If possible, the choice of
antibiotics is based on the results of culture and
sensitivity testing.
RESTRICTED ACTIVITY
The cat’s activity is restricted while the fracture is
healing. Although early return to limb and joint
function is beneficial, excessive loads should be
avoided. Restriction is usually achieved by confining
the cat to a small room in the house, with good
footing, where it cannot run or jump. Confinement to
a small cage may be required in cases where stability at
the fracture site is suspect. Sedation is rarely needed to
limit activity in cats. Cats with external fixators are
confined to ensure the fixator frame does not become
caught on furniture, fences, or other objects in the
environment.
PHYSICAL REHABILITATION
Postoperative physical rehabilitation is helpful to
encourage early limb function and prevent muscle
contracture66. Rehabilitation can be difficult in some
cats because of their independent nature and
reluctance to be handled during therapy67. The
procedures should be performed in a quiet room away
from loud noises and distractions. Cold compresses
are applied to the limb 3–4 times a day (10–15
minutes) for the first 24 hours after surgery. Warm
compresses are then applied several times daily for the
next week. Limited exercise and passive joint motion
are introduced gradually as the patient becomes
more comfortable. Passive range-of-motion exercises
(10 repetitions) can be performed several times daily,
along with mild massage of the muscles of the affected
limb. Controlled activities and games may also be
used to encourage limb function. NSAIDs help
reduce inflammation and pain and increase the cat’s
tolerance for physical therapy. Rehabilitation exercises
should be performed carefully so as not to cause
pain or disrupt the fixation. Aquatic therapy or
hydrotherapy can also be performed, using the same
selection criteria and protocols that are used in dogs,
but is not tolerated by all cats.
POSTTRAUMATIC OSTEOMYELITIS
Posttraumatic bacterial osteomyelitis is uncommon
in cats and usually occurs after open reduction
of fractures, treatment of open fractures, or bite
wounds. In comparison with dogs, local extension of
40

soft tissue wound infections involving the
distal extremities is a more frequent cause of
osteomyelitis. Staphylococcus sp., Streptococcus sp.,
and Escherichia coli are common isolates from
infected bones. Proteus sp., Klebsiella sp.,
Pseudomonas sp., Pasteurella sp., and anaerobes, such
as Actinomyces sp., Clostridium sp., Bacteroides sp.,
and Fusobacterium sp., are frequently isolated
from bone infections caused by bite wounds28,68.
Multiple organisms may be present. Young male cats
are overrepresented, reflecting the disproportionate
incidence of fractures and bite wounds in this section
of the cat population.
DIAGNOSIS
The diagnosis of bacterial osteomyelitis is based on
clinical signs, characteristic radiographic findings,
culture of samples collected from the site by aspirate
or biopsy, and, in some cases, blood culture. Clinical
signs of osteomyelitis may include pain, swelling,
erythema, and poor limb function. Initially, these
signs may be difficult to distinguish from early
recovery from fracture repair or an incision
complication, although an acute onset of more
severe lameness or failure of the patient to improve
as expected after fracture repair may be an indication
of infection. A persistent fever may be present in
some cats. With chronic infections, muscle atrophy
and muscle fibrosis may be observed. Eventually,
draining tracts may develop in the skin over the
infected bone.
Radiographic signs of osteomyelitis depend on
the chronicity and severity of the infection (16).
Radiographs obtained early in the disease process may
be inconclusive, as signs may be difficult to distinguish
from the normal healing process. However, as the
infection progresses, loss of the normal trabecular
pattern, bone lysis, sclerosis, and a periosteal response
separate from the healing callus may be appreciated69.
With the passage of time, coalescence of adjacent foci
of lysis leads to larger irregular areas of bone loss.
Bone resorption is most marked around implants and
at the fracture site. Eventually, sequestration of bone
may occur. Sequestered bone maintains its increased
density and sharp borders and thus appears denser
than the surrounding bone. A more radiolucent
region comprised of infected exudate usually
surrounds the sequestrum. Surrounding this is the
involucrum, comprised of new bone and fibrous tissue
laid down as the body attempts to isolate the

16

A B C D E
16 Osteomyelitis of the long bones. A Lateral radiographic view of an ulna with osteomyelitis secondary to a bite wound.
Sclerosis and a bony sequestrum are visible. B Lateral radiographic view of a stifle joint with osteomyelitis affecting the tibial
tuberosity. C Lateral radiographic view of a humerus with osteomyelitis of the proximal metaphysis and diaphysis. Note
the bony sclerosis and periosteal proliferation. D Craniocaudal radiographic view of a humerus with pyogranulomatous
osteomyelitis. Note the bony lysis and loss of the normal trabecular pattern in the proximal humerus. E Lateral radiographic
view of a tibia, with osteomyelitis secondary to a bite wound. Lysis, periosteal reaction, and sclerosis are evident in the
diaphysis and distal metaphysis.
 Management of the orthopedic trauma patient
infection. Unfortunately, radiography alone is neither
highly sensitive nor specific in the diagnosis of
osteomyelitis. Nuclear scintigraphy, although not
specific, is very sensitive and can be helpful.
If infection is suspected, confirmation should
always be sought by culture of the wound. Culture
and sensitivity testing is performed on samples
collected by deep aspirates of the infected site or
biopsy samples of bone or periosteum collected
during surgical debridement. Aspiration of the site is
performed using a 20–21 gauge needle following
aseptic surgical preparation of the skin. The sample is
placed in blood culture medium for culture and
sensitivity testing. The efficacy of this technique is
supported by a study in dogs in which its use resulted
in bacterial growth in 86% of cases. The samples
should be examined for aerobic and anaerobic
bacteria28,68,69. Cultures from draining tracts usually
isolate contaminant or opportunistic bacteria and
provide little information about the organism
affecting the bone. Blood cultures are rarely needed
but can be helpful in identifying the pathologic
organism in cats with osteomyelitis.
PREVENTION
Prevention of bacterial osteomyelitis is better than
cure and all bite wounds and abscesses should be
treated aggressively, especially in locations where there
is underlying bone. Further soft tissue trauma during
fracture repair should be minimized by appropriate
debridement and the use of an atraumatic surgical
technique. The vascularity of bone fragments should
be preserved by avoidance of periosteal stripping and
by leaving muscle attachments to bone fragments
undisturbed. Intraoperative inoculation by bacteria
occurs when there is a breach in aseptic surgical
technique. Prolonged operating time, associated with
attempted anatomic reconstruction of comminuted
fractures, increases the extent of bacterial
contamination of wounds and also has a detrimental
effect on the vitality of the soft tissues around the
fracture. Metallic implants and suture material
should be used judiciously where there is wound
contamination or infection. External fixators are
useful for the treatment of open fractures and shearing
injuries, especially those distal to the elbow and stifle
joints. Avascular bone fragments should be removed
unless they make a significant contribution to the
stability of the reconstructed fracture.
TREATMENT
Treatment of osteomyelitis requires long-term
systemic antibiotic therapy using appropriate drugs at
41
adequate dosages, debridement and lavage of the
infected site (including removal of dead bone), and
rigid stabilization of the fracture (including the
placement of cancellous graft in bone deficits).
Antimicrobial therapy
Systemic antibiotic therapy is indicated in all cats with
bacterial osteomyelitis. The selection of drugs is based
on culture and sensitivity testing.
• Gram-positive organisms cause the majority of
infections and cefazolin or amoxicillin/clavulanate
are often used pending sensitivity results.
• Metronidazole or clindamycin may be administered
in cases where anaerobic infection is identified or
suspected. Long-term or high-dose therapy with
metronidazole should be restricted to refractory
cases because of potential neurotoxicity70.
• Aminolgycoside or fluoroquinolone antibiotics
should only be used for refractory infections
caused by Gram-negative organisms, because of
the potential for toxicity.
• Fluoroquinolones are chondrotoxic in immature
cats and long-term administration should be
avoided in geriatric cats or cats with impaired renal
function because of potential retinal toxicity32.
Systemic antibiotic therapy is continued for 5–7 weeks
or until clinical and radiographic signs of active
infection have resolved. Rarely, the infected site is
re-cultured after several weeks of treatment to identify
resistant organisms that may have developed
during prolonged antibiotic therapy, particularly if
radiographic and clinical signs of infection are not
improving or worsen during the course of therapy. Cats
should be monitored carefully for complications
associated with long-term antibiotic treatment. In cases
of severe chronic osteomyelitis, local antibiotic therapy
may be used in conjunction with systemic treatment by
placing polymethylmethacrylate beads impregnated
with gentamicin or tobramycin into the infected site37.
Debridement and lavage
All necrotic tissues are surgically excised. In chronic
osteomyelitis, dead fragments of bone (sequestra) may
be present and are often surrounded by a pocket of
infected fluid and a layer of fibrous tissue and new
bone (involucrum). All sequestra are removed and the
involucrum is debrided to healthy, bleeding bone.
Previously placed orthopedic implants that do not
contribute significantly to fracture stability are also
removed. Stable implants may be left in place until
healing is complete. The wound is lavaged with sterile
saline or Ringer’s solution.
42
Fracture stabilization
Infected fractures will generally heal if they are stable
and have adequate blood supply. If the fracture has
not been previously stabilized (or if previously placed
implants were removed during debridement), rigid
fixation is applied. In most cases, an external fixator is
used since it can be applied with minimal disruption to
the fracture site’s blood supply and the transfixation
pins are placed remote from the infected fracture site.
Plates are occasionally used because they provide rigid
fixation for the long period of time required for
infected bone to heal. However, the extensive soft
tissue dissection required to position the plate
properly can be a disadvantage when stabilizing
infected fractures. Intramedullary pins and cerclage
wires are not recommended for stabilizing infected
fractures.
Once the fracture is stabilized, cancellous bone
graft is placed in all bone defects. Alternatively,
grafting can be delayed until the initial inflammation
and suppuration is resolved71. The wound or incision
made to place implants can be closed primarily (after
thorough debridement and lavage) in most cases. In
more severe cases, open wound management or
closure of the incision over a drain may be
preferred71. The orthopedic implants are removed
once the fracture is healed, since they may act as a
nidus for infection, by harboring bacteria, and prevent
complete resolution of the osteomyelitis. Culturing
from the implants at the time of removal may help
determine whether there is a need for longer
antimicrobial therapy.
PROGNOSIS
The prognosis for osteomyelitis is variable depending
on the stage and extent of the infection. Low-grade
osteomyelitis may be resolved with appropriate
antibiotic therapy and delayed removal of implants.
More severe and extensive infection carries a much
more guarded prognosis and may require prolonged
and expensive treatment with an uncertain outcome.
Such cases may require multiple surgical procedures for
removal of sequestra, fracture stabilization, cancellous
bone grafting, and eventual removal of all metallic
implants. Even if the infection can be resolved, the
legacy of infection and chronic disuse may be poor
limb function associated with muscle atrophy and
fibrosis, soft tissue adhesions, and joint stiffness.

CHAPTER 4
FRACTURE CLASSIFICATION,
DECISION MAKING, AND
BONE HEALING
FRACTURE CLASSIFICATION
Numerous systems have been devised to classify
fractures, including cause, anatomic location, severity,
fracture configuration, and contamination1. In most
cases, more than one classification system is used to
describe fully a given fracture. Accurate and complete
description of a fracture provides useful information
when selecting repair options and facilitates
communication among clinicians.
CAUSE
Traumatic (direct or indirect)
Direct trauma to a bone is the most common cause of
fractures and frequently occurs when the cat is hit by
an automobile or falls from a significant height.
Indirect trauma to bone may lead to fractures by
transmitting force through bones or surrounding
muscles, tendons, and ligaments. Femoral neck
fractures and avulsion fractures of the calcaneus are
A B
17 Salter–Harris classification of growth plate injuries.
A Type I involves the growth plate only.
B Type II involves the growth plate and the metaphysis.
C Type III involves the growth plate and the epiphysis.
D Type IV involves the growth plate, metaphysis, and epiphysis.
E Type V is a compression injury of the growth plate.
43
examples of fractures often caused by indirect trauma.
Fractures caused by repeated low-grade trauma (stress
fractures) are uncommon in cats.
Pathologic
Pathologic fractures occur when a disease process
weakens the bone. Causes may include neoplasia,
infection, and nutritional or metabolic bone diseases.
ANATOMIC LOCATION
The location of a fracture in a long bone may be
described as diaphyseal, metaphyseal, or epiphyseal.
Other anatomic nomenclature is often used to describe
specific fractures more completely, including terms
such as condylar, supracondylar, subtrochanteric, and
articular.
Physeal fractures involve the growth plate in
immature animals and are described using the
Salter–Harris classification system (17)2.
17
C D E
44
SEVERITY OF FRACTURE
Incomplete
The fracture involves only one cortex of the bone
and displacement is minimal (e.g. fissure fractures that
disrupt a single cortex and often course longitudinally
in a bone) (18A).
Complete
The fracture disrupts the entire circumference of
the bone and may lead to significant displacement
(18B). Displacement of a fracture is described based
on how the distal fragment moves relative to the
proximal fragment.
Comminuted
Multiple fragments are present (18C). Comminuted
fractures can be further characterized by the number
of fragments and whether or not reduction of
the fracture results in contact between the primary
proximal and distal ends of the bone.
Segmental
There are two or more separate fractures in the bone
and the fractures lines do not connect (18D).
18
A B C D
18 Fracture classification based on the severity of bone
disruption. A Incomplete. B Complete. C Comminuted.
D Segmental.
FRACTURE CONFIGURATION
Transverse
The length of the fracture line is approximately equal
to the diameter of the bone (19A).
Short oblique
The length of the fracture line is less than two times
the diameter of the bone (19B).
Long oblique
The length of the fracture line is greater than two
times the diameter of the bone (19C).
Spiral
This is a long oblique fracture in which the fracture
line curves around the diaphysis (19D).
Impacted
The fracture fragments are compressed together.
Avulsion
The origin or insertion site of a tendon or ligament is
pulled from its parent bone (19E). The greater
trochanter, tibial tuberosity, calcaneus, and olecranon
are sites where avulsion fractures occur in cats.
CONTAMINATION
Closed fracture
No communication exists between the exterior and
the fracture site. The skin is intact, although
contusion may be present.
Open fracture
A communication exists between the exterior and the
fracture site3.
• Type I: a small puncture (<1 cm) is present in the
skin. The puncture occurs from the inside when
a fragment of bone briefly penetrates the skin.
• Type II: a wound (>1 cm) is present and
communicates with the fracture site. The wound
is a result of external trauma. Contusion of the
surrounding soft tissues is common.
• Type III: an extensive wound is present and is
caused by high-energy external trauma. Soft
tissues surrounding the fracture site are severely
damaged or absent.
• Type IIIa: significant soft tissue injury is
present, but adequate tissue remains to allow
closure of the wound.
• Type IIIb: extensive soft tissue injury with
insufficient skin and soft tissue remaining to
allow primary wound closure (i.e. degloving
injuries).
 Fracture classification, decision making, and bone healing
45

• Type IIIc: extensive soft tissue injury with FRACTURE DECISION MAKING
compromised vascular supply to the distal Fractures are diagnosed based on the cat’s history,
extremity. Loss of the limb may occur physical examination findings, and radiographs of the
without immediate intervention. affected limb. In many cases, fracture stabilization is
delayed to allow treatment of trauma-related injuries,
AO VET FRACTURE CLASSIFICATION SYSTEM such as shock, hypothermia, cachexia, external
The AO Vet has adopted a numerical fracture wounds or hemorrhage, thoracic injuries, abdominal
classification system modeled after the one used by injuries, neurologic injuries, and concurrent ortho-
the AO/ASIF for computerized documentation of pedic injuries5,6 (see Chapter 3).
human fractures4. The long bones are referred to by Two orthogonal radiographic views of the
number: fractured limb are obtained to document the type and
• Humerus = 1. location of the fracture and gather information on
• Radius/ulna = 2. feasible repair options. Sedation or short-duration
• Femur = 3. general anesthesia may be required to obtain
• Tibia/fibula = 4. radiographs without causing pain. If necessary,
radiography should be delayed until the cat is stable.
The fracture location is also referred to by number: In some instances, a single radiographic view of the
• Proximal = 1. fracture site can be obtained without sedation and can
• Shaft = 2. be used to confirm the fracture location, help
• Distal = 3. determine appropriate repair options, and provide the
owner with an estimated cost for treatment. The
Fracture severity is classified as follows: second view is then obtained prior to treatment.
• A = simple. Oblique views are occasionally helpful to identify the
• B = wedges. presence of articular fractures or to further delineate
• C = complex fracture configuration.
• Each further graded from 1–3 based on the Fractures occur when intrinsic or extrinsic forces
degree of fragmentation. are applied that exceed the material and structural
properties of the bone. The configuration of the
This classification system is used in some veterinary fracture depends on the magnitude, speed, and
literature to classify fractures and in reported data on direction of the force applied7,8. The bone’s inherent
fracture treatment methods. strength and any loads applied to the bone at the time

19 Common fracture configurations. 19

A Transverse.
B short oblique.
C Long oblique.
D Spiral.
E Avulsion.

A B C D E
46

of injury also influence the fracture configuration.
Compressive, tensile, bending, torsional, and shear
forces may act alone or in combination to disrupt the
support function of the bone (i.e. cause fracturing),
and may cause instability once the fracture is
repaired (20)7,8.
Successful fracture repair requires knowledge
of regional anatomy (including blood supply), an
understanding of basic bone healing physiology,
information on the fracture type and the forces acting
at the fracture site, and familiarization with the
advantages and limitations of all available repair
methods8,9. Each repair method chosen must provide
adequate stabilization while preserving blood supply
and soft tissue attachments to the bone. When selecting
the most appropriate repair method for a given fracture,
the surgeon must understand the ability of each
available fixation technique to neutralize disruptive
forces (Table 11). Bone plates, external fixators, and
interlocking nails can counteract all disruptive forces
when properly applied. Intramedullary pins do not
adequately control rotational forces when used alone,
so cerclage wires or an external fixator should be added
to provide adequate stabilization. External coaptation

20 20 Forces acting on bone.

A Compression (collapse
and overriding).
B Tension(distraction).
C Bending (angulation).
D Torsion (rotation).
E Shear (collapse and
overriding).

A B C D E

TABLE 11 FRACTURE REPAIR METHODS AND CONTROL OF DISRUPTIVE FORCES.

Disruptive forces acting on the fracture site
Fixation method Bending Shear Torsion Compression Tension
External coaptation (casts/splints) + – +/– – –
Single intramedullary pin + +/– – – –
Multiple intramedullary pins (stacked pins) + +/– +/– – –
Full cerclage wire alone – + + – –
Hemicerclage wire alone – + + – +/–
External fixators (linear and circular) + + + + +
Bone plates + + + + +
Lag screws alone – – – – –
Plate rod fixation + + + + +
Interlocking nail + + + + +
+ = good control of the disruptive force; +/– = partial control; – = poor control
 Fracture classification, decision making, and bone healing
47

devices may reduce forces applied to the fracture site
(depending on the fracture location and configuration),
but may not completely neutralize disruptive forces9. In
comminuted fractures, disruptive forces acting at
the fracture site may be quite large, particularly
if weight-bearing load is not shared between the bone
and the implants after fracture reduction. Fracture
configuration, available implants and equipment,
surgeon preference and experience, expense, and owner
compliance with postoperative care procedures are also
considered when selecting an appropriate repair
method.
FRACTURE HEALING
Bone healing is affected by mechanical factors
(reduction, stability) and biological factors (blood
supply, fracture location, soft tissue injury)10,11. Bone
healing can be classified into a number of types.
INDIRECT BONE HEALING
Indirect healing (secondary healing or classical healing)
of cortical bone is by callus formation and occurs when
small gaps or instability exist at the fracture site (21).
The bridging callus exists as medullary callus,
intercortical callus, and periosteal callus. Typically,

21

Hematoma

Granulation Connective
tissue tissue

A B C

Fibrocartilage
Haversian
remodeling

Woven
Cancellous bone
bone

D E F

21 Indirect bone healing. Fracture healing occurs by progressive bridging of the fracture gap by more strain-tolerant tissues.
A Hematoma. B Granulation tissue. C Connective fibrous tissue. D Fibrocartilage, which mineralizes to form cancellous
bone. E Woven bone. F Cortical bone forms by Haversian remodeling and the callus is eliminated.
48

indirect bone healing occurs when fractures are
immobilized by external coaptation.
The fracture gap is first filled with a hematoma.
Pluripotential mesenchymal cells in the region then
proliferate to form a ‘fracture callus’, comprised
sequentially of granulation tissue, fibrous connective
tissue, cartilage, mineralized cartilage, woven bone,
lamellar bone, and, finally, cortical bone. This process
is regulated by the amount of interfragmentary strain
placed on tissues in the fracture gap and by numerous
cellular mediators, chemoattractants, and growth
factors12,13. Repair tissues within the fracture gap are
subjected to interfragmentary strain when motion
occurs at the fracture site13. Strain is defined as the
ratio between the change in gap width to the total gap
width during this motion. Various tissue types can
withstand differing levels of strain: fibrous tissue
tolerates up to 20% strain, cartilage tolerates up to
10% strain, and bone tolerates up to 2% strain7,11.
Thus, the level of interfragmentary strain determines
the tissue types that may form within the gap. Strain-
tolerant tissues, like granulation tissue and fibrous
tissue, will survive in a gap under conditions of high
strain, while bone will not. Thus, strain-tolerant
tissues initially form in fracture gaps where motion
exists and strain is high. As interfragmentary strain is
reduced by increasing callus size or strength (or by
fracture fixation), less strain-tolerant tissues, like
cartilage and bone, begin to form.
Clinically, when a fracture is well reduced (small
gap), it is essential to provide rigid stabilization to
prevent motion and high strain levels that may prevent
bone formation in the gap. Excessive strain can lead to
tissue rupture and delayed healing. When larger gaps
are present between fragments, strain is distributed
over a larger area, thus reducing the strain on
individual cells. If rigid fixation is impossible due to
the fracture configuration, a bigger fracture gap is
preferred to distribute strain over a larger area and
reduce strain on each cell within the gap. The
resorption of fragment ends that occurs in fractures
that are reduced, but not completely stable, has the
effect of reducing interfragmentary strain. As the
callus matures, there is gradual replacement of each
tissue type by progressively stiffer and stronger tissue
until bony union is completed. In unstable fractures, a
large callus forms to provide early stability to the
fracture site. The potential drawback of indirect bone
healing is the slow return to function that may be
associated with instability of the fragments during the
healing process; this predisposes to the development
of fracture disease (muscle atrophy, joint stiffness,
disuse osteopenia, soft tissue adhesions).
DIRECT BONE HEALING
Direct healing (primary healing) of cortical bone
occurs when bone ends are in contact (<0.1 mm gap)
and under compression, as may be achieved with bone
plating (22). Internal remodeling of the Haversian
systems unites the apposed cortical ends (rather than
callus formation). Metaphyseal fractures involving
cancellous bone heal by increased osteoblastic activity

22

<0.1mm gap <1.0 mm gap

A B

22 Direct bone healing.

A Contact healing occurs when the bone ends are compressed together and rigidly fixed (<0.1 mm gap). Healing occurs
by Haversian remodeling.
B Gap healing occurs when the bone ends are apposed with a <1.0 mm gap. The gap fills with lamellar bone oriented
perpendicular to the longitudinal axis, which then undergoes Haversian remodeling to restore normal bone architecture.
 Fracture classification, decision making, and bone healing
49

and the deposition of new bone on existing bony 23

trabeculae. Gap healing is a type of direct healing
that occurs under similar prerequisite conditions to
contact healing but where the fractured bone
fragments are separated (<1.0 mm gap). The gaps are
filled with lamellar bone oriented perpendicular to the
longitudinal axis, which is then integrated into the
normal architecture of the bone during the process of
remodeling.
Although direct bone union was once considered
to be the ultimate goal of fracture repair, it is now
recognized that it is not a panacea. There are, in
fact, a number of disadvantages associated with this
approach. Rigid stabilization and compression of
fractures requires an invasive surgical procedure for
the application of a plate, with a consequent
disruption of the blood supply and soft tissue
envelope. Bone strength is regained very slowly with
direct healing, so implants need to be left in place for
a long time and the rigid stability they provide may
protect the bone from stress and lead to osteopenia. 23 Craniocaudal radiograph of a
The main advantage lies in an earlier return to tibial fracture stabilized with an
function since the bone fragments are stable in external fixator to achieve biological
compression. The limb can therefore be loaded while fixation and bridging osteosynthesis.
the bone is healing, thus fracture disease is avoided.
Direct bone healing should be the goal when dealing disturbance to the fracture hematoma, the soft tissue
with intraarticular fractures and simple transverse envelope, and the blood supply to the bone. Thus
fractures of long bones where compression can be interfragmentary strain is reduced and the fracture is
achieved readily by means of a plate. encouraged to heal in an environment of relative
stability where there is sufficient micromotion to
BRIDGING OSTEOSYNTHESIS stimulate bone callus formation.
The concept of bridging osteosynthesis has arisen in Stability can be achieved by application of an
an attempt to harness the rapid bone healing that external fixator in a closed fashion or by using a
occurs with indirect bone healing whilst reducing the minimally invasive (or biological) ‘open but do not
risk of fracture disease (23)14. Bridging osteosynthesis touch’ approach in which the fracture site is inspected
is most applicable to comminuted mid-diaphyseal for reduction of the main fragments without
long bone fractures where there are multiple small interfering with the intermediate fragments. A plate
fragments that are not amenable to reconstruction. (with or without an intramedullary pin) or an
The two ends of a fractured bone are immobilized in interlocking nail can also be applied using the same
their correct anatomic positions relative to one principles. Plates specifically designed for this purpose
another, without stabilization of the intervening generally have a central solid section to avoid placing
fragments. Implants are applied with minimal empty screw holes over the fracture site.
50
CHAPTER 5
INSTRUMENTS
IMPLANTS
The armamentarium of the feline orthopedic surgeon
must include a range of instruments and implants that
have been designed to be suitable for use on the bones
of the cat. Injuries to the distal extremities, in
particular, pose a challenge owing to the small size of
the bones, which may compromise both implant
application and implant security. It is essential that a
range of the correct sizes and types of implants is
available if adequate implant security is to be achieved,
whilst minimizing the risk of iatrogenic fracture.
INSTRUMENTS
Fracture repair requires the correct instrumentation to
approach and surgically expose fractured bone. In
addition, various instruments are required to achieve
and maintain fracture reduction before implants can
be applied.
Cat bone cortices are relatively thin and can easily
be fractured or fissured when being manipulated1.
Bone holding forceps should be the correct size and
must be designed to be able to grip without crushing
(24, 25). Similarly, bone-cutting instruments should
be sharp to avoid inadvertent crushing of bone. Many
of the instruments designed specifically for dogs or
adapted from human surgery are too large and
cumbersome and are unsuitable.
A range of small instruments should be included
24 25
AND
in the standard instrument pack for fracture
repair and joint surgery including retractors,
rongeurs, bone-cutting forceps, bone-holding
forceps, Hohmann retractors, and periosteal
elevators. A minimum of two pairs of small self-
retaining Gelpi retractors is invaluable in the surgical
approaches to most bones and joints. Small, serrated
bone-holding forceps, small pointed fragment or
reduction forceps, and mini Kern bone-holding
forceps are ideal for the manipulation of feline long
bones and small bone fragments. In addition,
instrument sets are required for the application of
intramedullary pins, cerclage wire, 2.7 mm, 2.0 mm,
and 1.5 mm plates and screws, external fixators, and
interlocking nails, if available.
A power drill is needed to drill a hole in the
cortical bone to allow screw insertion. Air-powered,
electrical, and battery-powered drills are available.
The drill must be properly sterilized using steam or
gas, or it may be placed into a sterile shroud to
prevent contamination of the surgical site. Drill bits,
drill guides, cortical taps, a measuring device to
determine the appropriate screw length, instruments
to contour the plate to the bone surface, and a screw
driver are also required. Many of these instruments are
specific for the size of screw and plate being used.
24 Very small fragment (reduction)
forceps with step down tips
(Veterinary Instrumentation). The
forceps are used to hold small bone
fragments in position while the
permanent fixation is being applied.
25 Small serrated bone holding
forceps (Veterinary Instrumentation).
The tips are sharp and may be used as
small fragment forceps.
 Instruments and implants
51

IMPLANTS longitudinal fins to increase rotational stability

A variety of implants is available for use in cats.
Implants are commonly made of stainless steel or
titanium. Details of those that are appropriate are
given below. A more detailed description of their use
is given in Chapter 6.
INTRAMEDULLARY PINS
Intramedullary or Steinmann pins are available from
various manufacturers and are usually 300 mm in
length. Pin diameters from 1.6 mm, up to a maximum
of 4.8 mm, are suitable for fracture repair in cats. Pins
with a smooth shaft and a trocar point at each end are
preferred.
TRILAM NAIL
The Trilam nail is a new type of intramedullary pin
that has been modified by the addition of three
26
(Rotec Medizintechnik) (26). The smaller diameter
nails (3 mm, 4 mm, and 5 mm outer diameter) are
suitable for repair of diaphyseal and metaphyseal
fractures of the humerus, femur, and tibia. The
results of fracture repair using the technique has
been described in a large series of cases, which
included 62 cats2.
KIRSCHNER WIRES, ARTHRODESIS WIRES, AND
SMALL FRAGMENT PINS
Kirschner wires and arthrodesis wires are like small,
flexible intramedullary pins. They are 120 mm long
and are available in 0.9 mm, 1.1 mm, 1.4 mm,
1.6 mm, and 2.0 mm diameter. Kirschner wires have
a bayonet point at one end and a trocar point at the
other, whereas arthrodesis wires have a trocar point
at each end. Threaded small fragment pins are
2.0 mm in diameter and have a threaded portion
ranging from 5–20 mm in length (Veterinary
Instrumentation). A small fragment pin washer is
available, which can be used to give the pin a screw-
like function.

ORTHOPEDIC WIRE
Orthopedic wire is available as a spool or with a
preformed loop at one end in a wide range of
diameters. Wire is used for cerclage and
hemicerclage, for interfragmentary fixation, and as a
tension band. The ideal size wire for most
applications in the cat is 0.8 mm (20 American wire
gauge [AWG]) but a range of diameters between
0.5 mm and 1.0 mm (24–18 AWG) should be
available. Gauge sizes are not universal since there
are two different systems of measurement in
common usage (Table 12).
26 Trilam nail. Instruments and implants set (Rotec
Medizintechnik).

TABLE 12 THE DIAMETER AND RESPECTIVE STRENGTHS OF WIRE USED IN CATS.

Diameter (mm) Gauge AWG Gauge SWG Relative tensile strength*
1.0 18 19 1.0
0.8 20 21 0.64
0.6 22 23 0.36
0.5 24 25 0.25

AWG = American wire gauge

SWG = Imperial standard wire gauge
* The tensile strengths are given in a ratio that compares the other sizes to 1.0 mm diameter wire.
52

BONE PLATES
Plates that are suitable for use in the cat include round
hole and dynamic compression plates (DCPs), which
are available to accommodate 2.7 mm, 2.0 mm, and
1.5 mm screw sizes (27). The Mini Bone Plating Set
and Small Bone Plating Set (Veterinary Orthopedic
Implants Inc.) provide plates that take screws ranging
from 1.5–3.5 mm and includes small DCPs and
cuttable plates. The Mini Fragment Instrument and
Titanium Implant Set (Synthes) includes 1.5 mm, 2.0
mm, and 2.7 mm straight and T plates. Lengthening
(Synthes) and biological healing plates (Veterinary
Instrumentation) are produced in 2.0mm and 2.7mm
versions, and 1.5 mm and 2.0 mm mini plates are
available, in a variety of shapes, including T, L, and
acetabular. Biological healing and lengthening plates
have a central solid section to avoid placing empty
screw holes over the fracture site; these are available in
4 sizes that are suitable for cats (2.0 mm/8 hole and
2.7 mm/6, 7, 8 hole (Veterinary Instrumentation)
(28). These plates can be used for nonreconstructable
mid-shaft long bone fractures. For certain
metaphyseal fractures it may only be possible to
achieve stable fixation with a plate by customizing the
plate. Conversion of the veterinary cuttable plate
(VCP) into a hook plate for use in cats has been
described3. Human maxillofacial mini plates have
been used to stabilize fractures of small bones in cats4.
Similarly bone plates may be applied to very small
bones using the human Modular Hand System
(Synthes). These plates are available as DCPs (straight
and T plates) in 1.0 mm, 1.3 mm, 1.5 mm, 2.0 mm,
and 2.4 mm sizes5. Limited-contact dynamic
compression plates (LC-DCPs) that accommodate
2.4 mm screws are also available and are useful for
repair of long bone fractures (Synthes).
buttress fashion by using the drill guide with the
arrow pointing away from the fracture line. When
using DCPs in buttress fashion, plate holes
positioned over the fracture gap must be left empty
and plate failure can occur at the empty holes.
A graft is placed in the defect to speed healing and
the cat’s activity is restricted to prevent premature
failure through empty screw holes.
A 1.5 mm/2.0 mm hybrid DCP has recently
been introduced for performing carpal arthrodesis
(Veterinary Instrumentation). The plate allows for the
placement of 2.0 mm screws in the radius and 1.5 mm
screws in the metacarpal bone, and it is also narrower
and thinner distally.
Reconstruction plates
Reconstruction plates have small notches on each
side of the plate between the oval screw holes (29).
They are available for use with 2.7 mm screws and are
quite easily contoured to fit the bone surface. They
are most commonly used for stabilization of pelvic
fractures.
27

Dynamic compression plates 27 Bone plates commonly used in cats: 2.7 mm DCP,
DCPs accommodating 1.5 mm screws (Veterinary mini-dynamic compression plate, T plates, L plates,
Orthopedic Implants Inc.) and 2.0 mm and 2.7 mm tubular plate, acetabular plate.
bone screws (Synthes) are often used in feline long
bone fractures. They are available in various lengths
and may be applied in neutralization, buttress, or
compression function. To create compression, the 28
plate screw is placed eccentrically in the oval screw
hole, causing the plate to slide as the screw is
tightened. When DCPs are used in buttress function
to span defects in the bone, a drill sleeve is used
(rather than the DCP drill guide) to position the
hole near the steep wall of the plate hole (as opposed
to the neutral or compression position). This rigidly 28 A 2.0 mm biological healing plate (Veterinary
fixes the plate and screw to minimize collapse of the Instrumentation) used to repair a simulated femoral
fracture gap. LC-DCPs may also be applied in fracture.
 Instruments and implants
53

Tubular plates Veterinary cuttable plates (VCPs)

One-third tubular plates with 2.7 mm bone screws VCPs are a unique and versatile specialty plate
are useful in the repair of many cat long bone indicated for repair of long bone fractures in
fractures1. Tubular plates are relatively thin, which cats7–9. They are available in numerous different
facilitates closure of the soft tissues over the plate, sizes, can be custom cut to the appropriate length
particularly when the plate is placed on the distal at the surgery table, and accommodate either
extremities. However, they have relatively high 2.7/2.0 mm screws or 2.0/1.5 mm screws (30)
torsional and bending strengths because of their
partial tubular shape. They can be flattened
somewhat, if necessary, to conform to the bone
surface; however, the partial tubular shape should be
preserved over the fracture site, to maintain
mechanical strength. The screw holes in the plate are
further apart than in most other bone plates, so they
can be used to span defects without placing empty
screw holes over the fracture site.
29
Mini plates
Mini plates are designed for use with 1.5 mm and
2.0 mm cortical screws6. Several types of mini plates
are available, including mini DCPs, round-hole plates
of various lengths, T plates, L plates (angled mini
plates), acetabular plates, and cuttable T plates
(Veterinary Orthopedic Implants Inc.; Synthes). The 29 A 2.7 mm reconstruction plate.
mini T plates and L plates are designed for use in
metaphyseal fractures of cats where only a small
epiphyseal fragment is present. The use of these plates
allows the surgeon to place two screws into very small 30
bone fragments. Specialized handles are used to hold
the smaller drill bits, taps, and screwdriver used to
insert the 1.5 mm and 2.0 mm screws. The specialized
screwdriver has a +-shaped tip. Care is taken while
drilling, tapping, and inserting these small screws to
prevent stripping (in most cases, the holes are drilled
and tapped by hand rather than with power tools).
Traditional and self-tapping screws are available in
both titanium and stainless steel.

AO/ASIF maxillofacial mini plates

Maxillofacial mini plates (Synthes) are specially A
designed, very small titanium plates available in a
variety of shapes and lengths. The plates are only
0.7 mm thick. Screws used with this system have a
thread diameter of only 1 mm (core diameter
0.7 mm) and are self-tapping. These plates are too
small for long bone fixation, but they have been used
successfully to stabilize mandible and metatarsal
fractures in cats4. B
30 Veterinary cuttable plates (Synthes).
A Large cuttable plate (top) that accommodates 2.7 mm
or 2.0 mm screws and small cuttable plate (bottom) that
accommodates 2.0 mm or 1.5 mm screws.
B Two cuttable plates stacked to increase stiffness.
54

(Table 13). The versatility of VCPs provides several
advantages when repairing fractures in cats. While
other small bone plates accepting 1.5 mm or 2.0 mm
screws are often too short or too weak to stabilize
long bone fractures, the VCP can be custom cut to
achieve the proper plate length. Regular bone plates
accepting 2.7 mm screws are often too thick or
require too large a screw hole for repair of small bone
fragments; the VCP accepts various screw sizes.
Additionally, the VCP has more screw holes per unit
length of plate, allowing the placement of more
screws in a small bone fragment than would be
possible with a 2.7 mm plate.
Another advantage of VCPs is that they can
be ‘stacked’ to achieve a variety of thicknesses
(1.0–3.0 mm for Synthes plates) and strengths (30).
This is particularly important when VCPs are used in
buttress fashion9. Mechanical testing of individual
and stacked cuttable plates found them to be more
resistant to bending than mini plates and 2.0 mm
DCPs, although they are still weaker than 2.7 mm
plates10. When the plates are stacked, they should be
contoured simultaneously to ensure the holes remain
aligned. The smaller plate then dictates the proper
screw size. Stacking plates of different lengths can also
be used to alter the rigidity of the fixation. The thicker
or longer plate is placed on the bone and the shorter or
thinner plate is stacked on top. This method gradually
transmits load from the implants to the bone at the
plate ends. The cuttable malleable plate is a notched
version of the VCP that is similar to the reconstruction
plate (Veterinary Instrumentation). This plate can be
readily contoured to irregularly shaped bones in the cat.
BONE SCREWS
Bone screws are made of stainless steel or titanium and
consist of a head, a shank, and the threads. Nonself-
tapping screws, 1.5 mm, 2.0 mm, 2.4 mm, and 2.7 mm
diameter, are most often used in cats and they are
available in many lengths. Screws with self-tapping flutes
have recently become available for use with the same
instrumentation as the nonself-tapping screws. The use
of self-tapping screws is likely to become commonplace
in the future.
Cortical screws are designed to maximize holding
in rigid cortical bone and have a thick shaft with many
small threads per unit length. Cancellous screws have a
wider thread pitch and provide holding power in
trabecular bone. The appropriate screw size is selected
based on the plate being applied and the size of the
bone. Screws are usually inserted by first drilling a hole
in the bone the same size as the shank of the screw.

TABLE 13 CUTTABLE PLATES FOR USE IN CATS.

Plate type Plate width Plate thickness Screws accepted Initial plate length
(mm) (mm) (mm) (number of holes)
Synthes
7.0 1.0 1.5/2.0 50
7.0 1.5 2.0/2.7 50
Veterinary Orthopedic Implants Inc.
3.8 0.8/1.0 1.5 20
5.0 1.0 2.0 20
5.0 1.5 1.5/2.0 25
6.5 1.8 2.0/2.7 25/40
7.0 1.0 1.5/2.0 50
7.0 1.5 2.0/2.7 50
Veterinary Instrumentation
5.0 1.4 1.5/2.0 30
6.0 2.0 2.0/2.7 24
Securos Veterinary Orthopedics
5.0 1.2 1.5/2.0 20
5.0 1.2 2.0/2.7 20
 Instruments and implants
The depth of the hole is measured to determine the
proper screw length. A tap is then passed through
the drill hole to cut threads into the bone matching the
threads on the screw. The correct diameter drill
bit and tap are used to ensure the screw is tight
(Tables 14, 15). The screw is then inserted and tight-
ened with the screwdriver. Self-tapping screws cut
threads in the bone as they are inserted and do not
require the hole to be pretapped.
EXTERNAL SKELETAL FIXATORS
Transfixation pins penetrate the bone, stabilize
fragments, and attach to the external frame
(connecting bars). The diameter of transfixation pins
used for linear external skeletal fixation is limited by
the small size of the bones. It is generally accepted
that there is a risk of iatrogenic fracture if the diameter
of the pin exceeds 25–30% of the diameter of the
bone. Small diameter pins reduce the risk of iatrogenic
fracture but there is a trade off in terms of reduced
frame strength. Pins 1.2–2.0 mm in diameter are most
often used in cats. Smooth pins, end-threaded pins,
and centrally threaded pins are available (31).
Threaded pins may have either a negative or
a positive (enhanced) profile11–15. Negative profile
pins are those in which the threads are cut into the
pin surface. The junction between the smooth and
threaded portions of pin is a weak area susceptible
to breaking. Ellis pins have a negative profile thread
at the tip of the pin. This tip is inserted into the
transcortex (second cortex) such that the junction
between the smooth and thread portions of the pin
TABLE 14 DRILL BIT AND TAP SELECTION FOR STANDARD CORTICAL SCREWS (HEXAGONAL HEAD)*.
1.5 mm cortical screws
Drill bit diameter – thread hole 1.1 mm
Tap diameter 1.5 mm
Drill bit diameter – glide hole 1.5 mm
TABLE 15 DRILL BIT AND TAP SELECTION FOR CORTICAL SCREWS (CRUCIFORM HEAD)*.
1.0 mm
Drill bit diameter – thread hole 0.8 mm
Tap diameter – 1.3 mm+
Drill bit diameter – glide hole 1.0 mm
+ For hard cortical or cancellous bone
* Synthes
55
is protected within the medullary cavity. Positive
profile pins are those in which the threads are added
to the shank, thus increasing the diameter of the
pin. Positive profile pins have significantly greater
holding power in bone and their use can help
prevent premature pin loosening11,13,14.
The size of pin most suitable for the cat has
a shank diameter of 2.0 mm with a thread profile
designed for cortical bone. These pins are used with
the mini (IMEX Veterinary Inc.) or small (Securos
Veterinary Orthopedics and Kirschner–Ehmer) fixa-
tor system. Because of their larger diameter, the use
of these positive profile pins is sometimes limited to
the metaphyseal regions of the long bones in adult
cats16–18. For kittens and for the small bones of the
31
31 Transfixation pins used for external fixation: (from top
to bottom) acrylic half pins, negative profile end-threaded
pin (Ellis pin), positive profile centrally-threaded pin,
positive profile end-threaded pin, smooth pin.
2.0 mm cortical screws 2.7 mm cortical screws
1.5 mm 2.0 mm
2.0 mm 2.7 mm
2.0 mm 2.7 mm
1.3 mm 2.4 mm
1.0 mm 1.8 mm
2.4 mm+
1.3 mm 2.4 mm
56
distal extremities, smaller diameter pins must be used
to avoid iatrogenic fracture. Small positive profile,
usually end-threaded pins are preferred for this
purpose. These are available as Miniature Interface™
fixation half pins (IMEX Veterinary Inc.) or as part of
the Small External Skeletal Fixator System (Securos
Veterinary Orthopedics). Miniature Interface™
fixation half pins are designed for use with acrylic
frames and have a central roughened area on the pin
shank to enhance acrylic grip. These pins are
available in a range of diameters (0.9 mm, 1.2 mm,
1.6 mm, 2.0 mm, and 2.4 mm). They have a smaller
diameter thread profile than the standard
transfixation pins.
Predrilling is recommended when inserting positive
profile pins using a drill bit a size smaller than the
shank of the pin (Table 16). Smooth pins (Kirschner
wires or arthrodesis wires) are available in diameters
including 0.9 mm, 1.1 mm, 1.4 mm, and 1.6 mm, and
are commonly used as transfixation pins, but they are
not ideal. In many cases, a combination of smooth and
threaded pins is used to improve holding power while
reducing cost. Trocar and chisel point pins are the
most frequently used to repair fractures in cats.
A circular external fixator is now available in a size
which is suitable for use in cats with fractures or limb
deformities. The Miniature Circular External Fixator
(IMEX Veterinary Inc.) provides 35 mm rings and
accommodates 0.9 mm and 1.1 mm Kirschner wires
TABLE 16 DRILL BIT SELECTION FOR IMEX
VETERINARY INC. POSITIVE PROFILE
TRANSFIXATION PINS.
Shank Thread ^Drill bit
diameter (mm) diameter (mm) diameter (mm)
0.9* 1.2 - Femoral diaphysis
1.2* 1.4 1.0 or 1.1
1.6* 1.8 1.5
2.0* 2.3 1.5
2.0 2.5 2.0
2.4* 2.9 2.0
2.4 3.2 2.3
* Miniature Interface fixation half pins suitable for use
with acrylic frames
^ Recommended drill bit diameter for predrilling
or arthrodesis wires and 1.0 mm stopper wires
(IMEX Veterinary Inc.). It can be used on its own or
as a hybrid device in combination with components
from a linear fixator.
Transarticular external skeletal fixation is the
temporary placement of a frame across a joint. The
addition of a hinge (Hofmann s.r.l.) to form a hinged
transarticular external skeletal fixator may avoid many
of the detrimental effects of prolonged joint
immobilization by allowing joint motion and early
weight bearing19.
Recommended pin diameters for adult cats of
average lean body weight (4–5 kg) are given
(Table 17). The metaphyseal regions of some long
bones (the proximal humerus and tibia and the
proximal and distal femur) may accommodate larger
diameter pins. Pin diameters should always be assessed
from preoperative radiographs and size selection
adjusted accordingly. Pins with a slightly larger
diameter shank can be used if they are smooth or have
a negative thread profile. Larger diameter pins may
also be used, with less risk of fracture where the pins
are introduced into the metabones because the stress
is distributed through multiple bones. The metatarsals
are larger than the metacarpals and can, therefore,
accommodate larger pins. Smaller transfixation pins
are used if external fixation is used in combination
with an intramedullary pin, for femoral, humeral, and
tibial fractures, to allow space for the pin.
TABLE 17 RECOMMENDED POSITIVE PROFILE
TRANSFIXATION PIN SHANK DIAMETERS FOR
LINEAR FIXATORS.
Bone Pin shank
diameter (mm)
2.0
Tibial diaphysis 2.0
Calcaneus 1.6
Metatarsals 1.6
Humeral diaphysis 2.0
Humeral condyle 1.6
Radius (craniocaudal placement) 1.6
Radius (mediolateral placement) 1.2
Radial carpal (mediolateral placement) 1.2
Radial carpal (dorsopalmar placement) 0.9
Metacarpals 1.2
 Instruments and implants
57

INTERLOCKING NAILS TOTAL HIP REPLACEMENT

Small diameter interlocking nails (4.0 mm and A modular cemented hip prosthesis system
4.7 mm) are available in seven different lengths (BioMedtrix CFX™ Micro hip system) suitable for use
(68 mm, 79 mm, 91 mm, 101 mm, 112 mm, 123 mm, in cats has recently become available. The system
134 mm) and are suitable for repair of femoral, comprises specialized instrumentation for implanta-
humeral, and tibial diaphyseal fractures (Small tion of the prostheses, a choice of three sizes of
Interlocking Nail System, Innovative Animal Products acetabular component (12 mm, 14 mm and 16 mm),
LLC.) (32). Each nail accommodates either standard and two sizes of femoral prosthesis.
2.0 mm cortical bone screws or 2.0 mm solid cross- The surgical technique is basically the same as for
locking bolts in three or four interlocking holes. Bolts larger dogs receiving a cemented total hip
are stronger and stiffer than screws because they do replacement except that the patient is smaller. Cats
not have a thread cut into their surface. The four-hole with a body weight less than 4 kg are unlikely to be
nails have two screw holes at each end (spaced 11 mm suitable candidates for total hip replacement.
apart). The three-hole nails have either a single
proximal or a single distal screw hole. Three-hole nails
are applicable where there is a small distal or proximal
bone fragment, a situation that is commonly
encountered in the cat. The 4.7 mm interlocking nail
is most frequently used for femoral fractures and the
4.0 mm nail for humeral and tibial fracture repair.
Interlocking nails function like an intramedullary plate
but require a more limited surgical approach. They
provide adequate axial and rotational stability and,
because they are placed at the neutral axis of the bone,
they provide better bending stiffness than comparable
bone plates20.

32

32 Interlocking nail. 4.0 mm and 4.7 mm instruments and

implants set (Innovative Animal Products LLC.).
58
CHAPTER 6
FRACTURE FIXATION
METHODS: PRINCIPLES
AND TECHNIQUES
PREOPERATIVE CONSIDERATIONS
ANALGESICS
Analgesic drugs are administered to increase comfort
and reduce stress in all cats with fractures.
Preemptive balanced analgesia is used before
surgery to prevent the ‘wind-up’ of pain, reduce drug
dosages and complications, and achieve a synergistic
analgesic effect. Opioids, α2-adrenergic agonists, and
nonsteroidal anti-inflammatory drugs (NSAIDs) are
often used (see Chapter 3)1–7.
ANTIBIOTICS
The use of prophylactic antibiotics in fracture repair
is controversial, but antibiotics are commonly
administered for open fractures, when severe trauma has
occurred, and when surgical intervention is required
(particularly if anticipated surgical time exceeds
2 hours). Cefazolin (22 mg/kg) is the antibiotic most
often used prophylactically during fracture repair,
although other antibiotics may be equally effective. The
chosen antibiotic should be effective against common
bacteria isolated from surgical wounds, including
coagulase-positive Staphylococcus spp. and Escherichia
coli. To achieve and maintain adequate blood levels
during surgery, antibiotics are typically administered
intravenously when the patient is anesthetized and the
dose is repeated every 2–4 hours throughout the
surgical procedure. Antibiotics are not continued after
surgery (except in open fractures) unless contamination
occurred during the procedure.
RADIOGRAPHS
Two orthogonal views of the fracture site are obtained
to classify the fracture accurately and to determine the
appropriate fixation options. In most cases, radiographs
obtained to diagnose the fracture are adequate. In some
cases, additional films are taken once the cat is
anesthetized to improve positioning, enhance detail, or
collect views not previously attainable. Radiographs
should be present in the operating room or casting
room for reference during the reduction and
stabilization procedure. Intraoperative radiographs, if
available, are extremely helpful in assessing reduction
and alignment and confirming implant positioning.
ASEPTIC PREPARATION FOR SURGERY
After induction of anesthesia, the fractured limb is
clipped and aseptically prepared for surgical reduction
and stabilization. Sufficient hair should be removed to
provide a generous surgical field and to allow collection
of autogenous cancellous bone graft if needed.
Chlorhexidine gluconate and povidone-iodine are
commonly used scrubbing solutions. A hanging-limb
preparation is preferred for most limb fractures and
allows the entire limb to be draped into the surgical field
and manipulated during surgery (33).
FRACTURE REDUCTION
CLOSED TECHNIQUE
Closed reduction is indicated when a fracture is to be
stabilized by external coaptation, closed intramedullary
pinning, or the application of an external skeletal fixator.
Reduction may be difficult (particularly in fractures that
are several days old) and requires careful traction,
countertraction, and manipulation of the limb. Muscle
relaxants may be helpful but are rarely needed in cats.
During reduction, soft tissue trauma should be
minimized to avoid damaging vessels, nerves, and
muscles. Reduction is best achieved by slowly applying
constant steady pressure to fatigue the muscles until the
fragments are realigned. Initially, traction can be
achieved using gravity by tying the distal aspect of the
fractured limb to the ceiling or an infusion stand. The
table is then lowered such that the patient is partially
‘hanging’ by the limb. Muscles are usually fatigued in
15–30 minutes and this facilitates reduction. During
application of traction to the limb, the soft tissue
envelope surrounding the bone will guide fragments
 Fracture fixation methods: principles and techniques
59
33

A B C
33 Hanging-limb technique for preparing limbs prior to surgery.
A Tape stirrups are applied to the foot and the limb is suspended for clipping and scrubbing.
B After draping, the foot is wrapped in sterile bandage material and the limb is released.
C The entire limb is in the sterile field and can be manipulated during surgery.

into an anatomic position. In some cases, the bone
segments can be toggled into proper alignment.
With closed fixation techniques, perfect anatomic
reduction of the fragments is not necessary for fracture
healing. The goal is to achieve rotational alignment, axial
alignment, and normal limb length. Ideally, the primary
bone segments should be in contact after reduction to
prevent collapse at the fracture site. Fifty percent overlap
of the primary bone fragments is preferred. Reduction
and alignment are confirmed radiographically.
OPEN TECHNIQUE
Open reduction is used when internal fixation of the
fracture is indicated and in articular fractures where
anatomic reduction is essential. Open reduction may
also be necessary in older fractures that cannot be
adequately reduced closed. The bone segments are
manipulated into alignment using bone forceps and
digital pressure. Levering fragments with a periosteal
elevator is also helpful, although care is needed to
prevent fracturing the bone. As with closed reduction,
slow, steady, constant pressure is the most effective
means of moving bone segments. It is imperative to
preserve soft tissue attachments and blood supply to
the bone fragments during reduction and fixation.
FRACTURE STABILIZATION
METHODS
EXTERNAL COAPTATION
Bandages, casts, splints, and slings can be useful in repair
of many types of fractures, particularly in the tibia,
radius/ulna, and more distal fractures8–13. Casts and
splints stabilize fractures by controlling motion of the
joints proximal and distal to the fracture site. They
should prevent rotation, angulation, and collapse of the
fracture site and maintain proper alignment and
reduction during healing. Minimally displaced fractures
respond well to external coaptation, as do fractures in
younger animals. The location and configuration of
a fracture dictates how effective external coaptation will
be at providing stability. External coaptation is used
primarily for fractures distal to the elbow or stifle joint.
Fractures of the femur and humerus are not amenable to
repair using external coaptation.
A major advantage of using external coaptation
devices to stabilize fractures is that the fracture site,
surrounding soft tissues, and blood supply to the
fragments are not disturbed by surgical manipulation.
External coaptation may also be a less expensive means of
stabilizing some fractures if the coaptation device is
applied properly, well cared for, and does not require
frequent changes. However, external coaptation devices
may not adequately control all of the forces acting on the
fracture site, which may lead to instability, increased pain,
reluctance to use the limb, and delayed healing14.
Potential complications associated with the use of
external coaptation include prolonged immobilization
of joints leading to joint stiffness and osteoarthritis,
muscle contracture, soft tissue trauma such as cast sores,
and inadequate stabilization of the fracture site15.
Frequent cast changes may be required in growing
animals or if the cast gets wet or soiled. Some cats are
intolerant of casts, bandages, splints, and slings. They
may refuse to walk for a period of time or may roll and
struggle to remove the coaptation. Mild sedation may
be used until the cat becomes accustomed to the device.
60

Casts 50%. Sufficient padding is placed to protect the limb and

Full-limb casts are usually applied as a primary fixation
after closed fracture reduction or as ancillary stabilization
following open reduction and internal fixation11,12.
Fiberglass resin-impregnated casting tape is commonly
used and is lightweight, easy to apply, and resistant to
impact. Fiberglass casts are also radiolucent, so the
fracture is readily monitored for complications and
healing without removing the cast. It also dries readily
should it become wet after application. For fractures of
the radius/ulna or tibia, the cast is placed from the toes
to the level of the mid-humerus or mid-femur. For more
distal fractures, the cast is placed from the toes to the
level of the proximal radius/ulna or tibia. The fracture
should be reduced and the limb should be in a functional
position before application of the cast. Placing joints in
a hyperextended position should be avoided.
Application
Tape stirrups are first placed to apply traction on the limb
and to prevent the cast from slipping. Long hair is shaved
if necessary. A small stockinette is placed over the limb
extending from the toes to the proximal extent of the
cast. Care is taken to eliminate folds in the stockinette
that may cause pain or pressure on the underlying skin.
Cast padding is then placed around the limb from distal
to proximal with each wrap overlapping by approximately
prevent cast sores. However, too much padding will
prevent the cast material from conforming to the limb
and may cause motion beneath the cast, instability of the
fracture, and trauma to the skin. Care is taken to ensure
all bony prominences are adequately padded. Roll gauze
may be applied over the cast padding but this is optional.
The fiberglass casting material is immersed in water and
squeezed to remove excess water. The cast material will
harden more slowly if cold water is used and more
quickly if warm or hot water is used. The cast material is
gently wrapped circumferentially around the limb,
beginning at the toes and progressing proximally,
overlapping each wrap by 50%. The distal portions of
phalanges 3 and 4 are left exposed to monitor for
swelling. Two or three layers of casting material may be
used to ensure the cast is sufficiently strong. The cast
should be applied quickly enough to allow the layers to
laminate together for added strength. Care is taken not
to pinch or squeeze the cast as it is hardening, or
depressions in the cast may place focal pressure on the
underlying skin. When the cast material is in place, the
stockinette is folded over proximally and distally to cover
the ends of the cast and the stirrups are reflected and
stuck to the outside of cast. Elastic adhesive tape or
Vetwrap (3M Animal Care Products) may be placed over
the cast (34).

34

C E
34 Full-limb cast application technique.
A Tape stirrups are placed medially and laterally on the foot and traction is applied. B A stockinette is placed over the limb.
C Cast padding material is applied. Avoid excessive padding or the cast will be loose. Roll gauze may be placed over the cast
padding if desired. D Casting material is applied and conformed to the limb. Overlap each wrap by 50%. Additional layers
are applied as needed for strength. E The tape stirrups and stockinette are reflected and a layer of elastic adhesive tape or
Vetrap is applied to cover the cast. The distal aspects of the 3rd and 4th phalanges are left exposed to monitor for swelling.
 Fracture fixation methods: principles and techniques
61

Care of casts Mason metasplints (metal or plastic) are commonly

After application, the cast is kept clean and dry and the
toes are monitored for swelling. The cast is checked
regularly for odor. The cat should be confined and
must not be permitted to lick or chew the cast.
If possible, the cast remains in place until healing is
complete, since loss of fracture reduction may occur if
the cast is removed prematurely. However, the cast
must be replaced if it becomes loose or causes irritation
to the skin. The cat is sedated and the cast is cut
medially and laterally with an oscillating saw (bivalve).
The two halves of the cast can then be removed. The
skin is treated appropriately and the bivalved cast is
re-applied. Tape can be used to hold the two halves of
the cast together. In some case, only one half of the
bivalved cast is reapplied and this serves as a splint.
Splints
Various types of splint are available and may be used
to stabilize fractures distal to the elbow and stifle
joints. Splints are placed on the caudal/palmar aspect
of the forelimb for fractures distal to the elbow.
used and have a ‘spoon’ shape to fit the distal aspect
of the limb. Alternatively, thermomoldable plastics
(X-Lite, AOA Kirschner Medical Corp.; Veterinary
Thermoplastic (VTP), IMEX Veterinary Inc.; or
Orthoplast, Johnson & Johnson) can be used to
customize a splint for each individual cat. Splints are
placed on the lateral aspect of the hindlimb for
fractures distal to the stifle. Fiberglass casting tape or
thermomodable plastics may be used to create a splint
that conforms to the limb.
Application
Tape stirrups are placed on the limb followed by cast
padding. Excessive padding should be avoided. Roll
gauze is then applied, ensuring the bandage is not too
tight. The commercial or custom-made splint is
positioned and secured to the limb with elastic
adhesive tape or Vetwrap (3M Animal Care Products).
The stirrups are folded up and stuck to the outer
wrap. If possible, the distal aspect of phalanges 3 and
4 are left exposed to monitor for swelling (35).

35

C E
35 Splint application technique.
A Tape stirrups are applied to the limb. B Cast padding material is applied (ensuring that all bony prominences are well
padded) with the limb in a functional position. C Roll gauze is applied. Avoid applying the material too tightly. D The tape
stirrups are reflected and the splint is placed. Commercially available splints or custom splints made from casting material or
thermomoldable plastics may be used. E Elastic adhesive tape or Vetwrap (3M Animal Care Products) is used to attach the
splint securely. The distal aspects of the 3rd and 4th phalanges are left exposed to monitor for swelling.
62
Care of splints
Care of splints is identical to that recommended
for casts. Splints are easier to change than casts and
are particularly useful for fractures of the
metacarpals, metatarsals, and phalanges and when
wounds are present that necessitate frequent
bandage changes.
INTRAMEDULLARY PINS, KIRSCHNER WIRES,
AND CERCLAGE WIRES
Intramedullary pins, Kirschner wires, and cerclage wires
are commonly used to repair fractures in cats. The
straight medullary cavity typical of most cat bones
makes them very amenable to intramedullary pin
placement. Pins and wires are relatively inexpensive
and easy to implant with minimal equipment.
Intramedullary pins provide axial alignment and resistance
to bending but do not control rotational forces. The
friction between the pin and the bone provides limited
control of compressive and tensile forces. Therefore,
intramedullary pinning can result in a slower return to
limb function and may involve more aftercare than
bone plating16. Intramedullary pins and full cerclage
wires work well for fractures of the tibia, femur, and
humerus. Placing an intramedullary pin in the radius is
discouraged because of the oval shape of the bone,
the limited medullary cavity, and the likelihood of
damaging the elbow or radiocarpal joints during
insertion.
Intramedullary pins
Intramedullary pins are often used to stabilize fracture
of the humerus, femur, and tibia in cats13,17–24.
Steinmann pins are the most common type of
intramedullary pin used. They are round, come in
a variety of lengths, and are 1.5 mm to 6.5 mm in
diameter. Pins with a ‘trocar’ point have better cutting
action and are used most often for intramedullary
pinning. Threaded pins are of little value as
intramedullary pins and are susceptible to breaking at
the junction of the threaded and smooth portions of
the pin.
Selection of the appropriate pin depends on the
size of the intramedullary cavity, the bone being
repaired, the fracture configuration, and whether
ancillary methods of fixation are to be used. Pin
diameters of 1.6 mm to 4.8 mm are suitable for use in
most cats. Generally, when a single intramedullary pin
is to be placed, it should be large enough to fill at least
60–70% of the medullary cavity at its narrowest point.
Larger pins provide greater resistance to bending
forces and are preferred in straighter bones. In larger
bones, two pins may be placed in the medullary cavity
to provide stability (‘stack pinning’)25. In some
fracture configurations in cats, it may be easier to
insert two smaller pins without disrupting the
fragments than to insert a single large pin. However,
stack pinning has not been shown consistently to
improve rotational stability25–28. This is particularly
true when both pins exit the cortex through the same
hole and function essentially like a single pin. A
modified intramedullary pin has recently been
described for use in cats that has three lamellae along
its shaft, giving it a triangular cross-sectional shape
(Trilam Nail, Rotec Medizintechnik) (26)29. The
lamellae engage the inner cortical bone to control
rotation.
Pin insertion
Intramedullary pins are inserted in a closed or open
fashion20,23. When open pinning is used, a limited
approach is made to the fracture site to achieve
reduction and ensure proper pin placement while
minimally disrupting the fragments. This is the more
commonly used method to place an intramedullary
pin and allows anatomic reduction of the fragments
and the application of cerclage wires. Intramedullary
pins may be inserted in either normograde or
retrograde fashion depending on the bone being
repaired. For normograde insertion, the pin is
inserted from one end of the bone, across the fracture
site, and into the opposite bone segment. For
retrograde insertion, the pin is started at the fracture
site and directed out of the proximal cortex of the
bone. The fracture is reduced and the pin is then
driven in the opposite direction and seated into the
distal segment of bone.
Intramedullary pins are typically inserted with
a hand-chuck, using a smooth internal and external
rotation of the wrist and forearm to minimize
‘wobble’. They may also be inserted with a power drill,
but care is needed to prevent thermal necrosis of the
bone, inadvertent penetration of the cortex, and
entrance into a joint. The pin is inserted until it
engages the cancellous bone at the far side of the
fracture. The depth of the pin can be estimated by
placing a pin of the same length along the outside of
the bone. The joints on either end of the long bone
should be manipulated through a full range of motion
and evaluated for crepitus indicative of pin penetration
into the joint. Final pin position is evaluated
radiographically.
Once the pin is in place, the end of the pin is cut
short and should not protrude from the skin.
Alternatively, the pin can be partially precut with
a saw based on the preoperative radiographs of the
 Fracture fixation methods: principles and techniques
normal contralateral bone. Following insertion the
pin is snapped off flush with the bone surface and
left in situ. This prevents soft tissue injury, pain, and
seroma formation.
Dynamic intramedullary pinning (Rush pinning)
Dynamic intramedullary pinning or Rush pinning is
a modification of the intramedullary pinning
technique23,30. Rush pins are specifically designed
intramedullary devices originally used in humans. They
have a hook on one end and are flat and skid-like on
the opposite end. A pair of these pins is inserted from
the end of a long bone into the medullary cavity to
create dynamic compression (36). In cats, small
Steinmann pins or Kirschner wires can also be inserted
in ‘Rush fashion’. This technique is used primarily for
metaphyseal or epiphyseal fractures.
To insert pins in Rush fashion, pilot holes are
drilled medially and laterally near the end of the
bone. The pins are inserted at an angle 20° to
the long axis of the bone. The fracture is reduced and
the pins are alternately advanced across the fracture
line. Each pin should cross the fracture line, glance
off the far cortex, and bend back toward the cortex in
which it was inserted. Blunting the ends of the pin,
placing a slight bend in the pin prior to insertion, and
tapping the pin into the bone rather than twisting it
can aid insertion and prevent the tip of the pin from
36 Pins placed in ‘Rush fashion’ 36
to repair a distal femoral
fracture.
63
sticking into the far cortex. The stability provided by
pins placed in Rush fashion depends on the elasticity
of the pins and proper positioning within the
medullary cavity.
Kirschner wires
Kirschner wires and arthrodesis wires are small,
flexible pins shaped much like Steinmann pins. They
are available in a range of sizes, 0.9–2.0 mm in
diameter. They can be inserted by hand-chuck or with
a power drill and are used in several ways to stabilize
fractures.
Figure-of-eight skewer technique
The figure-of-eight skewer technique is a modification
of the hemicerclage wiring technique (37)31.
A Kirschner wire is placed across the fracture line
with the ends of the Kirschner wire protruding
approximately 2 mm from each cortex. The Kirschner
wire is positioned either perpendicular to the fracture
line or perpendicular to the long axis of the bone,
whichever will provide the greatest fracture stability.
A cerclage wire is then placed in a figure-of-eight fashion
around the tips of the Kirschner wire, against the outer
cortex of the bone. The wire is tightened, with care
taken to keep even tension on the two wire ends. The
protruding ends of the Kirschner wire can be bent to
help retain the cerclage wire and prevent slippage.
37
37 Figure-of-eight skewer technique. A Kirschner wire is
placed perpendicularly across the fracture (black line). Wire
is placed in a figure-of-eight fashion around the protruding
ends of the Kirschner wire and tightened. The ends of the
Kirschner wire are bent over to prevent slippage and
reduce soft tissue trauma.
64
Cross pinning
The cross pinning technique is commonly used to
stabilize metaphyseal and physeal fractures. The
distal femur, proximal tibia, distal tibia, and distal
radius are sites where cross pinning is often
employed. Two Kirschner wires are inserted across
the fracture line from the epiphysis into the
metaphysis. The joint surface is avoided when
starting the pins. The Kirschner wires should cross
on the metaphyseal side of the fracture line and not
directly in the fracture32,33.
Tension band wire fixation
Tension band wiring is used to stabilize avulsion
fractures or osteotomies of the olecranon, greater
tubercle of the humerus, greater trochanter of the
femur, tuber calcaneus, tibial tuberosity, and the
medial and lateral malleoli34. Distractive forces
applied to the bone by tendon or ligament
attachments are converted to compressive forces by
the tension band fixation. The avulsed fragment is
reduced and two Kirschner wires are inserted across
the fracture line to maintain alignment and
neutralize shear forces. The pins should be parallel to
each other. A hole is drilled transversely across the
parent bone. Orthopedic wire (0.6 mm [22 AWG] or
38
A B
38 A Tension band wire fixation for stabilization of an olecranon fracture.
B Lateral radiographic view of an olecranon fracture repaired with tension band wire fixation.
0.8 mm [20 AWG]) is placed in a figure-of-eight
pattern (through the hole and around the
protruding ends of the Kirschner wires) and twisted
to tighten. A single or double twist can be placed in
the figure-of-eight wire. The protruding ends of the
Kirschner wires are then bent over, cut, and rotated
to prevent soft tissue irritation (38).
Cerclage wires
Cerclage wiring is a useful and versatile technique
used for fracture repair19,23,34. When applied
properly, cerclage wires neutralize specific forces at
the fracture site and do not compromise cortical
blood supply or interfere with bone healing35.
However, when used alone, cerclage wires are unable
to withstand load-bearing and muscle-generated
forces. Therefore, they are typically applied in
conjunction with other fixation methods, including
intramedullary pinning or plate fixation. Cerclage
wires are used alone only in certain situations, such as
in the repair of mandibular fractures. The key to
successful cerclage wiring is careful case selection and
strict attention to proper application techniques. The
most common wire used in cat fracture repair is
0.8 mm (20 AWG), although 0.6 mm (22 AWG) and
0.5 mm (24 AWG) wires are occasionally needed
 Fracture fixation methods: principles and techniques
(see Chapter 5). Cerclage wire is available as a spool
of wire or with preformed loops on one end (loop
cerclage).
Full cerclage wires
Full cerclage wires are placed completely around the
long bone. They are used to stabilize fissure fractures
and long oblique and spiral fractures, where the
fracture line is at least twice the diameter of the bone.
If a full cerclage wire is placed on a short oblique
fracture, shear forces are created and the fracture will
be unstable. The wire is likely to loosen and can slide
into the fracture line where it will interfere with
healing. Full cerclage wires are not used on transverse
fractures. The application of full cerclage wires to
a long oblique fracture creates interfragmentary
compression and enhanced stability. Several important
principles should be followed when applying full
cerclage wires:
• The cerclage wires are placed perpendicular to
the long axis of the bone. If the wire is not
perpendicular, it is likely to shift and become
loose. Loose wires provide no mechanical support
and interfere with revascularization and healing.
• Disruption of the soft tissues surrounding the
bone is minimized. Forceps or a wire-passer are
used to position the wire around the bone,
ensuring the wire is against the periosteal surface
of the bone and that soft tissue, vascular
structures, and nerves are not entrapped.
Entrapped soft tissue will suffer necrosis, leading
to loosening of the wire.
• Wires must be tight!
• A minimum of two full cerclage wires are placed
on each fracture line. A single wire simply creates
a fulcrum around which the fragments can move.
• Wires are placed a minimum of 0.5 cm from the
end of the fracture line and 1 cm apart along the
entire fracture line. Cerclage wires should never
be placed within the fracture line itself.
Full cerclage wiring is often used to stabilize
comminuted fractures (along with an intramedullary
pin, external fixator, or bone plate) (Table 18). The
full circumference of the cortical shaft must
be reconstructed for the wires to be effective. If
the reconstruction is incomplete, the fragments will
simply collapse into the medullary cavity as the wire
is tightened. If cerclage wires are placed on a bone
that is conical in shape, they may tend to shift
toward the narrower portion of the bone, resulting
in a loose wire. Placing a small Kirschner wire
through the bone at the level of the cerclage wire
can prevent slippage. Alternatively, a small notch
65
may be cut into the cortical bone and the cerclage
wire placed in the notch as it is tightened. If
cerclage wires are used to stabilize fragments prior
to application of a bone plate, the knot in the wire
should be placed such that it does not interfere with
proper plate positioning.
Hemicerclage wires
Hemicerclage wires are placed through the holes
drilled in the bone and are tightened to create
compression. Overtightening may damage the bone
where the wire exits the drill hole. These
interfragmentary wires should be placed perpendicular
to the fracture line to maximize compression between
the fragments and prevent wire movement and
loosening. In most cases, hemicerclage wires provide
little rotational stability and their use is limited to
specific situations, such as stabilization of nonweight-
bearing bones, such as the mandible or maxilla.
Tightening cerclage wires
Loop cerclage wires are tightened by placing the free end
of the wire through a preformed loop (‘eye’) created in
TABLE 18 OPTIONS FOR REPAIR OF DIAPHYSEAL
FRACTURES IN CATS.
Transverse/short oblique fractures
Bone plate
Interlocking nail
Intramedullary pin with an external fixator
External fixator
Long oblique fractures
Bone plate
Bone plate and cerclage wires or lag screws
Interlocking nail
Intramedullary pin and cerclage wires
Intramedullary pin and external fixator
External fixator
Comminuted fractures
Bone plate in buttress fashion
Bone plate and intramedullary pin (plate-rod)
Interlocking nail
External fixator (rigid frame configuration)
Bone plate and cerclage or lag screws
Intramedullary pin and cerclage wires
Intramedullary pin and external fixator
Autogenous cancellous bone graft in all defects
66

the opposite end (39). A specially designed tightening
device is available that creates maximum tension on the
wire around the bone. Once the wire is tight, the free end
of the wire is bent 180° to lock it in place, and the excess
is removed. Loop cerclage wires can be placed more
tightly than twist type wires36,37. However, since the knot
is secured simply by bending the wire, loop cerclage wires
may be susceptible to premature loosening.
Twisting the two ends of the wire is a common
method of securing a cerclage wire (40). Several
instruments are available for this purpose: a strong pair
of needle holders is commonly used. Tension is applied

39 39 Loop cerclage wire.

A Loop cerclage wire positioned
in the AO wire-tightening
device. The handle on the
tightening device is turned to
put tension on the wire.
B Loop cerclage wire placed on
a long bone. The end is bent
over to lock the wire in place.

A B

40

A B C
40 Twist cerclage wire. A The proper method to tighten the cerclage wire. Tension is applied by pulling
perpendicularly away from the bone surface as the wire is twisted. Equal tension is applied to both strands of wire to
create an interlocking twist. B Improper twist: one strand of wire is wrapping around the other. C Bending the wire
twist significantly reduces the tension and often results in a loose cerclage wire. Instead, the wire should be cut leaving
two to three twists in place.
 Fracture fixation methods: principles and techniques
by pulling perpendicularly away from the bone surface
as the twist is created. The tension in the wire and the
securing knot are thus created at the same time. Equal
tension is applied to both strands of wire to create an
interlocking twist in which each strand of wire wraps
around the other. Wires secured using this twist- knot
method provide only 40–60% of the static tension
created when using a loop cerclage38. Twist-knots are,
however, significantly more resistant to slippage37.
After completing the twist, the wire is cut leaving two
to three twists in place. Cutting the twist has been
shown to reduce the wire tension by up to 21%, but
bending the twist over decreases tension by as much
as 70%34. In most cases, this small projection causes
minimal soft tissue injury. If a twist wire must be bent
because of minimal soft tissue coverage at the fracture
site, it is best to continue to twist the wire as the
bending motion is applied.
Anatomic reconstruction of the fragments and
proper wire positioning are essential to prevent
premature loosening. Once a wire is placed, it is
checked to ensure it is tight. It is not uncommon for
a wire to become loose as other wires are tightened
along the bone. Frequent checks and replacement
of all loose wires are essential. Complications from the
use of cerclage wires generally result from the use of
undersized wire, use of a single wire on a fracture, or
from technical errors in application31. Most technical
errors result in loose wires that can migrate into the
fracture lines, disrupting vascular ingrowth and
delaying the healing process. Wires can become loose
if they are not tightened sufficiently, are not placed
perpendicular to the long axis of the bone, or if the
underlying bone fragments are not reduced
adequately. The wire knots should not be placed
where they may damage vessels and nerves.
EXTERNAL SKELETAL FIXATORS
External skeletal fixators are a versatile method of
fracture repair39–45. Both linear and circular fixation
systems are available for use in the cat44,46,47. They are
easily customized into a variety of configurations
to stabilize almost any type of fracture, require little
additional equipment for proper placement, are well
tolerated by most cats, and are ideal for stabilization of
comminuted, infected, and nonunion diaphyseal
fractures (Table 18). External fixators may be used as a
primary means of stabilization or in conjunction with
internal fixation methods. Fixators can control all forces
acting on a fracture site and are easily removed when
fracture healing is complete. When possible, external
fixators are applied in a closed manner to minimize
disruption of the soft tissues and blood supply at the
67
fracture site. In some cases, a limited open approach to
the fracture site is performed to improve reduction and
alignment. If the fracture site is opened, cortical defects
are filled with autogenous cancellous bone graft. Typical
components of an external fixator system include the
transfixation pins, clamps, and connecting bars.
Transfixation pins
Transfixation pins penetrate the bone, stabilize
fragments, and attach to the external frame (connecting
bars). Pins 1.2–2.0mm in diameter are most often used
in cats. They are inserted through small stab incisions in
the skin and must penetrate both cortices of the bone or
they will loosen prematurely. Pins that penetrate the skin
on only one side of the limb are termed ‘half pins’. Pins
that penetrate the skin on both sides of the limb are
termed ‘full pins’. A minimum of two transfixation pins
are inserted on each side of the fracture line, although
three or four pins are preferred if space allows.
Knowledge of the regional anatomy and careful
palpation are important to ensure pins are not placed in
the fracture line and to avoid damaging vessels, nerves,
and muscles48. When placed after open fracture
reduction, pins are inserted through separate stab
incisions rather than through the surgical incision.
Transfixation pins 25–30% of the diameter of a bone can
be inserted without significantly weakening the
bone44,49–52. Positive profile threaded pins have
significantly greater holding power in bone than smooth
pins and their use can help prevent premature pin
loosening49,53–55. However, their larger diameter may
limit their use to the metaphyseal regions of the long
bones. A combination of smooth and threaded pins may
be used to improve holding power while reducing cost.
Transfixation pins should be inserted using slow-
speed power insertion (<150rpm) with a variable speed
power drill56,57. High-speed power insertion results in
thermal necrosis of the bone and premature pin
loosening. Predrilling the hole in the bone with a drill
bit one size smaller than the transfixation pin will also
reduce the heat created during pin insertion58,59
(see Table 16). A hand-chuck may also be used to insert
the pins, but the slight wobble that occurs when pins are
inserted in this manner can lead to premature pin
loosening. ‘Backing-up’ the pin once it is inserted
should be avoided, as this can also cause pin loosening60.
Linear fixator systems
The small Kirschner–Ehmer (KE) fixator system is,
perhaps, the fixator system most often used for
fracture stabilization in cats. A 3.2 mm diameter steel
connecting bar is used and the clamps (used to
attach the transfixation pins to the connecting bar)
68
will accommodate pins up to 2 mm in diameter.
Unfortunately, positive profile threaded pins cannot
be inserted through the KE clamps, and additional
clamps cannot be added to the bar once the proximal
and distal pins are attached. The small Secur-U
External Fixator Clamp (Securos Veterinary
Orthopedics Inc.) can be used with the 3.2 mm
connecting bar and will accommodate 1.6–2.3 mm
transfixation pins. These clamps can be added to the
bar between previously placed clamps and they are
more resistant to slippage than KE clamps61,62. The
mini IMEX-SK System (IMEX Veterinary Inc.) uses
a 3.2 mm diameter connecting bar. The mini SK
clamp has a two-piece design that can be
disassembled to allow the addition of a clamp
between two existing clamps on the connecting bar.
It accommodates transfixation pins from 0.9–2.5 mm
in diameter.
Frame configurations
Various frame configurations can be used when
applying a linear fixator (41)12:
• Type Ia: a unilateral frame in which half pins are
placed in a single plane.
• Type Ib: a unilateral frame in which half pins are
placed in two planes (two type Ia frames placed
60–90° to each other). The two frames can be
connected to increase stiffness.
• Type IIa: a bilateral frame (connecting bars used
on both sides of the limb) in which all of the
transfixation pins are full pins (penetrating the
skin on both sides of the bone).
• Type IIb: a bilateral frame in which both full pins
and half pins are used.
• Type III: bilateral and biplanar frame (the most
rigid of the frame configurations).
• Tie-in configuration: a connecting bar is used to
attach the external fixator frame to an
intramedullary pin. Used in femoral and humeral
fracture repair.
Frame stiffness
Stiffer fixator frames enhance stability at the fracture
site and reduce the incidence of pin loosening and pin
sepsis59. Type III frames are stiffer than both type
I and II frames. Type II frames are approximately
twice as stiff as type I frames63,64. Type I and type II
frames are commonly used in cats, while type III
frames are only occasionally required65. Several
techniques can be used to increase the stiffness of any
fixator configuration59,66,67:
• Increasing the number of transfixation pins in
each fragment (three to four pins is ideal).
• Using larger diameter transfixation pins (up to
30% of bone diameter).
• Placing the innermost transfixation pins close to
the fracture site and the outermost pins near the
bone ends.
• Increasing the number and size of the connecting
bars.
• Placing the connecting bars closer to skin. The
connecting bar is typically placed approximately
1–2 cm from the skin surface to allow for
postoperative swelling. In some situations, the
connecting bar is slightly contoured to fit the
patient better.
• Reducing the fracture so that the fixator frame
shares load with the bone segments.
Fixator application techniques
Type Ia frame
1. A hanging-limb technique is used for preparing
and draping the limb. This will fatigue the
muscles, provide distraction, and facilitate fracture
reduction. In many cases, the limb is left hanging
during the initial steps of the application process
to maintain proper limb length.
2. The proximal and distal transfixation pins (half
pins) are inserted through small stab incisions in
the skin near the ends of the long bone. Placing
these pins parallel to the joint surfaces
will help ensure proper alignment. Positive profile
end-threaded pins may be used if their diameter is
less than 30% that of the bone. Predrilling the
holes with the appropriate sized drill bit will
reduce the incidence of thermal necrosis and pin
loosening.
3. Empty clamps are placed on the connecting bar
(to accommodate the expected number of
additional pins to be placed) and the
connecting bar is loosely attached to the
proximal and distal pins.
4. The fracture is reduced (ensuring proper bone
length and alignment of the joints proximally and
distally) and the clamps on the proximal and
distal pins are tightened. This will hold
the fracture in reduction while additional
transfixation pins are inserted through the empty
clamps on the connecting bar.
5. A minimum of two pins is inserted in each bone
segment, using three or four pins if the size of
the fragments will permit. The pins can be
inserted at an angle 20° to the long axis of the
bone if preferred.
6. Adequate alignment and reduction of the fracture
are confirmed using radiographs and careful
 Fracture fixation methods: principles and techniques
69

palpation, then all of the clamps are tightened.
If necessary, minor adjustments in fracture
reduction can be made by loosening the clamps
and manipulating the fragments.
Type Ia frame and intramedullary pin68,69
1. The fracture is reduced and the intramedullary
pin is inserted using either a closed or an
open technique. A pin less than 70% of the
diameter of the medullary cavity is used to
allow room to insert the transfixation pins. If
an open approach is used for a comminuted
fracture, absorbable suture can be used to pull
the bone fragments gently into alignment, or
cerclage wires can be placed to stabilize the
fragments. Cancellous bone graft is placed in
any defects.

41

A B C D

E F G
41 Fixator frame configurations. A Type Ia frame. B Type Ia frame with double connecting bar.
C Type Ib frame. D Type IIa frame. E Type IIb frame. F Type III frame. G Tie-in configuration.
70
2. The intramedullary pin is cut below the skin
surface.
3. The type Ia external fixator is applied (as
described). The transfixation pins are placed
through stab incisions in the skin (not through
the surgical incision).
Type Ia frame and intramedullary pin, tie-in
configuration70–72
1. The fracture is reduced and the intramedullary
pin is inserted using either a closed or an open
technique. A pin less then 70% of the diameter of
the medullary cavity at its narrowest point
is used.
2. The proximal end of the intramedullary pin is left
exposed (2–3 cm) above the skin surface.
3. The type Ia external fixator frame is placed (as
described).
4. Clamps and a connecting bar are used to attach
the intramedullary pin to the fixator frame, or the
proximal end of the frame’s connecting bar is
contoured so that it contacts the intramedullary
pin (connected with a clamp).
Type Ib frames
A type Ia frame is applied to the fracture as described.
A second type Ia frame is placed approximately
60–90° degrees to the first. The two frames can be
attached using short connecting bars to increase
stiffness.
Type IIa frames
1. A hanging-limb technique is used for preparing
and draping the limb. This will fatigue the
muscles, provide distraction, and facilitate fracture
reduction. The limb can be left hanging during
the initial steps of the application process to
maintain limb alignment.
2. The proximal and distal pins (full pins) are
inserted through stab incisions in the skin near
the ends of the long bone. The pins are placed
parallel to the joint surfaces. Centrally threaded
pins may be used to enhance holding power.
Predrilling the holes with an appropriate sized
drill bit will ease insertion and reduce thermal
injury to the bone.
3. The connecting bars (with the necessary
allotment of empty clamps) are clamped to
the two transfixation pins on each side of
the limb.
4. The fracture is reduced, ensuring proper limb
length and rotational and angular alignment.
A minimal surgical approach may be used gently
to align the fragments and place cancellous bone
graft if necessary.
5. The four clamps are tightened. This rectangular
frame will maintain reduction while the remaining
pins are inserted.
6. The remaining full pins are inserted through stab
incisions in the skin. To ensure the full pins
contact the connecting bars bilaterally:
• An aiming device is used to direct the pins61.
(Secur-Aim Fixator Pin Application Tool,
Securos Veterinary Orthopedics Inc.). The
device is attached to the fixator frame and
serves as a guide to allow placement of pilot
holes in the bone. Additional transfixation pins
are then inserted through the guide (and pilot
holes) in the proper orientation to contact
both connecting bars.
• An additional connecting bar (with empty
clamps) is attached to the proximal and distal
pins, forming a ‘double bar’ on one side of the
limb. Since the three connecting bars are in the
same plane, transfixation pins inserted through
the empty clamps on the double bar (and then
through the bone) will connect with the empty
clamps on the opposite side of the limb.
7. At least two full pins are inserted in each bone
segment (3–4 pins are preferred).
8. All the clamps are tightened.
9. The additional connecting bar is removed (or it
may be left in place as a double bar if additional
stiffness is required).
Type IIb frames
Type IIb frames are placed in the same manner as
type IIa, except that an additional connecting bar or
aiming device is not needed. Once the rectangular
frame is in place, and the fracture is reduced, half pins
(rather than full pins) are inserted through the empty
clamps on the two connecting bars. The half pins can
be inserted at an angle approximately 20° to the long
axis of the bone.
Type III frames
Type III frames (bilateral and biplanar) are the most
rigid of the frame configurations and are rarely required
in cats. However, they may be used to stabilize severe or
infected fractures of the distal extremities (particularly
the tibia) when delayed healing is expected65. The
fracture is reduced and a type II frame is placed from
medial to lateral on the limb. A second frame (type I) is
placed on the cranial aspect of the limb, at approximately
90° to the type II frame. Clamps and connecting bars
are used to connect the two frames together.
 Fracture fixation methods: principles and techniques
71

Acrylic frame fixators tubing, pediatric anesthetic tubing, or silastic tubing

Acrylic frame fixators (rather than those of metal or
carbon fiber rods) may be used as connecting bars to
grip the transfixation pins and stabilize the frame
(42). Acrylic frames are particularly useful in cats
because they are lightweight, less bulky, and can be
contoured to any shape bone or fracture configu-
ration. Positive profile threaded pins can be inserted
anywhere along the frame without passing through
clamps, and the connecting bar can be of any shape,
so transfixation pins need not be aligned in a single
plane to attach properly. Pins of various sizes can also
be used in the same frame19,41,73,74.
Smooth or threaded pins can be used with acrylic
fixators. The external portion of the pin is often bent
or slightly notched with a pin cutter so that the acrylic
can grip the pin more firmly. Specially designed pins
are available for use with acrylic fixators; they have
a roughened surface to strengthen the interface
between the pin and the acrylic (Miniature
InterfaceTM fixation half pins, IMEX Veterinary Inc.).
Flexible tubing of the appropriate diameter is placed
over the external portion of the transfixation pins to
contain the acrylic as is hardens. Thin-walled, flexible
tubing is preferred and rubber or polyvinyl medical
(Silastic Medical Grade Tubing, Dow Corning) is
often used. The appropriate diameter of the tubing
depends on the bone being repaired, fracture
configuration, frame configuration, and the size of the
cat. A 2 cm diameter acrylic bar is stronger than the
medium sized metal KE bar73.
Numerous products can be used to create the acrylic
connecting bars, including dental-grade nonsterile
methylmethacrylates and dental acrylics (LB Caulk
Co.), methylmethacrylates used for prosthesis
implantation or hoof repair (Simplex-P, Howmedica
International; Technovit, Jorgensen Laboratories), and
various epoxy putties73,75. Most acrylic materials have a
liquid and a powder component that are mixed
together and injected into the tubing using a catheter-
tipped syringe. Alternatively, the acrylic is allowed to
reach a doughy stage and is molded to the transfixation
pins (free-form). The acrylic undergoes an exothermic
reaction as it hardens, which can cause thermal injury to
soft tissues and bone by conduction along the
transfixation pins76,77. Placing the acrylic bar at least
1 cm from the skin surface and lavaging the pin/acrylic
interface with saline during the exothermic reaction
reduces thermal injury73.

42

A B C
42 Acrylic external fixators.
A Free-form acrylic fixator. Acrylic material or PMMA is allowed reach a doughy state and applied to
the ends of the transfixation pins.
B Acrylic fixator formed by placing flexible tubing on the transfixation pins. Acrylic or PMMA fills the
tubing and is allowed to harden, forming rigid connecting bars.
C Acrylic fixator on a cat femur.
72

When performing open reduction of the fracture, 43

the use of a commercially available acrylic fixator kit
(APEF System, Innovative Animal Products LLC.)
simplifies the procedure because the necessary tubing
and acrylic are sterile. Transfixation pins are inserted
into the bone at the locations desired for maximum
stability and minimal soft tissue injury. The fracture is
reduced and stabilized using the alignment frame
clamps and bars, which temporarily attach to the
transfixation pins close to the skin. If open reduction
was necessary, the skin incision can be closed at this
time. The corrugated tubing is then impaled on the
external ends of the transfixation pins outside the
alignment frame. The pins may be shortened to ensure
that only one wall of the tubing is penetrated. Acrylic is
then mixed within its plastic bag and poured into one
end of the tubing. The other end of the tubing is
occluded using plugs to prevent leakage. Once the
acrylic has hardened (10–12 minutes) the temporary
alignment frame is removed.
When using nonsterile acrylic or polymethyl-
methacrylate (PMMA), care must be taken to avoid 43 Transarticular external fixator used to stabilize a distal
contamination of the fracture site13. The transfixation femoral fracture. The articular component of the fracture is
pins are inserted and flexible tubing of the appropriate repaired with a lag screw to ensure a congruent joint surface.
diameter is placed over the pins. The tubing must be
sterilized if it is to be used during open fracture
reduction, or the incision is closed before handling the repair. Triangular frame configurations can be used or
tubing or nonsterile PMMA. The fracture is reduced the connecting bars (metal or acrylic) can be bent to
and a temporary connecting bar is placed on some of immobilize the joint in a weight-bearing position78. It
the pins (outside of the tubing) to maintain reduction. may be difficult to slide the clamps onto the bars once
The PMMA is mixed to liquid phase, placed in a large the bar is bent, so the surgeon should ensure the clamps
catheter-tipped syringe, and injected into one end of are properly positioned first. The transarticular fixator is
the tubing. The other end of the tubing is occluded removed as soon as healing is complete and physical
with gauze or cotton to prevent leakage. Leakage therapy is initiated to restore joint motion and prevent
through the holes in the tubing created by the pins is permanent joint injury. Ideally, the joint is immobilized
also controlled with gauze or cotton to prevent cement for a only a short period of time to minimize joint
from contacting the skin. Alternatively, the PMMA can injury79.
be mixed until it reaches a doughy phase and then
conformed on to the pins. When the PMMA has Circular fixator frames
hardened, the temporary connecting bar is removed Circular external fixators available for use in cats are
and the pins are cut short against the PMMA bar. The based on the ring fixator system used by the Russian
bar is wrapped to cover the cut ends of the pins. surgeon Gavriil A Ilizarov (IMEX Ring Fixator
System, IMEX Veterinary Inc.; Small Bone Fixator,
Transarticular fixators Hofmann s.r.l.)47,80,81. Circular frames are applied
Transarticular fixators are used for joint arthrodesis and in a closed fashion and are very stiff under shear
to stabilize metaphyseal or epiphyseal fractures where and bending loads. However, they allow axial
insufficient bone length is available to immobilize the micromotion at the fracture site, which encourages
fracture fragments adequately using internal fixation healing10,43. Circular fixators can be used to stabilize
(43)78. When transarticular fixators are used to stabilize very small fragments and they are extremely adjustable
articular fractures, the fracture involving the articular after application.
surface is reduced and stabilized using internal fixation The basic circular frame consists of metal rings,
and a transarticular fixator is applied to minimize partial rings, or arches interconnected by threaded
loading of the fracture site and protect the internal rods and nuts. Wires (1.0 mm wires are preferred in
 Fracture fixation methods: principles and techniques
73

cats) are placed through the bone and attached to 44

the rings with slotted or cannulated bolts. One or
two rings (with two wires per ring) are placed on
each side of the fracture. Many variations of the basic
frame are possible and they are readily adjusted after
application, making circular external fixator systems
very useful in stabilizing complex fractures,
transporting bone segments to fill defects, or
correcting angular and rotational deformities (44). A
common variation is to combine components of a
circular fixator with those of a linear fixator (‘hybrid
fixator’)46,47. These hybrid frames are particularly
useful when stabilizing fractures with short segments
near joints or repairing fractures proximal to the
elbow or stifle.
A B
Complications of external fixators 44 Circular external fixator.
Complications are common with the use of external A Circular external fixator on a cat tibia.
skeletal fixation, but are easily avoided or managed B Hybrid circular external fixator on a cat tibia.
with proper care (Table 19)16,43,45,77,82. Limb function (Photograph courtesy of Dr. Robert Radasch.)

TABLE 19 COMPLICATIONS OF EXTERNAL FIXATORS.

Complication Prevention/treatment
Pin tract sepsis/premature Use proper pin insertion techniques:
pin loosening • Place pins through stab incisions to reduce skin tension
• Place three to four pins on each side of the fracture
• Reduce thermal necrosis by predrilling holes and using slow-
speed power insertion (rather than hand insertion or high-speed
power)
• Avoid placing pins in fissures or fractures
Use adequately stiff frame configuration
Reduce the fracture so that the bone and fixator are load sharing
Prevent thermal bone injury when using acrylic fixator frame
Restrict patient activity after surgery
Daily cleaning of pin/skin interface or bandage to reduce pin/skin
movement
Limited limb function Avoid penetrating muscles and tendons during pin insertion
Focal osteomyelitis, ring sequestrum Avoid by using proper pin insertion techniques
Treat by removing the loose pin, systemic antibiotics, and curettage of
the necrotic bone. A cancellous graft is placed in the defect.
Pressure necrosis of skin Place frame 1–2 cm from skin surface
Reduce limb swelling with hot compresses or bandage
Iatrogenic fractures Avoid placing pins in fissures
Avoid placing pins too close to fracture
Use pins <25–30% of the diameter of the bone
Delayed or nonunion Place cancellous graft in bone defects
Use proper pin insertion techniques to avoid premature pin loosening
Select adequately stiff fixator frame
Staged removal of the fixator to encourage healing
Frame disruption Confinement and restricted activity
Bandage the fixator and limb
74
may be decreased after fixator application to the femur
or humerus if the transfixation pins penetrate large
muscles. Pin sepsis and premature loosening is a
common complication, particularly in comminuted
fractures where the fixator frame bears most of the load
or when a fixator is applied across a mobile joint.
Restriction of the patient’s activity after surgery and
strict owner compliance are important to prevent
premature loosening at the pin–bone interface and to
ensure the frame is not damaged in the patient’s
environment. Drainage from the pin tracts is often
a sign of pin loosening. Nonunion or delayed union of
the fracture may occur if the fracture is inadequately
stabilized or if the fracture site is infected43,82. Delayed
healing may also occur if frame stiffness is excessive83.
Staged removal of the frame can gradually transmit
load to the bone and encourage healing.
BONE PLATES AND SCREWS
Bone plates and screws are commonly used to
stabilize simple and comminuted fractures in cats
(see Table 18). One of the primary advantages of plate
fixation is that early return to limb function is
expected and encourged. Early limb function
minimizes complications such as muscle atrophy,
joint stiffness, and muscle contracture. It is also
important in cats with multiple injuries when early
use of the fractured limb is essential.
Plates and screws are available in a variety of sizes
and shapes, and when properly applied will control all
of the forces acting on the fracture site (see Chapter 4).
Plate and screw selection depends on the size of the
bone and the fracture configuration. Specific fracture
configurations may require the use of specialized plates
or plating techniques. Knowledge of the basic
techniques and when to use special implants or
methods are the keys to successful bone plating.
Plate application requires that the surgeon expose
a large portion of the fractured bone, which can
significantly disrupt soft tissue attachments and blood
supply. When deciding to use plating techniques for
a given fracture, the advantages of rigid stabilization
and early return to limb function must be weighed
against the disadvantage of delayed healing caused by
surgical invasion of the fracture site. Plate failure is
rarely a result of applying a plate in the ‘wrong’
situation, but rather a result of improper implant size
or errors in application. Plates and screws can be
applied to almost all fracture types, but successful
repair still requires the use of proper surgical
technique and strict attention to the principles of
plate/screw fixation84,85. In most cases, plates are not
removed after healing unless complications develop86.
Plating principles
• Aspetic technique is important since infection
around the implants can lead to delayed healing,
nonunions, draining tracts, and pain.
• The disruption of soft tissue attachments and
blood supply to the bone should be minimized.
• Appropriate sizes and shapes of implants should
be used.
• Placing screws in the fractures lines should be
avoided.
• A minimum of three screws (five to six cortices)
should be placed though the plate on each side of
the fracture line to ensure stable fixation. Longer
plates distribute the stresses over more of the
loaded bone and should be used where possible.
• Autogenous cancellous bone graft (or substitute)
should be placed in all defects if possible.
Screw functions (45)
Plate screws
Plate screws are used to secure the plate to the
bone surface87. The screw passes through a hole in
the plate, compressing the plate to the bone and
providing stability. Cortical screws are used in
most cases, but cancellous screws may also be used as
plate screws. The stability and rigidity of plate
fixation is dependent on the number of cortices
grasped by the screw threads. A minimum of three
screws on each side of the fracture lines is preferred to
ensure adequate fixation. The appropriate screw size
is selected for the plate being used.
Lag screws
Screws placed in lag fashion compress two fragments
together and provide the stability needed for
healing85,87. They are commonly used to stabilize
articular fractures and secure butterfly fragments in
long bone fractures. Lag screws may be placed through
a bone plate or separately from the plate. Both cortical
and cancellous screws may be placed in lag fashion. The
principle of a ‘lag screw’ is that the threads engage only
the cortex on the side of the fracture line opposite the
screw head. The threads engage the far cortex while the
screw head engages the near cortex. As the screw is
tightened, the two fragments are compressed.
Partially threaded screws are readily placed in lag
fashion because they have threads on only the distal
end of the screw. Fully threaded screws are placed in
lag fashion by overdrilling the near cortex (‘glide
hole’) so that the threads do not engage the bone.
The far hole is drilled and tapped to allow the threads
to grasp the bone (‘thread hole’). A drill sleeve is
inserted into the glide hole when drilling the thread
 Fracture fixation methods: principles and techniques
75

hole to ensure it is properly centered. The size of drill
bits used to create a glide and thread holes varies with
screw size (see Tables 14, 15). When lag screws are not
placed through a plate, countersinking the near cortex
maximizes contact between the screw head and the
bone and decreases stress concentration. When
possible, lag screws are placed perpendicular to the
fracture line.
Apophyseal or avulsion fractures can also be
stabilized with lag screws. The screw will compress
avulsion fractures and counteract the distractive forces
created by tendon or ligament attachments.
Position screws
Position screws are used to maintain fragment
position and prevent bone fragments from collapsing
into the medullary cavity during fracture repair. The
fracture is reduced and a thread hole is drilled and
tapped in both of the fragments. When the screw is
tightened, the fragments are fixed in position by the
threads engaging both fragments.
Bone plates
Bone plates are made of stainless steel or titanium
and come in a variety of sizes and shapes (see
Chapter 5)88–94. Plates vary in length, width,
thickness, number of holes, shape of the holes (round
or oval), and shape of the plate. Commonly, 2.7 mm
plates are used to repair femoral, tibial, and humeral
fractures in cats. 2.0 mm plates are often used to
stabilize radial fractures. The application of 2.4 mm
limited-contact dynamic compression plates
(LC-DCP) may be advantageous in many cats because
of the reduced bone contact and the smaller screw size
compared with the 2.7 mm implants. Depending on
how they are applied, plates are used to neutralize
forces, compress fractures together, or bridge gaps in
the bone.

45

A B

D E F

45 Screw functions. A Plate screws anchor the plate to the bone. B Position screw. Threads engage both fragments and
maintain position, preventing collapse of the fragment into the medullary cavity. C Lag screws compress fragments
together. The screw threads engage only the cortex opposite the screw head (thread hole). The near cortex is overdrilled
(glide hole). D Bone fragments are stabilized with lag screws to reconstruct the shaft of the bone. A neutralization plate is
then applied. E A lag screw is placed through the plate to compress the oblique fracture. F A lag screw is used alone to
stabilize a humeral condylar fracture.
76
Plate functions (46)
Neutralization
Plates are applied in neutralization fashion to ‘neutralize’
forces across the fracture site86. They are used when the
fracture is reduced or when fragments are anatomically
reconstructed using lag screws or cerclage wires. The
plate is then applied over the reconstructed bone to share
load and protect the fracture fragments and implants
from excessive loads generated during weight bearing.
Compression
Plates are applied in a compression fashion when the
fracture segments are reduced, and compressing the
fragments together enhances stability. This is most
often achieved through proper use of the oval holes
in a dynamic compression plate (DCP). The screw is
eccentrically placed in the oval hole, causing the plate
to shift as the screw is tightened. As the plate shifts,
the bone ends are compressed to enhance stability.
Buttress (bridging)
Plates are applied in buttress fashion to bridge defects
in a long bone fracture, support joint fractures, and
restore normal limb length after malunion or angular
limb deformity. When a gap exists at the fracture site
such that bone fragments do not share in load
bearing, the plate supports the fractured bone and
maintains normal limb length by preventing collapse
at the fracture site. The plate bears the entire
functional load applied through the bone until healing
46
A B C
occurs. Plates placed in buttress fashion are often
used to repair severely comminuted fractures when
reconstruction of the fragments is impossible, would
be too time consuming, or would significantly disrupt
the blood supply to the fracture site (Table 18). When
this technique is employed, normal bone length is
maintained, less time is spent reducing the fragments,
and disruption of the fracture site and its blood supply
is minimized.
Many types of plates can be used in buttress fashion
in cats, including DCP plates and cuttable plates.
Screw holes positioned over the fracture gap must be
left empty, and plate failure through the empty holes
can occur. Autogenous cancellous bone graft should
be placed in all fracture defects to encourage healing
before plate failure occurs. Specially designed
lengthening plates are also available for use in buttress
fashion (2.0 mm, 8 hole and 2.7 mm, 6, 7, 8 hole
Biological Healing Plates, Veterinary Intrumentation).
The central portion of the plate is devoid of holes to
prevent implant failure through empty plate holes.
A plate also serves as a ‘buttress plate’ when used
to stabilize joint fractures. The plate supports the
metaphyseal portion of the bone and maintains proper
joint alignment during fracture healing.
Plate and screw application techniques
Simple fractures
The fracture segments are identified and reduced,
avoiding disruption of the soft tissues and vascular
46 Plate functions.
A Plate used in bridging (buttress)
fashion to prevent collapse of the
fracture gap.
B Plate applied in compression fashion
to stabilize a transverse fracture.
C Plate applied in neutralization
fashion after reconstruction of the
fracture with lag screws.
 Fracture fixation methods: principles and techniques
supply. Care is also taken to prevent further fissuring
of the fragments. Once the bone ends are reduced
and properly aligned, a plate is applied in compression
fashion to compress the fracture ends together,
increasing stability and promoting healing. The
stability provided by such rigid internal fixation allows
early return of limb function.
Comminuted fractures
In comminuted fractures, several options exist for
plate stabilization:
• The fragments are reduced and stabilized with lag
screws or cerclage wires and a neutralization plate
is applied. Care must be taken to avoid damage
to the blood supply and surrounding soft tissues.
• If the comminuted area constitutes a small area of
the overall bone length, the primary fracture ends
can simply be apposed and plated (compression
plate) without significantly shortening the limb.
The small, comminuted fragments are discarded
or packed around the fracture site as bone graft.
• If the area of comminution is too great to allow
shortening of the bone and too severe to permit
reconstruction, a plate is applied in buttress
(bridging) fashion. Fragments are left in place if
they have a blood supply or can be gently moved
closer to the fracture site using absorbable suture
material. Alternatively, they can be morselized using
a rongeur and used as graft to fill the defect.
Autogenous cancellous graft is placed in the defect.
47
47 T plate applied to the proximal tibial metaphysis.
77
Metaphyseal fractures
Metaphyseal fractures can be stabilized using T plates
or L plates (47). These specialized plates are designed
for use on fractures located near the ends of long bones,
when only a small fragment of bone exists between the
fracture site and the joint. The plate allows several
screws to be placed in the small fragment of bone.
Articular fractures
Interfragmentary compression at the articular surface of
the fracture is achieved with lag screws or with screws
placed through a buttress plate. Placement of a buttress
plate on the metaphyseal region of a bone to support an
articular fracture can be difficult because of the limited
bone available for screw placement. T plates, L plates,
and cuttable plates may be used. The plate must be
carefully contoured to ensure the articular fracture is
not displaced when the plate is applied.
Irregularly shaped bones
Fractures of curved or flat bones like the ilium, scapula,
and mandible can be stabilized using regular DCP
plates, the more easily contoured reconstruction plates,
mini plates, cuttable plates, or cuttable malleable plates.
Plate–rod fixation
A combination of an intramedullary Steinmann pin
and a bone plate may be used to stabilize severely
comminuted diaphyseal fractures (Table 18) (48)95–97.
This technique provides adequate stability while
48
48 Plate-rod fixation of a femoral fracture. An
intramedullary pin and plate are used in combination.
78
minimizing trauma to the fragments and soft tissues at
the fracture site. The intramedullary pin is first
inserted normograde to restore proper bone length
and alignment, and to maintain distraction while the
plate is applied. A pin that fills 35–40% of the
medullary cavity is used. This smaller pin provides
room to insert the plate screws and prevents excessive
rigidity of the plate–rod construct, which can delay
healing. The bone fragments and fracture hematoma
are not disturbed. However, if large fragments are far
from the bone column, they may be gently brought
closer using absorbable suture material. No attempt is
made to reduce the fragments anatomically. A bone
plate is then contoured to the tension surface of the
bone and applied in buttress fashion. Radiographs of
the contralateral normal bone may be helpful when
contouring the plate. The most proximal and distal
screws are inserted to engage both cortices of the
bone (bicortical). The remaining screws need only
engage the near cortex (monocortical). A minimum
of three monocortical screws and one bicortical screw
should be used on each side of the fracture. The pin
reduces the strain on the plate and increases fatigue
life of the plate as the bone heals.
INTERLOCKING INTRAMEDULLARY
NAIL FIXATION
Interlocking nails (ILNs) are inserted into the
medullary cavity like an intramedullary pin98–102. They
provide greater bending stiffness than plates and screws
because the nail is placed in the medullary cavity along
the neutral axis of the bone102. The ILN can also be
inserted through a limited approach, reducing injury to
soft tissues and blood supply at the fracture site. The
relatively long, straight bones of the cat are well suited
for fracture repair using intramedullary fixation (49).
Small nails (4.7 mm and 4.0 mm diameter) are
available for stabilization of simple and comminuted
fractures of the femur, tibia, and humerus in cats (Small
Interlocking Nail System, Innovative Animal Products
LLC.)101–104. The nails are made of 316L stainless steel
and have a trocar point on one end for normograde
insertion. They are solid except for the screw holes
drilled near each end. Using a specially designed
insertion guide, screws are inserted through the bone
and the nail to provide axial and rotational
stability98–100. The nails are available in 68 mm,
79 mm, 91 mm, 101 mm, 112 mm, 123 mm and
134 mm lengths. Each has either four screw
holes (two proximal and two distal) or three screws
holes. Three-hole nails may have a single distal or
proximal screw hole. The holes are 11 mm apart and
accommodate either 2.0 mm diameter screws or
2.0 mm solid self-tapping cross-locking bolts
(Innovative Animal Products LLC.) (see Chapter 5).
ILN insertion technique
Radiographs of the contralateral, unfractured bone are
used to determine the size of the medullary cavity and
select the appropriate diameter and length of nail. The
larger 4.7 mm nail will fit into the medullary cavity in
some cats. However, the smaller 4.0 mm nail will
generally fit more easily (particularly in the tibia),
preserving endosteal blood supply and reducing
iatrogenic trauma to the bone during insertion102. The
nail should be long enough to ensure that the screws
can be placed through the ILN on both ends of the
bone and that the screw holes are 1–2 cm from the
fracture site. For fractures near the ends of the long
bone, ILNs with a single hole are used to avoid placing
a screw hole near the fracture site. Using a single screw
at one end of the nail does not significantly alter the
stability provided at the fracture site and is preferred
over placing a screw too close to the fracture100.
The fracture is exposed via a limited surgical
approach. The proximal cortex and medullary cavity are
opened using the nail or a Steinmann pin of the same
diameter. For many fracture types, it is easier to create
an opening into the medullary cavity by using
a Steinmann pin drilled through the proximal cortex in
a retrograde fashion from the fracture site. A series of
pins with increasing diameters is used until a hole is
created large enough to accommodate the desired nail.
This retrograde approach is more disruptive to the
fracture site, but often facilitates proper nail insertion19.
The extension rod and insertion handle are then
attached to the nail and it is introduced into the cavity
in a normograde fashion. Ideally, the nail is placed
with minimal disruption of the fracture site. The ILN
is passed across the fracture line and seated distally
without penetrating the articular surface. Another nail
of the same length can be used to estimate the depth
of insertion. Careful examination of the radiographs
and visualization of the fracture may also help ensure
that the nail is inserted to the proper depth. The
proximal end of the nail should be seated below
the proximal cortex. This is important in femoral
fractures to prevent sciatic entrapment and seroma
formation; and in tibial fractures to avoid trauma to
the articular cartilage of the femoral condyles.
Once the nail is adequately seated, the insertion
handle is removed and the drill-aiming guide is
attached to the nail via the extension rod. The
extension rod allows the nail to be fully seated within
the bone while still attached to the aiming device.
The drill-aiming guide lies parallel to the nail, on
 Fracture fixation methods: principles and techniques
79

the outside of the limb, and has guide holes corre-
sponding to the screw holes in the nail. This allows the
surgeon to drill a hole accurately through the cortical
bone that is in line with the holes in the intramedullary
nail. Special sleeves fit into the holes in the aiming guide
to allow the surgeon accurately to drill, tap, and insert
the screws without visualization of the holes in the nail.
The distal screw or bolt is generally placed first via
a small stab incision over the appropriate portion of
the bone. The trocar guide and sharp trocar are
inserted through the appropriate hole in the aiming
guide, which corresponds to the distal screw hole in
the nail. The sharp trocar separates the soft tissues to
allow access to the bone. It is pushed against the bone
surface to create a starting point for the drill bit. Care
is taken not to move the aiming device during this
procedure. The drill sleeve and appropriate drill bit
(1.5 mm for screws and 2.0 mm for bolts) are then
inserted into the same hole in the aiming device.
A hole is drilled, with the bit passing through the near
cortex, the hole in the nail, and through the far cortex
of the bone. The surgeon must be careful not to allow
the drill bit to ‘walk along’ the bone surface before
engaging the cortex, or the misplaced screw or bolt
may miss the hole in the ILN. The depth of the drill
hole is then measured with a depth gauge, the hole is
tapped if using a screw with a 2.0 mm tap, and the
appropriate length screw or bolt inserted through the
bone and ILN. After insertion of one of the distal
screws or bolts, the fracture reduction is checked.
Proper rotation, alignment, and axial bone length are
confirmed and the remaining implants are inserted.
The extension rod and aiming device are removed
from the proximal end of the ILN.

49

A B C
49 Interlocking nail fixation.
A Interlocking nail attached to the extension rod and drill-aiming guide. Holes in the aiming guide are aligned with the
screw holes in the interlocking nail.
B Screw placement in the interlocking nail. The nail (1) is attached to the extension rod (2) and inserted in the medullary
canal. The drill-aiming guide (3) is attached. A drill bit is passed through the drill sleeve (4) to create a hole in the bone
that is in line with the screw hole in the nail.
C Interlocking nail in the femur secured with two screws proximally and distally.
80
When repairing comminuted fractures, the
fragments can be left in situ and the nail serves as
a buttress function to maintain bone length.
Alternatively, the fragments can be anatomically
reduced with cerclage wires and the nail inserted into
the distal portion of the fracture (neutralization
function). In many cases, it is preferable to avoid using
cerclage wires unless they contribute significantly to
the repair. Autogenous cancellous bone graft can be
placed at the fracture site if desired, or small fracture
fragments can be morselized using a ronguer and
packed around the fracture. The incision is closed
routinely and the fracture radiographed to confirm
reduction and ILN placement.
Postoperatively, the patient’s activity must be
restricted until bony union is confirmed radiogra-
phically. Radiographic evaluation at 4 and 8 weeks is
recommended. The implants are generally not
removed unless complications occur; however, a nail
extractor is available should removal be necessary.
Removal of screws or bolts from the end of the nail will
allow dynamic loading of the fracture site and can be
used to encourage healing102.
Complications of interlocking nails
Complications reported with ILN fixation include
breakage of the nail at the screw holes, breakage of
the screws, missing the screw holes during screw/bolt
placement, and delayed healing99,101,102. Failure at the
screw holes is usually associated with using an
undersized ILN or placing screw holes too near the
fracture site. Missed screw holes in the nail usually
occurs distally and is avoided by attaching the aiming
guide tightly to the nail, ensuring the aiming device
does not shift during drilling, using a sharp drill bit, and
marking the cortex with the trocar to prevent the drill
bit from slipping on the cortical surface when drilling19.
Delayed union can occur with any fixation method
and can be minimized by disrupting the fracture
hematoma and the bone’s soft tissue attachments as
little as possible during the surgical procedure. Careful
technique and attention to the rules of biologic fixation
is perhaps the best way to prevent delayed healing.
Sciatic neuropathy can occur when using an ILN to
stabilize femur fractures and is prevented by inserting
the nail completely into the trochanteric fossa.
CANCELLOUS AND
CORTICOCANCELLOUS
BONE GRAFTING
Cancellous and corticocancellous bone grafts are
used to fill cortical defects or are placed around the
fracture site to promote healing. Autogenous grafts are
collected from the same patient and have the
advantage of early revascularization and early
osteoinduction105–110. Allografts are also available
(Veterinary Transplant Services Inc.). Cancellous and
corticocancellous grafts do not provide structural
support like cortical grafts, but they do promote
bone healing by osteogenesis, osteoinduction, and
osteoconduction. Osteogenesis is the term given to the
graft’s ability to promote healing by delivering live,
bone-producing cells to the fracture site. A small
percentage (approximately 10%) of the transplanted
bone cells survive the transfer and produce new bone in
the recipient site. The percentage of cells that is viable
after transplantation depends on proper collection
methods and care of the graft material. Osteoinduction
is the term given to the graft’s ability to promote
healing by encouraging undifferentiated cells at the
fracture site to produce bone. Components of the graft
recruit mesenchymal cells in the recipient site to
differentiate into cartilage or bone-forming cells. Bone
morphogenic protein and other vital components of
the graft are likely to be responsible for inducing bone
production at the fracture site. Osteoconduction is
the term given to the graft’s ability to encourage bone
healing by providing a scaffold for ingrowth of
capillaries and osteoprogenitor cells from the
surrounding bone and soft tissues110.
INDICATIONS
Cancellous and corticocancellous bone grafts are
commonly used to encourage healing of comminuted,
delayed union, and nonunion fractures and to promote
arthrodesis of joints111. They have also been described
for use in the treatment of chronic osteomyelitis. In
fracture repair, autogenous bone graft is indicated to fill
gaps at the fracture site, replace missing bone fragments,
or promote healing by being placed around the fracture
site. Cancellous and corticocancellous bone grafts are
particularly helpful in fractures that have the potential
for delayed union or nonunion. Unlike cortical bone
grafts, cancellous grafts can be placed in contaminated
fracture sites without concern for sequestration.
AUTOGENOUS GRAFT COLLECTION
An autogenous bone graft must be collected properly
to maximize its effectiveness and prevent complications.
If a graft collection is anticipated, the donor site (or
sites) must be selected and prepared before surgery.
Collection of graft from several sites may be required if
a large quantity of graft is needed. The sites selected
may depend on the amount of graft required, the sites
that are readily accessible when the patient is positioned
on the surgery table for fracture repair, and any
 Fracture fixation methods: principles and techniques
morbidity associated with the donor site. The sites must
be clipped and scrubbed to prevent infection of the
donor site during collection. In most cases, the graft is
collected just before it is needed. However, if the
recipient site is infected or contains neoplastic cells, the
graft can be collected first to prevent contamination of
the donor site. A separate surgical pack or a separate
surgery team may be used to collect the graft.
In cats, autogenous cancellous graft may be
collected from the greater tubercle of the humerus, the
proximal tibia, the proximal femur, and the iliac crest
(50)108,109,112,113. These areas contain sufficient
quantities of cancellous bone and are readily accessible.
The proximal humeral site provides more graft than the
tibia and has been found to heal more quickly after graft
collection. For some surgeons, the iliac crest is the
preferred site for graft collection in cats.
A small incision is made in the skin and
subcutaneous tissues over the donor site. A trephine,
Steinmann pin, or drill bit is used to create a hole in
the near cortex of the bone. When collecting graft
from the iliac crest, a saw, rongeur, or osteotome may
be used to remove the dorsal cortex and permit access
to the medullary cavity. A bone curette is used to
remove the cancellous bone from the medullary cavity
(51). Corticocancellous graft is readily collected from
the iliac crest. The cortical bone removed from the iliac
crest to gain access to the medullary cavity is saved. It
is morselized using a bone rongeur and mixed with the
cancellous bone removed from the medullary cavity. In
some cases, small bone fragments from the fracture site
can be used as corticocancellous graft.
GRAFT PLACEMENT
The autogenous bone graft is immediately placed in the
recipient site or stored briefly by wrapping it in a moist
50
50 Cat skeleton showing the proper collection sites for
cancellous graft: greater tubercle of the humerus, proximal
tibia, proximal femur, and iliac crest.
81
sponge. A sponge moistened with blood is ideal. The
graft should not be allowed to desiccate and should not
be immersed in fluid. The graft should be placed in the
recipient site as soon as possible after collection, as
minimum storage time ensures maximal graft survival.
The graft is gently packed into the recipient site and the
surrounding soft tissues help hold the graft in place.
Overfilling the defect with cancellous bone does not
enhance healing114. Once a sufficient quantity of graft
is collected, the incision over the donor site is closed
routinely. Cancellous or corticocancellous allografts or
graft substitutes may be used instead of autograft
placement. In some cases, allografts or graft substitutes
are used as extenders for autografts in cats115.
COMPLICATIONS
Complications after collection of autogenous
cancellous graft are rare. Infection of the donor site,
seroma formation, or fracture of the donor bone are
potential risks but are uncommon if the collection is
performed properly. Collection of the graft may also
increase operative time if a separate surgical team is
not available.
51
A B
C
51 Technique for collection of autogenous cancellous
bone graft.
A A small surgical approach is made to the bone and
a hole is drilled in the cortex with a pin or drill bit.
B Cancellous bone is removed with a small bone curette.
C Autogenous cancellous bone removed from the greater
tubercle of the humerus in a cat.
82

IMPLANT REMOVAL interfere with healing. Complications that may warrant

Staged removal of external fixator pins may be used
to destabilize the frame gradually, thus increasing the
load on the bone and preventing stress protection.
This is particularly helpful in cats where rigid frame
configurations can slow healing83. Staged removal is
advocated when fracture healing is slow and would be
stimulated by gradually loading the fracture site.
Otherwise, the external fixator pins are simply
removed when healing is complete. In most cases, the
fixator can be removed with the patient under
sedation, although a short-acting general anesthetic
may be needed to remove positive profile pins.
During fracture healing, loose pins may need to be
removed if they cause pain and tissue reaction50.
Internal implants (plates, screws, intramedullary
pins, and wires) may be removed when healing
is complete, but are often left in place unless
complications develop, since removal requires addi-
tional surgery and added expense. Complications that
may warrant removal of intramedullary pins include
pin migration, seroma formation, soft tissue irritation,
and persistent lameness. Sciatic irritation after
intramedullary pinning or interlocking nail fixation of
the femur necessitates implant removal. Pins should
also be removed if they become loose and interfere
with fracture healing. Cerclage wires are rarely
removed unless they become loose or break and
plate removal include infections, stress protection of
the bone by the rigid implants, implant failure, and
lameness that occurs in cold weather when plates are
applied to the distal extremities86.
DELAYED AND NONUNION
FRACTURES
Delayed unions and nonunions occur infrequently
in cats. The reported incidence ranges from approxi-
mately 2–4.3%116,117. Nonunions occur most often in
fractures of the tibia and proximal ulna116. Delayed
unions are those fractures that are healing slowly and
have failed to unite in the expected period of time.
Nonunion fractures are those in which the bone ends
have failed to unite and all signs of repair (osteogenic
activity) have ceased118,119. The cat’s age, the length of
time since repair of the fracture, and the fixation
method employed are considered when distinguishing
a delayed union from a nonunion.
NONUNION FRACTURES:
CLASSIFICATION (52)120
Biologically active or viable
• Hypertrophic – a large, nonossified callus is
present, caused by motion at the fracture site.
• Moderately hypertrophic – a callus is present but
is not overly large.

52

A B C D E F G

52 Nonunion fracture classification system described by Weber/Cech.

Biologically active (viable) nonunions include:
A Hypertrophic nonunion with a large, nonossified fracture callus. B Moderately hypertrophic nonunion.
C Oligotrophic nonunion with minimal fracture callus. Biologically inactive (nonviable) nonunions include:
D Dystrophic nonunion. E Necrotic nonunion. F Defect nonunion. G Atrophic nonunion.
 Fracture fixation methods: principles and techniques
• Oligotrophic – the fracture callus is minimal
or absent. Oligotrophic nonunions are distinguished
radiographically from nonviable nonunions by the
irregular, hazy appearance of the bone ends
indicative of vascularity.
Biologically inactive or nonviable
• Dystrophic – fragments fail to heal because of
a loss of blood supply.
• Necrotic – fragments fail to heal because of
infection or sequestration.
• Defect – fragments fail to heal because of an
excessive fracture gap.
• Atrophic – as nonviable nonunions progress,
they may become osteoporotic and lose blood
supply and osteogenic activity. Resorption of
the bone ends occurs.
CAUSES OF DELAYED AND NONUNION
FRACTURES
Delayed and nonunion fractures are typically caused by
biologic or biomechanical factors (or a combination of
both). Predisposing factors include the severity
of initial trauma, the extent of soft tissue injury,
comminution, bone loss, devascularization of fracture
fragments, poor reduction, poor fixation, and
infection118,119. Nonunions are more likely to occur in
older cats and heavier cats116.
Inadequate stabilization of the fracture
Instability is the most common cause of delayed
unions and nonunions in cats and is generally a result
of selecting an inadequate fixation method or
improper application of the implants. Premature
loosening of orthopedic implants may also lead to
instability and poor healing.
Large fracture gap
Repair tissues are unable to bridge large fracture gaps
caused by bone loss, surgical resection, or distraction.
The resultant gap fills with fibrous tissue or cartilage
and fails to mineralize.
Loss of blood supply to the fragments
Devascularization caused by the initial trauma, surgical
intervention, excessive periosteal stripping, soft tissue
retraction, desiccation of soft tissues and bone, and
liberal use of electrocautery can contribute to a loss of
blood supply to the fracture site.
Infection of the fracture site
Bone fragments will heal in the presence of infection
only if they are stable and have adequate blood supply.
83
Implants are more likely to loosen in an infected
fracture site, leading to instability. Proper wound care
and surgical technique are essential in preventing
infection during fracture treatment.
Other causes
Other less common causes of delayed and nonunion
fractures in cats include osteopenia, neoplasia, radia-
tion therapy, glucocorticoid medication, metabolic
abnormalities, and nutritional deficiencies.
DIAGNOSIS
Delayed union and nonunion fractures are diagnosed
by physical examination and radiography. Physical
examination findings can include disuse muscle
atrophy, lameness, limb deformity (angular,
rotational, or shortening), pain, and reluctance to
use the limb. Drainage from the fracture site may
occur if infection is present. Delayed unions are
characterized radiographically by the presence of a
fracture gap, although signs of progressive healing
(i.e. callus formation) are evident. Common
radiographic features of nonunion fractures include
sclerotic fracture ends, the presence of a gap between
fragments, and smooth, well defined fracture
surfaces (53). Radiographs should be evaluated for
53
A B C
53 Radiographs of a nonunion radius and ulna fracture in a
cat. A Lateral radiograph obtained 4 months after an
intramedullary pin was inserted in the radius to stabilize
a diaphyseal fracture. The cat was nonweight-bearing on the
limb. B Lateral radiographic view after removal of the pin.
No callus is evident and the fracture has failed to heal. The
bone ends are sclerotic and atrophied. C The nonunion
fracture is stabilized with a compression plate applied to the
cranial surface of the radius. Autogenous cancellous bone
graft was packed around the fracture during surgery.
84
evidence of infection when a nonunion is suspected.
Varying degrees of callus are present at the fracture
site in viable nonunions. In nonviable nonunions,
the bone ends may appear atrophied and
osteopenic 118,120. Nuclear scintigraphy can be
helpful to determine whether bone ends are
vascularized.
TREATMENT OF DELAYED UNION
In many cases, delayed unions are managed by simply
allowing more time for healing to occur. The cat’s
activity is restricted to prevent implant failure and the
fracture is monitored radiographically. If instability at
the fracture site is contributing to delayed healing,
additional support may be provided using an external
fixator or external coaptation device. However,
if instability is severe, an entirely new fixation method
should be applied to the fracture. Autogenous
cancellous bone graft can also be placed to stimulate
more rapid healing. Infection is controlled by
antibiotic therapy (based on culture and sensitivity
testing) if indicated.
TREATMENT OF NONUNION FRACTURES
Successful treatment of a fracture nonunion is
contingent upon correcting the biomechanical and
biological factors that influence bone healing118,119.
Viable nonunions
Viable nonunions often result from instability.
Treatment involves neutralization of the forces acting
on a fracture site by proper internal fixation. In some
cases, the existing fixation method can simply
be enhanced to provide additional stability. For
example, an external fixator can be applied to provide
rotational support in a fracture previously repaired
with intramedullary pin. This is most beneficial if
performed before the healing process ceases, however,
and may be inadequate to encourage healing once
a nonunion has developed. In other cases of viable
nonunion, the initial fixation method is abandoned
and rigid fixation is applied, often using a bone plate
(53). Sufficient callus is removed to position the plate
properly and the callus and bone are compressed.
Debridement of the fibrous pseudoarthrosis between
the bone ends and opening the medullary cavity is not
essential but may be performed if it is required to
achieve adequate reduction, if it will not interfere with
blood supply, and does not result in significant
shortening of the limb. In some cases, the bone ends
are simply removed with a bone saw and the resultant
transverse fracture is plated under compression.
Stable, rigid fixation should be achieved even if
compression is not possible. External fixators can also
be used to stabilize viable nonunions.
Nonviable nonunions
Treatment of nonviable nonunions requires proper
alignment and stabilization of the fracture site and
steps to promote the biological healing process by
encouraging revascularization of the fragments. Bone
plates (and occasionally external fixators) are used to
stabilize the fracture rigidly. Revascularization of the
fracture site is enhanced by opening the medullary
cavity with a Steinmann pin or drill bit, placing
autogenous cancellous bone graft at the fracture site,
and drilling holes in dense cortical bone to allow
vascular ingrowth. Onlay bone grafts may also be used
to encourage healing and provide stability. The
surrounding soft tissues are handled with care during
surgery to preserve blood supply. Electrical stimulation
has also been used to promote healing of nonunions,
since bone growth is associated with electronegativity
and an electrical current may encourage bone
deposition. However, the lack of clinical trials, and the
additional expense, has limited the use of electro-
stimulation to treat nonunions in cats.
In infected nonunions, rigid fixation and pres-
ervation of blood supply are very important.
Additionally, all dead bone (sequestra) must be removed
and infected bone is debrided using rongeurs and
curettes. Infected soft tissues, draining tracts, and fistulas
are debrided and aerobic and anaerobic samples are
collected for culture and sensitivity testing. Rigid
fixation is applied, the wound is lavaged, and autoge-
nous cancellous bone graft is placed at the fracture site.
Delayed grafting may be indicated if infection is severe.
Appropriate antibiotics are administered systemically.
Local therapy with antibiotic-impregnated methyl-
methacrylate beads may also be used. The wound is
closed if possible; however, open wound management
may be preferred in some cases. The surgical implants
may be removed when the fracture heals or if they
become loose.
Early return to function, proper physical therapy,
appropriate antibiotic treatment (if indicated), and
owner compliance are essential for a successful
outcome. Many patients will require multiple surger-
ies to provide stability, place additional cancellous
grafts, and remove implants.
ARTICULAR FRACTURES
Articular fractures are treated with open reduction and
internal fixation to achieve proper alignment, ensure
stability necessary for early postoperative motion, and
restore normal joint function. Malarticulation,
 Fracture fixation methods: principles and techniques
85

osteoarthritis, joint pain, and limited function may
result if articular fractures are poorly reduced or
unstable. Adequate surgical exposure is created to
visualize the joint and the fractures fully. Small
cartilage fragments devoid of subchondral bone are
removed. Articular fragments with attached subchon-
dral bone are manipulated into reduction, taking care
not to damage the articular cartilage. Large gaps or
steps in the articular surface are prevented by accurate
reduction. Fragment stabilization is provided using one
of several methods (54):
• Ideally, screws are placed in lag fashion to provide
interfragmentary compression and counteract
shearing forces at the fracture site; 2.7 mm screws
are preferred, although 1.5 mm or 2.0 mm screws
are often used for small fragments. The screws are
placed through the subchondral bone, avoiding
damage to the articular surface. If necessary, the

54

A B C D E

F G H I

54 Repair of intraarticular fractures. A A transcondylar lag screw is inserted to compress the intraarticular fracture.
Accurate anatomic reduction is required to prevent gaps or steps in articular surface. B A transcondylar lag screw is
inserted to stabilize the intraarticular fracture. The supracondylar portion of the fracture is stabilized with cross pins.
C A lag screw is inserted from the metaphysis into the articular fragment. The screw does not penetrate the articular
surface. D A lag screw is inserted from the articular surface. The screw head must be countersunk below the cartilage
surface. E Kirschner wires are inserted from the metaphysis into the articular fragment. Interfragmentary compression is
not achieved with pin fixation. F A single Kirschner wire inserted through the femoral neck and into the osteochondral
fragment to stabilize a fracture of the femoral head. G Two Kirschner wires inserted from the articular surface. The wires
are countersunk below the cartilage surface to reduce trauma to the opposing cartilage. H A plate is applied to the
metaphysis of the bone to buttress the articular surface. A plate screw may be placed in lag fashion through the plate to
compress the fracture line. I A transarticular external fixator is applied to protect the internal joint fixation during healing.
86
screws can be inserted through the articular
cartilage and the heads countersunk below the
surface. However, damage to the opposing
articular surface may occur.
• Kirschner wires may be used to maintain
reduction of very small fragments, but they do
not provide compression. If Kirschner wires are
inserted through the articular cartilage, they must
be countersunk below the surface to avoid trauma
to the opposing cartilage.
• If necessary, a plate or external fixator may be
used to support (buttress) the joint fixation
during healing. Transarticular fixators may be
applied if needed, but are removed once initial
healing has occurred to allow joint motion.
Joint motion is encouraged soon after surgery to
preserve function and cartilage health. Early joint
function without disruption of the fracture site
obviously requires adequate internal fixation of
osteochondral fragments and restoration of normal
ligamentous structures and joint capsule. Passive
motion exercises may be used until the cat is able to
bear weight on the limb. If fracture fixation is
inadequate to permit early joint function, the joint is
immobilized with a splint, cast, sling, or external
fixator to protect the repair until partial healing has
occurred. Typically, the external support can be
removed in 3–4 weeks121.
Complications after an articular fracture repair may
include implant failure, reduced range of motion, and
osteoarthritis. Osteoarthritis is more severe in cases
with malalignment of the cartilage surface. Fortunately,
the progression of osteoarthritis is often slow and most
cats function well, with limited range of motion. Cats
rarely require arthrodesis for adequate, pain-free
function even if moderate osteoarthritis develops.
JOINT ARTHRODESIS
Joint arthrodesis (fusion) is rarely required in cats. It
may be an alternative to limb amputation in some
cases to preserve function in cats with compli-
cated intraarticular fractures or joint luxations, painful
joint instability, severe osteoarthritis unresponsive to
medical therapy, or postural abnormalities caused
by neurologic dysfunction122,123. Various techniques
used for arthrodesis of specific joints are discussed in
the pertinent chapters. The steps to achieve arthrode-
sis of any joint include:
1. Removal of the articular cartilage with curettes,
rongeurs, power driven burrs, or a bone saw to
expose the subchondral bone. Sclerotic
subchondral bone is removed to expose bleeding
cancellous bone.
2. Placement of autogenous cancellous bone graft at
the arthrodesis site to promote bony union across
the joint.
3. Application of rigid fixation. Bone plates, external
fixators, lag screws, and, in some cases, Kirschner
wires can be used. Where possible, compression
should be applied between the exposed
subchondral bone surfaces to enhance healing.
The joint should be fused in a weight-bearing
position.
4. Support of the fixation with external coaptation
or a transarticular external fixator if necessary.
 87

CHAPTER 7
ARTHROLOGY

Feline arthrology has been an overlooked subject in
the past with most reviews of joint disease in small
animals focusing on the dog. However, cats are now
known to suffer from many different types of joint
disease and, although there are many similarities with
the dog, there are also many features that are unique
to the feline patient.
CLASSIFICATION OF JOINT DISEASE
The terms arthritis and arthropathy literally mean joint
inflammation and joint disease, respectively. These terms
are used interchangeably in this chapter to describe
a number of well defined joint diseases characterized
by a combination of inflammatory and degenerative
changes. The terms degenerative joint disease (DJD)
and osteoarthritis are also often used synonymously. In
this chapter, DJD is used as a general descriptive term to
encompass degenerative changes in any joint in the
axial or appendicular skeleton, including synovial,
cartilaginous, and fibrous types. When DJD affects the
fibrocartilaginous intervertebral joints of the spine, it is
known as spondylosis deformans (see Chapter 11). The
term osteoarthritis is reserved for the specific type of
DJD that affects diarthrodial synovial articulations.
Diseases of synovial joints can conveniently be
divided into degenerative arthritis and inflammatory
arthritis on the basis of the predominant pathologic
process (Table 20). Degenerative arthropathies are the
most common types and include traumatic arthritis and
osteoarthritis. Inflammatory arthropathies are less
common than degenerative arthropathies and have
either an infective or immune-mediated etiology.
Infective arthritis caused by bacterial infection (septic
arthritis) is the commonest type of inflammatory arthritis
in the cat. Septic arthritis is classed as an erosive type of
arthritis because there is destruction of articular cartilage
in joints infected by bacteria. Immune-mediated
arthropathies can be subdivided into both erosive
and nonerosive forms. Differentiation between the
infective and immune-mediated forms of inflammatory
arthritis is essential since the therapeutic approaches
to these conditions are diametrically opposed.
Inappropriate treatment of an infective arthritis with
immunosuppressive drugs will have disastrous results.

TABLE 20 CLASSIFICATION OF JOINT DISEASE.

Degenerative Inflammatory Miscellaneous
arthritides arthritides joint disorders
Infective Immune-mediated Synovial sarcoma
Osteoarthritis arthritides arthritides Secondary neoplasia
Traumatic Primary Bacterial (septic) Systemic lupus erythematosus Hypervitmainosis A
arthritis Secondary Bacterial L-form Polyarthritis/meningitis Osteochondroma
Mycoplasmal Idiopathic Synovial osteochondromatosis
Calicivirus Periosteal proliferative Synovial cysts
Lyme disease Rheumatoid Patellar malformation
Tubercular Meniscal calcification
Fungal Osteochondritis dissecans
Osteochondrodysplasia in
the Scottish Fold cat
88

INVESTIGATION OF JOINT DISEASE then to stop interpreting the radiograph before the
SYNOVIOCENTESIS whole film has been assessed. All three components of
For details of synoviocentesis and analysis of synovial the joint should be evaluated radiographically: the
fluid see Chapter 2. bones, the soft tissues, and the joint space. The specific
features that should be examined are the bony anatomic
RADIOGRAPHY relationships, subchondral bone plates and subchondral
Radiography is the most frequently used ancillary bone of the epiphyses, the width and contents of the
diagnostic aid in the investigation of joint disease. joint space, the articular margins and periarticular
Radiographs should be interpreted in the light of the regions, and the periarticular soft tissues. The
clinical findings and not used as a substitute for a radiographic appearance of some disorders that are
correctly performed clinical examination. Radiography familiar to the canine clinician may differ in the cat. For
is usually used to confirm a suspected clinical diagnosis example, the predominant radiographic signs of feline
or to differentiate between two or more joint diseases hip dysplasia are a shallow acetabulum with remodeling
that have similar clinical characteristics. However, of the craniodorsal margin but with minimal
radiographic surveys of multiple joints might be remodeling of the femoral neck (55)1.
indicated to evaluate the overall status of the patient in • The anatomic relationships of the bones making
conditions that are frequently polyarticular, such up the joint may be altered with joint luxation,
as osteoarthritis or immune-mediated arthritis. subluxation, and intraarticular fracture. Reference
Radiographs of other body regions may be indicated; to a radiographic atlas, a file of normal cat
for example, in cats with joint trauma or neoplasia or radiographs, or a radiograph of the contralateral
some of the immune-mediated arthritides to check for joint may be helpful, especially for the smaller
evidence of lesions elsewhere. more complex joints of the distal extremities.
Feline joints are small so it is essential to obtain high • The subchondral bone plate should appear as a
quality radiographs if they are to be of diagnostic value. thin radiopaque line parallel to and adjacent to
Radiographs of joints should be correctly collimated to the joint space. Erosion of the subchondral plate
minimize scatter and obtained using fine detail screens
in two orthogonal planes (i.e. at right angles to
each other). Human mammography film/screen
combinations are especially useful for radiographs of the 55
distal extremities. Additional stress views may be
performed in the evaluation of joint instability. Oblique
projections and special views to outline certain
structures are performed less frequently in the cat than
in the dog. It is often useful to radiograph the
contralateral joint to provide a normal radiograph for
comparison or because some conditions occur
bilaterally. General anesthesia or heavy sedation is usually
required for optimal positioning.
Radiographic interpretation must be thorough and
complete so that each structure is assessed according to
its Roentgen signs. Radiographic lesions in feline joint
disease are often subtle and the use of a magnifying
glass and a bright light in addition to a normal viewer is
recommended. The radiologist should be familiar with
normal feline osteology and with the radiographic
appearance of normal feline joints. Accessory centers of
ossification and sesamoid bones may be present in or
around joints and these ossicles should not be confused
with chip fractures. For example, an accessory center of
ossification may be present as a normal anatomic variant
in the shoulder joint on the caudal or medial rim of the 55 Ventrodorsal radiograph of the pelvis of a cat with
glenoid. Methodical examination is essential; the most coxofemoral osteoarthritis secondary to hip dysplasia. Note
common error is to find the expected abnormality and the remodeling of the cranial margins of the acetabula.
 Arthrology
occurs with erosive immune-mediated or infective
arthritides, osteomyelitis, and joint neoplasia.
Localized areas of sclerosis and remodeling of the
subchondral plate may be seen at the margins of
destructive lesions, such as osteomyelitis.
However, sclerosis is more commonly seen as a
generalized change in chronic osteoarthritic joints
where there is loss of articular cartilage and
eburnation of the opposing joint surfaces.
• The subchondral bone of the epiphysis
subadjacent to the subchondral plate should have
a homogenous appearance. In comparison with
the dog, the cancellous bone of cats has a coarse
trabecular pattern. Osteomyelitis, neoplasia, and
articular fracture will cause an alteration in the
internal architecture of the trabecular bone.
Subchondral cysts are occasionally seen in
osteoarthritic joints in cats as discrete radiolucent
defects in the subchondral bone.
• Joint space width may be increased with joint
subluxation or luxation. Narrowing of the joint
space is indicative of loss of articular cartilage but
cannot be appreciated on normal nonweight-
bearing radiographs.
• Joint space structures are contained between the
subchondral bone plates of the opposing bones
that comprise the joint. This space, therefore,
includes the articular cartilage, synovial fluid, and
intracapsular fat (and intraarticular ligaments,
menisci, and synovial effusion when present).
Intraarticular structures are only visible when they
become mineralized2 or when increased joint mass
results in distension of periarticular soft tissues or
alteration of other intraarticular structures. An
example of the latter would be a reduction in size
of the infrapatellar fat pad in the stifle, associated
with a synovial effusion. Differentiation between
increased joint mass associated with the presence
of soft tissue or fluid cannot be made
radiographically and requires synoviocentesis.
• The articular margins and the periarticular areas
where ligaments and tendons attach should have
a regular, smooth cortical outline. Osteophytes
generally develop at the articular margins where
they appear as characteristic bony outgrowths.
Osteophytes are most commonly associated with
osteoarthritis. Osteophytes that develop at the
site of bony attachment of the joint capsule or at
ligament or tendon insertions are known as
enthesiophytes.
• Periarticular soft tissues are assessed for swelling,
thickening, and mineralization. Swelling most
commonly occurs as a result of acute trauma, for
89
example joint sprain, whereas thickening is a
chronic change most often associated with joint
instability, such as chronic cranial cruciate
ligament (CrCL) rupture. It is not possible to
differentiate between thickening and swelling
radiographically. Mineralization of periarticular
tissue is a rare occurrence. It is occasionally seen
as a sequela to chronic inflammation, for example
bacterial infective arthritis, and is also a feature of
synovial osteochondromatosis.
Contrast arthrography
Contrast arthrography is rarely performed in the cat.
Positive contrast arthrography involves the injection of
a contrast agent into a joint space so that it mixes with
the synovial fluid and delineates the internal margins of
the joint. The contrast agent of choice is iohexol
(Omnipaque 300; Nycomed), which is diluted 50:50
with sterile water to give a concentration of 150 mg of
iodine per ml. The technique is most useful for
investigation of shoulder joint pathology. The volume
of contrast agent required for suspected articular
cartilage lesions (0.5–1.0 ml) is less than that required
to detect capsular defects or to outline the biceps
tendon of origin (2.0–3.0 ml).
SONOGRAPHY
Ultrasonography has potential value for the
investigation of joint disease but there are few reports
of its use in cats3–5. The evaluation of bone is limited
because of the inability of ultrasound to penetrate
osseous tissues. However, sonography may be useful
in the identification of joint effusion, joint
thickening, articular or bone destruction, and joint
instability using a dynamic examination. Periarticular
soft tissue structures that may be examined with
ultrasound include muscles, tendons, abscesses, cysts,
foreign bodies, and tumors. Use of the technique is
likely to remain restricted to specialized centers
because of the small size of the structures under
investigation and the difficulty in the interpretation
of the images obtained.
ARTHROSCOPY
Arthroscopy is rarely used in the investigation and
treatment of feline joint disease. Examination of the
shoulder and stifle joints is possible6,7 but so far there
are mostly only anecdotal reports of its success. There
is one report of the successful evaluation and
debridement of the elbow joints of a cat with
intraarticular osteochondral fragments8. Application
of arthroscopy to other feline joints is likely to remain
limited because of their small size.
90
LABORATORY TESTS
A minimum database for investigation of a suspected
inflammatory arthropathy would include a bio-
chemistry and hematology panel and tests for feline
leukaemia virus (FeLV) and feline immunodeficiency
virus (FIV). This may help to identify cats that are
immunosuppressed or those that have involvement of
other body systems, such as may be seen with some
immune-mediated arthritides, (systemic lupus
erythematosus and idiopathic polyarthritis types II,
III, and IV). Further investigation of joint disease
requires synoviocentesis and synovial fluid analysis
(see Chapter 2). Individual tests, such as measurement
of titers for rheumatoid factor, antinuclear antibody,
or antibodies to Borrelia burgdorferi, may be indicated
in appropriate circumstances. These tests are discussed
more fully with the relevant joint disorders.
SYNOVIAL MEMBRANE BIOPSY
Biopsy of the synovial membrane or synovium is rarely
performed in the cat. The procedure can provide an
invaluable insight into the pathology affecting a joint
and is the only way of achieving a definitive diagnosis
in some cases. Samples are usually collected by means
of an arthrotomy and should be obtained from several
different sites to ensure that the changes seen are
representative of the pathologic process in the entire
joint.
The histologic appearance of feline and canine
synovial membrane is similar9. Histopathologic
examination can provide precise information about
the extent and type of cellular infiltrate, allowing
differentiation between degenerative and inflam-
matory joint disease. Although there is considerable
overlap between diseases, the nature of an inflam-
matory cell infiltrate may help in determining the type
of inflammatory arthritis. Histopathology is the only
way of achieving a definitive diagnosis of joint
neoplasia. Samples of the synovium can also be
submitted for bacterial culture and may be more likely
to yield organisms than synovial fluid.
DEGENERATIVE ARTHRITIDES
TRAUMATIC ARTHRITIS
Cause and pathogenesis
Traumatic arthritis follows a single acute joint injury
caused, for example, by vehicular trauma, an awkward
fall, gunshot wounds, or fights with other animals.
The least severe form of injury is a joint sprain, in
which there is variable stretching or tearing of
ligaments and joint capsule. Joint luxation involves a
more severe disruption of peri- and intraarticular
structures, with tearing of ligaments and joint capsule
and disruption of articular cartilage. Intraarticular
osseous and/or cartilage fractures are associated with
the more severe traumatic injuries and may occur in
isolation or combined with joint luxation or
subluxation. Following a traumatic incident there will
be hemorrhage within the joint and synovitis, which
may be localized to the site of injury.
Clinical signs
Clinical signs include lameness, joint swelling, joint
deformity, and pain on manipulation. Crepitus will be
present if there is fracture or luxation.
Diagnosis
If fracture or luxation is suspected, radiography
should be performed. Joint instability and ligamentous
disruption are evaluated by manipulation under
general anesthesia and stress radiography. Injury to
individual ligaments is most commonly encountered in
the stifle and tarsocrural joints. Joint sprains are
classified according to the severity of the ligamentous
injury as first, second, and third degree.
Treatment and prognosis
A more detailed discussion of the treatment of
traumatic disorders relating to specific joints can be
found in Chapters 8 and 9. In general, treatment
of joint trauma depends on the severity of the injury.
First degree sprains are mild and only require rest
and/or anti-inflammatory medication. Second and
third degree sprains and more severe types of joint
injury such as intraarticular fracture usually require
external coaptation or surgical repair. Osteoarthritis
will occur as a sequela to traumatic arthritis if there are
repeated mild to moderate episodes or if a single
episode is severe enough to cause significant damage to
the joint.
OSTEOARTHRITIS
Osteoarthritis is a type of DJD that is defined as a
disorder of diarthrodial synovial articulations
characterized by degeneration of articular cartilage,
bone remodeling, pathologic changes in periarticular
tissues, low-grade nonpurulent inflammation, and the
formation of new bone at the articular margins.
Osteoarthritis may be classified into primary and
secondary forms. Primary osteoarthritis is thought to
occur as a consequence of an inherent defect in the
articular cartilage so that it is unable to cope with
normal joint forces, whereas secondary osteoarthritis
is secondary to some other joint disorder. Most
osteoarthritis is thought to be secondary in the cat. In
a recent retrospective study of cats over 1 year of age
 Arthrology
radiographed for any reason, 22% showed evidence of
osteoarthritis of an appendicular synovial joint,
although this was not clinically apparent in 67% of
cases10. In another study of 100 cats over
12 years of age, radiographic evidence of DJD was
found in 90% of cats and severe osteoarthritis was
found in 17% of elbow joints11. The realization that
osteoarthritis is a common clinical problem in the cat
is a relatively recent phenomenon12.
Cause and pathogenesis
Osteoarthritis as a cause of chronic pain is common in
the geriatric cat, but it may be seen in any cat with joint
abnormality or following injury. It is postulated that
the inciting cause is repeated joint trauma associated
with the cat’s agile life style and ability to jump. In
accordance with this theory, some studies have found
that the shoulder and elbow joints of geriatric cats are
preferentially affected. Osteoarthritis may also be
secondary to gross trauma, such as joint fractures,
luxations, and ligamentous disruption. Developmental
diseases, such as hip dysplasia or patellar luxation, may
lead to osteoarthritis. Osteoarthritis has been reported
in multiple joints as part of feline mucopolysac-
charidosis VI13 and associated with acromegaly in
middle-aged cats caused by a pituitary adenoma14. The
pathogenesis of acromegalic arthropathy is not fully
understood but it is thought that cartilage hypertrophy
may interfere with cartilage metabolism, thereby
causing cartilage degeneration.
Despite multiple etiologies, the pathologic changes
of osteoarthritis share a final common pathway
that serves to perpetuate the degenerative processes.
Attention usually focuses on the articular cartilage but,
typically, all of the joint structures are involved.
Cartilage becomes fibrillated and ultimately may be
completely lost, exposing the underlying subchondral
bone, which responds by becoming thickened. The
other main feature of osteoarthritis is the production of
osteophytes, which initially develop outside the
epiphysis of the joint, but eventually become
incorporated into the joint, so that the joint assumes a
different shape. This process is known as remodeling
and is thought to be a mechanism that allows the joint
to cope better with the altered stresses placed on it.
Osteophytes are usually thought of as a chronic change
in osteoarthritis, but they have been shown to start to
develop within 1 week of experimental induction
of joint instability15. Enthesiophytes are soft tissue
mineralizations that develop when there is pathology of
the entheses, which are osseous insertion sites of
ligaments and tendons. Additional soft tissue
mineralization may occur as a result of capsular
91
dystrophic calcification or synovial metaplasia.
Degenerative enthesiopathy and intraarticular or
periarticular soft tissue mineralization often accompany
osteoarthritis, but may also occur independently. Other
pathologic changes include thickening of the joint
capsule, an increase in vascularity with hypertrophy and
hyperplasia of the lining layer of the synovial
membrane, and degeneration of intraarticular menisci.
The degeneration of articular cartilage that occurs in
osteoarthritis may be associated with the formation of
osteocartilaginous bodies that remain free in the joint,
disappear, or become embedded in the synovium.
Subchondral cysts are an occasional feature of
osteoarthritic joints in cats. A cyst develops when there
is replacement of subchondral bony trabeculae by
mixed connective tissue.
Clinical signs
Osteoarthritis is an emerging disease of the older cat.
Osteoarthritis has long been recognized
radiographically in cats but, because the disease may
be asymptomatic, the changes were often considered
incidental. The lack of attention to feline
osteoarthritis may be explained by a tendency to
extrapolate information from the dog where the
cardinal sign of osteoarthritis is lameness. It is now
believed that behavioral changes reflecting chronic
pain are more relevant to the diagnosis of
osteoarthritis in the cat. Because cats are small, light,
and agile they compensate well for musculoskeletal
disease and are able to adapt by redistributing weight-
bearing forces to other limbs. Additionally, because
the cat’s lifestyle prevents critical analysis of the gait by
the owner, mild lameness or joint stiffness usually
passes unnoticed. Behavioral changes reported by
owners of cats with osteoarthritis are nonspecific and
include those associated with attitude (hides away,
resents handling, bad tempered, less playful) and
those associated with disability (reduced grooming,
cannot jump, inactive). Lameness and stiffness
associated with osteoarthritis typically have an
insidious onset and are chronic and progressive in
nature. As in other species, signs are worse on rising
after a period of rest following exercise and initially
wear off after the animal warms up. The signs may
tend to wax and wane and are usually exacerbated by
cold and damp weather. Acute flare-ups of the signs of
established osteoarthritis may occur as part of the
natural history of the disease or be associated with
joint sprain or sepsis. Osteoarthritic joints are
susceptible to trauma and are also at increased risk of
infection spread hematogenously from a septic focus
elsewhere in the body.
92
Diagnosis
In advanced cases the diagnosis of osteoarthritis may
be obvious, especially if there is overt lameness.
Affected joints will be thickened on palpation owing
to bony remodeling, joint capsule fibrosis, and
synovial effusion. It is not usually possible to
appreciate this in the shoulder and hip joints because
of the surrounding soft tissues. Manipulation of a
joint with osteoarthritis will usually be resented and
there may be crepitus and a reduced range of joint
motion. The subtler behavioral changes associated
with osteoarthritis may be caused by many other
diseases, and careful assessment of the geriatric cat is
required to establish their significance. This may
include radiographic and laboratory evaluation to
confirm the presence of osteoarthritis and rule out
intercurrent disease.
The radiographic changes of osteoarthritis are
similar to those of the dog (56). The most striking
56
A B
56 Osteoarthritis. A Plantarodorsal radiograph of a cat with osteoarthritis of the hock joint secondary to previous trauma.
B Plantarodorsal view of the contralateral normal hock joint. C Mediolateral radiograph of a cat with osteoarthritis of the
elbow. D Craniocaudal view of the joint in C.
feature is the presence of osteophytes. These are
visualized as roughening of the joint margins, as
obvious bony masses (spurs or exostoses) projecting
beyond the normal bony outline, or as irregular bony
densities when superimposed on the normal osseous
architecture. There will be secondary soft tissue
swelling with thickening of the joint capsule and there
may be an increase in joint mass owing to synovial
effusion. Although enthesiophytes and/or soft tissue
mineralizations are commonly seen in osteoarthritic
joints, these features alone are not indicative of
osteoarthritis. With advanced osteoarthritis there will
be changes in bone shape due to remodeling,
accompanied by sclerosis of subchondral bone and,
occasionally, subchondral bone cysts visualized as
discrete radiolucent defects.
Analysis of the synovial fluid from affected joints
can be performed to rule out inflammatory joint
disease. The fluid from joints with osteoarthritis is
D
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93

normal or has only a slight reduction in viscosity and
a minimal increase in cell numbers, with macrophages
and lymphocytes predominating.
Treatment and prognosis
The approach to the management of osteoarthritis in
the cat is similar to that for dogs. Options include
exercise modification, weight control, the use of
drugs, and surgical intervention. Potential problems
with the management of osteoarthritis include lack of
familiarity with the disease in cats, difficulties with
lifestyle modification, and the toxicity of available
drug therapies. Despite this, the prognosis for
osteoarthritis is generally better than that for the dog
because cats are smaller and more athletic.
Modification of a cat’s exercise regimen may be
difficult but some control is possible; for example, by
altering the environment or by only allowing the
cat out at set times each day. Strategies used in the dog,
such as restricted leash exercise and aquatic therapy, are
sometimes appropriate for the cat. Lameness associated
with flare-ups of osteoarthritis should be managed by
enforcing strict confinement for a few days.
Weight loss is essential if the cat is obese and use of
a commercial low-calorie diet is recommended.
Conversely, geriatric cats that are underweight should
be fed a calorie-dense diet, since osteoarthritis will
worsen if they stop exercising as energy levels decline.
Pain control in cats with osteoarthritis has been a
problem in the past because of a lack of drugs
specifically licensed for long-term use in the cat
(Table 21). Cats are more susceptible than other
species to the adverse effects of nonsteroidal
antiinflammatory drugs (NSAIDs) because of a
deficiency of glucuronide conjugation. Slower drug
metabolism and a longer half-life lead to accumulation
of toxic amounts much faster in cats than other
species16,17. Currently the only drugs for which safe
chronic doses have been established by clinical usage
are aspirin and meloxicam. Even with these drugs it is
essential that dosing is performed accurately if
toxic effects are to be avoided18,19. Aspirin is
only available in human formulation and it is not
commonly used in the cat for the treatment of
osteoarthritis. Meloxicam is available in an injectable
form and as a syrup, which is palatable to cats and

TABLE 21 ORALLY ADMINISTERED DRUGS AND NUTRACEUTICALS USED IN THE MANAGEMENT OF

OSTEOARTHRITIS.
Drug Dose (mg/kg) Dose (5 kg/cat) Remarks
Meloxicam 0.1 mg/kg once daily 5 drops once daily Suspension is
1.5 mg/ml suspension for 5 days then for 5 days then 1–2 palatable
0.02–0.04 mg/kg drops once daily
Tolfenamic acid 4 mg/kg 20 mg once daily Do not exceed
20 mg tablet 3 days’ use
Ketoprofen 1 mg/kg 5 mg once daily Do not exceed
5 mg tablet 5 days’ use
Flunixin 1 mg/kg 5 mg once daily Do not exceed
meglumine 5 mg tablet 3 days’ use
Aspirin 15 mg/kg 75 mg every May cause
75 mg & 300 mg tablets 48 hours gastrointestinal
side-effects
Prednisolone 0.1–0.5 mg/kg 0.5–2.5 mg once Taper to every
1 mg & 5 mg tablets or twice daily 48 hours
Butorphanol 0.5–1 mg/kg 2.5–5.0 mg two Sedative side-effects
5 mg tablets or three times daily
Cosequin 1 capsule once Contains glucosamine,
regular strength daily for 6 weeks chondroitin sulphate,
then once daily glycosaminoglycans,
or 1 every 48 hours manganese ascorbate
94
facilitates accurate dosing in the food. Meloxicam is
currently only licensed for use in cats as a single
injection for reduction of postoperative pain and as
an antipyretic. The clinical efficacy of the syrup has
been demonstrated for cats with acute and chronic
painful locomotor disorders20. The authors have
found the oral form of the drug to be both safe and
effective when administered at a loading dose of
0.1 mg/kg (1 drop/kg) once daily for 5 days,
followed by a maintenance dose of 0.02–0.04 mg/kg
(1–2 drops/cat). This dosage can be used safely
long term, but, like all NSAIDs, meloxicam should
preferably be used strategically for a few weeks at a
time. In cases where medication is required on a
permanent basis, the lowest effective dose is titrated
against the clinical signs, if necessary, by reducing the
frequency of administration.
The use of glucocorticoids is controversial in the
treatment of osteoarthritis and there is evidence that
high doses cause deterioration by promoting cartilage
degeneration. However, glucocorticoids are well
tolerated by the cat and obvious clinical improvement
can often be produced by the use of relatively
low doses for short periods of time. Prednisolone
or prednisone at a dose rate of 0.1–0.5 mg/kg
once or twice daily is the drug of choice for
severe osteoarthritis unresponsive to NSAIDs or for
acute flare-ups when infection has been ruled out. If
long-term administration becomes necessary, the drug
should be administered on an alternate day basis and
the minimum effective dose should be titrated against
the clinical signs. The combined administration of
glucocorticoids and NSAIDs confers no therapeutic
advantage and is contraindicated because of the
greatly increased risk of side-effects.
The use of the so-called matrix supplements or
viscosupplements is poorly documented in the cat. The
injectable drugs, pentosan polysulphate and
polysuphated glycosaminoglycans, are unlicensed for
use in the cat, although the authors have used them
with some success. Pentosan polysulphate is
administered at a dose rate of 3 mg/kg subcutaneously
(SC) on four occasions 5–7 days apart. These drugs
should not be combined with NSAIDs since they have
anticoagulant properties that are potentiated by
NSAIDs. In one trial no short-term problems were
identified when polysuphated glycosaminoglycan was
administered to healthy cats21. There is also a number
of nutritional supplements available for oral
administration that are recommended for use in the cat
for the treatment of osteoarthritis. These preparations
are classed as nutraceuticals and are not subject to the
same rigorous licensing procedures applied to
pharmaceutical drugs22. Most nutraceutical products
marketed for osteoarthritis contain glucosamine and
chondroitin sulphate as the main ingredients. Their
mode of action is not fully understood but products
such as Cosequin (Nutramax Laboratories Inc.) may
have some benefits in the treatment of cats with
chronic pain due to osteoarthritis23. Although their
efficacy is not proven, they appear to be safe. They can
be used in combination with NSAIDs when they may
have the effect of reducing the minimum effective dose
of the NSAID.
Joints that are poorly responsive to medical
therapy may benefit from irrigation with sterile
normal saline or lactated Ringer’s solution. The
procedure can be combined with synoviocentesis and
is performed by insertion of an intravenous cannula
into the joint under general anesthesia followed by
lavage with up to 200 ml of fluid. This may be
beneficial because of the temporary removal of joint
debris and inflammatory mediators.
The goal of surgical intervention should be the
correction of the underlying causes of osteoarthritis,
such as cruciate rupture or intraarticular fracture,
in order to prevent or slow the progression of
the disease. Joints that are chronically painful and
nonfunctional may be salvaged by arthrodesis, or
excision arthroplasty in the case of the hip or
mandibular condyle. These procedures are discussed
in detail in the relevant chapters.
INFECTIVE INFLAMMATORY
ARTHRITIDES
An infective arthritis is a type of inflammatory
arthropathy caused by a living microbial agent, which
can usually be isolated from the joint. The microbial
agent in cats may be a bacterium, mycoplasma, virus,
fungus, or spirochaete.
BACTERIAL ARTHRITIS
Bacterial or septic arthritis is the most common type
of infective arthritis. The bacteria involved are those
commonly found in the oral cavity (Pasteurella
multocida, Streptococcus spp., Staphylococcus spp.,
coliforms, anaerobes).
Cause and pathogenesis
Septic arthritis is usually the result of a bite wound
sustained in a fight with another cat. Cat bites are a
common occurrence contributing to 4.7% of all feline
consultations in one North American study24. Other
causes include traumatic injuries, such as vehicular
trauma, extension of infection from adjacent soft
tissues, hematogenous spread, or iatrogenic following
 Arthrology
joint surgery. Intervertebral disc joints are rarely
affected causing discospondylitis. In line with the
etiology the joints of the distal extremities, particularly
the carpus, are most commonly affected.
Hematogenous spread from an infected focus
elsewhere in the body is uncommon. This type of septic
arthritis is usually mono-articular and infection is more
likely to localize to a joint that is already damaged.
Bacterial arthritis may thus be a complication of
traumatic joint injury, such as a sprain, and
osteoarthritic joints are predisposed to infection.
Multiple joint involvement may occur secondary to
bacterial endocarditis, although this is very rare in the
cat. Young kittens occasionally suffer from polyarticular
septic arthritis as a result of hematogenous spread from
an infected umbilicus or associated with postparturient
metritis or mastitis.
Clinical signs
The main presenting sign is lameness of a single limb,
which is usually acute and severe. If septic arthritis
follows a cat bite, initial lameness may fail to resolve or
there may be relapse after initial improvement. In some
cases the primary injury may have passed unnoticed by
the owner and evidence of a bite wound may only be
discovered on closer inspection. The affected joint will
be hot, swollen, and painful, with a reduced range of
motion. In advanced cases there may be crepitus
indicating extensive damage to articular cartilage and
bone. The cat is often, but not invariably, systemically
ill and pyrexic. In chronic cases there may be secondary
ligament rupture and disuse atrophy of the muscles of
the limb, and joint ankylosis may eventually develop.
Diagnosis
Diagnosis is based on the history and clinical findings,
radiography, and synovial fluid examination.
Radiography in the early stages shows nonspecific
changes associated with the accumulation of exudate,
soft tissue swelling, and joint distension. Osseous
changes become evident within a few weeks. Loss of
articular cartilage may be evident as a loss of joint
space, although changes in joint space are difficult to
assess in nonweight-bearing radiographs. Periarticular
osteophytes develop and these may be extensive. In
more chronic cases there is destruction of bone, with
erosion of the subchondral plate and, eventually,
complete loss of bone with an irregular widening of
the joint space. Osteomyelitis may extend into the
metaphyses of the adjacent bones, with a mixed
pattern of lysis and sclerosis as attempts are made to
wall off the infection (57). Bony ankylosis of the joint
may eventually develop.
95
Synovial fluid should be obtained from any joint
when infection is suspected. Suppurative fluid will be
increased in quantity, turbid, and watery, and may
be hemorrhagic. White blood cell numbers will be
increased and these will be predominantly degenerate
neutrophils. Culture of synovial fluid may reveal the
organism, although organisms cannot be grown in
some cases. The likelihood of a positive culture is
much greater if the sample is inoculated into blood
culture medium and if prior antibiotic therapy has not
been given.
Treatment and prognosis
Cat bites involving a joint or adjacent to a joint should
be treated aggressively, using lavage and drainage, if
necessary, to prevent infection becoming established
in the joint. Bacterial cultures of deep tissues should
be performed to determine appropriate antibiotic
therapy. Joints that are already septic should be
lavaged copiously under anesthesia with normal saline
or Ringer’s solution, either percutaneously or via a
mini arthrotomy. If infection is more chronic, an
arthrotomy is performed and a drainage tube placed
in the joint to permit continued drainage and
irrigation of the joint. Antibiotic therapy, preferably
57
A B
57 A Dorsopalmar radiograph of a cat with septic arthritis
of the carpus with osteomyelitis in the adjacent radial
metaphysis.
B Mediolateral view of the carpus of the same cat. Lysis,
periosteal reaction, and sclerosis are evident in the distal
radius. Note the soft tissue swelling and loss of the
radiocarpal joint space.
96
guided by culture and sensitivity, is continued for a
minimum of 4 weeks. Commonly used antibiotics
include cephalexin, potentiated amoxicillin,
clindamycin, fluoroquinolones, and metronidazole.
The prognosis is dependent on the degree of
permanent damage to the joint. If there has been
considerable destruction of articular cartilage, joint
function will be poor and excision arthroplasty,
arthrodesis, or even amputation may be necessary.
Persistent low-grade lameness may be a sequela
because of osteoarthritis or synovitis caused by the
presence of nonviable bacterial antigens. In the latter
case glucocorticoids may be beneficial provided
bacterial infection has been completely eliminated.
These drugs also help to relieve joint stiffness
associated with soft tissue swelling and fibrosis.
BACTERIAL L-FORM ARTHRITIS
Bacterial L-forms are a rare cause of inflammatory
polyarthritis in cats. Subcutaneous abscesses and
arthritis associated with a probable bacterial L-form
have been described25. Clinical signs were seen in
three cats from one household and included pyogenic
subcutaneous abscesses, inflammatory joint disease,
pyrexia, and systemic illness. The infection spread
locally and hematogenously to involve other joints
and subcutaneous sites. The exudate was
characterized by pyogranulomatous inflammation.
Radiography of affected joints revealed destructive
changes consistent with erosive joint disease.
Bacterial L-forms are bacteria that lack a cell wall
and are resistant to many broad-spectrum antibiotics,
although they are susceptible to tetracycline. A
number of reasons for the loss of the cell wall have
been proposed, including therapy with certain
antibiotics and interaction between the host’s immune
system and the bacterium. Because of the lack of cell
wall the bacterial L-forms cannot be identified using
routine light microscopy. The organisms are very
difficult to grow in the laboratory and routine cultures
of joints and abscesses will be negative.
MYCOPLASMAL ARTHRITIS
Mycoplasmas are found naturally in the upper
respiratory and urogenital tracts of healthy cats. There
are a number of reports of the organisms causing
polyarthritis and tenosynovitis, usually in debilitated or
immunosuppressed individuals26,27. Affected cats are
presented with lameness, swollen limbs, painful joints,
and pyrexia.
The synovial fluid is watery and turbid, and cytology
reveals large numbers of white blood cells with
nondegenerate neutrophils predominating. Culture of
the organism from the synovium or the synovial fluid
may be possible on special media. A tentative diagnosis
is possible if the organism can be visualized by
light microscopy after staining with Wright–Leishmann
or Giemsa. Treatment with tylosin, erythromycin,
tetracycline, or gentamycin may be successful.
CALICIVIRUS ARTHRITIS
Cause and pathogenesis
Calicivirus is a cause of acute arthritis in cats, either
following natural infection or live virus vaccination.
The role of calicivirus in chronic arthritis is unknown.
The arthritis may be infective, associated with
intraarticular live virus, or immune-mediated,
associated with intraarticular nonviable virus antigens.
Disease is most commonly seen in cattery kittens
infected with field strains of calicivirus. It can occur in
spite of vaccination since immunity to at least one
strain of calicivirus is not conferred by the more
commonly used vaccine strains. Lameness has been
reproduced experimentally using two separate strains
of calicivirus in young kittens28. Viraemia was
demonstrated but no lesions were found in muscles,
joints, or the central nervous system; increased
numbers of macrophages were found in the synovial
fluid. In the past, vaccine-associated calicivirus
arthritis was commonly seen associated with certain
strains of calicivirus included in live vaccines. This is
now a rare cause of disease since manufacturers have
removed these strains from their vaccines.
Clinical signs
Infective arthritis associated with certain field strains
of calicivirus is seen mainly as a transient lameness and
pyrexia in kittens between the ages of 6 and 12
weeks29,30. Affected kittens are usually ill for 1–2 days
and demonstrate a stiff gait with pain on manipulation
of affected muscles and joints. Less than half of the
kittens have, or subsequently develop, ulceration of
the tongue or hard palate. Kittens experimentally
infected displayed generalized hyperesthesia with
evidence of joint pain on manipulation and, in some
cases, cutaneous erythema over the tarsal joints28.
Immune-mediated arthritis is seen mainly as a
polyarthropathy 5–7 days after vaccination with live
vaccines containing feline calicivirus31,32. Affected cats
have a shifting lameness, a stiff gait, and pyrexia. Signs
generally occur after the first vaccination and most
affected cats are less than 6 months of age.
Diagnosis
Diagnosis is generally attempted on the basis of
clinical signs and, in the case of the vaccine-associated
 Arthrology
form of arthritis, the history of recent inoculation.
Serology is generally unhelpful because of the
widespread presence of antibody as a result of
vaccination. Cytology of synovial fluid from
affected joints may reveal an increased number of
macrophages, many of which contain phagocytosed
neutrophils28.
Treatment and prognosis
The prognosis for infective calicivirus arthritis is good
since the disease is self-limiting and only symptomatic
therapy is indicated. Immune-mediated calicivirus
arthritis is also usually transient, although some
cats develop a more protracted inflammatory
polyarthropathy. Disease is usually self-limiting but
administration of glucocorticoids may be indicated for
persistent cases. This form of polyarthritis is similar to
type II idiopathic polyarthritis.
LYME DISEASE
Cause and pathogenesis
Lyme disease is a multisystemic inflammatory disorder
of humans and domestic animals caused by infection
with the tick-borne spirochaete Borrelia burgdorferi.
Lyme disease was first recognized in the United
States, where it is endemic in certain areas, but has
since been described worldwide. Cats appear to be
resistant to the development of clinical signs of Lyme
borreliosis. Although they can become infected and
develop high levels of serum anti-borrelia antibodies,
the natural disease has not been described as a distinct
clinical entity in the cat.
Clinical signs
Clinical signs were not observed in experimental cats
inoculated by various routes with laboratory-derived
strains of Borrelia33. In contrast, when cats were
inoculated with the organism directly from ticks they
developed polyarthropathy and had joint, lymphoid,
pulmonary, and central nervous system inflammation
on postmortem examination34. In acute infections in
dogs, clinical lameness is frequently localized to
one or more joints, although chronic nonerosive
polyarthritis is the main finding in more prolonged
infections. The course of disease may be intermittent
and spontaneous resolution may occur. There is no
information on the clinical manifestations of natural
infection in cats but clinical signs are likely to be
similar to those described in the dog.
Diagnosis
The clinical signs are often vague and infection can
be asymptomatic, so accurate diagnosis of Lyme
97
disease is difficult. A positive serologic test merely
signifies exposure to the organism and is not proof
that the clinical signs are caused by the spirochaete.
In two North American studies serum samples taken
from cats that had been infected with ticks were
positive for antibodies to the organism in 14%35 and
15%36 of cases. The proportion of positive results was
the same irrespective of lameness. In the UK 4.8% of
cats, screened as clinical patients, were seropositive37.
None of the seropositive cats in the latter study had
clinical signs of lameness.
Treatment and prognosis
Therapy for Lyme disease is given empirically because
of the difficulty in making a definitive diagnosis. The
organism is susceptible to a number of antibiotics but
doxycycline (10 mg/kg twice daily for 4 weeks) is
currently the drug of first choice for adult cats.
Clinical improvement should always be viewed with
suspicion because the clinical signs may be
intermittent or may resolve spontaneously. Based on
the information available from other species, prompt
improvement in clinical signs is to be expected with
appropriate antibiotic therapy. Treatment is more
likely to be successful if antibiotics are given in the
initial acute phase of the infection.
TUBERCULAR ARTHRITIS
Tubercular arthritis is an occasional manifestation
of tuberculosis. In a recent series of cats diagnosed
with tuberculosis, one cat presented with
involvement of an elbow joint38. There was a history
of malaise, weight loss, and forelimb lameness.
Diagnosis was made by radiography and biopsy of the
synovium. The cat was successfully treated with
isoniazid, rifampicin, and streptomycin, although
there was residual lameness.
FUNGAL ARTHRITIS
Histoplasma capsulatum and Crytococcus neoformans
are rare causes of hematogenously disseminated
infective arthritis39. There is usually multisystemic
involvement and multiple joints may be affected.
Histoplasmosis is discussed in Chapter 13;
cryptococcosis is discussed in Chapter 11.
IMMUNE-MEDIATED
INFLAMMATORY ARTHRITIDES
Immune-based arthritides are uncommon causes of
lameness in the cat. There are a number of different
types but they are all characterized by chronic
synovitis affecting multiple joints in a bilaterally
symmetrical fashion. Although the underlying cause
98
of these disorders is unknown and they are classed as
noninfective, persistent intraarticular microbial
antigens may play a role in their etiopathogenesis. It is
useful to subdivide them into erosive and nonerosive
types based on the degree of damage to bone
and articular cartilage40. Joint inflammation in
nonerosive immune- mediated polyarthritis is thought
to be due to the deposition of immune complexes of
antibody, antigen, and complement in the synovial
membrane. Treatment of the various types of
immune-mediated polyarthritis is similar and is
discussed at the end of this section.
NONEROSIVE TYPES
Systemic lupus erythematosus (SLE) and idiopathic
polyarthritis are both more common in young adult
cats. The clinical signs of cats with nonerosive immune-
based polyarthritis are very similar irrespective of type
and generally have a rapid onset. Affected cats typically
appear very stiff and uncomfortable and may have a
history of shifting lameness. They are usually reluctant
to exercise, resent handling, and may be uncooperative
and bad tempered. There is usually inappetence,
malaise, and pyrexia unresponsive to antimicrobial
therapy. Affected joints are painful on manipulation
and distal limb joints may be obviously thickened and
swollen. In some cases it may be more difficult to
appreciate synovial effusion or periarticular thickening.
Cats with SLE and idiopathic polyarthritis may show
other signs of immune complex disease reflecting
involvement of other body systems. Idiopathic type II
cats may show signs of infection elsewhere in the body,
type III cats will have gastrointestinal signs, and type
IV cats may have signs relating to an underlying
neoplasm. Cats with type IV idiopathic polyarthritis
usually have myeloproliferative disease, which can be
diagnosed by bone marrow biopsy. A proportion of
these cases will be positive for FeLV.
Systemic lupus erythematosus
SLE is a multisystemic disease in which nonerosive
polyarthritis may be a feature. The antigen involved in
the pathogenesis of the polyarthritis, dermatitis, and
glomerulonephritis that may be seen with SLE is
believed to be nucleic acid. In one study, definite SLE
was diagnosed in only two of 31 cats with polyarthritis
and it is a rare cause of joint disease41.
Diagnosis
Three criteria must be satisfied to diagnose definite
SLE. Criteria 1 and 2 must always be satisfied; if
criterion 3 is not fulfilled a diagnosis of probable SLE
is made.
1. There should be multisystemic involvement,
although it is rare to have more than two body
systems affected at any one time. Common
manifestations include polyarthritis,
thrombocytopenia, hemolytic anemia, leucopenia,
pyrexia, dermatitis, glomerulonephritis, and
meningitis.
2. There should be a positive antinuclear antibody
(ANA) titer. A 1:40 titer is considered positive in
cats. The ANA test is very sensitive but has poor
specificity. The background level of ANA is
relatively high in the cat and false positive results
may occur during the acute phase of infectious
diseases such as FeLV, FIV, and feline infectious
peritonitis (FIP). It should be noted that a
diagnosis of SLE cannot be made by positive
ANA alone, regardless of titer.
3. The immunopathologic features should be
consistent with the clinical involvement. For
example, antibodies against red blood cells or
platelets should be demonstrable in cats with
anemia or thrombocytopenia; immune complex
deposition should be shown in tissue biopsies of
the synovial membrane or kidney in cats with
polyarthritis or glomerulonephritis respectively.
Polyarthritis/meningitis syndrome
Polyarthritis/meningitis syndrome (PMS) is a rare
condition with clinical manifestations similar to SLE.
However, there is joint and central nervous system
involvement only and affected cats test negative for
serum ANA. The typical presentation is an immature
or young adult cat with neck pain, depression,
pyrexia, and stiffness in addition to polyarthritis.
Cerebrospinal fluid (CSF) analysis reveals increased
protein and pleocytosis.
Idiopathic polyarthritis
Cats with polyarticular noninfective inflammatory joint
disease that does not satisfy the diagnostic criteria for
other types of polyarthritis are included in this broad
classification. Idiopathic polyarthritis is the commonest
of the immune-mediated arthritides in dogs but is rarely
reported in the cat41–43. Idiopathic polyarthritis can be
subdivided into four types based on the presence of
concurrent disease:
• Type I: uncomplicated idiopathic polyarthritis.
• Type II: reactive idiopathic polyarthritis
associated with infection elsewhere in the body;
for example, urinary or respiratory tract infection,
chlamydial conjunctivitis.
• Type III: enteropathic idiopathic polyarthritis
associated with gastrointestinal disease.
 Arthrology
99

• Type IV: neoplasia-related idiopathic polyarthritis 58

associated with neoplastic disease.
All types are believed to be the result of immune
complex hypersensitivity reactions. The different
associations in types II through IV may represent the
antigenic source for the immune complexes or may be
coincidental. Multisytemic involvement occurs in
some cats; these cases may resemble SLE but they are
consistently negative for ANA. Some cases of type I,
and occasionally type II, may eventually progress to
an erosive rheumatoid or periosteal proliferative A
polyarthritis.

EROSIVE TYPES
Erosive immune-mediated arthritis is also known as
chronic progressive polyarthritis44,45. There are two
types of disease: a more common periosteal
proliferative type and an uncommon deforming type
with many of the features of human and canine
rheumatoid arthritis46. With both types of disease the
clinical signs have a tendency to wax and wane.

Periosteal proliferative polyarthritis B

Periosteal proliferative polyarthritis (PPP) is seen in
young entire and neutered male cats less than 5 years
of age.

Cause and pathogenesis

The etiology is uncertain but there may be links with
FeLV, FIV, and feline syncytia forming virus (FeSFV)
infections45,47. It has been suggested that FeLV-
(or FIV-) induced immunosuppression allows multipli-
cation of FeSFV in the joints of predisposed
individuals, which causes the disease. However, an
increased incidence of FeLV or FIV virus in infected
cats has not been demonstrated. It has also been
reported that all cats with PPP are infected with
FeSFV48. It has not, however, been possible to
reproduce the disease experimentally45 and the virus
can be cultured from the joints of many normal cats. It
is possible that the presence of FeSFV is incidental,
since an already inflamed joint with many actively
dividing cells is an ideal environment for the virus to
multiply.
Clinical signs
There is typically an acute onset of pyrexia and malaise
with a stiff gait, joint effusion, and joint pain. There
may also be generalized muscle atrophy and generalized
or localized lymphadenopathy. Within several weeks of
this early acute phase the disease enters a more chronic
phase in which there is extensive periosteal new bone
formation, especially around the hocks and carpi (58).
C D
58 A Mediolateral radiograph of the hock joint of a cat
with early changes of PPP. Note the erosive changes on
the tuber calcis and the periarticular periosteal new bone
formation on the plantar aspect. (Radiograph courtesy of
Davies Veterinary Specialists.)
B Mediolateral radiograph of the elbow joint of the cat
in A showing erosive changes in the olecranon.
(Radiograph courtesy of Davies Veterinary Specialists.)
C Mediolateral radiograph of the elbow joint of a cat
with advanced changes of PPP. Note the extensive
remodeling of the joint and the periarticular periosteal
new bone formation.
D Marked swelling and thickening of the hock joints of
the cat in C.
100
Rheumatoid arthritis
Rheumatoid arthritis is a rare chronic progressive
destructive polyarthritis.
Cause and pathogenesis
The pathogenesis of the synovitis involves the
production of autoantibodies against immunoglobulin
(rheumatoid factor). The synovitis is caused by the
formation of immune complexes, including rheumatoid
factor and immunoglobulin, within the joint. However,
there is not always serologic evidence of rheumatoid
factor and its presence is not specific for rheumatoid
arthritis.
Clinical signs
Cats with rheumatoid arthritis have generalized
stiffness, progressive lameness, and debility of
increasing severity over a period of many months. The
onset is generally gradual and, unlike PPP, there is
no malaise and no significant synovial effusion.
Palpation reveals joints that are thickened and painful,
with crepitus and reduced range of motion on
manipulation.
Diagnosis
The criteria used to diagnose rheumatoid arthritis
in cats are based on those used in human
rheumatology:
1. Stiffness after rest.
2. Pain or tenderness on motion of at least one
joint.
3. Swelling of at least one joint.
4. Swelling of one other joint within a period of
2 months.
5. Symmetrical joint swelling.
6. Radiographic changes suggestive of rheumatoid
arthritis.
7. Serologic evidence of rheumatoid factor.
8. Abnormal synovial fluid.
9. Characteristic histologic changes in the synovial
membrane.
Characteristic radiographic changes include severe
subchondral bone lysis, joint deformity, and joint
subluxation or luxation. Subcutaneous nodules seen
in humans with rheumatoid arthritis have not yet been
reported in the cat. Seven criteria must be satisfied to
make a diagnosis of classical rheumatoid arthritis and
five to make a diagnosis of definite rheumatoid
arthritis. In addition, two of criteria 6, 7, and 9 should
be fulfilled and criteria 1–5 should have been present
for at least 6 weeks.
DIAGNOSIS OF IMMUNE-MEDIATED
ARTHRITIDES
Radiography
All clinically affected joints should be radiographed.
In cats with suspected multisystemic involvement,
radiography of other body regions may be indicated;
for example, the thorax for evidence of respiratory
infection in idiopathic type II polyarthritis. The
radiographic changes seen in the joints of cats with the
different types of immune-mediated arthritis are very
similar, especially in the early stages of disease.
Common features of both erosive and nonerosive
arthritis are periarticular soft tissue swelling,
distension of the joint capsule, and loss of
intraarticular fat shadows. With chronicity the erosive
forms show a more characteristic combination of
destructive and proliferative changes.
In rheumatoid arthritis the destructive changes
predominate. There is erosion of the joint margin
visualized as an increased irregular joint space or an
overall loss of mineralization of the bones forming the
joint. In comparison with the dog, the coarse trabecular
pattern of feline bones may make it more difficult to
appreciate the destructive changes in the early stages.
In PPP there are also destructive changes but the
proliferative changes predominate. PPP is characterized
by periarticular periosteal new bone formation, which is
so extensive in some cats that affected joints become
partially or sometimes completely ankylosed. There are
also erosive changes in the joints and bony deposits and
erosions at the point of attachment of ligaments or
tendons (enthesiopathies).
Serial radiography is useful to monitor the
progression of the arthritis. For example, some
nonerosive forms may progress to erosive disease and
secondary osteoarthritis may become apparent as joints
become more damaged and less stable.
Laboratory features
In cats with multisystem involvement the laboratory
features will be consistent with the underlying nature
of the immune complex disease, such as anemia and
thrombocytopenia. There is generally a nonspecific
absolute or relative increase in serum globulin levels.
Synovial fluid should be obtained from multiple
joints to confirm that there is an inflammatory
polyarthropathy. There is typically an increased volume
of turbid synovial fluid, with reduced viscosity, a poor
mucin clot, and a positive fibrinogen clot test. The
fluid has an increased white cell count, the majority of
which will be nondegenerate polymorphonuclear cells,
and is negative on culture (see Chapter 2). If there is
 Arthrology
still doubt about the diagnosis, multiple synovial
membrane biopsies from different parts of one or more
joints should be submitted for histopathologic
examination. However, the histologic changes can be
variable and are not specific for one particular type of
inflammatory arthropathy.
Serologic tests are performed for suspected cases of
rheumatoid arthritis and SLE. Rheumatoid factor may
be present in the blood of cats with rheumatoid arthritis
and ANA must be present in the blood of cats before
SLE can be diagnosed. Cats with SLE may also show red
cell autoantibodies or autoantibodies against leucocytes
or platelets. It is important to check with the diagnostic
laboratory that species-specific reagents are available
before submitting samples for immunologic testing.
TREATMENT AND PROGNOSIS FOR
IMMUNE-MEDIATED ARTHRITIDES
Nonspecific treatment of cats with immune-mediated
arthritis is the same as that for cats with osteoarthritis
(exercise restriction, weight control).
Specific treatment is directed towards the
underlying cause in cats with idiopathic polyarthritis
types II, III, and IV. Successful treatment of the
infective, gastrointestinal, or neoplastic process may
resolve the arthritis without the need for additional
immunosuppressive therapy.
Cats with chronic PPP or rheumatoid arthritis are
usually treated with anti-inflammatory doses of
prednisolone for short periods when there is a flare-up
of the clinical signs.
Immunosuppressive therapy with glucocorticoids
is the mainstay of treatment for all other types of
immune-mediated arthritis. The drug of choice is
prednisolone administered at a starting dose of
4 mg/kg divided twice daily for acute cases. This dose
is continued for 2 weeks and then gradually reduced
over a period of 8 weeks, provided the disease stays
in clinical remission. In some cats the drug can be
discontinued but in others a continuous low dose is
required to maintain remission. The maintenance
dose should preferably be given on an alternate day
basis to minimize side-effects. If remission cannot be
achieved, or can only be maintained with excessively
high doses, a combination of prednisolone and a
cytotoxic drug should be used. Cyclophosphamide at
a dose of 2.5 mg/kg is the most commonly used
cytotoxic drug. The drug is administered orally once
daily on 4 consecutive days of each week in
combination with prednisolone at an anti-
inflammatory dose of 1.0 mg/kg divided twice daily.
Cytotoxic drugs are stopped 4 weeks after complete
101
remission is achieved, although prednisolone may be
continued longer. Cyclophosphamide should never be
given for more than 4 months because of the potential
bladder toxicity.
The response to treatment should be monitored by
repetition of synovial fluid cytology 2 weeks after
starting treatment or introducing a different therapeutic
regimen. A low white cell count with a preponderance
of mononuclear cells is a good prognostic indicator and
the therapeutic regimen should be continued. If this is
not the case, the therapy should be modified; for
example, by addition of cyclophosphamide. Complete
blood counts should be performed weekly for cats
receiving cytotoxic therapy. If the white blood cell
count falls below 6.0 × 109/l the dose is reduced by one
quarter, if it falls below 4.0 × 109/l the drug should be
stopped for one week and then reinstated
at half the original dose. It is also advisable to monitor
the urine of cats receiving cyclophosphamide on a
weekly basis, for the presence of blood. Patients that are
immunosuppressed should be regularly checked for
and, as far as possible, protected from secondary
infections, especially of the urinary and respiratory
tracts. Vaccination is advisable but should not be given
until the immunosuppressive drugs have been stopped
or suspended.
The prognosis is variable and differentiation
between types of immune-mediated arthritis is
essential when attempting to predict the likely
outcome of treatment. The idiopathic polyarthritides
carry the best prognosis, with the exception of type
IV, which is secondary to a neoplastic process. The
prognosis tends to be worse for erosive than for
nonerosive forms, especially rheumatoid arthritis.
However, SLE often carries a poor prognosis because
of the involvement of other body systems.
MISCELLANEOUS DISORDERS
OF JOINTS
SYNOVIAL SARCOMA
Feline synovial sarcoma is a rare articular tumor with
only three putative and two definite cases reported
in the English language literature49–53. Synovial
sarcomata originate from mesenchymal synovioblastic
cells in the joint capsule, tendon sheath, or bursa and
invade the joint cavity secondarily. Clinical signs include
chronic progressive lameness, with periarticular soft
tissue thickening and swelling, pain on joint
manipulation, and reduced range of motion. All
reported cases have involved the joints of the distal
extremities or the elbow. Radiography typically reveals a
poorly defined periosteal reaction and multiple punctate
102
osteolytic lesions involving the epiphyses of more than
one bone adjacent to the affected joint. Diagnosis may
be confirmed in some cases by cytologic examination of
synovial fluid53 but otherwise requires incisional biopsy.
The tumor should be staged before surgery by
performing chest radiographs and needle aspiration of
the regional lymph node. Biopsy may suggest that the
tumor is a benign synovioma, but, in those cases where
local excision was performed, the neoplasm
recurred51–53. In dogs, survival may depend more on
the aggressiveness of treatment rather than on clinical
staging or tumor grading54 and the recommended
method of treatment is amputation. The metastatic
potential of the tumor in cats is unknown, although in
dogs 41–54% of cases have metastases at the time of
diagnosis or will develop metastasis subsequently55,56.
SECONDARY NEOPLASIA
Periarticular and juxta-articular malignancies, such as
osteosarcomata and fibrosarcomata, may arise from
extraarticular tissues and invade joints secondarily.
Transarticular involvement of fibrosarcoma has been
reported57. The presentation, diagnosis, and treatment
of these tumors are similar to synovial sarcoma.
Metastasis of malignant tumors to joints is very rare.
HYPERVITAMINOSIS A
The classical sign of vitamin A toxicity is neck stiffness
associated with cervicothoracic vertebral lesions, but
exostoses of limb joints may cause lameness and, in
severe cases, joint ankylosis. The elbow is most
commonly affected but involvement of the stifle and
hips, with no spinal lesions, has been reported58.
(See Chapter 13.)
OSTEOCHONDROMA
Osteochondromas have been reported as a rare cause of
lameness especially in the Burmese breed. The condition
usually affects one or both elbows and originates from
the medial humeral epicondyle59. (See Chapter 13.)
SYNOVIAL OSTEOCHONDROMATOSIS
Synovial osteochondromatosis (also known as synovial
chondrometaplasia) is a rare condition characterized by
the formation of chondral or osteochondral nodules
within the synovial tissue of a joint, tendon sheath, or
bursa. Lesions resembling synovial osteochon-
dromatosis have been reported in the stifle and elbow
joints of two cats60. The condition is typically
monoarticular and is thought to occur as a primary
idiopathic abnormality or secondary to joint disease.
There is chronic progressive lameness and joint
stiffness. The radiographic appearance varies according
to the stage of the condition. Initially there may be
only soft tissue swelling as a result of the cartilaginous
nodules and joint effusion. As the condition
progresses, calcified deposits become visible in and
around the joint and there will be evidence of
osteoarthritis (59). Treatment may be palliative using
NSAIDs or surgical treatment may be attempted by
total synovectomy with removal of all loose bodies. In
advanced cases excision arthroplasty or arthrodesis may
be performed. Synovial osteochondromatosis has been
reported affecting the elbow joint of a Bengal tiger61.
SYNOVIAL CYSTS
Synovial cysts have been reported affecting the elbow
joints of four geriatric cats5,62. The etiopathogenesis of
the condition in the cat is unknown, although in
humans it has been theorized that synovial cysts are
related to herniations of the joint capsule,
inflammation, or osteoarthritis. All of the cats presented
with fluid-filled swellings centered on the medial aspect
of a single elbow joint. Three of the cats had mild or
moderate lameness and showed radiographic evidence
of osteoarthritis. The osteoarthritis may have been the
cause of the lameness in these cases. Plain radiography
is inconclusive but contrast arthrography or
ultrasonography will outline the cystic extensions of the
synovial joint capsule. Confirmation of the diagnosis
requires aspiration of synovial fluid and biopsy. Surgical
excision was curative in one case but not in three cases
treated by excision or drainage.
59
59 Mediolateral radiograph of the stifle joint of a cat with
synovial osteochondromatosis. Note the extensive
intraarticular and periarticular mineralized deposits.
(Radiograph courtesy of Davies Veterinary Specialists.)
 Arthrology
PATELLAR MALFORMATION
Acute traumatic fractures of the patella are discussed in
Chapter 9. Malformation is occasionally encountered,
usually as an incidental finding on stifle radiographs.
The bone is divided into two (bipartite), three
(tripartite), or more (multipartite) parts and the
abnormality may be unilateral or bilateral. In bilateral
cases it would seem most likely that the etiology is
congenital. The lack of patella continuity is thought to
be associated with an area of reduced vascularity. In
some unilateral cases the lesion may represent chronic
nonunion patella fracture.
MENISCAL CALCIFICATION
Calcification within the cranial pole of the medial
meniscus is a common incidental radiographic finding
in the stifle joint of cats2,63,64 and has also been
reported in the tiger65. It is thought to occur either as
a normal anatomic variant or secondary to joint
trauma. The radiographic appearance, visualized on
the mediolateral view, is of single or multiple foci of
calcification in the cranial compartment of the
joint (60). The condition may be unilateral but is
frequently bilateral; it is sometimes associated with
lameness or may be seen in combination with other
disorders of the stifle, such as CrCL rupture. In the
absence of any other cause of stifle lameness,
medial meniscectomy may be curative63. The
60
60 Mediolateral radiograph of the stifle joint of a cat
showing mineralization and cranial luxation of a meniscus.
103
recommended treatment for cats with CrCL rupture
and concurrent meniscal calcification is meniscectomy
and stabilization of the stifle7.
OSTEOCHONDRITIS DISSECANS
There are two reports in the English language literature
of cats with lesions resembling osteochondritis
dissecans (OCD) of the proximal humerus, as
commonly seen in dogs66,67. There is also a single
report of bilateral OCD of the lateral femoral condyle
of the stifle joint68. All the reported cases were
immature cats that presented with lameness, which
resolved after surgical treatment.
OSTEOCHONDRODYSPLASIA IN THE SCOTTISH
FOLD CAT
Osteochondrodysplasia is an inherited defect in the
Scottish Fold cat caused by a simple autosomal
dominant gene69. The characteristic folding of the
ears is due to an abnormality of the aural cartilage.
Kittens affected by osteochondrodysplasia develop
an arthropathy of the hindlimbs with extensive
exostosis formation around the tarsal and metatarsal
joints (61). The resulting lameness can be treated
surgically either by excision of the exostoses70 or by
performing bilateral pantarsal arthrodesis 71.
Palliative radiation therapy has also been used to
resolve the clinical signs of the disorder72.
61
A B
61 A Mediolateral radiograph of the hock joint of a
Scottish Fold cat with osteochondrodysplasia. Note the
extensive periarticular exostosis and ankylosis.
B Plantarodorsal view of the hock joint of the cat in A.
(Radiographs courtesy of Malcolm McKee.)
104
LIGAMENTS AND TENDONS
In the musculoskeletal system ligaments
predominantly function to join bones and provide
support for joints. Ligaments may also perform
other functions of importance to the orthopedic
surgeon, such as the ligaments that are associated
with the menisci in the stifle joint. Ligaments that
unite bones are strong bands consisting of
longitudinally oriented bundles of collagen fibers.
The collagen fibers undergo a transition to
fibrocartilage where they attach to bone and are
known as Sharpey’s fibers. Ligaments supporting a
joint may be intraarticular, as in the case of the
cruciate ligaments, or, more commonly, are found as
cord like thickenings incorporated into the joint
capsule or separated from it by extensions of the
synovial lining, termed bursae. Injuries to ligaments
are known as sprains. When a ligament is avulsed
from its attachment site to bone with a small
fragment of bone this is known as a sprain-avulsion
fracture. Ligaments and tendons heal in a similar
fashion, which is described below.
Tendons function to attach muscles to bone and
may also provide ancillary support for joints.
Although the terms are not synonomous, some parts
of tendons are also known as ligaments. For
example, the portion of the tendon of the quadriceps
femoris muscle between the patella and the tibial
tuberosity is commonly known as the patellar
ligament. A muscle tendon unit (MTU) comprises a
muscle belly, its origin and insertion, and the
musculotendinous junction. Injury to any
component of the MTU is termed a strain. Tendons
consist of bundles of crimped collagen fibers and
parallel rows of fibroblasts. The crimping of the
fibers confers a spring-like function so that
deformation occurs in a nonlinear fashion when the
tendon is loaded under tension. A sac containing
synovial fluid, known as a tendon sheath, surrounds
the tendon where it crosses a joint. Nonsheathed
tendons are enclosed in loose connective tissue
known as the paratenon, which allows the tendon to
glide.
HEALING OF TENDONS AND LIGAMENTS
Strains and sprains are associated with rupture of
collagen fibers and hemorrhage from torn blood
vessels. There is an inflammatory response with
neovascularization and invasion of fibroblasts, which
lay down new collagen fibers. These fibers are at first
randomly oriented but become organized within
about 12 weeks of the injury. The collagen fibers
regain their longitudinal orientation in response to the
direction of tension within the healing tissues.
Optimum healing of tendons and ligaments is
promoted by complete immobilization during the
initial stages of fibroplasia (4–6 weeks) and
progressive loading of the tendon during the process
of maturation and organization of the healing tissue
(6–8 weeks). The gliding function of severely injured
tendons is often compromised by excessive formation
of fibrous tissue. Loss of function can be minimized
by early repair, gentle tissue handling, control of
infection, and appropriate rehabilitation. Any delay in
surgical repair will increase the likelihood of
complications.
REPAIR OF TENDONS
Tendon disorders are relatively uncommon in the cat
with the exception of injury to the tendons of the
distal extremities by sharp objects. In contrast to the
dog, disorders of the biceps tendon have rarely been
reported73,74. Severed tendons are repaired by
suturing using fine monofilament suture materials.
The tendons that most commonly require suturing
are the digital flexor tendons over the palmar and
plantar aspects of the metacarpus and metatarsus
respectively. Severance or avulsion of the common
calcanean tendon from its attachment on the tuber
calcis is occasionally seen as a result of trauma and may
be associated with a tendinopathy in older cats.
Severance of digital flexor tendons can occur in
association with small wounds and it is important to
check the integrity of the tendons at the time of first
presentation. The main concern is usually hemorrhage
and it is easy to overlook the tendon injury until the
wound has healed. The wound should be enlarged, if
necessary, to gain access to the severed ends of tendon
so that they can be sutured. Polypropylene (Prolene,
Ethicon) is the suture material of choice but
absorbable suture (PDS, Ethicon) may be preferred
where there are concerns about wound contamina-
tion. Size 3 metric suture is used for large tendons
such as the calcanean tendon, smaller diameter suture
may be required for other tendons. Several suture
patterns are suitable for tendon repair, including the
Pennington locking-loop pattern, Bunnell–Meyer
pattern, and the three-loop pulley pattern (62). The
most commonly used suture pattern in the cat is the
locking-loop suture. The locking-loop is preferred
because it is the easiest to apply to small flat tendons.
The three-loop pulley causes less tendon distortion
and is stronger (as might be expected since there are
six strands of suture material) than the locking-loop
pattern. However it is more difficult to apply and is
only suitable for large round tendons such as the
 Arthrology
105

calcanean tendon. Tendon repairs should be
supported postoperatively by placing the limb in a
short splint or cast for 6 weeks.
REPAIR OF LIGAMENTS
The ends of torn or avulsed ligaments are repaired in
the same fashion as tendons using a locking-loop
suture pattern, Bunnell–Meyer suture, or continuous
cruciate suture pattern. Alternatively, when there is
sufficient ligament substance remaining, the ligament
is reattached to bone. If the ligament cannot be
sutured, it is substituted by a prosthetic ligament.
Similarly, ligament repairs are usually protected by
using nonabsorbable suture anchored by screws,
bone tunnels, or bone anchors placed at the origin
and insertion sites of the ligament. Additional
protection of ligament repairs may be provided by the
use of a transarticular external skeletal fixator (TESF).
In cats there are many instances when ligaments are
not repaired or substituted and joint function is
restored by periarticular fibrosis alone. In the latter
situation, temporary joint alignment and stability
may be provided by alternative means, such as the
application of a TESF or by placing a transarticular
pin. Unilateral linear TESF frames are used for
immobilization of the stifle and elbow joints and
bilateral frames are used for the carpal and tarsal
joints. The addition of a hinge to form a hinged
transarticular external skeletal fixation frame
(HTESF) allows continued joint mobility and weight
bearing of the affected limb. The use of HTESF on
8 cats with tarsal or stifle joint injuries led to good
functional results75. The technique of transarticular
pinning can be applied to the stifle and tarsal joints
but is probably best reserved for the treatment of hip
luxation.
MISCELLANEOUS TENDON DISORDERS
Tendon avulsions, tendinopathies, and tendon
displacements are relatively uncommon. This
probably relates to the small size of the cat and the
low incidence of conformational abnormalities in
comparison with the dog. Tendon avulsions are
known as strain-avulsion injuries. They occur when
a tendon is pulled away from bone at its origin
or insertion, often with a small fragment of bone
attached. Strain-avulsion fractures are most frequently
seen in immature cats as physeal injuries. Common

62

5
3
3
5
3
1 1
1

6
4 4

2 2 2
i ii iii
A B

62 Two tendon suture patterns.

A Pennington locking-loop tendon/ligament suture. When placing the suture the needle should enter the cut end of the
tendon and exit at a distance from the cut end approximately equal to the width of the tendon. The transverse bites are
made superficial to the longitudinal bites.
B Three-loop pulley tendon suture. The three bites on the tendon should be rotated 120° from each other to completely
encircle the tendon. (i) The first bite is placed in a near–far pattern, (ii) the second is placed mid-way between near and
far, (iii) the third is placed in a far–near pattern.
106
63
63 Triceps tendinopathy. Flexed mediolateral radiograph
of the elbow joint showing multiple mineralized fragments
proximal to the olecranon (arrow).
sites of this type of injury are the supraglenoid
tubercle, the tibial tuberosity, and the olecranon
process. Physeal avulsion fractures are occasionally
bilateral and symmetrical76. Less common strain-
avulsion injuries include tendinopathies of the triceps
insertion (63) and traumatic avulsion of the triceps
tendon from the olecranon77.
Avulsion of the calcanean (Achilles) tendon is
occasionally seen in older cats and may occur
64
64 Calcanean tendinopathy. Mediolateral radiograph of the
hock showing an enthesiophyte on the tuber calcis of a cat
with avulsion of the calcanean tendon of insertion (arrow).
bilaterally following trivial trauma. In these cases there
is frequently a tendinopathy (or enthesiopathy) with
chronic degenerative changes in the tendon in
association with enthesiophytes on the tuber calcis
(64). Tendon displacements are very rare in the cat.
There is one report in the English language literature
of lateral displacement of the superficial digital flexor
tendon, which was thought to have had a traumatic
etiology78.

CHAPTER 8
FRACTURES AND
DISORDERS OF
THE FORELIMB
PART 1: SCAPULA AND SHOULDER JOINT
SCAPULAR FRACTURES
CAUSE AND PATHOGENESIS
Scapular fractures occur as a result of trauma.
CLINICAL SIGNS
The majority of cats with scapular fractures have
concurrent, trauma-related injuries, which may
include pulmonary contusions, rib fractures,
pneumothorax, and hemothorax1,2. Injuries to the
brachial plexus and suprascapular nerve may also
occur. Forelimb lameness, pain, swelling, and crepitus
in the scapular region are common clinical signs.
DIAGNOSIS
The diagnosis is confirmed radiographically.
65 Repair of scapular body fractures.
A Transverse scapular body fracture stabilized with
interfragmentary wires. Suture material may be used
instead of wire if desired.
B Scapular body fracture stabilized with a cuttable
bone plate applied to the base of scapular spine. The
screws are angled to maximize bone purchase
(insert).
107
TREATMENT AND PROGNOSIS
Scapular fractures are managed with conservative
therapy or surgery depending on their location and
degree of displacement.
Fractures of the body and spine
Fractures of the body and spine of the scapula are
usually managed conservatively. The surrounding
musculature (subscapularis, suprapinatus, and
infraspinatus muscles) provides internal support
and prevents severe displacement. Confinement
and restricted activity are adequate in most cases and
cats are typically walking well within 4 weeks of the
injury. The limb may be immobilized in a Velpeau
sling for 2 weeks if the cat is in particular pain.
If displacement of the fracture fragments is marked,
internal fixation may be indicated to reduce the
fracture, provide stability, and minimize pain during
healing (65). In most cases, orthopedic wire (0.6 mm
65
A B
108

[22 AWG]) or monofilament suture material (size 0) is
passed through holes drilled in the fragments3,4. The
wire (or suture) aligns the fragments and should not be
overtightened or it will tear through the thin bone.
Occasionally, a cuttable plate is used to achieve stability
of scapular body fractures. The plate is applied at the
base of the scapular spine where the bone is slightly
thicker. The screws are angled to maximize bone
purchase. Care is taken when placing the screws to
avoid penetrating the thoracic wall with the drill bit.
The cat’s activity is restricted for 4 weeks after surgery.
Fractures of the acromion
The acromion in cats has both a hamate and supra-
hamate (metacromion) process. The hamate process
projects from the distal aspect of the acromion. The
suprahamate process projects caudally from the
proximal aspect of the acromion (66). When fractured,
the acromion is typically distracted distally by the
acromial head of the deltoid muscle. Surgery is
indicated to achieve anatomic reduction, stabilize the
fracture, and prevent the suprascapular nerve from
becoming entrapped in a fracture callus. The
suprascapular nerve courses beneath the acromion
process and is protected during surgery. The acromion
process in some cats can be stabilized using tension
band wire fixation. A single Kirschner wire is placed
from the avulsed fragment into the spine of the scapula.
The tension band wire is placed around the Kirschner
wire and through a holed drilled approximately 1–2 cm

66

2 1

2
3

A B
66 The feline shoulder joint.
A Lateral view. 1 Metacromion, 2 Hamate process.
B Craniocaudal view. Note the scapular spine. The hamate process
projects from the distal aspect of the acromion. The suprahamate
(metacromion process) projects caudally from the proximal aspect of the
acromion. (Photograph courtesy of Tom Thompson.) 1 Metacromion,
2 Hamate process, 3 Coracoid process.
 Fractures and disorders of the forelimb
109

dorsally in the scapular spine. In cats too small to
accommodate a tension band, the avulsed acromion
process is reattached using orthopedic wire (0.6 mm
[22 AWG]) or monofilament suture material (0 or 2-0)
(67). The wire or suture should not be overtightened
or it will tear through the bone. It is not essential, but
the limb may be immobilized in a Velpeau sling or Spica
splint for 2–3 weeks after surgery to protect the repair.
Fractures of the scapular neck
Fractures of the scapular neck are often transverse and
are usually displaced medially. Pain and swelling are
evident in the region and the acromion process
feels prominent on palpation4. The suprascapular
nerve can be damaged during the trauma or by
the subsequent movement of bone fragments. If
displacement is significant, internal fixation is
indicated to restore anatomic alignment and prevent
the suprascapular nerve from becoming entrapped in
the healing callus. A craniolateral approach is used,
including ostectomy of the acromion process or
tenotomy of the acromial head of the deltoid5. The
suprascapular nerve is protected during the
procedure. Fixation is usually achieved using
Kirschner wires placed in a cross-pin configuration
(68). Careful pin placement is required to ensure the

67

A B

67 Repair of acromion process fractures.

A The avulsed acromion process is stabilized with interfragmentary suture or wire. The suprascapular nerve must be
preserved during fixation.
B The avulsed acromion process is stabilized with a tension band wire fixation.

68

A B C

68 Repair of scapular neck fractures.

A Scapular neck fracture stabilized with two Kirschner wires in cross-pin fashion. The wires should cross proximal to the
fracture line.
B Scapular neck fracture stabilized with a small cuttable plate.
C Scapular neck fracture stabilized with a mini T plate. The ostectomy of the acromion process is stabilized with
interfragmentary wires or suture.
110

pins engage the thin bone of the scapular body
proximal to the fracture. Ideally, the Kirschner wires
should cross proximal to the fracture line.
Occasionally, a mini plate (T plate or L plate) or small
cuttable plate is placed across the fracture line using
1.5 or 2.0 mm screws6. If an ostectomy of the
acromion process was performed, it is reattached with
a tension band wire fixation or interfragmentary wire.
If a tenotomy was performed, a locking-loop or
Bunnel–Meyer suture pattern is placed in the acromial
head of the deltoid and sutured to holes drilled in the
scapular spine.
Fractures of the glenoid and supraglenoid
tubercle
Glenoid fractures involve the articular surface of the
distal scapula. Extremely small fragments may simply
be removed. However, fragments large enough to
accept implants are stabilized with small screws
(2.0 mm) placed in lag fashion or Kirschner wires
(69 A)7. Anatomic reduction is important and care
is taken to avoid placing implants in the glenoid
cavity.
Fractures of the supraglenoid tubercle are usually
displaced by the tendon of origin of the biceps brachii
muscle. Careful reduction is required to prevent gaps
or steps in the articular surface. A cranial approach is
performed and the avulsed tubercle is reattached
using a 2.0 mm screw placed in lag fashion from the
tubercle to the scapular neck (69 B)3,5. The screw is
oriented parallel to the biceps tendon to reduce
bending loads. Alternatively, the tubercle can be
reattached using a tension band wire fixation (69 C).
A craniolateral approach is used and two Kirschner
wires are inserted through the tubercle and into the
scapular neck. A tension band wire is placed around
the Kirschner wires and through a hole drilled in the
cranial border of the scapular body. The tension band
wire will cross over the suprascapular nerve, which
must be carefully protected during surgery.
After fixation, the limb is immobilized in a
Velpeau sling for 2 weeks (if tolerated by the cat) and
the cat’s activity is restricted for 4–6 weeks. If the
articular comminution is severe and irreparable, or if
pain persists after fixation, excision arthroplasty or
shoulder arthrodesis may be indicated4,8,9.

69

A B C

69 Repair of glenoid and supraglenoid tubercle fractures.

A Glenoid fracture. A lag screw is placed to compress and stabilize the articular component of the fracture. The scapular
neck component of the fracture is stabilized with Kirschner wires in cross-pin fashion.
B Supraglenoid tubercle avulsion fracture stabilized with a lag screw. The screw is placed parallel to the biceps tendon to
reduce bending loads.
C Supraglenoid tubercle avulsion fracture stabilized with a tension band wire fixation. The suprascapular nerve must be
protected.
 Fractures and disorders of the forelimb
DORSAL DISPLACEMENT OF
THE SCAPULA
CAUSE AND PATHOGENESIS
Traumatic rupture of the serratus ventralis,
rhomboideus, and trapezius muscles can result in
dorsal displacement of the scapula4,10. The muscles
usually tear near their insertions on the scapula when
the cat falls or jumps from a significant height.
CLINICAL SIGNS AND DIAGNOSIS
The cat will typically have an acute, nonweight-
bearing lameness that progresses to weight bearing
over time. The scapula visibly displaces dorsally when
weight is placed on the limb (70).
TREATMENT AND PROGNOSIS
Most cats eventually regain pain-free limb function
after conservative therapy consisting of restricted
activity. The abnormal gait characterized by dorsal
displacement of the scapular persists, however.
Surgical intervention is required to stabilize the
scapula and restore normal gait. A craniodorsal
approach to the scapula exposes the damaged
muscles5. Primary repair of each muscle is performed
using monofilament, nonabsorbable suture material.
If the muscles are avulsed from the scapula, the suture
is anchored to holes drilled through the scapular
70
70 Dorsal displacement of the scapula.
111
body. Additional support can be provided by placing a
wire or suture through holes drilled in the caudal
scapular body and around an adjacent rib. The suture
material is passed cautiously around the rib to avoid
injury to the lungs or intercostal vessels. The limb is
immobilized in a Velpeau sling for 2 weeks and the
cat’s activity is restricted for 4 weeks.
SHOULDER LUXATIONS
CAUSE AND PATHOGENESIS
Shoulder luxation results from trauma and is
uncommon in the cat4,11.
CLINICAL SIGNS
Clinical signs may include pain in the shoulder region
and a nonweight-bearing lameness with the limb
flexed at the elbow.
DIAGNOSIS
A disparity in the relative positions of the acromion
process and the greater tubercle is usually palpable,
although the diagnosis of shoulder luxation is
confirmed radiographically. Radiographs should also
be evaluated for concurrent fractures of the scapula
and humerus12. A complete neurologic examination is
important to detect brachial plexus or other nerve
injuries.
Chronic mild shoulder joint instability has also
been reported in a cat13. With mild instability, laxity of
the shoulder joint in the craniocaudal or mediolateral
directions may be elicited by palpating the joint with
the cat under anesthesia.
TREATMENT AND PROGNOSIS
Closed reduction
Closed reduction is successful for the treatment
of shoulder luxation in most cats. The joint is
stabilized by external coaptation for 2–3 weeks and
the cat’s activity is restricted for 4–6 weeks. For medial
shoulder luxation, the limb is immobilized in a
Velpeau sling. The sling distracts the humeral head
laterally to maintain joint reduction. For lateral
luxations, the limb is immobilized in a Spica splint.
The humerus is positioned in slight abduction within
the splint to maintain shoulder reduction.
Surgical repair
Surgical repair is indicated if the joint is markedly
unstable after reduction, or remains unstable after
external coaptation, or if the cat will not tolerate
coaptation. Several surgical procedures may be used to
stabilize the shoulder joint in cats.
112

Transarticular pinning
The shoulder joint is reduced and placed in a normal
weight-bearing position (approximately 110°).
A small Steinmann pin is inserted normograde
through a stab incision over the distal aspect of the
greater tubercle, across the joint, and into the scapular
neck (71 A). The pin is cut short to reduce soft tissue
trauma. The limb is placed in a Spica splint for added
stability. The splint and pin are removed after
2–3 weeks4,14. The cat’s activity is restricted for an
additional 2–3 weeks. Transarticular pinning is a
relatively simple procedure, which is effective in
stabilizing the shoulder joint in cats, but damage to
the articular cartilage is caused by pin placement.
Imbrication of the joint capsule and glenohumeral
ligament
The torn joint capsule and glenohumeral ligaments
are sutured and imbricated with monofilament,
absorbable suture material (2-0). A simple interrupted
or continuous mattress pattern is used (71 B)14,15.
The glenohumeral ligaments are closely associated
with the joint capsule and appear as thickened bands
within the lateral and medial joint capsule13. The
medial glenohumeral ligament is torn more often than
the lateral. Imbrication is often performed along with
other internal fixation methods to stabilize the
shoulder joint.
Collateral support with suture
The joint is explored through combined craniolateral
and craniomedial approaches5. A hole is drilled from
lateral to medial through the center of the scapular
neck, avoiding the suprascapular nerve. A second hole
is drilled from lateral to medial through the proximal
humerus, between the humeral head and greater
tubercle. One or two strands of suture material are
passed laterally to medially through the hole in the
scapular neck and medially to laterally through the
hole in the proximal humerus. The suture is tied
under moderate tension on the lateral aspect of the
humerus (71 C)16. Monofilament polybutester suture
material (Novafil, Davis, & Geck) has been recom-
mended for its elasticity16. The limb is placed in a
Velpeau sling or Spica splint for 2–3 weeks after
surgery.

71

110°

A B C D
71 Techniques for stabilizing shoulder joint luxation.
A Transarticular pinning. The joint is placed at an angle of 110° prior to pin placement.
B Imbrication of the joint capsule and glenohumeral ligament with monofilament absorbable suture material placed in an
interrupted mattress pattern (medial view).
C Collateral support. Suture material is placed through holes drilled in the scapular neck and proximal humerus and tied
on the lateral side.
D Prosthetic medial glenohumeral ligament replacement (medial view). Suture material is attached to the proximal
humerus just distal to the insertion of the glenohumeral ligament using a bone anchor or bone tunnel. Bone tunnels are
drilled through the scapular neck at the cranial and caudal origins of the glenohumeral ligament. The suture is passed
from medial to lateral through the caudal bone tunnel, beneath the infraspinatus and supraspinatus muscles, and then
from lateral to medial through the cranial bone tunnel. The suture is tied medially.
 Fractures and disorders of the forelimb
Prosthetic medial glenohumeral ligament
Medial glenohumeral ligament replacement is
used to stabilize medial shoulder instability17,18.
A craniomedial approach to the shoulder is per-
formed. A hole is drilled just distal to the insertion of
the medial glenohumeral ligament on the proximal
humerus. A suture anchor (Bone Biter, Innovative
Animal Products LLC.) loaded with monofilament,
nonabsorbable suture material is inserted into the
hole. Alternatively, a bone tunnel is drilled to anchor
the suture to the humerus. Two bone tunnels are then
drilled in the scapula at the origins of the caudal and
cranial components of the glenohumeral ligament.
The medial glenohumeral ligament is replaced by
tying the suture using one of two methods:
• Two strands of suture are loaded in the bone
anchor. One strand is passed through the cranial
bone tunnel and tied. The second strand is passed
through the caudal bone tunnel and tied.
• A single strand of suture is loaded in the bone
anchor. The strand is passed through the caudal
bone tunnel, beneath the infraspinatus and
supraspinatus muscles along the lateral aspect of
the scapular neck, and back through the cranial
bone tunnel (71 D). The suture is tied18.
Postoperative care
Postoperatively, the limb is supported in a Velpeau sling
for 2–3 weeks. Exercise is restricted for 4 weeks. If
irreparable articular fractures are present, or instability
persists after repair, excision arthroplasty or arthrodesis
of the scapulohumeral joint may be required8,15.
72 Excision arthroplasty of the shoulder
joint.
A Ostectomy sites for excision of the
glenoid and proximal humerus.
B The proper angle for ostectomy of
the glenoid. The lateral edge should be
slightly longer than the medial edge.
The suprascapular nerve and caudal
circumflex humeral artery are preserved.
113
EXCISION ARTHROPLASTY
Excision arthroplasty is a salvage procedure per-
formed for shoulder injuries unresponsive to medical
or other surgical treatments3,8. Excision arthroplasty
is easier to perform than shoulder arthrodesis. A
craniolateral approach is performed, with tenotomies
of the infrapinatus and acromial head of the deltoid
muscle. The origin of the biceps brachii is removed
from the supraglenoid tubercle. The joint capsule is
incised close to the glenoid rim. An ostectomy of the
glenoid is performed, using an oscillating saw or
osteotome, to remove the articular surface (72). The
ostectomy is made at an angle such that the lateral
edge is slightly longer than the medial edge. The
suprascapular nerve and caudal circumflex humeral
artery are preserved. If desired, the proximal portion
of the humeral head can also be removed with a saw
or osteotome3. The infraspinatus is reattached. The
teres minor is placed over the glenoid ostectomy site
and sutured to the biceps tendon and medial joint
capsule. The acromial head of the deltoid muscle is
attached to the scapular spine using standard tendon
suturing techniques. Early use of the limb is encour-
aged after surgery to promote pseudoarthrosis.
SHOULDER ARTHRODESIS
Shoulder arthrodesis is indicated for traumatic joint
injuries, chronic subluxation unresponsive to surgical
repair, severe degenerative joint disease, and
congenital abnormalities9,19,20. The angle of fusion
should allow advancement of the limb and weight
bearing without overextension of the elbow.
72
Suprascapular
nerve
Osteotome
A B
114

Arthrodesis of the shoulder joint in cats is usually
performed at an angle of 110°; however, the correct
angle is best determined by evaluating the cat
preoperatively in a normal standing position19.
The shoulder joint is exposed through a combined
cranial and craniolateral approach, including ostectomy
of the acromion process and greater tubercle, and
tenotomy of the biceps brachii, infraspinatus, and
deltoideus muscles5. The suprascapular nerve is
protected. The articular surfaces of the humeral head
and glenoid are removed with an oscillating saw at the
correct angle, using care to avoid lateral or medial
angulation of the ostectomies. The distal scapula and
proximal humerus are opposed and temporarily fixed
with Kirschner wires. Autogenous cancellous bone
graft, collected from the ostectomized humeral head
and glenoid, is placed around the ostectomy site.
Several methods of arthrodesis are described in the
cat (73):
• Lag screw fixation: a lag screw is placed from the
cranial aspect of the distal scapula into the
proximal humerus to compress the cut surfaces20.
A 3.5 mm cortical screw or a 4.0 mm cancellous
screw may be used in most cats.
• Bone plating: a dynamic compression plate
(DCP) or cuttable plate (8–10 holes) can be
contoured and applied to the cranial aspect of the
proximal humerus and the dorsocranial junction
of the spine and body of the scapula. One or two
of the screws is placed in lag fashion through the
plate and across the joint19.
• Cross-pins and tension band wire fixation: two
or three Kirschner wires are inserted in cross-
pin fashion from the distal scapula into the
proximal humerus. Orthopedic wire (0.8 mm
[20 AWG]) is placed in a figure-of-eight pattern
through holes drilled in the cranial border of
the distal scapula and cranial surface of the
humerus. The wire serves as a tension band and
is tightened to help compress the ostectomy
sites together.
After fixation, the ostectomized greater tubercle is
re-attached with Kirshner wires or a small lag screw.
The ostectomized acromion process is reattached
with wire or suture material. A Spica splint is applied
to the limb for 4–6 weeks after surgery and exercise
should be restricted until union has occurred. In most
cases, function of the limb after arthrodesis is very
good. The mobility of the scapula on the body wall
allows the forelimb to move normally even after
arthrodesis.

73

110°

A B C D

73 Techniques for shoulder arthrodesis.

A The proper ostectomy sites on the distal scapula and proximal humerus. The arthrodesis angle is approximately
110° in cats. Osteotomies of the greater tubercle and acromion process are shown.
B Shoulder arthrodesis using a lag screw and a Kirschner wire. The ostectomized greater tubercle is reattached with
Kirschner wires or a small screw.
C Shoulder arthrodesis by plate fixation. Two of the plate screws are placed in lag fashion across the ostectomy site.
D Shoulder arthrodesis using cross-pins and a tension band wire fixation. The tension band wire is placed through
bone tunnels on the cranial surfaces of the scapula and humerus.
 Fractures and disorders of the forelimb
115

PART 2: HUMERUS AND ELBOW JOINT

HUMERAL FRACTURES growth plates4. If displacement is minimal, the limb

CAUSE AND PATHOGENESIS can be immobilized in a Velpeau sling for 3–4 weeks.
Humeral fractures in cats generally result from trauma When fragments are displaced, internal fixation is
and most occur in the distal portion or aspect of the preferred to achieve anatomic reduction and fixation.
bone1,2.
Greater tubercle
CLINICAL SIGNS Avulsion of the greater tubercle in immature cats can
Clinical signs include lameness, reluctance to bear be repaired in a closed or open fashion. Reduction of
weight on the limb, swelling, and pain. the displaced tubercle is facilitated by extension of the
shoulder joint. The fracture is stabilized using two
DIAGNOSIS Kirschner wires driven through the tubercle into the
The diagnosis is confirmed radiographically. The cat medullary cavity of the humerus. The Kirschner wires
must be carefully evaluated for concurrent injury to are bent over and cut short to reduce irritation to the
the thorax and nervous system (brachial plexus, radial overlying soft tissues. In mature cats, a tension band
nerve, median nerve)3. wire fixation or lag screw may be used (74).

TREATMENT AND PROGNOSIS Humeral head

Proximal fractures Salter-Harris type I and II fractures of the humeral
Proximal humeral fractures are uncommon in the cat head are repaired using two Kirschner wires. The
and may involve the greater tubercle and the humeral fracture is reduced (open or closed) and the wires are
head. They generally occur in young cats with open driven from just distal to the greater tubercle, across

74
Supraspinatus
tendon

A B C D

74 Repair of fractures of the greater tubercle.

A Avulsion fracture of the greater tubercle.
B Stabilization of the greater tubercle in an immature cat with two Kirschner wires.
C Stabilization of the greater tubercle in a mature cat with a tension band wire fixation.
D Stabilization of the greater tubercle in a mature cat with a single lag screw and a Kirschner wire.
116

the physis, and into the humeral head. Care is taken
not to penetrate the articular surface. In mature cats,
fractures of the neck of the humerus are stabilized
with a lag screw (2.7 mm) and a single Kirschner wire
(75, 76).
75
Humeral head and greater tubercle
Fractures of the proximal humeral growth plate
involving both the humeral head and the apophysis
of the greater tubercle occur rarely in cats. Open
or closed reduction is used to achieve proper
alignment. In immature cats, stabilization is achieved
by internal fixation using Kirschner wires placed from
the greater tubercle into the medullary cavity of the
humerus. In mature cats, Kirschner wires, lag screws,
or a tension band wire fixation may be applied (77).

Articular surface of humeral head

A B
75 Repair of humeral head fractures.
A Growth plate fractures of the humeral head in immature
cats are stabilized with Kirschner wires inserted from just
distal to the greater tubercle, across the physis, and into
the humeral head.
B In mature cats, a lag screw and Kirschner wire are
inserted.
Fractures involving the articular surface of the
humeral head are rare. Fragments are reduced and
stabilized using Kirschner wires or a lag screw driven
from the humeral shaft or greater tubercle into the
base of the fragment. If the articular fragment is very
small, the Kirschner wires can be inserted from the
articular surface into the subchondral bone and
countersunk below the articular cartilage using a small
nail-set (78)5. This technique injures the articular

76

A B C D
76 Fracture of the humeral head and greater tubercle.
A Lateral radiographic view of a Salter–Harris type I fracture of the humeral head. The greater tubercle is mildly displaced.
B Craniocaudal radiographic view. Note the medial displacement of the proximal humeral epiphysis.
C Postoperative lateral radiographic view. The humeral head is reduced and stabilized with Kirschner wires inserted from
distal to the greater tubercle. A Kirschner wire is inserted across the greater tubercle.
D Postoperative craniocaudal view.
 Fractures and disorders of the forelimb
117

surface and is used only when necessary. Migration of
the implants into the joint can result in severe
cartilage damage.
Diaphyseal fractures
Diaphyseal humeral fractures in the cat are typically
transverse or oblique. Open reduction and internal
fixation is preferred in most cases since it is difficult to
immobilize the humerus adequately with casts or
splints. The humeral diaphysis is exposed through
either a craniolateral or medial approach6–8. Care is
taken to avoid injury to the radial nerve during the
lateral approach to the bone. In the cat, the median
nerve and brachial artery pass through the
supracondylar foramen, located on the medial surface
of the humerus just proximal to the medial
epicondyle. The nerve is easily damaged by bone
fragments or implants and must be protected during

77

A B C D

77 Repair of proximal fractures of the humeral head and apophysis of the greater tubercle.
A Fracture involving the humeral head and greater tubercle.
B Stabilization in an immature cat using two Kirschner wires.
C Stabilization in a mature cat using a lag screw and a single Kirschner wire.
D Stabilization using a tension band wire fixation.

78

A B C

78 Repair of articular fracture of the humeral head.

A Kirschner wires are inserted from the great tubercle into the articular fragment. The articular surface is not penetrated
by the implants.
B A lag screw and Kirschner wire are placed to stabilize the articular fragment.
C Small Kirschner wires are inserted through the fragment from the articular surface and into the subchondral bone. The
wires are countersunk beneath the cartilage with a nail-set.
118

surgical repair of distal diaphyseal and metaphyseal 79

fractures. The ulnar nerve, located beneath the short
part of the medial head of the triceps brachii muscle,
must also be protected7. Stabilization of diaphyseal
humeral fractures can be achieved using several
methods.

External coaptation
External coaptation is indicated for stabilization of
nondisplaced fractures in immature cats. A Spica splint
or Velpeau sling is applied until the fracture is healed.
Complete immobilization of the proximal humerus is
difficult in mature and active cats.

Intramedullary pinning
Insertion of an intramedullary Steinmann pin is a
common and effective method of stabilizing humeral
fractures in cats9–11. The relatively straight humerus in
cats allows easy pin placement. Two important
anatomic features of the feline humerus must be
considered when placing an intramedullary pin:
• Narrow medullary cavity distally – a pin is
selected that will completely fill the distal aspect
of the medullary cavity.
• Supracondylar foramen – the location of the
supracondylar foramen precludes driving the pin
distally into the medial aspect of the condyle.
A B
Instead, the pin is positioned approximately 7–9
mm proximal to the medial epicondyle12. Pins 79 Normograde intramedullary pin insertion.
placed more distally can enter the supracondylar A The fracture is reduced and stabilized with bone clamps
foramen, damaging the median nerve and or cerclage wires.
brachial artery and penetrating the elbow joint13. B The pin is inserted at the proximolateral aspect of the
greater tubercle, driven distally across the fracture, and
Intramedullary pins may be inserted normograde seated into the distal humerus proximal to the
or retrograde into the humerus. For normograde supracondylar foramen.
insertion, the fracture is reduced and stabilized with
bone clamps or cerclage wires (if they are to be used)
(79). The pin is started at the proximolateral aspect of
the greater tubercle and driven distally across the
fracture and into the distal humerus (just proximal to
the supracondylar foramen). A second pin of identical For retrograde insertion, the pin is directed
length is used to determine how far distally the pin has proximally from the fracture site before final reduction
been placed, and the elbow is manipulated through a of the fracture (80). The pin should be inserted along
range of motion to ensure the pin has not penetrated the cranial surface of the medullary cavity to exit at the
the joint. Radiographs are also used to confirm tip of the greater tubercle. The pin is inserted until its
pin placement. The pin is then cut short to reduce soft distal end is just proximal to the fracture line. The
tissue trauma. Closed insertion of the intramedullary fracture is then reduced and stabilized with a bone
pin may be possible if the fracture is minimally clamp. Cerclage wires can be applied at this time if
displaced or if adequate reduction of the fragments is needed. The pin is driven distally and seated into the
achieved by palpation alone. Swelling of the soft distal humerus just proximal to the supracondylar
tissues surrounding the humerus and interposition of foramen. Proper insertion is confirmed and the pin is
soft tissues between the fragments may prevent closed cut short to reduce trauma to the soft tissue over the
reduction in some cases. tubercle.
 Fractures and disorders of the forelimb
119

80 Retrograde intramedullary 80
pin insertion.
A The pin is directed proximally
from the fracture site and exits
the medullary cavity at the
greater tubercle.
B The pin is inserted until its
distal end is proximal to the
fracture line.
C The fracture is reduced and
stabilized with a bone clamp or
cerclage wires. The pin is driven
distally and seated into the distal
humerus just proximal to the
supracondylar foramen.
D Craniocaudal view of the
humerus depicting pin
placement from the greater
tubercle to the distomedial
aspect of the humerus proximal
to the supracondylar foramen.

A B C D

81 Intramedullary pin fixation 81

of humeral diaphyseal fractures.
A A single intramedullary pin
may be used alone if reduction
is good and interdigitation of
the fragments provides
rotational stability.
B Ancillary fixation with full
cerclage wires is indicated in
long oblique fractures to
control rotation.
C Ancillary fixation with
hemicerclage wires.
D Ancillary fixation with a type
Ia external fixator to prevent
rotation around the single
intramedullary pin and collapse
of the fracture site.
A B C D

Intramedullary pins may be used alone if reduction
is good and interdigitation of the fragments provides
rotational stability12. In many cases, however, ancillary
fixation with full cerclage wires, hemicerclage wires, or
an external fixator is warranted to control rotational and
compressive forces at the fracture site (81). Application
of cerclage wires is not feasible if the fracture is stabilized
in a closed manner, but is easily performed during open
fracture repair. A type I external fixator can be applied to
prevent rotation if closed or open pinning is used. Stack
120

pinning (placing several pins into the medullary cavity) inserted with the dynamic intramedullary cross-pinning
does not completely prevent rotation but has been used technique achieve three-point fixation that provides
with success in cats (82)10,11. rotational and axial stability.

Dynamic intramedullary cross-pinning External fixation

(Rush pinning) A type I external fixator can be applied to the
Dynamic intramedullary cross-pinning is used to craniolateral aspect of the humerus as a primary means
stabilize fractures of the proximal or distal diaphysis and of fixation or in conjunction with an intramedullary
metaphysis in cats (83)14. Two Kirschner wires are pin9,15. Either acrylic or traditional connecting bars
inserted into the medullary cavity. For proximal may be used. A double connecting bar may be used
fractures, the first Kirschner wire is started at the for increased rigidity, although this is rarely necessary
proximolateral aspect of the greater tubercle and in cats. The fixator may be applied in a closed manner
the second wire is started the proximomedial aspect if the fracture can be reduced by palpation, or if
of the tubercle. For distal fractures, one wire is started intraoperative imaging is available to help ensure
just cranial to the medial epicondyle and the other just adequate alignment. Fixators may also be applied after
cranial to the lateral epicondyle. The wires are inserted open reduction (84).
at an angle to the median plane of the humerus so that
they will glance off the inner cortical wall and continue
in the medullary cavity (rather than penetrate the
cortex). The wires can be advanced by alternately
tapping them into place with a small mallet. 83
Alternatively, they can be inserted with a hand-chuck.
Minimal rotation of the hand-chuck is used to prevent
the wires from penetrating the cortex. Another means
of assuring the wires pass up the medullary cavity and
do not penetrate the humeral cortex is to blunt the tips
of the wires prior to insertion. This requires predrilling
of the insertion sites for each wire. Kirschner wires

82

A B
83 Dynamic intramedullary cross-pinning for repair of
proximal and distal diaphyseal or metaphyseal fractures of
the humerus.
A Proximal fracture repair (craniocaudal view). One
Kirschner wire is inserted from the proximolateral aspect of
the greater tubercle and the other from the proximomedial
aspect of the tubercle. The wires are inserted at an angle to
the median plane of the humerus and glance off the inner
cortical wall, continuing distally in the medullary cavity.
A B B Distal fracture repair (craniocaudal view). One wire is
82 Repair of a humeral diaphyseal fracture with stack inserted just cranial to the medial epicondyle and the other
pinning. just cranial to the lateral epicondyle. Kirschner wires
A Lateral view. inserted with the dynamic intramedullary cross-pinning
B Craniocaudal view. technique achieve three-point fixation that provides
rotational and axial stability.
 Fractures and disorders of the forelimb
121
84

A B C D E

F G H I
84 External fixation of humeral diaphyseal fractures.
A Type Ia external fixator applied to the craniolateral aspect of the humerus to stabilize a short oblique fracture. Care is
taken to avoid entering the supracondylar foramen.
B Acrylic external fixator (type Ia frame) for stabilization of a transverse humeral fracture.
C Type Ia external fixator with double connecting bars for stabilization of a comminuted humeral fracture.
D Type Ia external fixator used in conjunction with an intramedullary pin.
E External fixator and intramedullary pin used in a tie-in configuration.
F Stabilization of a comminuted humeral fracture using a hybrid type I–II external fixator frame. The distal full pin is
attached to the lateral frame with a curved connecting bar.
G Lateral radiographic view of a comminuted distal humeral fracture caused by gun shot.
H Lateral radiographic view after stabilization with a hybrid type I–II external fixator with tie-in configuration.
I Photograph of a cat with a hybrid type I–II external fixator with tie-in configuration.
122

To apply the fixator, a half pin is inserted across the
humeral condyle, starting just distal and cranial to
the lateral epicondyle. The pin is driven parallel to the
joint surface to a point just cranial and distal to
the medial epicondyle. Pins 1.5–2.2mm in diameter are
recommended for transcondylar use13. A second half
pin is inserted in the proximal humerus. When the
fixator is used in conjunction with an intramedullary
pin, this two-pin frame configuration is generally
adequate (84 D). The pin helps maintain alignment and
protects the frame from bending forces. The external
fixator controls rotational forces around the pin. For
additional stability, the external fixator frame can be
attached to the proximal portion of the intramedullary
pin (tie-in configuration) (84 E)16. If the fixator is
being used alone, particularly in comminuted fractures
where the fragments do not share in load-bearing, a
more rigid frame is indicated. In these cases, a minimum
of two transfixation pins are placed on each side of the
fracture line. Distally, the second pin is placed proximal
to the condyle. Care is taken to avoid entering the
supracondylar foramen or damaging the brachial artery
and median, ulnar, and radial nerves. Unfortunately, it
is often difficult to place two transfixation pins distally
in the cat humerus, particularly in comminuted distal
fractures. The distal pin may also be inserted completely
through the condyle (full pin). The pin exits the skin
medial to the condyle and is attached to the lateral
frame with an additional connecting bar9,17. This type
of frame is often referred to as a hybrid type I–II
external fixator (84 F–I).
Bone plate and screw fixation
Bone plates and screws may be used to stabilize
diaphyseal humeral fractures in cats18. Dynamic com-
pression plates (2.7 mm), cuttable plates, and tubular
plates are commonly used12,19–21. For fractures
involving the proximal half of the humerus, the plate is
usually applied to the cranial surface of the bone, thus
avoiding the insertions of the pectoral muscles
(85 A). For mid-diaphyseal fractures, the plate may be
applied to the lateral, medial, or cranial aspect of the
humerus (85 B–D). Lateral plating is achieved via a
craniolateral approach and requires that the plate be

85

A B C D
85 Plate application to the humeral diaphysis.
A Bone plate applied to the cranial humeral cortex to stabilize a proximal diaphyseal
fracture.
B Bone plate applied to the lateral humeral cortex to stabilize a mid-diaphyseal fracture.
C Bone plate applied to the medial humeral cortex. The median nerve and brachial
artery are protected during medial plate application.
D Bone plate applied to the cranial humeral cortex.
 Fractures and disorders of the forelimb
123

positioned beneath the radial nerve and brachialis
muscle7,8. Plate contouring is often easier when
applying a plate to the medial cortex, but the median
nerve and brachial artery must be protected as they
pass through the supracondylar foramen6,14. For
fractures involving the distal third of the humerus, the
plate may be applied either laterally or medially6,14.
However, contouring the plate to the distal aspect of
the humerus in a cat can be difficult and other means
of fixation are often used to stabilize more distal
fractures (see Supracondylar fractures and Condylar
fractures).
The plate needs to be long enough to ensure
the screws engage a minimum of five cortices on each
side of the fracture line. Plates may be used in
neutralization, compression, or bridging (buttress)
function depending on the fracture configuration.
• Transverse fractures – the fracture is reduced and
the plate is contoured to the cortex, ensuring that
at least three screws can be placed proximal and
distal to the fracture. A 2.7 mm DCP is commonly
used. The oval holes in the DCP plates allow the
fracture line to be compressed to enhance stability
and promote healing. Cuttable plates and tubular
plates may also be used (85 A).
• Oblique fractures – the fracture is reduced and
temporarily stabilized with a bone clamp. The
plate may be applied as described for transverse
fractures. Alternatively, a lag screw or cerclage
wires can be placed to compress the fracture line
and maintain reduction while the plate is applied
(86). If the orientation of the oblique fracture
line permits, one of the plate screws can be placed
in lag fashion across the fracture line.

86

A B C D
86 Stabilization of oblique humeral fractures with bone plates.
A Neutralization plate applied to the lateral cortex of the humerus after fracture reduction.
B The oblique fracture is stabilized with full cerclage wires and a neutralization plate is applied
to the lateral cortex.
C The oblique fracture is stabilized with a lag screw and a neutralization plate is applied to the
lateral cortex.
D Bone plate applied to the cranial surface of the humerus. A plate screw is applied in lag
fashion across the oblique fracture.
124
• Comminuted fractures – a bone plate can be
applied in several ways to stabilize comminuted
fractures of the humerus (87):
• Controlled collapse – if the area of
comminution is small, the primary
fragments are apposed, as in a transverse
fracture, and the comminuted fragments
are used as autogenous graft. This
results in minor shortening of the
limb and clinical function is normal.
• Fragment reconstruction – if the area of
comminution is too large to permit
shortening of the bone, the fragments
may be reconstructed using cerclage wires
or lag screws. The plate is then applied in
a neutralization function. This method
provides anatomic reduction and ensures
load sharing between the plate and bone.
However, it requires manipulation of
the fragments and possible interference
with soft tissue attachments and blood
supply.
• Bridging (buttress) plating – the plate is
applied in buttress fashion to bridge the
area of comminution. The proximal and
distal fragments are stabilized, leaving
the comminuted fragments undisturbed
within the fracture gap. This preserves
soft tissue attachments and blood supply,
but also requires the plate to bear additional
load until healing occurs. When applying a
plate in buttress fashion, plate failure can
occur through empty screw holes and
the cat’s activity must be restricted
postoperatively. Cuttable plates may be
stacked to increase rigidity when used in
buttress fashion19–21. Autogenous cancellous
bone graft is placed in the defect to promote
healing22.
• Plate–rod fixation – an intramedullary pin
is placed in normograde fashion to maintain
length and alignment of the bone while the
bone plate is applied. The pin should fill
approximately 35–40% of the medullary
cavity. The plate is contoured and applied in
buttress fashion on the medial or lateral aspect
of the humerus. The most proximal and distal
screws engage both humoral cortices
(bicortical). The remaining screws engage
only the near cortex (monocortical).
A minimum of three monocortical screws and
one bicortical screw are placed on each side of
the fracture. Comminuted fragments and the
fracture hematoma in the fracture site are not
disturbed.
Interlocking nail fixation
The relatively long, straight humerus in the cat
makes it well suited for fracture repair using a
4.7mm or 4.0 mm interlocking nail (ILN)23. (Small
Interlocking Nail System, Innovative Animal
Products LLC.) When possible, the ILN is inserted
normograde into the medullary cavity through a
limited approach at the greater tubercle, thus
reducing injury to soft tissues and blood supply
at the fracture site. ILNs are available in various
lengths (see Chapters 5 and 6) and have either
four screw holes (two proximal and two distal) or
three screws holes (a single distal or proximal screw
hole). For fractures near the metaphysis of the
humerus, an ILN with three screw holes is preferred
to avoid placing a screw within 1–2 cm of the
fracture site.
Once the nail is inserted, the drill-aiming guide is
attached to the nail via the extension rod to allow
placement of 2.0 mm diameter screws. The distal
screw is generally placed first via a small stab incision
over the appropriate portion of the humerus. The
remaining screws are then inserted. For comminuted
fractures, the fragments are typically left in situ and
the nail serves a buttress function. Alternatively,
fragments can be anatomically reduced with cerclage
wires (requiring an open approach) and the ILN
serves a neutralization function. It is preferable to
avoid using cerclage wires, however, unless they
contribute significantly to the repair. Autogenous
cancellous bone graft can also be placed at the fracture
site if desired.
 Fractures and disorders of the forelimb
125
87

A B C D

E F G

87 Stabilization of comminuted humeral fractures with bone plates.

A Comminuted diaphyseal humeral fracture.
B The fracture site is collapsed and stabilized with a compression plate. Bone fragments are used as bone graft around the
fracture site.
C The comminuted portion of the fracture is stabilized with cerclage wires and a neutralization plate is applied.
D The comminuted portion of the fracture is stabilized with lag screws and a neutralization plate is applied.
E A DCP plate is applied in bridging (buttress) fashion to maintain bone length. The comminuted fragments are
minimally disturbed to preserve blood supply. Plate failure may occur through empty plate holes placed over the
comminuted fracture.
F A lengthening (biologic healing) plate is applied to bridge the comminuted fracture. The central portion of the plate is
devoid of screw holes to prevent failure through empty holes.
G Plate–rod fixation of a comminuted humeral fracture.
126
Supracondylar fractures
Supracondylar fractures are relatively common in
cats and often involve the supracondylar foramen.
Many of the fractures are comminuted and can be
challenging to repair 24,25. A medial or lateral
approach to the distal humerus is performed to
expose the fracture 7. In many cases, the two
approaches are combined to allow reduction and
proper implant placement. When approaching the
distal humerus in a cat, care is taken to protect the
median nerve and brachial artery as they pass
through the supracondylar foramen. Occasionally,
the medial wall of the supracondylar foramen
is excised with a rongeur to prevent nerve
entrapment12. The ulnar nerve, located beneath the
short part of the medial head of the triceps brachii
muscle, must also be protected7. Several techniques
are described for repair of supracondylar fractures in
cats (88)25.
Cross-pin fixation
The fracture is reduced and temporarily stabilized
with pointed reduction forceps. If the fracture is
oblique, cerclage wires may be used to stabilize the
fracture line. Some comminuted fractures may also
be reconstructed using cerclage wires. Kirschner
wires (1.1–1.6 mm) are then placed in cross-pin
fashion from the lateral and medial aspects of
the condyle26. The wires are inserted from the
nonarticular portion of the condyle, just caudal to
the epicondyles, and advanced across the fracture
line, exiting the metaphyseal cortex proximal to the
fracture line. The wires are cut and bent over against
the condyle to avoid soft tissue and ulnar nerve
irritation12.
Dynamic intramedullary cross-pinning
Two Kirschner wires (1.1–1.6 mm) are started as
described above for the cross-pinning technique.
The wires are inserted at an angle to the median
plane of the humerus so that they will glance off the
inner cortical wall and continue proximally within
the medullary cavity (rather than penetrating the
cortex as cross-pins). To prevent the wires from
penetrating the cortex, the sites for wire placement
are predrilled and the tips of the wires are blunted.
The wires are advanced by alternately tapping them
into place with a small mallet. A hand-chuck may be
used, although minimal rotation of the chuck
is required to prevent the wires from engaging
the cortex. If comminution is present, the pins may
enter the fracture site rather than glance off the
cortex and continue proximally. If the comminuted
segment cannot be reconstructed with cerclage
wires, dynamic intramedullary cross-pinning may not
be feasible.
External fixator with an intramedullary pin
A small Steinmann pin or Kirschner wire is driven into
the medullary cavity of the humerus from the medial
aspect of the condyle24. In most cats, the pin must be
relatively small (less than 1.6 mm) to avoid entering
the supracondylar foramen13. If possible, the pin is
advanced up the medullary cavity to the greater
tubercle. It is then recessed below the surface of the
condyle to prevent injury to the ulnar nerve12. The
small pin maintains alignment while a type I or hybrid
type I–II external fixator is applied to the craniolateral
aspect of the humerus17. Either acrylic or traditional
connecting bars may be used. A half pin is inserted
across the humeral condyle (starting just distal and
cranial to the lateral epicondyle) parallel to the joint
surface. If possible, a second transfixation pin is
inserted distal to the fracture. One or two additional
half pins are inserted in the humerus proximal to the
fracture.
External fixator alone
If an intramedullary pin cannot be positioned,
the external fixator may be used alone. A type I
external fixator is used for most simple fractures. A
hybrid type I–II external fixator provides greater
rigidity and is used for comminuted fractures. If the
supracondylar fracture is comminuted, several
options exist:
• The fragments may be stabilized with cerclage
wire before application of the fixator.
• The fracture site may be collapsed to appose the
primary fragments and the fixator applied,
resulting in minimal limb shortening.
• The fragments are left undisturbed and the
fracture gap is maintained. The fixator is applied
to prevent collapse. Cancellous bone graft may
be placed in the fracture site to encourage
healing.
Condylar fractures
The feline humeral condyle is relatively straight and
wide, and lacks the supratrochlear foramen seen in
other carnivores9. As a result, fractures of the humeral
condyle are uncommon in cats. Open reduction and
internal fixation are required to reconstruct the
articular surface accurately and stabilize the fracture.
A lateral approach is usually adequate. The medial and
lateral aspects of the condyle are reduced and held
with a bone clamp. Small pointed reduction forceps or
 Fractures and disorders of the forelimb
127
88

A B C D

E F G H

88 Stabilization of supracondylar humeral fractures.

A Cross-pin fixation. The wires are inserted just caudal to the medial and lateral epicondyles and advanced across the
fracture line to exit the metaphyseal cortex proximal to the fracture line.
B Dynamic intramedullary cross-pinning. The wires glance off the inner cortical wall and continue proximally within the
medullary cavity.
C Type Ia external fixator and intramedullary pin. A small pin is used to avoid entering the supracondylar foramen.
D Hybrid type I–II external fixator and intramedullary pin.
E Type Ia external fixator. If possible, two transfixation pins are placed on each side of the fracture.
F Oblique supracondylar fracture stabilized with cerclage wires and a type Ia acrylic external fixator.
G A comminuted supracondylar fracture stabilized with a hybrid type I–II external fixator. The fracture gap is maintained
to preserve bone length.
H A comminuted supracondylar fracture stabilized by collapsing the fracture to appose the primary fracture segments and
applying a type Ia external fixator.
128
vulsellum forceps are effective. A small, transcondylar
Kirschner wire may also be placed to provide
rotational stability during screw placement.
Stabilization of condylar fractures is achieved by
placing a 2.0 mm or, preferably, a 2.7 mm cortical
screw across the humeral condyle (89)24. In most
cases, the screw is placed from lateral to medial using
one of two methods:
• The condyle is reduced and temporarily stabilized
with clamps or a Kirschner wire. A drill bit is used
to drill a screw hole, starting just cranial to the
lateral epicondyle. The hole is placed parallel to
the joint surface and exits the condyle just distal
and cranial to the medial epicondyle. Ideally, the
screw will be centered in the condyle. The hole is
measured (and tapped if necessary) and the
appropriate length screw is inserted. The screw
will maintain the interfragmentary compression
created by the clamps. In larger cats, the screw
can be inserted in lag fashion by ‘overdrilling’ the
hole in the lateral condyle to the same size as the
outer diameter of the screw (glide hole).
However, in smaller cats, overdrilling to create a
glide hole may remove too much bone from the
condyle12.
• The intracondylar fracture line is exposed. A drill
bit is used to drill a screw hole from the fracture
89
A B
line to a point just cranial to the lateral
epicondyle. The hole should be centered in the
condyle and parallel to the articular surface. The
hole may be drilled to the same size as the outer
diameter of the screw if a lag effect is desired
(and if overdrilling will not remove too much
bone from the condyle). The fracture is then
reduced and temporarily stabilized with a clamp.
The drill bit is then passed through the hole
drilled in the lateral condyle (using a drill sleeve if
overdrilled) to begin drilling a hole in the medial
condyle. The hole is measured (tapped if
necessary) and the appropriate length screw is
inserted.
After placement of the transcondylar screw, a
Kirschner wire is placed to prevent rotation around
the screw. The Kirschner wire may be positioned
parallel to the screw (across the condyle) or inserted
from the condyle into the supracondylar portion of
the humerus.
Combination supracondylar and condylar
fractures
Supracondylar and condylar fractures may occur
simultaneously and are often referred to as T- or
Y fractures. This type of fracture is rare in cats. Open
reduction and internal fixation are required to restore
89 Repair of humeral condylar fractures.
A The fracture is reduced and temporarily
stabilized with a bone clamp. A 2.0 mm or
2.7 mm bone screw is inserted across the
humeral condyle, parallel to the joint
surface. In larger cats, the screw can be
inserted in lag fashion by drilling a glide
hole in the lateral portion of the condyle.
A Kirschner wire is inserted to prevent
rotation around the screw.
B Lateral view showing the proper screw
placement for repair of a condylar
fracture. The screw is inserted just cranial
to the lateral epicondyle and exits the
medial aspect of the condyle, just cranial
to the medial epicondyle.
 Fractures and disorders of the forelimb
129

joint function. Repair consists of combining
techniques used for each fracture type. A lateral
approach to the elbow and distal humerus is usually
adequate, although an additional medial approach
may help in some cases7. First, the condylar fracture is
repaired to ensure the articular surface is accurately
reconstructed. A cortical bone screw (2.0 mm or
2.7 mm) is placed across the condyle as previously
described. Then, the supracondylar portion of the
fracture is stabilized using Kirschner wires placed in
cross-pin fashion, dynamic intramedullary cross-
pinning, an external fixator, or bone plating (90).

90

B C D E
A
90 Stabilization of T- or Y fractures of the distal humerus.
A Combination supracondylar and condylar fracture of the distal humerus.
B Repair using a 2.0 mm or 2.7 mm cortical bone screw inserted across the
condyle and two Kirschner wires inserted in cross-pin fashion to stabilize the
supracondylar portion of the fracture.
C Repair using a transcondylar screw and dynamic intramedullary cross-pinning.
D Repair using a transcondylar screw and a type Ia external fixator.
E Repair using a a hybrid type I–II external fixator.
F Craniocaudal radiographic view of a Y-fracture stabilized with a transcondylar
screw and two bone plates.

F
130

Placing a bone plate on the medial and lateral aspects 91

of the humerus may be indicated when stabilizing
severely comminuted fractures. Careful planning is
required to ensure all of the implants can be
positioned in the small, distal fragment without
penetrating the joint.

POSTOPERATIVE CARE OF HUMERAL FRACTURES

Postoperatively, the cat is restricted until bony
union is complete. Radiographic evaluation at 4 and
8 weeks is performed to assess healing and monitor for
complications. In most cases, external coaptation is
not used after internal fixation to allow limb function
and early joint motion. If it is necessary to augment
the fixation, however, a Velpeau sling or Spica splint
can be applied for 2–4 weeks (91). External fixators
are removed when healing is complete. Other
implants are left in place unless complications develop. 91 Spica splint applied to immobilize the elbow and
shoulder joints.
TRAUMATIC ELBOW LUXATION
CAUSE AND PATHOGENESIS
The elbow is a ginglymoid joint composed of
the humeroradial, humeroulnar, and proximal
radioulnar articulations (92). Weight-bearing force is
transmitted primarily across the humeroradial joint. The

92

A B C
92 Feline elbow joint.
A Lateral view.
B Medial view.
C Craniocaudal view.
 Fractures and disorders of the forelimb
collateral ligaments and position of the anconeal process
within the olecranon fossa provide stability. Elbow
luxation is relatively common in cats, generally as a
result of significant trauma. Lateral luxation is most
common. The medial epicondyle is larger than
the lateral epicondyle and the size and shape of
the medial epicondyle prevents medial movement of the
ulna27. Caudal luxation also occurs commonly in cats12.
CLINICAL SIGNS
Cats with elbow luxation may have a history of recent
trauma. Most are acutely nonweight-bearing and hold
the limb with the elbow slightly flexed and adducted.
The antebrachium is abducted and externally rotated.
Palpation of the elbow region reveals reduced range of
motion, pain, and swelling.
93 Radiographic views of an elbow luxation.
A Lateral view.
B Craniocaudal view.
131
DIAGNOSIS
Lateral and craniocaudal radiographic views of the
elbow are obtained to confirm the presence of a
luxation and evaluate for articular fractures or
fractures of the humerus, radius, or ulna (93).
TREATMENT AND PROGNOSIS
Joint reduction
The cat is stabilized and evaluated for other soft
tissue, neurologic, and orthopedic injuries before
joint reduction is performed. In acute injuries, closed
reduction is attempted first and is usually successful
in cats12,27. The cat is placed under general
anesthesia and the limb suspended from a stand for
5–10 minutes to fatigue the muscles and aid in
reduction of the joint.
93
A B
132

Lateral luxation Joint stabilization

The elbow is flexed to 110° and the antebrachium is
abducted and pronated. Medial pressure is applied to
the caudal ulna to engage the anconeal process within
the olecranon fossa, medial to the lateral epicondylar
ridge (94). The elbow is then extended slightly to
engage the anconeal process fully, allowing it to be
used as a fulcrum to lever the radial head into
position. The elbow is then slowly flexed and the
antebrachium is pronated and adducted while
applying medial pressure to the radial head. Several
attempts may be required before the joint is
reduced28. After reduction, the limb is maintained in
extension to prevent reluxation.
Caudal luxation
In caudal luxations, the proximal radius and ulna
are positioned caudal to the humeral condyle.
Palpation of the relative locations of the epi-
condyles and the radial head will usually confirm the
luxation. Reduction is often achieved when the limb is
suspended to fatigue the muscles. If this does not
occur, reduction may be achieved by placing traction
on the antebrachium until the humeral condyle is
aligned with the ulnar notch. The elbow is then flexed
to seat the condyle fully. After reduction, moderate
flexion of the elbow joint is usually required to
prevent reluxation.
After reduction of the luxation, the stability of the
joint is assessed. The collateral ligaments are evalu-
ated by flexing both the carpus and elbow to 90°27.
The foot is then internally and externally rotated and
the amount of rotation compared with the contralat-
eral normal limb. The foot will rotate excessively
internally if the lateral collateral ligament is damaged;
and will rotate excessively externally if the medial
collateral ligament is damaged. The collateral
ligaments may also be evaluated by placing valgus and
varus stress on the antebrachium with the elbow joint
extended.
Joints that are reasonably stable after closed
reduction are managed with external coaptation.
Joints that cannot be reduced closed, or easily reluxate
after closed reduction, are managed with internal
fixation27.
External coaptation
Lateral luxations are stabilized by placing the limb
in a Spica splint for 2–3 weeks. Immobilizing the
limb with the elbow in approximately 140° of
extension places the anconeal process within
the olecranon fossa for added stabililty. Caudal
luxtions are stabilized by placing the limb in
a Velpeau sling for 2–3 weeks to maintain elbow
flexion12.

94

Engage anconeal
process
110°
Flexion
Pronation

Medial pressure on
radial head
A B
94 Closed reduction of a lateral elbow luxation.
A The elbow is positioned in 110° of flexion and then pressure is applied to the proximal
ulna to engage the anconeal process within the olecranon fossa of the humerus.
B The joint is then pronated, adducted, and slowly flexed while exterting medial pressure
on the radial head.
 Fractures and disorders of the forelimb
133

Internal fixation locking-loop pattern. Severely damaged

Internal fixation is indicated when closed reduction is
unsuccessful or when elbow instability persists after
closed reduction. The joint is approached through a
lateral incision over the elbow. Hematoma, torn
remnants of the joint capsule, and muscle are removed
from the joint and the articular surfaces examined.
The elbow is reduced as described for the closed
methods. An olecranon ostectomy may be performed,
if necessary, to facilitate reduction, but is rarely
required. (The olecranon is reattached using a tension
band fixation after the joint is stabilized.) The joint is
stabilized by reconstruction of the periarticular soft
tissues (with or without a transarticular pin) and
external coaptation (95).
• Soft tissue reconstruction – after joint reduction,
the joint capsule and collateral ligaments are
reconstructed as needed to insure joint stability.
Several interrupted mattress sutures are placed
in the joint capsule. Torn collateral ligaments are
apposed with nonabsorbable suture material in a
ligaments are replaced with suture material
(prosthetic ligament). This is achieved by
placing the suture through bone tunnels
drilled at the origin and insertion sites of
the ligaments. Alternatively, bone anchors or
screws and washers may be placed to affix the
suture in the proper anatomic location28.
Nonabsorbable suture material (2–0) in a
figure-of-eight pattern is used. The radial and
ulnar nerves should be protected during
reduction and stabilization of the elbow joint.
The limb is placed in a Spica splint for 2 weeks
after surgery. The cat’s activity is restricted
for 4 weeks after splint removal. Passive range-
of-motion exercises are used to restore full
mobility to the joint.
• Transarticular pin – in some cats, soft tissue
reconstruction alone is inadequate to maintain
reduction. A transarticular Kirschner wire
(1.1–1.6 mm) may be inserted from the

95

A B C D

95 Surgical stabilization of elbow luxations.

A Soft tissue reconstruction with a locking-loop suture placed in the ruptured collateral ligament and several mattress
sutures in the torn joint capsule. The insert shows the locking-loop suture pattern. Nonabsorbable suture material in used.
B Soft tissue reconstruction using a prosthetic collateral ligament. Nonabsorbable suture material is placed in a figure-of-
eight pattern through bone tunnels drilled at the origin and insertion of the torn collateral ligament.
C Soft tissue reconstruction using a prosthetic collateral ligament. Bone screws and washers are used to anchor the suture
material in the proper location.
D Stabilization of an elbow luxation with a prosthetic collateral ligament, capsular inbrication, and a transarticular pin.
134

olecranon into the humeral condyle, or from the ELBOW ARTHRODESIS

humeral condyle into the radial head, as needed,
to stabilize the joint12. The elbow should be in a
functional position. The pin is cut but left long
enough to allow removal in 2 weeks. The limb is
placed in a Spica splint for 2 weeks. The cat’s
activity is restricted for 4 weeks after splint and
pin removal. Passive range-of-motion exercises
may be helpful in restoring joint mobility after
implant removal.
Prognosis
The prognosis after elbow luxation depends on the
severity of cartilage and periarticular soft tissue injuries,
chronicity of the luxation before repair, degree of
stabilization achieved, and owner compliance with
postoperative restriction and physical therapy. The
prognosis with elbow luxations is good to excellent if
treated early and physical therapy is begun soon after
reduction. Potential complications include reluxation,
reduced range of motion, osteoarthritis, and infection.
In cases of severe articular cartilage and periarticular
soft tissue injury, elbow arthrodesis may be considered.
Arthrodesis is an alternative to amputation for
treatment of irreparable comminuted intraarticular
fractures, chronic luxation unresponsive to surgical
stabilization, and severe degenerative joint disease29,30.
Unfortunately, limb function is significantly compro-
mised after elbow arthrodesis. Alhough the joint is
usually pain-free, most cats will use the limb only
intermittently, and the limb is circumducted during the
swing phase of each stride. Most cats function better
after amputation than after elbow arthrodesis27,30.
The elbow is usually fused at 110–135°, but the
angle should be individualized for each cat based on
preoperative evaluation29,30. The joint is exposed by a
combined lateral and caudal approach with ostectomy
of the olecranon process7. Transection of the ulnaris
lateralis, lateral collateral ligaments, and the joint
capsule allows removal of the articular cartilage from
the radial head, humeral condyles, and the trochlear
notch of the ulna using bone curettes or a power burr.
The joint space is filled with cancellous bone graft to
promote fusion. Rigid fixation is achieved with one of
several described techniques (96).

96

A B C

96 Elbow arthrodesis. A Lag screw fixation. A small pin is placed from the ulna to the humerus to maintain reduction at
the desired angle. Lag screws are inserted from the lateral epicondyle into the radial head, from the olecranon process to
the humerus, and from the ulna to the medial epicondyle. B Plate fixation. An eight- to ten-hole 2.0 mm or 2.7 mm bone
plate is applied to the caudal surface of the distal humerus and proximal ulna. Two screws are placed in lag fashion
through the plate and across the joint space. The olecranon process is reattached lateral to the bone plate. C Transarticular
external fixator. A small pin is inserted from the ulna, across the elbow joint, and up the medullary cavity of the humerus,
exiting the bone at the greater tubercle. A second pin is inserted normograde into the ulna from the olecranon process.
Transfixation half pins are inserted in the radius, ulna, and humerus. Flexible tubing is attached to the exposed ends of the
pins and filled with acrylic.
 Fractures and disorders of the forelimb
Lag screw fixation
A Steinmann pin is placed across the joint (from the
ulna to the humerus) to maintain reduction at the
desired angle. Stabilization is provided using lag
screws. One screw is inserted from the lateral
epicondyle into the radial head. A second screw is
placed from the olecranon process to the humerus.
A third screw is inserted from the ulna to the medial
epicondyle. An additional screw can be inserted from
the ulna to the humerus if sufficient room exists. After
surgery, the limb is immobilized in a Spica splint for
2–4 weeks. A transarticular external fixator can be
applied to protect the repair during healing but is
generally not required. Exercise must be restricted for
4–6 weeks after surgery or until radiographic evidence
of fusion is observed.
Plate fixation
A 2.0 mm or 2.7 mm bone plate is applied to the
caudal aspect of the distal humerus and proximal ulna
after ostectomy of the olecranon process30. An eight-
to ten-hole plate will suffice for most cats. Where
135
possible, screws are placed in lag fashion through the
plate and across the joint space. Separate lag screws
may also be placed outside the plate. The olecranon
process is reattached lateral to the bone plate using
Kirschner wires or a lag screw. After surgery, the limb
is immobilized in a Spica splint for 2–4 weeks.
Transarticular external fixator
A Kirschner wire (1.6–2.0 mm) is inserted across the
elbow joint from the ulna into the humeral medullary
cavity. The pin should exit the proximal humerus at
the greater tubercle. Both ends of the Kirschner wire
are left protruding from the skin. A second pin is
placed normograde into the ulna from the olecranon
process30. Several transfixation pins (half pins) are
inserted in the radius, ulna, and humerus. Flexible
tubing is then placed to connect the exposed ends of
the transfixation pins, ulnar pin, and both ends of the
humeral pin. The tubing is filled with acrylic and
allowed to harden. The fixator frame is wrapped. The
connecting bar and pins are removed when fusion is
complete.
136
PART 3: RADIUS AND ULNA
HEMIMELIA
Radial hemimelia (also called radial agenesis) is
a developmental anomaly characterized by the absence
or severe hypoplasia of the radius (97). It is reported
rarely in cats1,2. Although the etiology of radial
hemimelia is unknown, in utero mineral deficiencies
(including copper, manganese, and zinc), trauma to the
developing fetal skeleton, in utero drug toxicity, and
vaccination are potential causes. Genetics is also a likely
cause. A second breeding of the parents of kittens with
hemimelia produced another litter with affected kittens2.
Most kittens have an obvious limb deformity at
birth, characterized by shortening and curvature
of one or both forelimbs. The kittens are lame and
often have reduced range of motion of the elbow
and carpal joints. Carpal joint deformities may
occur concurrently. No effective treatment has been
reported, though some kittens will use the limb to
ambulate. Forelimb amputation may be performed in
97
A
97 A Cat with radial
hemimelia.
B Radiograph of
forelimbs from a cat
with radial hemimelia.
B B
cases of unilateral radial hemimelia if limb function is
poor or if trauma to the affected limb occurs.
Neutering is advised because of the potential genetic
component of the disease.
RADIAL HEAD LUXATION
Luxation of the radial head is rare in cats and is
associated with traumatic rupture of the annular
ligament. Clinical signs include lameness and elbow
pain. The displaced radial head is palpable in some
cases and the diagnosis is confirmed by radiographic
evaluation of the elbow joint (98). Treatment for
radial head luxation is open reduction and internal
stabilization. Once reduced, the radius is attached to
the ulna with a 2.0 mm cortical screw placed in lag
fashion (99). In most cases, the screw does not appear
to limit motion between the radius and ulna and
normal limb function is restored. The screw remains
in place unless complications develop.
98
A
98 Radial head luxation.
A Lateral radiographic
view.
B Craniocaudal
radiographic view.
 Fractures and disorders of the forelimb
137

FRACTURES cases. In most cases, proximal radial fractures can

CAUSE AND PATHOGENESIS
Fractures of the radius and ulna usually occur together
as a result of direct or indirect trauma to the
antebrachium. Most occur in the distal one-half of
the diaphysis or the distal metaphysis3,4. Open
fractures occur infrequently.
TREATMENT AND PROGNOSIS
In general, fractures of the radius are stabilized
preferentially over fractures of the ulna, since the radius
is the primary weight-bearing bone in the antebrachium.
Ulnar fractures are often left untreated if radial fixation
alone provides adequate stability. However, cats are able
to pronate and supinate the antebrachium and forepaw
to a greater degree than dogs, and stabilization of only
one bone provides less stability4.
be stabilized with Kirschner wires placed in
cross-pin fashion (100)5,6. The wires are inserted
just medial and lateral to the articular surface of the
radial head and driven into the opposite cortex distal
to the fracture site. If a portion of the articular surface
is involved, small screws (1.5mm or 2.0mm) are placed
in lag fashion to achieve interfragmentary compression.
If the epiphyseal fragment is large enough, mini T or L
plates can be applied (Synthes, Inc.; Veterinary
Orthopedic Implants Inc.). The surrounding soft
100

Proximal radial fractures

Fractures of the proximal radius may involve the
radial metaphysis, proximal radial growth plate, and the
radial head. The articular surface is involved in some

99

A A B
99 Surgical repair of a
radial head luxation.
A Lateral radiographic
view.
B Craniocaudal
radiographic view.

100 Repair of proximal radial fractures.

A Cross-pin fixation.
B Lag screw and Kirschner wire fixation.
B
C Mini T plate fixation.
138
tissues and collateral ligaments are sutured to ensure
joint stability. The limb may be immobilized in a soft
padded bandage or Spica splint for 2–3 weeks after
repair for additional support; however, early joint
motion is encouraged if fracture stability permits.
Diaphyseal radial fractures
Diaphyseal fractures of the radius can be stabilized
with external coaptation, external fixators, or a bone
plate and screws. If stability is adequate, additional
fixation of the ulna is not required in most cases.
External coaptation
External coaptation of radial and ulnar fractures is
indicated if the fracture can be adequately reduced
closed and the reduction is stable7. This is true of some
minimally displaced simple fractures, particularly those
in the distal half of the bone. External coaptation is very
effective in immature cats and in fractures in which the
ulna remains intact3. A cast or splint is placed from the
paw to the mid-humerus, immobilizing both the carpus
and elbow joints. Placing the splint on the lateral aspect
of the limb will allow immobilization of the elbow joint
at a functional angle.
External skeletal fixation
External fixators can be used to stabilize most fractures
of the radial diaphysis3,7–9. They are particularly useful
for repair of open and comminuted fractures. Where
possible, the fixator is applied closed or after a minimal
101
A B
101 External fixation of diaphyseal radial fractures.
A Type Ia external fixator. A minimum of two transfixation pins are applied to each side of the fracture.
B Type Ia acrylic external fixator. C Type IIb external fixator.
surgical approach to achieve fracture reduction8.
Because the feline radius is relatively flat in the
craniocaudal plane, placement of the transfixation pins
from medial to lateral can be challenging. Therefore,
the pins are often inserted from craniomedial to
caudolateral8. The craniomedial aspect of the radius
has minimal soft tissue coverage, which facilitates
pin placement. A minimum of two transfixation pins is
placed proximal and distal to the fracture (101).
Type Ia external fixators (unilateral frame/half pins)
with a single connecting bar are easy to apply and are
effective for most radial fractures in cats7. A hanging-
limb technique is used to fatigue the muscles, provide
distraction, and facilitate fracture reduction. The
proximal half pin is inserted parallel to the radiohumeral
joint through a stab incision in the skin over the
proximal, craniomedial aspect of the radius. The distal
half pin is inserted parallel to the radiocarpal joint
through a stab incision over the distal, craniomedial
aspect of the radius. These two pins are used to ensure
proper rotational alignment of the fracture and may be
used to provide distraction if needed. A connecting bar
(loaded with the desired number of empty clamps) is
placed on the proximal and distal transfixation pins.
The fracture is reduced and the clamps are tightened to
maintain reduction. A double connecting bar may be
added if additional frame stiffness is desired. Additional
half pins are then inserted through the empty clamps at
an angle of 20° to the long axis of the bone and the
clamps are tightened.
C
 Fractures and disorders of the forelimb
139

If an acrylic connecting bar is to be used, the
half pins are inserted and connected with flexible tubing
(APEF System, Innovative Animal Products LLC.).
Special pins designed for use with acrylic fixators may
be used (Miniature Interface™ fixation half pins, IMEX
Veterinary Inc.). The fracture is reduced and the tubing
is filled with acrylic. A temporary metal connecting bar
can be placed on the transfixation pins to maintain
reduction while the acrylic hardens.
A type IIb fixator (bilateral frame/full and half
pins) may be applied if additional stiffness is needed
to stabilize comminuted radial fractures (type III
frames are rarely indicated in cats). The proximal
full pin is inserted through the radius parallel to
the radiohumeral joint. The distal full pin is
inserted through the radius parallel to the radiocarpal
joint. Connecting bars (with the necessary allotment of
empty clamps) are attached to the transfixation pins on
each side of the limb. The fracture is reduced (using a
minimal surgical approach if necessary) and the clamps
are tightened. Additional half pins are inserted
through the empty clamps on the two connecting bars
and the clamps are tightened. Acrylic connecting bars
may be used instead of clamps if desired.
Bone plate and screw fixation
Diaphyseal radial fractures are amenable to repair with
bone plates and screws (102)3,4,7,10. The plate is

102

A
X

A B C D E F G

102 Plate fixation of diaphyseal radial fractures.

A Transverse fracture stabilized with a compression plate applied to the
cranial cortex of the radius.
B Transverse fracture stabilized with a compression plate applied to the
medial cortex of the radius.
C Oblique fracture stabilized with cerclage wires and a neutralization plate.
D Oblique fracture stabilized with lag screws and a neutralization plate.
E Comminuted fracture stabilized with a bridging plate.
F Comminuted fracture stabilized with a bridging plate and an
intramedullary pin in the ulna.
G Comminuted fracture stabilized with bridging plates applied to both the
radius and ulna.
H Lateral radiographic view of a diaphyseal radius and ulna fracture
stabilized with a bone plate applied to the medial aspect of the radius.
I Craniocaudal radiographic view of a bone plate applied to the medial
aspect of the radius.
H I
140
applied to the flat cranial surface of the bone through a
craniomedial surgical approach11. Application of a bone
plate to the medial surface has also been described12.
Cuttable plates, 2.0 mm DCPs, and tubular plates can
be applied to the radius in cats (Synthes, Inc.;
Veterinary Orthopedic Implants Inc.)13–15. Cuttable
plates and tubular plates are relatively thin, which
facilitates closure of the soft tissues after plate
application. Cuttable plates can be custom-cut to the
appropriate length at the surgery table and can be
stacked to achieve a variety of thicknesses (1.0–3.0 mm
with Synthes Inc. plates) and strengths.
In most cases, ulnar stabilization is not required
after radial plating. Occasionally, however, an
intramedullary pin is placed in the ulna to provide
additional support and to maintain reduction
of the radial fracture during plate application.
The pin may be inserted normograde from the
103
103 Intramedullary pin inserted into the radius. The pin
was placed retrograde from the fracture site causing severe
damage to the radiocarpal joint. Intramedullary pinning
for stabilization of radial fractures is not recommended.
olecranon process or retrograde from the fracture
site (following a minimal caudolateral approach to the
ulna). Alternatively, a bone plate may be applied to
the ulna if additional support is needed. However, the
small diameter of the distal ulna in the cat makes plate
application difficult. A soft padded bandage is applied
to the limb after surgery to reduce postoperative
swelling.
Intramedullary pinning
Intramedullary pinning is not recommended for repair
of radial fractures7,16. The narrow medullary cavity of
the radius will accommodate only a very small, flexible
pin that provides minimal stabilization and does not
control rotational forces. Additionally, insertion of the
pin is difficult without damaging the carpus or elbow
joints (103).
Distal radial fractures
Fractures of the distal radius include Salter–Harris
fractures of the distal radial growth plate, metaphyseal
fractures, epiphyseal fractures, and articular fractures.
Most are stabilized with external coaptation,
Kirschner wires placed in cross-pin fashion, external
fixators, bone plates, or lag screws (104). Pancarpal
arthrodesis may be indicated for irreparable, severely
comminuted articular fractures of the distal radius17.
External coaptation
External coaptation is indicated for fractures that
can be reduced closed and are relatively stable after
reduction. Distal radial fractures in immature cats and
fractures in which the ulna is intact are particularly
amenable to cast or splint fixation. The cast or splint
is applied to the limb from the paw to the mid-
humerus, immobilizing both the carpus and elbow
joints. Comminuted fractures tend to collapse and are
not ideally stabilized by external coaptation.
Cross-pin fixation
Distal metaphyseal fractures and fractures of the distal
radial growth plate may be stabilized using two
Kirschner wires (0.9–1.6 mm) placed in cross-pin
fashion5,6,16. The wires are inserted from the medial
and lateral aspects of the distal radius, avoiding the
articular surface. Removal of the implants may be
necessary if pin migration or soft tissue irritation occurs.
External skeletal fixation
A type Ia external fixator can be applied to the
craniomedial aspect of the distal radius if the distal
fragment will accommodate at least two transfixation
pins3,7. A lightweight acrylic bar is used to connect the
 Fractures and disorders of the forelimb
141

pins externally. Threaded pins will strengthen the
pin-bone interface and minimize premature loosening.
Bone plate and screw fixation
A bone plate is applied to the cranial or medial cortex
of the radius if the distal fragment will accommodate
at least two screws12. A mini T plate or small cuttable
plate with 1.5 mm or 2.0 mm screws is used in most
cases.
Lag screw fixation
Bone screws (1.5 mm or 2.0 mm) are placed in lag
fashion to compress fracture lines, particularly for
stabilization of articular fractures. The limb is placed
in a padded bandage for several days after surgery to
reduce swelling. If additional support is needed, a
caudal splint can be applied.
Ulnar fracture repair
Many ulnar fractures will heal after stabilization of
the concurrent radial fracture. Primary repair of a
fractured ulna is performed if:
• Stabilization is necessary to support a
comminuted radial fracture.
• The fracture involves the olecranon process or
trochlear notch.
• The fracture involves the styloid process and
carpal instability exists.

104

A B

C D E F G

104 Repair of distal radial fractures.

A Cross-pin fixation.
B Kirschner wire fixation.
C Tension band wire fixation.
D Lag screw fixation. A Kirschner wire may be placed to prevent rotation around the screw.
E Type Ia acrylic external fixator.
F Mini T plate applied to the dorsal cortex.
G Cuttable plate applied to the medial cortex.
142

Olecranon process fractures
The fractured olecranon process is usually displaced
proximally by the insertion of the triceps muscles. This
distractive force must be controlled to allow fracture
healing. Most olecranon fractures are transverse or
oblique and can be stabilized using a tension band
wire fixation (105)7,16. Reduction is facilitated by
extension of the elbow joint. Two Kirschner wires
(0.9–1.1 mm) are inserted from the tip of the
olecranon, across the fracture site, and into the
medullary cavity of the ulna. In smaller cats it may be
difficult to position two Kirschner wires in the narrow
olecranon. A single intramedullary pin may be placed
instead, but it will not control rotational forces in
many fracture configurations. A transverse hole is then
drilled from lateral to medial through the ulna distal
to the fracture to accommodate a strand of 0.8 mm
(20 AWG) orthopedic wire. The orthopedic wire is
placed in a figure-of-eight configuration through the
hole in the ulna and around the proximal ends of the
intramedullary Kirschner wires.
Comminuted olecranon fractures are repaired by
first reconstructing the fragments with Kirschner wires
(or lag screws) and then placing a tension band wire.
Alternatively, a bone plate may be applied to the
lateral or caudal surface of the ulna. A tubular plate,
cuttable plate, or 2.0 mm DCP can be used.
Trochlear notch fractures
Transverse and oblique fractures of the proximal ulna
involving the trochlear notch are repaired with a tension
band wire fixation or bone plate (105 B–E).
Comminuted fractures of the trochlear notch are
repaired with Kirschner wires or small lag screws to
ensure the articular surface is anatomically reconstructed.
A neutralization plate is then applied to the lateral
surface of the proximal ulna. If the joint surface cannot
be restored, the plate is applied in buttress fashion to

105

A B C D E

105 Repair of olecranon fractures.

A Tension band wire fixation (lateral and craniocaudal views). Two Kirschner wires are inserted normograde.
B Tension wire band fixation using a single intramedullary pin. This method provides less rotational stability at the
fracture site, but is often easier to apply to the narrow feline olecranon.
C Caudal plate fixation.
D Lateral plate fixation.
E Olecranon fracture with comminution of the trochlear notch. Fragments are stabilized with Kirschner wires or lag
screws prior to plate application.
 Fractures and disorders of the forelimb
143

bridge the defect and prevent collapse of the fracture site.
A tubular plate, cuttable plate, or 2.0 mm DCP can be
used. A cancellous bone graft is placed in the defect.
Monteggia fractures
Fractures of the ulna with concurrent radiohumeral
luxation are termed Monteggia fractures7,18. In cats,
they usually result from a fall7. The ulnar fracture may
be simple or comminuted. The radioulnar joint
remains intact in some cases, while in others the
annular ligaments and a portion of the lateral
collateral ligament are torn, resulting in radioulnar
luxation. Internal fixation is recommended to stabilize
the ulnar fracture and restore joint congruence (106).
If the radioulnar joint is intact, the ulnar fracture is
stabilized with an intramedullary pin placed
normograde or retrograde. A strand of 0.8 mm
(20 AWG) orthopedic wire is placed through two
holes drilled in the caudal cortex of the ulna (one
proximal and one distal to the fracture) as a tension
band. Bone plate fixation may also be used to stabilize
the ulnar fracture, and is particularly useful in
comminuted fractures. Stability of the ulna maintains
reduction of the radiohumeral joint if the radioulnar
joint is intact7. A splint or Robert Jones bandage may
be applied temporarily to the limb after surgery.
If the radioulnar joint is luxated, the ulnar fracture
is stabilized with an intramedullary pin or bone plate.
The annular ligament and torn portion of the lateral
collateral ligament are repaired with 2-0 monofil-
ament, nonabsorbable suture material. If the
ligaments cannot be repaired, a positional screw is
placed through the ulna into the proximal radius to
stabilize the radiohumeral joint. In most cases, this
screw does not significantly limit normal pronation
and supination of the antebrachium. However, if
movement is restricted, the screw may be removed in
3–4 weeks.

106

A B C D E F

106 Repair of Monteggia fractures (ulnar fracture with concurrent radiohumeral luxation).
A Monteggia fracture with an intact radioulnar joint.
B The ulnar fracture is stabilized with an intramedullary pin and tension band wire. The intact radioulnar joint maintains
reduction of the radiohumeral joint once the ulna is repaired.
C Stabilization using a lateral bone plate.
D Monteggia fracture with disruption of the radioulnar joint.
E The ulnar fracture is stabilized with a bone plate. The annular ligament and damaged portions of the collateral ligament
are sutured.
F The ulna is stabilized with a bone plate. A positional screw is inserted from the ulna to the proximal radius.
144
Diaphyseal ulnar fractures
Fractures of the ulnar diaphysis usually heal well after
reduction and stabilization of the concurrent radial
fracture (107). However, if ulnar repair is necessary to
provide additional stability, an intramedullary pin or
bone plate may be applied. The ulna is exposed
through a caudolateral surgical approach. Plate
application is easier on the proximal ulna where the
bone is larger. It may not be possible to apply a plate
to the small distal ulna in many cats. A tubular plate,
cuttable plate, or 2.0 mm DCP can be used.
Intramedullary pins may be inserted normograde or
retrograde through the olecranon process. This can
often be performed through a small incision (3–4 cm)
over the caudal aspect of the bone11. A pin of
adequate diameter to fill the distal ulnar medullary
canal should be selected4. Intramedullary pin fixation
of the ulna is not recommended for stabilization of
radius/ulna fractures without concurrent radial
stabilization. The small medullary cavity of the ulna
can accommodate only small, flexible pins that
provide inadequate bending and rotational stability
when used alone.
107
A B C D
107 Repair of ulnar diaphyseal fractures.
A, B Stabilization of the concurrent radial fracture with a
bone plate or external fixator allows healing of the
unrepaired ulnar fracture.
C A bone plate is applied to the radius. Inserting an
intramedullary pin in the ulna provides additional stability.
D Plate fixation of an ulnar fracture.
Styloid process fractures
The styloid process is the origin of the ulnar collateral
ligaments in the antebrachiocarpal joint. Fracture of
the distal styloid process may be associated with joint
instability or luxation7. Minimally displaced fractures,
particularly in immature cats, are immobilized in a
caudal splint for 4–6 weeks until healing is complete.
Styloid fractures may also be stabilized internally by
inserting a small Kirschner wire placed normograde
from the tip of the styloid process into the medullary
cavity of the distal ulna (108). A tension band wire is
often applied to prevent distraction at the fracture
site. In most cats, only a single Kirschner wire can be
inserted and small wire (0.5 mm [24 AWG]) is used
in a figure-of-eight pattern. Torn ligaments are
sutured if possible. The limb is placed in a caudal
splint for 3–4 weeks and the cat’s activity is restricted.
Severely comminuted styloid process fractures may be
repaired by attaching the distal styloid process to the
distal radius with a small lag screw. Pancarpal
arthrodesis may be required for irreparable styloid
process fractures accompanied by severe distal radial
fracture.
108
A B C
108 Repair of styloid process fractures of the ulna.
A Styloid process fracture stabilized with a Kirschner wire
inserted normograde.
B Styloid process fracture stabilized with a tension band
wire fixation.
C Comminuted styloid process fracture stabilized by
inserting a lag screw through the distal styloid process into
the radius.
 Fractures and disorders of the forelimb
145

PART 4: CARPAL, METACARPAL, AND PHALANGEAL INJURIES

CARPAL JOINT INJURIES Swelling and joint instability may be palpated

The carpal bones are anatomically arranged in in the carpal region. Radiographs are indicated
two levels (109, 110)1. Proximally, the radial to identify fractures and joint luxations. Stress
and ulnar carpal bones articulate with the distal radiographs are helpful in confirming instability.
radius and styloid process of the ulna to form
the antebrachiocarpal joint (radiocarpal joint
and ulnarcarpal joint). The accessory carpal bone
articulates with the palmar surface of the ulnar carpal 109
bone and serves as the insertion point for the
flexor carpi ulnaris muscle. The small carpal bones
(I through IV) articulate proximally with the radial and
ulnar carpal bones to form the middle carpal joint, and
distally with the metacarpal bones to form the
carpometacarpal joint. The spaces between each of the
carpal bones on a given level are called intercarpal
joints. Numerous ligaments maintain stability yet
permit joint motion. On the palmar surface of the
carpus, the joint capsule, palmar carpal fibrocartilage,
and ligaments support the joint while bearing weight.
Carpal injuries in the cat typically result from
trauma caused by falling, jumping, or being hit by an
automobile. Combined fracture/luxation of the
carpus is more common than isolated fracture or A B
luxation2. The cat is usually in pain and does not bear 109 Bones of the feline carpus and metacarpus.
weight on the injured limb. A Dorsal view. B Lateral view.

110
Ulna
Ulna Radius
Radius

Accessory
carpal bone
Radial carpal
bone
5th First
Carpals metacarpal metacarpal
Proximal
Metacarpals phalanx
Distal
phalanx
Digits Proximal
phalanx
Middle
phalanx
Distal
phalanx
A B C D

110 Bones of the carpus, metacarpus, and phalanges in a cat. A Dorsal view. B Lateral view. C Medial view. D Palmar view.
146
CARPAL BONE FRACTURES
Cause and pathogenesis
Carpal bone fractures are uncommon in cats; they
usually occur as a result of falling, jumping, or a road
traffic accident.
Diagnosis
Diagnosis is by palpation and radiography.
Treatment and prognosis
Fractures of the smaller carpal bones are managed by
closed reduction and external coaptation. The limb is
immobilized in a palmar splint (placed from the
phalanges to the proximal antebrachium) for 4 weeks.
A soft padded bandage is applied for an additional
2 weeks after splint removal. The cat’s activity is
restricted for 6 weeks.
Radial carpal bone fractures
Most fractures of the radial carpal bone are small chip
fractures of the dorsal surface. Small slab fractures
may also occur. Oblique fractures through the radial
carpal bone are rare. Generally, radial carpal
111
A B C D
111 Repair of radial carpal bone fractures.
A Doral slab fracture of the radial carpal bone.
B Lag screw fixation.
C Kirschner wire fixation.
D Chip fractures of the radial carpal bone. The fragments are excised via a dorsal surgical approach.
E Oblique fracture of the radial carpal bone repaired with a lag screw.
bone fractures are managed with external coaptation
in a palmar splint, particularly if the fragment is
minimally displaced. Displaced fragments are
excised through a dorsal approach to the carpus3.
The carpus is immobilized in a palmar splint for
2 weeks and then light exercise is encouraged. If the
fragment is large enough, it is reattached using a
1.5 mm bone screw placed in lag fashion (111).
Small Kirschner wires countersunk below the
cortical surface may also be used. The limb is
immobilized in a palmar splint for 3–4 weeks and the
cat’s activity is restricted for 6 weeks.
Accessory carpal bone fractures
The accessory carpal bone is less prominent in cats
than in dogs, and fractures of the accessory carpal
bone are rare in cats (112). In most cases, the
fracture fragment is very small. If the fracture does
not involve the articular surface (apical fractures) and
displacement is minimal, the limb is splinted with the
carpus flexed 20–25°. The splint remains in place for
3–4 weeks. A soft padded bandage may be applied
for an additional 2 weeks after splint removal if
E
 Fractures and disorders of the forelimb
112
A B C 1. Carefully cleaning and debriding the wound.
112 Surgical repair of accessory carpal bone fractures. In
most cases, the fragments are small and treatment consists
of external coaptation or fragment excision. If the
fragment is large enough, internal fixation with a lag screw
or Kirschner wire is indicated.
A Distal-basilar fracture of the accessory carpal bone
(involving the articular surface) stabilized with a 1.5 mm
lag screw.
B Proximal-basilar fracture of the accessory carpal bone
stabilized with a lag screw.
C Distal apical fracture of the accessory carpal bone
stabilized with a Kirschner wire.
needed. The cat’s activity is restricted during the
healing period. If the fracture involves the articular
surface of the accessory carpal bone (basilar
fractures), the fragment is removed through a
palmarolateral approach3. Larger fragments are
uncommon and may be reattached with a Kirschner
wire or a 1.5 mm lag screw. After surgery the limb is
immobilized in a palmar splint with the carpus flexed
20–25°. The splint remains in place for 2 weeks after
excision of bone fragments and for 4 weeks after
internal fixation. The cat’s activity is restricted for
6 weeks.
147
CARPAL SHEARING INJURIES
Cause and pathogenesis
Shearing (degloving) injuries occur less frequently on
the forelimb than on the hindlimb. Most occur when
the cat is hit by a car.
Clinical signs
The medial aspect of the carpus and metacarpus
is abraded by the pavement, destroying variable
amounts of tissue, including skin, muscle, tendons,
ligaments, and bone. One or more of the carpal joints
may be open and contaminated.
Treatment and prognosis
Shearing injuries of the carpus are managed by1,4:
2. Proper open-wound management.
3. Early stabilization of the joints.
Initially, the wound is covered with a sterile bandage
while the cat is stabilized and evaluated for other
traumatic injuries. The cat is then anesthetized and the
wound is examined under sterile conditions to assess
tissue damage. A sample is collected for culture
and susceptibility testing and a broad-spectrum
antimicrobial drug is administered. Cephalosporins
(cefazolin at 22 mg/kg IV every 8 hours) and
clindamycin (11 mg/kg IV every 12 hours) have been
recommended5. The wound is filled with sterile
lubricating jelly and the surrounding hair is shaved.
Copious lavage, with sterile saline, lactated Ringer’s, or
a 0.05% chlorhexidine solution, is used to remove hair
and debris from the wound and open joint spaces6.
Surgical debridement is then performed to remove
debris and devitalized tissues from the wound. Vessels
and nerves must be preserved. With some minor
shearing injuries, the wound is converted to a ‘clean’
wound by lavage and debridement and can be closed
primarily if adequate tissue remains. However, in most
cases, insufficient soft tissue remains to permit
primary closure, and progressive debridement over
several days is required to achieve a clean wound.
These cases are managed as open wounds4.
Stabilization of the joint is performed once the
wound is clean. Early stabilization encourages healing
of the periarticular soft tissues. The collateral
ligaments are repaired or replaced. Viable portions of
the ligaments can be sutured with monofilament
suture material. In most cases, however, the collateral
ligaments are too severely damaged and are replaced
with nonabsorbable, monofilament suture (2-0)
material placed in a figure-of-eight pattern. Bone
tunnels are drilled in the medial prominence of the
148

radial carpal bone and in the distal radius to anchor
the suture (113). Alternatively, bone anchors or small
screws may be placed at the origin and insertion of the
collateral ligament to attach the suture. If possible, the
joint capsule is sutured after lavage. The carpus is then
immobilized in a weight-bearing position with an
external fixator. A type Ia fixator (unilateral/half pins)
is adequate for most cats and is easily applied to the
craniomedial aspect of the carpus. Transfixation pins
are placed in the distal radius and the proximal
metacarpus. Small pins are used in the metacarpal
bones to prevent iatrogenic fracture7. An acrylic bar is
lightweight and can be contoured to allow proper pin
placement. The fixator remains in place for 3–4 weeks
until granulation tissue covers the wound. A palmar
splint can be used to immobilize the joint rather than
an external fixator, but the splint must be removed
daily to allow treatment of the open wound.
The open wound is managed daily. Wet-to-dry
dressings are applied to remove debris and encourage
granulation tissue formation8. Once granulation tissue
covers the wound, a dry nonadherent dressing is
applied. The bandage is changed less frequently and
may incorporate a splint for added support once the
external fixator is removed. In most cases, the wound
heals completely by epithelialization and contraction
in 10–12 weeks. If adequate soft tissue is present, the
wound may be secondarily sutured once a healthy
granulation bed has been established. Rarely, a skin
graft is required to cover unhealed soft tissue defects.
The cat’s activity is restricted until healing is
complete.
Arthrodesis is indicated in shearing injuries with
severe bone loss and irreparable damage to the distal
radius, radial carpal bone, and articular cartilage.
Arthrodesis is achieved with an external fixator or bone
plate (see Pancarpal arthrodesis). Bone grafting is
delayed until the joint space is covered with
granulation tissue. In some cases, arthrodesis is
performed only after primary treatment of the shearing
injury has failed to restore adequate, pain-free
function.
CARPAL LUXATIONS
Traumatic luxation or subluxation of the carpal joints
is uncommon in cats, and may accompany shearing
injuries. Because cats are relatively lightweight, most
carpal injuries respond well to conservative treatment
with external coaptation and restricted activity.
Internal fixation is indicated if the joint cannot be
reduced closed or is markedly unstable after closed
reduction.

113

Insertional
bone
anchors

A B C D E

113 Stabilization of carpal shearing injuries. A Shearing injury of the medial carpus. The radial styloid process, medial
portion of the radial carpal bone, and collateral ligaments are absent. The joint is stabilized by prosthetic replacement of
the collateral ligament. B Nonabsorbable monofilament suture material (figure-of-eight pattern) placed through bone
tunnels drilled in the distal radius and radial carpal bone. C Bone anchors are used to attach suture material to the distal
radius and radial carpal bone. D Bone screws are placed at the origin and insertion of the collateral ligament to attach
suture material. E The carpus is immobilized with a type Ia acrylic external fixator.
 Fractures and disorders of the forelimb
149

Radial carpal bone luxation include palmaroproximal luxation of the radial

Cause and pathogenesis
Luxation of the radial carpal bone occurs rarely in
dogs and has been reported in one cat9–11. The
luxation occurs secondary to a traumatic incident in
which the antebrachiocarpal joint is hyperextended
with pronation, followed by supination, of the joint11.
The short radial collateral ligament and dorsal joint
capsule rupture and the radial carpal bone luxates in a
palmar direction. It also rotates 90° about its
dorsopalmar and mediolateral axes.
Clinical signs
Clinical signs include acute lameness, soft tissue
swelling, and joint effusion.
Diagnosis
The carpus and foot are displaced palmarly, making
the styloid process of the distal radius prominent on
palpation. Manipulation of the foot causes pain, and
flexion is limited. Hyperextension of the carpal joint
can be induced with palpation. Radiographic findings
carpal bone and collapse of the antebrachiocarpal joint
space (114).
Treatment and prognosis
Anatomic reduction cannot be achieved with closed
methods because of the rotation of the luxated radial
carpal joint. Open reduction and internal fixation
are required. A dorsal approach to the carpus is
performed and visualization of the luxated radial carpal
joint is achieved by flexing the joint. Reduction is
achieved by first rotating the radial carpal bone about
its dorsopalmar axis and then about its mediolateral
axis. It is then repositioned by applying digital pressure
from the palmar aspect of the joint while extending the
carpus. After reduction, a small Kirschner wire is
inserted from medial to lateral through the radial
carpal bone and into the ulnar carpal bone. Clamping
the radial and ulnar carpal bones together during wire
insertion may prevent lateral displacement of the ulnar
carpal bone. Alternatively, a small lag screw can be
placed. The ruptured radial collateral ligament and

Luxated radial 114

carpal bone

A B

114 Luxation of the radial carpal bone.

A Dorsal and medial views depicting luxation of the radial carpal bone. The radial carpal bone is
displaced in the palmaroproximal direction and rotated about its dorsopalmar and mediolateral axes.
The carpus and foot are displaced palmarly, making the styloid process of the distal radius prominent
on palpation.
B Surgical stabilization of a radial carpal bone luxation. Reduction is achieved by rotating the radial
carpal bone about its dorsopalmar and mediolateral axes and then applying digital pressure to the
palmar aspect of the joint while extending the carpus. A Kirschner wire is inserted through the radial
carpal bone into the ulnar carpal bone. The ruptured radial collateral ligament and joint capsule are
sutured to restore joint stability.
150

joint capsule are sutured to restore joint stability. The
carpus is immobilized with a palmar splint or type Ia
external fixator for 4 weeks. The Kirschner wire may be
removed after 6 weeks if it causes complications or
migrates.
Follow-up evaluation of the single reported feline
case of radial carpal bone luxation revealed that the
cat’s function was good, although osteoarthritis and
decreased carpal flexion were evident. If radial carpal
bone luxation is accompanied by severe articular
cartilage damage or irreparable joint laxity, carpal
arthrodesis should be considered.
Antebrachiocarpal joint luxation and subluxation
Cause and pathogenesis
Trauma to the medial (radial) collateral ligament
is the most common injury associated with
antebrachiocarpal joint subluxation, resulting in
medial joint instability and palmar dislocation of the
radial carpal bone (115)12. In cats, the medial
collateral ligament consists of a single branch that
originates dorsoproximally on the distal radius
and courses obliquely in a palmarodistal direction to
insert on the radial carpal bone12. Complete
antebrachiocarpal luxation is rare.
Clinical signs
Clinically, the cat is lame.
Diagnosis
Pain and crepitus may be elicited on palpation of the
carpal region. Medial instability is palpable if rupture
of the collateral ligament is complete.
Treatment and prognosis
In most cases, the antebrachiocarpal joint is reduced
in a closed fashion and the limb is supported in a
palmar splint placed from the phalanges to the
proximal antebrachium. The splint remains in place
for 4–6 weeks. Alternatively, a small transarticular
Kirschner wire can be placed percutaneously prior to
splinting2. The wire is removed in 3–4 weeks.
If open reduction and internal stabilization are
required to maintain joint stability, a dorsal approach to
the distal radius and carpus is performed. If the joint is
severely damaged, pancarpal arthrodesis is considered.
However, in most cases, the antebrachiocarpal joint can
be reduced and stabilized using soft tissue
reconstruction or collateral ligament replacement:
• Soft tissue reconstruction – the torn radial
collateral ligament and joint capsule are repaired

115

A B C D

115 Repair of antebrachiocarpal luxation.

A Rupture of the radial collateral ligament resulting in medial joint instability.
B Stabilization of the antebrachiocarpal joint by primary repair of the torn radial collateral ligament and a transarticular pin.
C Stabilization of the antebrachiocarpal joint with a prosthetic ligament. Bone tunnels are drilled in the medial
prominence of the radial carpal bone and the distal radius. Monofilament, nonabsorbable suture material is placed in a
figure-of-eight pattern to replace the torn collateral ligament.
D Prosthetic ligament replacement using small screws placed at the origin and insertion of the collateral ligament to attach
the suture.
 Fractures and disorders of the forelimb
151

with monofilament, nonabsorbable suture
material (3-0 or 2-0). A locking-loop or
mattress suture pattern is recommended in
the ligament. Suturing the small ligament can
be difficult; and in many cases the ligament
is too damaged to be sutured adequately.
A transarticular pin may also be placed across
the joint, but is not usually required if the soft
tissues are anatomically reconstructed. The limb
is splinted for 4 weeks with the carpus in 15° of
flexion.
• Collateral ligament replacement - remnants of the
torn collateral ligament are sutured primarily if
possible. A prosthetic ligament is then placed to
protect the repair and stabilize the joint.
A bone tunnel is drilled in the medial prominence
of the radial carpal bone and distal radius.
Monofilament, nonabsorbable suture material
(2-0 or 0) is placed in a figure-of-eight pattern
through the tunnels to replace the torn collateral
ligament. Alternatively, bone anchors or small
screws may be placed at the origin and insertion
of the collateral ligament to attach the suture.
The joint capsule is imbricated and the incision is
closed routinely. The limb is placed in a palmar
splint (with the carpus flexed 15°) for 4 weeks.
The cat’s activity is restricted for 8 weeks.
Middle carpal and carpometacarpal joint luxation
and subluxation
Luxation and subluxation of the middle carpal and
carpometacarpal joints are rare.
Treatment and prognosis
In most cases, the joint is reduced in a closed fashion
and the limb is placed in a palmar splint for 4–6 weeks
with the carpus in 15–20° of flexion. The cat’s activity
is restricted for 8 weeks. If the joint is markedly
unstable after closed reduction, internal fixation may
enhance stability. A dorsomedial approach is performed
and the medial aspect of the joint is exposed. Bone
tunnels are drilled through the palmaromedial process
of the radial carpal bone and the base of metacarpal II.
Monofilament, nonabsorbable suture material (0 or
2-0) is placed through the tunnels in a figure-of-eight
fashion and tightened (116). The limb is immobilized
in a palmar splint for 4–6 weeks with the carpus in 15°
of flexion1. If pain and instability persist after closed or
open stabilization, partial carpal arthrodesis is
considered13.

116

A B C

116 Repair of middle carpal joint luxation.

A Medial instability of the middle carpal joint (arrow) caused by ligament rupture.
B Stabilization of the middle carpal joint with suture material placed through bone tunnels drilled in the
palmaromedial process of the radial carpal bone and the base of metacarpal II.
C Medial view: prosthetic ligament replacement.
152

HYPEREXTENSION INJURIES OF THE CARPUS antebrachiocarpal and carpometacarpal joints in

Cause and pathogenesis
Hyperextension injuries to the feline carpus are
uncommon and typically occur when the cat falls or
jumps from a great height. The trauma causes tearing of
the palmar carpal fibrocartilage and palmar ligaments.
Injury to any or all of the antebrachiocarpal, middle
carpal, or carpometacarpal joints can occur (117).
Clinical signs
Hyperextension of the carpus is usually palpable and
the cat may walk with a palmigrade stance.
Diagnosis
Stress radiographs will confirm the hyperextension
injury and may be used to determine which joints are
involved. Radiographs should be evaluated carefully
for concurrent fractures.
Treatment and prognosis
Carpal hyperextension injuries in cats are usually
treated conservatively. The limb is bandaged with the
flexion for 3–4 weeks. The carpal flexion bandage
prevents weight bearing and allows healing of palmar
fibrocartilage. After bandage removal, the cat’s
activity is restricted for an additional 3–4 weeks.
Jumping is discouraged during this period. Mild
physical therapy exercises (including stretching and
passive range-of-motion exercises) may be instituted
to restore normal joint motion. This technique is
usually successful in cats, although it is not effective in
dogs. If hyperextension recurs after bandage removal,
carpal arthrodesis may be indicated if the cat’s
function is limited or pain persists13,14.
PANCARPAL ARTHRODESIS
Pancarpal arthrodesis involves fusion of the antebra-
chiocarpal, middle carpal, and carpometacarpal
joints 15. Indications include luxation, hyper-
extension, debilitating osteoarthritis of the
antebrachiocarpal joint, shearing injuries with
significant loss of articular cartilage, and postural
deformity resulting from radial nerve paralysis16.

117

A B
117 Carpal hyperextension injury.
A Carpal hyperextension results from traumatic tearing of the palmar carpal fibrocartilage and palmar
ligaments. Increased separation between the palmar process of the ulnar carpal bone and the base of
metacarpal V may occur if the middle carpal joint is involved.
B A carpal flexion bandage for treatment of carpal hyperextension injury.
 Fractures and disorders of the forelimb
153

A hanging-limb preparation is used. Hemorrhage is
controlled by tightly wrapping the limb with sterile
Vetwrap (3M Animal Care Products), beginning at
the toes and progressing proximally to the proximal
antebrachium. An incision is made through the
Vetwrap and the joint is exposed via a dorsal
approach3. The articular cartilage is removed with a
small bone curette or burr. The joint is reduced in a
weight-bearing position (10–12° of carpal
extension) and a bone plate is applied to achieve
arthrodesis (118). The bone plate is applied to the
dorsal surface of the radius, radial carpal bone, and
metacarpal III. Three screws are placed in the
radius, one in the radial carpal bone, and
three in metacarpal III. Cuttable plates
(1.5/2.0 mm, 7–8 holes) are sufficiently small for
carpal arthrodesis in cats, accommodate several sizes
of small screws, and can be cut to the desired length
at the surgery table 17,18. If a DCP is used,
compression can be created across the joint space.
Care is taken during insertion of screws to avoid
fracturing the small metacarpal bones. Autogenous
cancellous graft is placed in the joint spaces and a
palmar splint is applied for 6 weeks after surgery.
Splinting will help reduce the incidence of
metacarpal bone fracture 19. Alternatively, after
preparation of the joint, a type IIb external fixator
with acrylic connecting bars can be applied instead
of a plate. However, premature pin loosening and
fractures of the metacarpal bones can occur.
Arthrodesis of the antebrachiocarpal joint alone
may result in the eventual breakdown of the
remaining carpal joints and is not recommended.
PARTIAL CARPAL ARTHRODESIS
Partial carpal arthrodesis involves fusion of the middle
and carpometacarpal joints. Indications include
trauma, debilitating osteoarthritis, and luxation or
hyperextension of the middle or carpometacarpal
joints20. If the antebrachiocarpal joint is normal,
partial carpal arthrodesis is preferred. After removing
the cartilage from the joint surfaces, small
intramedullary Kirschner wires are inserted from
metacarpals III and IV, across the joints, and into the

118

A B
118 Pancarpal arthrodesis.
A Dorsal and lateral views of pancarpal arthrodesis with a bone plate. The articular cartilage is removed
and the joint is plated in 10–12° of carpal extension. The bone plate is applied to the dorsal surface of
the radius, radial carpal bone, and metacarpal III. Three screws are placed in the radius, one in the
radial carpal bone, and three in metacarpal III. Autogenous cancellous graft is placed in the joint spaces
to promote arthrodesis.
B Dorsal view of pancarpal arthrodesis with a type IIb acrylic external fixator. Premature pin loosening
and metacarpal bone fractures are complications of external fixation for pancarpal arthrodesis.
154

radial carpal bone (119). A small slot is created
distally in the dorsal surface of the metacarpal bones
to access the medullary cavity. The Kirschner wires are
inserted with the carpus in full flexion to minimize
subluxation of the middle or carpometacarpal joints.
After insertion, the exposed ends of the Kirschner
wires are bent over to reduce trauma to the phalanges
and soft tissues. This technique is extremely difficult
because of the small size of the metacarpal bones.
Alternatively, the Kirschner wires can be inserted in a
cross-pin configuration13. The medial Kirschner wire
is placed from the medial-dorsal aspect of metacarpal
II into the ulnar carpal bone. The lateral Kirschner
wire is placed through the radial carpal bone and
through the lateral-dorsal aspect of metacarpal V. The
tip of the wire is countersunk below the articular
surface of the radial carpal bone. Autogenous
cancellous bone graft is placed and the incision is
closed routinely. The carpus is immobilized in a splint
for approximately 6 weeks after surgery, or until
radiographic evidence of fusion is present.
METACARPAL AND PHALANGEAL
INJURIES
METACARPAL FRACTURES AND LUXATIONS
Fractures of the metacarpal bones and luxations of the
carpometacarpal or metacarpophalangeal joint are
usually managed by splinting for 4–6 weeks. Spoon
splints work well in most cats. Splinting of metacarpal
fractures is particularly successful if one of the
metacarpal bones is intact and serves as an ‘internal
splint’. If all four of the metacarpal bones are
fractured, care must be taken to avoid angular
deviation of the paw within the splint. Metacarpal

119

II IV
III

II

A B

119 Partial carpal arthrodesis.

A Arthrodesis of the middle carpal and carpometacarpal joints with small intramedullary Kirschner wires inserted from
metacarpals III and IV, across the joints, and into the radial carpal bone. Slots are created distally in the dorsal surface of
the metacarpal bones to access the medullary cavity. The carpus is flexed during pin insertion. Autogenous cancellous bone
graft is placed in the joint spaces to promote arthrodesis.
B Partial carpal arthrodesis with Kirschner wires in cross-pin configuration. The medial Kirschner wire is inserted from the
medial-dorsal aspect of metacarpal II into the ulnar carpal bone. The lateral Kirschner wire is placed through the radial
carpal bone and through the lateral-dorsal aspect of metacarpal V. The tip of the wire is countersunk below the articular
surface of the radial carpal bone. Autogenous cancellous bone graft is placed in the joint spaces.
 Fractures and disorders of the forelimb
155

fractures may also be stabilized by inserting small carpal pads if possible. A surgical drain may be placed.
intramedullary Kirschner wires (120)21. Typically, the The digital and carpal pads are apposed on the palmar
Kirschner wires are placed in metacarpal bones III and surface of the paw with interrupted sutures. The skin is
IV only. A small slot or hole is drilled distally in the apposed on the dorsal surface of the paw.
dorsal surface of the metacarpal bone to access the
medullary cavity. A small, flexible Kirschner wire is
inserted normograde from the hole, across the
fracture line, and into the proximal metaphysis.
Placement of these pins is challenging because of the 120 Repair of metacarpal 120
narrow medullary cavity. Retrograde insertion is not fractures. Internal fixation
recommended as it may cause damage to the joints with small intramedullary
proximal and distal to the metacarpal bones. After pin Kirschner wires placed in
placement, the foot is splinted for 4–6 weeks and the metacarpal bones III and IV.
cat’s activity is restricted. A slot is created distally in
the dorsal surface of the
PHALANGEAL FRACTURES AND LUXATIONS metacarpal bone and a
Fractures and luxations involving the phalanges are flexible Kirschner wire is
usually managed by closed reduction and splinting for inserted normograde from
4–6 weeks. Spoon splints work well in most cats. If the slot, across the fracture
severe trauma to the phalanges has occurred, the loss of line, and into the proximal
soft tissues (including skin, tendons, ligaments, and metaphysis. The foot is
joint capsule) may complicate repair. Fusion podoplasty splinted for 4–6 weeks.
may be performed as a salvage procedure in the
treatment of degolving injuries of the digits (121)22.
The traumatized soft tissues are debrided dorsally and
palmarly between the digits, preserving the digital and

121

A B C D

121 Fusion podoplasty technique for repair of severe phalangeal soft tissue trauma.
A, B Traumatized tissue between the digits is debrided dorsally and palmarly, preserving the digital and carpal pads if
possible.
C The digital and carpal pads are apposed on the palmar surface of the paw.
D The skin is apposed on the dorsal surface of the paw. A surgical drain may be placed prior to closure.
156

Digit amputation (declawing) (see Onchyectomy). The foot is clipped

Digit amputation may be indicated as treatment
for comminuted fractures, nonunions, intraarticular
fractures, irreparable luxation, shearing injuries,
neoplasia, or chronic infections of the digit.
Amputation is usually performed at the metacarpo-/
metatarsophalangeal joint, although removal at the
proximal or distal interphalangeal joint can also be
performed (122, 123). Amputation at the distal
interphalangeal joint is as described for onychectomy
and aseptically prepared for surgery. Care is taken to
clean adequately the nail beds, pads, and skin between
the digits. A tourniquet is placed to control
hemorrhage. An elliptical skin incision is made around
the digit at the level of the amputation. The ellipse
begins proximodorsally and ends distally on the
palmar/plantar surface. The digital pad is preserved if
the level of the amputation is distal enough. Vessel
ligation and electrocautery are used to control

122

A B C D

122 Digit amputation at the metacarpo-/metatarsophalangeal joint. A Diagram of bones of the foot depicting the
location of the elliptical skin incision made for amputation of the third digit at the metacarpophalangeal or
metatarsophalangeal joint. B Diagram of a cat’s foot depicting incision location. The elliptical incision begins
proximodorsally and ends distally on the palmar/plantar surface of the foot. C The metacarpo-/metatarsophalangeal joint
is disarticulated to remove the phalanges. The distal condyle of the metatarsal/metacarpal bone is excised with a rongeur.
D Subcutaneous tissues and skin are closed.

123 123 Digit amputation at the proximal interphalangeal joint.

Diagram of bones of the foot depicting the location of the elliptical skin incision made for
amputation of the third digit at the proximal interphalangeal joint. The joint is
disarticulated to remove the second and third phalanges (shaded area). The distal condyle
of the first phalanx is removed with a rongeur. The digital pad is preserved if possible and
sutured to the skin to close the defect.
 Fractures and disorders of the forelimb
hemorrhage. The joint proximal to the desired level of
amputation is disarticulated by transection of the joint
capsule, collateral ligaments, and tendons traversing
the joint. The condyle proximal to the site of
amputation is also removed using a small rongeur. The
subcutaneous tissues and skin are closed. If the digital
pad remains, it is sutured to the skin to close the
defect. The foot is bandaged for 10 days and activity is
restricted to allow healing. Most cats function very
well after amputation of a single digit. Chronic
lameness may occur after amputation of more than two
digits, particularly if the third or fourth digit is
removed. Preservation of the digital pad will improve
postoperative function.
In some cases of severe phalangeal injuries, the
digits may be amputated at the metacarpophalangeal
joint and the metacarpal pad is advanced distally to
cover the distal palmar aspect of the foot, thus
preventing the need for a total limb amputation
(124)21. The phalanges are amputated at the
metacarpophalangeal joint (including excision of the
heads of the metacarpal bones). The carpal pad is
preserved. A surgical drain is placed and a subcuticular
suture pattern is used to rotate the carpal pad distally to
cover the ends of the metacarpal bones. The remainder
of the incision is closed with mattress sutures in the
skin. A splint is applied to the limb for 4 weeks to allow
complete healing and reduce the likelihood of pad
injury caused by shearing motion between the pad and
the metacarpal bone during weight bearing.
124 Metacarpophalangeal amputation and
distal transfer of the metacarpal pad for
treatment of irreparable phalangeal trauma.
A The phalanges are amputated at the
metacapophalangeal joint, preserving the carpal
pad. The heads of the metacarpal bones are
excised.
B A surgical drain is placed and a subcuticular
suture pattern is placed to rotate the carpal pad
distally to cover the ends of the metacarpal
bones.
C The remainder of the incision is closed with
mattress sutures in the skin. The limb is
splinted for 4 weeks.
157
ONYCHECTOMY (DECLAWING)
Declawing procedures are commonly performed in
domestic cats in some countries to prevent damage
or injury to furniture, other pets, the owners, and
the cat itself. The procedure is usually performed on
indoor cats between 3 and 12 months of age. In
most cases only the front claws are removed.
Thousands of cats are declawed each year in North
America. It is estimated that approximately
14 million of the 59 million owned cats in the
United States are declawed23. Other reports indicate
that as many as 45% of the owned cats are
declawed 24. Declawing procedures are not
performed in many countries23.
The humane considerations of onychectomy are
controversial25. Proponents consider it a justifiable
option to prevent scratching, particularly if the cat
cannot be retrained and is in danger of being removed
from the home. Opponents condemn onychectomy
on ethical grounds as a needless procedure
(performed strictly for owners’ convenience) that
renders the cat unable to engage in species-specific
behaviors, such as scratching, grooming, and self-
defense23. Alternatives to onychectomy should be
discussed with cat owners prior to surgery.
SURGICAL TECHNIQUES
Onychectomy is the removal of the distal phalanx
including the claw. Growth and development of the
claw is derived from the basal germinal cell layer
124
A B C
158
(stratum germinativum) located on the ungual crest
of the distal phalanx (125)26. It is essential to remove
the entire ungual crest (and all germinal cells) during
surgery to prevent regrowth of the claw. When
possible, onychectomy is performed in young,
growing cats (often at the time of neutering).
Generally only the claws on the front feet are
removed. The procedure is performed with the cat
under general anesthesia. Analgesic drugs are
essential to minimize intraoperative and
postoperative pain.
The cat is positioned in lateral recumbency and
the front paws are scrubbed prior to surgery. The hair
may be clipped in longhaired cats. A tourniquet is
applied to the proximal antebrachium, just tight
enough to control hemorrhage and maintain a clear
surgical field. Tourniquets applied proximal to the
elbow may provide insufficient hemostasis and
damage the radial, ulnar, or median nerves.
Tourniquets applied to the distal antebrachium may
damage the radial nerve26. The limb is draped and
the distal phalanx, including the claw, is excised from
each of the front digits using one of several described
techniques.
Amputation of PIII with a guillotine-type
nail trimmer
The claws are trimmed short to facilitate placement
of the sterile nail trimmer (Resco Nail Shears, Resco
Co.). The ring of the nail trimmer is placed over the
claw into the dorsal interphalangeal space between the
second and third phalanx (126). The claw is grasped
with a towel clamp or forceps and traction is applied to
open the joint space. The blade of the nail trimmer is
125 First phalanax
Collateral ligaments
Common digital extensor tendon
Dorsal elastic ligament
Ungual crest
Third phalanx
Collateral ligaments
Flexor process of PIII
Digital pad
125 Feline phalangeal anatomy (lateral view).
positioned palmarly, in contact with the skin distal to
the digital pad. The claw is lifted dorsally to rotate the
flexor process of the distal phalanx in a palmar direction.
As the claw is rotated, the blade reflects the digital pad
proximally. The nail trimmer is closed to complete the
amputation after ensuring that the ring is positioned in
the interphalangeal space dorsally and the digital pad is
reflected. The blade must be sharp to avoid crushing the
tissues. Cutting the pad or the distal aspect of the
middle phalanx will lead to greater postoperative
discomfort and lameness. With the distal phalanx
removed, the wound is inspected for complete excision
of the ungual crest. The distal articular surface of the
middle phalanx should be visible. In most cases, a small
remnant of the distal phalanx (the flexor tubercle)
remains in the wound and is visible just palmar to the
articular surface of the middle phalanx. This remnant
can be left in situ without concern for claw regrowth26.
However, if a large piece of the distal phalanx remains,
it may contain germinal cells of the ungual crest and
claw regrowth is possible. It should be excised with a
scalpel blade. All front claws are removed.
Disarticulation of the distal phalanx
Removal of the distal phalanx by disarticulation of the
distal interphalangeal joint is achieved using a scalpel
blade or surgical laser.
Scalpel method
The claw is grasped with a towel clamp or forceps.
Pushing up on the digital pad will also help extrude
the claw. A circumferential incision is made in the
hairless, cuticle-like skin along the dorsal aspect of the
claw with a number 11 or 12 scalpel blade (127).
Superficial digital
flexor tendon
Second phalanx
Distal annular ligament
Deep digital flexor tendon
 Fractures and disorders of the forelimb
159
126
Second phalanx

Third phalanx

Ungual crest
Third phalanx
Second
phalanx

Flexor
process

A B

126 Onychectomy performed with a guillotine-type nail trimmer.

A The ring of the nail trimmer is placed over the claw into the dorsal interphalangeal space between the second and third
phalanx. The blade of the nail trimmer is positioned ventral to the distal phalanx, distal to the digital pad. Before
performing the amputation, the claw is lifted dorsally to rotate the flexor process of the distal phalanx ventrally while the
blade reflects the digital pad proximally.
B With a proper amputation (dashed line), the entire ungual crest is removed to prevent regrowth of the claw. Inspection
of the incision will reveal the distal articular surface of the second phalanx. A small remnant of the flexor process of the
distal phalanx is seen palmar to the articular surface of the second phalanx.

127 Onychectomy by disarticulation of the distal 127

phalanx – scalpel method. The claw is grasped with
forceps and a circumferential incision is made along the
dorsal aspect of the claw with a scalpel blade (dashed Common digital
extensor tendon
line). The common digital extensor tendon and dorsal
elastic ligaments are transected. The incision is continued Dorsal elastic ligaments
along both sides of the digit, transecting the skin, joint
capsule, and collateral ligaments. Ungual crest
The dissection continues in the palmar direction around
Second phalanx
the flexor process of the distal phalanx to transect the
deep digital flexor tendon. The distal phalanx is then Deep digital
dissected from the digital pad and other soft tissue flexor tendon
attachments. All of the distal phalanx, including the
Third phalanx
ungual crest and flexor tubercle, is removed. Collateral ligaments
Flexor process
Digital pad
160
The skin is retracted proximally away from the claw.
The scalpel blade is then used to transect the common
digital extensor tendon and dorsal elastic ligaments
between the second and third phalanges. The incision
is continued along both sides of the digit (following
the contour of the proximal aspect of the distal
phalanx), cutting the skin, joint capsule, and palmar
collateral ligaments. The dissection continues in the
palmar direction around the flexor tubercle of the
distal phalanx to transect the deep digital flexor
tendon. The distal phalanx is then dissected from the
digital pad and other soft tissue attachments. Cutting
the digital pad is avoided. All front claws are removed.
Laser method
Laser disarticulation of the distal interphalangeal
joint is performed like the scalpel method, except
that the incisions are made with a carbon dioxide
(CO2) laser (Luxar Corporation). The laser (light
amplification by stimulated emission of radiation)
emits an intense beam of light to concentrate energy
on the target tissue27. The energy is converted to
heat and instantly raises the intracellular water
temperature above the boiling point, thus
vaporizing or ablating the tissue. Minimal collateral
damage is caused to surrounding tissues. Vessels are
sealed by tissue contracture to decrease bleeding.
For this reason, tourniquets are often not required
during laser onychectomy. Nerve endings and
lymphatic vessels are also sealed, resulting in less
pain and swelling after surgery27. In many cats,
postoperative discomfort after laser disarticulation is
reduced.
The paw is scrubbed prior to surgery and the
skin and hair is soaked with saline (alcohol is not
used!). A tourniquet may be applied, but is often
not needed. The surgeon and all assistants must don
protective eyewear and all routine safety measures
for laser usage are followed. A moistened gauze
sponge may be used to protect the surgeon’s fingers
from burns caused by the laser during the
procedure. The CO2 laser is set on a continuous
power setting of 6–8 watts. The claw is grasped with
a towel clamp or forceps and traction is applied to
the digit. The hair and cuticle-like skin are retracted
proximally from the dorsal aspect of the claw.
A horizontal cut is made through the tissue on the
dorsal aspect of the digit, proximal to the ungual
crest and between the second and third phalanges.
The laser beam is directed obliquely toward the
second phalanx to transect the common digital
extensor tendon and dorsal elastic ligaments. Care is
taken to avoid damaging the articular cartilage on
the distal aspect of the middle phalanx. Burned
tissue (char) is wiped away with a saline soaked
gauze sponge. Next, the incision is continued along
the lateral and medial sides of the digit, transecting
the skin, joint capsule, and palmar collateral
ligaments between the second and third phalanx.
Ventral traction is then applied to the claw to
subluxate the distal interphalangeal joint. The laser
beam is directed distally from within the joint space
(in a slight right-to-left sweeping motion) to
transect the attachment of the deep digital flexor
tendon on the flexor tubercle of the distal phalanx.
Care is taken to avoid the digital pad. Finally, the
remaining skin is severed and the distal phalanx is
removed. Ideally, the distal phalanx is removed with
very little soft tissue attached. Burned tissue is
removed with a moistened sponge.
WOUND CLOSURE
After amputation or disarticulation of each distal
phalanx from the front feet, the wounds on each digit
are closed with suture material or cyanoacrylate tissue
adhesive, or the paw is bandaged.
Suturing
One or two sutures are used to appose the skin
edges. Chromic catgut (3-0) or monofilament,
absorbable suture may be used2. Suturing after
onychectomy is not mandatory but may reduce the
incidence of postoperative hemorrhage in adult
and obese cats. A bandage is often applied after
suturing. In most cases, the cat will remove the
sutures 1–2 weeks after surgery. If the sutures remain
in place and cause irritation, removal is indicated.
Sedation may be required to allow suture removal in
some cats.
Cyanoacrylate tissue adhesives
Cyanoacrylate tissue adhesives (isobutylcyanoacrylate
and n-butyl monomers) may be used to appose the
skin edges after onychectomy26,28. Several brands
of tissue adhesive are available for use in cats
(Nexaband, Tripoint Medical; Vetbond, Animal Care
Products/3M) and can decrease surgical time, avoid
complications associated with suturing, and often
negate the need for bandaging after surgery. This is
particularly useful in fractious cats where bandage or
 Fractures and disorders of the forelimb
suture removal is problematic. The adhesive is used
sparingly and is applied to the skin edges only.
Cyanoacrylate adhesives placed subcutaneously can
cause foreign body reaction, infection, delayed healing,
and lameness26,29. Cyanoacrylates undergo slow
biodegradation (with 91% remaining after 156 days)
and should not be used in infected surgical sites26,30.
A bandage may be applied after wound closure with
adhesives, but is not required in all cases.
BANDAGING
Bandages may be applied to the front feet for 18–24
hours after onychectomy. They are applied after
closure of the wounds with suture or adhesive, or
are used alone in some cases. The bandage should
cover the foot and extend to the proximal
antebrachium. Placing bandages too tightly can
lead to swelling and necrosis of the foot. Mild
bleeding can occur at bandage removal. If bleeding
persists, the bandage is reapplied for an additional
24–48 hours. Bandages are not usually required
after laser onychectomy.
POSTOPERATIVE CARE
Litter is replaced with shredded paper or commercially
available paper litter for 2 weeks. Sutures are removed
in 10–14 days if not already removed by the cat.
Antibiotics are not routinely administered after
onychectomy unless lameness persists or signs of
infection develop. In general, recovery to pain-free
limb function is faster in young cats than in older or
obese cats.
ANALGESIA
Analgesics are required to control pain after
surgery 25,31,32. Cats given butorphanol
(0.2 mg/kg) IM before surgery, at extubation, and
every 4 hours for the first 12 hours after
onychectomy bear weight sooner and eat better
than unmedicated cats. The incidence of severe
lameness is also reduced with butorphanol
treatment 32. A recent study found that limb
function is better in cats treated with a transdermal
fentanyl patch or intramuscular injections of
butorphanol (0.4 mg/kg every 4 hours for the first
24 hours after surgery) than in cats treated with
topical bupivacaine33. This study also indicated that
limb function remained reduced 12 days after
onychectomy, suggesting that long-term analgesic
protocols may be warranted. Another study found
161
that the application of a transdermal fentanyl patch
(25 µg/hr) 18–24 hours prior to surgery is as
effective as butorphanol therapy for controlling
postoperative pain34,35. A fentanyl patch is less
sedating and does not require repeated injections to
control pain. Infiltration of a local anesthetic agent
(bupivacaine) in a ‘ring block’ pattern around the
distal antebrachium or irrigation of the wounds with
bupivicaine at the time of surgery may also reduce
pain associated with onychectomy36. However, local
analgesia and wound irrigation should not be used
as the sole means of providing postoperctive
analgesia in cats after onychectomy33.
COMPLICATIONS
Complications are common after onychectomy
and have been reported in up to 50% of cases25,29.
Early postoperative complications occur in approx-
imately 24% of cats and include hemorrhage and
pain26,29,37. Later complications occur in approx-
imately 20% of cats and include claw regrowth,
chronic draining tracts, radial neuropraxia or paralysis
secondary to tourniquet use, infection, wound
dehiscence, protrusion of the second phalanx, tissue
necrosis from improper bandaging, palmigrade stance,
persistent lameness, and possibly behavioral changes.
Complications are prevented or minimized by using
sterile technique, controlling hemorrhage, completely
excising the ungual crest, protecting digital pads
during surgery, and proper postoperative care.
Hemorrhage
Hemorrhage is common after declawing procedures
and is usually controlled by application of a bandage
to the foot for 18–24 hours. Significant hemorrhage is
most common in older cats and least common after
laser onychectomy and when the wounds are closed
with suture material or tissue adhesive.
Pain
Pain is managed with proper preemptive and
postoperative analgesic therapy (see Analgesia).
Claw regrowth
Claw regrowth results from inadequate removal of
the ungual crest and the germinal tissue responsible
for claw growth26. Regrowth may occur months to
years after surgery and is more common after
amputation of the distal phalanx with a guillotine-
type nail trimmer than after disarticulation26,29.
162
In most cases, the cat becomes lame and draining
sinuses develop on the dorsal axial and abaxial
surfaces of the affected digits. The drainage often
subsides with antibiotic treatment but recurs unless
the claw is excised. The newly developing claw
is usually palpable beneath the skin or, in some cases,
will protrude through the skin, leading to concurrent
infection. If claw regrowth is detected in one digit,
the others should be checked as well. Palpation and
radiographic evaluation of the digits will confirm if a
portion of the third phalanx was not excised (128). If
regrowth occurs, the claw and remaining ungual crest
are excised with a scalpel blade and the wound is
managed as an open wound. Antibiotics are
administered until the wounds are healed.
Chronic draining tracts
Draining tracts may occur as a result of claw regrowth
or if cyanoacrylate tissue adhesive was placed
subcutaneously in the wounds after onychectomy.
The wounds are debrided and remaining portions of
the distal phalanx are excised with a scalpel blade.
The wounds are left open to heal by second intention
and the foot is bandaged. Soaking the foot daily in
dilute chlorhexidine solution has been advocated.
128
A
128 Radiographs of the foot from a cat with regrowth of the claws after
onychectomy.
A Lateral radiographic view.
B Dorsopalmar radiographic view. Large portions of the distal phalanx are
visible. The ungual crest of the distal phalanx was not properly excised during
surgery, allowing regrowth of the claw.
Oral antibiotics are administered until wound healing
is complete.
Radial neuropraxia or paralysis
Injury to the radial nerve is usually associated with
use of a tourniquet during surgery. Clinical signs
can include obvious limb dysfunction after surgery
(dragging the limb, inability to extend the carpus) or
self-mutilation of the foot. In most cases, the nerve is
only temporarily injured (neuropraxia) and signs
resolve within 6–8 weeks. Radial neuropraxia is
avoided by tightening the tourniquet only enough to
control hemorrhage. It should be placed on the
proximal antebrachium where the radial nerve is
adequately protected by overlying muscles.
Infection
Infection can occur after onychectomy if improper
sterile technique is used, if the wounds failed to
close after surgery, or as consequence of claw
regrowth. Infections are more common after
amputation with a guillotine-type nail trimmer than
after disarticulation26,29. The use of cyanoacrylate
tissue adhesive has also been associated with higher
infection rates. Cyanoacrylate adhesives placed
B
 Fractures and disorders of the forelimb
163

subcutaneously may cause foreign body reaction
and infection, leading to delayed wound
healing26,29. Adhesives should be used sparingly and
applied to the skin edges only. Clinical signs of
infection include pain, swelling, and drainage.
Rarely, septicemia can occur in cats with abscessed
paws. Treatment consists of cleaning and debriding
the wound and allowing drainage by open wound
management. Intermittently soaking the infected
digits in dilute chlorhexidine solution is often
advocated. Systemic antibiotics are administered
until healing is complete.
Wound dehiscence
Wound dehiscence may occur if the sutures or tissue
adhesive fail to maintain reduction of the skin edges.
Wounds that are managed with bandages only
after surgery may also open. Occasionally, wound
dehiscence occurs when the cat licks or chews at the
surgical sites. The dehiscence rate is reportedly higher
after disarticulation with a scalpel blade than after
amputation with a nail trimmer, perhaps due to longer
surgery time and greater soft tissue trauma26. The
dehisced wounds are managed with open wound
therapy and systemic antibiotics are administered.
Protrusion of the second phalanx
Protrusion of the second phalanx through the
surgical wound may occur if the wound was not
closed after surgery or if the wound dehisces. The
exposed end of the second phalanx is visible and
palpable. Owners occasionally report hearing a
‘clicking’ sound when the cat walks on a hard
surface. The cat is anesthetized and the area is
cleaned. The distal end of the second phalanx is
removed with a small rongeur and the wound is
closed with two interrupted sutures (3-0 chromic
gut) placed in the skin edges. Lameness is often
prolonged after removing the distal end of the
second phalanx.
Tissue necrosis
Swelling and necrosis of the foot may occur if bandages
are placed too tightly or are left on too long (129).
Palmigrade stance
A palmigrade or ‘flatfooted’ stance develops in some
cats after onychectomy, though it rarely causes
clinically significant signs. The cause is unknown, but
it may be associated with removal of the entire third
phalanx, inflammation, and tendonitis29.

129

129 Tissue necrosis of the paw after onychectomy

procedure. Bandages applied to the paws after surgery to
control hemorrhage were too tight. (Photograph courtesy
of Dr. O. Lanz.)
164

Persistent lameness Deep digital flexor tenectomy

Up to 50% of cats are lame for 1–54 days after
onychectomy. Some cats demonstrate long-term
discomfort29,38. Acute lameness is more common
after disarticulation of the distal interphalangeal joint.
However, chronic lameness is more common after
amputation of the distal phalanx with a nail
trimmer26. Cutting the digital pad or distal aspect of
the second phalanx can prolong lameness and pain
after onychectomy. Overall, persistent lameness is
identified in only 0.86% of cats23. Computerized gait
analysis of cats shows that bilateral forelimb
onychectomy does not result in abnormal vertical
forces in the forelimbs when measured more than
6 months after surgery39.
The deep digital flexor tendon inserts on the flexor
tubercle of the distal phalanx. To extrude the claws
from the sheath, the deep digital flexor muscle is
contracted to flex the distal interphalangeal joint.
Surgical excision of a portion of the deep digital flexor
tendon prevents flexion of the distal interphalangeal
joint and extrusion of the claw. Severing the tendon
does not affect the cat’s ability to walk normally. After
tenectomy, the claws continue to grow and often
become thickened and blunted. The nails must be
trimmed regularly to prevent them from growing into
the digital pad37,43,44. Owners unable or unwilling to
trim the claws regularly should not elect tenectomy as
an alternative to onychectomy.

Behavioral changes Surgical technique

Onychectomy has reportedly lead to physical and
behavioral changes in some cats, including increased
aggression, biting, and house soiling23,36,40. Other
studies of cats undergoing declawing procedures
suggest that declawing causes no significant
behavioral changes in most cats41–43.
ALTERNATIVES TO ONYCHECTOMY
Alternatives to declawing are offered to owners
that have humane concerns regarding surgical
removal of the claws or are concerned with potential
complications associated with onychectomy procedures.
The palmar surface of each digit is clipped and
scrubbed from the digital pad to the metacarpal pad.
A tourniquet is applied to the proximal
antebrachium and tightened just enough to control
hemorrhage. A 3–5 mm skin incision is made over
the palmar surface of each digit (beginning 3–5 mm
proximal to digital pad) to expose the deep digital
flexor tendon (130). The tendon lies just beneath
the skin and is identified by its white, glistening
appearance. The tendon is isolated by blunt
dissection with a mosquito hemostat or curved iris
scissors. A 5 mm long segment of the tendon is

130

A B C

130 Deep digital flexor tenectomy.

A A 3–5 mm skin incision is made over the palmar surface of each digit to expose the deep digital flexor tendon.
B The deep digital flexor tendon lies just beneath the skin and is isolated with a mosquito hemostat or curved iris scissors.
C A 5 mm long segment of the tendon is exteriorized and excised with a scalpel blade. Surgical excision of a portion of
the deep digital flexor tendon prevents flexion of the distal interphalangeal joint and extrusion of the claw. After
tenectomy, the claws continue to grow and frequent trimming is necessary.
 Fractures and disorders of the forelimb
exteriorized and excised with a scalpel blade.
Hemorrhage is usually minimal and can be
controlled by direct pressure or electrocautery. The
edges of the skin incision are apposed and a single
drop of cyanoacrylate tissue adhesive is applied.
A bandage is not necessary44.
Complications
Complications reported after deep digital flexor
tenectomy include hemorrhage, infection, pain,
interphalangeal joint immobility and fibrosis, and
excessive nail growth37,44. Most cats appear in
significantly less pain 24 hours after tenectomy
(compared with onychectomy), but the incidence of
infection, persistent lameness, and minor behavioral
changes are the same for both procedures37. After
tenectomy, the claws continue to grow and are
usually thickened and rough. Frequent trimming is
required to prevent claws from growing into the
digital pads. Some cats can still use their claws
after tenectomy, though the ability to scratch is
limited36. Owner satisfaction rates of 70–94% are
reported after tenectomy 37,43. If complications
after tenectomy are severe, onychectomy may be
required.
Behavior modification
Retraining or behavior modification techniques may
help prevent cats with claws from damaging furniture
or scratching owners and other pets.
Capping
An alternative to surgical declawing is to place a
vinyl cap over the tip of each claw (Soft Paws). The
caps are attached with glue and must be replaced
approximately every 6–8 weeks as the claw grows.
Premature removal of the caps will also necessitate
replacement.
FORELIMB AMPUTATION
Limb amputation is a salvage procedure indicated for
irreparable fractures or when severe complications
occur after attempted fracture treatment.
Complications necessitating amputation may include
nonunion, osteomyelitis, severe muscle contracture or
joint dysfunction, and neurologic dysfunction.
Neoplasia affecting the soft tissues or skeleton is also
an indication for amputation. The cat should be
carefully evaluated to ensure the remaining three
limbs are healthy and can adequately support weight.
Cats are typically able to ambulate well after
amputation of one limb. Amputation of two limbs has
been described in cats.
165
FORELIMB AMPUTATION WITH SCAPULECTOMY
Removal of the entire forelimb, including the scapula,
provides excellent cosmetic results and is the preferred
method of forelimb amputation in cats. The entire
forequarter is clipped and prepared for surgery19.
A hanging-limb preparation is used to allow
manipulation of the limb intraoperatively. The skin
incision begins at the dorsal border of the scapula and
extends distally along the scapular spine to the
shoulder joint. The incision is then extended
circumferentially around the shoulder joint.
Electrocautery may be used to control small bleeding
vessels. Ligation is used to prevent hemorrhage prior
to transection of larger vessels. The cephalic vein on
the lateral aspect of the shoulder is ligated and
transected. The omotransversarius muscle is sharply
transected from the cranial border of the scapular
spine. The incision is continued dorsally along the
scapular spine, severing the cervical and thoracic
portions of the trapezius muscle. The rhomboideus
muscle is removed from the dorsomedial aspect of the
scapula. The ventral serratus muscle is elevated from
the scapula. The scapula is then abducted from the
body wall to expose the axillary space. The fascia is
bluntly dissected to allow transection of the insertions
of the latissimus dorsi, teres major, and cutaneous
trunci muscles near the humerus. The thoracodorsal
artery and vein are identified and separately ligated
and divided. The thoracodorsal nerve is transected.
The scapula is abducted further and rotated to
expose the axillary artery. It is double ligated and
transected. The lateral thoracic artery is ligated and
divided. The brachial and axillary veins are separately
ligated and divided. The nerves of the brachial plexus
are then transected in a caudal to cranial direction.
Branches of the superficial cervical artery are ligated.
The scapula is further abducted to allow transection of
the ventral musculature. The deep and superficial
pectoral muscles are removed from their insertions on
the humerus. The cleidobrachialis muscle is transected
to complete the amputation. Bupivacaine can be
injected into the cut ends of the brachial plexus prior
to wound closure. The fascia of the deep pectoral
muscle is sutured to the scalenus and latissimus dorsi
muscles. The fascia of the cleidobrachialis muscle is
sutured to the fascia of the superficial pectoral muscle.
Fascia of the trapezius and omotransversarius muscles
is sutured to the dorsal aspect of the latissimus dorsi
muscle. Subcutaneous tissue and skin are sutured.
Dead space is reduced during closure to minimize
seroma formation. A Penrose drain may be placed if
necessary and is removed 3–5 days after surgery. The
incision and body wall may be bandaged.
166
FORELIMB AMPUTATION MID-HUMERUS
Removal of the forelimb at the mid-humerus is
easier to perform but provides less satisfactory
cosmetic results than amputation with scapulec-
tomy. The remaining proximal humerus and scapula
become prominent as the shoulder muscles atrophy
after amputation, and the movement of these
structures beneath the skin is concerning to some
owners.
The hair is clipped and the skin prepared from the
dorsal mid-line to the ventral mid-line, and distally on
the limb to the carpus. A hanging-limb preparation is
used. A lateral skin incision is made from the
cranial aspect of the brachium, distally to just proximal
to the elbow joint, and then proximally to the caudal
aspect of the brachium19. The incision is continued in
a straight line on the medial aspect of the limb to
connect the cranial and caudal portions of the lateral
incision. Electrocautery may be used to control small
bleeding vessels. Ligation is used to prevent
hemorrhage prior to transection of larger vessels.
Medially, the brachial artery and vein are separately
ligated and transected proximal to the collateral ulnar
artery. The median, musculocutaneous, and ulnar
nerves are transected. The triceps tendon is transected
near the olecranon. The brachial and biceps brachii
muscles are transected near their insertions distal to
the elbow joint. The cephalic vein is ligated and
divided. The radial nerve is cut. The brachiocephalicus
muscle is elevated from the humeral crest to expose
the humerus. The bone is cut at its mid-shaft using
a power saw or wire saw. The distal aspect of the
triceps is sutured to the brachial and biceps brachii
muscles to cover the cut end of the humerus. The
subcutaneous tissues and skin are sutured. A bandage
may be applied to control swelling.
 167

CHAPTER 9
FRACTURES AND
DISORDERS OF
THE HINDLIMB
PART 1: PELVIS

The pelvis is comprised of two bilaterally symmetrical the cat and occur most often in young animals (mean
hemipelves, each consisting of the ilium, ischium, age 16.8 months)3,5,6. In most cases, two or more of
pubis, and acetabular bones (131). Each ilium is the pelvic bones are fractured, leading to displacement
attached to the spine at the sacrum, forming the of the fragments and narrowing of the pelvic canal.
sacroiliac joints. Weight-bearing loads are transmitted Displacement is minimal if only one of the pelvic
from the femoral head to the acetabulum, along the bones is fractured, but this is uncommon. Pelvic
body of the ilium, and through the sacroiliac joint to fractures are rarely open because the pelvis is
the spine. completely surrounded by muscle and other soft
tissues.
PELVIC FRACTURES (GENERAL) Concomitant injuries occur in the majority of
CAUSE AND PATHOGENESIS cats (59–72%) with pelvic fractures6,7. In one report,
Trauma to the pelvis is common in cats, often a result 56.4% of cats with pelvic fractures had other
of being hit by a car or falling from a great height1–4. musculoskeletal injuries; these may include sacral
Pelvic fractures account for 20–22% of all fractures in fractures, coxofemoral luxations, femoral head and
neck injuries, and femoral fractures3,7,8. Ischial
fractures often occur concurrently with sacral
fractures6. Twenty-three percent of cats with pelvic
fractures had concurrent injuries to the thorax or
131 abdomen, including pneumothorax, hemothorax,
urinary tract injuries, gastrointestinal injuries,
abdominal hernia, diaphragmatic hernia, and rupture
of the prepubic tendon7,9. Twenty percent had
5 injuries of the nervous system, including lumbosacral
1 1 plexus injury and sciatic nerve damage7,10,11. Many
4 cats with pelvic fractures have injuries to multiple
3 body systems. A complete physical examination,
2 orthopedic evaluation, and neurologic examination,
4 and radiographs of the thorax and abdomen should be
obtained to identify concurrent injuries and allow
2 initiation of proper treatment.
3
A B CLINICAL SIGNS
Cats with pelvic fractures are often unwilling to stand
131 Normal pelvic anatomy. 1 ilium, 2 pubis, 3 ischium, or ambulate, particularly immediately after the
4 acetabulum, 5 sacrum. A Ventrodorsal view. B Lateral trauma. However, cats with unilateral injuries, more
view. chronic injuries, or fractures involving only the pubis
168
or ischium will stand but appear uncomfortable. In
many cases, swelling, pain, and asymmetry are evident
in the pelvic region.
DIAGNOSIS
Pelvic fractures are readily diagnosed by physical
examination and radiography. Palpation of the
greater trochanter, ischial tuberosity, and ilial wings
often reveals crepitus and malalignment. Digital
rectal examination is helpful in assessing the
integrity of the pelvic canal, but can be difficult
because the cat will be in pain and because of the cat’s
small size.
Pelvic fractures can be confirmed on ventrodorsal
and lateral radiographic views. Oblique views prevent
overlap of the two hemipelves and are often helpful.
Sacroiliac fracture/dislocation is best observed on the
ventrodorsal radiographic view (132).
TREATMENT AND PROGNOSIS
The cat should be carefully evaluated for concurrent
injuries and stabilized before initiating treatment for
the pelvic fractures. Pelvic fractures are treated with
either conservative medical therapy or open surgical
stabilization.
132
132 Ventrodorsal radiographic view of the pelvis from a
cat with bilateral sacroiliac luxation and a comminuted
femoral fracture.
Conservative therapy
Conservative therapy is indicated for fractures of the
pelvis that do not involve the weight-bearing axis
(acetabulum, ilial body, sacroiliac joint). This includes
fractures of the ishium, pubis, and ilial wings.
Fractures of these bones are well supported by
the pelvic musculature and typically heal without
surgical intervention. Conservative therapy is also
used when there is minimal displacement of the
fracture fragments, or minimal narrowing of the pelvic
canal, or if financial considerations preclude surgery.
Conservative therapy involves cage confinement
for 4–6 weeks. Urination and defecation are
monitored and the cat is kept clean and dry to avoid
decubital ulcers. Oral administration of stool softeners
and laxatives may be used to ease defecation. Physical
therapy, including passive range-of-motion exercises,
can be used if tolerated by the cat. Analgesic
medications should be used if needed during the early
stages of healing, but caution is needed to avoid
complications. Fracture healing is monitored
radiographically to ensure healing is progressing.
Potential complications of conservative therapy for
pelvic fractures include prolonged pain during healing
and entrapment of the sciatic nerve in the healing
callus. Additionally, malunion of the pelvic bones can
lead to persistent gait abnormality and chronic
narrowing of the pelvic canal, resulting in obstipation,
constipation, and, eventually, megacolon12–14.
Surgical therapy
Surgical intervention is indicated to reduce and
stabilize pelvic fractures if:
• The fractures involve the weight-bearing axis of
the pelvis.
• Significant narrowing of the pelvic canal is
present.
• The fracture involves the articular surface of the
acetabulum.
• Concurrent orthopedic injuries require
stabilization for the cat to ambulate.
• Extreme pain or neurologic deficits indicate nerve
injury.
Reduction and stabilization of fractures involving
the acetabulum, ilial body, and/or sacroiliac joint
allow earlier return to function and minimize
narrowing of the pelvic canal. Repair of acetabular
fractures ensures earlier weight bearing and helps
reduce the development of osteoarthritis. Surgery
should be performed within 4–5 days of the injury
if possible, as longer delays can make proper
reduction of the fracture fragments more difficult.
 Fractures and disorders of the hindlimb
169

Surgical stabilization of ischial and pubic fractures is Surgical therapy

rarely indicated and most are managed with Several techniques have been described for surgical
conservative treatment. stabilization of sacroiliac fracture/dislocation in
cats8,13,16.
Postoperative management
After repair of pelvic fractures, the cat’s activity is Dorsolateral surgical approach
restricted for 4–6 weeks or until healing is A dorsolateral surgical approach to the sacroiliac
radiographically complete. Walking and limited activity joint allows anatomic reduction and stabilization of
are permitted to maintain muscle and joint health. If sacroiliac fracture/luxations (133)17,18. The ilial
the cat is unable to ambulate, a dry, well padded bed is wing, sacroiliac joint, and sacral body are visualized
important to prevent decubital ulcers. The patient to facilitate proper implant placement. The cat is
should be turned from side to side frequently.
Urination and defecation are monitored and the patient
is kept clean and dry. Stool softeners may be used to
ease defecation, though this is rarely needed if the pelvic 133
diameter is adequate. If neurologic deficits were
present, neurologic function is monitored regularly to
determine if function is improving. The fractures are
monitored radiographically to confirm healing and
observe for implant problems. The implants are not
removed unless complications develop.

SACROILIAC
A
FRACTURES/DISLOCATION
CAUSE AND PATHOGENESIS
Fracture/dislocation of the sacroiliac joint occurs when
the ilial body is displaced from its attachment to the
sacrum (132). This injury accounts for 19–27% of pelvic
injuries in cats15. The ilium is usually displaced cranially
and dorsally, although the degree of displacement can
Middle
vary from mild to severe. Fractures of the pubis and gluteal Sacrum
ischium are often present and allow displacement of the muscle
hemipelvis. Bilateral sacroiliac luxation is common
Wing of
(18–46% of cases) and often occurs without concurrent ilium
pelvic injuries8,11. Sacroiliac dislocation and ilial body Sacroiliac
fractures occasionally occur ipsilaterally, but in most joint
cases, one or the other is present.
Cranial gluteal
CLINICAL SIGNS artery, vein,
nerve
The injury is painful and is often associated with
neurologic deficits caused by injury to the lumbosacral
nerve trunk or sciatic nerve. B

TREATMENT AND PROGNOSIS
Conservative therapy
Conservative therapy is indicated in cases with minor
displacement, when no neurologic deficits are present,
or when the cat is ambulating well. Because cats are
lightweight, many respond well to conservative
treatment. However, stabilization of the sacroiliac
joint may improve the cat’s comfort, allows earlier
return of limb function, and reduces repeated trauma
to the lumbosacral nerve truck.
133 Dorsolateral approach to the sacroiliac joint. A The cat
is positioned in ventral recumbency and an incision is made
along the dorsal iliac spine. B Subcutaneous tissues are
incised and the origin of the middle gluteal muscle is
elevated from the lateral surface of the ilial wing. The cranial
gluteal vessels and nerve are avoided. The soft tissues
between the iliac crest and the sacrum are elevated.
The ilium is rotated slightly to visualize the sacroiliac
joint, the articular surface on the medial aspect of the
ilium, and the sacral body.
170

placed in ventral recumbency and the area over the during insertion of the Kirschner wire is important
sacroiliac joint is prepared for surgery. The hindlimbs to ensure it is accurately positioned at the edge of
may be positioned such that the hips and stifles are the sacral body. The Kirschner wire thus provides
flexed and the cat is resting on its knees. A pad placed temporarily stabilization of the joint and serves as a
beneath the pubis will elevate the patient’s body and landmark for screw placement. A lag screw is then
ease reduction by removing pressure from the placed into the sacral body next to the Kirschner
sacroiliac joint. wire. It is important to angle the screw correctly to
The incision is made over the iliac crest along the avoid entering the lumbosacral disc space cranially,
dorsal iliac spine. Subcutaneous tissues are incised the spinal canal dorsally, or exiting the sacral body
and the origin of the middle gluteal muscle is ventrally15. The Kirschner wire may be left in place
elevated from the lateral surface of the ilial wing. The to prevent rotation around the lag screw. In most
cranial gluteal vessels and nerve are located near the cats, the sacral body is too small to accommodate
caudal iliac spine and are avoided. The soft tissues two lag screws. Another method of inserting the lag
between the iliac crest and the sacrum are elevated screw is to drill a ‘thread’ hole into the sacral body
using blunt and sharp dissection, exposing the before reduction of the fracture. A ‘glide’ hole is
sacroiliac joint. The ilium is rotated slightly to allow then drilled from medial to lateral through the ilial
visualization of the articular surface, located on its wing at the appropriate location. The screw is then
medial side just ventral to the dorsal iliac spine. This inserted through the ilium from lateral to medial.
also allows visualization of the sacroiliac joint and The fracture is reduced as the screw is directed into
identification of the sacral wing. Ventral retraction the predrilled hole in the sacral body. If desired, a
of the ilium with a Hohmann retractor will also Kirschner wire may be inserted parallel to the screw
improve exposure. The articular surface of the sacral to prevent rotation, though this is not necessary in
wing consists of a semilunar synovial portion (which most cats.
is located caudoventrally and is covered with hyaline
cartilage) and a fibrocartilagenous portion which is
located craniodorsally. Careful removal of some of
this fibrocartilage will improve visualization. The
proper location to insert the screw in the sacrum is
just cranial to the cresent shaped hyaline cartilage15.
A bone clamp is placed on the ilial wing to allow the
application of force in a caudal and ventral direction, 134
thus re-aligning the articular surfaces of the ilium
and the sacrum (134). Countertraction on the
sacrum with a hemostat or other blunt instrument
will ease reduction.
A lag screw is then placed through the ilium and
into the sacral body to achieve compression and
maintain reduction (135). In most cats, a 2.7 mm
cortical screw is used and placed in lag fashion.
A 2.0 mm or 3.5 mm cortical screw may used instead,
depending on the size of the sacral body. The screw
should be long enough to extend 60% of the distance
across the sacrum. Measuring the distance on the
ventrodorsal radiograph is helpful in selecting a
screw of sufficient length. It can be difficult to
position this screw properly in the sacral body
and avoid inserting it into the sacral wings alone
(which have less holding power), the lumbosacral
disc space, or into the spinal canal. This is made 134 Reduction of a sacroiliac luxation. A bone clamp is
more difficult by the small size of the sacral body in placed on the ilial wing and force is applied in a caudal and
the cat. One helpful technique is to place a Kirschner ventral direction until the articular surfaces of the ilium
wire through the ilial wing and into the sacrum once and the sacrum are aligned. Countertraction is applied to
the joint is reduced. Visualization of the sacral body the sacrum with a hemostat to facilitate reduction.
 Fractures and disorders of the hindlimb
171
135

A B
Proper implant
placement Articular face

Cranial
Caudal Cranial
Articular face
Caudal
Proper implant
placement
C D

E F
135 Stabilization of a sacroiliac luxation.
A A 2.7 mm screw is inserted in lag fashion through the ilium and into the sacral body. The screw should extend at
least 60% of the distance across the sacrum. A Kirschner wire may be inserted to prevent rotation around the screw.
B Lateral view depicting proper placement of the lag screw in the sacral body.
C Lateral view of the sacrum depicting the proper anatomic location for inserting implants.
D Medial view of the ilium depicting the proper anatomic location for inserting implants.
E Ventrodorsal radiographic view of the pelvis after stabilization of the left sacroiliac joint with a single transsacral screw.
F Lateral radiographic view of the pelvis after transsacral screw placement.
172
Ventrolateral surgical approach
A ventrolateral surgical approach may be used to
visualize the ilium and allow stabilization of sacroiliac
fracture/dislocations (136)19. This approach is often
used when repair of ilial fractures will be performed
concurrently, since it is easily combined with a lateral
approach to the ilium.
The cat is placed in lateral recumbency and a skin
incision is made from the center of the iliac crest to
the greater trochanter. Subcutaneous tissues and
superficial fascia are reflected. The deep gluteal fascia is
incised. The intermuscular septum, between the
middle gluteal muscle and the tensor fasciae latae, is
incised from the ventral iliac spine to the cranial border
of the biceps femoris muscle. The middle gluteal
muscle is retracted dorsally to allow an incision to be
made in its origin on the ilium, beginning at the
caudoventral iliac spine and continuing cranially and
dorsally. A periosteal elevator is used to reflect the
muscle and expose the lateral aspect of the ilial wing.
Ligation of the iliolumbar vessels may be necessary to
control hemorrhage. The origin of the iliacus muscle is
incised along the ventromedial border of the ilium and
136
Middle
gluteal
muscle
136 Ventrolateral approach to the sacroiliac joint. The cat
is positioned in lateral recumbency and a skin incision is
made from the center of the iliac crest to the greater
trochanter. Subcutaneous tissues and superficial fascia are
reflected. The deep gluteal fascia in incised. The
intermuscular septum between the middle gluteal muscle
and the tensor fasciae latae is incised from the ventral iliac
spine to the cranial border of the biceps femoris muscle.
The middle gluteal muscle is retracted dorsally to allow an
incision to be made in its origin on the ilium, beginning at
the caudoventral iliac spine and continuing cranially and
dorsally. A periosteal elevator is used to reflect the muscle
and expose the lateral aspect of the ilial wing. The arrow
indicates the proper location for screw insertion.
elevated to allow digital palpation of the sacral body.
A lag screw and Kirschner wire are inserted as
previously described, although visualization of the
sacral body is limited and care must be taken to place
the implants properly.
Single transsacral screw
Bilateral sacroiliac fracture/dislocations can be
repaired using separate surgical procedures to place
lag screws bilaterally. Alternatively, a technique for
placing a single, long transsacral screw to stabilize
bilateral dislocations has also been described in
cats (137)20. The cat is positioned in ventral
re-cumbency after preparation of the dorsal lum-
bosacral region for surgery. A dorsolateral approach
is made to each sacroiliac joint. The first sacroiliac
joint is reduced and temporarily stabilized with a
transarticular Kirschner wire. From the contralateral
sacroiliac joint, a drill bit is placed in the center of
the sacral body. The drill bit is advanced parallel to
the surgery table and perpendicular to the spine,
traversing the sacrum and the previously reduced ilial
wing. The hole is measured and tapped. A glide hole
137
137 Stabilization of bilateral sacroiliac luxations using a
single transsacral screw. A dorsolateral approach is made to
each sacroiliac joint. The first sacroiliac joint is reduced
and temporarily stabilized with a transarticular Kirschner
wire. From the contralateral sacroiliac joint, a lag screw is
placed across both ilial wings and the sacral body. The
screw is placed in the center of the sacral body.
 Fractures and disorders of the hindlimb
is then drilled in the proper location in the remaining
ilial wing and a screw of sufficient length to pass
through both ilial wings and the sacrum is inserted.
A washer is placed over the screw prior to insertion.
Tension band technique
A tension band technique has also been described
for stabilization of sacroiliac luxation in cats19. The cat
is placed in ventral recumbency and a dorsolateral
approach is made to the injured sacroiliac joint.
Another small approach is made to the contralateral
iliac crest. Holes are drilled from lateral to medial
through the craniodorsal aspect of each iliac crest
(138). Using a straight needle, a strand of large
monofilament nylon suture is threaded through the
hole in one iliac crest, through the sacral muscles, and
through the hole in the other iliac crest. The suture is
then passed dorsal to the iliac crests and back through
the sacral muscles. The sacroiliac luxation is reduced
and a 1.5–2.0 mm Steinmann pin is inserted through
the ilium and into the sacral body. The pin is oriented
parallel to the surgical table and perpendicular to the
spine. The pin is inserted to penetrate at least one-half
138
138 Stabilization of a sacroiliac luxation with a tension
band technique. Holes are drilled through the craniodorsal
aspect of each iliac crest. A straight needle is used to place
a strand of monofilament nylon suture through the holes.
The sacroiliac luxation is reduced and a 2.0 mm
Steinmann pin is inserted through the ilium and into the
sacral body, extending at least one-half the distance across
the sacrum. The suture preplaced in the iliac crests is tied
to form a tension band.
173
the distance across the sacrum. Proper pin length is
determined from preoperative radiographs. Once the
pin is in place, the suture through the iliac crests is
tied to form a tension band. The tension band
technique was successful in stabilizing 24 sacroiliac
luxations in 19 cats21. Complications were few and
included pin migration.
Closed lag screw placement
Using intraoperative imaging (C-arm), the sacroiliac
luxation can be reduced and a lag screw placed
percutaneously22. This technique is less invasive than
the others described above, but requires specialized
equipment.
ILIAL FRACTURES
CAUSE AND PATHOGENESIS
Fractures of the ilium disrupt the weight-bearing axis
of the pelvis, leading to significant dysfunction. They
are usually accompanied by fractures of the pubis and
ishium, allowing the caudal segment of the fracture
to collapse into the pelvic canal (139). Ilial fractures
in cats are typically oblique, although comminuted
139
139 Ilial fracture. Ventrodorsal radiographic view
of a right ilial, pubic, and ischial fracture. The right
side of the pelvis is collapsed medially into the
pelvic canal.
174
fractures do occur. The sciatic nerve courses along
the medial aspect of the ilial body and can be trauma-
tized when the fracture occurs or during attempts at
repair.
TREATMENT AND PROGNOSIS
Surgical stabilization is recommended to restore limb
function, prevent narrowing of the pelvic canal, and
prevent injury to the sciatic nerve caused by motion of
the fragments or exuberant callus formation. The cat
is positioned in lateral recumbency. An area from the
dorsal mid-line to the hock and from cranial to the
ilial wing to the perineum is clipped and prepared for
surgery. A hanging-limb preparation allows the limb
to remain in the surgical field for manipulation as
needed during surgery.
A lateral surgical approach to the ilium is
performed, beginning with a skin incision from the
iliac crest to the greater trochanter (140) 18.
Subcutaneous tissues are incised to expose and allow
separation between the middle gluteal and the
tensor fascia lata muscles. The deep and middle
140
Middle gluteal muscle
Cranial gluteal
artery, vein,
and nerve
Shaft Deep gluteal
muscle
of ilium
Sartorius
muscle
and tensor
fasciae Lateral
latae Iliolumbar
circumflex
muscle artery and vein femoral vessels
140 Lateral approach to the ilium. A skin incision is
made from the iliac crest to the greater trochanter.
Subcutaneous tissues are incised to expose the separation
between the middle gluteal and the tensor fascia lata
muscles. The deep and middle gluteal muscles are
reflected dorsally using a periosteal elevator to expose
the ventral and lateral surfaces of the ilium. The lateral
circumflex femoral vessels and the cranial gluteal vessels
and nerve are preserved. The iliolumbar vessels course
ventral to the ilial wing and are transected as the exposure
is extended cranially. The ventral portion of the gluteal
attachment on the ilial wing is cut to increase visualization
of the cranial ilium. A Hohmann retractor may be placed
over the dorsal aspect of the ilium to maintain retraction
of the gluteal muscles.
gluteal muscles are reflected dorsally using a
periosteal elevator to expose the ventral and
lateral surfaces of the ilium. The lateral circumflex
femoral vessels and the cranial gluteal vessels and
nerve are preserved. The iliolumbar vessels course
ventral to the ilial wing and are transected as the
exposure is extended cranially. The ventral portion
of the gluteal attachment on the ilial wing is cut
to increase visualization of the cranial ilium. A
Hohmann retractor is placed over the dorsal aspect
of the ilium to maintain retraction of the gluteal
muscles.
In most cases, the caudal fracture segment is
displaced medially and cranially. Reduction is achieved
by traction, levering, and rotation of the caudal
fracture fragment. Bone forceps placed on the ilium
just cranial to the acetabulum allow the fragment to
be manipulated into alignment. In cases where the
ischial attachment to the ilium is intact, a clamp can be
placed on the ischial tuberosity (via a small surgical
approach) to allow manipulation of the caudal ilial
segment (141). Traction on the greater trochanter
may also be used to manipulate the caudal ilial
fragment into alignment. Placement of clamps and
manipulation of the fracture fragments are performed
with care to avoid injuring the sciatic nerve. Once
reduced, the fracture is temporarily stabilized with
bone clamps.
Several methods of stabilizing ilial fractures have
been described, but plate fixation is preferred (141).
The bone plate is contoured to the lateral surface of
the ilium. It is important that the plate contour is
concave to ensure the normal diameter of the pelvic
canal is maintained. The plate should be positioned
on the ilium such that a minimum of two to three
screws are placed cranial and caudal to the fracture
site. Also, the cranial portion of the plate should
be positioned to allow a screw to be placed through
the ilium and into the sacral body. Since the bone of
the ilial wing is relatively thin, placing a screw
into the sacrum will increase the holding power of
the screw. Care is taken not to strip screws placed into
the thin bone of the cranial ilium. Various types of
bone plates can be used on the ilium, including
2.7 mm dynamic compression plates (DCPs), small
reconstruction plates, and cuttable plates. Mini
plates, T plates, and L plates are also used when small
fragments prevent the insertion of at least two screws
using a straight plate.
In some cases, the fracture cannot be stabilized
with bone clamps after reduction. The plate is
contoured appropriately. Evaluation of the intact
ilium on the ventrodorsal radiograph is helpful to
 Fractures and disorders of the hindlimb
175

ensure the plate is properly contoured. It is then on the ischial tuberosity) as medial force is applied to
attached to the caudal fracture fragment. The fracture the cranial aspect of the plate (142). When the
is then reduced by placing lateral traction on the fracture is reduced and the cranial portion of the plate
greater trochanter (or manipulation of a clamp placed contacts the ilium, the cranial screws are inserted.

141

A B

141 Stabilization of an ilial fracture with a bone plate.

A The fracture is reduced by traction, levering, and rotation of the caudal fracture fragment. A bone forceps placed on the
ilium just cranial to the acetabulum, on the greater trochanter, or on the ischium may be used to align the fracture.
B Reduction is maintained with a bone clamp and the plate is applied to the lateral surface of the ilium. A minimum of
two to three screws are placed cranial and caudal to the fracture site.

142

A B
142 Plate fixation of ilial fractures. A If fracture reduction cannot be maintained with a bone clamp, the plate is contoured
appropriately and applied to the caudal fracture segment. B The fracture is reduced by applying traction to the greater
trochanter while the cranial aspect of the plate is pushed medially. When the fracture is reduced, the cranial aspect of the
plate contacts the ilium and the remaining screws are inserted.
176

Other reported methods of stabilizing ilial ACETABULAR FRACTURES

fractures include the insertion of lag screws from the
ventral border of the ilium, insertion of small pins, and
application of cerclage wires (143). The narrow width
of the feline ilium makes placement of ventral lag
screws very difficult. Kirschner wires may be inserted
from ventral to dorsal across the ilium to stabilize
fractures. The Kirschner wires are properly positioned
by inserting them through the soft tissues ventral to
the ilium. Unfortunately, they provide less stability
than screws and tend to loosen before bone healing is
complete. Full cerclage wires are difficult to place
since the medial aspect of the ilium is not visualized
and blindly passing wires can endanger the sciatic
nerve and rectum. Hemicerclage wires may be placed
on the lateral aspect of the ilium and anchored with
screws or Kirschner wires. In most cases, pins and
wires are used only in conjunction with plate
stabilization, if at all.
CAUSE AND PATHOGENESIS
Acetabular fractures are typically unilateral in cats, and
most (77%) are two-piece fractures6.
TREATMENT AND PROGNOSIS
Treatment options include conservative therapy,
femoral head and neck excision arthroplasty, or open
reduction and stabilization.
Conservative management
Conservative management is indicated when there
is no displacement of the fragments evident
radiographically, no narrowing of the pelvic canal, and
no palpable crepitus with manipulation of the hip
joint23. Fractures involving the caudal third of the
acetabulum are treated conservatively often, though
this portion of the acetabulum is weight-bearing in cats.
Restricting activity and preventing weight bearing by

143

A B

C D

143 Alternative methods for internal fixation of ilial shaft fractures.

A Plate fixation with mini T plates or L plates.
B Lag screw fixation. Two bone screws are inserted in lag fashion from the ventral ilial border. This technique is difficult in cats
because the ilium is narrow.
C Kirschner wires and cerclage wire fixation. The Kirschner wires are inserted through the soft tissues ventral to the ilium, across
the fracture line, and into the dorsal aspect of the ilium. Orthopedic wire is placed around the protruding ends of the Kirschner
wires and tightened.
D Alternatively, the orthopedic wire can be anchored using small bone screws.
 Fractures and disorders of the hindlimb
177

placing the limb in a sling may allow healing. In most
cases, the cat will begin using the limb within 10–14
days. Excision arthroplasty may be indicated in cats that
fail to show improvement in pain level or limb function
after 10–14 days of conservative therapy23.
Femoral head and neck excision arthroplasty
Femoral head and neck excision arthroplasty is
indicated if the fragments are displaced, if anatomic
reconstruction of the acetabulum is not feasible
(comminuted fractures), when the cost of repair is
prohibitive, or in cats that fail to improve after
2 weeks of conservative therapy23. The procedure is
performed via a craniolateral approach to the hip
joint (144).
The cat is positioned in lateral recumbency and the
hip area and hindlimb are clipped and prepared for
surgery. A hanging-limb preparation is used. A skin
incision is made over the cranial aspect of the hip
joint. The subcutaneous tissues are incised. An
incision is made in the fascia lata along the cranial
border of the biceps femoris muscle. The incision
necessary for adequate exposure is slightly longer in
the cat than in the dog. The biceps femoris muscle is
retracted caudally (protecting the sciatic nerve) and
the superficial and middle gluteal muscles are
retracted dorsally. The deep gluteal muscle is also
retracted dorsally, although a partial tenotomy of its
tendon of insertion will enhance exposure. An incision
is then made in the joint capsule cranial to the femoral
head. This incision extends from the acetabular rim
and along the femoral neck to include a portion of the
origin of the vastus lateralis muscle. The joint capsule
and vastus lateralis muscle are elevated to expose
the entire femoral neck. More subperiosteal elevation
of the vastus lateralis muscle is needed in the cat than
in the dog to expose the femoral neck adequately. The
femur is externally rotated and curved scissors are
used to transect the ligament of the head of the femur.
The femur is then externally rotated 90° to luxate the

144

Incision in deep gluteal muscle

Middle gluteal muscle

Superficial gluteal muscle

Greater trochanter

Incision in origin of
vastus lateralis muscle
Articularis coxae
muscle

Biceps femoris
Rectus femoris muscle, retracted
muscle

Incision in
joint capsule

144 Craniolateral approach to the hip joint. A skin incision is made over the cranial aspect of the hip joint and the
subcutaneous tissues are incised. The fascia lata along the cranial border of the biceps femoris muscle is incised and the
biceps femoris muscle is retracted caudally (protecting the sciatic nerve). The superficial and middle gluteal muscles are
retracted dorsally. The deep gluteal muscle is retracted dorsally. A partial tenotomy of the tendon of insertion of the deep
gluteal improves exposure. The joint capsule is incised from the acetabular rim, along the femoral neck, and the incision
extends to include a partial tenotomy of the tendon of origin of the vastus lateralis muscle. The joint capsule and vastus
lateralis muscle are elevated to expose the entire femoral head and neck. The ligament of the head of the femur is cut and
the femur is externally rotated to luxate the femoral head from the acetabulum.
178
femoral head from the acetabulum and allow
visualization of the entire femoral head and neck.
In this position, the patella is pointing straight up and
the surgeon is seeing the cranial aspect of the femur
through the incision. This exposure and positioning is
important to ensure a proper ostectomy is performed.
A bone saw, sharp osteotome and mallet, bone cutter,
or rongeur is used to remove the femoral head and
neck. The ostectomy should be performed on a line
from the lateral aspect of the intertrochanteric notch
proximally to just proximal to the lesser trochanter
distally to ensure removal of the entire femoral head
and neck (145). Care is taken not to perform the
ostectomy along a line directed perpendicular to the
axis of the femoral neck, since this location does not
account for anteversion of the femoral head and will
fail to remove a portion of the caudal femoral neck. If
an ostectome is used, it should be the same width as
the femoral neck so that repeated cuts are not
required to complete the excision. It must also be
sharp to avoid iatrogenic fracture of the femur. When
the ostectomy is completed, the femoral head and
neck are grasped with forceps and the remaining soft
tissues are excised. The ostectomy site is palpated to
ensure it is smooth. A rongeur or small bone rasp can
be used to remove any bone spurs. The joint capsule
145
A (dashed line) will fail to remove a portion of
B C
is closed with absorbable suture and the partial
tenotomies of the deep gluteal and vastus lateralus are
sutured. Interposition of soft tissues (deep gluteal or
biceps muscle) into the ostectomy site has been
described, but is probably of minimal benefit.
After femoral head and neck excision arthroplasty,
exercise and movement of the hip are encouraged to
promote development of a pseudoarthrosis. However,
when excision is used for treatment of pelvic fractures,
care is needed to ensure such activity does not
interfere with healing or cause pain. Once the pelvic
fractures are stable, physical therapy and active
motion are encouraged to improve function of the
pseudoarthrosis. The prognosis for pain-free limb
function in cats after femoral head and neck excision
arthroplasty is excellent24.
Open reduction and internal stabilization
Open reduction and stabilization of acetabular
fractures are indicated when fragments are displaced,
crepitus is palpable, and surgical intervention will
adequately reconstruct the articular surface. In most
cases, internal stabilization is reserved for fractures
involving the cranial two-thirds of the acetabulum.
The goal of surgery is to reconstruct the fragments
anatomically to reduce pain, encourage early
145 Femoral head and neck excision
arthroplasty.
A The femur is externally rotated to visualize
the entire femoral head and neck. The
ostectomy is performed on a line from the
lateral aspect of the intertrochanteric notch
to just proximal to the lesser trochanter
(solid line). An ostectomy on a line
perpendicular to the axis of the femoral neck
the caudal femoral neck.
B The ostectomy is parallel to the sagittal
plane of the femur (rather than parallel to
the femoral neck) to avoid leaving a portion
the femoral neck in situ.
C Ventordorsal radiographic view of a
femoral head and neck excision arthroplasty.
 Fractures and disorders of the hindlimb
179

limb function, and minimize the development of Plate fixation

osteoarthritis. A dorsal approach to the hip by
ostectomy of the greater trochanter is preferred by
many surgeons and enhances visibility; however, many
acetabular fractures can be stabilized via a craniolateral
approach to the hip joint as previously described18.
The fragments are reduced and temporarily stabilized
using pointed reduction forceps. Manipulating the
caudal fragment with a bone clamp applied to
the ischium through a small caudal incision may
facilitate reduction in some cases. The sciatic nerve
must be identified and protected throughout
the procedure. Internal fixation is provided once the
articular surface is anatomically reduced and no steps
or gaps are present in the articular cartilage (146).
Plate fixation is commonly used and provides rigid
stabilization. A 2.0 mm bone plate, acetabular plate,
or L plate is contoured and secured to the dorsal
acetabular rim (146 B). The plate must be precisely
contoured to avoid displacement of the fracture site
when the screws are tightened. Small Kirschner wires
may be inserted across the fracture line to maintain
reduction while applying the plate. Care is taken to
avoid inserting screws into the acetabulum.
Lag screws
Oblique, two-piece fractures may be stabilized using
two lag screws placed perpendicularly to the fracture
line (146 C).

146

A B C

D E F

146 Repair of acetabular fractures.

A The fragments are reduced and temporarily stabilized using pointed reduction forceps. A clamp may be applied to the
ischium to manipulate the caudal fragment and facilitate reduction.
B Plate fixation. A Kirschner wire is inserted across the fracture line to maintain reduction while applying the plate. The
plate is applied to the dorsal acetabular rim. It must be precisely contoured to prevent displacement of the fragments as
the screws are inserted.
C Lag screw fixation. Two screws are inserted in lag fashion perpendicularly to the fracture line.
D Tension band wire fixation. Two Kirschner wires are placed across the fracture line to prevent rotation. A figure-of-
eight wire is then placed on the dorsal aspect of the acetabulum, anchored by the protruding ends of the Kirschner wires.
E Alternatively, the figure-of-eight wire can be anchored to two screws inserted in the dorsal acetabular rim cranial and
caudal to the fracture line.
F Screw–wire–polymethylmethacrylate composite fixation. A tension band using screws, Kirschner wires, and a figure-of-
eight wire is applied to the dorsal acetabular rim. Polymethylmethacrylate is then applied over the implants. The sciatic
nerve is protected from the heat created as the polymethylmethacrylate hardens.
180
Tension band wire fixation
Two-piece transverse fractures that are relatively stable
after reduction may be stabilized with a tension band
wire. One or two Kirschner wires are placed across the
fracture line to prevent rotation. A figure-of-eight
wire is then placed on the dorsal aspect of the
acetabulum. The figure-of-eight wire is anchored to
the protruding ends of the Kirschner wires or to
screws inserted in the dorsal aspect of the acetabulum
(146 D, E).
Tension band wire fixation is not as rigid as plates
or lag screw fixation, but is often adequate in cats.
Screws–wire–polymethylmethacrylate (PMMA)
composite fixation
A tension band fixation using screws, Kirschner wires,
and a figure-of-eight wire is applied as previously
described. PMMA is applied over the implants on the
dorsal acetabular rim to enhance stability (146 F)25.
The sciatic nerve must be protected from the heat
created by the exothermic reaction as the PMMA
hardens.
ISCHIAL FRACTURES
Ischial fractures in the cat rarely require surgical
fixation. Most occur in conjunction with other pelvic
fractures, and reduction of the concurrent injuries
(sacroiliac luxation, ilial fracture, or acetabular
fracture) usually aligns the ischial fracture as well.
However, in rare cases, the ischial tuberosity is
147
147 Repair of ischial fractures. The displaced ischial
fragment is reduced and stabilized using a tension band
wire fixation or two interfragmentary Kirschner wires.
markedly displaced by the origins of the biceps
femoris, semitendinosus, and semimembranosus
muscles. Fixation of the displaced ischial tuberosity
may restore function and reduce pain. Fixation is
achieved using either a tension band wire fixation or
interfragmentary wires (147).
PUBIC FRACTURES
Pubic fractures and pubic symphyseal separations in
the cat rarely require surgical fixation. Stabilization of
fractures present in other bones of the pelvis will
usually adequately reduce the pubic bones. Cage rest
and limited activity allow eventual bony union.
Hobbles can be applied to the hindlimbs to prevent
abduction during healing, but many cats tolerate them
poorly. Rarely, interfragmentary wires are used to
align and stabilize the pubis (148).
PELVIC MALUNION FRACTURES
Unreduced pelvic fractures may heal as malunions.
Malunions of the pubis and ischium often cause no
clinical abnormalities. However, malunion fractures of
the acetabulum may lead to poor joint congruence
and osteoarthritis (149). Malunions of the ilium often
cause gait abnormalities and marked narrowing of the
pelvic canal, leading to recurrent bouts of constipation
or obstipation. Pelvic collapse may also occur in cats
with nutritional secondary hyperparathyroidism
caused by eating a diet low in calcium or high in
phosphorus (as in all-meat diets) (150). In some
148
148 Repair of pubic fractures and pubic symphyseal
separations. Pubic fractures rarely require internal fixation,
but they may be stabilized using interfragmentary cerclage
wires anchored through holes drilled in the bone.
 Fractures and disorders of the hindlimb
181
149

A B
149 Radiographs of a pelvic malunion fracture involving the left ilium and acetabulum. Radiographic signs of
osteoarthritis are present in the left coxofemoral joint.A Ventrodorsal view. B Lateral view.

150 Treatment of pelvic canal 150

narrowing with pubic
symphysiotomy. A Ventrodorsal
radiographic view of the pelvis from a
jaguar with nutritional secondary
hyperparathyroidism. The pelvic canal
is collapsed causing obstipation. A
folding fracture of the right femur is
evident. B Surgical correction of the
pelvic collapse with pubic
symphysiotomy (intraoperative view).
A piece of high-density polyethylene
is wired to each half of the separated
A B C
symphysis to widen the pelvic canal
permanently. C Postoperative,
ventrodorsal radiographic view of the
pelvis after surgical correction of the
pelvic collapse. D Ventrodorsal
radiographic view of the pelvis from a
cat with pelvic canal narrowing
resulting from fracture malunion.
E Postoperative radiograph of the cat
after symphysiotomy and insertion of
a cortical bone autograft to widen the
pelvic canal. F Diagram depicting
symphysiotomy and placement of a
cortical autograft from the ulna or
D E F
ilium for treatment of pelvic collapse.
182

cases, stool softeners, proper diet, and occasional
enemas may resolve the clinical signs. However, if
signs are persistent or recur frequently, surgical
intervention to widen the pelvic canal is indicated.
Widening the pelvic canal may not return defecation
to normal in cats with neurologic deficits, idiopathic
megacolon, or where signs of obstipation have been
present for more than 6 months14. In these cases,
subtotal colectomy is recommended12.
Splitting and separating the pubic symphysis,
partial pelvectomy, and corrective ostectomy
procedures can widen the pelvic canal in cats with
obstipation secondary to pelvic malunion. In many
cases, continued medical therapy is required after
surgery.
PUBIC SYMPHYSIOTOMY
A ventral approach is performed and an osteotome or
saw is used to separate the two halves of the pubis.
Retractors are used carefully to spread the symphysis
and widen the pelvic canal. The sacroiliac joints limit
the amount of separation achieved by splitting the
pubic symphysis. A cortical graft from the ilium or an
ulnar autograft can be collected and wired into place
between the two halves of the pubic symphysis to
maintain separation17,26. Alternatively, a piece of
sterile high-density polyethylene can be placed within
the symphysis and secured with wires (150)27.
PARTIAL PELVECTOMY
A rectal examination is performed to ascertain the
location and volume of bone that must be removed
to enlarge the pelvic canal. In most cases, portions
of the pubis and ischium are resected, leaving the
acetabula, ilia, and sacroiliac joints intact if possible
(151). Bilateral resection may be performed if
necessary. Alternative procedures (symphysiotomy
and pelvic ostectomy) should be considered if repair
of the collapsed pelvis requires removal of the
acetabulum and ilium, since resection of these
structures would necessitate concurrent limb
amputation.
The cat is positioned in lateral recumbency and
a hanging-limb preparation is used to allow access to
the entire hindlimb during surgery. A urethral
catheter is placed to facilitate identification and avoid
injury to the urethra during surgery. A purse-string
suture is placed in the anus to reduce contamination
of the surgical site. Antibiotics (cefoxitin, 10 mg/kg)
are administered intravenously before surgery and

151

A B C

151 Surgical treatment of pelvic malunion.

A Malunion of pelvic fractures causing narrowing of the pelvic canal.
B Partial pelvectomy. Portions of the pubis and ischium are excised.
C Pelvic ostectomy. An ostectomy is made in the body of the ilium and the pubis and ischium are either osteotomized or
partially resected. The acetabular segment is displaced laterally and stabilized with a bone plate.
 Fractures and disorders of the hindlimb
every 2 hours during the procedure28. The portion of
the pelvis to be resected is exposed, using caution to
protect neurovascular structures. Hemostasis is
achieved with electrocautery and vessel ligation as
needed. The soft tissues are carefully elevated from the
bone with a periosteal elevator. The bone is removed
with a saw, rongeur, or osteotome and mallet. The
soft tissues are anatomically apposed to eliminate
dead-space. Closed suction drains may be placed
during surgery if necessary and are removed 24 hours
after surgery or when drainage is minimal28.
183
PELVIC OSTECTOMY
Pelvic ostectomy techniques may be performed alone
or in conjunction with partial pelvectomy to widen
the pelvic canal14,29. An ostectomy is made in the
body of the ilium and the pubis and ischium are either
osteotomized or partially resected. The resultant free
acetabular segment is displaced laterally and stabilized
with a bone plate (151). Care is taken to protect the
sciatic nerve during the procedure. An ostectomy may
be performed bilaterally if necessary to widen the
pelvis adequately.
184

PART 2: COXOFEMORAL JOINT

COXOFEMORAL LUXATION CLINICAL SIGNS

CAUSE AND PATHOGENESIS
The coxofemoral joint is a diarthrodial articulation
between the femoral head and acetabulum (152). It is
the most commonly luxated joint in cats. Luxations are
generally a result of trauma and result in obvious
mechanical dysfunction. The majority of hip luxations
are craniodorsal (153). Ventral and caudal luxations
occur infrequently, and may be accompanied by
avulsion fracture of the greater trochanter1. Articular
cartilage damage may result from the initial trauma to
the joint and from lack of lubrication and nourishment
normally provided by the synovial fluid.
Cats with coxofemoral luxations often present with a
history of observed or suspected trauma. A thorough
physical examination is needed to confirm the hip
luxation and identify concurrent trauma-related
injuries. The clinical findings in cats with coxofemoral
luxation may include:
• Pain in the hip region.
• Lameness (usually nonweight-bearing initially).
• External rotation and adduction of the affected
limb.
• Asymmetry of the hips due to displacement of the
trochanter.

152 152 Feline coxofemoral joint.

(Photograph courtesy of Tom
Thompson.)

153 153 Radiographs of

coxofemoral luxation.
A Ventrodorsal view.
B Lateral view.

A B
 Fractures and disorders of the hindlimb
• Increased distance between the greater trochanter
and tuber ischii.
• Apparent shortening of the affected limb with
craniodorsal luxations.
• Crepitus in the hip joint.
• Palpable laxity of the coxofemoral joint. This is
best evaluated by placing a thumb in the ischiatic
notch between the greater tochanter and ischial
tuberosity. External rotation of the femur will not
displace the thumb from the notch. This technique
is also valuable for assessing the joint after closed
reduction. With the femoral head seated in the
acetabulum, the thumb will be displaced from the
ischiatic notch with external rotation of the femur.
DIAGNOSIS
Radiographic evaluation of the hip is required
to confirm the luxation, determine the direction of
the luxation, and evaluate for other abnormalities
(acetabular fractures, femoral neck fractures, slipped
capital physis, hip dysplasia).
TREATMENT AND PROGNOSIS
Conservative treatment
Conservative treatment of coxofemoral luxation can
be successful in some cats2. Without reduction,
a pseudoarthrosis may develop between the luxated
femoral head and the caudal ilium, allowing limited,
pain-free function. However, reduction and stabilization
of the joint are recommended in cats that fail to bear
weight on the limb within 4–5 days of injury. Chronic
lameness often develops if the cats have not shown
consistent improvement within the first 2 weeks.
Reduction and stabilization
Closed or open reduction and stabilization of the
luxated joint are preferred in most cases. Joint
reduction should be performed soon after injury to
minimize destruction of cartilage and before muscle
spasticity and fibrosis prevent easy relocation. However,
diagnosis and management of concurrent injuries may
take precedence. Shock therapy, supportive care, and a
thorough evaluation (including thoracic radiographs)
should be performed in cats that have sustained recent
trauma. In most cases, closed reduction is attempted
first. Open (surgical) reduction is indicated if acetabular
or femoral head fractures are present, the joint reluxates
after closed reduction and internal stabilization is
required, other injuries require immediate return of hip
function, or if the luxation is chronic and visual
evaluation of the cartilage is necessary3. After
reduction, the hip joint is generally immobilized to
maintain reduction. This may be achieved by external
185
coaptation or internal stabilization. Stability may not be
possible in dysplastic joints.
Closed reduction and stabilization
Closed reduction is usually successful if performed in the
first few days after luxation. The cat is placed under
general anesthesia to relax muscles and eliminate pain
during hip manipulation. The cat is positioned in lateral
recumbency with the luxated limb uppermost. An
assistant places a small towel or rope in the cat’s inguinal
area beneath the luxated hip to provide countertraction
and stabilize the pelvis during reduction. Initially, in
cases of craniodorsal luxation, the femoral head is
disengaged from the dorsal acetabluar rim by grasping
the hock and stifle and externally rotating the limb. The
limb is then pulled distally and caudally to align the
femoral head over the acetabulum. The limb is then
internally rotated and abducted to reduce the joint.
Digital pressure applied to the greater trochanter is
helpful in directing the femoral head into the
acetabulum. Alternatively, the limb may be internally
rotated and pulled distally while the femoral head is
guided into the acetabulum by pressure on the greater
trochanter. Once the joint is reduced, medial pressure is
applied to the trochanter as the limb is manipulated
through a full range of motion. This removes blood
clots, joint capsule, and other soft tissues from the
acetabulum. The stability of the joint is also assessed
during this manipulation. Reduction is confirmed by
radiography.
After closed reduction, a nonweight-bearing sling
(Ehmer sling) is applied to maintain reduction
(154)2,4. Radiographs are obtained after the sling is
154
154 Ehmer sling applied to immobilize the limb after
closed reduction of a craniodorsal coxofemoral luxation.
The sling prevents weight bearing and internally rotates
the femur to maximize stability of the hip joint.
186

applied to ensure the joint is still reduced. The sling is
required for 10–14 days, until the joint capsule and
periarticular soft tissues are sufficiently healed to
maintain reduction. The sling must be monitored
closely for complications such as slipping, reluxation,
and soft tissue trauma. Some cats are intolerant of
Ehmer slings.
The insertion of an ischioilial pin (DeVita pin) has
also been used to stabilize the hip joint after closed
reduction5. A Steinmann pin is placed from ventral to
the ischium, over the femoral head, and imbedded in
the wing of the ilium. Unfortunately, the ilial wing in
cats is relatively flat, making it difficult adequately to
seat the pin cranially1. As a result, complications
occur frequently and include pin migration, reluxa-
tion, sciatic nerve injury, and damage to the femoral
head6.
Reluxation occurs in over 50% of cases after closed
reduction7. If the joint remains unstable or reluxation
occurs, open techniques or femoral head and neck
excision arthroplasty are indicated.
Open reduction and stabilization
Open methods of reduction allow exploration of joint,
removal of soft tissue entrapped in the acetabulum,
and internal stabilization. The success rate after open
reduction and stabilization (approximately 85%) is
significantly greater than after closed reduction7.
A craniolateral approach to the joint is usually
sufficient; however, a trochanteric ostectomy can be
performed to improve exposure and provide stability
after closure (dorsal approach). Once the joint is
reduced, stabilization techniques are used, alone or in
combination, to provide joint stability while the joint
capsule and periarticular soft tissues heal. Open
techniques useful for stabilization of coxofemoral
luxation in cats include:
• Capsulorraphy. A craniolateral or dorsal
approach to the hip is performed and the torn
joint capsule is sutured to provide joint stability
(155)8. Monofilament, nonabsorbable sutures
(2–0) are placed in a mattress or cruciate
pattern. An Ehmer sling may be applied for
10–14 days postoperatively to protect the
repair. Alternative methods will be required if
the joint capsule is severely damaged or torn
from its attachment to the femur or
acetabulum.
• Prosthetic capsule replacement9–11. Prosthetic
capsule replacement is performed through a
craniolateral or dorsal approach to the hip
joint8,9–12. If the joint capsule is damaged or
avulsed from the acetabulm, two bone screws
(2.0 mm or 2.7 mm screws with washers) are
placed in the dorsal acetabular rim at
approximately the 10 o’clock and 1 o’clock
positions for the left hip (or 11 o’clock and
2 o’clock for the right hip). The screws serve as
anchor points for suture attachment. A hole is
also drilled through the femoral neck to anchor
sutures. Monofilament suture material is ‘woven’
between the screw heads and the femoral neck

155

155 Capsulorraphy for stabilization of coxofemoral

luxations. A craniolateral approach to the hip is performed
and the torn joint capsule is sutured with monofilament,
nonabsorbable sutures in a mattress or cruciate pattern.
 Fractures and disorders of the hindlimb
187

to create a ‘web’ over the joint and prevent
reluxation (156). The sutures are tightened while
the limb is held in a weight-bearing position with
slight abduction and internal rotation. The limb
may be placed in an Ehmer sling after surgery;
however, the stability is generally adequate to
allow the cat to walk on the limb if needed. This
technique has been very successful in maintaining
joint reduction and has few complications when
performed properly. Complications may include
damage to the articular cartilage by the suture,
reluxation through the ‘web’, and infection.
• Transposition of the greater trochanter.
Ostectomy of the greater trochanter improves
exposure to the joint for capsulorraphy or
prosthetic capsule placement12. When closing
the incision, the trochanter is simply transposed
approximately 1 cm distally and caudally. This
transposition of the trochanter provides
ancillary stabilization by increasing the medial
pull of the gluteal muscles and abducting and
internally rotating the femur. The trochanter is
reattached with a tension band wire fixation or
a lag screw (157).

156 Prosthetic capsule replacement for stabilization of 156

coxofemoral luxations. A craniolateral or dorsal approach
to the hip joint is performed and two screws with washers
are inserted into the dorsal acetabular rim at approximately
the 10 o’clock and 1 o’clock positions for the left hip (or
11 o’clock and 2 o’clock for the right hip). A hole is
drilled through the femoral neck and monofilament suture
material is woven between the screw heads and the
femoral neck to prevent reluxation.

157 Transposition of the greater trochanter for 157

stabilization of coxofemoral luxations. The greater
trochanter is moved 1 cm distally and caudally and
re-attached with a tension band fixation or lag screw.
188

• Transarticular pinning. A small Steinmann pin or following pin removal. Complications of

Kirschner wire (1.6–2.0 mm diameter) is
inserted through the femoral head and neck into
the acetabulum to provide joint stability (158)13.
Typically, the pin is inserted in a retrograde
fashion, starting at the fovea capitis and exiting
near the third trochanter. The joint is then
reduced and the limb is held in a weight-bearing
position with slight abduction while the pin is
driven through the acetabular wall into the
pelvic canal. An assistant evaluates pin depth by
rectal examination. The lateral portion of the
pin is then bent over and cut short. Enough pin
length is left to allow later removal. A
capsulorraphy is performed if possible and the
incision is closed routinely. An Ehmer sling can
be applied after surgery but is not essential. The
sling if applied is removed after 10 days and the
pin is removed after 2–3 weeks. The cat’s
activity is restricted for an additional 4 weeks
transarticular pinning include pin migration,
perforation of the rectum, pin bending or
breakage, and osteoarthritis3,14.
• Toggle rod fixation. This allows early use of the
limb after surgery, which may be necessary if
injury to the opposite hindlimb is present15.
A dorsal approach to the hip joint with
ostectomy of the greater trochanter is the
preferred approach. However, the technique
may also be performed through a craniolateral
approach to the hip. A hole is drilled through
the femoral head and neck from the fovea capitis
to the region of the third trochanter. A second
hole is drilled in the center of the acetabular
fossa (penetrating the medial acetabular wall)
large enough to accommodate the toggle rod.
(Securos Veterinary Orthopedics Inc.; IMEX
Veterinary Inc.) One or two strands of suture
material are then inserted through the hole in

158

A B

C D

158 Transarticular pinning for stabilization of coxofemoral luxations.

A A 1.6–2.0 mm diameter pin is inserted retrograde, starting at the fovea capitis and exiting near the third
trochanter. The pin is advanced until the tip is at the level of the femoral head.
B The joint is reduced and the limb is held in a weight-bearing position with slight abduction while the pin
is driven through the acetabular wall into the pelvic canal.
C The lateral end of the pin is bent over and cut short, leaving enough pin length to allow later removal.
D Ventrodorsal radiographic view of the hip joint in a cat. The craniodorsal hip luxation is stabilized with a
transarticular pin.
 Fractures and disorders of the hindlimb
189

the center of the toggle rod. The suture may be
attached to the toggle rod by inserting a loop of
suture through the hole in its center and then
placing the ends of the suture back through the
loop to lock the suture in place15. The toggle
rod is then inserted through the hole drilled in
the acetabulum. By pulling on the ends of the
sutures, the toggle rod is positioned against the
medial acetabular wall and cannot pass back
through the hole. The free ends of the sutures
are then passed through the bone tunnel in the
femoral head and neck, exiting near the third
trochanter. The sutures are secured to the femur
by drilling another hole through the lateral
femoral cortex. One end of the suture is passed
through the hole and the two ends are tied.
Alternatively, the suture can be tied to a sterile
button on the lateral aspect of the femur (159).
The sutures are tightened while the hip is held
in a reduced position. A capsulorraphy is
performed and the greater trochanter is
reattached using a tension band wire fixation.
The suture material within the joint, which
maintains reduction until the periarticular soft
tissues are healed, eventually becomes
encapsulated in the regenerating round
ligament. A potential complication of toggle rod
fixation is premature suture breakage and joint
reluxation.
• Fascia lata loop stabilization. This technique is
similar to toggle rod fixation in many ways,
except that the fasica lata is used rather than
suture material16. A caudolateral approach to
the hip joint is performed and a long strip of
facia lata (1 cm wide) is harvested. One end of
the fascial strip is passed over the dorsal aspect
of the ilium and pulled into the acetabulum
(through a hole drilled in the acetabular fossa)
using a wire loop. Care is taken to protect the
sciatic nerve. The fascial strip is then passed

159

A B C

D E
159 Toggle rod fixation for stabilization of coxofemoral luxations.
A A hole is drilled through the femoral head and neck from the fovea capitis to the region of the third trochanter.
B A hole is drilled in the center of the acetabular fossa, penetrating the medial acetabular wall.
C Suture material is attached to the toggle rod and it is inserted through the hole in the acetabulum. The toggle rod is
positioned against the medial acetabular wall.
D The suture is then passed through the bone tunnel in the femoral head and neck, exiting near the third trochanter.
E The suture is secured on the lateral aspect of the femur either using a sterile button or by passing the suture through a
transverse hole drilled in the femoral cortex and tying the suture ends together.
190

through a tunnel drilled in the femoral head and
neck starting at the fovea capitis and extending
to the third trochanter. The luxation is reduced
and the two ends of the fascial strip are sutured
together near the trochanteric exit (160).
A capsulorraphy is performed and the incision is
closed routinely. The cat’s activity is restricted
for 6 weeks after surgery. External coaptation is
not required. Good results have been reported
in two cats using this technique16.
• Extraarticular iliofemoral suture. Suturing
techniques have been described for stabilization
of hip luxations in cats (161 A)17,18.
A craniolateral approach to the hip joint is
performed. Hematoma, remnants of the round
ligament, and other soft tissues are removed
from the acetabulum and the joint is reduced.
A capsulorraphy is performed if possible. Using a
drill bit or Stenmann pin, a hole is drilled from
lateral to medial in the ilium just cranial to the
acetabulum. A second hole is drilled from caudal
to cranial through the femur just distal to the
insertion of the gluteal muscles at the base of
the greater trochanter. A strand of large,
monofilament suture material (0 polypropylene;
Prolene, Ethicon) is passed from lateral to medial

160 160 Fascia lata loop stabilization of coxofemoral

luxations. A strip of fascia lata is harvested and passed
over the dorsal aspect of the ilium, into the acetabulum
through a hole drilled in the acetabular fossa, and
through a tunnel in the femoral head and neck. The
luxation is reduced and the ends of the fascial strip are
sutured together over the lateral aspect of the femur.

161

B C
161 Coxofemoral luxation.
A Extraarticular iliofemoral suturing technique for stabilization of coxofemoral luxations. Holes are drilled from lateral to
medial in the ilium just cranial to the acetabulum and caudal to cranial through the femur at the base of the greater
trochanter. A strand of large, monofilament suture material is passed from lateral to medial through the hole in the ilium
and from cranial to caudal through the hole in the femur. The suture is then passed beneath the insertion of the gluteal
muscles on the trochanter and the ends are tied, with the hip joint internally rotated and abducted.
B Lateral radiograph of the pelvis of a cat with coxofemoral luxation and concomitant fracture of the femoral head.
C Postoperative lateral radiograph of the same patient showing total hip replacement using the BioMedtrix CFXTM Micro
hip system.
 Fractures and disorders of the hindlimb
through the hole in the ilium. A curved
hemostat is placed under the ventral edge of the
ilial body to grasp the suture and bring it to the
lateral side of the ilium. The suture is then
passed from cranial to caudal through the hole in
the femur. The suture is then passed from caudal
to cranial beneath the insertion of the gluteal
muscles on the trochanter using a hemostat or
straight needle. The joint is internally rotated
and abducted and the suture is tied18. To avoid
drilling holes in the ilium and femur, an
alternative method of placing the suture has been
described17. Cranially, the suture is anchored in
the tendon of origin of the psoas minor muscle;
and caudally it is attached to the tendon of
insertion of the middle gluteal muscle. After
manipulating the joint to ensure stability, the
incision is closed. A nonweight-bearing sling is
applied for 7–10 days and the cat’s activity is
restricted for 6 weeks.
After open reduction and stabilization of a
coxofemoral luxation, the limb can be placed in
a nonweight-bearing sling (Ehmer or figure-of-eight)
for 7–14 days if tolerated by the cat. The sling must
be monitored closely for complications. Many of the
internal stabilization techniques can be used without
external coaptation if early postoperative use of
the surgically treated joint is required. Exercise is
restricted for 4–6 weeks after surgery. The prognosis
after coxofemoral luxation is good if reduction and
stability are achieved soon after injury. Osteoarthritis
is possible due to injury of the articular cartilage at the
time of luxation or surgical repair. Total hip
replacement or femoral head and neck excision should
be considered if closed and open techniques are
unsuccessful, or if severe femoral head damage is
present. These procedures may also be used as the
primary treatment method for hip luxations in cats.
Total hip replacement
Total hip replacement can now be performed on most
cats greater than 4 kg body weight as an alternative to
femoral head and neck ostectomy, using a modular
cemented prosthesis (BioMedtrix CFX™ Micro hip
system) (161 B, C). Indications include coxofemoral
osteoarthritis, luxation that cannot be maintained
using closed or open procedures, fractures of the
femoral head and neck that are not amenable to
surgical repair, and malunions.
191
Femoral head and neck excision arthroplasty
Surgical removal of the femoral head and neck is
indicated for treatment of recurrent hip luxations,
severe fractures of the acetabulum or femoral head
and neck, and coxofemoral osteoarthritis19 (see
Femoral head and neck excision arthroplasty
for acetabular fractures). It may also be used as a
primary means of treating coxofemoral luxation in
cats. The procedure is completed through a
craniolateral approach as previously described
(144, 145). The prognosis after excision arthro-
plasty in the cat with coxofemoral luxation is
good20,21. Most cats will walk well within 5 weeks
and return to function within 5 months of
surgery1,21.
HIP DYSPLASIA
Hip dysplasia is much less common in cats than
in dogs, although the actual incidence is undeter-
mined. The Orthopedic Foundation for Animals
reports that hip dysplasia is present in approximately
18% of Maine coon cats. It is a congenital disease that
usually affects both hip joints and may lead to pain
and osteoarthritis. It occurs more commonly in female
and purebred cats, though it has been reported in a
litter of domestic shorthair cats2,22–24.
Some cats with hip dysplasia show no clinical signs.
However, others present with hindlimb weakness,
reluctance to walk, or hip pain. The diagnosis of hip
dysplasia is based on radiographic findings of hip joint
laxity, shallow acetabula, and mild remodeling of the
craniodorsal acetabular margin. Remodeling of the
femoral neck, often seen in dysplastic dogs, is
uncommon in cats22,23,25–28. Hip joint laxity
is associated with the development of osteoarthritis
and may be confirmed using distraction radiography
or measurement of the Norberg angle from the hip-
extended ventrodorsal radiographic view. The mean
Norberg angle in normal cats is 92.4°28.
In most cases, cats with clinical signs of hip
dysplasia are treated with cage rest for 2–3 weeks.
Long-term medical management with the non-
steroidal antiinflammatory drug (NSAID),
meloxicam, can be used but is rarely indicated. Total
hip replacement or femoral head and neck excision
arthroplasty can be performed if clinical signs persist
after conservative therapy2.
192

PART 3: FEMORAL AND PATELLAR FRACTURES

Femoral fractures occur commonly in cats and are
readily diagnosed by palpation and radiography. In
almost all cases, surgical intervention is indicated to
reduce the fracture properly and provide stability.
PROXIMAL FEMORAL FRACTURES
FEMORAL HEAD FRACTURES
Cause and pathogenesis
Fractures of the femoral head are typically avulsion
fractures. A fragment of bone attached to the ligament
of the head of the femur remains within the joint
space while the remaining portion of the femoral head
is luxated craniodorsally.
Treatment and prognosis
Treatment of femoral head fractures is achieved by
reattaching the fragment with Kirschner wires or
a screw, by removing the bone fragment, or by
femoral head and neck excision arthroplasty1.
Kirschner wire/screw fixation
If the avulsed fragment of bone from the femoral head
is sufficiently large, it can be re-attached using
Kirschner wires or a small screw placed in lag fashion
(162). This may be accomplished by placing the
implants from just distal to the greater trochanter,
through the femoral neck, and into the avulsed bone.
Unfortunately, placing the implants in this manner is
difficult since the bone fragments are usually very
small and visualization of the fragment is impossible
when the femoral head is placed into the acetabulum.
Consequently, confirming proper reduction of the
fracture is difficult unless intraoperative imaging is
available. It is important that the implants do not
penetrate the articular surface of the hip joint. This is
checked by carefully manipulating the joint and by
palpating the joint surface with a smooth hemostat or
periosteal elevator.
An alternative method involves excising the
fragment from its attachment on the round ligament
and then anchoring it to the femoral head with
Kirschner wires or a 2.0 mm lag screw placed from
the articular surface into the femoral neck. This
method allows visualization of the fragment, assures
proper reduction, and allows the implants to
be countersunk below the articular surface. When
possible, the implants are placed in the fovea capitis
and countersunk to reduce damage to the cartilage.
The femoral head is then reduced into the acetabulum
and the joint capsule sutured to provide stability.
Complications after internal fixation of femoral
head fractures can include implant migration into
the joint, implant migration leading to fixation
failure, avascular necrosis of the femoral head,
recurrent coxofemoral luxation, and osteoarthritis of
the joint.

162

A B C D

162 Stabilization of femoral head fractures.

A Avulsion fracture of the femoral head. The avulsed fragment typically remains in the acetabulum, attached to the
ligament of the head of the femur.
B The fragment is re-attached with Kirschner wires or a screw placed from just distal to the greater trochanter, through
the femoral neck, and into the avulsed bone.
C The fragment is attached with Kirschner wires inserted from the articular surface into the femoral neck. The wires are
placed in the fovea capitis and countersunk to reduce damage to the cartilage.
D If the fracture configuration permits, a 2.0 mm screw may be placed in lag fashion to compress the fracture.
 Fractures and disorders of the hindlimb
193

Fragment excision 163

If the avulsed fragment is too small to allow fixation,
it is simply excised. The femoral head is then reduced
and stabilized. Since the fragment is small and
typically involves the region of cartilage surrounding
the fovea capitis, hip joint function is generally good,
although osteoarthritis may develop over time.

Femoral head and neck excision arthroplasty

Femoral head and neck excision arthroplasty is
performed if damage to the femoral head is severe
(see 145). The prognosis after femoral head and neck
excision arthroplasty is very good and it is often
recommended as the procedure of choice for fractures
of the femoral head in cats.

SEPARATIONOF THE PROXIMAL FEMORAL

GROWTH PLATE
Cause and pathogenesis
Separation of the proximal femoral growth plate
occurs uncommonly in immature cats, usually as
a result of trauma. Most are Salter–Harris type
I fractures in which the separation occurs along the
physeal line (163)2. This injury is also referred to as a
capital fracture or a slipped capital epiphysis. 163 Ventrodorsal radiographic view of a separation
Spontaneous femoral capital physeal fractures have (Salter–Harris type I fracture) of the proximal
also been described in adult cats, typically in heavier, femoral growth plate. This injury is also referred to
neutered males with delayed physeal closure3. as a capital fracture or a slipped capital epiphysis.

Diagnosis
In most cases of proximal femoral growth plate
separation, the epiphysis (femoral capitis) remains within
the joint space while the femoral neck is displaced
craniodorsally. Occasionally, displacement at the physis is
minimal and careful examination of the radiographs or
additional frog-limb and extended views, is required to
confirm the fracture. The ligament of the head of the
femur is purported to provide significant blood supply
to the femoral capital epiphysis4.
Treatment and prognosis
Treatment of proximal femoral growth plate fractures
is by conservative therapy, femoral head and neck
excision arthroplasty, or internal fixation using
multiple Kirschner wires1,4,5.
Conservative therapy
Some cats will return to adequate function without
surgical treatment, particularly when displacement of
the epiphysis is minimal. Activity is restricted and the
fracture is monitored radiographically. The hip may
function normally if the epiphysis heals in an
anatomic or near-anatomic position, although
osteoarthritis may develop over time. If the epiphysis
becomes more displaced or limb function is not
satisfactory, internal fixation or excision arthroplasty
is indicated.
Total hip replacement
Total hip replacement is indicated for femoral head
fractures that are not amenable to surgical repair. The
prognosis is likely to be excellent.
Femoral head and neck excision arthroplasty
Removal of the femoral head and neck is commonly
performed for separation of the proximal femoral
growth plate (see 145). The prognosis is fair to good
and complications are few.
Kirschner wire/screw fixation
If surgical stabilization is elected, it may be achieved
using three Kirschner wires1,5,6. A craniolateral
approach to the hip joint is performed to visualize the
fracture site. The Kirschner wires are inserted from just
distal to the greater trochanter and advanced through
194

the femoral neck until they are visualized at the physis
(164). Alternatively, they may be placed in a retrograde
fashion starting at the physis and exiting the lateral
femoral cortex distal to the greater trochanter. The
Kirschner wires may be positioned such that they are
divergent or parallel to each other. The fracture is then
reduced by manipulation of the femur, ensuring that
the epiphysis is properly positioned relative to the
femoral neck. The Kirschner wires are then advanced
into the epiphysis to provide stability. The joint is
manipulated through a range of motion and the
articular surface is palpated with a smooth periosteal
elevator to ensure the wires do not penetrate the
cartilage of the epiphysis. The Kirschner wires are bent
against the lateral femoral cortex to reduce soft tissue
trauma and prevent migration.

164

A B C

D E F

164 Stabilization of proximal femoral growth plate separations (slipped capital epiphysis).
A Salter–Harris type I fracture of the proximal femoral growth plate. The fracture occurs along the physis.
B Repair using Kirschner wires. Three Kirschner wires are inserted from the greater trochanter and through the femoral
neck to the physis.
C The fracture is reduced and the Kirschner wires are advanced into the epiphysis. Care is taken to ensure they do not
penetrate the articular surface.
D A screw and single Kirschner wire inserted through the femoral neck into the epiphysis.
E Small screws inserted through the articular surface into the femoral neck. The screw heads are countersunk to reduce
joint trauma.
F Craniocaudal radiographic view of a proximal femoral growth plate separation stabilized with three Kirschner wires.
(Radiograph courtesy of Dr. Mark Rochet.)
 Fractures and disorders of the hindlimb
Alternatively, a screw may be inserted rather than
Kirschner wires. A single Kirschner wire is placed
parallel to the screw to prevent rotation. Implantation
of screws from the articular surface into the femoral
neck has also been described. The screw heads must
be countersunk below the cartilage surface to reduce
joint trauma. After fixation, the joint capsule is
sutured with 3-0 or 4-0 monofilament suture material
and the incision is closed routinely. Postoperative care
should include restricted activity for 3–4 weeks.
FEMORAL NECK FRACTURES
Cause and pathogenesis
Fractures of the femoral neck are often the result of
trauma and may occur alone or in conjunction
with other fractures in the cat7. Pathologic femoral
neck fractures may occur secondary to metaphyseal
osteopathy or feline capital physeal dysplasia
(see Chapter 13)8–10.
Treatment and prognosis
Treatment of pathologic fractures is by total hip
replacement or femoral head and neck excision
arthroplasty. Treatment of traumatic femoral neck
fractures may be by conservative therapy, total hip
replacement, femoral head and neck excision arthroplasty,
or internal fixation using Kirschner wires or screws.
Conservative therapy
Incomplete and nondisplaced fractures of the femoral
neck may be treated by immobilization of the limb and
restriction of activity for 4 weeks. Radiographs of the hip
165 Radiographs of a femoral neck fracture.
A Ventrodorsal view of a right femoral neck
fracture.
B Postoperative ventrodorsal view showing
stabilization of the femoral neck fracture with
multiple Kirschner wires.
195
should be obtained with the femur in several positions
to determine if the fracture site is stable before selecting
conservative treatment. Hip-extended views and ‘frog-
limbed’ views are useful. If the fracture becomes
displaced or fails to heal, internal fixation or femoral
head and neck excision arthroplasty is indicated.
Total hip replacement
Total hip replacement is indicated for femoral neck
fractures that are not amenable to surgical repair. The
prognosis is likely to be excellent.
Femoral head and neck excision arthroplasty
Femoral head and neck excision arthroplasty is often
performed for unstable fractures of the femoral neck
(see 145). It is considered by many to be the
treatment of choice for these fractures in the cat.
Kirschner wire or screw fixation
A craniolateral approach to the hip joint is performed.
Reduction is achieved by manipulating the greater
trochanter with a bone clamp until the fractured
femoral neck is aligned. A Kirschner wire is then
inserted across the fracture line to maintain reduction
while the remaining implants are placed. Multiple
Kirschner wires are inserted normograde across the
fracture starting from the lateral femoral cortex distal
to the greater trochanter (165)5. The wires are
inserted into the femoral head without penetrating
the articular surface. They are cut and bent over
against the lateral cortex of the femur to reduce
muscle trauma and prevent migration.
165
A B
196

Alternatively, a 2.7 mm cortical bone screw can be
placed in lag fashion through the femoral neck and
into the femoral head. This is achieved by first drilling
a glide hole (2.7 mm) from the base of the greater
trochanter to the fracture line. A drill sleeve is
inserted into the glide hole to allow drilling of a
thread hole (2.0 mm) in the center of the femoral
head proximal to the fracture line. The drill bit
should not penetrate the articular surface of the
femoral head. The hole is measured and tapped and
the proper length screw is inserted. Care is taken not
to overtighten the screw. A Kirschner wire is inserted
across the fracture parallel to the screw to prevent
rotation (166). Postoperatively, the limb is placed in
a nonweight-bearing sling for 7–10 days and the cat’s
activity is restricted for 4 weeks.

166

A B C D

166 Stabilization of femoral neck fractures.

A Multiple Kirschner wires are inserted normograde across the fracture starting from the lateral femoral cortex distal to
the greater trochanter. The wires are inserted into the femoral head without penetrating the articular surface and are bent
over to reduce muscle trauma and prevent migration.
B A 2.7 mm cortical bone screw is placed in lag fashion through the femoral neck and into the femoral head. First,
a 2.7 mm glide hole is drilled from the base of the greater trochanter to the fracture line.
C The fracture is reduced and a Kirschner wire is placed to maintain reduction. A drill sleeve is inserted into the glide hole
and a 2.0 mm thread hole is drilled proximal to the fracture line.
D A screw is inserted to compress the fracture line. The Kirschner wire prevents rotation around the screw.

167 167 Radiographs of a fracture of the

greater trochanter.
A Lateral view of the proximal femur.
The greater trochanter is fractured and
displaced. The coxofemoral joint is luxated.
B Postoperative ventrodorsal view. The
coxofemoral joint was reduced. The
displaced greater trochanter was reduced
and stabilized with two divergent
Kirschner wires.

A B
 Fractures and disorders of the hindlimb
197

GREATER TROCHANTERIC FRACTURES
Cause and pathogenesis
Avulsion fracture of the greater trochanter may occur
with or without luxation of the coxofemoral joint or
separation of the proximal femoral physis.
Treatment and prognosis
Open reduction and internal stabilization are the
preferred treatment (167, 168). The fracture is
reduced through a lateral surgical approach over the
trochanter. The hip joint is not exposed unless an
open reduction of a coxofemoral luxation or repair of
a slipped capital epiphysis is required. The greater
trochanter is reduced and temporarily stabilized with
reduction forceps. Permanent fixation is achieved by
inserting a screw in lag fashion, tension band wire
fixation, or multiple Kirschner wires.
Lag screw fixation
A 2.7 mm bone screw is placed in lag fashion from the
trochanter to the femoral shaft. The glide hole
(2.7 mm) is placed in the trochanter and the thread
hole (2.0mm) is placed in the femoral metaphysis. The
screw should be sufficiently long to engage the medial
cortex of the femur. A second screw or Kirschner wire
is placed to prevent rotation around the screw.
Tension band wire fixation
Two parallel Kirschner wires (1–1.6 mm) are inserted
from proximal to distal across the fracture line and
into the medullary cavity of the femur. Compression
is achieved by placing a figure-of-eight orthopedic
wire around the proximal portion of the Kirschner
wires and through a hole drilled transversely across the
femur distal to the trochanter. The wire is twisted
until tight and the proximal tips of the Kirschner wires
are bent over and cut short.
Kirschner wire fixation
With the trochanter reduced, two or three Kirschner
wires (1.1–1.6 mm) are inserted from proximal to
distal through the trochanter and into the femur.
The wires should be placed at various angles rather
than parallel to each other. They should engage the
medial femoral cortex, although care is taken not to
penetrate the cortex excessively and traumatize tissue
on the medial aspect of the femur. The proximal
ends of the wires are bent over and cut short.

168

A B C D
168 Stabilization of greater trochanteric fractures.
A Avulsion fracture of the greater trochanter.
B Lag screw fixation. A 2.7 mm lag screw is inserted from the trochanter to
the femoral shaft. A 2.7 mm glide hole is drilled in the trochanter and a
2.0 mm thread hole is drilled in the femoral metaphysis. A Kirschner wire
is placed to prevent rotation around the screw.
C Tension band wire fixation. Two Kirschner wires are inserted across the
fracture line and into the medullary cavity of the femur. A figure-of-eight
wire is placed around the exposed ends of the Kirschner wires and through
a hole drilled transversely across the femur. The Kirschner wires are bent
over and cut short.
D Kirschner wire fixation. Two or three Kirschner wires are inserted at
divergent angles through the trochanter and into the femur, engaging the
medial femoral cortex. The ends of the wires are bent over and cut short.
198

INTERTROCHANTERIC FRACTURES ineffective since it is extremely difficult adequately to

Intertrochanteric fractures of the proximal femur
are typically stabilized with a combination of
intramedullary pinning and tension band wire
fixation (169). The fracture is reduced and two
Steinmann pins are inserted normograde through the
greater trochanter into the femoral medullary cavity.
The pins may be placed parallel to each other or as
dynamic intramedullary cross-pins (Rush pins). A
tension band wire is then placed around the exposed
proximal ends of the intramedullary pins and through
a hole drilled transversely across the femur distal to
the fracture site.
DIAPHYSEAL FEMORAL
FRACTURES
TREATMENT AND PROGNOSIS
Repair of fractures of the femoral diaphysis with open
or closed reduction and rigid stabilization is preferred
in most cases. External coaptation is generally
immobilize the femur with casts or splints. Femoral
fractures treated with external coaptation alone may
fail to heal or heal in a malunion (170).
The femoral diaphysis is visualized through a lateral
surgical approach (171)11. An incision is made through
the skin and subcutaneous tissue over the craniolateral
border of the femur from the greater trochanter to the
patella. The fascia lata is incised along the cranial edges
of the biceps femoris muscle and the biceps is retracted
caudally to expose the femur. The aponeurotic septum
on the lateral surface of the femur is incised to allow
cranial retraction of the vastus lateralis muscle. The
sartorius muscle is undivided in the cat (unlike the dog)
and may be encountered when performing a lateral
approach to the femur. Care is taken to preserve the soft
tissue attachments to the femur and bone fragments
wherever possible during reduction.
Intramedullary pins and cerclage wires, external
fixators, bone plates and screws, interlocking nails, or

169 170

A B
A B
169 Stabilization of intertrochanteric 170 Radiographs of a femoral malunion. Mild femoral shortening
fractures of the proximal femur. occurred as a result of the malunion.
A Two intramedullary pins are inserted A Lateral view.
normograde through the greater B Craniocaudal view.
trochanter into the femoral medullary
cavity. A tension band wire is placed.
B Alternatively, the pins may be placed
as dynamic intramedullary cross-pins
(Rush pins).
 Fractures and disorders of the hindlimb
combinations of these methods can be applied with
great success in stabilizing femoral diaphyseal fractures
in cats.
Intramedullary pins and cerclage wires
Placement of an intramedullary Steinmann pin
is a very common method of stabilizing femoral
fractures in cats12–14. The pin should be of a diameter
to fill 60–70% of the medullary cavity. Normograde
pin insertion is preferred because it allows proper
placement of the pin in the trochanteric fossa, may
reduce the possibility of injury to the femoral head
and sciatic nerve, and allows the pin to be cut short to
reduce trauma to the gluteal muscles and subsequent
seroma formation (172). For normograde insertion,
the fracture is reduced and stabilized with bone
clamps or cerclage wires (if they are to be used). The
pin is started at the medial aspect of the greater
trochanter (in the trochanteric fossa) and driven
171
Biceps femoris muscle
Vastus
lateralis
muscle
171 Lateral approach to the femoral diaphysis. An
incision is made over the craniolateral border of the
femur from the greater trochanter to the patella. The
fascia lata is incised along the cranial edges of the
biceps femoris muscle and the biceps is retracted
caudally. The aponeurotic septum on the lateral
surface of the femur is incised to allow cranial
retraction of the vastus lateralis muscle.
199
distally across the fracture and into the distal femur.
The pin is seated in the distal fragment without
entering the stifle joint. A second pin of identical
length can be used to measure how far distally the pin
has been inserted. Radiographs are also used to
confirm pin placement. The stifle joint is manipulated
through a range of motion to ensure the pin has not
penetrated the joint. Closed insertion of an
intramedullary pin is possible if the fracture is
minimally displaced or if adequate reduction of the
fragments can be achieved by palpation alone.
Excellent results can be achieved with closed pin
insertion, particularly in young cats when the fracture
is repaired within 1–3 days15. However, swelling of
the soft tissues surrounding the femur and interpo-
sition of muscle between the fragments may prevent
closed reduction in some cases.
For retrograde insertion, the intramedullary pin is
directed proximally from the fracture site before final
172
A B C
172 Normograde intramedullary pinning of the femur.
A, B A pin large enough to fill 60–70% of the medullary
cavity is selected. The pin is inserted at the medial aspect
of the greater trochanter in the trochanteric fossa.
C The pin is driven distally across the fracture and seated
into the distal femoral segment.
200

reduction of the fracture (173). It should be inserted
along the lateral surface of the medullary cavity to avoid
injury to the femoral head and neck as the pin emerges
proximally16. The pin should exit the medullary cavity
at the trochanteric fossa. The proximal femur is held in
adduction and in a normal standing angle (or slightly
extended) so that the pin does not damage the sciatic
nerve as it exits the proximal femur. The fracture is then
reduced and stabilized with a bone clamp. Cerclage
wires can be applied at this time if needed. The pin is
driven distally and seated into the distal fragment as
described for normograde insertion.
Intramedullary pins are rarely used alone as they
do not eliminate rotational forces at the fracture site.
Ancillary fixation with full cerclage wires or an
external fixator is often used to prevent rotation
(174). Application of cerclage wires is not feasible if
the fracture is stabilized in a closed manner, but is
easily performed during open fracture repair. An
external fixator can be applied to prevent rotation if
closed or open pinning is used (175, 176). Stack
pinning (placing several pins into the medullary
cavity) does not completely prevent rotation but it has
been used with success in cats17–20.

173 173 Retrograde intramedullary pinning of the femur.

A A pin large enough to fill 60–70% of the medullary cavity is selected. The
pin is inserted proximally from the fracture site and exits the medullary cavity
at the trochanteric fossa.
B The fracture is reduced and the pin is driven distally and seated into the
distal femur.

A B

174 174 Ancillary fixation with

intramedullary pins.
A Full cerclage wires.
B A type Ia acrylic fixator is
applied to prevent rotation
around the pin.
C A type Ia external fixator is
placed to prevent rotation and
collapse at the fracture site.
D A type Ia external fixator and
full cerclage wires for stabilization
of a comminuted femoral
fracture.
E Multiple intramedullary pins
A B C D E (stack pinning).
 Fractures and disorders of the hindlimb
201

Bone plates and screws
Bone plates are commonly used to stabilize femoral
fractures in cats and, when properly applied, are able
to counteract all of the forces acting at the fracture
site20,21. They are easily applied to the lateral surface
(tension surface) of the femur through a lateral
approach. DCPs and cuttable plates with 2.7 mm
cortical screws are commonly used. Limited-contact
dynamic compression plates (LC-DCP) with 2.4 mm
screws are also used for repair of femoral fractures.

175

A B C
175 Radiographs of a transverse, mid-diaphyseal femoral fracture stabilized with an intramedullary pin and type Ia
acrylic external fixator.
A Preoperative lateral view.
B Postoperative lateral view.
C Postoperative craniocaudal view.

176

A B C D
176 Radiographs of an oblique, distal diaphyseal femoral fracture stabilized with an intramedullary pin, full cerclage
wires, and a type I acrylic external fixator in a tie-in configuration.
A Preoperative lateral view.
B Preoperative craniocaudal view.
C 6-week postoperative lateral view.
D 6-week postoperative craniocaudal view. Fracture union is complete.
202

The screws should engage a minimum of five cortices Oblique fractures

on each side of the fracture line. Bone plates may
be applied to the femur to stabilize most fracture
configurations (177).
Transverse fractures
The fracture is reduced, ensuring proper angular and
rotational alignment of the proximal and distal fracture
segments. The linea aspera located along the caudal
border of the femur is an excellent landmark for
ensuring proper rotational alignment. The plate is
properly contoured and applied to the lateral femoral
cortex. In most diaphyseal fractures, sufficient room
exists proximally and distally to place a minimum of
three screws on each side of the fracture line. A 2.7 mm
DCP or 2.4 mm LC-DCP is commonly used. The oval
holes in DCP plates allow the fracture line to be
compressed to enhance stability and promote healing.
Cuttable plates and tubular plates may also be used
(178). Reconstruction plates (2.7 mm) may be useful
for stabilization of more distal diaphyseal fractures.
The fracture is reduced. The plate may be applied
as described for transverse fractures but without
compression. Alternatively, a lag screw or cerclage
wires can be placed to compress the fracture line and
maintain reduction while the plate is applied. If the
orientation of the oblique fracture line permits, one of
the plate screws can be placed in lag fashion across the
fracture line (177).
Comminuted fractures
A bone plate can be applied in several ways to stabilize
comminuted femoral fractures (179). When the area
of comminution is small, the primary fragments
are apposed as in a transverse fracture and the
comminuted fragments are used as autogenous graft.
This results in only minor shortening of the femur and
clinical function is normal.
If the area of comminution is too large to permit
shortening of the bone, the fragments may be
reconstructed using cerclage wires or lag screws. The

177

A B C D E
177 Bone plate stabilization of transverse and oblique femoral fractures.
A A transverse fracture stabilized with a DCP to achieve compression across the fracture line. A minimum of three screws
is placed on each side of the fracture line.
B A 2.7 mm reconstruction plate is easily contoured to the curvature of the distal femur to stabilize distal diaphyseal
fractures.
C An oblique fracture stabilized with a lag screw and bone plate.
D An oblique fracture stabilized with full cerclage wires and a bone plate.
E An oblique fracture stabilized with a bone plate. The plate screw crossing the fracture line is placed in lag fashion.
 Fractures and disorders of the hindlimb
203

178 Bone plate stabilization of a transverse 178

femoral fracture.
A Craniocaudal radiographic view of a transverse
femoral fracture.
B Postoperative craniocaudal view. The fracture
was stabilized with stacked cuttable plates. Two
full cerclage wires were placed on the distal
segment to compress a fissure fracture.

A B

179

A B C D E

179 Bone plate stabilization of comminuted femoral fractures.

A Comminuted diaphyseal femoral fracture.
B Stabilization with full cerclage wires and a neutralization plate.
C Stabilization with lag screws and a neutralization plate.
D Stabilization with a bridging (buttress) plate. Autogenous cancellous bone graft is placed in the defect.
E Stabilization with plate-rod fixation. An intramedullary pin is placed normograde in the medullary cavity to maintain
bone length and alignment. A plate is contoured and applied in buttress fashion on the lateral aspect of the femur. The
proximal and distal screws are bicortical. The remaining screws are monocortical. Suture material may be used gently to
move fragments into the fracture site if necessary.
204

plate is then applied in a neutralization function
(180). This method provides anatomic reduction and
ensures load sharing between the plate and bone.
However, it requires manipulation of the fragments
and there may be interference with soft tissue
attachments and blood supply.
The plate can alternatively be applied in bridging
(buttress) fashion to span the area of comminution
(181). The proximal and distal fragments are
stabilized, leaving the comminuted fragments
undisturbed within the fracture gap. This preserves

180

A B

C D
180 Comminuted femoral fracture repaired with lag screws and stacked cuttable plates
applied in neutralization function.
A Preoperative craniocaudal view.
B Preoperative lateral view.
C Postoperative craniocaudal view.
D Postoperative lateral view.
 Fractures and disorders of the hindlimb
205

soft tissue attachments and blood supply, but
also requires the plate to bear additional load until
healing occurs. The fracture heals by callus forma-
tion. When applying a plate in bridging fashion,
plate failure can occur through empty screw holes
and the cat’s activity must be restricted postopera-
tively. DCPs and cuttable plates applied in buttress
fashion have been used with success in comminuted
femoral fractures in cats22. Steel 2.4 mm LC-DCPs
may be applied in buttress fashion to comminuted
femoral fractures; however, titanium LC-DCPs are
not recommended for use in buttress fashion.
Stacking two cuttable plates increases their strength
and is helpful when applying cuttable plates
to comminuted fractures. Lengthening (Synthes
Inc.) and biological healing plates (Veterinary
Instrumentation) are devoid of screw holes centrally
and are ideal for use in buttress fashion. Autogenous
cancellous bone graft is placed in the defect to
promote healing23.
Another option for stabilization of comminuted
diaphyseal fractures is plate–rod fixation (179)24. An
intramedullary pin is placed in normograde fashion to
maintain length and alignment of the bone while the
bone plate is applied. The pin should fill approximately
35–40% of the medullary cavity. The plate is contoured
and applied in buttress fashion on the lateral aspect of
the femur. The most proximal and distal screws engage
both femoral cortices (bicortical). The remaining
screws engage only the near cortex (monocortical). A
minimum of three monocortical screws and one
bicortical screw are placed on each side of the fracture.
Comminuted fragments and the fracture hematoma in
the fracture site are not disturbed. However, suture
material may be used gently to move distant fragments
into the fracture site if necessary.

181

A B C D
181 Comminuted femoral fracture repaired with a cuttable plate applied in bridging (buttress) fashion.
Autgenous cancellous graft was placed at the fracture site.
A Immediate postoperative craniocaudal view.
B Immediate postoperative lateral view.
C 1-month postoperative craniocaudal view.
D 1-month postoperative lateral view.
206

External fixators pin–bone interface and reduce the incidence of

A type Ia external fixator applied to the lateral aspect of
the femur will provide adequate stability for most
fractures in cats (182)25. They may be applied in a
closed manner if the fragments can be reduced by
palpation or if intraoperative imaging is available to
help ensure adequate alignment. They may also be
applied after open reduction (183). A minimum of
two (and preferably three or four) transfixation pins are
placed on each side of the fracture line if the fixator
is the primary means of fracture stabilization (184).
Positive profile pins improve holding power at the
premature pin loosening. In some cases, the external
fixator is placed in conjunction with an intramedullary
pin to prevent rotation around the pin and increase the
resistance of the frame to bending forces (185). A
slightly smaller intramedullary pin may be used
to allow placement of the transfixation pins. The
external fixator frame can also be attached to the
proximal portion of the intramedullary pin (tie-in
configuration) using a connecting bar to increase
stability further26. Acrylic or traditional connecting
bars may be used.

182

A B C D

182 Stabilization of femoral diaphyseal fractures with external fixators.

A A type Ia external fixator applied to the lateral aspect of the femur. A minimum of two transfixation pins are placed on
each side of the fracture line. The fixator may be applied closed or after open reduction.
B A type Ia external fixator and full cerclage wires.
C An acrylic type Ia external fixator and an intramedullary pin.
D Tie-in configuration. The external fixator and intramedullary pin are attached proximally with a connecting bar.

183 183 A type Ia external fixator applied to the

femur after open reduction of the fracture.
The external fixator provides additional support
to the fracture repair and is easily removed when
healing is complete.
 Fractures and disorders of the hindlimb
207
184

A B
184 A type Ia acrylic external fixator applied to a transverse femoral fracture.
A Craniocaudal view.
B Lateral view.

185

A B
185 A type Ia external fixator and intramedullary pin applied to a comminuted femoral fracture.
A Craniocaudal view. Three transfixation pins are inserted on each side of the fracture line. Positive profile pins
are used to enhance the pin–bone interface and reduce pin loosening.
B Lateral view.
208
186
A Mark Rochet.)
B C
Some cats will be reluctant to use the limb for
a time after application of an external fixator to the
femur, presumably because of the pins penetrating
large muscles. The cat’s activity is restricted during the
healing period, although weight bearing and joint
motion are encouraged. Fracture healing is monitored
radiographically and the fixator is removed when
healing is complete. External fixators can generally be
removed with the cat under sedation or short-term
anesthesia.
Interlocking nails (ILNs)
4.7 mm and 4.0 mm diameter ILNs may be used to
stabilize simple and comminuted fractures of the
femur in cats (Small Interlocking Nail System,
Innovative Animal Products LLC.) 27,28. The
fracture is exposed via a limited surgical approach.
The appropriate length ILN (68–134 mm) is
selected based on radiographs and is inserted into
the medullary cavity in a normograde fashion. If
necessary, the proximal cortex and medullary cavity
can be opened using the ILN or a Steinmann pin in
a retrograde fashion, though this is more disruptive
to the fracture site. An insertion guide is then used
to place screws through the bone and the nail to
provide axial and rotational stability. 2.0 mm screws
are used for these small nails. The distal screw is
usually placed first. One or two screws are placed on
each side of the fracture line and should be at least
1–2 cm from the fracture site (186).
When stabilizing comminuted fractures, the ILN is
186 ILN fixation of femoral
fractures.
A Diagram of a comminuted
diaphyseal femoral fracture
stabilized with an ILN placed in
buttress fashion.
B, C Craniocaudal and lateral
radiographic views of a femoral
fracture stabilized with a 4.0 mm
ILN. The ILN is inserted
normograde into the femoral
medullary canal and attached to
the extension rod and drill-
aiming guide to allow insertion
of 2.0 mm screws through the
bone and ILN. One or two
screws may be placed on each
side of the fracture line.
(Radiographs courtesy of Dr.
usually placed to provide a buttress function and
the fracture fragments are minimally disturbed.
Autogenous cancellous bone graft is placed at the
fracture site if desired, or small fracture fragments can
be morselized and packed around the fracture.
Alternatively, the fragments can be anatomically
reduced with cerclage wires. The ILN then provides
a neutralization function. In most cases, however,
cerclage wires are not placed unless they contribute
significantly to the repair. The implants are generally
not removed unless complications occur.
DISTAL FEMORAL FRACTURES
Distal femoral fractures in cats include fractures of the
distal femoral growth plate, supracondylar fractures,
trochlear fractures, and condylar fractures. Clinical
signs include swelling, crepitus, and pain in the distal
femur. Most cats are initially nonweight-bearing,
though some will begin to place weight on the limb
if the injury is several days old. The diagnosis is based
on palpation and radiography of the femur.
External coaptation is ineffective in stabilizing
most distal femoral fractures because the epiphysis
is displaced by its muscular attachments. Internal
fixation allows better anatomic reduction and implant
placement stabilizes the fracture site.
With distal femoral fractures, the cruciate and
collateral ligaments (and other soft tissue support
structures of the joint) may be damaged as well,
requiring additional treatment to re-establish joint
function. In fractures involving the articular surface of
 Fractures and disorders of the hindlimb
187
A B
187 Radiographs of a Salter–Harris type I fracture of the
distal femoral growth plate.
A Lateral view.
B Craniocaudal view.
the femur, anatomic reduction, rigid fixation, and
early joint motion are essential for return of normal
joint function29,30. Inadequate treatment of intra-
articular fractures can lead to delayed or nonunion,
poor joint function, and progression of
osteoarthritis31. If an articular fracture is irreparable
or severe complications develop, limb amputation or
stifle arthrodesis may be indicated.
FRACTURESOF THE DISTAL FEMORAL
GROWTH PLATE
Cause and pathogenesis
Fractures involving the distal femoral growth plate
occur commonly in immature cats and are usually
Salter–Harris type I or II fractures (187)2,32,33. They
also occur with some frequency in young adult cats
and may result from late closure of the growth plate
after early neutering34. The epiphyseal segment is
usually displaced caudally and proximally.
Treatment and prognosis
Surgical stabilization of distal femoral growth plate
fractures is achieved through a parapatellar approach to
the stifle joint and distal femur. The epiphyseal
segment is pulled distally to achieve reduction. Smooth
pins are inserted across the growth plate to provide
stability yet allow continued growth35. Studies have
found that mild growth disturbance is common after
repair of Salter–Harris type I and II fractures of the
distal femur36–38. Fortunately, lameness is uncommon
and cats adapt well to minor changes in limb length
209
188
A B C
D E F
188 Repair of Salter–Harris type I and II fractures of the
distal femur. A Salter–Harris type I fracture of the distal
femoral growth plate. B Repair using a single
intramedullary pin placed normograde from the distal
femoral epiphysis. The pin is inserted just cranial to the
origin of the caudal cruciate ligament. The pin is advanced
to the proximal femur and countersunk below the articular
surface at the intercondylar notch of the stifle joint.
C Cross-pin fixation. Kirschner wires are inserted through
the nonweight-bearing cartilage lateral and medial to the
trochlear ridges. The wires cross and exit the cranial cortex
of the femur approximately 2 cm proximal to the fracture
line. D Parallel Kirschner wire fixation. E Lateral view
showing the proper angulation of the pins. F Dymanic
intramedullary cross-pinning (Rush pinning).
after fracture fixation39. Proper surgical technique is
essential since postoperative epiphyseal alignment is an
important factor influencing the outcome after surgical
repair36,37. Repair of Salter–Harris type I and II
fractures is usually achieved using one of several
described pinning methods (188).
210
Single intramedullary pin
A lateral parapatellar approach is made to the stifle
joint and distal femur. The patella is reflected
medially to visualize the fracture site and the
intercondylar notch. A Steinmann pin (50–70% of
the diameter of the medullary cavity) is inserted
normograde into the distal femoral epiphysis
immediately cranial to the origin of the caudal
cruciate ligament39,40. The fracture is reduced and
the pin is advanced across the fracture line and into
the medullary cavity of the metaphysis. The pin is
advanced until it engages the cancellous bone at the
proximal femur. It is then cut and countersunk
below the articular surface at the intercondylar notch
of the stifle joint. The joint is lavaged and closed
routinely. Complications with this technique are
uncommon but may include instability, infection,
pin migration into the joint, and iatrogenic fracture
of the femoral epiphysis39.
Crossed or parallel Kirschner wires
A lateral parapatellar approach is used to access the
fracture site and stifle joint. The fracture is reduced
and temporarily stabilized with pointed-reduction
forceps. A Kirschner wire (1.1–1.6 mm) is inserted
through the nonweight-bearing cartilage lateral to
the trochlear ridge and 3 mm cranial to the origin of
189
A B
189 Repair of a Salter–Harris type I fracture of the distal
femur using cross-pin fixation.
A Craniocaudal view.
B Lateral view.
the long digital extensor tendon. A second Kirschner
wire is inserted at a corresponding point just medial
to the medial trochlear ridge. They are both directed
to exit the cranial cortex of the femur approximately
2 cm proximal to the fracture line (189)1,40–42. The
Kirschner wires may be placed either parallel to each
other or in a crossed-pin fashion. Once the wires are
positioned, they are cut and countersunk below the
cartilage surface using a nail-set. The joint is lavaged
and closed routinely. The prognosis after internal
fixation of distal femoral growth plate fractures in cats
using two Kirschner wires is excellent, although
complications such as malalignment, implant failure,
nonunion, and patellar luxation have been
reported37.
Dynamic intramedullary cross-pinning
Two Kirschner wires (1.1–1.6 mm) are positioned in
a similar manner as described above for the cross-
pinning technique 40,43. However, rather than
penetrating the cranial femoral cortex proximal to
the fracture line, the wires glance off the inner
cortical wall and continue up the medullary cavity.
With this technique, the pins are often described as
having been inserted in ‘Rush fashion’. This is
achieved by first inserting the medial and lateral
Kirschner wires into the epiphyseal segment to the
level of the fracture line. The wires are inserted at a
10–15° angle to the median plane of the femur. The
fracture is reduced and the wires are alternately
pushed up the femoral shaft, directing them toward
the greater trochanter. During insertion, the
hand-chuck is only minimally rotated to prevent the
wires from penetrating the cranial femoral cortex. If
desired, the wires can be alternately tapped into
place with a small mallet rather than inserted with
the hand-chuck. Another means of assuring the wires
pass up the medullary cavity and do not penetrate
the femoral cortex is to blunt the tips of the wires
prior to insertion. This requires that the wire tracts
in the epiphyseal segment be predrilled using a small
drill bit. The wires are seated into the proximal
femoral metaphysis. A Kirschner wire of similar
length is used as a measuring-pin to ensure the wires
are adequately inserted. Kirschner wires inserted in
the dynamic intramedullary cross-pinning technique
achieve three-point fixation that provides rotational
and axial stability43.
Single Rush pin
A modification of the single intramedullary pinning
technique involves the insertion of a 2.4 mm Rush pin
into the medullary cavity44. A 2.4 mm hole is drilled
 Fractures and disorders of the hindlimb
211

into the distal femoral epiphysis immediately cranial to External fixators

the origin of the caudal cruciate ligament. The hole is
directed to the center of the growth plate. A second
2.4 mm hole is drilled in the metaphyseal surface of
the growth plate to open the medullary canal. The
fracture is reduced and the Rush pin is inserted
normograde into the drill hole and advanced across
the fracture line. The pin is advanced until it engages
the cancellous bone at the proximal femur. The hook
on the end of the Rush pin is positioned in the
intercondylar notch.
SUPRACONDYLAR FRACTURES
Cause and pathogenesis
Supracondylar fractures in adult cats are typically
transverse or short oblique and do not involve the
articular surface.
Treatment and prognosis
Repair is achieved using the pinning techniques
described for Salter–Harris fractures, external fixators,
or bone plates and screws (190).
Pinning techniques described for repair of distal
femoral growth plate fractures may be used to stabilize
supracondylar fractures in adult cats45.
External fixation may be used to stabilize simple or
comminuted supracondylar fractures if adequate
bone exists distal to the fracture site to place the
transfixation pins. External fixators may be applied in
a closed fashion if acceptable reduction can be
achieved. If open reduction is indicated, a lateral
approach to the femur is combined with a para-
patellar approach to the stifle. The fracture is reduced
and transfixation pins are placed through the femur in
a lateral to medial direction. A minimum of two pins
are placed proximally and distally to the fracture site.
The transfixation pins are then attached using acrylic.
Acrylic connecting bars are easily contoured
to accommodate the curved distal femur, are
lightweight, and eliminate the need to ensure all
transfixation pins are inserted in the same plane. They
also allow different sized transfixation pins to be used
in a single frame. A type I external fixator is suffi-
ciently strong to stabilize distal femoral fractures in
cats, particularly if the fracture is well reduced. An
intramedullary pin may be inserted to augment the
stability, although this is rarely necessary. A hybrid
type I–II external fixator frame may be used for more
distal fractures where two transfixation pins cannot be

190

A B C D E F

190 Repair of supracondylar femoral fractures.

A Cross-pin fixation.
B Dynamic intramedullary cross-pin fixation (Rush pinning).
C A type Ia acrylic external fixator. A minimum of two pins are placed proximally and distally to the fracture site.
D A hybrid type I–II external fixator and intramedullary pin for stabilization of a comminuted supracondylar fracture.
E Bone plate fixation with a reconstruction plate.
F Bone plate fixation with a mini L plate.
212
inserted into the epiphyseal segment. They are
also useful to buttress comminuted supracondylar
fractures. Rarely, a transarticular fixator is placed
across the stifle joint to support internal fixation of
a supracondylar fracture.
Bone plates and screws
Bone plates may be used to stabilize supracondylar
fractures if the epiphyeal segment is large
enough46,47. Cuttable plates, DCPs, and recon-
struction plates have been used for repair of distal
femoral fractures in cats 21,47 . Reconstruction
plates (2.7 mm) are more easily contoured to fit
the curved distal femur than standard bone plates
and can be positioned more distally on the femur
without interfering with the patella. Proper
contouring permits the insertion of three screws in
the small epiphyseal fragment of most fractures.
Mini plates can also be used to repair distal femoral
fractures in cats46. Various shapes are available
(straight, T plates, L plates) to ensure adequate
fixation of the distal fracture segment. Mini plates
also allow the insertion of small 2.0 mm screws
into the epiphyseal fragment.
CONDYLAR AND TROCHLEAR FRACTURES
Cause and pathogenesis
Condylar and trochlear fractures involve the articular
surface of the distal femur. Fractures involving a single
condyle are termed unicondylar. The medial condyle
is most commonly fractured, becoming separated
from both the femoral shaft and the lateral condyle. In
most instances, the caudal cruciate and medial
collateral ligaments remain attached to the fractured
medial condyle. Bicondylar fractures occur when the
medial and lateral condyles separate, and each is
fractured from the femoral shaft. They are often
termed ‘Y’ or ‘T’ fractures. Concurrent damage to the
cruciate ligaments or menisci is not uncommon
with bicondylar fractures. Trochlear fractures of the
distal femur may occur in conjunction with condylar
fractures and are usually transverse or oblique.
Diagnosis
Lateral, craniocaudal, and, occasionally, oblique
radiographic views are helpful to confirm the presence
of articular fractures and plan implant placement prior
to surgery.
Treatment and prognosis
Intraarticular fractures involving the femoral trochlea
or condyles require internal fixation to realign the
articular surface and preserve joint function. A
parapatellar incision is used and can be extended into
a lateral approach to the femur to improve exposure
of the supracondylar region. An arthrotomy allows
visualization of the intraarticular fractures.
If possible, screws (2.0 mm or 2.7 mm) placed
in lag fashion are used to stabilize the fractures.
Alternatively, Kirschner wires are used to hold
fragments in reduction, but they do not create
interfragmentary compression. Good anatomic
alignment is essential and gaps or steps in the articular
surface should be avoided.
Unicondylar fractures
Unicondylar fractures are repaired using inter-
fragmentary compression when possible. In a study of
experimentally induced unicondylar fractures, lack of
interfragmentary compression lead to instability and
caused delayed union, osteophyte formation, and
cartilage erosion31. A parapatellar approach to the
stifle joint is used and may be combined with a partial
horizontal capsulotomy to reduce the caudally
displaced condylar fragment. Once reduced, the
fragment is temporarily fixed with Kirschner wires or
bone forceps. Stabilization is achieved by placing a
lag screw from the femoral metaphysis into the
fractured condyle (191). Alternatively, the lag screw
may be started in the condyle and placed into the
femoral metaphysis, with care taken to avoid
damaging the articular cartilage. Ideally, the lag screw
is inserted perpendicular to the fracture line. Rotation
around the lag screw is prevented by the addition of
a Kirschner wire across the fracture line or the
placement of two screws in larger fragments. If
necessary, the lag screw may be placed transversely
into the other condyle to achieve fixation48.
Bicondylar fractures
Surgical treatment of bicondylar fractures requires
repair of both the intercondylar fracture and
the supracondylar portion of the femur (192).
A parapatellar approach to the stifle joint is used.
The two condyles are reduced and held in position
with Kirschner wires or bone-holding forceps. An
intercondylar lag screw is placed to create compression
between the condyles. Two screws provide better
rotational stability, but there is often insufficient room
for placement of two screws. Fortunately, rotation
around the lag screw is prevented when the
supracondylar portion of the fracture is stabilized.
Once the joint surface has been reconstructed, the
remaining supracondylar fracture is repaired using
crossed pins, crossed lag screws, a Steinmann pin, or
dynamic intramedullary cross-pins (Rush pinning). If
 Fractures and disorders of the hindlimb
213
191

A B C D E
191 Stabilization of unicondylar fractures of
the distal femur.
A A lag screw is placed from the metaphysis
into the fractured condyle. A Kirschner wire
is inserted to prevent rotation around the
screw (craniocaudal view).
B Lateral view.
C A lag screw and Kirschner wire are placed
from the nonarticular portion of the
condyle into the femoral metaphysis or the
intact condyle.
D Lateral radiographic view of a medial
condylar fracture of the distal femur.
E Craniocaudal radiographic view.
F Postoperative radiographic view (lateral)
of a medial condylar fracture repaired with a F G
lag screw and Kirschner wire.
G Craniocaudal postoperative view.

192 Stabilization of bicondylar fractures of 192

the distal femur.
A Fixation with an intercondylar lag screw
and dynamic intramedullary cross-pinning
(craniocaudal and lateral views).
B Fixation with a bone plate. One of the
distal plate screws is inserted in lag fashion
to compress the intercondylar fracture
(craniocaudal and lateral views).
C Fixation with an intercondylar lag screw
and a type Ia acrylic external fixator
(craniocaudal view).

A B C
214
the supracondylar portion of the fracture is
comminuted, an external fixator or bone plate applied
in buttress fashion may be applied. External fixators
may also be used as the primary means of fracture
stabilization, particularly in open or comminuted
supracondylar fractures, but these do not create
interfragmentary compression between the condyles.
A transarticular fixator may be used but is rarely
needed for additional support after internal fixation49.
Trochlear fractures
Fractures involving the femoral trochlea may be
simple (often transverse or oblique) or comminuted.
Internal fixation is required to realign and stabilize
the articular fragments (193)46. A lateral para-
patellar surgical approach is used. The fragments are
reduced to avoid gaps or steps in the articular
surface. Kirschner wires can be inserted to attach
193
A B
C D
193 Repair of femoral trochlear and articular
fractures.
A Kirschner wires are inserted and countersunk
to reattach small osteochondral fragments.
A mini L plate is applied to the lateral aspect of
the distal femur.
B, C Articular fractures are stabilized with
Kirschner wires inserted and countersunk below
the cartilage surface.
D A lag screw is inserted and countersunk
below the articular cartilage.
small osteochondral fragments to the underlying
subchondral bone. The wires are countersunk below
the articular surface with a nail-set. Those fragments
too small to stabilize are discarded. Stability is then
provided by the application of small bone plates and
screws (2.0 mm or 2.7 mm) to the lateral aspect of
the distal femur. Mini plates (Synthes) are
particularly useful and come in various shapes to
allow insertion of two screws in the distal segment.
Mini L plates and T plates are used commonly. In
cases where plate fixation is impractical, crossed lag
screws or multiple Kirschner wires may be applied.
Autogenous cancellous bone graft is placed in any
defects. Postoperatively, passive range-of-motion
exercises are used to restore joint mobility. If
external support is necessary after fixation, a
nonweight-bearing sling may be applied. Therapy is
initiated when the sling is removed. In a study of
seven cats operated on for repair of trochlear
fractures, 85% had good functional recovery46.
Comminuted articular fractures
Comminuted fractures of the distal femoral articular
surface are repaired using Kirschner wires or lag screws
(193). Osteochondral fragments are reduced and
stabilized using Kirschner wires placed through the
fragment into the subchondral bone. Lag screws can be
used to stabilize larger fragments50,51. The Kirschner
wires and screw heads are countersunk below the
articular surface to minimize cartilage damage during
joint motion50,51. Fragments which cannot be stabilized
are discarded51. Larger articular fragments may also be
stabilized using Herbert bone screws (Zimmer Inc.)52.
They have threads at both ends and no head, enabling
them to be implanted completely beneath the cartilage
surface. The threads at either end of the screw have a
different pitch so that, as the screw is tightened, the
pitch differential between the screw ends compresses
the bone fragments together. Herbert bone screws are
available in 16–30mm lengths, have a shank diameter of
1.85 mm, and a thread diameter of 3 mm or 4 mm.
Bioabsorbable implants have also been used to reattach
osteochondral fragments53. Pins made of polydioxanone
(PDS, Ethicon) and composites of polyglycolide or
polylactide (BIOFIX VET-rods, Bioscience Ltd.) are
inserted through the osteochondral fragment into
the underlying subchondral bone53,54.
 Fractures and disorders of the hindlimb
POSTOPERATIVE CARE OF
FEMORAL FRACTURES
The cat’s activity is restricted after surgery to prevent
disruption of the repair. Early passive motion and
controlled exercise are encouraged after repair of
articular fractures to maintain range of motion and
improve joint function. In cases where a transarticular
external fixator was applied to augment stabilization,
the fixator is removed as soon as the fracture site is
stable to allow initiation of physical therapy. Fracture
healing is monitored radiographically until complete.
Implants are typically not removed unless compli-
cations develop.
COMPLICATIONS OF FEMORAL
FRACTURES
Complications of femoral fracture repair include
malunion, delayed union, infection, implant failure,
stifle or hip joint stiffness, quadriceps contracture,
and sciatic nerve injury 55. The application of
a 90–90 flexion splint has been recommended for
1–2 weeks after surgery in young cats and cats with
severe trauma that are at risk for joint stiffness and
quadriceps contracture (194)56. Hindlimb ampu-
tation is often required if quadriceps contracture
develops after fracture fixation, although successful
treatment with a dynamic flexion apparatus in a cat
has been reported57. Osteoarthritis may develop
after surgical repair of articular fractures, although it
is rarely severe in cats and is minimized by good
surgical technique, anatomic reduction, rigid
fixation, and early postoperative joint motion.
194 Photograph of a 90–90 flexion splint applied to
the hindlimb of a cat. The stifle and hock joints are
maintained at 90° of flexion to prevent quadriceps
contracture and minimize joint stiffness after femoral
fracture repair.
215
PATELLAR FRACTURES
CAUSE AND PATHOGENESIS
Patellar fractures are uncommon and occur as a result
of direct trauma to the patella or, in some cases, from
extreme traction applied by the quadriceps mechanism
when the stifle joint is extended to break a fall. Patellar
fractures are typically closed and usually involve
the articular surface of the patella. Comminuted,
longitudinal, and transverse fractures of the patella can
occur, and some are minimally displaced58. Transverse
fractures are the most common type.
CLINICAL SIGNS
Cats with patellar fractures are acutely nonweight-
bearing and may have a history of a fall or
other trauma. The cat will eventually begin to bear
weight on the limb but will usually remain lame.
Many are unable to extend the stifle fully or to
support weight with the stifle in extension59. Pain,
swelling, and crepitus in the stifle joint are common
clinical signs.
DIAGNOSIS
The diagnosis of patellar fractures is confirmed
radiographically. Mediolateral, craniocaudal, and
tangential views are used to determine the type of
fracture and the presence of comminution.
TREATMENT AND PROGNOSIS
Patellar fractures are repaired to preserve the
quadriceps extensor mechanism, reestablish continuity
of the articular cartilage surface to minimize the
development of degenerative joint disease, and to
provide fixation sufficient to allow bone healing.
194
216
Conservative treatment
External coaptation may be used in some nondis-
placed fractures, maintaining the stifle in extension to
prevent movement of the fragments caused by
contraction of the quadriceps muscles. A bandage
should remain in place for 4–6 weeks. Physical therapy
is then needed to reestablish quadriceps muscle
strength and joint mobility.
Surgical treatment
In most cases, the tension created by the quadriceps
muscles necessitates internal stabilization of patellar
fractures. Internal fixation provides increased stability,
allows proper alignment of the articular surface to
minimize the development of osteoarthritis, and
allows earlier return of stifle function, thereby
decreasing muscle atrophy and loss of joint range
of motion that can occur with prolonged
immobilization37,58,60. A lateral or medial stifle
arthrotomy is performed to visualize the articular
surface of the patella. Accurate reduction of the
articular surface is important to reestablish joint
congruity. The stifle is held in extension while
reduction forceps are used to realign the fracture
fragments. Small chondral or osteochondral fragments
are discarded if they cannot be incorporated into the
repair (partial patellectomy)61. The tendon ends
are sutured to preserve the quadriceps mechanism if
a partial patellectomy is necessary. Complete
patellectomy has been reported in the cat but is not
recommended and may lead to pain, decreased stifle
function, ligament instability, osteoarthritis, and
muscle atrophy59,62.
Cerclage wiring or tension band fixation is used for
stabilization of patellar fractures (195).
Cerclage wire
A cerclage wire may be used to stabilize nondis-
placed fractures of the patella. A large-bore
hypodermic needle is used to pass a cerclage wire
(0.8 mm [20 AWG]) through the quadriceps tendon
(proximally) and the straight patellar tendon
(distally) to encircle the patella completely. The
tension band wire is positioned on the cranial surface
of the patella (tension side) to prevent displacement
of the fracture line during weight bearing.
Tightening the wire until the fracture is slightly
overreduced will create compression at the fracture
when the stifle is flexed60.
Tension band fixation
A tension band device can be used to repair transverse
and comminuted patellar fractures since it will
counteract the distracting forces created by the
quadriceps muscles60. The fragments are reduced
and a Kirschner wire is inserted normograde or
retrograde through the patella to realign the
fragments prior to placement of the tension band
wire. Predrilling with a 1.1 mm drill bit may be
necessary to place the Kirschner wires in the
extremely hard bone of the patella. The Kirschner
wire must not penetrate the caudal articular surface of
the patella, but should protrude from the patella
proximally and distally59,60. A single Kirschner wire is
usually adequate, although double Kirschner wires
minimize rotational forces between fragments. They
may be crossed or placed parallel as dictated by the
fracture lines. A cerclage wire is then placed encir-
cling the protruding ends of the Kirschner wire in
either a mattress or figure-of-eight fashion. The
cerclage wire is tightened and the pins are cut short
to minimize soft tissue trauma.
Postoperative care
Postoperatively, the cat’s activity is restricted until
clinical union is achieved. If necessary, the stifle can be
immobilized in a padded bandage for 1–2 weeks to
protect the incision site and prevent flexion of
the joint early in the healing process. However,
the bandage should be removed as soon as possible
to allow joint movement and rehabilitation of
the quadriceps muscles. Mild, passive flexion and
extension of the stifle may be started as early as 5 days
after surgery in most cases. Activity is gradually
increased starting 2 weeks after surgery. The implants
are removed once the fracture has healed if pin
migration or irritation of the surrounding soft tissues
occurs.
Complications and prognosis
Seroma formation, implant migration, and osteoarthritis
are possible complications of surgical repair of patellar
fractures. Limb function is usually good if accurate
reduction and rigid stability are achieved59.
 Fractures and disorders of the hindlimb
217

195

A B

195 Stabilization of patellar fractures.

A Cerclage wire is placed encircling the patella. A hypodermic needle may be
used to pass a cerclage wire through the quadriceps tendon proximally and the
straight patellar tendon distally. The wire is positioned on the cranial surface of
the patella to prevent displacement of the fracture line during weight bearing
(craniocaudal and lateral views).
B Tension band fixation of a patellar fracture. A Kirschner wire is inserted
normograde or retrograde through the patella to realign the fragments. A
cerclage wire is placed (mattress or figure-of-eight pattern) encircling the
protruding ends of the Kirschner wire.
218
PART 4: STIFLE DISORDERS
The stifle joint is comprised of the femorotibal and
femoropatellar joints, their common joint capsule,
and ligamentous support structures (196). The
cruciate ligaments (cranial and caudal) and collateral
ligaments (medial and lateral) provide stability to the
stifle joint. Traumatic disruption of these ligaments
and luxation of the patella (traumatic or congenital)
are common causes of stifle pain and lameness in cats.
PATELLAR LUXATION
CAUSE AND PATHOGENESIS
Congenital medial patellar luxations occur in Devon
Rex, Abyssinian, and domestic shorthair cats1–4. Most
are bilateral and may be associated with a shallow
trochlear groove, slight medial deviation of the tibial
tuberosity, and an underdeveloped medial femoral
condyle5. Coxa vara, lateral bowing of the distal
femur, and tibial torsion are not typically seen in cats
with patellar luxation6,7. A weak association between
medial patellar luxation and hip dysplasia is described
in cats8.
Patellar luxations may also occur as a result of
trauma, although the trauma is often unobserved9.
Minor trauma may produce clinical signs in cats with
previously subclinical patellar laxity. Medial luxation
is most common and may occur unilaterally or
bilaterally. Lateral luxation occurs less frequently and
196
A B
196 Feline stifle joint.
A Lateral view. B Craniocaudal view. (Photographs
courtesy of Tom Thompson.)
is usually unilateral. Patellar luxation affects both male
and female cats2. Most affected cats are less than
3 years of age, and, in one report, 66% were less
than 1 year of age2,7. Patellar luxation may also occur
secondary to femoral fracture repair, surgical
treatment of other stifle injuries, or congenital defects
affecting the femur or tibia7.
CLINICAL SIGNS
Mild patellar laxity is normal in cats. Slight subluxation
of the patella is often elicited during palpation and
rarely causes clinical signs unless aggravated by trauma8.
In many cats, patellar luxation causes no clinical signs
and is detected incidentally during physical
examination. In other cats, however, patellar luxation
causes gait abnormalities, pain, acute lameness, locking
of the limb in extension, or a crouching stance.
A review of 21 cats with patellar luxation reported
that 66% were markedly lame or had noticeable gait
abnormalites7. The lameness is intermittent in
some cats. Cranial cruciate ligament (CrCL) rupture
secondary to patellar luxation is rarely described in cats.
DIAGNOSIS
The diagnosis of patellar luxation is made by palpation
of the joint and evaluation of patellar stability.
A grading system is used to describe the clinical
severity of the patellar luxation:
• Grade I: the patella is manually luxated using
digital pressure, but reduces spontaneously when
pressure is released. Cats with grade I luxation
rarely show clinical signs.
• Grade II: the patella is manually luxated using
digital pressure or with rotation of the tibia. The
patella can be reduced easily and will remain in
place until the limb is manipulated. Not all cats
with grade II luxation show clinical signs.
• Grade III: the patella is luxated at the time of the
examination. It may be positioned into the
trochlear groove using digital manipulation, but
spontaneously reluxates. The degree of lameness
is variable with grade III luxations, but is often
persistent.
• Grade IV: the patella is permanently luxated and
cannot be reduced with digital manipulation or
rotation of the tibia. Grade IV luxations are
uncommon in cats.
Patellar luxation may also be identified on cranio-caudal
radiographic views of the stifle joint. The position of the
tibial tuberosity and development of the medial femoral
condyle are assessed on lateral and craniocaudal
radiographs. A ‘skyline’ radiographic view may be used
to assess the depth of the femoral trochlea.
 Fractures and disorders of the hindlimb
219

TREATMENT AND PROGNOSIS Retinacular imbrication

Conservative or surgical treatment may be used to
treat patellar luxation in cats. Conservative therapy is
recommended for treatment of cats without clinical
signs or if signs are mild or infrequent. Confinement
and limited activity is encouraged during bouts of
intermittent, mild lameness.
Surgical treatment is recommended for cats with
more severe luxation and those with persistent clinical
signs2,7,10. A lateral parapatellar approach is made to the
stifle joint. Depending on the severity of the luxation,
soft tissue procedures and bony reconstructive proce-
dures are used alone or in combination to restore
normal anatomy, prevent patellar luxation, and improve
stifle joint function.
Soft tissue procedures
In cats with grade II luxation, soft tissue procedures
alone are often adequate to maintain patellar reduction.
Capsular imbrication
A portion of the joint capsule is excised and the edges
are sutured to increase tension10. Monofilament,
absorbable suture material (3–0) is often used. The
lateral joint capsule is imbricated to stabilize medial
patellar luxations; the medial joint capsule is
imbricated to stabilize lateral patellar luxations.
Monofilament, nonabsorbable suture material (2–0)
is placed in the retinacular fascia (Lembert or mat-
tress pattern) to achieve imbrication (197 A)9.
Alternatively, a narrow strip of the retinacular fascia is
excised and the resultant edges are sutured. The
lateral retinaculum is imbricated to stabilize medial
patellar luxations; the medial retinaculum is imbri-
cated to stabilize lateral patellar luxations. The region
of imbrication should begin at the distal aspect of the
stifle joint and continue proximal to the patella.
Fabellar–tibial antirotational suture
An antirotational suture is used to prevent internal
rotation of the tibia and maintain proper alignment of
the quadriceps mechanism. A suture is placed around
the lateral fabella and through a hole drilled
in the tibial tuberosity (197 B). Monofilament,
nonabsorbable suture material (2-0 to 0) is often
used. An antirotational suture may also be used to
stabilize joints with concurrent CrCL rupture.
Fabellar–patellar suture
A suture is passed in a figure-of-eight pattern from
the fabella to the patella (197 C). The suture can
be passed around the patella or placed through the
patellar tendon. The suture is tightened just enough
to stabilize the patella.

197
Fabella
Fascia lata

Patella

Patella
Patellar Fabella
ligament Patella
Patellar
ligament

Tibial
Tibial tubercle
tubercle
A B C

197 Soft tissue re-constructive procedures for stabilization of patellar luxations.

A Retinacular imbrication. Suture material (mattress or Lembert pattern) is placed in the retinacular fascia from proximal to
the patella to the distal aspect of the stifle. B Fabellar–tibial antirotational suture. A suture is placed around the lateral fabella
and through a hole drilled in the tibial tuberosity. C Fabellar–patellar suture. A suture is passed in a figure-of-eight pattern
from the fabella to the patella. The suture may be passed around the patella or through the patellar tendon beside the patella.
220
Releasing incision
A releasing incision is made through the fascia on the
side opposite the luxation to relieve tension on
the tissues that may lead to postoperative reluxation.
In some cases, the releasing incision is made as part
of the surgical approach to the joint. The synovial
membrane is sutured to reduce leakage of
synovial fluid from the joint, but the fibrous joint
capsule and retinacular fascia are left open.
Bony reconstructive procedures
Trochleoplasty
Trochleoplasty techniques are used to deepen the
trochlear sulcus and improve patellar stability. Several
techniques have been described, although techniques
that preserve the articular cartilage are preferred.
• Sulcoplasty: the articular cartilage and
subchondral bone of the trochlear sulcus are
198
A B
198 Femoral sulcoplasty for stabilization of patellar
luxations. A The articular cartilage and subchondral bone
of the trochlear sulcus are removed with a file.
B Completed sulcoplasty. The procedure adequately
deepens the trochlea, but destroys the articular cartilage.
removed with a file, bone rasp, or rongeur (198).
The procedure is easily performed and adequately
deepens the trochlea, but destroys the articular
cartilage11. Techniques which preserve the
articular cartilage are preferred.
• Trochlear wedge recession12,13: a small saw is used
to excise a wedge-shaped osteochondral fragment
from the trochlea, preserving the articular surface
(199). A small amount of bone is removed from
the resultant femoral defect and from the apex of
the excised wedge of bone using a saw, scalpel
blade, or rongeur. The osteochondral fragment is
then positioned back into the defect. The replaced
wedge is thus recessed, creating a deeper trochlear
sulcus. Fixation of the wedge is not necessary. The
proximal aspect of the trochlear sulcus may not be
altered with the technique, and may need to be
widened or deepened with a small file.
199
Caudal
cruciate
ligament
Patella
Bone
cartilage
wedge
A B
199 Trochlear wedge recession.
A A saw is used to excise a wedge-shaped osteochondral
fragment from the trochlea, preserving the articular surface.
B Bone is removed from the wedge and the femoral defect
and the osteochondral fragment is replaced (recessed),
deepening the trochlear sulcus.
 Fractures and disorders of the hindlimb
221

• Block recession trochleoplasty14,15: a small saw
and osteotome are used to remove a rectangular
osteochondral fragment from the trochlear sulcus,
preserving the articular surface of the trochlea
(200). A small section of bone is removed from
the resultant femoral defect (and from the base of
the excised ostechondral block) with a rongeur
prior to replacing the fragment. Block recession
trochleoplasty increases the depth of the proximal
sulcus and recesses a larger percentage of the
articular surface than wedge recession. Care must
be taken to avoid damaging the cartilage,
especially in smaller cats.
Tibial tuberosity transposition
Transposition of the tibial tuberosity is rarely required
in cats. However, in cases of severe or recurrent
luxation, transposing the insertion of the straight
patellar ligament will align the quadriceps mechanism
(and thus the patella) over the trochlear groove to

200

A D
B C

E F G
200 Block recession trochleoplasty.
A A saw and small osteotome are used to remove a rectangular osteochondral fragment from the trochlear
sulcus (preserving the articular surface).
B, C Diagrams depicting the proper cuts performed in the trochlear sulcus.
D Photograph showing the excised osteochondral block and resultant defect in the trochlear sulcus.
E Bone is removed from the defect in the trochlear sulcus and from the base of the excised osteochondral
block with a rongeur (shaded areas).
F The osteochondral block is replaced in the defect.
G Completed block recession trochleoplasty. Block recession trochleoplasty increases the depth of the
proximal sulcus and recesses a larger percentage of the articular surface than trochlear wedge recession.
222
improve patellar stability. The tibial tuberosity is cut
with a small osteotome, beginning just caudal to the
insertion of the straight patellar ligament (201). The
osteotome is directed distally to free the tuberosity.
Alternatively, the tuberosity can be cut with a small
bone cutter. It is preferred to leave the fascial
attachments at the distal aspect of the tuberosity
intact. The tuberosity is then displaced laterally to
correct medial patellar luxation (or medially to correct
lateral patellar luxation). Alignment is confirmed
by viewing the limb from its cranial aspect. The
tuberosity is moved until the hip joint, femoral
trochlea, and tibial tuberosity are in a straight line. In
most cases, the tuberosity is only displaced a few
millimeters to achieve proper alignment. It is then
reattached using two small Kirschner wires driven
through the tuberosity and into the underlying tibia.
Care is taken not to place the Kirschner wires into the
stifle joint or into the soft tissues on the caudal aspect
of the tibia. With the tuberosity transposed, the tibia
is internally and externally rotated to confirm patellar
stability.
Prognosis
The prognosis after surgical repair of patellar luxation
in cats is good to excellent6,7. The limb may be
bandaged for 1 week after surgery, although many cats
201
A B
resent bandages and immobilization is not necessary
for a satisfactory outcome. Exercise is restricted for
4 weeks to allow healing.
CRUCIATE LIGAMENT INJURIES
CRANIAL CRUCIATE LIGAMENT INJURY
Cause and pathogenesis
The CrCL in the cat prevents stifle hyperextension,
excessive internal rotation of the tibia, and cranial
translation of the tibia (cranial draw motion)16.
Rupture of the ligament causes joint instability lead-
ing to pain, effusion, and osteoarthritis. Complete
rupture of the CrCL occurs relatively infrequently in
cats, perhaps because the CrCL is relatively larger than
the caudal cruciate ligament in the cat (unlike dogs
and humans)17. Partial tears of the CrCL are also
reported infrequently in cats, perhaps because cats
develop few clinical signs with partial tears or recover
quickly when they occur. Trauma is thought to be the
most common cause of CrCL rupture in the cat.
The exact mechanism of rupture is unknown, but
severe internal tibial rotation, stifle hyperextension, or
supraphysiologic loading of the ligament may cause
rupture. The influence of hormones, genetics, joint
inflammation, and conformation on CrCL rupture in
cats has not been evaluated. However, cats with CrCL
rupture are often overweight9.
201 Tibial tuberosity
transposition. A The tibial
tuberosity is removed with an
osteotome, beginning just caudal
to the insertion of the straight
patellar tendon. The osteotome is
directed distally to free the
tuberosity (dashed line), leaving
the distal fascial attachments intact.
B, C The tuberosity is moved
laterally (to correct medial patellar
luxation) and reattached with two
Kirschner wires inserted through
the tuberosity and into the
proximal tibia. Placing the
Kirschner wires into the stifle joint
or the soft tissues caudal to the
tibia should be avoided. The hip,
femoral trochlea, and tibial
tuberosity should be in alignment
C when the limb is viewed from its
cranial aspect.
 Fractures and disorders of the hindlimb
Clinical signs
Signs of acute CrCL rupture include a sudden
onset lameness (may be nonweight-bearing), stifle pain,
and joint effusion. The lameness usually improves
with rest, but may worsen after exercise.
Diagnosis
The diagnosis of CrCL rupture is based primarily on
clinical signs, physical examination findings, and
radiographs. Physical examination reveals a positive
cranial draw sign, positive tibial compression test,
joint pain, and stifle joint effusion (202). With
more chronic ruptures, crepitus and periarticular
thickening may be noted on palpation of the joint.
Joint laxity usually persists even in chronic cases of
CrCL rupture. A ‘click’ may be noted during
palpation and is indicative of a meniscal tear.
Radiography of the stifle may reveal joint effusion or
signs of osteoarthritis. Calcification or ossification of
the medial or lateral meniscus is reported in cats
with CrCL rupture and can be observed
radiographically18,19.
Treatment and prognosis
Treatment of CrCL rupture in the cat is either
conservative therapy or surgical stabilization.
202 Diagnosis of
CrCL ruptures.
A Cranial draw
sign.
B Positive tibial
compression test.
A B
223
Conservative therapy
Conservative therapy is the treatment of choice for
most cats with CrCL rupture. The cat is confined
to limit activity and, if necessary, placed on a diet to
reduce weight. Normal limb function and pain-free
range of motion usually return within 4–5 weeks20.
However, many cats treated conservatively will have
persistent joint laxity, mild muscle atrophy, thickening
of the joint capsule, and mild osteoarthritis20.
Surgical stabilization
Stabilization of the stifle after CrCL rupture is
recommended only in cats with persistent lameness
unresponsive to conservative therapy. Obese cats may
be reluctant to ambulate during conservative therapy
and may benefit from early surgery. The presence of
meniscal calcification alone does not warrant surgical
intervention, since some cats with this condition
have no clinical signs20. However, removal of the
mineralized meniscus is beneficial if pain and lameness
persist after conservative therapy18. Cats should
be evaluated for cardiomyopathy before being
anesthetized for surgery21. Intracapsular and
extracapsular surgical techniques have been used for
repair of CrCL deficient stifles in the cat; however,
extracapsular stabilization is simple to perform, is less
invasive, and provides good results9,16,22.
202
224

Extracapsular stabilization imbricates the lateral bony tunnel. One end of the suture is then passed
joint tissues to prevent cranial draw motion and from lateral to medial, caudal to the patellar tendon,
minimize internal rotation of the tibia. The limb is and back through the bone tunnel to the lateral
shaved and prepared from the hip to the metatarsus. side. The suture should be placed in a mattress
A hanging-limb preparation is used to allow fashion such that the free ends are positioned
manipulation of the stifle joint during surgery. A caudally, thus allowing the knot to be buried
lateral parapatellar arthrotomy is performed. A small beneath the biceps fascia.
Hohmann retractor or mosquito hemostat is placed Once the suture is properly placed through the tibial
in the intercondylar notch and over the tibial plateau crest and around the lateral fabella, it is tightened and
to displace the tibia cranially during joint exploration. secured. The stifle joint is placed in a weight-bearing
Torn remnants of the CrCL and damaged portions of position with the tibia externally rotated. The suture is
the menisci are excised. The joint is then lavaged and tightened until no draw motion can be elicited before
the joint capsule is sutured with absorbable suture the suture is secured. A pointed reduction forceps may
material (3-0) in a continuous pattern. The be used to clamp the stifle joint in the proper position
extracapsular suture is then placed. Monofilament before tightening the suture. Traditionally, the suture is
suture material is preferred; 2-0 or 0 suture material secured by tying a knot. A slip-knot may be used initially
is used for most cats. To place the extracapsular to ‘slide’ the suture into a tight position. A square knot
suture proximally, the fascia of the biceps femoris is then placed to complete the knot. Alternatively, the
muscle is elevated from the joint capsule and first throw of the knot can be clamped to hold it tight
retracted laterally and caudally. The fabella is palpable while a second throw is placed, although care is needed
just proximal to the femoral condyle at the origin of to ensure the suture material is not weakened. The knot
the gastrocnemius muscle. The suture is placed
around the fabella through the surrounding
femorofabellar ligament (203). This is best
accomplished using a strong, curved suture needle.
Needles specially designed for placing extracapsular
sutures are available as eyed-needles (Anchor
Products Co.) or with monofilament nylon suture
already swaged on (Securos Veterinary Orthopedics 203
Inc.). A taper needle is preferred to avoid damaging
the femorofabellar ligament, adjacent vessels, or the
peroneal nerve. Entrapment of the peroneal nerve in
the suture causes pain and possible neurologic
dysfunction. The curve of the needle should allow the
suture to be placed with minimal entrapment of
the soft tissue surrounding the fabella. Encircling
soft tissue will eventually result in loosening of
the suture. Once the suture is positioned around the
fabella, proper suture placement is confirmed by
placing tension on the suture and ensuring stability.
The suture should be repositioned if necessary.
Alternatively, the suture can be anchored to
the lateral femoral condyle using a suture anchor
system (Bone-Biter Anchors, Innovative Animal
Products LLC.). This technique does not require
surgical exposure of the fabella and minimizes the 203 Extracapsular stabilization of the cruciate-deficient
potential complications associated with placing the stifle joint. Monofilament suture material (2-0 or 0) is
suture around the lateral fabella. placed in a mattress pattern around the lateral fabella
To place the extracapsular suture distally, the (through the femorofabellar ligament) and through a hole
cranial tibial muscle is elevated and a hole is drilled drilled in the tibial tuberosity. The suture passes beneath
through the tibial tuberosity. The hole may be the patellar tendon. The suture is tied caudally near the
drilled transversely or at a slight angle to reduce fabella. The lateral fascia is then advanced and imbricated
stress on the suture material as is passes through the over the extracapsular suture.
 Fractures and disorders of the hindlimb
should be positioned caudally under the biceps muscle
to minimize soft tissue irritation.
Once the extracapsular suture is in place, the
lateral fascia is imbricated. Monofilament, absorbable
suture (3-0) is placed in a Lembert or vest-over-pants
pattern to tighten the lateral fascia and advance the
biceps. Alternatively, a narrow strip of the fascia can
be excised and the edges apposed to achieve
imbrication. Imbrication provides additional support
to the joint and adequately covers the knot in the
extracapsular suture with soft tissue. Care is taken not
to overtighten the tissue proximal to the patella or
patellar luxation may occur. The subcutaneous tissue
and skin are sutured routinely.
Postoperatively, the cat’s activity is restricted for
6 weeks16. Running and jumping should be avoided.
External coaptation is not required during the
postoperative recovery period.
CAUDAL CRUCIATE LIGAMENT INJURY
Isolated caudal cruciate ligament injuries are rare in cats
and may cause lameness and stifle joint pain23,24. The
diagnosis is based on palpation of a caudal draw sign,
joint effusion, and pain. Conservative management will
usually result in return of normal function9.
More often, caudal cruciate ligament ruptures occur
in conjunction with ruptures of the cranial cruciate or
collateral ligaments as a result of severe trauma to the
stifle (see Stifle luxation). The stabilizing function
of the caudal cruciate ligament is replaced using
extracapsular sutures. Large (0 or #1) monofilament,
nonabsorbable suture material is placed from a hole
drilled in the fibular head to the patellar ligament just
distal to the patella. A second suture is placed from
a hole drilled in the caudomedial tibial plateau to the
patellar ligament just distal to the patella25.
COLLATERAL LIGAMENT INJURY
CAUSE AND PATHOGENESIS
Injuries to the collateral ligaments of the stifle joint
result from trauma. The medial collateral ligament is
injured more frequently than the lateral collateral
ligament25. Concurrent meniscal injury and CrCL
tearing may occur with collateral ligament rupture.
CLINICAL SIGNS
Most cats are nonweight-bearing on the limb and
painful in the stifle region.
DIAGNOSIS
The diagnosis of collateral ligament injury is based on
physical examination findings and radiography.
The cat should be heavily sedated or anesthetized
225
to allow a complete evaluation of the joint and
proper positioning for radiographs. Stabilization
of respiratory and cardiovascular signs associated
with trauma should be performed first if necessary.
Palpation of the injured stifle usually reveals effusion
and obvious joint laxity. All ligamentous structures of
the joint are assessed during palpation. To assess
collateral ligament integrity, varus and valgus stress
is applied to the stifle with the joint in flexion
and extension25. Normally, the medial collateral
ligament is taut in stifle flexion and extension. The
lateral collateral ligament is taut in stifle extension, but
slightly lax in stifle flexion. Loss of medial collateral
ligament integrity results in valgus instability of the
stifle and excessive internal rotation of the tibia when
the joint is flexed. Loss of lateral collateral ligament
integrity results in varus instability.
Radiographic evaluation of the stifle joint may
identify intraarticular fractures or small fragments of
bone associated with avulsion injuries to the collateral
ligaments. Stress radiographs are used to confirm join
instability caused by collateral ligament disruption.
When varus or valgus stress is applied to the joint, the
joint space will appear widened radiographically if the
collateral ligament is ruptured.
TREATMENT AND PROGNOSIS
Proper treatment of collateral ligament injuries
depends on the degree of joint instability and the
severity of the ligament damage26.
• First-degree ligamentous sprains: first-degree
sprains are mild11,26. Hemorrhage and edema
are present within the parenchyma of the
ligament and a few collagen fibers may be
ruptured, but the ligament is intact. The
function of the ligament is preserved and the
joint is stable. First-degree sprains are managed
conservatively with rest and external
coaptation to support the ligament for
4 weeks during healing. A lateral splint is used
to immobilize the stifle joint. NSAIDs may be
administered to reduce swelling and control
pain, although caution is needed to avoid drug
side-effects27.
• Second-degree ligamentous sprains: the ligament
is grossly intact but its function is disrupted. Joint
instability is present and surgical stabilization is
indicated9.
• Third-degree ligamentous sprains: the
parenchyma of the ligament is disrupted or
avulsed from its point of origin or insertion on
the bone. The joint is unstable and surgical
stabilization is indicated9.
226

No studies describing the results of conservative Reattaching avulsed ligaments

therapy for treatment of second- and third-degree
collateral ligament sprains in cats have been reported;
surgical repair is preferred to prevent persistent joint
instability, pain, lameness, and osteoarthritis9,16,28.
The stifle joint is explored through a parapatellar
incision to confirm the collateral ligament damage and
evaluate other structures, including the articular
cartilage, cruciate ligaments, and menisci. Repair of
the collateral ligament is achieved by one of three
techniques:
• Primary repair of ligament.
• Reattachment of the ligament to the bone if an
avulsion injury is present.
• Replacement of the damaged ligament using
suture material16.
Primary ligament repair
With traumatic disruption of the ligament,
parenchymal damage usually precludes primary repair.
However, primary repair may be feasible in cases of
ligament laceration. Nonabsorbable suture material
(2-0 or 3-0) is placed to approximate the traumatized
ends of the ligament. A locking-loop, Bunnel–Meyer,
or continuous cruciate suture pattern may be used
(204 A)9,29.
If a large enough bone fragment remains attached to
the avulsed ligament, it is anchored to its original site
with a lag screw or divergent Kirschner wires
(204 B–D). Unfortunately, in many cases, the avulsed
fragment is too small to accommodate the implants. If
the bone fragment is too small, the ligament is
reattached to the bone using 2-0, monofilament,
nonabsorbable suture material. The suture is
placed though the ligament in a locking-loop or
Bunnel–Meyer pattern. The suture is then placed
through a bone tunnel drilled at the ligament’s
normal site of attachment (204 E). Alternatively,
a bone anchor can be used to attach the suture to the
bone at the proper location.
Ligament replacement
In most cases of stifle collateral ligament disruption,
replacement with a prosthetic ligament is necessary
(205). Even in cases where the damaged ligament
is reattached or sutured, a prosthetic ligament is
placed to protect the ligament during healing.
Nonabsorbable, monofilament suture material (0 or
2-0) is placed in a figure-of-eight pattern to restore
collateral ligament function. The suture is attached
proximally and distally at the normal anatomic

204

A B C D E
204 Collateral ligament repair.
A Primary ligament repair. Nonabsorbable suture material is placed in a locking-loop suture pattern to approximate the
traumatized ends of the ligament. The insert shows a close-up view of the locking-loop suture pattern. B Collateral ligament
avulsion. C Avulsion re-attached with a lag screw. D Avulsion re-attached with divergent Kirschner wires. E Re-attachment of
an avulsed collateral ligament with a locking-loop suture placed in the tendon and through a bone tunnel.
 Fractures and disorders of the hindlimb
227

locations of the ligament’s origin and insertion using
one of several methods:
• Bone tunnels are drilled to allow passage of the
suture. The suture is tightened with the stifle in
extension.
• Screws (2.7mm) and washers are inserted into the
ligament origin and insertion sites on the femoral
condyle and the proximal tibia. The suture is
wrapped around the screw heads (beneath the
washers) and tied with the stifle in extension (206).
• Bone anchors are inserted to attach the suture to
the bone (207).
Postoperatively, the cat’s activity is restricted for
4–6 weeks to allow healing. If tolerated by the cat,
a lateral splint is applied for several weeks to protect
the repair.

205

A B C
205 Collateral ligament replacement (prosthetic ligament placement). Nonabsorbable, monofilament suture material is
placed in a figure-of-eight pattern. A The suture is attached to the bone through bone tunnels located at the ligament’s
origin and insertion. B Figure-of-eight suture placed around 2.7 mm bone screws. Washers are used to prevent the suture
from slipping off the screw heads. C Figure-of-eight suture attached with bone anchors inserted into the cortical bone.

206 207

A B
207 A, B Stifle medial collateral ligament rupture repaired
with a prosthetic ligament. Bone anchors are used to
A B attach suture to the bone.
206 A, B Stifle medial collateral ligament rupture repaired
with a prosthetic ligament placement. Two bone screws
(with washers) are inserted into the bone at the ligament’s
origin and insertion. Suture material is placed around the
screws in a figure-of-eight pattern.
228
STIFLE LUXATION
CAUSE AND PATHOGENESIS
Stifle luxation (stifle derangement, stifle dislocation)
occurs infrequently in cats when multiple ligamen-
tous injuries lead to gross instability of the joint.
Luxation may occur bilaterally30. In some cases, the
four primary stabilizing structures of the stifle
(cruciate ligaments and collateral ligaments) are
ruptured. More commonly, the medial collateral
ligament and both cruciate ligaments are damaged.
Secondary stabilizers of the joint, including the joint
capsule, menisci, and muscles and tendons that
traverse the joint, may also be damaged25,31. Serious
vascular and neurologic damage to the limb is rare25.
CLINICAL SIGNS
Most cats with stifle luxation present after a significant
trauma. The stifle region is swollen and painful. The
majority of stifle luxations are closed, though open
wounds may be present in some cases.
DIAGNOSIS
Obvious stifle instability is present, but it is difficult
accurately to determine which ligaments are ruptured
from physical examination and radiography alone.
Radiographs are obtained to confirm the luxation and
evaluate the joint for articular fractures (208).
208
A B
208 Stifle luxation.
A Lateral view.
B Craniocaudal view.
Surgical exploration and careful examination of each
ligament are needed to confirm the extent of the
ligamentous injury25.
TREATMENT AND PROGNOSIS
The injured limb is placed in a Robert Jones bandage
for 48 hours to reduce swelling and limit motion
while the patient is stabilized. The joint is then
surgically explored through a lateral parapatellar
approach to assess the articular surface, cruciate
ligaments, and menisci. Ruptured cruciate ligaments
and damaged portions of the menisci are excised.
The medial and lateral collateral ligaments are
assessed through separate surgical approaches. Each
ligament is carefully examined and palpated while
applying stress to the limb. The joint is thoroughly
lavaged and then stabilized by transarticular pinning
or extraarticular suture stabilization. Rarely, stifle
arthrodesis is performed if damage to the articular
cartilage and joint support structures is severe and
irreparable.
Transarticular pinning with coaptation
After exploration and debridment of the joint, the stifle
joint is reduced and held in a functional, weight-
bearing position (30–40° of flexion). A 3.0 mm or
3.5 mm Steinmann pin is inserted across the joint to
 Fractures and disorders of the hindlimb
229

provide stability (209). Alternatively, a positive profile
threaded pin may be used to prevent pin migration.
The pin may be inserted in one of several ways:
• The pin is driven proximally from the distal
aspect of the tibial crest until it enters the stifle
joint through the nonarticular intercondylar area
cranial to the intercondyloid eminence. The joint
is reduced and the pin is advanced across the
joint, into the intercondylar fossa of the distal
femur, and through the femur. The pin exits the
cranial femoral cortex proximal to the patella.
The pin is cut flush with the tibia9.
• The pin is first inserted in a retrograde fashion
from the nonarticular intercondylar eminence of
the tibial plateau to exit at the distal aspect of the
tibial plateau. The joint is reduced and the
direction of pin insertion is then reversed, driving
the pin into the distal femur32,33.
• Two pins are placed. The first is positioned across
the joint from the tibia to the femur as described.
The second pin is inserted from the craniomedial
aspect of the tibial crest, through the intercondylar
area, and into the lateral femoral condyle33.
After pin placement, the joint capsule is imbricated
with absorbable, monofilament suture (2-0) and the
subcutaneous tissues and skin are closed routinely.
A lateral splint is applied to the limb to provide
additional support during the healing period and is
important in the prevention of complications33. Strict
confinement is enforced for 1 month. The transar-
ticular pin(s) and splint are removed in 4 weeks and
confinement is continued for an additional 8–10
weeks33.
Excellent results have been reported with the
use of transarticular pinning and concurrent
coaptation for the repair of stifle luxations32,33.
Reported complications include bending, migra-
tion, or loosening of the pins, iatrogenic cartilage
damage, reduced range of motion, and
osteoarthritis32,33.
Extraarticular suture stabilization
After exploration and debridment of the joint,
the arthrotomy incision and tears in the joint capsule
are sutured with absorbable, monofilament suture
material (3-0 or 2-0). Large monofilament,

209

209 Stabilization of a stifle luxation with a

transarticular pin. The joint is placed in a functional
position and a 3.0 mm or 3.5 mm Steinmann pin is
driven proximally from the distal aspect of the tibial
crest, across the stifle joint, and into the
intercondylar fossa of the femur. The pin exits the
cranial femoral cortex proximal to the patella.
230
nonabsorbable sutures (0 or #1) are then placed
outside of the joint capsule to replace the function of
the various ruptured or damaged ligaments
(210)25,34,35:
• CrCL – a suture is placed from the lateral fabella
to a hole drilled in the tibial tuberosity. Another
suture is placed from the medial fabella to the
hole in the tibial tuberosity. A third suture is
placed from the lateral fabella to the patellar
ligament just distal to the patella.
• Caudal cruciate ligament – one suture is placed
from a holed drilled in the fibular head to the
patellar ligament just distal to the patella.
Another suture is placed from a hole drilled in
the caudomedial tibial plateau to the patellar
ligament just distal to the patella.
210
A B
210 A medial view; B lateral view. Extraarticular suture
stabilization of a stifle luxation. Large monofilament,
nonabsorbable sutures are placed outside of the joint
capsule to replace the function of the ruptured ligaments.
To replace function of the CrCL, sutures are placed from
the medial and lateral fabellae to a hole drilled in the tibial
tuberosity and from the lateral fabella to the patellar
ligament. To replace function of the caudal cruciate
ligament, sutures are placed from the fibular head and the
caudomedial tibial plateau to the patellar ligament. The
medial collateral ligament is replaced with suture material
anchored with screws, bone tunnels, or bone anchors. The
joint is reduced and positioned in 150° of extension. The
collateral ligament sutures are tightened first. The sutures
augmenting the CrCL and caudal cruciate ligament are
then tightened.
• Collateral ligaments – suture material is placed in
a figure-of-eight pattern from the distal femur to
the tibial plateau, using the normal origin and
insertion points of the ligament as landmarks.
The suture is anchored to the bone using bone
tunnels, screws and washers, or bone anchors
(see Collateral ligament rupture).
All of the sutures are preplaced and the joint
is reduced. The stifle joint is positioned in a functional,
standing angle (approximately 150° of extension in
most cats) and the sutures are tightened. The
collateral ligament sutures are tightened first. The
sutures augmenting the CrCL and caudal cruciate
ligament are then tightened9.
Postoperatively, the limb is bandaged for 10–14
days. The cat’s activity is restricted for 10 weeks9. If
the cat will not tolerate long-term bandaging,
a transarticular external fixator can be placed to
provide stability (211)25,31. The fixator is removed
after 4 weeks and a soft padded bandage is applied for
an additional 4 weeks25. Restricted activity is required
to reduce complications associated with use of an
211
A B
211 A transarticular external fixator applied to stabilize the
joint after internal repair of a stifle luxation.
A Craniocaudal view.
B Lateral view.
 Fractures and disorders of the hindlimb
231

external fixator, including pin loosening, disruption
of the fixator, and fractures of the tibia and
femur31. Good clinical function is reported after use
of extraarticular suture stabilization for treatment of
stifle luxation in cats, despite a reduction in joint
flexion and mild osteoarthritis25,31.
STIFLE ARTHRODESIS
Stifle arthrodesis is rarely performed in cats but
may serve as an alternative to amputation in the treat-
ment of irreparable joint luxations, severe osteoarthritis,
comminuted intraarticular fractures, and debilitating
fracture disease36–39. Stifle arthrodesis does not
restore normal limb function, but acceptable, pain-
free function can be expected if the procedure is
performed properly. Results are best if the ipsilateral
hip is normal and the stifle is fused at an angle that
allows the foot to contact the ground without
causing excessive flexion or extension of the
opposite limb40.
The stifle is fused at an angle of 120–125° for most
cats37,38. The ideal fusion angle is determined
preoperatively by measuring the contralateral stifle joint
in a normal standing position. To compensate for bone
shortening caused by ostectomy of the femur and tibia,
5° degrees is added to the measurement obtained39.
Care must be taken not to shorten or lengthen the limb
significantly during the arthrodesis procedure.
Successful arthrodesis of the stifle requires sound
surgical technique, strict asepsis, and adherence to the
general principles of joint arthrodesis. If autogenous
cancellous graft is to be collected, a donor site is
prepared and draped. Cancellous grafting is not
essential because of the large contact area created
between the femur and tibia during arthrodesis.
Commercial allogenic graft material may also be used
or can be added to autogenous graft as an extender.
The ipsilateral proximal humerus and iliac crests are
commonly used donor sites in the cat.
A bilateral parapatellar approach to the stifle joint is
performed. Exposure is improved by ostectomy of the
tibial tuberosity. The fat pad, cranial and caudal
cruciate ligaments, medial and lateral menisci, and
intermeniscal ligaments are excised. The collateral
ligaments are preserved, if possible, to facilitate
manipulation of the limb. Kirschner wires are inserted
as markers for the ostectomies of the proximal tibia and
distal femur to ensure the proper fusion angle (212).

212
#3

#4 30°

120°

#2
30°
#1

A B C D
212 Stifle arthrodesis.
A Kirschner wire #1 is inserted in the sagittal mid-line plane of the tibia perpendicular to the long axis of the bone. Wire
#2 is inserted in the sagittal plane 30° from the first. Wire #3 is inserted in the sagittal plane of the femur perpendicular
to the long axis. Wire #4 is inserted 30° from the third wire. Ostectomy of the proximal tibia is performed parallel to wire
#2; ostectomy of the distal femur is performed parallel to wire #4 (ensuring a fusion angle of 120°). B The femur and
tibia are apposed using the Kirschner wire markers to maintain rotational alignment. Temporary reduction is maintained
with crossed Kirschner wires. Cancellous graft is placed. C Two screws are placed in lag fashion across the joint (one
from the lateral femoral condyle to the cranial–medial aspect of the tibia, the other from the medial femoral condyle to
the cranial–lateral aspect of the tibia). A small pin is placed from the proximal aspect of the trochlear sulcus into the
proximal tibia. A transverse hole is drilled through the proximal tibial crest and a tension band wire is placed.
D Alternatively, Kirschner wires may be inserted in cross-pin fashion across the joint. Cerclage wire is placed in a figure-
of-eight fashion around the ends of the Kirschner wires medially and laterally.
232
The first wire is inserted in the median plane of the
proximal tibia, perpendicular to the long axis of the
bone. A second wire is placed in the median plane 30°
from the first. A third wire is placed in the median
plane of the femur, perpendicular to the long axis. A
fourth wire is inserted 30° from the third wire. Using
an oscillating bone saw, ostectomies of the distal femur
and proximal tibia are performed to remove the
articular cartilage (exposing subchondral bone) and to
provide good bone contact between the femur and
tibia. Ostectomy of the proximal tibia is performed
parallel to the second wire; ostectomy of the distal
femur is performed parallel to the fourth wire. This will
ensure a fusion angle of 120°. The popliteal vessels and
peroneal nerve must be avoided. The femur and tibia
are apposed, using the wire markers to ensure proper
rotational alignment. Kirschner wires are inserted in a
cross-pin configuration to maintain reduction
temporarily. Cancellous bone may be removed from
the ostectomized portions of the femur and tibia and
placed at the site of arthrodesis prior to fixation.
Additional cancellous graft may be harvested from the
prepared donor site if needed.
Once the ostectomies are completed and the femur
and tibia are aligned, two screws are placed in lag
fashion across the joint. One screw is placed from the
lateral femoral condyle to the cranial–medial aspect of
the tibia. The second screw is placed from the medial
femoral condyle to the cranial–lateral aspect of the
tibia. The screws should penetrate the tibial cortex to
ensure stability. Next, a small pin is inserted from the
proximal aspect of the trochlear sulcus into the
proximal tibia, and a transverse hole is drilled
through the proximal tibial crest. A tension band wire
(0.6–0.8 mm [20–22 AWG]) is placed through the
hole in the tibia and around the proximal end of the
pin protruding from the femur.
Alternatively, Kirschner wires can be used instead of
screws. The Kirschner wires are placed in cross-pin
fashion across the joint. Cerclage wire (0.8–1.0 mm
[18–20 AWG]) is placed in a figure-of-eight fashion
around the ends of the Kirschner wires medially and
laterally to create compression36. A lateral splint or
transarticular external fixator may be applied for 4
weeks for added support36,41. The cat is restricted until
radiographic union is achieved (typically 8–10 weeks).
 Fractures and disorders of the hindlimb
PART 5: TIBIAL AND FIBULAR FRACTURES
Tibial and fibular fractures are common in the cat,
accounting for 5–19% of all fractures1–3. Most result
from various types of trauma, including automobile
trauma, bite injuries, gunshot wounds, and falling
from a great height (high rise syndrome)2–4. With
high rise syndrome, cats falling from the fourth to
the seventh storey are most likely to sustain fractures
and other injuries3,4. Because of the minimal soft
tissue coverage on the medial aspect of the tibia,
open fractures occur frequently (17–46%)4,5. Tibial
fractures are managed using a variety of fixation
methods depending on the location and configu-
ration of the fracture. More severe fractures take
longer to heal and have a higher frequency of
complications, including infection, delayed union,
malunion, and nonunion 4. Generally, fibular
fractures are not treated with internal fixation and
heal readily once the tibia is stabilized. However,
fibular head fractures causing stifle instability and
distal malleolar fractures causing tarsal instability are
often surgically repaired6.
PROXIMAL TIBIAL FRACTURES
Fractures of the proximal tibia include avulsion
fractures of the tibial tubercle or cruciate ligament,
tibial plateau fractures, and proximal metaphyseal
fractures. Salter–Harris fractures of the proximal
tibial growth plate occur in immature cats. Fracture
configuration is determined by radiographic
evaluation. Physical examination should also include
a complete evaluation of the ligamentous structures of
the stifle joint.
TIBIAL TUBERCLE AVULSION FRACTURES
Cause and pathogenesis
The tibial tubercle is the insertion point for the
straight patellar tendon. Hyperflexion of the stifle
joint can cause separation (avulsion) of the growth
plate of the tibial tuberosity in immature cats
(usually those less than 10 months of age). Bilateral
avulsions may occur. Avulsion fractures of the tibial
tuberosity are uncommon in skeletally mature
cats7,8.
Clinical signs
Clinical signs of avulsion of the tibial tubercle include
lameness, pain in the stifle region, and a limited ability
to extend the stifle joint. The displaced tubercle is
233
palpable in some cases. Cats with bilateral avulsion
often present with a crouched posture and are
reluctant to walk7.
Diagnosis
Lateral and craniocaudal radiographs of the stifle joint
confirm the diagnosis. The radiolucent line normally
present between the tubercle and the tibia prior to
fusion of the tubercle should not be mistaken for
a fracture. With an avulsion, the tibial tubercle is
displaced proximally and the patella is positioned
more proximally in the trochlear sulcus. In unilateral
cases, comparison with radiographs of the contralat-
eral limb is helpful.
Treatment
Conservative therapy or surgical stabilization of
the tubercle may be used depending on the severity
of the displacement and the chronicity of the
fracture9,10.
Conservative therapy
Strict confinement and external coaptation are
recommended for tibial tubercle avulsions if
displacement is minimal (<3 mm) and in chronic cases
when healing is evident radiographically7,11. The limb
is immobilized in a cast or padded bandage with the
stifle joint in slight extension to reduce tension in the
quadriceps muscles. Immobilizing the stifle joint in
a hyperextended position should be avoided. The
joint is immobilized for 2–3 weeks10. When the
bandage is removed, physical therapy is initiated
gradually to regain joint function.
Open reduction and stabilization
Surgical repair is recommended for treatment of
tibial tuberosity avulsion fractures with moderate or
severe displacement (>3 mm). Surgery permits
anatomic reduction of the tubercle to restore
quadriceps function and allows earlier return of
stifle flexion8,10. A parapatellar incision is made,
extending down the tibia to ensure adequate
exposure of the tubercle. The hematoma is carefully
removed from the fracture site to avoid
traumatizing the zone of dividing cartilage cells
at the physis. Extension of the stifle joint and
slow traction on the straight patellar tendon
fatigues the quadriceps muscles and allows
234
reduction of the tubercle on the proximal tibia.
The tubercle is reattached using one of several
methods (213).
• Ligament–bone suture technique: nonabsorbable,
monofilament suture material (2-0 or 0) is placed
in a locking-loop or Bunnel–Meyer type suture
pattern in the distal portion of the straight
patellar tendon. The suture is then placed
through holes drilled in the bone of the proximal
tibia to reattach the patellar tendon at its
insertion. This technique is particularly useful for
stabilization of small bone fragments.
• Cerclage wire fixation: two holes are drilled from
lateral to medial through the avulsed tubercle,
one proximal and one distal. Corresponding holes
are also drilled in the proximal tibia. Two small
wires (0.6 mm [22 AWG]) are placed through
the holes to cerclage the fragment in place.
Because of the soft bone in young cats, the wires
can tear through the bone, resulting in a loss of
fixation.
• Kirschner wire fixation: two Kirschner wires are
driven through the tubercle and into the tibia.
The wires are placed at divergent angles. Seating
213
A B
213 Stabilization of tibial tubercle avulsion fractures.
A Avulsion of the tibial tubercle. The tubercle is displaced proximally.
B Ligament–bone suture technique.
C Cerclage wire fixation.
D Kirschner wire fixation.
E Tension band fixation.
the wires into the caudal tibial cortex will
increase holding power. Care is taken to avoid
placing the wires into the proximal physis or
stifle joint.
• Tension band wire fixation: application of a tension
band to the avulsed tubercle will counteract the
pull of the quadriceps muscles and is the preferred
method of fixation8,10. Two small Kirschner wires
are placed through the tubercle and into the tibia.
Orthopedic wire (0.6–0.8 mm [20–22 AWG]) is
then placed in a figure-of-eight fashion around the
exposed ends of the Kirschner wires and through a
hole drilled more distally in the tibia.
Postoperatively, the cat is confined and the limb is
immobilized in a soft padded bandage for 2 weeks.
The bandage is then removed and exercise is restricted
for an additional 2 weeks. Physical therapy is initiated
to promote joint motion. In immature cats, implants
are removed as soon as healing is complete to help
avoid premature closure of the growth center and
disfiguration of the proximal tibia7,10. The prognosis
for limb function after repair of an avulsion fracture of
the tibial tuberosity is good to excellent if the
C D E
 Fractures and disorders of the hindlimb
235

condition is treated early and anatomic reduction and
rigid fixation are achieved. Complications are
uncommon and typically result from implant failure or
growth abnormalities7. Pin bending or migration,
wire breakage, avulsion of the tuberosity from the
implants, and patellar luxation may occur9,11.
Flattening and distal translocation of the tibial
tuberosity is common after fixation, but causes
minimal loss of function in most cases7.
CRUCIATE LIGAMENT AVULSION FRACTURES
Avulsion fractures of the CrCL occur rarely in cats,
and usually in conjunction with severe trauma to the
stifle joint8. A positive cranial draw motion, joint
effusion, and pain are detected on palpation.
Radiographically, a small bony fragment may be visible
within the joint. A stifle arthrotomy is indicated if
bone fragments are observed within the joint on
radiographs. In most cases, the bone fragment is too
small to allow primary fixation and it is removed along
with the cruciate ligament. The cruciate-deficient
stifle is then stabilized with extracapsular sutures (see
Cranial cruciate ligament repair).
TIBIAL PLATEAU AND PROXIMAL GROWTH
PLATE FRACTURES
Cause and pathogenesis
Fractures of the tibial plateau often involve the articular
surface and may occur as an extension of oblique or
longitudinal fractures of the tibial metaphysis.
Salter–Harris fractures of the proximal tibial growth
plate are typically type I or II fractures12.
Clinical signs
The cat is typically nonweight-bearing on the limb,
and pain, swelling, and crepitus are evident on
palpation of the stifle joint.
Diagnosis
The diagnosis is confirmed by radiography. Oblique
radiographic projections may help to reveal
intraarticular fractures.
Treatment and prognosis
If the fracture can be anatomically reduced in a closed
manner, external coaptation may be applied for
3–4 weeks until union occurs. Lateral splints and full
casts have been used. However, in most cases, internal
fixation is indicated to reduce the fracture anatomically
and stabilize it adequately. Articular fractures are
surgically repaired to ensure accurate reduction and
prevent gaps or steps in the articular surface.
A craniomedial approach to the proximal tibia and
stifle is performed. A second craniolateral incision is
helpful in some cases8. The fracture is reduced by
careful manipulation of the fragments to prevent
injury to the growth plate in immature cats. Fixation
is achieved using an intramedullary pin, Kirschner
wires, or small screws (214). The implants should not
enter the joint. In immature cats, Kirschner wires may

214

A B C D E F

214 Stabilization of fractures of the proximal tibial growth plate and tibial plateau.
A Lateral and craniocaudal views of a fracture of the proximal tibial growth plate (Salter–Harris type I).
B Intramedullary pinning. C Kirschner wires in cross-pin configuration.
D Dynamic intramedullary pinning. E Lag screw fixation.
F Two screws placed in lag fashion to compress an articular fracture of the proximal tibial plateau.
236
be placed in cross-pin or dynamic cross-pin configu-
ration to stabilize growth plate fractures13–15. In
mature cats, Kirschner wires or lag screws (2.7 mm)
are used. Articular fragments are stabilized with lag
screws if possible, or with small Kirschner wires.
Fixation of the fibular head is performed only if it is
needed to provide additional stability or to restore
lateral collateral ligament function. In some cases, it is
helpful to place a plate in buttress fashion on the
proximal tibia to support the tibial plateau and
stabilize the metaphyseal portion of the fracture, if
present10.
Postoperatively, the limb is immobilized in a soft
padded bandage for 1–2 weeks. The bandage is then
removed and the patient’s activity is restricted until
union is complete.
PROXIMAL METAPHYSEAL FRACTURES
Cause and pathogenesis
Fractures of the proximal tibial metaphysis are often
transverse or short oblique. Longitudinal fractures
may extend into the stifle joint. In some cases,
impaction of bone at the fracture site occurs.
Treatment
Closed reduction and stabilization
In many cases the fracture can be reduced closed. If
the fracture configuration is inherently stable,
215
A B
stabilization is provided by an external splint, closed
intramedullary pinning, or an external fixator (215).
• External coaptation. The lateral splint or cast
must immobilize the stifle joint adequately.
Rotational forces may not be controlled with
external coaptation.
• Closed intramedullary pinning. A small stab
incision is made medial to the insertion of the
straight patellar tendon. The stifle is flexed 90°
and a Steinmann pin is started at the medial
aspect of the tibial plateau (approximately 5 mm
caudal to the point of the tibial tubercle)16. The
fracture is reduced and the pin is inserted along
the medial tibial cortex and seated into the distal
metaphysis. A second pin of equal length (or
intraoperative radiograph) is used to measure the
depth of pin insertion. The pin is then retracted
5 mm, cut short with a pin cutter, and reseated
using a countersink and mallet to reduce trauma
to the stifle.
• Closed application of an external fixator. A type
Ia external fixator may be applied to the proximal
medial aspect of the tibia if at least two to three
transfixation pins can be inserted proximal to the
fracture17,18. Acrylic fixators allow more freedom
in pin placement and are lighter than traditional
metal fixators. The fixator is easily removed when
healing is complete.
215 Stabilization of proximal metaphyseal tibial fractures
after closed reduction.
A Closed insertion of an intramedullary pin. The pin is cut
and countersunk to reduce trauma to the stifle.
B Application of a type Ia acrylic external fixator. A
minimum of two transfixation pins are placed on each side
of the fracture.
 Fractures and disorders of the hindlimb
237

Open reduction and stabilization
Surgical fixation is required if the fracture cannot
be adequately reduced closed or if rotational
forces are not controlled with a splint or single
intramedullary pin. Methods of open fixation useful
for repair of proximal metaphyseal fractures include
intramedullary pins and cerclage wires, lag screw
fixation, external fixators, and small bone plates and
screws (216).
• Intramedullary pinning: a Steinmann pin is
inserted normograde from the medial aspect of
the tibial plateau19,20. Retrograde insertion is also
feasible, although the pin should be directed
toward the craniomedial aspect of the tibial
plateau to avoid injury to the patellar tendon or
cruciate ligaments1,20. Cerclage wires may be
used to stabilize bone fragments and control
rotational forces in long oblique fractures
(216 A). To prevent the cerclage wires from
slipping on the conical proximal tibia, the bone
may be notched with a file or a Kirschner wire
can be placed across the bone to support the
cerclage wire.
• Lag screw fixation: a single lag screw or two lag
screws placed in a crossed-screw fashion can be
used to stabilize some proximal metaphyseal
fractures (216 B–D). In most cases, the screws are
inserted from the tibial plateau into the cortical
bone of the tibia. A buttress plate can be applied to
protect the screws from excessive forces if necessary.
• External fixator: as with closed application, an
acrylic external fixator can be applied to the
proximal–medial aspect of the tibia if at least two
to three transfixation pins can be inserted
proximal to the fracture (215 B)17,18. A type Ia
fixator is mechanically strong enough for most
metaphyseal fractures in cats. The fixator is
removed when healing is complete.
• Bone plate and screws: a small DCP, cuttable plate,
or mini plate (T plate or L plate) accommodating
2.0mm or 2.7mm screws is applied to the medial
aspect of the tibia (216 E)21,22. At least three
screws should be placed on each side of the
fracture. The plate may serve as a neutralization,
buttress, or compression plate depending on the
fracture configuration and reduction.

216

A B C D E

216 Stabilization of proximal metaphyseal tibial fractures after open reduction.

A Intramedullary pin (placed normograde) and full cerclage wires. The bone of the tibial crest is notched to prevent
the cerclage wires from slipping.
B A single screw placed in lag fashion. A Kirschner wire is inserted to prevent rotation around the screw.
C Two screws placed in cross-screw fashion.
D A lag screw and Kirschner wire placed across the metaphysis to compress a fracture extending into the stifle joint.
E A bone plate applied to the medial aspect of the proximal tibia to stabilize a comminuted metaphyseal fracture. One
of the plate screws may be placed in lag fashion across the fracture line. T plates and L plates are commonly used to
stabilize metaphyseal fractures.
238
Postoperative care
Postoperatively, the limb is immobilized in a soft
padded bandage for 1–2 weeks. The bandage is then
removed and the patient’s activity is restricted until
union in complete.
DIAPHYSEAL TIBIAL FRACTURES
Diaphyseal tibial fractures are very common in cats.
TREATMENT AND PROGNOSIS
Diaphyseal tibial fractures are amenable to repair
using numerous methods5.
External coaptation
Splinting and casting are often used to stabilize tibial
fractures that have minimal displacement, and
fractures in young kittens. The presence of an intact
fibula increases the chances of success with external
217
A B
217 Stabilization of a comminuted tibial fracture with
external coaptation.
A Craniocaudal view of a comminuted tibial fracture
stabilized with a full cast. The fibula is intact, which
prevents collapse at the fracture site and controls
rotational and shearing forces.
B Craniocaudal view of the fracture after 4 weeks in a
cast. Healing is evidenced by mineralizing callus at the
fracture site.
coaptation, since the fibula serves as an internal splint,
preventing collapse at the fracture site and helping to
control rotational and shearing forces (217). Rarely,
fracture of the fibula can occur after treatment of tibial
fractures with external coaptation4. Since complete
immobilization of the stifle joint is difficult, proximal
metaphyseal and diaphyseal fractures are more
difficult to stabilize with external coaptation than
more distal fractures. The splint or cast is applied with
the stifle and hock joints in weight-bearing, functional
positions. When the coaptation device is removed,
physical therapy may be required to restore full
function of the stifle and hock joints.
Intramedullary pinning
Intramedullary pinning is a common and typically very
successful technique for repair of tibial fractures
(218)5. The pin provides control of bending forces at
218
A B C
218 Stabilization of tibial disphyseal fractures with
intramedullary pinning.
A A single intramedullary pin is inserted after closed or
open fracture reduction. Normograde pinning is preferred
to avoid damage to the stifle joint. A single intramedullary
pin does not control rotational forces at the fracture site,
but may be effective if the fracture fragments interdigitate.
B An oblique tibial fracture stabilized with an
intramedullary pin and full cerclage wires.
C A comminuted tibial fracture stabilized with an
intramedullary pin and a type Ia external fixator.
 Fractures and disorders of the hindlimb
the fracture site and maintains proper bone length.
The relatively straight tibia in the cat generally permits
easy insertion. However, a single intramedullary pin
will not prevent rotation at the fracture site.
Closed pinning
Closed pinning is used if the fracture can be satisfactorily
reduced with minimal trauma to the overlying soft
tissues and if interdigitation of the fracture segments will
provide rotational stability with a single intramedullary
pin16. The pin is inserted in a normograde fashion from
the proximal end of the tibia and should fill 60–70% of
the medullary cavity. The stifle is flexed 90° and the pin
is placed through a stab incision in the skin just medial
to the patellar tendon. It enters the proximal, medial
aspect of the tibial plateau approximately 5mm caudal to
the point of the tibial tubercle. It is inserted along the
medial tibial cortex and seated into the distal metaphysis.
Once the pin is fully seated distally, it is retracted
approximately 5mm, cut short, and then reseated using
a counter-sink and mallet. A type Ia external fixator can
be applied to the medial aspect of the tibia if additional
stability is needed.
Open reduction and pinning
Open reduction and pinning is necessary in some cases
to achieve anatomic reduction and to allow the
insertion of cerclage wires to control rotation at the
fracture site19. A craniomedial approach to the tibial
shaft is performed to allow visualization of the fracture
and reduce the fragments. Care is taken to prevent
undue injury to the soft tissues. Once the fracture is
219 Stabilization of tibial
diaphyseal fractures with external
fixators.
A A type Ia external fixator.
Postive profile pins enhance
holding at the pin–bone interface.
B A type IIa external fixator. All of
the transfixation pins are full pins.
C A type IIb acrylic external
fixator. Both full and half pins are
inserted.
A B
239
reduced and temporarily stabilized with bone clamps,
the intramedullary pin is inserted normograde as
described for closed pinning. Alternatively, the pin
may be inserted in a retrograde fashion starting at the
fracture site. Retrograde insertion is easier to perform;
however, the shape of the medullary cavity determines
where the pin will exit the tibial plateau. Damage to
the patellar tendon, cruciate ligaments, or articular
cartilage may occur20, 24. The effects of retrograde
pin insertion in the tibia have been evaluated in
the dog1,23. A study investigating retrograde
tibial pinning in cats found injury to the straight
patellar tendon occurred in most cases and was not
recommended20, 24. Once the pin is in place, ancillary
fixation with cerclage wires or an external fixator can
be applied if needed. Open fixation also allows the
placement of bone graft to promote healing,
particularly in comminuted fractures25.
Postoperatively, a soft padded bandage may be
applied for several days to reduce swelling. The patient’s
activity is restricted until bony union is complete.
External fixators
External fixators may be used for stabilization of most
tibial fractures and are generally well tolerated by cats
(219)17. They are particularly useful in the repair of
comminuted fractures, open or infected fractures,
and nonunion fractures, as they provide rigid fixation
without placing implants near the fracture site17,18. If
the fragments can be reduced adequately, the fixator
is applied in a closed fashion. In other cases,
a minimal approach to the fracture is performed to
219
C
240
allow reduction of the fragments before applying the
fixator. Cerclage wires may be used to reduce the
fragments primarily if an open approach is used.
However, in most cases, the fragments are aligned
and temporarily stabilized with small clamps, which
are removed once the fixator is in place.
Type Ia (unilateral) frames are easily applied to the
medial or craniomedial aspect of the tibia and are
sufficiently rigid to stabilize most cat fractures.
The fixator may be used in conjunction with an
intramedullary pin (218 C). The intramedullary pin
aligns the fragments, preventing collapse of the
fracture site, while the fixator provides resistance
to bending and rotational forces. Type II frames
(bilateral, uniplanar) may be used in severely
comminuted fractures, but cause more soft tissue
trauma (220). Ring fixators may also be used for
repair of tibial fractures. In most cases, a hybrid ring
fixator is used with a ring placed at the distal aspect of
the tibia and traditional linear connecting bars placed
proximally (221).
Acrylic, carbon fiber, or metal connecting bars
may be used. The lightweight acrylic and carbon
fiber connecting bars are ideal for use in cats. Double
220
A B
connecting bars are rarely needed. At least three
transfixation pins are placed on each side of the
fracture. The cat’s activity is restricted to prevent
accidental damage to the fixator frame. The fixator is
removed when the bone is radiographically healed.
Bone plates and screws
Bone plates are typically applied to the medial surface
of the tibia and may be used in compression,
neutralization, or bridging (buttress) function
depending on the fracture configuration (222).
A medial approach is used, with care taken to preserve
blood supply and soft tissue attachments where
possible26. The fracture is reduced and stabilized with
clamps if possible. Cerclage wires or lag screws can be
placed to stabilize fragments, or the plate can be
applied over the area of comminution in a bridging
fashion. Cuttable plates and 2.7 mm DCPs are often
used21. 2.0 mm mini plates are often too short for use
in diaphyseal fractures in cats. The principles of
plating must be followed, including insertion of at
least three screws on each side of the fracture.
Plate–rod fixation is useful for stabilization of severely
comminuted tibial fractures27.
220 A, B Stabilization of a tibial
diaphyseal fracture with a type IIa
external fixator. Full and half pins are
inserted. Positive profile pins are used
to enhance the pin–bone interface
and prevent premature pin loosening.
 Fractures and disorders of the hindlimb
241
221

A B
221 A hybrid external ring fixator applied to the tibia to stabilize a comminuted
diaphyseal fracture (Photos courtesy of Dr. Robert Radasch.)
A Medial view.
B Cranial view.

222 Stabilization of tibial 222

diaphyseal fractures with bone
plates.
A A bone applied in compression
function for stabilization of a
transverse fracture.
B A bone plate applied in
neutralization function after
reconstruction of a comminuted
fracture with full cerclage wires.
C A bone plate applied in
neutralization function after
reconstruction of a comminuted
fracture with lag screws.
D A bone plate applied in bridging
(buttress) function. Cancellous
bone graft is placed in the
fracture gap.

A B C D
242
ILN fixation
A 4.0 mm ILN may be used to stabilize tibial
diaphyseal fractures in some cats (Small Interlocking
Nail System, Innovative Animal Products LLC.)28,29.
The fracture is exposed via a limited surgical approach.
The ILN is inserted into the medullary cavity and
across the fracture line in a normograde fashion,
ensuring that the end of the ILN is countersunk
below the surface of the tibial plateau to avoid trauma
to the femoral condyle. The drill-aiming guide is
attached to the tibial extension rod on the end of the
ILN to allow insertion of 2.0 mm screws through
the bone and nail. In most cases, the distal screw is
inserted first. One or two screws are placed on each
side of the fracture line. The screws should be at least
1 cm from the fracture site.
DISTAL TIBIAL AND MALLEOLAR
FRACTURES
DISTAL TIBIAL METAPHYSEAL AND GROWTH
PLATE FRACTURES
Treatment and prognosis
Fractures of the distal metaphysis (including growth
plate fractures in immature cats) are often managed
by external coaptation30,31. These fractures tend to
heal quickly, probably due to the cancellous bone
in the metaphysis. The fracture is reduced and a cast
or lateral splint applied until union in complete.
In some cases, however, open techniques are needed
to reduce the fragments adequately and achieve
stabilization (223).
Cross-pin fixation
Two Kirschner wires are inserted from the lateral and
medial malleoli across the fracture line, and into the
223
A B C D
tibia. The wires should cross proximal to the fracture
line and exit the tibial cortex13.
Dynamic intramedullary cross-pinning
(Rush pinning)
Two Kirschner wires are inserted from the lateral and
medial malleoli at a 10–15° angle to the median plane
of the tibia. The fracture is reduced and the wires are
alternately pushed up the tibial shaft. The wires are
inserted either by pushing the hand-chuck with
minimal rotation, or tapping with a small mallet to
prevent them from penetrating the tibial cortex. The
wires can also be prevented from penetrating the
cortex by blunting the tips of the Kirschner wires prior
to insertion. Holes are then drilled in the malleoli to
permit insertion of the blunted wires. The wires are
seated into the proximal tibial metaphysis, using a wire
of similar length as a measuring pin. Dynamic
intramedullary pins achieve three-point fixation with
rotational and axial stability15.
Single intramedullary pin
A single Steinmann pin is inserted in a normograde
fashion from the proximal tibia, across the fracture line,
and into the small epiphyseal segment. Retrograde
insertion of the pin from the fracture site may also be
used, though damage to the straight patella tendon is
likely20. Rotation at the fracture site may not be
adequately controlled with a single pin, and the bone
purchase in the small epiphyseal segment is often
limited. A variation of this technique is to insert the
Steinmann pin through the tarsocrural joint and into
the medullary cavity of the tibia. Satisfactory results
have been reported, but the technique damages
the articular cartilage and should be avoided if possible.
223 Stabilization of distal tibial growth plate and
metaphyseal fractures.
A Cross-pin fixation. The Kirschner wires cross proximal to
the fracture line and exit the tibial cortex.
B Craniocaudal radiographic view of a distal tibial fracture
stabilized with cross-pin fixation.
C Dynamic intramedullary pinning. Three-point fixation
provides rotational and axial stability.
D Single intramedullary pinning. A single Steinmann pin is
inserted normograde or retrograde. Rotation at the fracture
site may not be adequately controlled with a single pin and
bone purchase in the epiphyseal fragment is limited.
 Fractures and disorders of the hindlimb
243

External fixator MALLEOLAR FRACTURES

Rarely, a transarticular external fixator is applied across
the tarsocrural joint to provide temporary support for
metaphyseal and epiphyseal fractures32. A fixator may
also be used to stabilize comminuted articular fractures
of the distal tibia. If possible, the fixator is removed in
3–4 weeks to minimize damage to the tarsocrural joint.
Postoperative care and prognosis
A soft padded bandage or splint may be applied
postoperatively for additional support if needed. The
cat’s activity is restricted until bony union is complete.
Potential complications of distal tibial fractures include
pin migration, implant failure, irritation to the skin
over the implants, malunion, and delayed union. The
implants may be removed if complications develop.
Fractures of the lateral and medial malleoli lead to
instability of the tarsocrural joint and subsequent
osteoarthritis and pain if not properly repaired. If the
malleolus is minimally displaced, external coaptation
may be sufficient to restore joint function. In many
cases, however, internal stabilization using Kirschner
wires, small screws placed in lag fashion, or tension
band wire fixation is indicated to provide rigid fixation
(224, 225). The implants are inserted through the
malleolus (after reduction) and through both cortices
of the tibia. The limb is placed in a padded bandage or
splint after surgery. Because of the minimal soft
tissue coverage over this region, the implants may
need to be removed once the fracture has healed if
complications occur.

224

A B C D

24 Stabilization of lateral malleolar fractures. A Avulsion fracture of the lateral malleollus. B Stabilization with a screw
and Kirschner wire. C Stabilization with two Kirschner wires. D Stabilization with tension band wire fixation.

225

A B C D
225 Stabilization of medial malleolar fractures.
A Avulsion fracture of the medial malleolus. B Stabilization with a screw and Kirschner wire. C Stabilization with two
Kirschner wires. D Stabilization with a tension band fixation.
244

PART 6: TARSAL, METATARSAL, AND

PHALANGEAL INJURIES

Fractures and luxations of the tarsus, metatarsus, and
phalanges occur as a result of trauma1. The tarsus
consists of numerous joints and their supporting
ligaments (226, 227). From proximal to distal, the
joints of the hind foot include:
• Tarsocrural joint: articulation between the tibia
and fibula and the talus and calcaneus.
• Talocrural joint – between the talus and tibia.
• Talocalcaneal joint – between the talus and the
calcaneus.
226
• Intertarsal joints: articulations between the tarsal
bones.
• Talocalcaneal joint – between the talus and
calcaneus.
• Talocalcaneocentral joint – between central tarsal
bone and the base of the talus and calcaneus.
• Calcaneoquartal joint – between the calcaneus
and the fourth tarsal bone. The combined
calcaneoquartal and talocalcaneocentral joints are
often referred to as the proximal intertarsal joint.
• Centrodistal joint – between the central tarsal
bone and tarsal bones I, II, and III. This is
often referred to as the distal intertarsal joint.

226 Feline tarsus.

A Lateral view.
B Dorsal view.
C Plantar view. (Photographs courtesy of Tom
A B C Thompson.)

227 227 Diagram of the

feline tarsus and
Calcaneus metatarsus.

IV III II
Talus

Central tarsal
bone I II III
IV
}
Tarsals

III II

II
I IV III
A Dorsal view.
B Plantar view.
C Medial view.
D Lateral view.

}
III
III
V IV III IV V
II Metatarsals Sesamoid
V
II III IV
bones
Proximal phalanx

Middle phalanx

Distal phalanx
} Digit

A B C D
 Fractures and disorders of the hindlimb
245

• Tarsometatarsal joints – between the distal tarsal Tension band fixation

bones and metatarsal bones.
• Metatarsophalangeal joints – between the
metatarsal bones and first phalanges.
• Interphalangeal joints – between phalanges.
FRACTURES OF THE TARSUS
CALCANEAN FRACTURES
Cause and pathogenesis
Calcanean fractures are uncommon in cats and cause
disruption of the extensor apparatus for the tarsus.
Fractures occur more often near the base of the
calcaneus than in the shaft or tuber.
Clinical signs
The cat may present either nonweight-bearing or
walking with the foot in a plantigrade stance.
Treatment and prognosis
External coaptation of calcanean fractures is successful
in some cases. The hock is immobilized in extension to
reduce the distracting force applied to the calcaneus by
the common calcanean tendon. However, the common
calcanean tendon often displaces the proximal fragment
proximally and internal fixation is needed properly to
reduce and stabilize the fracture. Several methods of
internal fixation can be used (228).
Tension band fixation is the preferred method of
fixation because it converts the tensile force applied
by the common calcanean tendon into compressive
force to encourage healing. The cat is prepared for
surgery using a hanging-limb preparation. A
plantarolateral approach to the calcaneus is
performed. The superficial digital flexor tendon is
reflected medially to allow normograde insertion of
Kirschner wires into the calcaneus. Two Kirschner
wires (1.1 mm diameter) are placed from the
plantarlateral and plantarmedial aspects of the
calcanean tuber, driven distally across the fracture site,
and seated into the base of the calcaneus. A hole is
then drilled from lateral to medial across the base of
the calcaneus. Orthopedic wire (0.6 mm [22 AWG])
is placed in a figure-of-eight pattern through the hole
and around the proximal ends of the Kirschner wires
protruding from the calcanean tuber. The wire is
tightened and the twist is bent over and placed against
the cortex of the bone to minimize irritation to the
overlying soft tissues. The Kirschner wires are bent
over to stabilize the wire and reduce irritation to the
superficial digital flexor tendon.

228
Calcaneus

IV Tarsal
bone

A B C D
228 Stabilization of calcanean fractures.
A Lateral and plantar views of a fracture of the calcanean tuber stabilized with a tension band wire fixation. Orthopedic
wire is placed in a figure-of-eight pattern around the proximal ends of the Kirschner wires and through a hole drilled in
the base of the calcaneus. The Kirschner wires are bent over to stabilize the wire and reduce irritation to the superficial
digital flexor tendon. B Lateral and plantar views of a calcanean body fracture stabilized with a tension band wire fixation.
A Kirschner wire is inserted normograde from the calcanean tuber into the base of the calcaneus and countersunk into the
tuber. A figure-of-eight wire is passed through two holes drilled in the base of the calcaneus and in the tuber calcaneus.
This technique reduces irritation of the superficial digital flexor tendon. C Plantar view of a fracture of the base of the
calcaneus stabilized with a tension band wire fixation. A Kirschner wire is inserted normograde from the tuber calcaneus
into the fourth tarsal bone. The figure-of-eight wire is then placed through holes drilled in the tuber calcaneus and the
fourth tarsal bone. D Plate fixation of a calcanean body fracture.
246
Alternatively, one or two Kirschner wires can be
inserted normograde from the calcanean tuber into
the base of the calcaneus. Two Kirschner wires
provide greater rotational stability. The Kirschner
wires are countersunk into the tuber. The figure-of-
eight wire is then passed through two holes drilled
from lateral to medial in the base of the calcaneus and
in the tuber calcaneus. Countersinking the Kirschner
wires and placing the figure-of-eight wire through
a bone tunnel in the tuber avoids irritation to the
superficial digital flexor tendon.
If the fracture is at the base of the calcaneus, one
or two Kirschner wires are inserted normograde from
the tuber calcaneus, through the base of the calcaneus
across the calcaneoquartal joint, and into the fourth
tarsal bone. The figure-of-eight wire is then placed
through holes drilled in the tuber calcaneus and the
fourth tarsal bone.
Plate fixation
A small bone plate may be applied to the lateral aspect
of the calcaneus, although this is rarely necessary in
cats. Mini plates and cuttable plates (with 2.0 mm
screws) may be used. Small lag screws or Kirschner
wires are placed to stabilize comminuted fragments at
the base of the calcaneus if necessary.
Postoperative care
Postoperatively, the limb is placed in a soft padded
bandage for several days to reduce swelling. The cat’s
activity is restricted until union is complete. A lateral
splint may be applied for 3–4 weeks to provide
229
A B
229 Stabilization of talar fractures.
A Stabilization of a trochlear ridge fracture. Two Kirschner wires are inserted through the osteochondral fragment and
countersunk below the cartilage surface. B Lateral and dorsal views of a talar neck fracture stabilized with a positional
screw inserted from the head of the talus into the calcaneus. C Medial and dorsal views of a fracture of the base of the talus
stabilized with two Kirschner wires placed in cross-pin fashion.
additional stabilization if needed for comminuted
calcanean fractures.
TALAR FRACTURES
Fractures of the talus are relatively common in cats and
may involve the neck, body, base, or trochlear ridges.
Comminuted fractures occur frequently. Fractures of
the trochlear ridges (medial or lateral) are intraarticular.
Diagnosis
The diagnosis is based on careful radiographic
evaluation of the joint. Oblique views with the joint
flexed and extended may help confirm the presence of
a fracture.
Treatment and prognosis
External coaptation
Fragments are often too small for internal fixation and
the fractures are treated by external coaptation. A cast
or lateral splint is placed for 4–6 weeks. The joint
should be immobilized in a functional, weight-
bearing position. External coaptation does not
provide rigid fixation and may allow fragments to heal
in malalignment. With intraarticular fractures,
osteoarthritis and reduced range of motion are
possible sequelae.
Internal fixation
If the fragments are of sufficient size, they may
be stabilized using small Kirschner wires (0.9 mm)
or bone screws (1.5 mm) (229). To stabilize trochlear
fractures, Kirschner wires are inserted and
C
 Fractures and disorders of the hindlimb
247

countersunk below the articular surface. To stabilize Malleolar fracture repair

talar neck fractures, Kirschner wires or a positional
screw are inserted from the head of the talus into the
calcaneus. Stabilization of basal fractures of the talus is
achieved with Kirschner wires placed in cross-pin
fashion. Postoperatively, a lateral splint or external
fixator is applied for 4 weeks and exercise is restricted.
• Immobilization and arthrodesis: in cases of
comminuted talar fractures, the tarsus may be
initially immobilized in proper alignment with an
external fixator. Once consolidation of the
fragments has occured, surgical arthrodesis of the
joint may be performed if pain or dysfunction
persist.
In many cases, collateral ligament function is restored
by repairing the fractured malleolus (224, 225).
A small lag screw or tension band fixation is used to
reattach the malleolus to the distal tibia. A lateral
splint may be applied after surgery for additional
support. Removal of the splint in 10–14 days and
earlier return of function, including physical therapy,
have been shown to improve function in cats after
repair of talocrural luxation2.

OTHER TARSAL BONE FRACTURES

Surgical fixation of fractures of the smaller tarsal bones
is difficult in cats. Treatment of these fractures is
usually achieved by external coaptation (230). This is
most successful if the fracture is minimally displaced or
can be adequately reduced prior to stabilization. The
limb is placed in a splint or external fixator and activity
is restricted for 6 weeks.

LUXATIONS OF THE TARSUS

TALOCRURAL LUXATION
Cause and pathogenesis
Traumatic luxation of the talocrural joint often 230
occurs with fractures of the medial or lateral
malleolus (or both)2,3. Less commonly, luxation
occurs with rupture or avulsion of the collateral
ligaments. In cats, the medial and lateral collateral
ligaments are each comprised of two short ligaments;
there is no long component as seen in dogs.

Clincal signs
Clinical signs of talocrural luxation include pain,
swelling, and palpable joint instability.

Diagnosis
Radiographs are obtained to evaluate the malleoli for
fractures. Varus or valgus stress can be applied to the
tarsocrural joint during radiography to demonstrate
laxity.

Treatment and prognosis

The joint is explored to evaluate the cartilage and
remove hematoma and debris. Any articular fractures
are stabilized with small Kirschner wires countersunk
below the articular surface. The joint is then reduced 230 Fractures of the distal tarsal bones.
and stabilized using one of several methods. Lateral radiographic view.
248
231

A B C D

231 Stabilization of talocrural luxations.

A Collateral ligament repair. Monofilament, nonabsorbable suture material is placed in a locking-loop pattern through the
ligament and passed through a hole drilled in the malleolus. B Reattachment of an avulsed fragment of bone with two
Kirschner wires. C Prosthetic collateral ligament replacement (medial). Nonabsorbable, monofilament suture material is
placed in a figure-of-eight pattern to replace both components of the collateral ligament. Bone tunnels, bone anchors, or
screws with washers are used to attach the suture. The origin of the collateral ligament is the medial malleolus. The
insertion points for the collateral ligament are the head and body of the talus. D Prosthetic collateral ligament
replacement (lateral). The origin of the collateral ligament is the lateral malleolus. The insertion is on the dorsal aspect of
the base of the calcaneus and the coracoid process of the calcaneus.

Collateral ligament repair
If the collateral ligament is avulsed from the
malleolus, its function may be restored by reattaching
the ligament to its origin (231 A). This is difficult to
accomplish due to the small size of collateral ligaments
in the cat. Monofilament, nonabsorbable suture
material (2-0) is used to place a locking-loop or
Bunnel–Meyer suture in the ligament. The suture is
then passed through a hole drilled in the distal aspect
of the malleolus. If an avulsed fragment of bone is
present and is large enough to accommodate
implants, it is re-attached with Kirschner wires
(231 B). The limb is immobilized for 10–14 days in a
splint, padded bandage, or transarticular external
fixator. Physical therapy is encouraged when the splint
is removed2.
Prosthetic collateral ligament replacement
If the collateral ligament is damaged, it is replaced
with suture material to restore joint stability4.
Nonabsorbable, monofilament suture material (2-0) is
placed in a figure-of-eight pattern to replace both
components of the collateral ligament (231 C, D).
Bone tunnels are drilled at the origin and insertion
points of the collateral ligaments to serve as anchor
points for the sutures (prosthetic ligament).
Alternatively, small screws with washers or bone
anchors may be used to attach the suture, though this
is difficult in smaller cats. On the lateral side, the origin
of the collateral ligament is the lateral malleolus. The
insertion is on the dorsal aspect of the base of the
calcaneus and the coracoid process of the calcaneus.
On the medial side, the origin of the collateral is the
medial malleolus. The insertion is on the head and
body of the talus. In most cases, remnants of the
damaged ligament help identify the anatomic sites of
ligament attachment. After placement of the prosthetic
ligaments, the joint is immobilized in a splint or
transarticular external fixator for 10–14 days.
Transarticular pin fixation
A Steinmann pin is inserted through the base of the
calcaneus, across the joint, and into the distal tibia
(232). The limb is placed in a lateral splint or cast and
the cat’s activity is restricted for 4 weeks while the
periarticular soft tissues heal. The external splint and
pin are removed after 4 weeks and a soft padded
bandage is applied for an additional 2 weeks. This
technique is effective in stabilizing tarsocrural luxations
in cats, but causes damage to the articular cartilage.
Transarticular external fixation
A transarticular external fixator may be applied to
stabilize tarsocrural luxations, either as a primary
 Fractures and disorders of the hindlimb
249

232 Stabilization of a talocrural 232

luxation with a transarticular pin.
A Preoperative lateromedial view.
B Preoperative dorsoplantar view.
C Postoperative lateromedial view.
D Postoperative dorsoplantar view.

A B C D

233

A B C
233 Stabilization of talocalcaneal luxations.
A Lateral radiographic view of a talocalcaneal luxation. Talocentral luxation with plantar displacement of the head of the
talus and subluxation of the calcaneoquartal joint are also present. B Diagrams of a talocalcaneal luxation stabilized with a
2.0 mm positional screw placed from the head of the talus into the distal aspect of the calcaneus. C Lateral radiographic
view of a talocalcaneal luxation stabilized with a 2.0 mm positional screw. (Radiographs courtesy of Carlos Macias.)

means of repair or in conjunction with internal
fixation techniques. Transfixation pins are inserted
through the tibia proximally and through the base of
the calcaneus and metatarsal bones distally. A type I
frame is usually sufficient. Metal connecting bars
may be used, although acrylic bars are more easily
contoured and are sufficiently strong. If the external
fixator is the primary means of stabilization, it should
remain in place for 3–4 weeks to allow healing of the
periarticular soft tissues. Physical therapy is initiated
after fixator removal to restore full joint motion.
Arthrodesis
Arthrodesis is rarely performed for treatment of
tarsocrural luxation in cats. However, it is considered
in cases with severe soft tissue injury, irreparable
articular fractures, or chronic osteoarthritis (see Tarsal
arthrodesis). After removing the articular cartilage
and placing bone graft, the joint is stabilized using lag
screw fixation, a bone plate and screws, a Steinmann
pin, or an external fixator.
TALOCALCANEAL LUXATIONS
Cause and pathogenesis
The talocalcaneal joint has three pairs of cartilage-
covered facets and two talocalcanel ligaments5. The
proximal ligament is located between the proximal and
middle articulations. The distal ligament is located at
the proximolateral aspect of the distal articulation.
Traumatic rupture of the talocalcaneal ligaments leads
to luxation. Talocalcaneal luxations are associated
with concurrent luxation of either the talocentral or
calcaneoquartal joints (233). The head of the talus
may displace either dorsally or plantarly, with
250
concurrent talocentral luxation; or the distal calcaneus
may displace dorsally or plantarly, with concurrent
calcaneoquartal luxation6. Concurrent fractures of the
talar neck and collateral ligament ruptures occur rarely.
Clinical signs
Luxation of the talocalcaneal joint is uncommon in
cats and causes a nonweight-bearing lameness.
Diagnosis
Palpation of the tarsus reveals pain, crepitus, and
swelling. Lateral and dorsoplantar radiographic views
are obtained to confirm the luxation and identify
concurrent injuries of the tarsus.
Treatment and prognosis
Closed reduction and stabilization with external
coaptation may be possible in some cases. However, if
the luxation cannot be reduced, open reduction and
internal stabilization is recommended. The cat is
positioned in dorsal recumbancy and a hanging-limb
preparation is performed. A dorsomedial approach to
the tarsus is made via an incision from the medial
malleolus to the base of the second metatarsal bone.
The joint capsule on the dorsal aspect of the tarsus is
incised and retracted. Manipulation of the limb, digital
pressure, and pointed reduction forceps are used to
reduce the luxation. Stabilization is achieved by placing
a positional screw (2.0 mm) from the head of the talus
into the distal aspect of the calcaneus5,6. The limb is
immobilized in a Robert Jones bandage or splint for 4
weeks. The cat’s activity is restricted for 8 weeks.
INTERTARSAL AND TARSOMETATARSAL
SUBLUXATION/LUXATION
Cause and pathogenesis
Luxation or subluxation of the intertarsal joints or the
tarsometatarsal joints results from hyperextension and
tearing of the plantar ligaments and fibrocartilage.
Such luxations are very rare in cats. Luxation of the
proximal intertarsal joint is not reported in the cat7.
Diagnosis
Diagnosis is based on palpation of joint laxity and
stress radiography.
Treatment and prognosis
External coaptation
The joint is reduced and a cast or lateral splint is
placed, extending from the toes to the proximal
tibia, for 4–6 weeks. Because of the disruption of
the plantar ligaments, external coaptation may be
ineffective in many cases.
Pin fixation
A small Steinmann pin is placed retrograde from the
luxated joint, through the base of the calcaneus, to
exit at the tuber calcis. The joint is reduced. The
direction of the pin is then reversed and it is inserted
through the fourth tarsal bone and into the
proximal metatarsus (234 A, B)8. The pin is cut
short to prevent injury to the superficial digital
flexor tendon. A lateral splint is applied for 4–5
weeks.
Kirschner wire fixation
Two Kirschner wires are inserted in cross-pin fashion
across the luxated joint. Cerclage wire may be placed
in a figure-of-eight around the exposed ends of the
Kirschner wires if desired (234 C, D).
Arthrodesis
If instability and pain persist after external coaptation
or pinning, arthrodesis of the joint may be required.
Arthrodesis is accomplished by removing the articular
cartilage, placing bone graft, and creating rigid
fixation using a bone plate, pin and tension band wire,
or Steinmann pin and cross-pins (see Tarsal
arthrodesis) (234 E)9.
METATARSOPHALANGEAL AND
INTERPHALANGEAL LUXATION
Luxation of the metarsophalangeal and inter-
phalangeal joints is managed by external coaptation. A
spoon splint is applied for 4–6 weeks. Digit
amputation is performed if healing is incomplete and
pain persists after external coaptation.
SHEARING INJURIES OF
THE TARSUS
CAUSE AND PATHOGENESIS
Shearing (degloving) injuries of the tarsus can occur
when an automobile hits the cat. The medial
(and occasionally lateral) aspect of the tarsus is
abraded by the pavement, destroying variable
amounts of tissue, including skin, muscle, tendons,
ligaments, and bone. In many cases, one or more of
the tarsal joints are open and severely contaminated.
Often the medial malleolus and collateral ligaments
are destroyed.
TREATMENT AND PROGNOSIS
The principles of managing shearing injuries are as
follows:
• Careful cleaning and debridement of the wound.
• Proper open wound management.
• Early stabilization of the joints.
 Fractures and disorders of the hindlimb
251
234

E B C D
234 Stabilization of intertarsal and tarsometatarsal luxations.
A Lateral radiographic view of a tarsometatarsal luxation.
B Pin fixation. A Steinmann pin is placed in a retrograde fashion from the luxated joint, through the base of the calcaneus,
and exits at the tuber calcis. The joint is reduced and the pin is inserted through the fourth tarsal bone and into the
proximal metatarsus.
C Kirschner wire fixation. Two Kirschner wires are inserted in cross-pin fashion across the luxated joint.
D Cerclage wire may be placed in a figure-of-eight fashion around the exposed ends of the Kirschner wires.
E Lateral radiographic view of a tarsometatarsal luxation stabilized with a bone plate.

At initial presentation, the wound is covered with
a sterile bandage while the cat is stabilized and evaluated
for other traumatic injuries. The cat is then anesthetized
and the wound is examined under sterile conditions to
assess tissue damage. A sample is collected for culture
and susceptibility testing and broad-spectrum
antimicrobial drugs are administered. Cephalosporins
(cefazolin at 22 mg/kg IV every 8 hours) and
clindamycin (11 mg/kg IV every 12 hours) have been
recommended10. The wound is filled with sterile
lubricating jelly and the surrounding hair is clipped.
Copious lavage with sterile saline, lactated Ringer’s, or a
0.05% chlorhexidine solution is used to remove hair and
debris from the wound and open joint spaces11.
Surgical debridement is then performed to remove
debris and devitalized tissues from the wound. Vessels
and nerves must be preserved. With some minor
shearing injuries, the wound is converted to a ‘clean’
wound by lavage and debridement and can be closed
primarily if adequate tissue remains. However, in most
cases, insufficient soft tissue remains to permit primary
closure, and progressive debridement over several days
is required to achieve a clean wound. These cases are
managed as open wounds12.
Stabilization of the joint is performed once the
wound is clean. Early stabilization encourages healing
of the periarticular soft tissues. The collateral
ligaments are repaired or replaced (231). Viable
portions of the ligaments can be sutured with
monofilament suture material. In most cases, how-
ever, the collateral ligaments are too severely damaged
and are replaced with nonabsorbable, monofilament
suture material (2-0) placed in a figure-of-eight
pattern. Bone tunnels or screws are placed at the
origin and insertion points of the collateral ligaments
to serve as anchor points for the sutures. On the
medial side of the talocrural joint, the origin of
the collateral ligament is the medial malleolus, the
insertion is the head of the talus and the body of
the talus. On the lateral side of the joint, the origin
of the collateral ligament is the lateral malleolus, the
insertion is at the dorsal aspect of the base of
the calcaneus and the coracoid process of the
calcaneus (see Talocrural luxation).
The tarsus is then immobilized at a normal,
weight-bearing angle with an external fixator. In cats,
a simple frame configuration consisting of full
transfixation pins placed through the tibia and
252

proximal metatarsal bones is sufficient (235)7. If 235

added strength is needed, an additional pin can be
placed through the tuber calcis. The transfixation pins
are connected bilaterally with acrylic or clamps and
metal bars. The fixator remains in place for 3–4 weeks
until granulation tissue covers the wound. A lateral
splint can be used to immobilize the joint rather than
an external fixator. The splint provides less stability,
however, and must be removed daily to allow
treatment of the open wound.
The open wound is managed daily. Wet-to-dry
dressings are applied to remove debris and
encourage granulation tissue formation13. Perforating
the cortical bone may enhance granulation tissue
formation over exposed bone surfaces14. Once granu-
lation tissue covers the wound, a dry nonadherent
dressing is applied. The bandage is changed less
frequently and may incorporate a splint for added
support once the external fixator is removed. In most
cases, even those with large soft tissue deficits, the
wound heals completely by epithelialization and
contraction in 10–12 weeks. If adequate soft tissue is
present, the wound may secondarily be sutured once a
healthy granulation bed has been established. Rarely, 235 A type II external fixator applied to immobilize the
a skin graft is required to cover unhealed soft tissue tarsus after collateral ligament replacement for repair of a
defects. The cat’s activity is restricted until healing shearing injury. The transfixation pins are connected
is complete. bilaterally with acrylic or clamps and metal bars.
Arthrodesis is indicated in shearing injuries
with severe bone loss and irreparable damage to
the malleolus, trochlea, and articular cartilage.
Arthrodesis is achieved with an external fixator
(see Tarsal arthrodesis). Bone grafting is delayed until CLINICAL SIGNS
the joint space is covered with granulation tissue. In Complete laceration of the common calcanean tendon
some cases, arthrodesis is performed only after results in a plantigrade stance (the plantar surface of
primary treatment of the shearing injury has failed to the tarsus contacts the ground), and must be
restore adequate, pain-free function. differentiated from fracture of the calcaneus and
rupture of the Achilles tendon.
CALCANEAN TENDON
LACERATIONS TREATMENT AND PROGNOSIS
CAUSE AND PATHOGENESIS Surgical repair of the lacerated tendons is indicated.
The common calcanean tendon consists of three parts. The wound is lavaged and antibiotic therapy is
The superficial digital flexor tendon courses over the initiated. An incision is made over the common
tuber calcis and inserts on the plantar surfaces of the calcanean tendon, from the mid-tibia to the tuber
second phalanges. The combined tendon of calcis. The exposed ends of the tendon are identified
the gracilis, biceps femoris, and semitendinosus and sutures are placed in the tendon ends to facilitate
muscles inserts on the medial aspect of the tuber manipulation. Devitalized tissue is debrided.
calcis15. The calcanean tendon (Achilles tendon) is the Extension of the tarsocrural joint will facilitate
largest component and is the tendon of insertion of apposition of the tendon ends. The ends are sutured
the triceps surae muscle (the combined gastrocnemius separately in a locking-loop pattern using monofil-
and soleus muscles in the cat). It inserts on the lateral ament, nonabsorbable suture material (2-0). If the
aspect of the tuber calcis. tendon is avulsed from the tuber calcis (or the
laceration is near the tuber), it may be reattached by
placing the suture through holes drilled through the
 Fractures and disorders of the hindlimb
253
236

A B C

236 Repair of calcanean tendon injuries.

A Tendon lacerations may be sutured with nonabsorbable, monofilament suture material in a locking-loop pattern. Each
tendon is sutured separately.
B, C Tendon injuries near the tuber calcis are repaired by reattaching the tendon to the bone. A locking-loop suture is
placed in the tendon and passed through holes drilled in the tuber calcis. Medial and lateral bone tunnels are drilled
from tip of the tuber calcis to the medial and lateral cortices to prevent interference with the superficial digital flexor
tendon.

bone (236). Medial and lateral bone tunnels are 237

drilled from the tip of the tuber calcis to the medial
and lateral cortices to prevent interference with the
superficial digital flexor tendon as it passes over
the tuber calcis. To protect the repair during healing,
the tarsocrural joint is immobilized in extension. This
is achieved using a lateral splint or external fixator, or
by placing a 2.7 mm screw or 0.8 mm (20 AWG)
cerclage wire from the tuber calcis to the distal tibia
(237)8. The limb is placed in a splint for 4 weeks. The
cat’s activity is restricted for 10 weeks.

237 Immobilization of the tarsus with a screw placed

from the calcaneus to the tibia after repair of a calcanean
tendon injury.
254

AVULSION OF THE 238

ACHILLES TENDON
CAUSE AND PATHOGENESIS
Avulsion of the Achilles (calcanean) tendon from the
calcaneus in cats is usually a result of trauma. The
condition may occur bilaterally.

CLINICAL SIGNS
The condition causes a characteristic gait abnormality
(238)15. When the cat bears weight on the limb, the
tarsus and digits are simultaneously hyperflexed. On
palpation of the limb with the stifle fully extended, the
tarsus will flex beyond 90°. As the tarsus is flexed, the 238 Cat with an avulsion of the Achilles tendon. Note the
digits will also flex because the superficial digital flexor plantigrade stance.
tendon remains intact. Radiographic evaluation may
reveal an avulsion fracture of the tuber calcis and soft
tissue swelling at the insertion of the gastrocnemius 239
tendon. Enthesiophytes and periosteal bone prolifer-
ation are often seen at the end of the calcaneus in cats
with tendon avulsion (particularly in older cats),
suggesting that a chronic tendinopathy may con-
tribute to the acute failure of the tendon’s insertion
on the tuber calcis (239)15.

TREATMENT
Both external coaptation and internal fixation have
been used for treatment of gastrocnemius avulsion in
the cat15.

External coaptation
Cats with avulsion of the Achilles tendon can be
successfully managed with external coaptation, 239 Radiograph of the tarsus from a cat with an avulsion of
particularly if the luxation is chronic15. A lateral splint is the Achilles tendon. Note the enthesiophyte and periosteal
applied from the toes to the proximal tibia. The tarsus is bone proliferation at the tuber calcis.
placed in a normal weight-bearing position or in slight
extension. The splint is removed after 6 weeks and the
cat’s activity is restricted for an additional 4 weeks. 240

Internal fixation
If an avulsed fragment of bone is evident radio-
graphically, a tension band wire fixation is used to
stabilize the fracture and restore function of the
Achilles tendon (240). The avulsed tendon may also
be reattached to the tuber calcis using a locking-loop
suture pattern16. Monofilament, nonabsorbable
suture material (0 or 2-0) is preferred. The tendon in
sutured to the bone through a hole drilled in the
calcaneus. Medial and lateral bone tunnels are drilled
from the tip of the tuber calcis to the medial and
lateral cortices. A splint is applied for 4–6 weeks.
Alternatively, an external fixator may be used to
immobilize the joint while the tendon heals, but is not 240 Stabilization of an avulsion injury of the Achilles
usually necessary in cats. tendon with a tension band wire fixation.
 Fractures and disorders of the hindlimb
255

LUXATION OF THE SUPERFICIAL calcanean tendon, and debilitating osteoarthritis18,19).

DIGITAL FLEXOR TENDON
Lateral luxation of the superficial digital tendon has been
reported in the cat17. Clinical signs may include
intermittent lameness and swelling over the tuber calcis.
Palpating the superficial digital flexor tendon while
internally and externally rotating the tarsus may confirm
the luxation. Treatment is achieved by suturing the
retinaculum near the tuber calcis using monofilament,
nonabsorbable suture material (3-0). The medial
retinaculum is repaired to stabilize a lateral luxation17.
TARSAL ARTHRODESIS
Arthrodesis may be required as treatment for
comminuted tarsal bone fractures or when previous
external coaptation or internal fixation have failed,
leading to pain, lameness, or osteoarthritis. Important
principles of arthrodesis include removal of the
articular cartilage, placement of an autogenous
cancellous bone graft, and rigid fixation.
TALOCRURAL ARTHRODESIS
Talocrural arthrodesis is indicated for severe shearing
injury, comminuted intraarticular fractures, joint
laxity or hyperextension, irreparable damage to the
The joint may also be fused along with transposition
of the long digital extensor tendon for injury to the
sciatic nerve. Arthrodesis of the talocrural joint
eliminates the majority of tarsal joint movement and
results in a persistent gait abnormality. Additional
stress is imparted to the remaining distal tarsal
joints, which may lead to the development of
osteoarthritis20.
The talocrural joint is exposed by a medial
malleolar ostectomy and the joint surfaces are
prepared by removing the cartilage with a curette or
power-driven burr. The joint is aligned and initial
fixation is achieved by placing two Kirschner wires
across the joint. The angle of talocrual arthrodesis is
115–125° in cats7,18. Rotational and angular
deformity is avoided. Rigid fixation is achieved using
one of several techniques.
Lag screws
A 3.5 mm cortical screw is placed in lag fashion
from the distal tibia, across the joint, and through
the talus and calcaneus (241). The drill hole is
started at the caudomedial aspect of the tibia
(1–1.5 cm proximal to the joint space) and angled

241

115 + 125°

A B C D
241 Talocrural arthrodesis.
A The articular cartilage is removed from the distal tibia and talus with a curette or power-driven burr.
B, C Medial and dorsal views of the talocrural joint. The joint is aligned (115–125°) and temporarily stabilized with
Kirschner wires. A 3.5 mm cortical screw is placed in lag fashion from the distal tibia, across the joint, and through the
talus and calcaneus. A positional screw is placed from the tuber calcis into the distal tibia.
D Talocrural arthrodesis with an intramedullary pin and transarticular type II external fixator. Cancellous bone graft is
placed at the site
256
approximately 15° from the sagittal plane of the tibia
to enter the talus and calcaneus. The screw should
exit the bone at the plantarolateral cortex near the
base of the calcaneus. The glide hole (3.5 mm) is
placed in the distal tibia and the thread hole
(2.5 mm) is placed in the talus and calcaneus. The
appropriate length, fully threaded cortical screw is
inserted and tightened. A second screw may be
inserted across the joint if possible. A positional
screw is then placed from the tuber calcis into the
distal tibia to protect the lag screw from bending and
shearing forces. Alternatively, a transarticular
external fixator may be applied (242). The medial
malleolus is reattached with a tension band wire or
morselized with a rongeur and used as bone graft.
Autogenous cancellous bone graft is collected from
the proximal tibia and placed at the site. If an
external fixator was not applied, the limb is placed in
a lateral splint for 6 weeks or until radiographic signs
of union are evident.
242
A
242 Talocrural arthrodesis with a
lag screw and transarticular acrylic
external fixator.
A Lateromedial view.
B Oblique view.
B
Steinmann pin and a transarticular
external fixator
The joint surfaces are prepared as previously described
and the joint is positioned at an angle of 115–125°. A
Steinmann pin is inserted from the base of the
calcaneus, through the talus, and into the distal tibia
(241). In most cases the pin will enter the tibial
medullary cavity and is inserted to engage the
proximal tibial metaphysis. A type II external fixator is
then applied. Transfixation pins are inserted medially
to laterally through the tibia and proximal metatarsal
bones. The transfixation pins are attached bilaterally
to connecting rods (using clamps) or with acrylic bars.
Cancellous bone graft is placed at the site to speed
fusion. The cat’s activity is restricted until fusion is
complete and the fixator is removed. The Steinmann
pin is removed if irritation to the soft tissues over the
calcaneus develops. This technique is particularly
useful in open injuries because the implants are easily
removed when fusion is complete.
 Fractures and disorders of the hindlimb
257

PARTIAL TARSAL ARTHRODESIS is then reversed and it is driven across the

Partial tarsal arthrodesis involves fusion of the
proximal intertarsal, distal intertarsal, and tar-
sometatarsal joints. Indications include hyper-
extension injuries and subluxation of the intertarsal
and tarsometatarsal joints, comminuted intraarticular
fractures of the tarsal bones, shearing wounds, severe
osteoarthritis, and treatment of lameness associated
with Scottish Fold osteodystrophy18,21. Movement in
the tarsocrural joint is spared and limb function after
partial tarsal arthrodesis is good.
The joint is exposed and the articular cartilage is
removed with a curette or small power burr. The joint
is aligned and cancellous bone graft is placed at the
site of arthrodesis. Stabilization is achieved using one
of several techniques (243).
Pin and cross-pin fixation
A Steinmann pin is inserted normograde from the tuber
calcis, across the tarsus, and into the fourth metatarsal
bone. Alternatively, the pin is inserted in a retrograde
fashion from the fourth tarsal bone, through the
calcaneus, and out at the tuber calcis. The pin direction
tarsometatarsal joint into the metatarsus9. The tip of
the pin is countersunk into the tuber calcis to avoid
trauma to the superficial digital flexor tendon. Two
Kirchner wires are then placed in cross-pin fashion
across the tarsus. One Kirschner wire is inserted
through the fourth tarsal bone and driven medially
and distally into the second metatarsal bone. The
second Kirschner wire is started at the head of the fifth
metatarsal bone and driven proximally and medially
into the central tarsal bone. A lateral splint is placed for
4–5 weeks.
Pin and tension band wire fixation
A Steinmann pin is inserted (either normograde or
retrograde) from the tuber calcis into the metarasus.
Holes are drilled from lateral to medial through the
calcanceus and through the plantar tubercle of the
fourth tarsal bone (or the head of the metatarsal
bone). Orthopedic wire (0.8 mm [20 AWG]) is placed
through the holes in a figure-of-eight fashion. The
wire is tightened to lie along the plantar surface of the
tarsus as a tension band.

243

A B C D E
243 Arthrodesis of the proximal intertarsal, distal intertarsal, and tarsometatarsal joints (partial tarsal arthrodesis).
A Pin and cross-pin fixation. A Steinmann pin is inserted from the tuber calcis into the fourth metatarsal bone. The pin is
countersunk into the tuber calcis. A Kirschner wire is inserted from the fourth tarsal bone into the second metatarsal
bone. A second Kirschner wire is inserted from the head of the fifth metatarsal bone into the central tarsal bone.
B, C Pin and tension band wire fixation. A Steinmann pin is inserted from the tuber calcis into the fourth metatarsal
bone. A tension band wire is placed in a figure-of-eight fashion on the plantar surface of the tarsus through holes drilled
through the calcaneus and the heads of the metatarsal bones.
D, E Bone plate and screw fixation. A bone plate is applied to the lateral surface the tarsus from the calcaneus to the fifth
metatarsal bone with 2.0 mm or 2.7 mm screws. Three screws are placed in the calcaneus, one or two screws in the tarsal
bones, and three screws in the metatarsal bones. Cancellous bone graft is placed prior to closure.
258

Bone plate and screws joints22. Indications include shearing injuries,

A bone plate is placed along the lateral surface of the
tarsus from the calcaneus to the fifth metatarsal bone.
Cuttable plates work well and can be cut to the
appropriate length at the surgery table. 2.7 mm or
2.0 mm screws can be used. To improve contact
between the plate and the bone, the base of the fifth
metatarsal bone and the calcaneus may be leveled with
a power burr. Typically, three screws are placed into
the calcaneus (one also engages the talus) and one or
two screws are inserted into the tarsal bones. The
three distal screws are placed into the metatarsal
bones. External coaptation is recommended for
4–6 weeks after surgery.
PANTARSAL ARTHRODESIS
Pantarsal arthrodesis involves fusion of the tibiotarsal,
proximal and distal intertarsal, and tarsometatarsal
osteoarthritis, and painful unstable conditions
unresponsive to reconstruction. Because of the
degenerative joint disease that often develops in the
more distal tarsal joints, pantarsal arthrodesis may be
preferred for diseases of the tarsocrural joint over
tarsocrural arthrodesis alone23. The joints are exposed
through a lateral incision from the distal one-third of
the tibia to the metatarsus. The joints are prepared by
removing the articular cartilage and placing cancellous
bone graft. The preferred angle of arthrodesis is
115–125° in cats. Rigid fixation is provided with one
of several techniques (244).
Dorsal bone plate and screws
A 2.7 mm DCP is applied to the cranial/dorsal surface
of the tibia, tarsus, and metatarsus22. Bending forces
applied to the plate in this position may lead to plate

244

A B C D E
244 Pantarsal arthrodesis. The cartilage is removed from the joint surfaces and cancellous graft is placed. The joint is
positioned at an angle of 115–125°.
A Arthrodesis with a dorsal bone plate and screws.
B Arthrodesis with a medial (or lateral) bone plate. The plate should be long enough to allow insertion of three screws in
the tibia and three screws in the metatarsal bones.
C Arthrodesis with a pin and external fixator. A Steinmann pin is inserted from the base of the calcaneus to the proximal
tibial metaphysis. Kirschner wires are inserted across the tarsus in cross-pin fashion from the fourth tarsal bone to the
second metatarsal bone and from the fifth metatarsal bone to the central tarsal bone. A type II external fixator is applied.
D, E Arthrodesis with screws and Kirschner wires. A lag screw is placed across the talocrural joint. A position screw is
placed from the calcaneus to the tibia. Kirschner wires are inserted in cross-pin fashion from the fourth tarsal bone to the
second metatarsal bone and from the fifth metatarsal bone to the central tarsal bone.
 Fractures and disorders of the hindlimb
failure or screw loosening. A cast or lateral splint is
applied to the limb during the healing period to
reduce the likely of implant failure. The plate may be
removed when fusion is complete to avoid
complications.
Medial bone plate and screws
A bone plate is applied to the medial (or lateral) aspect
of the tibia, tarsus, and metatarsus. The distal fibula
must be ostectomized to allow application of the plate
to the lateral aspect of the distal tibia. Reconstruction
plates are readily contoured to allow arthrodesis
at an angle of 115–125°. Tarsal arthrodesis plates are
also available that are custom-made based on
the radiographs (Veterinary Instrumentation, UK).
The plate should be long enough to allow insertion of
three screws in the tibia and three screws in the
metatarsal bones. The limb is placed in a lateral splint
for 8 weeks or until fusion is complete. The cat’s
activity is restricted during the healing period.
Removal of the bone plate is recommended after
fusion to prevent implant loosening and breakage.
Pin and external fixator
The articular cartilage is excised from the joints and
bone graft is placed. The tarsus is positioned at an
angle of 115–125°. A Steinmann pin is inserted from
the base of the calcaneus and into the distal tibia. The
pin is seated in the proximal tibial metaphysis.
Kirschner wires are then inserted across the tarsus in
cross-pin fashion. The first wire is inserted through
the fourth tarsal bone and into the second metatarsal
bone. The second wire is started at the head of the
fifth metatarsal bone and inserted into the central
tarsal bone. A type II external fixator is then applied.
Transfixation pins are inserted medially to laterally
through the tibia and proximal metatarsal bones and
connected bilaterally with acrylic or connecting bars.
The cat’s activity is limited until fusion is complete
and the fixator is removed. The Steinmann pin is
removed if irritation to the soft tissues over the
calcaneus develops. A potential complication of using
external fixators is fracture of the metatarsal bones.
Screw and Kirschner wire fixation
One or two lag screws are placed across the
talocrural joint as described for talocrural arthrodesis.
A positional screw is inserted from the calcaneus
to the tibia. Kirschner wires are inserted in cross-pin
fashion to stabilize the intertarsal joints and
tarsometatarsal joints. The first wire is inserted
through the fourth tarsal bone and into the second
metatarsal bone. The second wire is started at the
259
head of the fifth metatarsal bone and inserted into the
central tarsal bone. The limb is placed in a cast or
lateral splint for 6–8 weeks to protect the implants and
provide additional support.
METATARSAL AND PHALANGEAL
FRACTURES AND LUXATIONS
Metatarsal and phalangeal fractures and luxations of the
hindlimb are managed in the same manner as the
metacarpal and phalangeal injures in the forelimbs (see
Chapter 8). In most cases, the fracture or luxation is
reduced closed and the limb is splinted for 4–6 weeks.
Spoon splints work well and are available to fit most
cats. Splinting of metatarsal fractures is particularly
successful if one of the metatarsal bones is intact and
serves as an internal splint. If all four of the metatarsal
bones are fractured, care must be taken to avoid angular
deviation of the paw within the splint. Alternatively,
small intramedullary Kirschner wires can be inserted
into the third and fourth metatarsal bones to maintain
alignment, though this can be difficult in the cat
because of the small diameter of these bones (see 120).
A small hole is drilled in the dorsal surface of the distal
aspect of the metatarsal bone to access the medullary
cavity. The fracture is reduced and a Kirschner wire is
inserted normograde from the hole into the proximal
metaphysis. The limb is then splinted and the cat’s
activity is restricted until fracture healing is complete.
With severe trauma to the phalanges, the loss of soft
tissues (including skin, tendons, ligaments, and joint
capsule) may complicate repair. Fusion podoplasty may
be performed as a salvage procedure in the treatment of
degolving injuries of the digits (see Chapter 8)24. Digit
amputation may be indicated as treatment for
comminuted fractures, nonunions, intraarticular
fractures, irreparable luxation, shearing injuries,
neoplasia, or chronic infections of the digit (see
Chapter 8). In some cases of severe phalangeal injuries,
the digits are amputated at the metatarsophalangeal
joint and the metatarsal pad is advanced distally to cover
the distal plantar aspect of the foot, thus preventing the
need for a total limb amputation25. A splint is applied
to the limb for 4 weeks to allow complete healing and
reduce the likelihood of pad injury caused by shearing
motion between the pad and the metatarsal bones
during weight bearing.
HINDLIMB AMPUTATION
Hindlimb amputation is a salvage procedure indicated
for irreparable fractures or when severe complications
occur after attempted fracture treatment. Complications
necessitating amputation may include nonunion,
osteomyelitis, severe muscle contracture or joint
260
dysfunction, and neurologic dysfunction. Neoplasia
affecting the soft tissues or skeleton is also an indication
for amputation. The cat should be carefully evaluated to
ensure the remaining three limbs are healthy and can
adequately support weight.
Amputation through the mid-shaft or proximal
one-third of the femur is preferred. This technique
provides cosmetic results and protection of the
inguinal area26. The limb is prepared from the dorsal
mid-line to the ventral mid-line, caudally to the tail
head and cranially to the last rib. A hanging-limb
preparation is used so the limb can be manipulated
during surgery. A semicircular skin incision is made
over the lateral surface of the thigh starting at the
flank, extending over the distal third of the femur, and
ending near the tuber ischii. A semicircular medial
skin incision starts in the flank, extends distally to the
mid-shaft of the femur, and ends at the tuber ischii,
connecting the cranial and caudal points of the lateral
incision and completing the circular incision around
the limb. Medially, the sartorius and gracilis muscles
are transected mid-belly. Electrocautery may be used
to control small bleeding vessels. Ligation is used to
prevent hemorrhage prior to transection of larger
vessels. The femoral artery and vein and saphenous
vein are separated, ligated, and transected. Retraction
of the vascular stump allows transection of the
pectineus muscle near its musculotendinous junction.
The cranial belly of the sartorius muscle and
the quadriceps muscles are transected proximal to the
patella. Laterally, the fascia lata and biceps femoris
muscles are transected along the same line as the
lateral skin incision. Dorsal retraction of the biceps
femoris muscle allows visualization and transection of
the ischial nerve at the level of the greater trochanter.
The semitendinosus, semimembranosus, and adduc-
tor muscles are then transected at mid-femur. The
femur is cut at the junction of its proximal and middle
thirds using a bone saw or wire saw. The distal limb is
removed. The bone is covered during closure by
suturing the distal aspect of the quadriceps muscles to
the adductor muscle and the biceps femoris to the
gracilis. The caudal sartorius muscle is sutured to
the fascia lata prior to suturing the subcutaneous
tissues and skin. The longer skin flap on the lateral
aspect of the limb provides a more cosmetic closure
and places the thicker, hair-covered lateral skin over
the end of the stump.
Alternatively, for severe fractures involving the
proximal femur, amputation of the hindlimb can be
achieved by disarticulation of the coxofemoral joint.
Hemipelvectomy with limb amputation is occasionally
indicated for treatment of neoplasms of the proximal
limb and pelvis in cats.
 261

CHAPTER 10
FRACTURES AND
DISORDERS OF THE
SKULL AND MANDIBLE
MANDIBULAR FRACTURES
CAUSE AND PATHOGENESIS
Mandibular fractures are common in cats and
comprise approximately 11–23% of all feline
fractures1,2. They usually occur as a result of blunt
trauma (often vehicular trauma), a fall, or a fight with
another animal. Mandibular fracture caused by severe
periodontal disease or neoplasia is rare in cats. The
majority of mandibular fractures are open3,4.
CLINICAL SIGNS
Cats with mandibular fractures tend to hold the
mouth open and the mandible may be deviated
toward the side of the injury. In bilateral fractures, the
rostral aspect of the mandible will be displaced
ventrally. Blood in the saliva and excessive salivation
are noted in most cases. Pain and crepitus are elicited
if attempts are made to palpate the mandible.
DIAGNOSIS
Radiography is helpful to identify fractures caudal
to the molar teeth that cannot be seen on
oral examination. To evaluate the mandible
and temporomandibular joints, a lateral view, a
dorsoventral view, and, if necessary, left and right 20°
oblique lateral views should be obtained (245). The
zygomatic arches, maxilla, and cranium should also be
evaluated for fractures.

245

B
245 Fracture of the vertical ramus of the mandible.
A Dorsoventral view.
B Lateral view.

A
262
TREATMENT AND PROGNOSIS
Cats with mandibular fractures must be carefully
evaluated for evidence of cranial trauma and skull
fractures. Other potential problems in cats with
mandibular fractures include airway obstruction
and inability or reluctance to eat and drink. Full
assessment and stabilization of the patient should
be performed before initiating treatment of the
mandibular fracture.
Anesthesia is often required to allow a complete
oral examination and radiography, and to enable
definitive repair of the fracture. Initially, the
endotracheal tube is placed through the oral cavity.
However, once repair of the fracture has begun, the
endotracheal tube is redirected and placed via a
pharyngostomy incision to allow assessment of dental
occlusion during the repair5,6. Alternatively, a
tracheostomy tube can be placed, but this is only
needed when the airway is compromised and a
tracheostomy will be required after surgery.
Antibiotics are indicated because mandibular
fractures are usually open to the oral cavity. Fortunately,
despite the open nature of most fractures, osteomyelitis
is rare. Antibiotics directed at microorganisms common
to the oral cavity are preferred, including ampicillin
(25 mg/kg IV) or cefazolin (22 mg/kg IV).
Amoxicillin/clavulanate, clindamycin, or metronidazole
may be given to cats with severe periodontal disease6.
Culture of the fracture site will often reveal a wide
variety of organisms, and determining which are
likely to cause infection can be difficult. In general,
defects in the gingival and other soft tissues of the
mouth are left open to allow drainage and healing
by second intention. If the defect is large, it may be
sutured after copious lavage and debridement.
A number of repair methods may be applicable for a
given fracture configuration. The choice of technique
will be based on the location and stability of the
fracture, the age of the patient, concurrent injuries,
financial considerations, the preferences and experience
of the surgeon, and the equipment available.
Principles of mandibular fracture repair
Numerous techniques are described for stabilization
of mandibular fractures. With all techniques,
anatomic reduction and occlusive alignment, stable
fixation, preservation of soft tissues, and avoidance of
iatrogenic tooth damage are essential. In most cases,
proper occlusion is achieved by providing adequate
reduction of the fragments. Occlusion should not be
sacrificed for better reduction, since fractures will
heal even if slight gaps are present in the fracture line.
However, seemingly minor malocclusion can lead to
difficulty eating and pain postoperatively. After
fixation, the oral cavity should be thoroughly
lavaged.
Stable teeth are generally not removed, even if
the root is exposed. Leaving teeth prevents further
damage at the fracture site and aids in occlusion,
which helps stabilize the fracture7. Early stabilization
of the fracture supports compromised teeth and
allows quicker healing of soft tissues. In the unlikely
event that a nonunion fracture develops, removal of
the tooth at the fracture site may be indicated.
Diseased teeth should be removed from the fracture
site at the time of fixation.
Implants should be placed to avoid damaging
the teeth and roots, which occupy the dorsal half to
two-thirds of the mandibular body. It is also preferable
to avoid further injury to the neurovascular bundle in
the mandibular canal, which occupies most of the
ventral one-third of the bone. Hence there are few
safe corridors for implant placement.
Conservative treatment without stabilization of
the fracture is more applicable to the cat than the dog
and can produce surprisingly good results. Many
fractures of the mandibular ramus are treated
conservatively. Stable minimally displaced unilateral
fractures of the mandibular body without
comminution in young cats can also be treated
conservatively. A degree of residual malocclusion may
occur but can usually be resolved by extraction of one
or more teeth to permit full jaw closure.
Symphyseal separations
Symphyseal separations are common, accounting for
73% of mandibular fractures in cats8. The majority are
separations of the mandibular syndesmosis caused by
trauma (246).
Symphyseal separations are readily stabilized with
a single cerclage wire placed around the rostral
mandible. A 16 gauge needle is used as a wire passer
to position the wire. The needle is passed through
a small stab incision made in the skin on the mid-line,
ventral to the mandibular symphysis. The needle is
passed adjacent to the lateral aspect of the mandible
and exits the gingiva just caudal to the canine tooth.
Orthopedic wire (0.8 mm [20 AWG]) is inserted
through the needle to exit the stab incision. The
process is repeated on the opposite side with the other
free end of the wire. The wire is then tightened by
twisting ventral to the symphysis to compress the
fracture. The wire should be tightened sufficiently
to prevent shearing forces between the mandibles.
Overtightening should be avoided as this may cause
displacement of the canine teeth and malocclusion.
 Fractures and disorders of the skull and mandible
263

246

A B

C D
246 Placement of a cerclage wire for mandibular symphyseal fracture repair. (Photographs courtesy of Carlos Macias.)
A The cat has a concomitant median fracture of the hard palate, which has necessitated pharyngostomy intubation to
allow assessment of dental occlusion during fracture repair.
B A 16 gauge hypodermic needle is passed from the mid-line ventral to the mandible to exit from the caudolateral aspect
of the canine tooth. Orthopedic wire (0.8 mm, 20 AWG) is passed through the needle from the tip and the needle is
withdrawn.
C On the opposite side the needle is placed in similar fashion. The wire is passed through the needle taking care to avoid
kinking the wire, and the needle is withdrawn.
D The fracture is aligned and the wire is tightened taking care to ensure that the wire is pushed down flat against the
intermandibular soft tissues. Although the wire should be tight, overtightening may cause loss of alignment. The wire is
cut, bent over, and buried under the skin surface.
264

When tight, the wire twist is cut (leaving 3–4 twists),
bent over to reduce soft tissue injury, and buried
under the skin surface. The intraoral portion of the
wire is flattened against the intermandibular soft
tissues. Irritation to the skin over the wire twist and
mild drainage from the site is common. The wire is
removed in 4–6 weeks when healing is complete. To
remove the wire, the site of the previous stab incision
is explored to find the twist, which is grasped with
forceps. The intraoral portion of the wire is cut and
straightened as the wire is pulled ventrally by the twist
and out through the previous stab incision.
A technique using a Kirschner wire inserted across
the symphysis and a figure-of-eight wire has been
described for stabilization of symphyseal separations.
However, the lower canine teeth occupy most of the
width of the mandible in cats, and approximately 70%
of these teeth lie beneath the gingiva and are not
visible to the surgeon. As a result, inserting the
Kirschner wire without hitting a tooth root is difficult.
Mandibular body fractures
Muzzle fixation
Application of a tape muzzle is an inexpensive and
noninvasive technique for stabilizing mandibular
fractures (247)3,4. Muzzles are used to prevent
movement of the fracture site temporarily and reduce
further soft tissue injury while the cat is prepared for
surgery. Alternatively, they are used as a definitive
form of stabilization or to provide additional support
following internal fixation. When used alone, muzzles
are applied to fractures that are relatively stable and
minimally displaced. They typically do not provide
adequate stability for rostral fractures of the mandible.
Commercially available feline muzzles are often too
large for use in fracture stabilization and may interfere
with breathing or eating. The relatively short maxilla
in cats can make maintaining a tape muzzle difficult.
An Elizabethan collar is used to prevent the cat from
removing the muzzle.
To apply a tape muzzle, the jaw is closed ensuring
proper occlusion. Three pieces of 12 mm adhesive
tape are used. The tape is folded to conceal the
adhesive. The first piece of tape forms a strap around
the mandible and maxilla. It should be tight enough
to hold the mouth shut while allowing approximately
5 mm of space between the upper and lower incisor
teeth. The upper and lower canine teeth will
interdigitate to prevent excessive lateral movement of
the mandible. If the strap is too tight, the cat will be
unable to open its mouth sufficiently to drink or eat
gruel. A second piece of tape, forming a strap around
the cat’s head and ears, attaches to the muzzle strap to
hold it against the bridge of the nose and prevent it

247

A B C

247 Muzzle fixation for fracture stabilization.

A The first piece of tape forms a strap around the mandible and maxilla. It should be tight enough to hold the mouth shut
while allowing approximately 5 mm of space between the upper and lower incisor teeth.
B A second piece of tape, forming a strap around the cat’s head and ears, attaches to the muzzle strap to hold it against the
bridge of the nose and prevent it from sliding rostrally. The muzzle strap should not contact the eyes.
C A third piece of tape, forming a strap under the cat’s throat, prevents the head strap from slipping over the head and ears.
 Fractures and disorders of the skull and mandible
265

from sliding rostrally. The muzzle strap should not
contact the eyes. A third piece of tape, forming a strap
under the cat’s throat, prevents the head strap from
slipping over the head and ears. It should not be too
tight or it will interfere with respiration. To prevent
the muzzle strap from slipping rostrally, a fourth strap
may be placed dorsally in the mid-line or the muzzle
strap may be loosely sutured to the skin.
After application of a tape muzzle, occlusion may
be imperfect. However, the fragments are usually
guided into adequate alignment by the occlusion of
the teeth. If significant malocclusion develops, an
alternative form of fixation may be required. This can
occur if the fracture is inherently unstable or if the
muzzle is too loose. Failure of the canine teeth to
interdigitate may also allow the mandible to displace
laterally, leading to malocclusion. Complications with
tape muzzles can include malocclusion, aspiration
secondary to vomiting, and dermatitis around the
muzzle. Daily cleaning of the skin beneath the tape
will reduce the severity of the dermatitis.
External fixators
An external fixator can be applied to one or
both mandibles to stabilize fractures (248). Fixators
have been used in multiple, comminuted, and open
mandibular fractures3,6,9. The fixation pins are
inserted through stab incisions in the skin over the
mandible. It is important to ensure that the pins are
not placed in the fracture line and do not damage
tooth roots, the tongue, and other oral soft tissues. If
the pin accidentally hits a tooth root, it may glance off
and proceed through the bone, or the tooth enamel
will prevent further insertion. The tooth may be
damaged and the heat generated during the drilling
can lead to premature pin loosening. Pins are typically
placed ventrally on the mandible to avoid the tooth
roots. Unfortunately, pins placed ventrally may enter
the mandibular canal and damage the neurovascular
structures within. Pins placed caudally are associated
with increased morbidity because they penetrate the
large masseter muscle. A minimum of two pins should
be placed on each side of the fracture line. The
mandible is quite thin with poorly defined cortices
and threaded pins are recommended since they will
enhance holding power and minimize premature
loosening of the fixator.
When external skeletal fixation is used for
mandibular fracture repair, an acrylic or epoxy resin
fixator is preferred since it is lightweight, can be
conformed to the shape of the mandible, and allows
pins to be inserted in variable locations and still attach
to the connecting bar9. Small diameter pins are used
to avoid damaging tooth roots and the structures in

248

A B

248 External skeletal fixation of comminuted mandibular fractures.

A Unilateral acrylic external fixator.
B Bilateral acrylic external fixator. The rostral pins are angled ventrally so that the
acrylic side bar does not interfere with eating.
266
the mandibular canal. Once the transfixation pins are
inserted, flexible tubing is placed over the protruding
ends of the pins. The fracture is held in reduction (and
the teeth are held in proper occlusion) while the
tubing is filled with acrylic or polymethylmethacrylate
(PMMA) and allowed to harden. Alternatively, epoxy
resin (or acrylic when it reaches a doughy consistency)
is packed over the ends of the pins. Small positive
profile pins specially designed for use with acrylic
frames (Miniature Interface fixation half pins, IMEX
Veterinary Inc.) are preferred. Other types of fixation
pin should be bent or notched to improve the
interface between the pin and the connecting bar. The
fixation pins are cooled using saline-soaked swabs
during exothermic setting of the acrylic. The acrylic
side bar should be 1–1.5 cm from the skin surface to
help prevent thermal necrosis and allow for soft tissue
swelling. Complications of external fixators used in
mandibular fracture repair include premature pin
loosening, infection, and damage to the frame by
objects in the environment. To remove the fixator, the
pins are cut between the mandible and the connecting
bar and then each pin is pulled out.
Plates and screws
Plates and screws are rarely needed to stabilize
mandibular fractures in cats. They are applied through
a ventral incision over the mandibular body. Plates and
screws provide rigid fixation, but implantation is
invasive and placement of the screws can damage
the tooth roots or neurovascular structures in the
mandibular canal6. When placing a plate on
the mandible, it is important to preserve dental
249
249 Plate fixation of a mandibular body fracture using a
2.0 mm mini plate. The plate is placed ventrally on the
lateral aspect of the mandible to avoid the tooth roots.
occlusion. Unfortunately, because of plastic
deformation of the bone at the time of injury, normal
occlusion is not necessarily achieved even when the
fracture is perfectly reduced. Therefore, the fracture
may need to be stabilized with a small defect at the
fracture site to ensure proper occlusion of the teeth.
This occasionally requires visualization of the oral
cavity during plate placement. If infection occurs, a
second surgical procedure may be necessary to remove
the implants once the fracture has healed. Mini plates,
cuttable plates, and human 1.0 mm and 1.5 mm
maxillofacial mini plates (Chapter 5) can be used to
stabilize mandible fractures in cats (249)10,11.
Interdental fixation
Interdental fixation involves the application of wires,
or acrylic, or both, around the teeth to stabilize
fractures of the mandible (250)6.
This technique avoids iatrogenic trauma to tooth
roots and neurovascular structures in the mandibular
canal, is minimally invasive, preserves blood supply and
soft tissues, and restores occlusion. It is also mechanically
strong since the tension side of the mandible is the
alveolar border. Unfortunately, the dental anatomy of
the cat does not lend itself to this technique because
of the large interdental spaces, the shape of the crowns of
the teeth, and the paucity of premolar and molar teeth
(there are only three cheek teeth in each hemimandible).
An adequate number of healthy teeth must be present
for interdental fixation to be effective. A composite
intraoral dental restorative splint is stronger than either
interdental wire or restorative alone.
The mouth is cleaned and small diameter wire
 Fractures and disorders of the skull and mandible
267

(0.5mm [24 AWG]) is intertwined around the crowns of
the teeth rostral and caudal to the fracture site. The Stout
multiple loop wiring technique is a commonly used
method of wire placement. The wire is twisted on the
labial side to tighten it against the teeth (and to create
small loops of wire that will engage the restorative).
Overtightening of the wires is avoided to prevent
gapping of the fracture on the ventral mandibular border.
Depending on the material being used, the teeth may
need to be cleaned, acid etched, and rinsed. Etching is
performed on the buccal and lingual surfaces of the teeth
except for the carnassial tooth, where it is performed only
on the lingual surface. A thin layer of dental adhesive may
then be applied and cured with an ultraviolet light to
allow proper occlusion with the mandibular arcade. Self-
curing composite restoratives (for example, Protemp
Garant, ESPE Dental Medizin; Build-It, Pentron
Clinical Technologies LLC.) are nonexothermic and do
not produce the toxic fumes associated with acrylic
monomers. The restorative material is applied (using a
syringe or gun) to the appropriate surfaces of the teeth
and around the wire loops. The fracture is held in
reduction until the restorative has hardened. If necessary,
the material can be shaped using a burr.
The appliance will accumulate food debris (and
exudates from open fractures). Daily rinsing by the
owner can reduce the severity of this complication.
The wires and restorative are removed when the
fracture has healed.

250

B C

250 Interdental wiring of mandibular fractures.

A The Stout multiple loop wiring technique consists of buccal and lingual wire loops. These loops are connected by
multiple wire loops formed from the lingual strand and tightened around the buccal strand.
B Wire is first applied to the teeth on either side of the fracture line.
C The teeth are acid etched and dental acrylic is applied over the teeth and wire. Acrylic is applied to the buccal and
lingual dental surfaces except for the carnassial tooth, which is not covered on the buccal surface.
268

Interarcade fixation (maxillary–mandibular fixation)
This is a form of biological osteosynthesis that
involves using wires, screws, and elastic or dental
acrylic to fix the mandible and maxilla together to
provide stability (251)3,4,12–14.
When wire is used, the jaws are closed and the
fracture is reduced. Wire (0.6–0.8 mm [22–20 AWG])
is passed through transverse holes drilled bilaterally in
the alveolar bone of the mandible and maxilla, being
careful to avoid tooth roots. Depending on the
fracture location, the wires may be placed just caudal
to the canine teeth or between the roots of the
carnassial teeth. The wire is tightened (twisted) until
stable occlusal alignment is achieved. Sufficient space
is left between the incisors to allow the cat to drink
and eat gruel. Nutrients may be provided via
esophagostomy or gastrostomy tube if necessary. The
wires are removed after 4 weeks or when fracture
healing is complete.
When screws and elastic are used, the screws are
positioned caudal to the canine teeth, avoiding the
tooth roots (252)14. Elastic bands are then placed
over the protruding screw heads to achieve alignment.
The technique is useful for comminuted caudal
mandibular fractures but can also be applied to
temporomandibular joint (TMJ) luxations that remain
unstable after closed reduction. If the screws are
positioned unilaterally, they should be positioned
strategically to oppose any malalignment of the jaw.
Generally the mandibular screw is positioned caudal
to the maxillary screw so that the fracture is distracted.
Implant positioning is reversed for most TMJ
luxations (i.e. the maxillary screw is more caudal than
the mandibular screw). The client should be
instructed how to remove the elastic bands in an
emergency; for example, if the cat is attempting
to vomit.
A method of interarcade fixation described more
recently involves the use of dental restorative (for
example Protemp Garant, ESPE Dental Medizin;
Build-It, Pentron Clinical Technologies LLC.) to
bond the ipsilateral mandibular and maxillary canine

251

B C
251 Interarcade fixation of mandibular fractures.
A Interarcade wiring between the roots of the carnassial teeth.
B Cat showing interarcade bonding of the canine teeth.
C Gun containing resin-based fiber-reinforced dental restorative material used to
bond the canine teeth.
 Fractures and disorders of the skull and mandible
teeth together for up to 6 weeks12. Interarcade canine
acrylic bonding is particularly applicable if all four
canine teeth are intact, but it may still be effective if
there are two opposing canine teeth. Bonding has the
same functional effect as external coaptation but,
unlike the application of a tape muzzle, it is ideally
suited to the cat. It is the authors’ preferred technique
for the majority of mandibular fractures because it is
simple, inexpensive, easy to perform, and produces
excellent results. Unfortunately, it is less suitable for
252
252 Screws placed in the mandible and maxilla for the
treatment of an unstable temporomandibular joint
luxation. (Photograph courtesy of Mark Tonzing.)
A B
253 Interfragmentary wire fixation of a mandibular fracture.
A In all but the most stable fractures it is preferable to use two wires.
B For oblique fractures a triangular configuration can be very effective.
269
brachycephalic cats because of their jaw conformation
and the small size of the canine teeth in these breeds.
Alternative techniques must also be used for very
rostral (and symphyseal) fractures. Depending on the
material used, the canine teeth may need to be
cleaned, pumiced, and acid etched to allow adherence
of the restorative. A thin layer of dental adhesive may
then be applied and cured with an ultraviolet light.
The fracture is reduced and the restorative material is
applied to bridge the upper and lower canine teeth on
one side. The mouth remains open (approximately
1 cm between the mandibular and maxillary incisors)
to allow the cat to eat and drink. Several thin layers
of restorative are applied and cured until fixation is
adequate. The procedure is repeated to bridge the
upper and lower canine teeth on the other side. A
modification of the technique involves placing plastic
cylinders (portions of a drinking straw) on the
ipsilateral canine teeth and filling the cylinders with
chemical cure restorative. Interarcade canine acrylic
bonding does not harm the teeth and avoids the
possible damage to the tooth roots associated with
some other mandibular stabilization techniques. The
restorative sometimes breaks or loosens before the
end of the 6-week period but, by this time, healing is
usually sufficiently advanced so that replacement is
not required.
Interfragmentary wires
Interfragmentary wires are useful in stabilizing
transverse or oblique mandibular fractures, particularly if
the contralateral hemimandible is intact (253)3.
Interfragmentary wires are not recommended in
comminuted fractures where fixation is difficult or
253
270
when bone loss has occurred. A ventral approach is
made to the bone and the periosteum is reflected
from the fracture site. The wire (0.6 mm [22 AWG])
is passed through transverse holes drilled through
the mandible on each side of the fracture line
(avoiding tooth roots). Two wires are placed across
each fracture line to enhance stability. One wire is
placed close to the alveolar border (tension surface)
of the mandible. The wires are placed perpendicular
to the fracture line to provide interfragmentary
compression and reduce shearing forces. It is
important that the wires are tight, otherwise motion
will soon cause cyclic failure of the implants. Once
tightened, the wires are bent over and cut short to
reduce soft tissue trauma. In most cases, the
interfragmentary wires are not removed unless
complications develop15.
Mandibulectomy
Mandibulectomy is indicated as a salvage procedure
for mandibular fractures with irreparable damage
to the bone or soft tissues, severe infection
and sequestration, nonunion, and severe bone loss.
Sufficient mandible is excised to remove infected bone
and soft tissues and to permit tension-free closure of
the oral mucosa. Medial drift of the mandible
will occur in some cases, but is often minimal
and temporary16. Overall, function after partial
mandibulectomy in cats is good.
Fractures of the ramus
Most fractures of the (vertical) ramus are managed
conservatively using a tape muzzle or interarcade
fixation3,6. Internal fixation of ramus fractures is
problematic because the bone of the ramus is much
254
254 Interfragmentary wire fixation of a mandibular
fracture. For fractures of the mandibular ramus the thin
central portion of the bone is avoided and implants are
placed near the periphery.
thinner and weaker than that of the mandibular body
(less than 1.0 mm thick in most of its central
portion) and implant placement involves
considerable elevation of soft tissues. Because of the
extensive musculature surrounding the ramus,
displacement of bone fragments is often minimal. If
internal fixation is necessary to provide stability,
interfragmentary wiring or a small bone plate may be
used (254)11,15.
Bone screws and external fixator pins hold poorly
in the thin cortical bone of the ramus. Fortunately,
dental malocclusion as a complication of fracture is
less common in this region of the mandible8. The
presence of significant malocclusion at the time of
presentation is often an indication that there is
concomitant TMJ luxation.
Condylar fractures are uncommon and when they
do occur they are often associated with fractures of the
symphysis or rostral mandibular body. The principles
of articular fracture repair dictate rigid internal
fixation with accurate anatomic realignment and
early return to function. However, because of the
inaccessibility of the joint and the small size of the
fracture fragments, internal fixation is rarely indicated.
Despite being an articular fracture, good results are
normally achieved with conservative management and
postsurgical periarticular fibrosis is avoided17.
If a functional outcome is not achieved following
conservative management, excision arthroplasty can
be performed with good results18.
Postoperative management
Most cats with mandibular fractures will eat soon after
stabilization of the fractures. A liquid diet should be
fed for the first 4–7 days after surgery and hard food
 Fractures and disorders of the skull and mandible
should be avoided for at least 4 weeks.
If damage to the mouth and pharynx is severe, or if
the fracture fixation technique prevents opening of the
mouth, a nasopharyngeal feeding tube can be placed to
allow tube alimentation before and after surgery.
Alternatively, an esophagostomy or gastrostomy
feeding tube can be placed while the cat is anesthetized
for radiographs or fracture repair. Although the goal is
rapid return to enteral nutrition, tube feeding using
liquidized tinned foods or commercial diets may be
required to maintain the animal’s caloric intake during
the first few days or weeks after surgery. (For further
discussion of feeding tubes see Chapter 3.)
Complications of mandibular fracture
Complications are common and were reported in
24.5% of mandibular fractures in 62 cats8. The most
frequent complication was dental malocclusion
secondary to malunion, which is most easily resolved by
extraction of the offending teeth if they interfere with
eating. The use of intraoral appliances for fracture repair
will inevitably be associated with a degree of stomatitis
and gingivitis secondary to food entrapment, but this
will resolve rapidly once the appliance is removed.
MAXILLOFACIAL FRACTURES
CAUSE AND PATHOGENESIS
Fractures of the maxillofacial bones and palate occur
as a result of trauma.
CLINICAL SIGNS
Swelling, epistaxis, and subcutaneous emphysema
are common clinical signs4. Dyspnea and airway
obstruction can occur due to intranasal hematomas and
swelling, or if bone fragments are markedly displaced.
DIAGNOSIS
Cats with maxillofacial fractures should be carefully
evaluated for concurrent injuries, particularly neurologic
deficits from cranial trauma. Radiographic examination
is helpful to assess the extent of the injury to the skull.
TREATMENT AND PROGNOSIS
The majority of maxillofacial fractures are stable and
minimally displaced and can be treated conservatively.
The nares are kept clean to ease respiration and
oxygen may be provided initially if needed. Anti-
inflammatory drugs are administered to reduce
swelling and pain. Most cats will drink and eat soft
food, although nutritional support via esophagostomy
or gastrostomy tube may be required in more severe
cases. A tape muzzle can be used to stabilize the
fracture site if needed.
271
Surgical treatment of maxillofacial fractures
is indicated when the nasal cavity is occluded,
when marked displacement of bone fragments causes
disfigurement, or when malocclusion with the mandible
is present. Surgery is performed once the initial swelling
has resolved. If the fracture is reconstructable, bone
fragments are reduced and stabilized with inter-
fragmentary wires (0.5 mm [24 AWG]). Non-
reconstructable comminuted fractures are treated using
interdental acrylic splinting or application of a bilateral
acrylic external fixator. Rarely, sequestrum will form at
the fracture site and require excision. Avulsion fractures
of the alveolar bone typically retain some mucosal or
gingival attachments and are stabilized using Kirschner
wires. If fragments must be removed, mucosal flaps are
used to cover the defect and prevent oronasal fistula
formation3. Mandibular symphyseal realignment and
stabilization using cerclage wire has been described for
correction of malocclusion secondary to impaction
fractures of the maxilla19.
Palatine fractures
Fractures of the hard palate and nasal bones in the
median plane are common in traumatized cats (255).
The fracture is a component of the triad of injuries
(thoracic trauma, facial trauma, and extremity fractures)
termed ‘high rise syndrome’20. Injury occurs when a
cat jumps or falls from a height of two storeys or more
255
255 Anesthetized cat with fracture of the hard palate in
the median plane. The endotracheal tube has been placed
via a pharyngostomy incision. (Photograph courtesy of
Carlos Macias (same cat as 246).)
272

and lands on its forelimbs and chin. Ventral trauma
forces the mandible dorsally, creating distraction forces
between the hemimaxillae, which results in fracture in
the median plane often accompanied by a cleft palate.
The fracture is characterized by a cleft in the soft tissue
and bone of the hard palate and is readily diagnosed on
oral examination. Cats with palatal fractures may have a
nasal discharge and may have blood in the saliva.
Conservative treatment of palatine fractures has been
recommended21. Defects less than 2–3mm in width
may heal within 4 weeks. However, surgery is the
preferred option in most cases, especially for larger
lesions or if the defect fails to close3,4. Surgical repair will
prevent food and water from entering the nasal cavity
during healing. In most cases, the defect is reduced
using digital pressure on each side of the maxilla. With
the palate reduced, a Kirschner wire is driven across the
maxilla, dorsal to the bony palate, avoiding the tooth
roots. The angle of the pin should be maintained parallel
to the hard palate and carefully controlled to avoid
penetration of the contralateral orbit. Ideal pin
placement is between the third and fourth premolars
(just rostral to the roots of the maxillary carnassial
tooth). The Kirschner wire should protrude approxi-
mately 2 mm on each side between the teeth. An
intraoral figure-of-eight wire is then placed around the
protruding ends of the Kirschner wire (256). Rather
than leaving the figure-of-eight wire exposed it is prefer-

256

A B

C D
256 Palatine fracture repair. A With the fracture reduced, a Kirschner wire is driven across the maxilla just dorsal to the
hard palate between the roots of the third and fourth premolar teeth. Approximately 2 mm is left protruding at each end.
B A figure-of-eight of orthopedic wire is placed around the protruding ends of the Kirschner wire and tightened. It is
preferable to bury this wire beneath the mucoperiosteum of the hard palate. C An additional Kirschner wire may be placed
in the same fashion caudal to the canine teeth if necessary as shown on this radiograph. (Radiograph courtesy of Malcolm
McKee.) D A Kirschner wire has been placed caudal to the canine teeth just dorsal to the hard palate. A figure-of-eight of
orthopedic wire has been placed around the protruding ends of the Kirschner wire (and the canine teeth) and tightened. An
additional Kirschner wire was placed in the same fashion between the roots of the third and fourth premolar teeth. The
caudal figure-of eight of wire was buried beneath the mucoperisoteum. (Photograph courtesy of Carlos Macias (same cat as
246 and 255).)
 Fractures and disorders of the skull and mandible
273

able to bury the wire by passing it between the bone and
the mucoperiosteum before looping it around the ends
of the interfragmentary pin. The ends of the pin are bent
over to prevent migration and avoid trauma to the labial
mucosa. If desired, the oral mucosa overlying the palate
is apposed with absorbable suture material.
Alternatively, palatine fractures can be stabilized
using intraoral wire loops or large monofilament
sutures placed around the right and left maxillary
canine teeth and between the roots of the right and
left carnassial teeth (257)3. It is preferable to bury the
more caudal wire by passing it between the bone and
the mucoperisoteum.
Postoperatively there is rapid relief from pain and
patients are usually willing to eat the day after surgery.
The cat should be fed soft food and observed for signs
of rhinitis. If the intraoral wire is left exposed, the
surgical site may be lavaged daily with water using a
syringe; however, this is not essential and may not be
tolerated by some cats. The implants are removed
after 3–4 weeks when healing is complete.
Zygomatic arch fractures
Fractures of the zygomatic arch cause pain and
swelling of the periorbital region8. In most cases,
zygomatic arch fractures are managed conservatively,
using cold compresses to reduce swelling. If the cat is
unable to blink properly, topical eye ointment may be
applied to protect the cornea until periorbital
swelling subsides. Medially displaced fragments can
displace the globe and interfere with movement of
the mandible. They can be reduced and stabilized
using interfragmentary wires or, if comminution is
severe, they can be removed. The arch is exposed via
a lateral skin incision and elevation of the platysma
muscle, avoiding the palpebral nerve and facial
vessels.
TEMPOROMANDIBULAR
JOINT INJURY
TEMPOROMANDIBULAR JOINT LUXATION
Cause and pathogenesis
The TMJ is a condylar joint that has a simple
hinge-like function in the cat. The joint is inherently
stable as a result of the close congruity between
the condyloid process and the relatively deep
mandibular fossa22. Rostral condylar displacement
is prevented by a well developed bony process
analogous to the human articular eminence.
Likewise the well developed retroarticular process
prevents caudal displacement. Interposed between
the articulating surfaces is a fibrocartilaginous
meniscus dividing the joint into two separate
compartments. There is a loose joint capsule that is
strengthened laterally by fibrous bands forming a
lateral ligament. Luxation is presumed to occur
when there is traumatic overextension of the TMJ.
In most cases there is unilateral luxation of the
mandibular condyle from the mandibular fossa in a
rostrodorsal direction.

257

A B

257 Alternative method of palatine fracture repair.

A Orthopedic wire is placed between the roots of the left and right maxillary carnassial teeth and around the base of the
maxillary canine teeth. It is preferable to bury the more caudal wire beneath the mucoperiosteum.
B The two figure-of-eight wires are tightened to close the defect.
274

Clinical signs Treatment and prognosis

Typically an affected cat is presented with an inability
to close the mouth and with the lower jaw deviated
away from the affected TMJ. Unilateral, caudoventral
luxation is occasionally encountered, in which case the
jaw will be deviated toward the side of the lesion. TMJ
luxations may occur alone or with other fractures of
the mandible3. Luxation as a component of multiple
mandibular injury may be more difficult to detect but
should be suspected in any patient with head trauma
where there is significant unexplained malocclusion.
In contrast to the dog, isolated TMJ luxation is said to
be common, although many cases have concurrent
fracture of either the condyloid process, the caudal
retroarticular process, or the rostral articular
eminence23. Bilateral luxations may also occur.
Diagnosis
Intraoral examination may reveal swelling and contusion
in the region of the TMJ and mediolateral laxity can
be palpated in most cases. Radiography (lateral,
ventrodorsal, and oblique views) is used to confirm the
luxation and evaluate for concurrent fractures.
Right and left lateral oblique projections with the
cat’s head rotated dorsally by 20° will usually permit
evaluation of both TMJs23,24. To obtain these views
the head is rotated along its median axis so that the
TMJ nearest the film will be projected clear of the
skull ventrally. The radiographs should be checked
carefully for periarticular fracture since this will
complicate treatment.
Closed reduction of TMJ luxations is possible in most
cases (258).
With the cat under general anesthesia, a
tuberculin syringe or small dowel is placed
transversely across the jaw at the level of the molar
teeth. The rostral mandible and maxilla are then
squeezed together, partially closing the jaw and
levering the caudal mandible against the syringe to
disengage the luxated condyle. While maintaining
pressure on the rostral mandible, it is pushed in
the appropriate direction to reduce the luxation.
For caudoventral luxations, the rostral mandible is
pushed away from the side of the luxation; for the
more common rostrodorsal luxations, the rostral
mandible is pushed toward the side of the luxation.
Once the luxation is reduced, pressure on the
mandible is released. Reduction is confirmed by
proper occlusion of the upper and lower canine teeth
and by radiography.
In an alternative reduction method, the thumb is
placed in the oral cavity and the mandibular body is
grasped between the thumb and forefinger4. Traction
is applied to manipulate the TMJ into reduction.
Manipulating the mandible with the mouth closed as
much as possible will ease reduction.
In most cases, the TMJ will be stable after closed
reduction. If there is instability, additional support is
provided by the application of a tape muzzle for
2 weeks or an interarcade fixation technique is used.
Rarely, the TMJ cannot be reduced or reluxation

258

258 Reduction of a rostrodorsal temporomandibular luxation. A wooden

dowel or tuberculin syringe is placed between the carnassial teeth to act as
a fulcrum. The mouth is forced closed to disengage the condyle and the
affected side is pushed caudally to reduce the luxation.
 Fractures and disorders of the skull and mandible
275

occurs after reduction. Open reduction and
imbrication of the joint capsule or condylar resection
is indicated and may be achieved through a lateral
approach6,18. A condylar tethering technique using
polyester suture has been described and was
successfully applied to a cat with recurrent luxation
and fracture of the articular eminence25.
TEMPOROMANDIBULAR JOINT ANKYLOSIS
Cause and pathogenesis
TMJ ankylosis can result from trauma, infection, or
neoplasia, although the majority of reported cases have
occurred as a sequela to TMJ trauma26–30. It is prudent
to warn clients of all cats suffering craniofacial trauma
of the risk of subsequent TMJ ankylosis. The ankylosis
may be intraarticular (true ankylosis) or extraarticular
(false ankylosis) but the presentation is the same31.
Clinical signs
The primary clinical sign is the inability to open the
mouth completely, leading to an inability to eat,
weight loss, an unkempt staring coat because of
difficulty grooming, and atrophy of the masticatory
muscles. Typically there is a progressive reduction
in the range of jaw motion, usually over a period
of many months. If ankylosis occurs in an immature
cat, altered development of the mandible may
occur, causing brachygnathism or other abnormalities
in facial appearance27. Ankylosis may occur
unilaterally or bilaterally.
glucocorticoids fails to prevent recurrence of
ankylosis after this maneuver.
Endotracheal intubation may not be possible and
alternative arrangements should be made for the
maintenance of anaesthesia; for example, by repeated
infusion of an intravenous agent such as propofol.
Provision should be made for an emergency
tracheotomy if the airway becomes obstructed during
the procedure.
Before approaching the TMJ it is advisable to
split the mandibular symphysis to verify normal
functioning of the contralateral joint28. Mandibular
symphysiotomy is easily performed using an
osteotome via a mid-line incision on the chin. If the
TMJ ankylosis is unilateral, the unaffected
hemimandible can then be opened to allow
endotracheal intubation and maintenance with
gaseous anaesthesia. If ankylosis is bilateral, surgery is
performed on both joints simultaneously.
259

Diagnosis
Radiographic examination should be performed
using a dorsoventral view of the skull and lateral
oblique views of both TMJs. However, radiographic
evaluation of the feline TMJ for ankylosis is difficult
and the changes may be missed or their extent may
be underestimated. Expected radiographic changes
include loss of joint space and periarticular new bone
production and there may be evidence of previous
trauma (259).

Treatment and prognosis

Treatment for TMJ ankylosis is surgical resection of
the abnormal tissue to allow more normal range of
jaw motion. It may be necessary to excise the
mandibular condyle, the coronoid process, part of
the zygomatic arch, and the periarticular
osteophytes. Treatment by stretching the jaws open
under general anaesthesia (so-called brisement 259 TMJ ankylosis. Dorsoventral radiograph of a cat
forcée) carries the risk of jaw fracture and is with bilateral TMJ ankylosis. There is periarticular
associated with a high frequency of recurrence. periosteal new bone formation affecting both TMJs
Parenteral or periarticular administration of (arrows).
276

With the patient in lateral recumbency, a curved Postoperative care

skin incision is made along the ventral border of the
zygomatic arch, crossing the TMJ caudally (260).
The origin of the masseter muscle on the zygomatic
arch is incised and subperiosteal reflection of the
muscle is performed taking care to avoid the dorsal
branch of the facial nerve. In most cases there is
extensive bone formation around the caudal portion
of the zygomatic arch, necessitating removal of its
caudal portion and adjacent periarticular new bone
to gain access to the TMJ. This exposes the lateral
surface of the joint and the dorsal portion of the
condyloid process. Proceeding in a ventromedial
direction, further proliferative bone and fibrous
tissue, the mandibular condyle, and as much of the
dorsal portion of the ramus as necessary are excised
in order to re-establish jaw movement. In those cases
that have undergone preliminary symphysiotomy,
this is repaired in a conventional manner using
cerclage wire.
Postoperatively a soft diet is fed for 4 weeks and
physical therapy is commenced after the first week
to help improve range of motion and reduce the
likelihood of recurrence of the ankylosis. Physical
therapy for the jaw may be achieved by feeding
frequent small meals and gently forcing the mouth
open and closed several times a day. The prognosis
after surgical resection of the ankylosis is generally
good. A pseudoarthrosis develops as the area is filled
with fibrous connective tissue27. Potential com-
plications include re-ankylosis, facial nerve paralysis,
and malocclusion.
TEMPOROMANDIBULAR JOINT FRACTURES
Fractures of the TMJ are managed in several ways.
Fixation may be unnecessary in fractures with
minimal displacement and normal occlusion. The cat
is fed soft food for 3–4 weeks to allow healing.
Highly comminuted fractures of the TMJ are

260

Zygomatic arch
Platysma muscle
Palpebral nerve
Transverse facial vein

Dorsal Nerve to tactile and sinus hair

branch Condyloid process of mandible
of facial Platysma muscle
nerve Masseter muscle
A B

260 Surgery for TMJ ankylosis.

A TMJ ankylosis showing the surgical approach (inset).
B Treatment by excision of the condyloid process including a portion of the vertical ramus and the zygomatic arch.
 Fractures and disorders of the skull and mandible
difficult to stabilize because of the small size of the
fragments. In most cases, these fractures are treated
with a tape muzzle or interarcade fixation 17.
Immobilization for 3–4 weeks is usually adequate. If
adequate function does not return, excision
arthroplasty of the condyle is performed18. The
condyle is removed with a rongeur or osteotome to
allow development of a functional pseudoarthrosis
and prevent contact between the mandible and the
temporal bone.
INTERMITTENT OPEN MOUTH LOCKING
Cause and pathogenesis
This condition is recognized in certain breeds of dog
and there are a number of single case reports of the
condition in the cat32–35. Three of the four reported
cases have been in Persian cats and it may be that the
brachycephalic conformation of this breed is a
predisposing factor.
The condition in dogs is associated with TMJ
dysplasia and joint laxity, which allows the coronoid
process of the mandible to contact the ventral or lateral
aspect of the ipsilateral zygomatic arch, preventing
closure of the mouth. Mandibular symphyseal laxity may
also contribute to excess lateral movement of
the hemimandible and the resulting impingement.
The etiology is assumed to be the same for the
cat, although in one case (the only non-Persian)
a deformity of the zygomatic arch was presumed to be
the cause of the impingement.
Clinical signs
All reported cases have had a history of
repetitive open mouth jaw locking, especially after
yawning. There may be signs of mild discomfort
when the jaw is locked. Palpation in the locked state
reveals a unilateral protuberance along the
ventrolateral aspect of the zygomatic arch on the
affected side.
Diagnosis
Diagnosis is based on physical examination and
radiographic findings, including displacement of the
mandible, impingement of the coronoid process on
the zygomatic arch, and, in some cases, bony dysplasia
of the TMJ.
Treatment and prognosis
If the cat is presented with the jaw locked, reduction
is achieved by opening the mouth a little further and
pressing the protruding coronoid process medially.
Treatment is by partial zygomatic arch ostectomy.
Locking is recreated during surgery in order to
277
identify the site of impingement. An approach is made
over the ventral border of the zygomatic arch at this
point, using blunt dissection and periosteal elevation
to expose the bone. Rongeurs are used to remove a
small rectangular segment of the bone, 10–15 mm
long, from the ventral aspect, leaving the dorsal
border intact, if possible, to support the orbit. The
mouth is opened again to confirm that it is not
possible to induce locking. An alternative technique
involves ostectomy of only the locking part of the
coronoid process32. In severe cases it may be necessary
to excise the entire zygomatic arch and the coronoid
process of the mandible.
FRACTURES OF THE
NEUROCRANIUM
Fractures of the neurocranium are uncommon,
presumably due to the fact that most cats are killed
outright or die soon afterwards. Emergency
treatment of animals with head trauma has recently
been reviewed 36. All cats with head trauma
constitute a medical emergency and surgical
intervention may be indicated in a small proportion
of cases. Mortality, even in treated cases, is high,
with death typically resulting from a progressive
increase in intracranial pressure.
The goals of therapy are to alleviate brain swelling
and prevent damage to vital brainstem structures.
Surgical intervention may be indicated for treatment of
fractures of the skull when they are open or depressed
sufficiently to impinge on the underlying neurologic
structures. Cats have a remarkable ability to
compensate for loss of cerebral tissue and it is important
not to make hasty decisions based on the initial
appearance of a patient with severe head trauma.
The initial approach to management is the same
for any acutely traumatized cat and is directed
at concurrent life-threatening injuries. Hypoxia
is addressed by maintaining a patent airway,
and placing the patient in an oxygen-enriched
environment. Despite concerns about exacerbation
of cerebral edema, hypovolemia should be corrected
by administration of intravenous fluids. In addition,
specific medical therapy may be initiated, although
there is considerable controversy surrounding the
use of drugs for head injury. Mannitol is an osmotic
diuretic that has been shown to reduce brain edema
and intracranial pressure. Theoretical concerns
about exacerbation of intracranial hemorrhage
by the osmotic action of mannitol are clinically
unfounded and should not prevent its use 36.
Once the patient is hemodynamically stable,
mannitol is administered as a slow intravenous
278
infusion over 10–20 minutes at a dose of 2.0–4.0 g
for the average cat. Mannitol has a rapid onset of
action, which persists for 2–5 hours. The drug may
be repeated if necessary to a maximum of three
boluses in a 24-hour period.
The use of glucocorticoids is contraindicated
for head trauma victims because they exacerbate
hyperglycemia. Hyperglycemia can potentiate
neurologic injury in patients with head injury,
so iatrogenic hyperglycemia should be avoided37.
High-dose methylprednisolone sodium succinate
therapy may provide beneficial therapeutic effects solely
because of its free-radical scavenging activity.
Methylprednisolone sodium succinate should be given
as an adjunctive treatment within 8 hours of injury
and, because of concerns about induction of
hyperglycemia, its use should probably be restricted to
nonhyperglycemic cats that are not responding to fluid
and oxygen therapy and mannitol administration.
Prediction of outcome is based on an assessment of
261
Burr/drill holes
261 Surgical decompression for head injury.
the level of consciousness and brainstem reflexes and
the results of serial neurologic examinations following
treatment. Loss of consciousness, dilatation of one or
both pupils, and motor dysfunction, such as paresis or
decerebrate rigidity, are bad prognostic indicators.
Deterioration in the neurologic status despite medical
therapy indicates progressive brain edema and/or
hemorrhage and, under these circumstances, surgical
decompression should be considered.
Decompression is achieved by trephining the skull
close to the fracture (261). Depression fractures are
treated by insertion of small instruments around the
periphery of the fracture to elevate and remove
the fragments. Meticulous hemostasis is essential,
followed by closure of the dura mater, either by direct
suturing or by the application of a temporal fascia graft
if a defect is present. Unstable bone fragments should
not be replaced since the temporal muscle provides
adequate protection for the brain parenchyma.
Bone
fragment
Elevator Drill hole Meninges
Cerebral parenchyma

CHAPTER 11
FRACTURES AND
DISORDERS OF THE SPINE
SURGICAL ANATOMY
VERTEBRAE
The vertebral column is composed of a series of
51–54 vertebrae, most of which are joined by
intervertebral discs, ligaments, and the synovial
joints between the articular processes. The basic
structure of each vertebra is similar, although the
morphology varies from one region of the spine to
another. Each vertebra has a vertebral arch
comprising two pedicles and a dorsal lamina. The
vertebral canal is formed from the vertebral arch
laterally and dorsally and the vertebral body
ventrally. Most vertebrae have transverse processes
projecting laterally from the vertebral body, a
spinous process projecting dorsally from the lamina,
and cranial and caudal articular processes on the
vertebral arch. Other bony processes vary according
to region. The synovial articulations lie dorsally
except for those between the first and second
cervical vertebrae (C1–2), where they are ventral,
and the sacrum, where they are fused. These
262 Articulated cranial lumbar vertebrae.
279
articulations are standard diarthrodial joints with
articular cartilage, a joint capsule, and synovial fluid
(262). Spinal nerves and blood vessels exit the
vertebral canal between each pair of vertebrae
through their respective intervertebral foramina.
The first two cervical vertebrae, the atlas and
axis, have a distinct morphology that reflects their
more specialized function. There is no
intervertebral disc between the atlas and axis. With
the exception of C7, the vertebral arteries pass
through transverse foramina in the transverse
processes of the cervical vertebrae. The axis has a
very large dorsal spinous process that extends over
the atlas and is connected to it by the atlantoaxial
ligament. The dens arises embryologically from the
atlas and has a separate growth plate. It projects
cranially from the body of the axis and lies on the
floor of the vertebral canal. Thoracic vertebrae
articulate with the ribs and have small vertebral
bodies and large dorsal spinous process. Lumbar
vertebrae have very long vertebral bodies with short
262
280
spinous processes angled cranially. The lumbar
transverse processes project cranioventrally,
overlapping the preceding vertebra. The ventral
deflection of these processes is more pronounced in
the cat than the dog. The transverse processes are
short on the first lumbar vertebra (L1) but become
progressively narrower and longer on more caudal
vertebrae. The ribs and the transverse processes of
L1 at the thoracolumbar junction are important
landmarks when performing surgery in this region
of the spine. The three sacral vertebrae are fused to
form one body, which articulates with the pelvis at
the sacroiliac joints.
SPINAL CORD
The spinal cord extends from the foramen magnum
to L7 in the vertebral canal. The cord is surrounded
by the meninges, which comprise three layers. The
most superficial and substantial layer is the dura
mater. Lying adjacent to the dura is the thin
arachnoid mater and internal to this is the pia mater,
which is closely apposed to the cord. Cerebrospinal
fluid (CSF) is contained intrathecally in the
subarachnoid space between the pia and arachnoid
maters. This space is traversed by the arachnoid
trabeculae, which suspend the spinal cord in the CSF.
The termination of the spinal cord is known as the
conus medullaris and the meninges caudal to the
conus medullaris form the filum terminale, which
extends into the sacrocaudal vertebral canal.
The cord is divided into a central core of gray
matter, comprising the cell bodies of lower motor
neurons, and an external portion of white matter,
composed of ascending and descending groups of
axons called tracts. The tracts or pathways that
ascend (afferent) to the brain have a sensory function
263
L3 L4 L5 L6 L7
L3 L4
L5
263 Lumbosacral spine showing the relationship between spinal cord segments
and vertebrae. Segment L4 is dorsal to the L4 vertebral body, segment L5 is
dorsal to the L4–5 intervertebral disc, segments L6 and L7 are dorsal to the L5
vertebral body, and the three sacral segments are dorsal to the L6 vertebral body.
and those that descend (efferent) from the brain
have a motor function. The spinal cord is segmental
(eight cervical, thirteen thoracic, seven lumbar, three
sacral, five caudal) with each paired dorsal and
ventral nerve root emanating from its respective
segment and joining to form the paired segmental
spinal nerves, which exit at the corresponding
intervertebral foramina. The C1 spinal nerves exit
through the lateral foramina in the atlas. The
remaining cervical spinal nerves exit through
the intervertebral foramina cranial to the vertebra of
the same annotation, with the exception of the C8
nerves, which exit between the C7 and T1 vertebrae.
Thus the thoracic and lumbar segmental spinal
nerves exit through the intervertebral foramina
caudal to the vertebra of the same annotation. Spinal
cord segments C6–T2 and L4–S3 contain the cell
bodies for the lower motor neurons forming the
brachial and lumbosacral plexuses innervating the
forelimb and hindlimb musculature respectively.
These two regions of the spinal cord are thicker and
are known as intumescences. It is essential to
understand the relationship between spinal cord
segments and vertebrae in order to determine the
anatomic location of a lesion; neurologic lesion
localization refers to spinal cord segments and not
vertebrae (263).
In contrast to the dog, where the lumbosacral
spinal cord is considerably foreshortened, the feline
conus medullaris was found to terminate in the
sacrum in over 90% of adult cats1. As a consequence
of this there is closer correlation between the
vertebrae and their respective spinal cord segments,
and a focal compressive lesion will tend to affect fewer
spinal cord segments and nerve roots than a lesion in
the same location in the dog.
S1 S2 S3 CD1
S3
S2
L6 L7 S1
 Fractures and disorders of the spine
INVESTIGATION OF
SPINAL DISEASE
APPROACH TO THE SPINAL PATIENT
Spinal disease is uncommon in the cat compared
with the dog, largely because of the infrequency of
intervertebral disc disease. This may appear to be
good news for the cat, but the consequences for the
veterinarian are unfamiliarity with the procedures
for diagnosis and investigation of spinal diseases
when they do occur. There is also a lack of
consensus on the optimum methods of management
for many disorders. Spinal disease should be
suspected in any cat presented with spinal pain,
hindlimb weakness, or paralysis. Neuromuscular
diseases must also be considered if there is
generalized weakness or paralysis affecting all four
limbs.
SIGNALMENT AND HISTORY
The signalment is important in the initial assessment
of any neurologic disease but this information can be
misleading and should be used with care. Breed
predispositions are less important in the cat than the
dog since pedigree cats are less common than their
canine counterparts. In general, trauma is more
frequent in young cats, whereas degenerative and
neoplastic conditions tend to increase in frequency
with age. However, there are exceptions; for example,
spinal lymphoma, which is more prevalent in young
cats. A full history is an important prerequisite to the
neurologic examination and will provide information
about the nature, duration, and progression of the
disease in addition to antecedent disease and the
response to previous therapy.
PHYSICAL EXAMINATION
A carefully performed routine physical examination
should provide information about relevant concurrent
or intercurrent disease and will assist in ruling out a
number of disorders that may mimic spinal disease. In
practice it is easier to perform a screening neurologic
examination as part of this routine physical
examination. If there are concurrent signs referable to
the head, such as altered consciousness, seizures, or
cranial nerve deficits, then the disease can either be
localized to the brain or it is diffuse or multifocal in
origin.
Observation of gait, posture, and general
demeanor should precede the hands-on part of the
examination. The patient should be allowed to relax
and should be gently coaxed to move around the
examination room, unless a traumatic spinal injury is
suspected, in which case movement should be
281
restricted. This part of the examination is particularly
relevant to the cat, as latter parts of the examination
may be more difficult to perform. The presence of any
spinal pain or deformity should be noted at this stage.
It is also important to check the color of the footpads
and the quality of the femoral pulses in any cat with
acute paraparesis or paraplegia to rule out ischemic
neuromyopathy.
NEUROLOGIC EXAMINATION
If neurologic abnormality is suspected during the
initial physical examination, a more thorough
neurologic examination is performed with the goal
of establishing whether spinal disease is present and,
if it is, to determine its location and assess its severity.
A full description of how to perform a neurologic
examination is contained in standard neurology texts
and only those aspects of the examination that are
pertinent to feline spinal disorders will be discussed
here. A methodical approach is followed and this
generally makes the clinical syndromes in cats with
neurologic dysfunction caused by spinal disease easy
to recognize. The investigation of cats presenting
with nonspecific signs of pain and lameness not
caused by orthopedic disease may be more
problematic.
Performing a neurologic examination on any
patient can seem daunting for the novice.
Additional difficulties include the potentially
uncooperative nature of the feline patient and the
fact that some of the tests used in the dog are either
not applicable to the cat or must be interpreted with
caution. It is essential that the clinician develops
familiarity with the responses of normal cats by
regular practice before drawing conclusions about
the altered responses seen in clinical cases. The
examination should be performed in a quiet
environment with the patient initially in the upright
position. Once the cat has become more
accustomed to being handled, the remainder of the
tests are performed with the patient in lateral
recumbency. Patients must not be sedated or
anesthetized prior to neurologic examination since
this will alter the responses seen to many of the
stimuli.
Localization of spinal lesions
Spinal cord lesions display a range of signs based on
their location and severity. On the basis of
the neurologic examination it may be possible to
localize the lesion to one of five functional regions of
the spinal cord. These regions are cervical (C1–C5),
cervicothoracic (C6–T2), thoracolumbar (T3–L3),
282

lumbosacral (L4–S3), and sacral (S1–S3) (264). The
cervical and thoracolumbar regions of the spinal cord
convey the upper motor neurons whereas those of the
cervicothoracic and lumbosacral regions also contain
the cell bodies of the lower motor neurons to the
forelimbs and hindlimbs respectively. Lesions in these
different regions will produce different permutations
of neurologic signs (Table 22).
The tests used to localize neurologic signs include
postural reactions and assessment of reflexes
(Table 23). Postural reactions are sensitive but
relatively nonspecific indicators of neurologic

264 264 The five functional

Cervical Lumbosacral
regions of the spinal cord:
intumescence intumescence
cervical, cervicothoracic,
thoracolumbar, lumbosacral,
and sacral.

C1–C5 C6–T2 T3–L3 L4–S3 S1–S3

TABLE 22 THE EXPECTED REFLEX RESPONSE TO SPINAL CORD LESIONS.

Lesion location* Forelimb Hindlimb Bladder, anus, and tail
C1–C5 UMN UMN UMN
C6–T2 LMN UMN UMN
T3–L3 Normal UMN UMN
L4–S3 Normal LMN LMN
S1–S3 Normal Normal LMN

* Based on spinal cord segments rather than vertebrae

UMN = upper motor neuron
LMN = lower motor neuron.

TABLE 23 COMMONLY ASSESSED SPINAL REFLEXES.

Site Reflex Spinal cord segments
Forelimb Extensor carpi radialis C7–T2
Forelimb Flexor (withdrawal) C6–T2
Hindlimb Patellar L4–L6
Hindlimb Cranial tibial L6–S1
Hindlimb Flexor (withdrawal) L6–S1
Anus Perianal S1–Cd1
Bladder Sphincter tone S1–S3
Dorsum Cutaneous trunci (panniculus) T3–L1 (afferent)
C8–T1 (efferent)
 Fractures and disorders of the spine
dysfunction. A positive test merely indicates loss of
integrity of either the lower motor neurons of the
local reflex arc or the upper motor neuron tracts to
the brain. Some postural reactions such as hopping on
individual limbs, hemistanding, hemiwalking, and
wheel-barrowing are difficult to perform and interpret
because of the temperament of the cat. Other tests,
such as proprioceptive placing, extensor postural
thrust, and the crossed extensor reflex, are more
consistently useful.
The segmental cutaneous trunci (panniculus)
reflex is unreliable in the cat and it is therefore
important not to ascribe too much significance to its
absence since it cannot be elicited in some normal
individuals. Assessment of flexor (withdrawal) and
myotatic (tendon stretch) reflexes is used to localize
a lesion to the area of the spinal reflex tested. These
segmental tests do not rely on the integrity of
pathways to the higher centers and these reflexes
will be intact even if portions of the spinal cord
cranial to the reflex arc are completely destroyed.
The most reliable forelimb myotatic reflex is the
extensor carpi radialis although even this is variable
in normal cats. In the hindlimb, the patellar reflex is
the most reliable myotatic reflex and can generally
be assessed accurately in all cats. Myotatic reflexes
are graded on the basis of the strength of the motor
response. Lesions that affect the lower motor
neurons of the reflex arc cause depression or
absence of the reflex tested. This type of neurologic
dysfunction is referred to as lower motor neuron or
flaccid paresis or paralysis since the tone in the
affected muscles is reduced. It is important to note
that the finding of lower motor neuron deficits in all
four limbs is usually indicative of neuromuscular
disease rather than spinal disease. Lesions cranial to
the segmental site of the reflex arc spare the spinal
reflex and the motor response may be increased
because of the loss of the inhibitory influence of the
upper motor neurons. The neurologic dysfunction
in these cases is referred to as upper motor neuron,
or spastic paresis or paralysis, since the tone in the
affected muscles is increased. However, the
distinction between hyperactive and normal
responses is not clear-cut and caution should be
exercised in the interpretation of an apparently
hyperactive response.
The flexor reflex is elicited by applying a painful
stimulus to the digit using fingers or a hemostat. A
positive response is shown by flexion of all of the
joints in the tested limb. It should be stressed that
this reflex indicates functional spinal cord segments at
this level but does not require conscious perception
283
of noxious stimuli. The crossed extensor reflex may
also be observed when testing the flexor reflex. A
positive response is seen when the contralateral limb
rapidly extends as the tested limb flexes. This
abnormal reflex is seen in most cats that have a severe
lesion at a site cranial to the segments involved in the
flexor reflex. Assessment of the perianal reflex is
accomplished by stimulating the anus or perianal
skin. The normal reaction is contraction of the anal
sphincter and flexion of the tail. Bladder function
should be assessed when urinary retention or
incontinence is suspected by attempted manual
evacuation. Increased urethral sphincter tone is
associated with lesions involving the upper motor
neuron supply to the bladder. There will be urinary
retention with overflow and manual evacuation of the
bladder will be difficult. Loss of urethral sphincter
tone is associated with lower motor neuron lesions
affecting the sacral spinal cord segments. The bladder
will be large and flaccid, with little resistance to
manual evacuation.
Assessment of severity and prognostic indicators
The severity of a lesion is inferred from the degree of
neurologic dysfunction and has an important bearing
on the prognosis. Cases are assigned to a grade based
on the results of the neurologic examination. The
specific criteria used to assign patients to a grade are
spinal pain, unassisted walking ability, voluntary limb
movement, and perception of deep pain. The grading
system used by the authors is as follows:
• Grade 1: spinal pain with no evidence of
neurologic dysfunction.
• Grade 2: ambulatory paresis.
• Grade 3: nonambulatory paresis.
• Grade 4: plegia.
• Grade 5: plegia and absence of deep pain
perception.
• Grade 6: ascending/descending myelomalacia.
Perception of deep pain is dependent on functional
ascending tracts in the spinal cord and a positive
response is shown by a conscious reaction to the
stimulus. Positive responses include turning the head
in recognition of the pain, attempting to scratch or
bite the examiner, or an autonomic effect, such as
dilatation of pupils or increased respiratory or heart
rate. The small nonmyelinated nerve axons that carry
deep pain sensation are more resistant to the effects
of distortion than other nerve fibers. They are also
numerous and diffusely distributed in multisynaptic
tracts adjacent to the spinal cord gray matter.
Therefore, deep pain perception is the last modality
284
to be lost and its absence is a bad prognostic sign.
Because deep pain is a key prognostic indicator it is
important to apply a maximal stimulus such as
application of pliers to the distal limb (taking care
not to crush the tissues) before consigning a patient
to the grade 5 category. It is also important to assess
the presence or absence of voluntary bladder
function since this will affect the management of the
case and may have an influence on the prognosis.
In some cases with severe neurologic signs, such
as loss of deep pain perception, the prognosis may
be so bad that further investigation to determine
the etiology may be deemed unnecessary. In
general, the prognosis worsens as the severity of
neurologic dysfunction increases and is worse for
individuals displaying lower motor neuron rather
than upper motor neuron deficits. The nature of the
injury, and the duration and rate of onset of the
neurologic signs, are also factors that may have a
bearing on the prognosis. For instance, it is
generally accepted that the prognosis for patients
with no deep pain perception is poor if this has been
caused by an acute traumatic injury or if the pain
perception has been absent for more than
48 hours. In dogs with intervertebral disc extrusion
and absence of deep pain perception, one study
showed that the prognosis is better following
decompressive surgery if the onset has been
gradual2. There is no specific information available
in the cat but the situation is likely to be similar.
Cervical and cervicothoracic lesions
Compressive lesions affecting spinal cord segments
C1 through T2 cause neurologic dysfunction in
both the forelimbs and hindlimbs. Differentiation
between cervical (C1–5) and cervicothoracic
(C6–T2) lesions is attempted primarily on the basis
of whether the deficits are lower motor neuron or
upper motor neuron in nature. Unfortunately this
differentiation is not always clear-cut. A lesion that
causes irritation of the meninges and dorsal nerve
roots with minimal cord compression will cause
neck pain. The lesion can sometimes be localized
fairly accurately by determining the site of pain on
palpation.
A focal compressive lesion of spinal cord
segments C1–5 will produce signs affecting all four
limbs, with the extent depending on the severity of
the lesion. With mild compressive lesions the
hindlimbs often appear more ataxic than
the forelimbs because the afferent tracts from the
hindlimb are more superficial than those from the
forelimbs. A unilateral lesion will produce signs of
hemiparesis on the ipsilateral side.
A cervicothoracic lesion may affect the nerve roots
of the brachial plexus as well as the spinal cord so that
the forelimbs may appear more severely affected than
the hindlimbs. This distinction is not absolute,
however, since the forelimbs may also appear more
severely affected when there is a mid-line cranial
cervical compressive lesion. In this instance the
afferent spinal cord tracts from the forelimbs that are
located in the mid-line are preferentially affected. A
unilateral lesion that impinges predominantly on one
of the nerve roots comprising the brachial plexus will
cause forelimb lameness known as a ‘root signature’
that may mimic lameness associated with orthopedic
disease.
Progressive paresis is noted with increasing severity
of spinal cord compression, although voluntary
movement is initially retained. The paresis may then
be classed as ambulatory or nonambulatory according
to the ability of the patient to stand and walk
unassisted. Hemiparesis is seen with unilateral
involvement and tetraparesis with bilateral lesions.
Voluntary movement ceases with more severe
impairment of neurologic function but perception of
deep pain is retained and the patient becomes
hemiplegic or tetraplegic. Spinal causes of hemiplegia
are very rare and usually result from a unilateral
intramedullary cord lesion.
The most severe lesions of the cervical and
cervicothoracic spinal cord will affect urinary and
respiratory function and are rarely seen. Lesions
above C5 affect the upper motor neurons of the
phrenic and intercostal nerves. At C5–7 the lower
motor neurons of the phrenic nerve are also affected
and caudal to C7 the upper and lower motor neurons
of the intercostal muscles are affected. A cervical
lesion severe enough to cause loss of deep pain
perception would also cause death from respiratory
paralysis and such cases rarely survive long enough to
receive veterinary attention.
Lesions of the cervical and cervicothoracic regions
can be difficult to differentiate, particularly if they are
mild. The vertebral canal, especially in the caudal
cervical region, is more spacious relative to the
diameter of the spinal cord than elsewhere; a
compressive lesion must, therefore, be larger before it
impinges on the cord. The myotatic reflexes in the
forelimb are difficult to obtain, making depressed
responses difficult to interpret. The flexor reflex is easy
to test for and is reliable but it has low sensitivity and
specificity. It is derived from five spinal cord segments
 Fractures and disorders of the spine
and nerve roots (C6–T2) extending over four
vertebral bodies (C5–T1), so it takes a severe lesion
spread over multiple vertebral bodies to depress or
abolish this reflex.
Thoracolumbar, lumbosacral, and sacral lesions
Compressive lesions of spinal cord segments T3
through S3 will cause neurologic dysfunction in the
hindlimbs with normal forelimbs. Differentiation
between thoracolumbar (T3–L3) and lumbosacral
(L4–S3) lesions is attempted primarily on the basis of
whether the deficits are upper motor neuron or lower
motor neuron in nature. This is generally easy to
accomplish by evaluating the hindlimb reflexes and
assessing bladder and bowel function. A mild focal
compressive lesion in these regions, which only
irritates the meninges and dorsal nerve roots with
minimal spinal cord compression, will produce signs
of back pain. Localization is based on evidence of pain
or hyperpathia on paravertebral muscle palpation or
hyperesthesia elicited by pin pricking along the
dorsum.
Mild spinal cord compression in the
thoracolumbar region results in conscious
proprioceptive deficits in the hindlimbs. There is
progressive hindlimb weakness or paraparesis with
increasingly severe lesions and, eventually, there is
difficulty in supporting body weight, although
voluntary movement is retained. Paraparesis
progresses to paraplegia with more severe lesions, as
voluntary movement is abolished. Neurogenic urinary
incontinence usually develops at this stage, as the
bladder fills and then overflows. Palpation
characteristically reveals a tense bladder that is difficult
to express because urethral sphincter tone is increased.
Superficial pain (pinprick pain) is usually lost but deep
pain perception is only abolished when the lesion is
very severe.
The Schiff–Sherrington phenomenon may be seen
in acute severe lesions of the thoracolumbar spine that
result in paraplegia. The forelimbs become rigidly
extended when the patient is placed in lateral
recumbency. The phenomenon is thought to occur
because of the removal of the influence of ascending
inhibition on the extensors of the forelimb from a
center in the lumbar spinal cord. Postural reactions
and reflexes will be intact, despite the increased
extensor tone in the forelimbs, although they may be
hyperactive. Spinal cord integrity has been maintained
if deep pain perception is present in the hindlimbs.
Lesions involving the lumbosacral segments are
localized by the alterations in the spinal reflexes seen
285
on the neurologic examination. The spinal cord is
foreshortened relative to the vertebral column so
that segments L4–C5 are housed in vertebrae
L4–S1; but, as already mentioned, the disparity is
less than that seen in the dog1. In the cat, spinal cord
segment L4 is located in the corresponding vertebral
body, whereas segment L5 is positioned over the
L4–L5 intervertebral disc, segments L6 and L7 in
the L5 vertebral body and the three sacral segments
in the L6 vertebral body. The nerve roots from these
segments run caudally in the vertebral canal forming
the cauda equina before exiting caudal to the
vertebra of the same annotation. The nerve roots are
vulnerable to injury at several sites but there is more
space in the lumbosacral region of the vertebral canal
and the nerve roots are more tolerant of deformation
than the spinal cord. Recovery is unlikely if there is
severe damage. The spinal cord segments S1–3 and
nerve roots contribute to the pelvic nerve, which
supplies sensory and motor innervation to the
bladder, descending colon, and rectum. The same
segments and nerve roots also contribute to the
pudendal nerve, which transmits sensory
information from the external urethral sphincter,
anal sphincter, and perineal region, and motor
innervation to the external urethral sphincter and
the anal sphincter.
Mild compressive lesions between L4–S3 may
cause pain and depress reflexes in the hindlimbs,
anus, or tail. More severe lesions affecting these
segments may cause paraparesis or paraplegia, with a
reduced or absent patellar reflex if segments L4–6
are involved. Tests for sacral spinal cord segments
and their associated nerves rely on sensory stimuli
applied to the various regions supplied by these
nerves and motor responses originating in the sacral
spinal cord. A lesion between segments S1–3 will
spare the hindlimbs but there will be no reflex
urination or defecation. The so-called lower motor
neuron bladder is arreflexic, feels flaccid, and is
generally easy to express manually. The anal
sphincter will be dilated and the tail atonic. There
will be some autonomous function because of the
intrinsic ability of smooth muscle to contract but this
is usually not effective in emptying the bladder.
Caudal vertebral lesions may produce only an atonic
tail with normal urination, hindlimb function, and
defecation.
DIFFERENTIAL DIAGNOSIS
Once a lesion has been localized to one of the
four areas of the spinal cord on the basis of the
286
neurologic examination, a differential diagnosis list
should be drawn up embracing all of the disease
conditions that may be present at that location. It is
helpful to formulate this checklist using the mnemonic
DAMNIT V (or VITAMIN D) (Tables 24, 25).
DIAGNOSTIC TESTS
The cause of some spinal disorders may be apparent
on the basis of the signalment, history, and the
findings of the physical and neurologic examinations
but, in most cases, further investigation will be
required to achieve an accurate diagnosis and
prognosis. A minimum database would include a
complete blood count, serum biochemistry profile,
urinalysis, and tests for feline leukemia virus (FeLV)
and feline immunodeficiency virus (FIV). These tests
may shed some light on the cause of the spinal cord
dysfunction or identify significant intercurrent
disease that may have a bearing on the management
of the case. Hypergammaglobulinemia and
neutrophilia may be associated with infection or
neoplasia. If an inflammatory disease is suspected,
serum antibody titers to Toxoplasma, Cryptococcus
spp. and feline infectious peritonitis (FIP) can be
evaluated. Additional diagnostic tests include
radiography, myelography, CSF analysis, and
advanced imaging techniques. These latter tests are
generally performed if the cat is showing signs of
moderate to severe or progressive neurologic
dysfunction or spinal pain that is not responding to
conservative management.
Radiography
Plain radiographic changes may be diagnostic with
some conditions, such as spinal trauma, vertebral
neoplasia, and discospondylitis. In the case of
intervertebral disc disease, myelography will be
required to assess the significance of changes seen on
plain radiographs and to identify the site of the lesion
before surgical intervention. Plain radiographic
changes may be subtle and good quality radiographs
should be obtained in two orthogonal planes to allow
full assessment. This requires administration of a
general anesthetic, unless contraindicated because of
concurrent injury in the trauma patient or if spinal
fracture/luxation is suspected. Radiographs should
be obtained of the area of interest following
localization by neurologic examination. In some cases
it may be necessary to obtain survey radiographs of
the complete spine to check for multiple lesions; for
example, where the neurologic signs indicate a
multifocal disease or in cats with spinal trauma. In
this case two or three radiographs should be obtained
centered on different regions of the spine; for
example, lumbosacral, thoracolumbar, and
cervicothoracic junctions. The temptation to obtain a
single survey radiograph of the whole spine should be
avoided.
Myelography
Myelography is the injection of positive contrast
medium into the subarachnoid space. The technique
has been widely reported in the dog but there are few
descriptions of myelography in the cat3–5.
Myelography is an essential tool in the investigation of
many feline spinal diseases but it is not a substitute for
radiography. High quality plain radiographs of the
spine should always be evaluated before performing
myelography.
The procedure is performed either by injection
at the cisterna magna (cerebellomedullary cistern)
or by injection at L6–7 into the lumbar cistern,
using a 22 gauge × 3.8 cm spinal needle. Iohexol, at
a concentration of 240–300 mg/ml of iodine
(Omnipaque, Nyegaard), is the contrast agent of
choice. It is administered at a dose rate of
approximately 0.5 ml/kg depending on the site
of injection and the suspected location of the lesion;
2–3 ml is the dose range for adult cats. The
technique is essentially the same as that for the dog
except for the option of a more caudal location for
the site of the lumbar injection. It has been
suggested that the accurate diagnosis of spinal
lesions may be compromised by rapid dissipation of
the contrast medium after the injection6. This is
probably related to the small size of the feline
patient rather than more rapid clearance of the drug
from the subarachnoid space. Delineation of lesions
can be improved by obtaining radiographs during
the injection of the contrast medium or, when this
is not feasible, the radiographs are taken as soon as
possible after the injection has been completed.
Indications and contraindications
The indications for performing myelography are the
same as those for the dog and can be briefly summa-
rized as follows:
• To identify a spinal lesion not visible on plain
radiographs.
• To determine if spinal cord compression is
present following identification of a lesion on
plain radiographs.
• To determine the significance of multiple lesions
identified on plain radiographs.
• To assist with planning the type of procedure to
be performed.
 Fractures and disorders of the spine
287

TABLE 24 DIFFERENTIAL DIAGNOSIS OF SPINAL CORD LESIONS.

Disease category Differential diagnosis (examples)
D Degenerative Inter vertebral disc disease
Spondylosis deformans
Degenerative myelopathy
A Anomalous (congenital) Atlantoaxial subluxation
Sacrocaudal dysgenesis
Spina bifida
Miscellaneous vertebral malformations
Subarachnoid cysts
Syringomyelia and hydromyelia
Vertebral angiomatosis
M Metabolic L ysosomal storage diseases
N Neoplastic Spinal tumors
Vertebral tumors
N Nutritional Hyper vitaminosis A
I Inflammatory Feline infectious peritonitis (FIP)
Toxoplasmosis
Cryptococcosis
Discospondylitis
Bacterial meningomyelitis
Immune mediated (FIP? FIV? FeLV?)
I Iatrogenic Incorrect/contaminated spinal puncture!
I Idiopathic The etiology of many disorders is not fully
understood
T Traumatic Fracture/luxation
Intervertebral disc extrusion
V Vascular Fibrocartilaginous embolism

TABLE 25 DIFFERENTIAL DIAGNOSIS BASED ON RATE OF ONSET AND AGE.

Acute Chronic
Immature Adult Immature Adult
Trauma IVDD Lymphoma Hypervitaminosis A
IVDD
Lymphoma Lymphoma Inflammatory Inflammatory
Inflammatory Neoplasia (nonlymphoid) Discospondylitis Neoplasia (nonlymphoid)
Congenital anomalies FCE Congenital anomalies Lymphoma
Trauma Arachnoid cyst Discospondylitis
Degenerative myelopathy
Inflammatory Spina bifida Syringomyelia
Vertebral angiomatosis
Lysosomal storage
IVDD = intervertebral disc disease Syringomyelia
FCE = fibrocartilaginous embolism
288

Myelography is contraindicated in cats where the
risk of anesthesia or spinal puncture is unacceptable
and is inadvisable in cats with severe inflammatory
spinal disease. Epileptogenic drugs, such as
acepromazine, are not used for premedication
because of the risk of postmyelographic seizures.
After myelography, patients should be recovered in
sternal recumbency with the head raised to promote
the flow of contrast away from the brain.
Postmyelographic seizures are controlled by
administration of diazepam.
Choice of site for myelography
In general, cisternal puncture is performed for
cervical and lumbosacral lesions and lumbar
puncture for thoracolumbar lesions. The advantages
of cisternal puncture are that it is technically easier
and it is more likely that a satisfactory CSF sample
will be obtained. However, seizures are more likely
to occur, the flow of contrast caudally may be
problematic, and it will not be possible to outline an
acute compressive lesion, particularly in the
thoracolumbar region. In lumbar myelography the
injection can be made under pressure, so the contrast
can be made to outline an acute compressive lesion
regardless of location. The disadvantages are that it
is technically more difficult to perform, it frequently
is not possible to obtain a CSF sample, and epidural
leakage of contrast is more likely to occur, making
interpretation difficult. A degree of epidural leakage
of contrast is inevitable and tends to make lumbar
injection unsuitable for the investigation of
suspected lumbosacral lesions.
Cisternal myelography
The site is clipped and aseptically prepared for
injection into the cerebellomedullary cistern. The
cat should be in right lateral recumbency for
the right-handed operator. It is preferable to tilt the
patient 5–10° to promote the caudal flow of
contrast medium. The head is held by an assistant at
an angle of 90° with the nose parallel to the
tabletop. Maximal flexion is not necessary and is
avoided since it may occlude the endotracheal tube.
The site of injection is in the dorsal mid-line at
a point bisecting a line joining the cranial edge of
the wings of the atlas and the occipital protuberance
(265). The needle is inserted perpendicular to the
neck and the stylet is removed once the skin has
been penetrated. The needle is then slowly advanced
until a slight pop is felt as it passes through the
ligamentum flavum and the hub is observed for the
appearance of CSF. A sample of CSF is collected
and, if it is clear, the contrast agent is injected. If the

265

A B

265 Technique for cisternal puncture.

A Lateral view. B Dorsal view. The needle is inserted in the dorsal mid-line at a point
bisecting a line between the cranial edge of the wings of the atlas as shown by the lower
dots and the external occipital protuberance as shown by the upper dot.
 Fractures and disorders of the spine
289

CSF is contaminated with blood it is allowed to flow
until it clears before injecting the contrast agent.
Cervical radiographs are obtained immediately after
injection of contrast. Poor filling of the
cervicothoracic junction with contrast medium may
be a problem. This can be overcome by taking a
dorsoventral projection with the head raised rather
than the standard ventrodorsal projection of this
region. Note that the endotracheal tube will be
overlying the region of interest and it must be
removed unless it is radiolucent. To image the
lumbosacral cord the patient should be tilted by up
to 60° for a few minutes with the head end raised
before radiography.
Lumbar myelography
The site is clipped and prepared aseptically for
lumbar injection. The cat is positioned in lateral
recumbency and the spine is hyperflexed by drawing
the hindlimbs cranially between the forelimbs. The
main landmark is the dorsal spinous process of L7,
which lies between the wings of the ilium and is
shorter than the other lumbar spinous processes.
Placement of the spinal needle can be made in one of
several ways. The authors’ preferred method is to
puncture the skin slightly off the mid-line caudal to
the L7 dorsal spine and advance the needle
cranioventrally towards the mid-line, sliding it down
the spinous process (266). If bone is palpated, the
needle is walked cranially off the vertebral lamina
and advanced through the ligamentum flavum into
the vertebral canal. A muscular twitch is felt and seen
in the hindlimbs and tail as the needle penetrates the
meninges and spinal cord. The needle is advanced
through the spinal cord to the floor of the vertebral
canal. If CSF does not flow the needle may be
withdrawn very slightly until CSF appears in the
hub. The injection of contrast agent may require
more pressure than a cisternal puncture, particularly
if there is a thoracolumbar compressive lesion.
Tilting of the patient is not required before imaging
but the head should be raised to reduce the amount
of contrast agent reaching the brain. The likelihood
of obtaining a diagnostic image will be increased if
the radiographs are taken either during or
immediately after the injection of contrast,
particularly if the lesion is acute and associated with
intramedullary swelling. The ventrodorsal projection
may provide important information about the
lateralization of the lesion in cases where surgical
decompression is contemplated. Left and right 20°
lateral oblique projections are a useful aid in
determining lateralization of a lesion if this is not
clear from the ventrodorsal projection.

266

266 Lumbar injection technique. The needle is inserted

slightly off mid-line caudal to the L7 dorsal spinous
process and directed cranioventrally towards the mid-line.
290
Myelographic interpretation
The appearance of the normal myelogram in the cat
is similar to that of the dog (267)5. There should be
two continuous lines or columns of contrast, which
are situated dorsal and ventral to the spinal cord on
the lateral view and on the right and left of the spinal
cord on the orthogonal view. On the lateral
myelogram the contrast columns are widest at the
level of C2–3, whereas the separation of the two
columns is at its greatest at the level of the brachial
and lumbosacral intumescences, in the
cervicothoracic and caudal lumbar regions,
respectively. A degree of attenuation and indentation
of the ventral column is a normal finding over the
cervical and thoracolumbar intervertebral disc spaces.
The two columns of contrast converge at the level of
the L6 vertebral body where the sacral segments of
267
A B
C D
267 The myelographic appearance of the normal feline spine. (Radiographs courtesy of Davies Veterinary Specialists.)
A Lateral view of the cervical spine.
B Lateral view of the thoracic spine.
C Lateral view of the thoracolumbar spine.
D Lateral view of the lumbosacral spine.
the spinal cord are situated. The contrast usually
continues well into or beyond the sacrum around the
cauda equina and should terminate in a fine point.
Spinal cord lesions may produce deviation,
attenuation, or absence of one or both contrast
columns. An attempt is made to classify lesions into
one of three categories according to their anatomic
relationship to the subarachnoid space based on the
myelographic appearance (268):
• Extradural: deviation of both columns in the
same direction, commonly accompanied by
attenuation of one or both columns.
• Intradural/extramedullary: absence of one column
with a split contrast column on either view (the
so called golf-tee or island sign).
• Intramedullary: divergence of the contrast
columns on both views.
 Fractures and disorders of the spine
291

The information gleaned from the myelogram common, followed by intradural/extramedullary

concerning the anatomic features of the lesion, in
conjunction with the signalment and history, is often
sufficient to make a putative diagnosis. For example,
intradural/extramedullary lesions are almost exclusively
due to tumors, the most common being nerve sheath
tumors and meningiomas. Extradural lesions are most
lesions; intramedullary lesions are seen less frequently.
Cerebrospinal fluid analysis
CSF examination is a useful diagnostic tool in the
investigation of feline spinal disease but it does have
limitations. Abnormal CSF is a strong indicator of

268
Spinal Contrast
cord column

Lesion

Lesion
ii iii
Lesion i
A

Lesion

Lesion

Lesion
i ii iii
B

Lesion

Lesion

Lesion ii
i iii
C
268 Myelographic appearance of extradural ventral mid-line, intradural/extramedullary ventral mid-line,
and intramedullary lesions in both orthogonal planes
A i Cross-sectional illustration of an extradural lesion. ii Lateral myelographic appearance.
iii Ventrodorsal myelographic appearance.
B i Cross-sectional illustration of an intradural/extramedullary lesion.
ii Lateral myelographic appearance. iii Ventrodorsal myelographic appearance.
C i Cross-sectional illustration of an intramedullary lesion. ii Lateral myelographic appearance.
iii Ventrodorsal myelographic appearance.
292
spinal cord or nerve root inflammatory diseases but
no other type of spinal disease consistently produces
any change in the CSF.
Indications and contraindications
Indications for CSF analysis include cats with
suspected meningomyelitis or with multifocal signs on
neurologic examination. CSF analysis should always
be performed when myelography has failed to
demonstrate a lesion. Spinal puncture is an invasive
procedure with a degree of risk and should only be
performed when there is a definite indication. CSF
collection is always performed with the patient
anesthetized and is, therefore, contraindicated if the
risk of general anesthesia is unacceptable. Other
contraindications include cats with spinal injury or
instability at the proposed site of collection and cats in
which raised intracranial pressure may lead to caudal
brain herniation following removal of CSF.
Intracranial pressure is typically normal in cats with
spinal disease but may be elevated if there is
concurrent head injury, severe multifocal
inflammatory disease, or neoplasia. Concurrent
intracranial disease should be suspected when the
signs include an altered state of consciousness, dilated
pupils with reduced pupillary light reflexes, or
respiratory depression.
Collection procedure
CSF is collected either by cisternal puncture at the
cerebellomedullary cistern (cisterna magna) or by
lumbar puncture, as previously described for
myelography. The choice between the two sites is
largely the preference of the clinician. The caudal flow
of CSF means that a lumbar sample may be more
representative of a disease localized to a site cranial to
the puncture. This advantage is generally outweighed
by the greater difficulty in obtaining a sufficient
quantity of CSF and the frequency of blood
contamination at the lumbar site. In many cases the
pathologic changes are sufficiently generalized or are
multifocal so that abnormalities are present
throughout the CSF. When performing a myelogram,
CSF should always be collected prior to injection of
contrast medium. The CSF can subsequently be
submitted for analysis if the myelogram does not
provide a diagnosis.
Laboratory analysis
CSF should be collected into EDTA for cytology and
a plain container for biochemistry. The examiner
should observe the gross appearance of the CSF at the
time of collection. Normal CSF is clear on gross
examination unless there has been blood
contamination during sampling. A yellowish
discoloration is caused by the presence of free
bilirubin as a result of previous hemorrhage and is
known as xanthochromia. Turbidity is caused by an
increase in the white cell count above approximately
500 cells/µl.
Cytology and measurement of protein levels is
performed routinely and culture and sensitivity is
performed if clinical signs suggest bacterial infection
or if there is an increase in the number of neutrophils
in the CSF. CSF contains low levels of protein so it
is a hypotonic fluid with poor cellular stability. It is
usually recommended that cytology should be
performed within 30 minutes of collection because
of rapid cellular deterioration. Submission of freshly
prepared air-dried smears of sediment is helpful in
cases where laboratory examination is likely to be
delayed. The addition of autologous serum and
storage at 4°C was found to result in satisfactory
preservation of cells for up to 48 hours in a recent
study7. An elevation in the number of cells, termed
pleocytosis, occurs when there is inflammatory
disease; this is normally accompanied by a
corresponding increase in the amount of protein. In
general, neutrophils are indicative of bacterial
infection. Mixed pleocytosis tends to be associated
with fungal or protozoal disease. Disease resulting in
degeneration of the spinal cord or nerve roots
without inflammation will produce an elevation in
protein with little or no pleocytosis, termed
albuminocytologic dissociation. Electrophoresis may
be utilized to determine the levels of different
protein fractions. An elevation of albumin suggests
leakage into the CSF as a result of a disturbance of
the blood–brain barrier, whereas elevated
immunoglobulin indicates intrathecal synthesis.
Normal values for CSF are given in Table 26.
Interpretation of abnormal values is given in
Table 27.
Advanced imaging techniques
These techniques are increasingly becoming more
available and are being used at specialist centers for
the investigation of spinal disorders. Computed
tomography (CT) uses X-rays generated by an anode
rotating around the patient at high speed.
Computer-generated images are produced that
represent transverse sections through the patient at
that level. An alternative method that has been
proposed for cats, when detailed examination of the
entire spine is required, involves the acquisition of
sagittal rather than transverse images 9. CT is
 Fractures and disorders of the spine
293

TABLE 26 NORMAL VALUES FOR CEREBROSPINAL FLUID ANALYSIS8.

Color Transparent
Clarity Clear
Specific gravity 1.004–1.006
Urinary reagent strips pH 8 +/– 1
Protein trace to 30
Glucose trace to +
Blood negative
Cell number <3/µl (cisternal)
Cell type RBC 0
Lymphocytes
Monocytes
Neutrophils (rare)
Eosinophils (rare)
Choroid plexus or ependymal cells (rare)
Total protein 10–27 mg/dl (cisternal)
<45 mg/dl (lumbar)
Albumin 1–20 mg/dl

TABLE 27 ABNORMAL VALUES AND THEIR INTERPRETATION8.

Cell type <50 cells/µl 50–500 cells/µl >500 cells/µl
Neutrophils Bacterial Bacterial Bacterial
Neoplasia Neoplasia Neoplasia
IVDD FIP Cryptococcosis
Spinal cord trauma Cryptococcosis
Lymphocytes – Bacterial (after antibiotic Bacterial (after antibiotic
therapy) therapy)
Toxoplasmosis
Eosinophils Toxoplasmosis Toxoplasmosis
Cryptococcosis
Mixed cell population FIP FIP FIP
Toxoplasmosis Toxoplasmosis Cryptococcosis
Cryptococcosis Cryptococcosis Neoplasia
Neoplasia Neoplasia
IVDD
Spinal cord trauma
Cerebral infarction
IVDD = intervertebral disc disease
FIP = feline infectious peritonitis
294
particularly useful for showing osseous rather than
soft tissue detail but the technique can be improved
for investigation of the spinal cord by myelographic
enhancement.
Magnetic resonance imaging (MRI) is a computer-
assisted technique that depends on the magnetic
properties of atomic nuclei in body tissues. A variety
of different forms of image can be produced, but the
principle ones are T1-weighted and T2-weighted.
Tissues with high water content, such as CSF, appear
dark (hypointense) on T1-weighted and bright
(hyperintense) on T2-weighted images. Images can be
enhanced by the use of a paramagnetic contrast agent
such as gadolinium. MRI is particularly useful for
examining the spinal cord and nerve roots and the
other nonosseous structures of the spine. In recent
years there has been an increasing number of reports
of the use of MRI in the investigation of feline spinal
disease10–12.
Electrophysiologic testing
The electromyogram (EMG) is a recording of the
electrical activity of resting muscle in the
anesthetized patient. Any disease process affecting
the ventral horn cells in the spinal cord, the ventral
nerve root, the peripheral nerve, the neuromuscular
junction, or muscle can produce changes in this
electrical activity. Assessment of spontaneous
electrical activity may be used to help differentiate
upper motor neuron and lower motor neuron
deficits but the technique is rarely used in the
evaluation of feline spinal disease. Abnormalities in
individual muscles can be used to localize pathology
to specific nerves or nerve roots, which may be used
in the investigation of neuromuscular disorders.
These investigations are usually undertaken at
specialist centers13,14.
TREATMENT OF SPINAL
DISORDERS
The success of treatment for a spinal disorder is
dependent on accurate diagnosis and is predicated by
the nature of the underlying cause and the extent of
the injury to the spinal cord and nerve roots. Some
conditions, such as FIP and spinal lymphoma, carry a
poor prognosis whereas others, such as spinal trauma
and intervertebral disc disease, may carry a good
prognosis for return to function with appropriate
treatment.
CONSERVATIVE TREATMENT
Conservative and/or medical treatment is indicated
for a number of conditions, particularly in cases
where neurologic dysfunction is mild (trauma and
intervertebral disc disease) or where the primary
condition either cannot be addressed (fibrocarti-
laginous embolism) or can be addressed without
resort to surgery (discospondylitis, lymphoma).
Details of medical treatment are given in the
appropriate section. Conservative treatment entails
cage rest, nursing care, and pain relief. Good
conservative treatment of a paralyzed patient is
demanding and should not be undertaken lightly.
Analgesia can be provided by the use of opiates
and/or nonsteroidal anti-inflammatory drugs
(NSAIDs) but the latter must not be combined with
glucocorticoids.
SURGICAL TREATMENT
Surgical intervention is indicated to restore the
normal anatomy of the vertebral canal, to relieve
compression of nervous tissue, and, in some cases, to
confirm or establish a definitive diagnosis.
Decompressive procedures performed on the spine
are essentially the same as those for the dog and
include dorsal laminectomy, hemilaminectomy, and
ventral slot. With the exception of thoracolumbar
hemilaminectomy, there are few indications for these
procedures and this is the only technique that will be
described in any detail. Surgical treatment of vertebral
fracture/luxation is described in the appropriate
section.
Dorsal laminectomy and hemilaminectomy
Dorsal laminectomy is the surgical removal of the
dorsal spinous process and the dorsal lamina. Both
sets of dorsal articular facets should be left intact, if
possible, to preserve stability of the spine.
Hemilaminectomy is the removal of one pair of
articular facets and the surrounding bone of the
vertebral pedicle to gain access to the vertebral canal
(269). Laminectomy is performed to enable
visualization of the contents of the vertebral canal for
diagnostic purposes, to obtain biopsy samples, and for
the removal of compressive lesions such as extruded
disc material. Hemilaminectomy is usually preferred,
especially if the lesion is ventral to the cord, since
manipulation of nervous tissue is avoided. Dorsal
laminectomy is usually performed for cervical and
thoracic lesions and lesions at the lumbosacral
junction.
Hemilaminectomy is most easily performed in the
thoracolumbar region, with the cat positioned in
sternal recumbency and using a dorsal approach. The
skin and subcutaneous tissues are incised slightly to
one side of the mid-line. The lumbodorsal fascia is
 Fractures and disorders of the spine
295
269

A B

269 Thoracolumbar hemilaminectomy.

A The articular facets are first removed with bone cutters or rongeurs.
B Bone is removed with a high-speed burr down to the periosteum. The remaining wafer-thin bone and periosteum are
removed using fine instruments to expose the spinal nerve and extruded disc material on the floor of the vertebral canal.

incised on one side of the dorsal spinous processes
and the epaxial muscle attachments are reflected from
the vertebrae in the region of interest. The correct
location is ascertained by reference to the myelogram
and by palpation of the last rib and the first lumbar
transverse process, which are important landmarks.
The articular facets are removed using rongeurs or a
bone cutter and the bone is removed from the pedicle
using a high-speed burr to expose the spinal cord. If
there is a compressive lesion, such as extruded disc
material, this is removed using fine instruments and
suction, taking care not to touch the spinal cord or
nerve root. Particular care should be taken not to
damage the nerve roots at or caudal to the L4–5
intervertebral disc, since these contribute to the
nerves that innervate the hindlimbs. If the lesion is an
intervertebral disc herniation, the procedure is
completed by cranial retraction of the spinal nerve
from the lateral aspect of the intervertebral disc.
A window is then created in the annulus fibrosus of
the disc and the remaining nucleus pulposus is
removed with a small dental tartar scraper or similar
instrument. Wound closure is performed using simple
interrupted or continuous absorbable sutures in the
lumbodorsal fascia and the rest of the wound closure
is routine.
NURSING AND PHYSICAL THERAPY
Irrespective of whether treatment is conservative or
surgical, cats with severe spinal cord dysfunction
should be hospitalized initially and their progress
should be constantly monitored and re-evaluated by
performing serial neurologic examinations. Once it
has been established that the cat is showing
progressive neurologic improvement, owners can be
shown how to perform nursing at home.
Adequate nursing care of the paralyzed cat is
crucial to achieve a successful outcome. The single
most important aspect of nursing care is management
of the urinary bladder. If voluntary movement in the
limbs is weak or absent, it can be assumed that the
bladder is paralyzed; this will require manual
emptying three or four times daily or use of an
indwelling catheter. If the bladder is not emptied,
stretching, as a result of urinary retention, will cause
irreversible damage to the detrusor muscle so that it
will not contract even when voluntary motor function
returns. A lower motor neuron bladder is easier to
manage since there is less resistance to manual
expression.
Other aspects of nursing care include keeping
the cat clean and dry, grooming the coat, and
ensuring adequate nutritional and fluid intake.
Pressure sores should be prevented by the provision
of soft absorbent bedding and by regular turning
every 4–6 hours if the cat cannot move for itself or
maintain sternal recumbency. It is imperative that
cats that are being treated conservatively for spinal
fracture/luxation or intervertebral disc disease
should be confined in a cage and movement should
296
be severely restricted for the first 4 weeks. Passive
flexion–extension exercise and massage of paralyzed
limbs should be performed with great care during
this period. Rehabilitation can be started after
4 weeks but cats should be confined indoors for at
least a further 8 weeks.
Physiotherapy and rehabilitation can be more
aggressive for cats that have undergone surgical
stabilization following spinal trauma or decompressive
surgery in the case of disc disease. Weight bearing and
walking movements should be encouraged in these
patients by supporting the cat under the abdomen
with the hands or by the use of a sling. Aquatic
therapy or hydrotherapy can also be beneficial during
recovery from spinal injury but is not tolerated by
all cats.
COMMON DISORDERS OF
THE SPINE
VERTEBRAL FRACTURE/LUXATION
Spinal cord trauma is probably the most frequent
cause of spinal disease in cats. In spite of this there
are relatively few reports of treatment in the
literature and many of those cases that have been
reported have been treated conservatively rather
than surgically15–17. There is a predisposition in
young male cats, as with all traumatic incidents.
Unfortunately many traumatic spinal injuries in the
cat result in severe spinal cord injury or even
severance.
Cause and pathogenesis
The usual cause is road traffic accidents, but spinal
injury may also occur as a result of dog bites, jumps or
falls from a height, and bullets. The type of injury will
be determined by the extent of the trauma and the
size and direction of the forces involved.
The primary tissue of concern following spinal
trauma is nervous rather than osseous, in contrast to
fractures and luxations affecting the appendicular
skeleton. There are two components to any acute or
primary traumatic spinal cord injury. The first is the
concussive effect of the forces applied at the time of
the trauma and, to a lesser extent, the ongoing
instability that follows disruption of the vertebral
column. The second is the residual compressive
effect of the tissues surrounding the spinal cord.
Severe spinal cord compression is addressed by
restoration of the normal anatomy of the vertebral
column and, if necessary, by decompressive surgery.
The pathophysiology of severe concussive injury
involves a cascade of events known as secondary or
delayed injury mechanisms, which involve the release
of large amounts of oxygen-free radicals. Secondary
injury ultimately results from a reduction in the flow
of blood to the spinal cord.
Biomechanics and classification of spinal injury
Spinal fractures and luxations generally occur at the
junctions between a flexible and relatively inflexible
region of the vertebral column, i.e. adjacent to the
skull, thorax, and pelvis. The thoracic region
constitutes the most stable region of the spine and
many of these injuries occur at the thoracolumbar
junction, with 50–60% of injuries occurring between
T11 and L6. Another common location for injury in
the cat is the junction of the sacrum and the caudal
vertebrae.
Forces induced by violent trauma may result in
severe hyperextension, hyperflexion, axial
compression, or rotation of the spine, or a
combination of these. The biomechanics of the injury
and the forces that have to be counteracted during
the healing process can be inferred from the
radiographic appearance of the fracture. For the
purposes of assessing the stability of the injury it is
convenient to divide the vertebral column into two
compartments. The dorsal compartment comprises
all of the structures dorsal to the floor of the vertebral
canal and the ventral compartment comprises all of
the structures ventral to the floor of the vertebral
canal (270).
• Dorsal compartment injuries with fracture of the
articular facets usually result from hyperextension
of the spine and are generally stable unless there
has been extensive tearing of the intervertebral
disc.
• Ventral compartment injuries, with wedge
compression fracture of the vertebral body or
traumatic disc extrusion, usually result from
hyperflexion of the spine and are generally
stable.
• Minimally displaced combination dorsal and
ventral compartment injuries with fracture of
the articular facets, compression fracture of
the vertebral body, and extrusion of the
intervertebral disc usually result from axial
compression of the spine and are often
unstable.
• Grossly displaced combination dorsal and
ventral compartment injuries with fracture of
the articular facets and fracture of the vertebral
body or complete disruption of the
intervertebral disc usually result from a mixture
of rotation and flexion of the spine and are
extremely unstable.
 Fractures and disorders of the spine
Clinical signs
Clinical signs vary from sudden onset spinal pain to
paraplegia or tetraplegia, depending on the severity
and the location of the injury. Sacrocaudal fractures
and luxations may produce urinary incontinence
and paralysis of the tail, with or without hindlimb
paresis.
The various types of traumatic spinal injury
include:
• Vertebral fracture.
• Vertebral luxation or subluxation.
• Intervertebral disc extrusion.
• Spinal cord concussion.
• Spinal cord hemorrhage and hematoma.
Diagnosis
In cases where spinal fracture or luxation is
suspected, handling of the patient should be
minimized until stability of the spine can be assessed
radiographically. A full neurologic examination is
contraindicated because of the risk of inflicting
further injury on the spinal cord. It is possible to
perform a modified examination involving testing of
myotatic and flexor reflexes and deep pain
perception to help determine the location and
severity of the lesion. Patients should be assigned to
a grade on the basis of the degree of neurologic
dysfunction as previously discussed. Cats with
absence of deep pain perception in the limbs
Flaval
ligament
Vertebral lamina
Dorsal
Pedicle
Dorsal
longitudinal
ligament
Ventral
Intervertebral disc
Vertebral body Ventral longitudinal ligament
270 The two compartments of the vertebral column in spinal injury. The dorsal compartment comprises the vertebral lamina
and pedicles, the articular facets and joint capsule, and the flaval, interspinous, and supraspinous ligaments. The ventral
compartment comprises the vertebral body, intervertebral disc, and the dorsal longitudinal, ventral longitudinal, and
intertransverse ligaments.
297
following traumatic injury carry a poor prognosis
for return of deep pain perception.
An initial radiographic assessment is performed on
the conscious patient, if possible, but precautions
must be taken to avoid struggling. The
administration of sedation or general anesthesia may
be necessary if this is not contraindicated; for
example, because of hypovolemia or the presence of
other injuries. If the initial radiographs show that the
spinal injury is likely to be stable, further radiographs
may be obtained under general anesthesia. In some
cases the lesion may be subtle and good quality, well
positioned radiographs in two planes are essential to
allow a proper evaluation. When radiography shows
marked displacement of the vertebrae the spinal cord
injury will be severe. If there is greater than
50% displacement of the vertebral canal on both
orthogonal radiographs, it is assumed that there is
functional, if not anatomic, spinal cord severance and
the prognosis is generally hopeless. Greater vertebral
displacement can be tolerated in the lumbosacral
spine because there is more space in the vertebral
canal relative to the neural structures and the cauda
equina is more tolerant of deformation than the
spinal cord.
It is important to be aware of the limitations of
spinal radiography; assessment of the prognosis is
based on the degree of spinal cord injury and cannot
be reliably predicted from the radiographic
270
Supraspinous Interspinous Articular facets
ligament ligament and joint capsules
Dorsal
Ventral
Intertransverse
ligament
298
appearance of the vertebral column alone (271, 272).
Furthermore, radiographs do not show the maximum
degree of displacement achieved so it is possible to
underestimate the extent of the spinal injury.
Despite these reservations, radiography is an
essential tool for assessing the extent of the injury and
determining treatment options. It is advisable to
radiograph the whole spinal column because multiple
injuries are not uncommon; in one study, 20% of
patients had a second spinal fracture/luxation18.
Myelography is not performed routinely but is
specifically indicated either when the radiographs
reveal no abnormalities or when the findings fail to
correlate with the results of the neurologic
examination. Lesions that can only be identified by
myelography include some traumatic intervertebral
disc extrusions, spinal hemorrhage, and spinal cord
concussion. Myelography is indicated when cord
decompression by hemilaminectomy is planned to
facilitate lateralization of the lesion. Myelography may
also be helpful where further assessment of spinal
instability is considered desirable by the use of stressed
views. However, great care must be taken to avoid
further injury to the spinal cord when performing the
manipulations required for such studies. Advanced
imaging techniques, such as MRI and CT, may provide
much additional information but are rarely used at
present because of their expense and lack of availability.
Treatment and prognosis
The goals of treatment are to relieve spinal cord
compression, maintain stability during healing, and
mitigate the effects of secondary spinal cord injury. The
choice of treatment is based on the duration, severity,
and progression of the neurologic dysfunction and an
assessment of the stability at the site of injury. Additional
concerns include financial constraints, the experience of
the veterinarian, and the availability of referral.
The options available for management of spinal
fracture/luxation include:
• Conservative treatment.
• External splinting or casting.
• Internal fixation.
• Internal fixation plus spinal cord decompression.
There is currently no satisfactory method of treatment
for secondary injury despite the fact that it has been the
focus of much research19. Methylprednisolone sodium
succinate (MPSS) is the only available drug that has
been shown to have any neuroprotective effect, albeit
only in human clinical trials. The potential benefits of
this drug are because of its free radical scavenging
ability and not because of its glucocorticoid action.
Dexamethasone, although frequently used, is not a
suitable substitute for MPSS since evidence of any
therapeutic benefit from its use in acute spinal cord
injury is lacking. MPSS should be administered within
8 hours of the injury as a slow intravenous bolus
injection. The timing of administration is crucial and its
use beyond 8 hours may be detrimental. The initial
dose is 30mg/kg (i.e. a 125mg vial for the average cat)
followed by half this dose 3 and 6 hours later. Dosage
regimens vary but treatment should not exceed
24 hours. The benefits of treatment with MPPS have
not been quantified in cats but are likely to be small.
Conservative treatment
Provided deep pain perception is still present, many
cats with spinal fractures and luxations will return to
satisfactory function with time, strict cage rest, and
good nursing care (273)15,17. It should be borne in
mind that the cost saving with conservative treatment
may be less than expected. The expense of surgery
should be weighed against the extra costs likely to be
incurred, as a result of the increased duration of
nursing care required, if the same patient is managed
conservatively.
Conservative treatment is indicated if radiographic
assessment shows that the injury is likely to be stable
and there is strong voluntary movement in the limbs.
Single dorsal or ventral compartment injuries are
generally stable, whereas injuries involving both
compartments are generally unstable. In cases where
there is doubt the patient may be hospitalized for
conservative treatment and observed carefully for
progression of neurologic signs. Worsening of the
neurologic status in a cat undergoing proper
conservative treatment is generally a sign of spinal
instability and is an indication for surgical intervention.
If the patient has no voluntary movement, but deep
pain perception is present and the spinal injury is stable
with little displacement, there is a fair prognosis for
return to function with conservative treatment. Surgical
decompression and stabilization will likely improve the
prognosis for a successful outcome however, and there
will be a more rapid and complete return to function.
The prognosis for complete return of function in
patients with an absence of deep pain perception as a
result of trauma is very poor. However, failure to regain
deep pain perception does not always preclude recovery
of hindlimb motor function (although urinary and fecal
incontinence are likely to persist). Recovery of motor
function can still occur if descending axons survive the
injury. Survival of as few as 5–10% of axons is sufficient
for restoration of basic locomotion in cats. In cats with
spinal cord transection a degree of locomotor function
may return as a result of the activity of local spinal
circuits (spinal reflex walking).
 Fractures and disorders of the spine
299

External splinting or casting
External coaptation can be used as the sole method of
treatment or may be used to supplement internal
fixation. To the authors’ knowledge there are no
descriptions of the use of external coaptation in a series
of feline spinal fractures and luxations. Back splinting
has been used with some success in the dog, where the
main indication is for thoracolumbar injuries20. The
cat’s small stature and propensity to rest means that
cage confinement may be sufficient for many of
the injuries where splinting would be indicated for the
equivalent canine injury. Nevertheless, splinting may

271 Spinal fracture/luxation. 271

Despite the relatively mild degree
of vertebral displacement, the cat
had no deep pain perception
caudal to the lesion.
A Lateral view of the thoracic
spine showing a spinal
fracture/luxation at T7–8 (arrow).
Note the rib fracture just ventral
to T7 (arrowhead).
B Ventrodorsal view of the same
lesion. The spinal lesion is much A
less apparent on this view.

272 273

A
272 Mid-thoracic spinal fracture/luxation. This degree of
displacement is inevitably associated with spinal cord
transection. The cat had no deep pain perception caudal to
the lesion. (Radiograph courtesy of Malcolm McKee.)

B
273 Caudal thoracic spinal fracture/luxation.
(Radiographs courtesy of Malcolm McKee.)
A Lateral view showing spinal fracture/luxation at T11–12.
B Lateral view of the same lesion following successful
conservative management.
300
occasionally be applicable particularly for cats with
thoracolumbar injuries. The ideal candidate would be
one where there is still voluntary movement in the
hindlimbs and the injury is confined to the dorsal
compartment of the vertebral column, with an intact
vertebral body and intervertebral disc providing a
ventral buttress.
The goal of splinting is to immobilize the spinal
segments cranial and caudal to the site of injury.
Various materials can be used but thermoplastic
material (Orthoboard, Millpledge) is ideal since it can
be molded to fit the patient (274). The splint is
conformed to the shape of the body along the dorsal
spine, extending from the withers to the base of the
tail. It is preferable to apply the splint with the patient
sedated rather than anesthetized so that the protective
muscle tone of the epaxial muscles is maintained. The
splint is first held against the spine with the cat lying
on its side restrained by two people. The cat is then
gently rolled into dorsal recumbency synchronously
with the splint so that the splint cradles and supports
the spine. Application is completed by the addition of
Elastoplast strips cranially and caudally, encircling the
splint and incorporating the forelimbs and the
hindlimbs, respectively. If the cat struggles and will
not tolerate the splint, it should be removed.
Internal fixation and reduction
Internal fixation is the recommended method of
treatment in unstable fractures and luxations of the
spine, especially those cases where there is a combined
dorsal and ventral compartment injury. Many
techniques have been described but the most
commonly used options for internal fixation in the cat
274
274 Back splinting for thoracolumbar spinal injury.
Application of a back splint made from thermoplastic
material.
are pins and polymethylmethacrylate (PMMA),
vertebral body plating, and modified segmental
fixation using pins and wire.
Reduction of cervical vertebral fracture/luxations
can be facilitated by the use of a small Gelpi retractor
placed in the intervertebral disc spaces cranial and
caudal to the lesion after partial fenestration.
Alternatively, a small hole can be drilled in the ventral
vertebral body either side of the lesion to accommodate
the points of small pointed reduction forceps.
Reduction of fracture/luxations of the thoracic and
lumbar spine can be achieved by placing traction on the
spine using very small pointed fragment (reduction)
forceps (Veterinary Instrumentation) attached to the
dorsal spinous processes of the vertebrae either side of
the lesion (275). Correct reduction is assessed by
noting the position of the articular facets and by
inspecting the floor of the vertebral canal if
hemilaminectomy has been performed. Reduction can
be maintained by continued traction on the bone
holding forceps or by temporary insertion of a small
Kirschner wire across the articular facet. Alternatively, a
small lamina spreader designed for human spinal
surgery can be used to reduce some fractures and
distract overridden vertebrae.
• Pins or screws and bone cement. This is a versatile
method of spinal stabilization that has been
described in dogs21. It does not require a great deal
of specialized equipment and can be performed on
all regions of the spine. However, it does require a
thorough knowledge of vertebral anatomy and
strict attention to aseptic technique. There is little
margin for error when placing the pins and
anatomic landmarks vary from one region of the
275
275 Reduction technique for displaced spinal
fracture/luxation. Traction is placed on the spinous
processes by an assistant using small fragment forceps or
towel clamps.
 Fractures and disorders of the spine
spine to another, so it is helpful to have an
anatomic specimen available for reference during
the procedure. A ventral approach is used for
cervical lesions whereas a dorsal approach is used
for thoracic and lumbar lesions. For the dorsal
approach, epaxial muscles are reflected from one or
both sides of the spine to the level of the transverse
process if the lumbar spine is involved. In the
thoracic region, dissection is continued to the costal
fovea taking care not to penetrate the pleural cavity.
If decompressive surgery is to be performed, then
this is done first. A minimum of two pins or screws
are then placed into the vertebrae to span the lesion
using a slow speed electric or air drill (276).
Unilateral placement requires less dissection and
often provides sufficient stability for cats. If the
lesion is mid-body (fracture), the pins are placed in
the adjacent vertebral bodies. If the lesion is at the
level of the intervertebral disc space
(fracture/luxation), the pins are placed in the
vertebrae either side of the disc. Positive profile
threaded pins will maintain stability longer than
smooth pins and are quicker and easier to place
than bone screws. Small-diameter threaded pins
that have a roughened area of pin shank to enhance
the interface with the bone cement are available
(Imex Miniature Interface™ fixation half pins). The
276 The use of pins and bone cement for repair
of spinal fractures and luxations.
A Optimal placement of pins in the lumbar
vertebrae.
B Optimal placement of pins in the thoracic
vertebrae.
C Optimal placement of pins in the cervical
vertebrae.
D Optimal placement of pins in two adjacent
vertebrae. If there is fracture of the vertebral
body, the pins are placed in the vertebral bodies
cranial and caudal to the lesion to span the
lesion.
301
pins are driven so that they emerge 2–3mm from
the ventral aspect of the vertebral body to engage
both bone cortices. The pins are then cut just
below the level of the dorsal spinous processes and
they are notched with a pin cutter if they have a
smooth shank. A small pack (20g) of PMMA bone
cement is mixed and about a quarter to half of the
cement is applied to connect the pins. Once it has
reached the doughy stage and does not stick to the
surgeon’s gloves, the cement is packed around the
pins taking care to avoid the spinal cord and nerve
roots. The amount of cement should not be so
excessive that it precludes subsequent closure. The
cement is lavaged with cool saline for five minutes
to dissipate the heat produced as it polymerizes.
The lumbodorsal fascia is sutured over the cement
mass with monofilament absorbable suture material.
Occasionally it may be necessary to place releasing
incisions in the lumbodorsal fascia to permit
closure. The remainder of the wound is closed
routinely. For cervical lesions a ventral approach is
made and the longus colli muscles are reflected
from the relevant vertebral bodies. The pins are
angled 20–25° from the mid-line away from the
vertebral canal to engage both cortices of the
vertebral body (276). The pins are cut and
notched, if necessary, and connected with bone
276
A B
C D
302

cement. The longus colli muscles are closed cranial
and caudal to the cement and the remainder of the
closure is performed routinely.
• Vertebral body plating. This is an effective means
of stabilization for vertebral body fractures or
luxations22. Application requires specialized
equipment and a thorough knowledge of vertebral
anatomy. It is the authors’ preferred technique for
injuries involving the thoracolumbar vertebral
column. A 2.0mm plate with 4–8 holes or a
2.0/2.7mm veterinary cuttable plate (VCP),
depending on the configuration of the
fracture/luxation, can be applied in most cases.
Approach to the thoracic vertebrae is restricted to
the caudal thoracic region and requires rib
resection to allow placement of the plate. Plating is
generally not performed caudal to the fourth
lumbar vertebra because the nerve root is resected
at the spanned intervertebral space and this would
affect the important nerve roots of the lumbosacral
plexus. A dorsolateral approach is made to the
spine, as described for hemilaminectomy, to the
level of the transverse process of the lumbar
vertebrae or the head of the rib in the case of the
thoracic vertebrae. The vessels and nerves exiting
from the intervertebral foramen at the disc space
to be spanned are cauterized using bipolar cautery
and then severed. A plate is chosen of a sufficient
length to allow placement of at least two screws in
the vertebral body cranial and caudal to the lesion.
If the lesion is mid-body (fracture), the screws are
placed in the adjacent vertebral bodies. If the
lesion is at the level of the intervertebral disc space
(fracture/luxation), the screws are placed in the
vertebrae either side of the disc. The screw holes
are drilled with reference to an anatomic specimen
so that they are angled away from the vertebral
canal (277). If a hemilaminectomy has been
performed, the holes are drilled using the anatomic
location of the spinal cord as a reference point.

277

A
B

D F

277 The use of a vertebral body plate to repair a spinal fracture or luxation. (Radiographs courtesy of Malcolm McKee.)
A Correct placement of a plate on the lateral aspect of lumbar vertebrae. B Cross-sectional view showing optimal
placement of a screw in the vertebral body. C Lateral radiograph showing a spinal fracture at L3.
D Ventrodorsal view of the case in C. Note the unilateral femoral neck fracture and the intestinal gas shadows indicating
abdominal wall rupture. E Lateral view showing repair using a plate and screws. F Ventrodorsal postoperative view.
 Fractures and disorders of the spine
303

• Spinal stapling or modified segmental spinal
fixation. Spinal stapling involves wiring of a
U-shaped pin to the dorsal spinous processes and
the articular processes or transverse processes of
the vertebrae. The technique can be used to
stabilize lesions in all regions of the spine with
the exception of the cervical region. It is relatively
easy to perform and requires no specialized
equipment. However, pin migration and loss of
fixation are potential complications. Application
requires extensive dissection, with exposure of
2–3 dorsal spinous processes and articular facets
cranial and caudal to the lesion. The technique
was originally described in 197123 but
modifications have since been made by a number
of workers24–26. Following a bilateral dorsal
approach, a Kirschner wire (or small
intramedullary pin) 1–1.6 mm in diameter is
passed through the skin and epaxial muscle and is
inserted through the dorsal lamina of a vertebra
adjacent to the lesion (278). The entire length
of the wire is passed through the opposite side
and then half withdrawn while retracting the
epaxial musculature to free it from the wire.
The wire is then bent to a U shape using
bending pliers and carefully contoured to fit
along the dorsal laminae between the spinous
and articular processes. The wire is held in place

278

B E

C F
278 Spinal stapling.
A The Kirschner wire is inserted through the skin and epaxial muscle into the dorsal lamina. B The Kirschner wire is bent
into a U shape and contoured to fit over the dorsal laminae between the spinous processes and the articular facets. A hole is
drilled in the dorsal lamina and a hemicerclage wire is placed to stabilize the free end of the Kirschner wire. C A figure-of-
eight wire is placed through holes drilled in the dorsal laminae of the vertebrae at the site of the lesion. D Lateral radiograph
of the thoracolumbar spine showing a spinal fracture luxation at T12–13. (Radiograph courtesy of Dr. Otto Lanz.)
E Intraoperative view showing placement of a spinal staple. (Photograph courtesy of Dr Otto Lanz.) F Lateral postoperative
radiograph of the thoracolumbar spine showing repair using a spinal staple. (Radiograph courtesy of Dr Otto Lanz.)
304
with a hemicerclage wire (0.6 mm [22 AWG])
passed through a hole drilled in the dorsal lamina
of the vertebra at its opposite end. The
fracture/luxation is stabilized with a figure-of-
eight wire passed through the dorsal laminae of
the vertebrae at the site of the lesion and placed
dorsal to the Kirschner wire to span the lesion.
The technique works well but care must be
exercised when drilling the holes in the dorsal
laminae not to penetrate the vertebral canal. The
fixation can be strengthened by placing
supplementary cerclage wires attaching the wire
to the transverse processes or the ribs but this
requires extra dissection and is rarely necessary.
• Spinal cord decompression. Accurate
anatomic realignment and stabilization of
fracture/luxations will automatically result in a
degree of spinal cord decompression. However,
additional decompression of the spinal cord should
be considered when there is no voluntary
movement in the affected limbs and/or there is
radiographic or myelographic evidence of bone
fragments, hematoma, or extruded intervertebral
disc in the vertebral canal. Decompressive surgery
is indicated most frequently in the thoracolumbar
region where the vertebral canal is at its narrowest
relative to the diameter of the spinal cord. Cats
with absent deep pain perception are usually
euthanased, but if they are treated surgically, spinal
cord decompression and durotomy are essential to
establish that the cord has not been transected.
Thoracolumbar decompression should be
performed by hemilaminectomy since this has less
of a destabilizing effect than dorsal laminectomy
(279). Hemilaminectomy allows visual assessment
of the condition of the spinal cord and removal of
compressive material. It is important to note that
because spinal cord decompression causes
iatrogenic spinal instability it is only ever
undertaken as an adjunct to internal fixation.
FRACTURES AND LUXATIONS OF THE SACRAL
AND SACROCAUDAL SPINE
Cause and pathogenesis
Sacral fracture is not uncommon in the cat and is usually
the result of vehicular trauma. Sacral fractures in dogs
and cats have recently been described and classified27. In
this study concomitant pelvic injuries were common,
with 65% of cats having unilateral or bilateral sacroiliac
luxation. Sacroiliac luxation is discussed in Chapter 9.
Sacrocaudal luxation or fracture/luxation is more
common than sacral fracture (279). The injury is
thought to occur as a result of traction forces on this
region of the spine when a cat, which is attempting to
escape, has its tail trapped under the tire of a moving
vehicle.
Clinical signs
Clinical signs of sacrocaudal injuries include pain and
swelling in the sacrocaudal region and tail paralysis.
There may be severe neurologic dysfunction
associated with transverse or comminuted sacral
fracture or when there has been traction on the nerve
roots of the cauda equina.
Diagnosis
It is important to obtain radiographs in two orthogonal
planes since the osseous injuries may be relatively mild
and may be obscured on the ventrodorsal view by fecal
material in the rectum.
Traction on any of the more cranial nerve roots of
the cauda equina (L6–S1) will cause paraparesis with
lower motor neuron deficits involving the sciatic
nerve. The pudendal and pelvic nerves originate from
the sacral nerve roots (S1–3) and innervate the
bladder, rectum, and colon. Injury to these nerve
roots may cause urinary retention, loss of anal tone
and urethral sphincter tone, and loss of perineal
279
A
279 Sacrocaudal
fracture/luxation in a cat.
A Lateral radiograph showing
fracture/luxation between the
sacrum and the first caudal
vertebra.
B Ventrodorsal view. The
injury is often less apparent
on this view.
B
 Fractures and disorders of the spine
sensation. Injury to the caudal nerve roots Cd1–5 in
isolation causes tail paralysis. In a study of a series of
51 cases with fracture/luxation of the sacrocaudal
region, cats were assigned to a grade on the basis of
the neurologic examination as follows28:
• Grade 1: tail base pain only.
• Grade 2: tail paralysis.
• Grade 3: tail paralysis and urinary retention
(bladder difficult to express manually).
• Grade 4: tail paralysis, urinary retention, and
loss of perineal sensation or reduced anal tone.
• Grade 5: tail paralysis, urinary retention, absent
anal tone, loss of perineal sensation, and loss of
urethral sphincter tone (bladder easy to express
manually).
Treatment and prognosis
Stabilization of sacral fractures is indicated when there
are neurologic deficits, obvious displacement of bone
fragments or instability likely to cause compression of
nervous tissue. Some sagittal fractures can be repaired
by placement of a lag screw or using a tension band
technique in conjunction with a transarticular pin in a
similar fashion to sacroiliac luxation (280) (see
Chapter 9). Transverse fractures or comminuted
fractures in which the landmarks for lag screw or pin
placement are obscured can be stabilized using
transilial brace fixation29. A dorsal surgical approach
280
A B
280 Sacral fracture.
A Ventrodorsal radiograph of the pelvis showing a type II
(foraminal) sacral fracture.
B Postoperative ventrodorsal radiograph of the pelvis
showing fracture repair using a 2.7 mm screw.
305
to the sacroiliac joints is performed bilaterally. The
sacral fracture is reduced using bone holding forceps
attached to the ilium and a small intramedullary pin is
driven through the iliac wings over the dorsal aspect
of the sacrum. The ends of the pin should be bent
over in order to prevent migration. If there is
concurrent contralateral sacroiliac luxation, a transilial
brace can be combined with a transsacral pin or a
contralateral transarticular pin or lag screw.
Medical treatment of cats with sacrocaudal spinal
injury involves pain relief and manual evacuation or
catheterization of the bladder 3–4 times daily to
prevent excessive bladder distension, which may cause
irreversible damage to the detrusor muscle.
Surgical treatment of cats with sacrocaudal
fracture/luxation is controversial, with some
authorities advocating immediate tail amputation or
surgical repair to reduce pain and eliminate further
traction on the nerve roots of the cauda equina. Other
options include repair of the osseous injury using pins
or wires or decompression of the cauda equina in
conjunction with amputation or stabilization of the
vertebrae. None of these has so far been conclusively
demonstrated to influence the outcome, although
stabilization will provide early pain relief. A simple
method of surgical stabilization involves the use of an
internal sling of polypropylene suture material placed
using a dorsal approach (281). The polypropylene
281
281 Repair of sacrocaudal fracture/luxation. Dorsal view
showing internal fixation of a sacrocaudal fracture/luxation
using polypropylene suture material as a sling. The suture
is passed through a hole drilled in the base of the second
dorsal spinous process of the sacrum and is then passed
around the transverse processes of the luxated vertebra
(Cd1 in this case).
306
(4 Metric [1 USP]) is passed through a hole drilled in
the second dorsal spinous process of the sacrum and is
then passed around the transverse processes of the
luxated vertebra (usually Cd1). Similarly, transverse
sacral fractures between the second and third sacral
vertebrae can be stabilized using a nonabsorbable
suture or hemicerclage wire passed through holes
drilled in the base of their respective spinous processes.
Dorsal laminectomy, in an attempt to visualize and
decompress the sacral nerve roots, has been advocated
for treatment of fractures of the sacrum and
sacrocaudal region30. Decompressive surgery allows
visualization of the cauda equina, which may help in
assessing the prognosis but does not have any
therapeutic benefit for cats with traction injury of the
cauda equina.
The prognostic information drawn from the study
described above28, based on the results of neurologic
examination, is as follows:
• The prognosis is excellent for grade 1 and grade
2 cases.
• The prognosis for grade 3 cases is good with the
majority recovering fully.
• The prognosis for grade 4 cases is fair to good,
with approximately 75% of cats making a
recovery.
• The prognosis for grade 5 cases is fair with a
recovery rate of approximately 50%.
Cats in the series that did not recover urinary function
within 4 weeks of the injury remained incontinent
during a 2–36 month follow-up period. However, it
was noted that tail function could take several months
or much longer to improve. An insufficient number of
cats were treated surgically to permit comparison
between the results of surgical and medical treatment.
The prognosis for recovery of tail function for cats
with sacrocaudal fracture/luxation is good with
conservative treatment, especially for grades 2–4, so
immediate tail amputation is difficult to justify. The
authors advocate early tail amputation if there has
been severe trauma to the tail itself or there is gross
displacement of the vertebrae on radiographs, on the
grounds that complete avulsion of the caudal nerve
roots is likely to have occurred. Hindlimb dysfunction
is usually the result of neuropraxia and generally
resolves completely within 2–4 weeks.
DISORDERS OF THE TAIL
The tail is comprised of 21–24 caudal vertebrae.
Traumatic injury of the tail is not uncommon. Causes
include road traffic accidents, bites, bullets, malicious
injury, and entrapment in doors. Concurrent soft
tissue injury is common and many fracture/luxations
of the middle and distal thirds of the tail are open.
Surgical reduction and stabilization of the osseous
component of tail injuries is rarely indicated. In cases
where there is instability, sufficient immobilization of
the caudal vertebrae can generally be afforded by
simple bandaging techniques. For more severe soft
tissue injuries, in cases where there is vascular
compromise or paralysis of the tail with marked
displacement, partial or total amputation is indicated.
Surgical reduction and stabilization of the tail base
either alone or in conjunction with more distal
amputation may be indicated in cases where the
proximal caudal vertebrae may impinge on the rectum
or anus31. A careful assessment of bladder function
and anal tone should be made in all cats with proximal
caudal vertebral fracture/luxations.
Cat bites in this region are common and occasionally
result in vascular compromise or osteomyelitis, which is
generally best treated by partial amputation.
Tail kink is as a congenital deformity in which
there is a kink, usually in the distal third of the tail.
The condition was formerly common in the Siamese
but has largely been eliminated from the modern
breed. Surgical correction is not indicated and is
fruitless if it is attempted. The range of tail
abnormalities seen in Manx and Manx-cross cats are
discussed in the section on sacrocaudal hypoplasia.
NEOPLASIA
Spinal neoplasia is probably the second most
important cause of feline spinal disease following
trauma. Many tumor types have been reported
affecting the feline spinal cord but, with the exception
of extradural lymphoma, spinal neoplasia is
uncommon. After meningioma, lymphoma is the
second most common form of neoplasia involving the
feline central nervous system. In one study of cats
with lymphoma, central nervous system involvement
was diagnosed in 26 (12.1%) of 214 cats and, of these,
23 (88.5%) had tumors in the vertebral canal, 22 of
which were solitary32.
Cause and pathogenesis
The combined results of two North American studies
showed that 89% of 36 cats with spinal lymphoma
tested positive for FeLV antigen32,33. However, there
may be geographical variations in prevalence of FeLV
and there appears to have been a decrease in the
prevalence of FeLV-positive cats during the past 10–15
years, probably because of the widespread availability
of an effective vaccine34. The proportion of cats with
FeLV may have a bearing on the prognosis, since
 Fractures and disorders of the spine
positive FeLV status has been shown to have a negative
influence on the outcome of chemotherapy35.
Nonlymphoid spinal tumors are rarely seen
compared with the dog. There are many reported
tumor types including osteosarcoma (OSA)36,
chondrosarcoma37, meningioma, lipoma, malignant
nerve sheath tumor, meningeal sarcoma38,
rhabdomyosarcoma39, and astrocytoma40. Of the
extradural spinal tumors, OSA is the most frequent
primary vertebral neoplasm. Meningiomas are the
most common intradural-extramedullary neoplasm,
whereas intramedullary neoplasia has been reported
very rarely40,41.
Although spinal lymphoma can occur at any age,
cases are typically less than 4 years old32,33. The
etiological association of spinal lymphoma with FeLV
probably explains the age bias in reported cases. In the
majority of cats with spinal lymphoma the neoplastic
tissue is confined to the extradural space and extends
over multiple vertebral bodies. In one study,
neoplastic tissue was present in an extradural location
in 20 of 23 cats32. The brachial plexus was involved in
the other three cats, and there was extension to the
subarachnoid space.
282 Radiographs of osteosarcoma in a cat.
A Lateral view of the lumbosacral spine showing an
osteosarcoma of L5. Note the presence of spondylosis
deformans and multiple narrowed intervertebral disc spaces.
B Ventrodorsal view.
283 Lateral myelogram of a cat with vertebral
osteosarcoma at T8 showing a dorsal
extradural compressive lesion (arrow).
(Courtesy of Malcolm McKee.)
307
Clinical signs
The clinical presentation of cats with spinal lymphoma
is variable. There may be evidence of spinal pain and
sudden or gradual onset paraparesis or tetraparesis. Cats
with cervical spinal cord or nerve root involvement
generally have acute tetraparesis and lower motor
neuron signs in the forelimbs. Signs typical of nerve
root lesions (root signature), such as lameness and pain
on shoulder extension, are infrequently reported. Some
cats may have extraneural clinical abnormalities, such as
anorexia and weight loss, lethargy, and peripheral
lymph node enlargement. Cats with nonlymphoid
tumors are typically much older (median age 12 years)
than cats with lymphoid tumors and do not show signs
of systemic illness or clinical evidence of metastasis33.
Intramedullary neoplasms are nonpainful initially
because the meninges are not affected.
Diagnosis
Survey radiography is most likely to be helpful
for nonlymphoid tumors, such as OSA or
chondrosarcoma, where there may be evidence of an
osseous lesion (282 and 283). Most soft tissue and
spinal cord nonlymphoid tumors will not cause any
282
A
B
283
308

changes on plain radiography. Myelography reveals duration of complete remission using a COP protocol
the typical pattern of an extradural compression in in six cats was 14 weeks, despite the fact that all of
75% of cats with lymphoma32,33. Cats with neoplastic these cats had severe neurologic deficits at the time of
infiltration from the spinal nerve roots across the treatment33. In the same study a single cat treated by
subarachnoid space may show an intramedullary dorsal decompressive surgery and chemotherapy had a
myelographic pattern. In a series of nonlymphoid more prolonged remission of 62 weeks. For further
tumors the most frequent site was intradural- details concerning chemotherapy of lymphoma,
extramedullary, followed by extradural, with one standard oncology texts should be consulted.
tumor having a combined extra and intradural
component (284)38. None of these tumors was
intramedullary.
CSF analysis is infrequently diagnostic of
neoplasia. There are usually mild nonspecific increases
in the white blood cell count and protein
concentration; neoplastic cells are sometimes seen in 284
cats with spinal lymphoma. Definitive diagnosis may
require fine needle aspiration of the mass under
fluoroscopic guidance42 or exploratory laminectomy
and histopathologic examination of a biopsy sample.
Bone marrow aspiration cytology will show evidence
of neoplastic infiltration in about 70% of cats with
lymphoma, even though a complete blood count may
be completely normal. In one report of 11 cats with
nonlymphoid tumors, all of the cats tested negative
for FeLV and FIV38.

Treatment and prognosis A

The long-term prognosis for cats with spinal neoplasia
is poor. Radiotherapy may be used to treat localized
epidural spinal lymphoma. In one study of 10 cats
with various forms of localized lymphoma, eight cats
achieved complete remission with a median duration
of over 2 years43. Remission of spinal lymphoma can
also be achieved with standard combination
chemotherapy, such as cyclophosphamide, vincristine
(oncovin), and prednisolone (COP). Doxorubicin
appears to be the single most effective agent for
treating lymphoma in cats, however, and the addition
of this drug to COP-based protocols has improved
the results of treatment. Cats are less tolerant of
doxorubicin than dogs and a dose of 1 mg/kg, or
25 mg/m2, IV every 3 weeks is recommended.
Cardiac toxicity has not been documented in the cat
and is unlikely to occur if the total cumulative dose of
doxorubicin is less than 150 mg/m2. Even cats with
severe neurologic dysfunction may respond well to
treatment and achieve complete or partial remission.
Long-term maintenance protocols have not been B
shown to give superior results and chemotherapy is 284 Spinal meningioma in a cat. (Radiographs courtesy of
discontinued after 25 weeks in cats that have attained Davies Veterinary Specialists.)
complete remission. Few studies have reported the A Lateral myelogram of the thoracolumbar spine showing
results of treating cats with spinal lymphoma so the an intradural-extramedullary lesion at L2–3.
number of cases is small. In one study the median B Ventrodorsal myelogram showing the same lesion (arrow).
 Fractures and disorders of the spine
To the authors’ knowledge only one report has
looked at the long-term outcome of a series of cases
undergoing surgical treatment for nonlymphoid
tumors38. In this series of 11 cats with a range of
different tumors, all underwent surgical removal of
tumor tissue via hemilaminectomy or dorsal
laminectomy but without extensive bony resection.
The median survival time following surgery alone was
180 days. The authors concluded that cases should be
critically evaluated in order to differentiate spinal
lymphoma from nonlymphoid tumors because the
latter may carry a better prognosis following
treatment.
INFLAMMATORY MENINGOMYELITIS
Inflammation of the meninges (meningitis) and the
spinal cord (myelitis) is a relatively common cause of
feline spinal disease. Inflammatory disease should be
suspected in a cat of any age presented with spinal
pain, progressive paresis, hypergammaglobulinemia,
iritis, chorioretinitis, and signs of systemic illness. The
commonest etiological agents responsible for
meningomyelitis are viral (FIP), with bacterial,
protozoal (toxoplasmosis) and fungal (cryptococcosis)
infections occurring only sporadically. Uncommon
causes of inflammatory meningomyelitis are covered
later in this chapter.
Feline infectious peritonitis
Cause and pathogenesis
FIP is an immune-mediated disorder associated with
coronavirus infection. Disease occurs following the
formation of immune complexes of virus, viral
antigen, antiviral antibodies, and complement and
affects multiple body systems in effusive and
noneffusive forms. Cats with the noneffusive form of
FIP may develop multifocal granulomatous
meningomyelitis, which is probably the most frequent
type of inflammatory spinal disease44.
Clinical signs
Cats of any age may be affected, although about 50%
of cats are less than 2 years of age. Purebred cats and
cats living in multicat households are predisposed. In
one study, signs of central nervous system
involvement were identified in 12.5% of cats with
FIP45. Paraparesis is one of the commonly reported
manifestations of noneffusive FIP, along with other
neurologic and systemic signs. When FIP causes spinal
meningitis there may be limb weakness and
incoordination, spinal pain, hyperesthesia, and
pyrexia. When FIP causes a pyogranuloma affecting a
peripheral nerve or the spinal cord there may be
309
lameness or progressive ataxia and paraparesis or
tetraparesis. Concurrent ocular signs are frequently
seen in noneffusive FIP, although Toxoplasma spp.,
FeLV, FIV, and systemic fungal infections may cause
similar changes.
Diagnosis
Diagnosis is based on the clinical signs and supportive
laboratory findings. At present there is no single
accurate diagnostic test for FIP, although various
algorithms have been devised that give a high
predictive value for diagnosis of the disease46.
Serologic testing is nonspecific because many healthy
cats and cats with conditions other than FIP may be
seropositive. However, cats with noneffusive FIP
usually have a high antibody titer to feline coronavirus
and are rarely seronegative. A seronegative result is
therefore helpful in ruling out a diagnosis of
noneffusive FIP. Total serum protein is usually elevated
and serum protein electrophoresis may reveal
polymonoclonal hypergammaglobulinemia, although
this may also occur in cats with lymphoma, multiple
myeloma, FIV, and some chronic infections. CSF
analysis reveals elevated protein (0.56–3.48 g/l
[56–348 mg/dl]) and pleocytosis with a mixed
population of neutrophils, lymphocytes, and
macrophages47. In some cases the CSF may not flow
easily through the needle at the time of collection
owing to the massive inflammatory cell accumulation.
Hydrocephalus was a postmortem finding in 75% of
24 cats with FIP and neurologic signs48. Advanced
imaging techniques may help to differentiate FIP from
lymphoma and other inflammatory diseases of the
central nervous system in which hydrocephalus has not
been reported.
Treatment and prognosis
Treatment of cats with FIP is aimed at suppressing the
immune response using appropriate drugs48. Cases
with concurrent FIV or FeLV or moderate to severe
neurologic dysfunction are unlikely to respond to any
treatment. Cats with mild clinical signs and minimal
neurologic dysfunction may show temporary
improvement and enjoy a good quality of life for
several months.
INTERVERTEBRAL DISC DISEASE
Intervertebral disc degeneration is a common
postmortem finding in cats but, until recently, there
were few reports of clinical intervertebral disc disease.
The literature concerning the subject has recently
been reviewed49. The incidence of disc disease in the
largest feline study so far was 0.12%50 compared with
310
a reported incidence of 2.3% in the overall canine
population51. The recent trend toward a greater
number of reports of disc disease in the literature may
have several explanations. The disease may be showing
a true increase in prevalence because of the increased
life expectancy of cats or, more likely, spinal
disease is being investigated and treated with
increasing frequency in the cat. It is important
to include disc disease in the differential diagnosis for
any cat with paresis or paralysis since it is a
potentially treatable condition, unlike many other
spinal disorders in the cat.
Cause and pathogenesis
Widespread disc degeneration was discovered from
about 10 years of age onwards in a series of
groundbreaking postmortem studies on the feline
intervertebral disc performed in the 1960s52–55. In
these studies Hansen type 1 disc extrusion and
Hansen type 2 disc protrusion were identified,
although the latter was much more common. In
contrast to dogs, the thoracolumbar area was not
affected and cervical protrusion was more common
than lumbar protrusion. None of these cats was
showing clinical signs of disc disease and it
was postulated that intervertebral disc degeneration
was of little clinical relevance in the feline. Since
these studies were performed there has been an
increasing awareness of feline disc disease as a clinical
entity with at least 27 cases reported in the English
language since 19805,11,50,56–63. The combined
results of these studies show a mean and median age
of 7 years (range 18 months–17 years). Ten of the
cats were pedigree and four of these were Siamese
but, because of the small number of cases and a
possible selection bias in favor of pedigree cats, it is
not possible to draw any definite conclusions about
breed predisposition. There was no clear sex
predisposition and most of the cats were neutered.
The thoracolumbar spine was affected in the
majority of cases. Two cats had multiple sites with
two discs affected in one cat and three in another. In
contrast to the postmortem studies, the majority of
cats (89%) had Hansen type 1 disc extrusion and
both of the cases confirmed as having Hansen type 2
disc disease were located in the cervical region at
C5–6. The anatomic distribution of disc disease was
different from the dog with the affected discs
grouped around two regions. The first region was
thoracolumbar, which is also the most common site
in the dog, with a peak incidence at T13–L1 (seven
cases). The second was the caudal lumbar region
with a peak incidence at L4–5 (eight cases), which is
similar to the peak incidence found in the
postmortem studies. It has been conjectured that
this distribution may be related to the cat’s ability to
jump, which places strain on the caudal lumbar
spine50. In the same study it was noted that the cats
with lumbar disc disease weighed considerably more
than those with thoracolumbar disease. The
additional weight would place additional strain on
the spine, especially during this maneuver. In
common with dogs, clinical cervical disc disease is
seen less frequently than thoracolumbar disc disease
with only two reported cases. Cervical disc disease
was a common postmortem finding, although most
of these were type 2 disc protrusions. The
explanation for this may be the greater diameter of
the vertebral canal relative to the spinal cord in this
region of the spine.
Clinical signs
The clinical signs of disc extrusion in the cat are very
similar to those in the dog. Typically the onset of
clinical signs was acute and severity ranged from two
cats with chronic back pain to three paraplegic cats in
which deep pain perception was reported to be
absent. Because of the propensity for caudal lumbar
disc disease, a significant number of cases will have
lower motor neuron deficits and localize to spinal
cord segments L4–S3. Spinal cord compression at or
caudal to the L5–6 intervertebral disc will cause lower
motor neuron signs and hypo- or arreflexia, associated
with cauda equina syndrome.
Diagnosis
Intervertebral disc disease should be included in the
differential diagnosis for any cat presented with
spinal cord disease, especially if it is of acute onset.
In comparison with cats presented with spinal
trauma or lymphoma, cats with intervertebral disc
disease tend to be older, are more likely to be kept
indoors, and test negative for FeLV. The
radiographic changes seen with intervertebral disc
disease are similar to those described for dogs.
Survey films typically show mineralization of the
nucleus pulposus of one or more discs in cats at risk
for the disease. Cats with clinical disease may show
narrowing of the extruded disc space, radiopacity in
the affected intervertebral foramen, and a reduction
in the width of the diarthrodial joint space.
Myelography typically shows an extradural
compressive lesion centered over the affected
intervertebral disc space (285). Since most cats have
acute onset thoracolumbar disc disease, the preferred
site of contrast injection is L6–L7. Cisternal
 Fractures and disorders of the spine
injection may be used if the lesion is chronic or has
been localized to the cervical region by neurologic
examination. The ventrodorsal myelogram is used
as an aid in determining lateralization of the
lesion, which is important when performing a
285
A disease is extensive, however, and, since the
B as a prophylactic measure, is not currently
285 Thoracolumbar intervertebral disc extrusion in a cat.
A Lateral myelogram of the thoracolumbar spine showing
a ventral extradural lesion at T12–13.
B Ventrodorsal myelogram of the cat in A.
311
hemilaminectomy, and should be obtained as soon
after the injection as possible. Left and right lateral
oblique views are then obtained as necessary.
Treatment and prognosis
Treatment can either be conservative or surgical.
Conservative treatment entails cage rest for 4 weeks
followed by house confinement for a further 8 weeks.
Conservative treatment of the paralyzed patient is
discussed earlier in this chapter. Surgical treatment
entails decompressive surgery with or without
fenestration of the affected intervertebral disc. Since
most clinical disc disease is located at the
thoracolumbar junction and the caudal lumbar
region, hemilaminectomy is usually the procedure of
choice.
The number of reported cases in the feline is too
low to draw definite conclusions about the optimum
method of management. The literature on canine
pathogenesis is similar, it is not unreasonable to
extrapolate this information to the cat. The experience
of the authors and reports of treatment in the
literature suggest that the prognosis following surgical
decompression by hemilaminectomy is good provided
deep pain perception is present. The authors’ protocol
for treatment based on the results of the neurologic
grading system described previously (see page 283) is
as follows:
• Mildly affected cases (grades 1 and 2) can be
treated conservatively by cage rest and the use
of analgesia if necessary. Clients should be
warned that sudden deterioration of signs might
occur, particularly if cage rest is not performed
correctly. There is also a risk of recurrence of
neurologic signs after successful conservative
treatment and these signs may be worse than
the original episode. Recurrence is thought to
occur in about 30% of dogs and there is no
reason to suppose that this figure will be any
lower in the cat.
• More severely affected cases (grades 3 and 4)
should be treated by hemilaminectomy and
fenestration of the affected disc. It should be
noted that there are no reported cases of
recurrent disc extrusion following successful
surgical treatment in the cat. Multiple disc
fenestration as frequently advocated in the dog,
indicated in the cat. Some of these cases would
recover with conservative treatment but the
recovery is less predictable, takes longer, and is
less likely to be complete, especially in those cats
312
with absence of voluntary movement. There will
be a risk of recurrence of signs following
resumption of normal activity. Cats that are not
improving with conservative therapy within a
period of 2 weeks and cats showing progression
of neurologic signs are also surgical candidates.
There is very little information concerning
treatment of cats with absent deep pain
perception but the recovery rate following
decompressive surgery was 62% in one canine
study2. The recovery rate following conservative
treatment of such cases is likely to be negligible.
The authors are not aware of any reports of cats
that have developed ascending/descending
myelomalacia following intervertebral disc
extrusion but there is no reason to suppose that
it does not occur and this possibility should be
discussed with the client before undertaking
surgery on cats with signs of severe neurologic
dysfunction.
SPONDYLOSIS DEFORMANS
Spondylosis deformans is less common in cats than in
dogs but is seen occasionally as an incidental finding
in cats from middle age onwards (286). The etiology
is presumed to be the same as in dogs where it has
been associated with degeneration of the annulus
fibrosus of the intervertebral disc64. However, the
pathogenesis of spondylosis deformans does not
include degeneration of the nucleus pulposus and
disc extrusion and its presence at a disc space is
286
286 Spondylosis deformans. Lateral radiograph of the
thoracolumbar spine showing spondylosis deformans from
T11 to L1. The intervertebral disc space is narrowed at
T12–13. The radiographic changes were incidental
findings in this 11-year-old cat.
therefore not proof of clinical disc disease at that site.
Spondylosis is seen most frequently in the
thoracolumbar region and at the lumbosacral
junction. Cats with neurologic dysfunction and
spondylosis on plain radiographs should always be
investigated thoroughly for other causes of spinal
disease.
CAUDA EQUINA SYNDROME
Cauda equina syndrome is defined as a neurologic
condition caused by compression, displacement, or
destruction of the nerve roots of the cauda equina.
The term lumbosacral disease and cauda equina
syndrome are often used synonymously, although any
pathology at or caudal to the L5–6 disc space in the
cat may cause cauda equina neuropathy. In
comparison with the dog, the condition is rarely
recognized in cats with the exception of spinal
fracture/luxation. Other causes include spinal and
vertebral neoplasia, especially lymphoma65, caudal
lumbar or lumbosacral disc protrusion66 or extrusion,
fibrocartilaginous embolism, cauda equina neuritis,
and discospondylitis. Cauda equina neuritis is caused
by inflammatory disease such as FIP or
toxoplasmosis. Spondylosis deformans is not an
uncommon finding at the lumbosacral junction and
sometimes appears to be associated with vague signs
of spinal discomfort suggestive of mild nerve root
compression (287). The principles for the
investigation of cauda equina syndrome are the same
as those for other regions of the spine. Delineation of
287
287 Lumbosacral DJD in a cat. Lateral radiograph of the
lumbosacral junction showing spondylosis deformans and
narrowing of the intervertebral disc space at L7–S1. The
cat presented with vague signs of hindquarter discomfort
with no evidence of neurologic dysfunction.
 Fractures and disorders of the spine
the lumbosacral region on plain ventrodorsal
radiographs can be improved by positioning the
hindlimbs cranially, thereby flexing the lumbosacral
spine. The clinician should be aware of the anatomy
of the lumbosacral spinal cord in the cat1.
Myelography is more useful in the cat than the dog
because the dural sac invariably crosses the
lumbosacral junction and continues well into or
beyond the sacrum (288). Surgical access to the
vertebral canal caudal to the L6–7 disc space is
generally made via dorsal laminectomy67.
UNCOMMON DISEASES OF
THE SPINE
TOXOPLASMOSIS
Cause and pathogenesis
Toxoplasma gondii is an intracellular protozoal
parasite that affects virtually all species of warm-
blooded animals. Domestic cats and other Felidae are
the definitive hosts for the organism and
toxoplasmosis in cats is usually subclinical. Disease is
caused by cell necrosis associated with intracellular
growth of Toxoplasma spp. and may affect multiple
body tissues with diverse clinical signs. Although
288
A inflammation.
B Cause and pathogenesis
288 Caudal lumbar intervertebral disc extrusion in a cat.
A Lateral myelogram of the lumbosacral spine showing a
ventral extradural lesion at L6–7.
B MRI scan of the lumbosacral spine. (Image courtesy of
Davies Veterinary Specialists.)
313
toxoplasmosis is always included in the differential
diagnosis of spinal disease, the nervous system was
the predominant organ of involvement in only 7% of
cases in 100 cats with histologically confirmed
toxoplasmosis68.
Clinical signs
Clinical findings may include limb weakness, paresis,
muscle pain, and hyperesthesia. Neurologic
examination may reflect a mixture of spinal cord and
muscle or peripheral nerve signs since all of these
tissues may be affected.
Diagnosis
Antemortem diagnosis is based on clinical signs,
serologic examination, laboratory findings, and the
response to antitoxoplasmic treatment. Unfortunately,
no single serologic test exists that can definitively
confirm a diagnosis of toxoplasmosis and, because
there is a delay in obtaining results, treatment is
usually initiated on the basis of other findings.
Treatment and prognosis
The drug of choice is clindamycin, which is
administered at a dosage of 40 mg/kg body weight in
divided doses for 4–6 weeks. Transient vomiting is a
common side-efffect of clindamycin in cats.
Glucocorticoids in clinical doses have not been
shown to exacerbate systemic disease69. The response
to treatment with clindamycin is fair to good if the
cat is negative for FeLV and FIV and is treated before
the development of paralysis. Systemic signs, if
present, usually begin to resolve within the first 48
hours of administration. Neurologic signs generally
improve more slowly and there may be residual
neurologic dysfunction as a sequela to nervous tissue
NEOSPOROSIS
Natural infection with Neospora caninum has not
been documented in the cat. Experimental infection
of prenatal and neonatal kittens produced lesions
similar to those seen in the dog, i.e. encephalomyelitis,
polymyositis, and hepatitis; the disease was subclinical
in adult cats70.
CRYPTOCOCCOSIS
Cryptococcus neoformans is the commonest cause of
systemic mycotic infection in the cat. Cats with
neurologic involvement generally have diffuse
meningoencephalitis, although a more localized
granulomatous lesion may develop occasionally.
314
It has been speculated that cats that are
immunosuppressed as a result of FeLV or FIV
infection may be more prone to infection. However,
underlying diseases are often not detected in cats with
clinical disease and factors that predispose to
infection remain elusive71.
Clinical signs
The clinical signs are variable according to the sites
affected. Signs of spinal cord and nerve root
infection are seen occasionally and include limb
weakness and paralysis. These may occur either alone
or be accompanied by signs of involvement of other
organs.
Diagnosis
Diagnosis is based on CSF analysis, serologic testing,
tissue biopsy, and isolation of the organism by fungal
culture. CSF cytology has revealed organisms in the
majority of canine cases72. CSF serology is preferred
to serum serology for cats with neurologic signs of
Cryptococcus spp. and may be more sensitive than
either CSF cytology or CSF culture. False-negative
cytology and serology results may be seen and, in
these cases, culture may be required to confirm a
diagnosis. Unfortunately culture has limited clinical
utility because there is a time delay of several weeks.
Treatment and prognosis
Treatment is by the administration of the antifungal
antibiotics, itraconazole or fluconazole, at a dosage of
5–10 mg/kg/day divided twice daily for 2–3 months
beyond the resolution of all clinical signs73,74. Studies
in cats have shown significant variability in the
absorption of itraconazole and the oral solution is
more consistently absorbed than the capsules.
Fluconazole is the drug of choice in the treatment of
cryptococcal meningitis in humans but is more
expensive than itraconazole. In one study,
seropositivity for FeLV or FIV was found to have a
negative influence on the prognosis75 and such cases
may require maintenance therapy.
FELINELEUKEMIA VIRUS AND FELINE
IMMUNODEFICIENCY VIRUS
Tests for both of these viruses are frequently
indicated as part of the investigation of spinal
disease. Positive FeLV or FIV tests may be
associated with spinal cord disease or could be
coincidental. Neurologic manifestations of FIV
infection are not common but a wide variety of
neurologic signs have been reported, including
paresis76. There is also a significant correlation
between FIV infection and the development of
leukemia and lymphoma77,78. Furthermore, both
viruses may cause immunosuppression and
predispose to infection with opportunistic
pathogens that may cause spinal disease, such as
coronavirus, Toxoplasma spp., or Cryptococcus spp..
BACTERIAL MENINGOMYELITIS
Cause and pathogenesis
Bacterial meningomyelitis is rare but may
occasionally occur when there is bacteremia
secondary to infection remote from the spine79.
Critically ill patients and cats that are
immunocompromised as a result of FeLV or FIV
infection may be predisposed. Other causes include
iatrogenic (as a result of a contaminated spinal
needle), or direct extension along the paraspinal
muscles into the vertebral canal from an infected bite
wound over the dorsum80. An epidural granuloma
has been reported as a rare cause of paraparesis81.
Fusobacterium and Bacteroides spp. were isolated
from the granuloma.
Clinical signs
Affected cats have spinal pain and hyperesthesia and
may show neurologic dysfunction predicated by the
location and severity of the infection. There are
frequently clinical signs caused by bacterial infection
elsewhere in the body.
Diagnosis
CSF analysis may show neutrophilic pleocytosis and
positive bacterial culture. Neutrophils show
degenerative changes and may contain phagocytosed
bacteria. False-negative culture results are not
uncommon. Pasteurella spp. and Staphylococcus spp.
are the most likely isolates, although anaerobic
bacteria may also be involved; definitive antimicrobial
therapy should be based on the results of culture and
sensitivity when available.
Treatment and prognosis
A broad-spectrum bactericidal antibiotic that
penetrates the CSF should be chosen initially, such as
a potentiated sulfonamide or enrofloxacin. If
anaerobes are suspected, metronidazole may be
added or a third generation cephalosporin can be
used instead. Cefotaxime and ceftazidime are usually
effective against anaerobes and are the drugs of
choice for Gram-negative infections. However, these
drugs are expensive and may have limited activity
 Fractures and disorders of the spine
against Gram-positive cocci. Antimicrobial therapy
should be continued for 2–4 weeks beyond the
resolution of clinical signs. For localized infections
antibiotics should be combined with drainage and
debridement of affected tissues. The outcome of
treatment will depend on the severity and duration
of the clinical signs and the ability to isolate the
organism responsible. The prognosis will be better
for those cases where the underlying cause is
identified and can be addressed.
FIBROCARTILAGINOUS EMBOLISM
Cause and pathogenesis
Fibrocartilaginous embolism (FCE), or ischemic
myelopathy, is a very rarely reported spinal disease in
the cat, the importance of which lies in its
differentiation from other more frequent causes of
acute spinal injury. The condition is not uncommon in
the dog and has been reported in a number of other
species, including humans. The pathogenesis involves
infarction of the spinal cord as a result of
fibrocartilaginous embolization from the
intervertebral disc. It is not known how the
intervertebral fibrocartilage enters the spinal cord
vasculature, although several theories have been
proposed. The precise etiology may differ between
species or even between different individuals in the
same species.
Clinical signs
There are only four published reports of feline FCE
in the English language82–85. All reported cases have
been over 8 years of age and there appears to be a
predisposition for either the cervical or the lumbar
intumescence. In the one case there was worsening
of signs over a period of 5 days, which was presumed
to be due to progressive ischemia and inflammation
secondary to the initial infarction. This finding has
been rare in cases documented in the dog, where the
presentation is usually acute to peracute and
nonprogressive. In common with the dog, all the
feline cases have shown asymmetric signs with no
evidence of spinal pain.
Diagnosis
CSF analysis performed in three cats showed
nonspecific changes with increased cell counts that
were predominantly neutrophilic and in two cats there
was also elevation of protein. Myelography in one case
showed obstruction to the flow of contrast medium
past the site of the lesion consistent with
intramedullary swelling83. Presumptive diagnosis is
315
based on the clinical signs and investigations to
exclude other causes of acute spinal injury. Definitive
diagnosis depends on postmortem and
histopathologic examination of the cord, so the
condition may be much more common than can be
inferred from the literature. FCE should be included
in the differential diagnosis for any cat with a
nonpainful acute spinal disorder with no clear history
of trauma, particularly where there are lower motor
neuron signs. Histopathologic examination of
suspected cases should include the vertebral bodies
and intervertebral discs in an attempt to elucidate the
underlying pathogenesis.
Treatment and prognosis
There is no convincing evidence that treatment has
any effect on the outcome in other species. All
reported feline cases were euthanased because of the
severity of the neurologic dysfunction and the poor
response to conservative management. However,
because of the low index of suspicion for FCE there
may be many cases that have recovered with
conservative management where the clinical signs
have been ascribed to trauma. Treatment entails good
nursing care, bladder management, and appropriate
physical therapy as for any paralyzed patient.
Administration of MPSS may have some value if the
case is seen within the first 8 hours using the protocol
for any acute spinal injury. Other glucocorticoids,
although frequently used, are unlikely to be of any
benefit. The prognosis would appear to be poor,
particularly where there are lower motor neuron
deficits.
DISCOSPONDYLITIS
Cause and pathogenesis
Discospondylitis is an inflammatory process
involving the intervertebral disc space and adjacent
end plates of successive vertebral bodies. The
condition is not uncommon in the dog but is very
rare in the cat. There are three case reports in the
English language literature86–88. In two of these
cases the infection was shown to extend into the
vertebral canal, which is an uncommon finding in
dogs. Streptococcus canis and Actinomyces viscosus
were cultured from a paravertebral abscess in one
cat; another cat had a concurrent Escherichia coli
urinary tract infection. The third report did not
describe culture results.
Discospondylitis in humans usually originates by
hematogenous spread of bacteria from a source of
sepsis elsewhere in the body, such as the urinary
316
tract. The infection is thought to start as an
osteomyelitis of the vertebral metaphysis and then
spread to the disc and adjacent soft tissues after
penetrating the vertebral end plate. The involvement
of multiple sites in the reported cases is consistent
with hematogenous spread rather than extension
from a local soft tissue infection.
Clinical signs
Clinical signs have included paresis, paraplegia,
inappetence, pyrexia, and, in one cat, hyperesthesia
with no neurologic deficits.
Diagnosis
In all the reported cases, osteolysis of adjacent
vertebral end plates was the predominant radiographic
feature with variable degrees of spondylosis and
sclerosis (289). Since immunosuppression might be
expected to play a role in the disease, all suspected
cases should be tested for FeLV and FIV.
Treatment and prognosis
Cases in the literature are too few to assess the
results of treatment. However, based on the
authors’ personal experience and extrapolation from
the dog, medical treatment is likely to be successful
if neurologic dysfunction is not severe. A broad-
spectrum bactericidal antibiotic should be chosen,
preferably based on the results of culture and
sensitivity if there is concurrent sepsis elsewhere. If
there is no clinical improvement within the first
7–10 days, the antibiotic should be changed or the
diagnosis reviewed. Treatment with a suitable
antibiotic is continued for a minimum of 6 weeks.
289
289 Discospondylitis. Lateral radiograph of the
thoracolumbar spine of a 7-month-old cat with spinal pain,
showing the characteristic osteolysis of the verterbal end
plates at L1–L2.
Follow-up radiographs should be obtained every
4–6 weeks to assess the efficacy of therapy.
Antimicrobial therapy is continued until the lesions
become radiographically silent. Bony changes lag
behind clinical improvement so worsening of the
radiographic features may be seen on the first set of
follow-up films.
The prognosis for cats with severe neurologic
dysfunction is likely to be guarded. These cases may
require surgical management for curettage of
affected disc spaces, to obtain samples for culture,
and to decompress the spinal cord. It has been
suggested that instability may play a role in the
pathogenesis, so concurrent surgical stabilization of
affected vertebrae should be considered. The
information in the literature suggests that spread of
the infection from the disc to the meninges occurs
early in the course of the disease when the
radiographic changes are subtle. If this is a particular
feature in cats, it is likely to have a strong negative
influence on the prognosis.
CONGENITAL ANOMALIES
Congenital anomalies of the vertebrae and spinal
cord are uncommon causes of spinal disease in the
cat. A variety of deformities may be found
incidentally during routine radiographic examination
(290, 291). The range of anomalies is similar to
those reported in the dog although they occur much
less frequently. Deformities that are generally
asymptomatic include hemivertebra, block vertebra,
butterfly vertebra, transitional vertebra, and
abnormalities of the sacrum such as fusion of S3 and
Cd1 or incomplete fusion of S2 and S3.
 Fractures and disorders of the spine
SACROCAUDAL HYPOPLASIA
Cause and pathogenesis
The bobtail of Manx and Manx cross cats is an
autosomal dominant trait that is also responsible for
other vertebral and neural anomalies of the
sacrocaudal region89. The so-called Manx cat is not a
pure breed and the morphology of the sacrocaudal
region in a litter of kittens may range from no tail
(‘rumpy’), a tail stump (‘rumpy riser’), a short tail
(‘stumpy’), and a normal length tail. The most
common vertebral malformation, apart from caudal
290
290 Congenital spinal anomaly. Ventrodorsal radiograph of
the pelvis showing a transitional vertebra at the lumbosacral
junction. There is unilateral sacralization with one side of the
seventh lumbar vertebra fused to the ilium and the sacrum.
This was an incidental finding in this cat.
317
dysgenesis, is sacrocaudal hypoplasia but spina bifida
may also occur (292). Spinal cord abnormalities
include absence or partial development of sacral and
caudal spinal cord segments or cauda equina,
myelodysplasia (disorganization of gray and white
matter), myeloschisis (cleft within the spinal cord),
diastematomyelia (duplication of the sacral segments),
syringomyelia in the lumbar and sacral spinal cord
segments, shortening of the spinal cord, meningocele,
myelomeningocele, and subcutaneous cyst formation.
291
291 Congenital spinal anomaly. Lateral radiograph of a
lumbar block vertebra. (Radiograph courtesy of Malcolm
McKee.)
292
292 Ventrodorsal radiograph of the pelvis of a Manx cat
with sacrocaudal hypoplasia and sacral spina bifida.
(Radiograph courtesy of Malcolm McKee.)
318
Clinical signs
The spinal cord and cauda equina malformations are
associated with a range of neurologic deficits. A bunny-
hopping gait is considered a normal characteristic of the
breed and even cats with no abnormality of the sacrum
have a degree of myelodysplasia. Cats with sacrocaudal
hypoplasia have more severe clinical signs reflecting
abnormal development of the nerves of the cauda
equina. In severe cases kittens may present at 3–6 weeks
of age with paraparesis and urinary and fecal
incontinence.
Diagnosis
The diagnosis can be confirmed by radiographic
examination and myelography may sometimes show
concurrent spinal cord abnormality such as
meningocele or attachment of the spinal cord to
tissues in the lumbosacral region. The severity of the
neurologic signs does not always correlate with the
degree of spinal deformity.
Treatment and prognosis
There is no specific treatment and the prognosis for
cats with severe neurologic impairment is poor.
Meningocele may be corrected surgically in cats with
minimal neurologic dysfunction.
ATLANTOAXIAL SUBLUXATION
Subluxation of the atlantoaxial articulation is a very
rare spinal disorder in the cat. There have only been
four reported cases in the English language,
including two cats with occipitoatlantoaxial
malformation90,91 and two cats with aplasia or
hypoplasia of the dens92,93. Clinical signs were the
same as those in the dog, ranging in severity from
chronic neck pain to tetraparesis. The diagnosis is
made by radiographic examination and a successful
outcome may be achieved using standard surgical
stabilization techniques described in dogs, such as
ventral cross-pinning. The condition should be
included in the differential diagnosis for any cat
presented with a spinal lesion localizing to the cranial
cervical region.
SPINA BIFIDA
Spina bifida is the incomplete closure or fusion of the
dorsal vertebral arches94. There may be protrusion of
the meninges (meningocele) or the spinal cord and
meninges (myelomeningocele) through the vertebral
defect. If the defect communicates with the skin
surface, there will be leakage of CSF onto the skin and
a risk of meningitis and electrolyte depletion95.
Concomitant anomalies include tethering of the spinal
cord and hydrocephalus. Spina bifida is most common
in the sacral region of the Manx cat but has been
described in the thoracic and lumbar vertebrae of a
litter of kittens96. Spina bifida not involving the spinal
cord or cauda equina is not associated with any
neurologic signs.
The diagnosis of spina bifida is made
radiographically. Myelography or ultrasonography are
required to confirm the presence of a meningocele or
myelomeningocele. Surgery is indicated to close the
meningocele and relieve spinal cord tethering, which
may be of benefit to prevent loss of urinary and fecal
continence and progressive paraparesis. There is a case
report of successful surgical treatment of a tethered
spinal cord associated with an intradural extra-
medullary lipoma and meningocele in a Manx cat97.
DEGENERATIVE MYELOPATHY
To the authors’ knowledge there is only one report of
this condition in the English language literature98.
The condition may be more common than realized
since definitive diagnosis requires histopathologic
examination of the spine. The history and clinical
signs and the histopathologic findings were similar to
those described in German shepherd dog degenerative
myelopathy, except that the pathology extended to
the white matter of the medulla and the cerebellar
peduncles.
LYSOSOMAL STORAGE DISEASES
Cause and pathogenesis
This is a diverse group of metabolic diseases affecting
multiple body systems linked by the common
pathologic feature of abnormal intracellular
accumulation of storage material. They are rare
congenital disorders caused by a deficiency of one or
more enzymes necessary for the hydrolysis of
proteins, polysaccharides, and complex lipids. The
enzymes are present in lysosomes, hence the
collective term of lysosomal storage diseases. All of
the lysosomal storage diseases of cats are inherited as
autosomal recessive traits99. They are classified into
subgroups on the basis of the metabolic pathway
affected and the type of storage found. The main
subgroups are the glycoproteinoses, the
sphingolipidoses, the mucopolysaccharidoses, and the
proteinoses.
Clinical signs
The enzyme deficiency leads to accumulation of
metabolite, causing a wide array of clinical signs.
Neurologic signs usually develop in the immature
animal in the first few months of life and are progressive
 Fractures and disorders of the spine
over the first year. However, delayed onset diseases have
been reported, particularly ceroid lipofuscinosis, and
their prevalence is probably underestimated. Clinical
signs include paraparesis or tetraparesis often with signs
of cranial involvement such as seizures, intention
tremor, and blindness. Sphingomyelinosis (Niemann–
Pick disease) is associated with a deficiency of the
enzyme sphingomyelinase, which results in a
demyelinating polyneuropathy (see Chapter 12).
Mucopolysaccharidosis VI (Maroteaux–Lamy disease)
is due to a defect in the metabolism of
mucopolysaccharides or glycoaminoglycans and is seen
predominantly in Siamese cats100. These cats present at
4–7 months of age with progressive paraparesis
associated with spinal cord compression. Affected
kittens are smaller than normal littermates and have
characteristic physical deformities, including a broad
face with small ears, corneal opacification, and pectus
excavatum. Skeletal abnormalities include fusion of
vertebrae and bony proliferation, with protrusion into
the thoracolumbar vertebral canal and the
intervertebral foramina, causing spinal cord and nerve
root compression.
Diagnosis
Lysosomal storage disease should be included in the
differential diagnosis for any cat with progressive
multifocal neurologic disease, particularly if
inflammatory disease has been excluded. Diagnosis is
based on biopsy of appropriate tissues according to
the nature of the disease. Lysosomal enzyme analysis
may be performed at specialist laboratories and will
provide a definitive diagnosis for most lysosomal
storage diseases. Molecular screening tests are likely to
become increasingly available in the future. Diagnosis
of mucopolysaccharidosis VI can be confirmed by
measurement of arylsulfatase enzyme activity in
leucocytes.
Treatment and prognosis
There is no effective treatment for any of the lysosomal
storage diseases but progression of neuronal storage
may be slow and some cats may survive months to
years after diagnosis. The skeletal changes seen in
mucopolysaccharidosis VI are nonprogressive after
physeal closure at around 9 months of age and
decompressive surgery may improve neurologic status.
SYRINGOMYELIA AND HYDROMYELIA
Hydromyelia and syringomyelia are terms used to
describe cystic fluid-containing cavities within the
spinal cord. The fluid is similar, if not identical, to
CSF. Hydromyelia is a dilation of the spinal cord
319
central canal, which is lined by ependymal cells and
often communicates with the ventricular system. The
term syringomyelia refers to cystic cavities within the
substance of the spinal cord. In practice the two may
be difficult to differentiate and the terms
syringohydromyelia or syringomyelia are often used to
encompass both conditions101. The clinical signs
reflect spinal cord dysfunction and depend on the size
of the lesion, the rate of onset, and the region of spinal
cord involved.
Syringohydromyelia may occur in association with
other congenital anomalies of the spinal cord or may
be secondary to compressive myelopathies.
Hydromyelia may be accidentally diagnosed during
routine myelography when contrast medium enters a
dilated central canal. In many cases, however,
myelography is normal or shows only intramedullary
enlargement of the cord. Definitive diagnosis is best
made using MRI. Although rarely reported in the
cat102, these conditions may be diagnosed more
frequently with the increased availability of advanced
imaging techniques. Treatment may be attempted by
shunting or surgical drainage of the syrinx but the
prognosis is usually poor.
SPINAL SUBARACHNOID CYST
Synonyms for this condition include arachnoid cyst,
subarachnoid cyst, meningeal cyst, and
leptomeningeal cyst. The condition is well known in
humans and is increasingly being reported in dogs,
but there are only three reported cases in the
cat103–105. All three cysts have been located in the
thoracolumbar region.
The condition should be included in the
differential diagnosis for any cat with progressive
spinal cord dysfunction, especially if this localizes to
the thoracolumbar region. Definitive diagnosis
requires myelography or advanced imaging
techniques. The myelographic appearance is
characterized by a bulbous expansion of the
subarachnoid space in the dorsal mid-line with
attenuation of the subadjacent spinal cord. The
pathogenesis of the condition is not known. Various
causes have been proposed, including trauma,
arachnoiditis, spina bifida, spinal dysraphism, and
congenital dural diverticula. Treatment by
decompressive dorsal laminectomy and drainage of
the cyst with or without marsupialization appears to
be successful.
VERTEBRAL ANGIOMATOSIS
Angiomatosis is a rare developmental anomaly
characterized by the formation of multiple
320

nonneoplastic tumors that form from blood vessels SPINAL DERMOID CYST
(angiomas). The pathogenesis is not fully understood There is one report of a dermoid cyst in the thoracic
but the condition is thought to be a vascular spine of a young adult Balinese cat108. Clinical signs
malformation. The condition has been reported in were consistent with a severe spinal compressive
four cats106,107. The vascular lesion arises in a vertebra lesion. The cyst was considered to be a congenital
and extends into the vertebral canal, causing anomaly.
compression of the spinal cord and nerve roots. All
cases have been between 1 and 2 years of age and have HYPERVITAMINOSIS A
presented with progressive spinal pain and paresis with Hypervitaminosis A is a rare nutritional disorder
localization to the caudal thoracolumbar region. The caused by an excessive intake of vitamin A. The
radiographic appearance shows a poorly circumscribed condition frequently causes cervical spinal lesions and
mixed pattern of bony proliferation and bone lysis is discussed in Chapter 13.
usually involving the pedicle of a single vertebra. The
response to surgical resection and decompression was
favorable in the two cases in which it was attempted.
The condition should be included in the differential
diagnosis for an apparently aggressive bone lesion
affecting the thoracolumbar region in a young cat,
especially if the pedicles are involved.

CHAPTER 12
NEUROMUSCULAR
DISORDERS
INTRODUCTION
Neuromuscular diseases affect muscles, peripheral
nerves or nerve roots, and neuromuscular junctions.
These diseases are all relatively uncommon but it
is important to be able to recognize the signs when
they do occur. With the exception of autonomic
neuropathies, such as dysautonomia, all neuro-
muscular disorders manifest as muscular weakness,
which may range from localized paresis to generalized
paralysis. A common nonspecific finding in cats with a
range of neuromuscular disorders is abnormal posture
with ventral neck flexion (293). Causes of neck
ventroflexion include myasthenia gravis, hypokalemia,
thiamine deficiency, hyperthyroidism, organophos-
phate toxicity, ethylene glycol toxicity, polyneu-
ropathy, and polymyopathy.
293 Cat with neck ventroflexion. (Photograph
courtesy of Andrew Sparkes.)
321
Diagnosis of a neuromuscular disorder is made
on the basis of physical and neurologic examination,
laboratory testing, electrophysiology, and biopsy.
Electrophysiologic evaluation of nerve and muscle
disorders is usually only performed at specialist centers.
Muscle and nerve biopsy and additional laboratory tests
are discussed in Chapter 2 (for laboratories see p. 334,
1–3). Neurologic examination should provide a clear
distinction between neuropathies and myopathies.
Hyporeflexia or arreflexia and possible impairment of
sensory pain perception are distinguishing features of
neuropathies and are not seen with myopathies or junc-
tionopathies. The distinction between myopathy and
junctionopathy may be more difficult to make.
Myasthenia gravis, in particular, may produce signs that
mimic those of a generalized myopathy, although it is a
junctionopathy.
293
322

CLASSIFICATION OF or paralysis, ataxia, hypo- or areflexia, tremors, altered

NEUROMUSCULAR DISORDERS
Neuromuscular disease is classified into three types
determined by the anatomic location of the lesion.
• Neuropathies – diseases of the peripheral nerves
or nerve roots.
• Myopathies – diseases of the muscles.
• Junctionopathies – diseases of the neuromuscular
junction.
Diseases are further subdivided according to whether
they are acquired or inherited. Inherited or congenital
neuromuscular diseases are less common than acquired
ones1. A detailed review of neuromuscular disease in
the dog and cat has recently been published2.
CAUSES OF NEUROMUSCULAR
DISEASE
Causes of neuromuscular disease are summarized in
Table 28.
NEUROPATHIES
Neuropathies can be divided into inherited and
acquired types. Clinical signs of both include paresis
muscle tone, and muscle atrophy (Table 29).
Impairment of sensation is variable and there may be
anesthesia, hyperesthesia, or paresthesia. The acquired
types may have immunologic, metabolic, or toxic
etiologies or may be idiopathic when the underlying
cause is never discovered. Feline polyneuropathies
have recently been reviewed3.
INHERITED POLYNEUROPATHIES
An inherited polyneuropathy should be suspected in
any cat less than 1 year of age with progressive tremors,
paraparesis, or tetraparesis with depressed or absent
spinal reflexes. Most congenital polyneuropathies are
untreatable, progressive, and fatal.
Hyperoxaluria
Affected cats have low concentrations of the enzyme D-
glycerate dehydrogenase, resulting in an unexplained
axonopathy with lower motor neuron dysfunction.
Affected cats have an intermittent oxalaturia and
usually die from renal failure due to deposition of
oxalate crystals in the kidneys before 1 year of age4.

TABLE 28 CAUSES OF NEUROMUSCULAR DISEASE.

Inherited Acquired
Neuropathies Hyperoxaluria Adult onset motor neuron disease
Hyperchylomicronemia Idiopathic polyneuropathy
Axonopathy of Birman cats Ischemic neuromyopathy
Sphingomyelinosis (Niemann–Pick disease) Diabetic polyneuropathy
Toxic polyneuropathy
Neoplastic neuropathy
Traumatic neuropathy
Iatrogenic neuropathy
Local tetanus

Myopathies Nemaline myopathy Myositis ossificans

Muscular dystrophy Hypokalemic myopathy
Devon Rex myopathy Infectious myopathy (bacteria,
Burmese hypokalemic myopathy protozoa)
Fibrodysplasia ossificans progressiva Fibrotic myopathy
Myotonia Quadriceps contracture
Idiopathic polymyopathy
Paraneoplastic myopathy
Junctionopathies Myasthenia gravis Myasthenia gravis
Organophosphate and carbamate toxicity
Snake bite and tick paralysis
 Neuromuscular disorders
323

TABLE 29 SUMMARY OF THE CLINICAL SIGNS OF NEUROMUSCULAR DISEASE.

Neuropathies
Muscle atrophy
Altered muscle tone
Paresis or paralysis
Proprioceptive deficits
Hyporeflexia or areflexia
Myopathies Junctionopathies
Muscle weakness or stiffness Reduced exercise tolerance
Variable muscle pain Intermittent weakness
Muscle atrophy or hypertrophy Flaccid paralysis
Reduced exercise tolerance
Stiff, stilted gait
Limited joint movement (contracture)

Hyperchylomicronemia electromyographic changes. Affected cats survived for

Affected cats have low lipoprotein lipase activity and
elevated plasma triglyceride and cholesterol. Clinical
signs, including monoparesis, facial paralysis, and
Horner’s syndrome, result from compression of
peripheral nerves by lipid granulomas that probably
develop subsequent to trauma. Feeding a low-fat diet
results in resolution of lipemia and neurologic
dysfunction5.
Distal axonopathy of Birman cats
Affected cats show a degenerative neuropathy of the
sciatic nerves and several areas of the brain and spinal
cord. The disease is seen in 6–10-week-old male
Birman kittens as a progressive hindlimb ataxia
and plantigrade stance. Postmortem examination
reveals a central and peripheral distal axonopathy.
An autosomal sex-linked mode of inheritance is
suspected6.
Sphingomyelinosis (Niemann–Pick disease)
Sphingomyelinosis is a lysosomal storage disease
associated with a deficiency of the enzyme
sphingomyelinase, which results in a demyelinating
polyneuropathy7. The disease has been reported in
three Siamese kittens of 6 weeks and 5–7 months of
age. Clinical signs include progressive lower motor
neuron paresis, ataxia, tremor, hypermetria, and
hepatosplenomegaly8.
ACQUIRED NEUROPATHIES
Adult onset motor neuron disease
Progressive weakness and generalized muscle atrophy
associated with motor neuron cell death has been
described in three unrelated adult cats of different
breeds and ages9. Clinical signs included chronic
progressive weakness, neck ventroflexion, generalized
muscle atrophy, and, eventually, hypo- or areflexia.
There is no effective treatment. Diagnosis was based
on the slowly progressive clinical signs and the
up to 5 years after the onset of signs. Another study
described the findings in two adult cats, which had
similar clinical signs for 1 and 3 years’ duration10.
Idiopathic polyneuropathy
Acute and chronic forms of polyneuropathy of
unknown etiology have been described in cats.
Acute idiopathic polyneuropathy
Acute-onset, areflexic, flaccid tetraparesis or tetraplegia
similar to coonhound paralysis in dogs has been reported
in cats11,12. The age of onset has varied from 3 months
up to 4 years. Clinical signs begin with paraparesis
progressing rapidly to tetraparesis within 72 hours.
Respiratory depression occurs in severely affected cases,
necessitating oxygen therapy or ventilation. Electro-
myography usually reveals evidence of denervation, in
the form of fibrillation potentials and positive sharp
waves 5–7 days after onset, in limb and paravertebral
musculature. Loss of axons, demyelination, and
macrophage accumulation were found in the ventral
nerve roots of cats with the condition that were
euthanased. Treatment with glucocorticoids is indicated
if an acute inflammatory or immune-mediated
polyneuropathy is suspected. Methylprednisolone
sodium succinate (MPSS) is administered at a dosage of
15 mg/kg IV every 6 hours for the first 24 hours,
followed by a reducing anti-inflammatory dosage of
prednisolone over a 2-week period. There is a single
report of a cat with an acute-onset, relapsing idiopathic
polyneuropathy of 12 weeks’ duration that improved
within 6–7 days following prednisolone therapy and
resolved completely within 6 weeks13.
Chronic idiopathic polyneuropathy
Chronic idiopathic polyneuropathy was described
in two cats with progressive tremors, ataxia, and
weakness14,15. Progression to severe flaccid tetra-
paresis occurred over several weeks. Fascicular nerve
324

biopsy demonstrated segmental demyelination and The ischemia is produced by vasoconstriction of

axonal loss15. Electromyography revealed positive
sharp waves and fibrillation potentials, suggesting
axonal and myelin disease. The etiology in some
cases of chronic polyneuropathy is presumed to be
immune-mediated and may respond to
immunosuppressive doses of glucocorticoids.
Prednisolone is administered at a dosage of
2–4 mg/kg divided twice daily for 2 weeks, followed
by a reducing dosage over a period of 2–3 months. If
glucocorticoids are discontinued too rapidly, there
may be a recurrence of clinical signs, but their
re-administration may again result in clinical
improvement. The long-term prognosis is guarded,
however, as signs tend to recur and may eventually
become refractory to glucocorticoids.
Ischemic neuromyopathy
Cause and pathogenesis
Ischemic neuromyopathy and paraplegia in cats are
commonly associated with aortic thromboembolism
secondary to hypertrophic cardiomyopathy. Occlusion
of the aorta by a foreign body has been described
as a rare cause of ischemic neuromyopathy16,17.
In cats with arterial thromboembolic disease,
occlusion of the distal aortic trifurcation occurs when
an embolus breaks free from a thrombus in the left
atrium or ventricle and enters the peripheral
circulation. The aorta is the commonest site, but
emboli may also lodge in other vessels, most
commonly the right brachial artery, causing ipsilateral
forelimb monoparesis or monoplegia (294 A).
collateral circulation induced by vasoactive substances,
such as serotonin and prostaglandins, released from
the platelets in the clot.
Clinical signs
Clinical signs include acute-onset paraparesis/paraplegia
with cold extremities, absent or weak femoral pulses,
and evidence of underlying congestive heart failure.
Other signs tend to develop 12–24 hours later and
include firm painful muscles, swelling of the limbs, and
cyanosis of the nails and footpads (294 B).
Diagnosis
Diagnosis of ischemic neuromyopathy is made
on the basis of the clinical findings and the
demonstration of underlying cardiac disease. The
clinical signs in cats with traumatic spinal/pelvic
and concurrent thoracic injury after an unobserved
road traffic accident may be superficially similar
to those in cats with ischemic neuromyopathy.
Differentiation can easily be made between the two
conditions by checking the femoral pulses and
comparing the color of the forelimb and hindlimb
footpads.
Treatment and prognosis
The approach to management of the acute case
includes the use of thrombolytic agents to lyse the
embolus in combination with analgesia as necessary.
Thrombolytic agents, such as streptokinase or tissue
plasma activator, are only of benefit if administered

294

A B
294 Ischaemic neuromyopathy. (Photographs courtesy of Dr John Tyler.)
A Cat with forelimb monoparesis as a result of embolization in the right brachial artery.
B Footpads of the forelimbs and hindlimbs of a cat with ischemic neuromyopathy.
 Neuromuscular disorders
early in the course of embolization, preferably within
the first 2–4 hours. Vasodilators have been used in
the past to promote collateral circulation by
arterial vasodilatation but their efficacy is doubtful.
Vasodilators may cause generalized hypotension and
are therefore not recommended. In the longer term
aspirin is commonly used at a dose of 25 mg/kg every
3 days to prevent further episodes, although there
are no studies to demonstrate the efficacy of any
medication to prevent thrombus formation.
The short-term prognosis is usually dependent on
the severity of the underlying heart failure. If the heart
failure is controlled, some cats will recover partial or
even complete function over a 4–6-week period after
the initial episode. However, because the embolus is
usually only a portion of the intracardiac thrombus, or
because additional thrombi form, recurrent episodes
are likely. The median survival time in a recent series
of 44 cases was 6 months18.
Diabetic polyneuropathy
A distal polyneuropathy affecting the hindlimbs is
occasionally seen in cats with diabetes mellitus and
may occur in advance of those signs more typically
associated with the disease19,20. The reported
incidence is 8% of diabetic cats but the true figure
may be much higher. Distal axons are primarily
affected with secondary demyelination. Affected cats
have a plantigrade posture, progressive paraparesis,
hyporeflexia, and hindlimb muscle atrophy (295).
Signs may progress to involve the forelimbs. Clinical
signs usually improve and may resolve within
295 Diabetic cat with a plantigrade stance. (Photograph courtesy of Jon Wray.)
325
6–12 months with strict glycemic control.
Acetyl-L-carnitine has been used in a few cats with
persistent clinical signs of neuropathy with
subjectively good results21.
Toxic polyneuropathies
Toxicity should be suspected in any cat with
polyneuropathy and a history of exposure to a toxic
substance or drug. Once the underlying toxic
substance is removed most cats recover from the
neuropathy with supportive care. Cats have been
used as an experimental model for studying
polyneuropathies associated with a number of toxic
substances. These include thallous acetate,
acrylamide, and organophosphates, which disrupt
axonal transport. Organophosphates and carbamates
cause a nonselective reduction in the activity of
acetylcholinesterase, allowing continuous cholinergic
stimulation. A peripheral neuropathy may occur as
a delayed form of neurotoxicity either after prolonged
exposure or sometimes days to weeks after even
minimal exposure to these agents22. Chronic toxicity
is manifested as reversible neuromuscular weakness
that may last 2–4 weeks.
In 1995 there was an outbreak of neurologic
dysfunction in cats in the Netherlands and Switzerland
associated with the accidental contamination of cat food
with salinomycin, an ionophore anticoccidial agent used
in poultry. The neurologic dysfunction ranged from
mild paresis to severe tetraparesis, dyspnea, dysphagia,
and autonomic signs23,24. A distal axonopathy was
found on histologic examination of peripheral nerves25.
295
326
The cytotoxic drug, vincristine, may induce
peripheral neuropathy ranging from change of voice to
sensory and motor polyneuropathy and tetraparesis26.
The signs resolve once the drug is discontinued.
Neoplastic neuropathy
Peripheral nerves can be compromised either by direct
neoplastic involvement or remote paraneoplastic
effects. Direct involvement may be the result of
primary neoplasia, compression by adjacent
neoplasms, or infiltration by neoplastic cells. Primary
nerve sheath neoplasms arise from the myelin-
producing cells (schwannomas) or the connective
tissue surrounding the nerve (neurofibromas,
neurofibrosarcomas) and are rare in the cat27.
Lymphoma has been reported involving peripheral
nerves and nerve roots, especially at the brachial
intumescence28. Clinical signs of neoplastic
neuropathy include paresis, muscle atrophy, and
paresthesia, which may manifest as excessive licking at
the site of the affected sensory dermatome.
The authors are not aware of any reports of
paraneoplastic polyneuropathy in the cat but the
condition has been identified in dogs and is likely to
occur in cats as well. The pathogenesis is uncertain,
although an immunologic mechanism is most likely.
Progressive polyneuropathy may be a sentinel for
a clinically silent malignancy and a diligent search
for primary neoplasia should be included in the
routine diagnostic work-up for these cases. In theory,
successful treatment of the primary neoplasm should
result in resolution of the associated polyneuropathy,
although this may take several months.
Traumatic neuropathies
Peripheral nerves consist of bundles of nerve fibers in
an arrangement of connective tissue. Individual nerve
fibers are surrounded by a myelin sheath. Traumatic
injuries to peripheral nerves are classified in increasing
degrees of severity as neuropraxia, axonotmesis, and
neurotmesis.
Neuropraxia occurs when there is a mild stretch or
compression injury. There is temporary loss of
function for a period of days to weeks. Axonotmesis
occurs when there is a severe compression or stretch
injury with complete disruption of axons but the
supporting connective tissues elements remain intact.
Return to function requires regeneration of proximal
axons distally to the end organ. This occurs at a rate
of 1 mm/day and recovery, if it occurs, takes many
months. Neurotmesis occurs when there is an avulsion
injury or severance of a nerve. There is complete
disruption of the neural and connective tissue
components of the nerve. Unless the nerve ends are
surgically reunited, the proximal axons lack direction
and regrow into the surrounding tissues, creating
a neuroma. After surgical repair (neurorrhaphy) up to
75% of the original function may be restored but this
takes many months.
A variety of traumatic injuries may be associated
with peripheral nerve dysfunction. Important
syndromes include brachial plexus avulsion, radial
neuropathy, ischiatic and sciatic neuropathy, and
sacrocaudal traction injuries. Traumatic neuropathies
commonly occur in association with orthopedic
injuries such as pelvic, humeral, and femoral fractures.
It is critical to evaluate these cases carefully for
peripheral nerve injury that may affect the functional
outcome before performing fracture repair. The
particular peripheral nerve or nerve roots affected by
an injury can be determined by neurologic
examination and be further evaluated using
electrophysiologic testing. The hallmarks of peripheral
nerve injury include lower motor neuron signs, such
as flaccid paresis or paralysis, hypo- or arreflexia, rapid
neurogenic muscle atrophy (within 7–10 days of the
injury), and sensory impairment. The prognosis
depends on the severity of axonal disruption and is
worst for nerve root avulsion injuries. Stretch and
compression injuries may resolve but recovery can
take from several weeks to several months. Serial
neurologic examinations are performed to monitor
regeneration after nerve injury.
Brachial plexus avulsion
Avulsion injury of the brachial plexus is a well
recognized syndrome that is usually caused by
vehicular trauma or falls from a height. Traction on the
forelimb results in the nerve roots comprising the
plexus being stretched and torn from the spinal cord.
The brachial plexus is derived from the last three
cervical and the first two thoracic nerve roots
(C6, C7, C8, T1, and T2). Injuries may be partial or
complete depending on the extent and the direction of
the traction. Injury to the caudal nerve roots (C8–T2)
or the entire plexus occurs most frequently, whereas
selective cranial root (C6–7) injury is uncommon.
Complete avulsion results in total paralysis of the
affected limb, often with Horner’s syndrome and
unilateral loss of the cutaneous trunci reflex (296).
Caudal avulsion will spare the flexors of the elbow and
the limb will be carried with the elbow flexed, but the
cat will be unable to extend the elbow to bear weight.
Cranial plexus injuries result in an inability to flex the
elbow. The prognosis is poor unless the injury is
confined to the cranial plexus. If nerve roots are not
 Neuromuscular disorders
completely avulsed, there may be some recovery of
neurologic function over a 1–3-month period. If there
is no improvement in limb function within a period of
3 months, amputation is generally indicated. Muscle
relocation techniques have been described for cases
with partial neuropathy29 but the results are often
unsatisfactory in the forelimb, probably because
denervation is frequently more widespread than
initially suspected.
Radial nerve paralysis
Radial nerve paralysis is sometimes used incorrectly as
a synonym for brachial plexus avulsion. True selective
distal radial nerve injury is occasionally seen in
association with humeral fractures. The entire radial
nerve is sometimes injured in conjunction with
fracture of the first rib. Distal injury is less serious
since it spares the innervation to the triceps muscle
and the elbow can still be extended to bear weight.
Options for the treatment of permanent neurologic
impairment are arthrodesis, muscle relocation, and
amputation. Amputation is indicated for entire radial
nerve injuries if there has been no recovery within
a period of 3 months. Distal radial nerve paralysis may
be managed by arthrodesis of the carpus in 20–30° of
hyperextension to prevent trauma to the digits.
296
296 Cat with left brachial plexus avulsion showing
Horner’s syndrome.
327
Ischiatic/sciatic neuropathy
Ischiatic neuropathy is most commonly observed as
a result of craniomedial displacement of iliac shaft
fractures with impingement on the underlying
ischiatic trunk30,31. Sciatic nerve injury is occasionally
seen in association with femoral or acetabular fracture
and hip luxation. The peroneal component of the
nerve is more susceptible to injury than its tibial
counterpart because of the greater diameter of its
fibers32. Peroneal nerve dysfunction causes partial
sciatic neuropathy, which manifests as reduced or
weak hock flexion during testing of the flexor reflex.
Selective involvement of the tibial component is rarely
seen as a result of trauma but does occur in cats with
diabetic neuropathy. If the nerve has not been
completely severed, recovery of partial or complete
neurologic function may occur over a period of 1–3
months. If it is known that the nerve has been
transected, for example if the injury is iatrogenic, the
ends should be surgically anastomosed. This is
relatively easy for true sciatic nerve injury, but
exposure is very difficult in the region where the
ischiatic trunk lies medial to the pelvis. Muscle
relocation techniques can only be used in selected
cases where there is remaining functional muscle that
can be transferred to replace the function of
a paralyzed muscle29. Injuries are more likely to
involve a single nerve, or a component of a single
nerve, in the hindlimb than the forelimb, so muscle
relocation is more appropriate for restoration of
hindlimb function. In cats with peroneal nerve
paralysis a side-to-side anastomosis is performed
between the tendons of insertion of the functional
long digital flexor and the nonfunctional long digital
extensor muscles. The relocated muscle acts as a
digital extensor and hock flexor. In cats with sciatic
neuropathy affecting both the peroneal and tibial
components, use can be made of the functional
femoral nerve by relocation of the tendon of origin
of the nonfunctional long digital extensor muscle
in combination with arthrodesis of the tarsus.
The tendon is relocated to the lateral aspect of the
patellar retinaculum so quadriceps contraction causes
synchronous extension of the digits.
Iatrogenic neuropathy
Iatrogenic injury most commonly involves the
sciatic nerve as a result of inadvertent penetration
during retrograde intramedullary pinning of femoral
fractures33,34 or injection of irritant substances into
the hamstring muscles35. The nerve may also be
injured during closed reduction of hip luxation and
procedures that involve a caudal approach to the hip
328
joint, such as internal stabilization of hip luxation,
internal fixation of acetabular fracture, and femoral
head and neck excision. The distal radial nerve may be
injured during internal stabilization of humeral
fractures.
Local tetanus
Cause and pathogenesis
Tetanus is caused by the obligate anaerobic
bacterium, Clostridium tetani, which produces the
neurotoxin tetanospasmin. The toxin undergoes
retrograde neuronal transport from the
neuromuscular junctions adjacent to the site of
infection to exert its effect on inhibitory
neurotransmission. Cats are less susceptible to
tetanus than most other domestic species because of
an inability of this neurotoxin to penetrate the
nervous system easily and attach to binding sites 36,37.
Generalized tetanus is easily recognized and
the diagnosis is usually straightforward. Localized
tetanus is a rare manifestation of tetanus that has
been reported predominantly in the cat38–42. The
clinical signs result from the action of the neurotoxin
on the inhibitory neurones, which innervate the local
muscle groups adjacent to the site of the infection.
Clinical signs
When a single limb is affected the condition presents as
a cause of nonweight-bearing lameness with continuous
involuntary contraction of the muscles innervated by
the same or adjacent spinal nerves. Sensory perception
is not impaired and affected cats are otherwise mentally
alert and healthy. There is usually a history of a
penetrating wound or surgery up to 3 weeks before the
onset of signs, close to or distal to the spastic muscle
groups (297). Localized tetanus occasionally
progresses to the generalized form and there is also a
single report of progression to severe spastic tetraparesis
with no intracranial signs43.
Diagnosis
The diagnosis may be confirmed by finding the organism
in Gram-stained smears (if a contaminated wound is still
present); serum concentrations of antitetanus antibody
will be elevated. Electromyography will show postneedle
insertion activity in the affected muscles.
Treatment and prognosis
Treatment is directed at controlling the infection,
neutralizing the toxin, and relieving the spasticity.
Penicillin G is traditionally the antibiotic of choice and
can be given both intravenously in the aqueous form and
intramuscularly as the procaine salt. Tetanus antitoxin is
also administered (10,000 I.U. IV). Metronidazole may
be more effective than penicillin G, although it carries
a higher risk of toxicity37. Diazepam may be used to help
reduce the spasticity at a dose of 2.5–5 mg orally three
times daily. The prognosis is good, although resolution is
gradual and may take 2–5 months.
MYOPATHIES
Cats with polymyopathies present with generalized
weakness causing exercise intolerance, fatigue, stiff
stilted gait, and, often, neck ventroflexion. Muscle
swelling, pain, or atrophy may also be present,
although muscle hypertrophy may occur in some
myopathies. In contrast to the polyneuropathies,
sensory pain perception, spinal reflexes, and
proprioception are not impaired (Table 29). Certain
disorders of the neuromuscular junction may mimic
the signs observed in a generalized myopathy. An
elevation of creatine kinase (CK) occurs when there is
myonecrosis associated with an inflammatory
myopathy but increased CK alone is not diagnostic
of myositis. Differentiation of many of these disorders
depends on the examination of a properly processed
muscle biopsy specimen. Myopathies can be divided
into inherited and acquired types. Idiopathic
myopathy is an acquired myopathy where the
underlying cause cannot be determined.
INHERITED POLYMYOPATHIES
Nemaline myopathy
Nemaline or rod myopathy is a congenital disorder
characterized by nemaline rods within myofibers.
Clinical signs, which appear at 6–18 months of age,
include muscle weakness with reluctance to walk and
297
297 Cat with local tetanus of the hindlimbs and tail
following castration.
 Neuromuscular disorders
a hypermetric gait. There is also muscle atrophy,
tremors, and hyporeflexia. Electrophysiology is
normal and CK is only marginally elevated, so
diagnosis is based on muscle biopsy44.
Feline muscular dystrophy
Muscle dystrophies are genetically determined
disorders characterized by progressive, mostly
noninflammatory, degeneration of skeletal muscle.
A dystrophic myopathy should be considered in any
kitten with muscle weakness, gait abnormality, muscle
atrophy or hypertrophy, or muscle contractures.
An X-linked inherited muscular dystrophy,
characterized by an absence of dystrophin, has been
reported in male cats less than 2 years of age45,46.
Clinical signs include marked symmetrical muscle
hypertrophy, tongue enlargement, difficulty in
walking, and a stiff bunny-hopping gait. A peculiarity
of the condition is the presence of calcified nodules on
the tongue. Serum CK levels are dramatically elevated
and there are severe generalized EMG changes.
Histopathologic examination of muscle biopsies
reveals muscle pallor and myofiber necrosis. Definitive
diagnosis requires dystrophin immunostaining.
Dystrophic myopathy and demyelinating
neuropathy associated with absence of laminin alpha2
has been described in two unrelated cats in the
USA47. One cat was a young female Siamese with
muscle atrophy and marked weakness and the other
was a young female domestic shorthair with
progressive spasticity beginning at 6 months of age.
There was moderate elevation of serum CK in both
cases. More recently, laminin alpha2 deficiency was
reported in a young European-bred Maine coon cat48.
The myopathy in this case was characterized by
progressive weakness, muscle atrophy, and joint
contracture.
Myopathy of the Devon Rex
An idiopathic polymyopathy with an autosomal
recessive pattern of inheritance has been reported in
Devon Rex cats49,50. Clinical signs, which appear from
3–23 weeks of age, include muscle weakness and
tremor, especially of the head. Affected kittens walk
with a hypermetric gait and develop ventroflexion
of the head and neck. The neck often remains
permanently flexed, causing difficulty in chewing
and swallowing food. Serum CK is not elevated.
Histopathologic examination of muscle biopsies shows
myopathy with the cervical and proximal limb muscles
preferentially affected. Affected individuals can have a
reasonable quality of life but premature death due to
asphyxiation when eating is not uncommon.
329
Fibrodysplasia ossificans progressiva
Fibrodysplasia ossificans is a rare condition
characterized by progressive ossification of the
connective tissues associated with skeletal muscle.
The disorder is always multicentric, is unrelated to
trauma, is often symmetrical, and, unlike ossifying
myositis, does not primarily involve muscle51–53.
There is hyperplasia and often ossification of
connective tissue, causing displacement of muscles
and entrapment of nerves with progressive
immobility. Radiography reveals extensive soft tissue
mineralization. The masses may be confused with
extraskeletal osteosarcomas. Muscle biopsy shows
differentiated cartilage and bone within the muscle
without inflammation. The prognosis is poor with
development of severe disability within a period
of several weeks to several months. There is no
treatment for the condition.
Myotonia
Myotonia is the continued active contraction of
a muscle after the cessation of voluntary effort or
stimulation. The condition is characterized by muscle
hypertrophy, spasm, stiffness, and inability to initiate
movement. Hereditary myotonia has been reported in a
series of domestic shorthair and longhair cats that may
have been related and is similar to congenital myotonia
in dogs54–56. Affected kittens walk with an awkward stiff
gait that is worse after rest and in cold weather. When
affected kittens are startled they may fall into lateral
recumbency in rigid hyperextension. Palpation reveals
widespread muscle hypertrophy. There is characteristic
dimpling of the tongue and skeletal muscle under
general anesthesia. Electromyography shows
spontaneous trains of repetitive waxing and waning
discharges after insertion of the electrode, producing an
audible dive-bomber or motorcycle sound. There is no
treatment and the prognosis is guarded, although
mildly affected cats may have a reasonable quality of life.
ACQUIRED MYOPATHIES
Traumatic myopathy
Skeletal muscle is composed of an arrangement of
striated muscle fibers or myofibrils and connective
tissue sheaths. Injuries heal by a combination of
fibrosis and regeneration of myofibrils. Excessive
postoperative scar tissue formation compromises
function and can be minimized by careful tissue
handling, debridement of necrotic tissue, and accurate
muscle apposition. Muscle should be sutured using an
absorbable material in a horizontal mattress pattern
placed through the holding layer, which is the external
connective tissue sheath or epimysium. Traumatic
330
injuries to muscles and tendons are called strains and
are classified as first degree (mild), second degree
(moderate), and third degree (severe). A strain can
affect any of the components of the muscle–tendon
unit, i.e. the tendon of origin or insertion, the
musculotendinous junction, or the muscle belly itself.
Such injuries are commonly seen in working or racing
dogs but are rarely recognized in the cat.
Injury causes disruption of muscle and/or
collagen fibers, hemorrhage, and inflammatory
edema. The goal of treatment in the acute phase is the
reduction of hemorrhage and swelling in an attempt
to limit subsequent scar tissue formation and muscle
contracture. This is achieved by restriction of activity
and application of cold to the site of injury.
A nonsteroidal anti-inflammatory drug (NSAID)
should be administered by injection to help reduce
swelling and relieve pain. Third degree strains
frequently involve rupture of the tendon or
musculotendinous junction and require surgical
repair.
Fibrotic myopathy of the semitendinosus muscle
Fibrotic myopathy is a condition in which muscle
tissue is replaced by fibrous connective tissue. A case
comparable to that affecting the semitendinosus
muscle in dogs has been reported in a Himalayan
cat57. The cat presented with lameness, characterized
by decreased abduction of the limb and marked
298
A B
flexion of the hip, stifle, and hock as the limb was
advanced. The limb could not be fully extended and
the foot was placed abruptly with intermittent
knuckling of the paw. Surgical exploration revealed
a firm pale semitendinosus muscle caused by fibrosis
of unknown origin. A full range of normal movement
was restored using a Z-plasty lengthening procedure.
The lameness recurred within 2 months of surgery but
limb abduction was maintained.
Quadriceps contracture
Quadriceps contracture occurs as either a congenital
abnormality or more commonly is acquired as
a complication of mid-diaphyseal femoral fracture
in immature cats (298)58. The condition
is characterized by rigid stifle hyperextension
and atrophy of the quadriceps muscles. Severe
contracture leads to the condition of genu
recurvatum, in which the stifle is bent backwards. The
etiology includes adhesion of the quadriceps muscle
group to an exuberant femoral callus, delayed fracture
repair, damage to muscles and nerves or vascular
compromise associated with trauma or fracture
repair, and osteomyelitis59,60. There may be an
increased risk of this complication when treating
femoral fractures in young cats following biologic
principles of repair, because of poor fragment
reduction and prolific callus formation associated with
these techniques61. Following contracture,
298 Quadriceps contracture.
A Mediolateral radiograph of the stifle
of a cat with quadriceps contracture
following a distal femoral fracture,
showing avulsion fracture of the tibial
tuberosity.
B Fracture repair using a Kirschner wire
and figure-of-eight tension band wire.
 Neuromuscular disorders
331

degenerative changes occur in articular and peri- intake in cats fed certain diets65,66. A congenital form of
articular tissues, which become irreversible if not the condition has also been described in Burmese
recognized and treated promptly59. Other sequelae kittens aged 2–6 months67,68. In Burmese kittens the
include proximal displacement of the patella, avulsion defect causes a shift of potassium between the
of the tibial tuberosity, disuse osteopenia, stifle intracellular and extracellular compartments. In cats
osteoarthritis, limb shortening, and coxofemoral with renal failure, hypokalemia further compromises
subluxation or luxation. The prognosis for return of renal function, thus establishing a vicious cycle of renal
full function is poor and conservative and surgical dysfunction and potassium depletion. Cats appear to be
treatments may be unrewarding. Surgical treatment particularly susceptible to electrolyte abnormalities,
options include release of adhesions, muscle- although the mechanisms to account for the weakness
lengthening procedures, vastus intermedius excision, are not fully understood.
stifle arthrodesis, and limb amputation. Successful
management has recently been described in a Clinical signs
6-month-old cat that developed contracture following Clinical signs include generalized muscle weakness
plating of a comminuted femoral fracture61. seen as cervical ventroflexion, reluctance to move, and
Treatment involved release of adhesions between the pain on palpation of muscle groups. Reduced exercise
quadriceps and the fracture callus, application of a tolerance and lethargy may be noticed before obvious
dynamic flexion apparatus, and an intensive weakness becomes apparent. Clinical signs of renal
physiotherapy program. Stifle arthrodesis produces a disease may also be present.
relatively good functional outcome in chronic cases.
Diagnosis
Ossifying myositis (myositis ossificans) Diagnosis is based on clinical signs, low serum
Ossifying myositis is a rare disorder characterized by potassium (less than 3.0 mmol/l), elevated CK and
osseous metaplasia or heterotopic ossification of assessment of renal function. Muscle biopsy may show
skeletal muscle. Localized and generalized forms of the evidence of myonecrosis.
disease have been described. The generalized form may
be confused clinically with fibrodysplasia ossificans
progressiva. The localized form of the disease is most
commonly seen about the elbow and may be a sequela 299
to trauma, although this is not an essential
prerequisite62. Clinical signs include lameness,
weakness, stiffness, muscle pain and swelling, and a
palpable firm calcified mass in affected muscles.
Radiographically, lesions tend gradually to develop a
roughly linear shape with clearly defined margins that
may be aligned with a specific muscle (299). Surgical
excision of focal masses may be curative. There is a
single case report of generalized myositis and
ossification in a 4-year-old cat with a history of
relapsing weakness63. Muscles were firm on palpation
and radiography revealed multiple areas of irregular
linear mineralized opacity. Postmortem examination
revealed that most skeletal muscles were affected.

Hypokalemic myopathy
Cause and pathogenesis
A generalized acute onset hypokalemic polymyopathy
has been recognized for some years. The condition
occurs most commonly in some cats with chronic renal
insufficiency where there is excessive loss of potassium 299 Lateral radiograph of the proximal hindlimb limb
in the urine64. Other causes of hypokalemia include of a cat with myositis ossificans showing extensive
thyrotoxicosis, diuretic therapy, chronic gastrointestinal mineralization in the muscle of the caudal thigh.
disease, hepatic disease, and inadequate potassium (Radiograph courtesy of Davies Veterinary Specialists.)
332
Treatment
Muscle weakness improves within 24–48 hours
of the commencement of treatment with oral
potassium gluconate (2–6 mmol/cat/day). Severely
affected cats may require potassium chloride (diluted
in lactated Ringer’s solution) at a dose of
0.5 mmol/kg/hour IV.
Infectious myopathy
Feline bacterial myositis is a common occurrence
secondary to wounds and bites. Cats with
deep abscesses or cellulitis of a limb typically present
with lameness, depression, and pyrexia. Pasteurella
multocida is the most frequently isolated
organism. Clostridial myositis has been described but
it is uncommon69,70. Clinical signs include severe
focal or multifocal muscle pain. Treatment involves
aggressive surgical debridement and appropriate
antibacterial therapy. Infectious myopathies caused by
fungal or viral proliferation are very rare.
Protozoal myopathy
Toxoplasma gondii can produce an inflammatory
polymyopathy often with respiratory, ocular, and
abdominal signs. In a large series of histologically
confirmed cases of toxoplasmosis the most frequent
presentation was persistent pyrexia unresponsive to
routine antibiotic therapy71. Most cats had
antemortem evidence of thoracic or abdominal disease.
Because intraocular inflammation is a common
finding, examination of the eyes should be performed
routinely in all cats with suspected toxoplasmosis.
Cats are the definitive host for this parasite
and pass oocysts in the faeces. Infection may
occur through ingestion of any of the three life stages
of the organism or transplacentally. Toxoplasmosis in
cats is generally subclinical; clinical signs are most
frequently associated with postnatal infection.
Immunosuppression in cats infected with FIV or
FeLV or on glucocorticoid therapy may allow
reactivation of latent toxoplasmosis.
Diagnosis of clinically active Toxoplasma infection
is based on clinical signs, muscle biopsy, and enzyme-
linked immunosorbent assay (ELISA) of serum or
CSF. Immunoglobulin M (IgM) levels increase within
2–4 weeks of infection but are negative by
16 weeks. IgM titers greater than 1:256 and/or
a fourfold increase in IgG titers indicate recent or
active disease.
The drug of choice for treatment is clindamycin
at a dose of 40 mg/kg orally or IM in divided doses
for 4–6 weeks. Transient vomiting is a common
side-effect of clindamycin in cats.
Neospora caninum does not appear to affect
cats naturally, although experimental infection of
kittens has resulted in fatal encephalomyelitis and
myositis72.
Idiopathic polymyopathy
Idiopathic polymyositis is an inflammatory
myopathy of unknown cause. Affected individuals
are usually older than 1 year and there is no
identified breed predisposition 73. There is a
presumed immune-mediated etiology, although the
antigenic cause has not been identified. Clinical
signs include persistent neck ventroflexion, exercise
intolerance, generalized weakness, and pain on
palpation of muscles. There may be regurgitation
and secondary aspiration pneumonia associated
with megaesophagus. The serum CK level is usually
moderately or markedly elevated and there is
EMG evidence of muscle disease. Muscle biopsies
demonstrate myonecrosis with lymphocytic
infiltrates. The prognosis for cats without
megaesophagus is generally good; some cats
recover spontaneously and others respond to
immunosuppressive doses of glucocorticoids
(prednisolone 2–4 mg/kg daily in divided doses).
Paraneoplastic myopathy
A low-grade polymyopathy is seen occasionally in
cats with thymoma and other malignancies. In a
series of 11 cats with thymoma, three cats had
polymyositis74. It has been postulated that
the neoplasm causes T cell proliferation against
an unidentified muscle antigen. Cats with
histopathologically confirmed myositis that fail to
respond to glucocorticoid therapy should be screened
for occult malignancy.
JUNCTIONOPATHIES
Neuromuscular junction diseases generally manifest
as progressive loss of muscle strength with
exercise or complete flaccid paralysis (Table 29).
Junctionopathies are uncommon in the cat.
MYASTHENIA GRAVIS
Cause and pathogenesis
Myasthenia gravis occurs as a result of reduced
numbers of functional acetylcholine receptors on the
postsynaptic membrane of the neuromuscular
junction. All breeds may be affected, but in one large
study Abyssinian and Somali cats were over-
represented75. The disorder is most commonly
immune-mediated, although congenital myasthenia
gravis has been reported76. Myasthenia gravis in cats is
 Neuromuscular disorders
more frequently associated with thymoma than it is in
dogs77. Acquired myasthenia gravis has been reported
2–4 months after initiation of therapy with the
antithyroid drug, methimazole, and should be
suspected in any hyperthyroid cat that develops
muscle weakness following drug therapy78.
Clinical signs
The spectrum of clinical signs is very similar to those
seen in dogs, but there are important differences.
The predominant clinical sign is generalized
exercise-induced muscle weakness. There is reduced
exercise tolerance, reluctance to exercise, and there may
be neck ventroflexion and muscle tremors. Affected cats
often move with a crouching gait and then flop over
onto their sides with the head resting on the paws. In a
large series of cases over half the cats presented with
either generalized weakness or generalized weakness
associated with a cranial mediastinal mass. An acute
fulminating form manifesting as severe appendicular
muscle weakness and respiratory muscle paralysis has
been recognized. Focal forms of myasthenia gravis
associated with megaesophagus or dysphagia are less
common in the cat than in the dog75.
Diagnosis
Diagnosis is based on clinical signs and the response
to intravenously administered edrophonium chloride
(Tensilon test). In positive cases there is a dramatic
improvement in muscle strength, which lasts for a few
minutes. Circulating antibodies to acetylcholine
receptors are usually found in the acquired form of the
disease. Samples must be submitted to a specialist
laboratory for analysis. There is a frequent association
with thymoma, so cats with a cranial mediastinal
mass should be tested for myasthenia gravis prior to
surgical removal of the mass, even in the absence of
muscle weakness. Conversely, all cats with myasthenia
gravis should be radiographed to screen for thymoma
even in the absence of clinical signs of esophageal
dysfunction or respiratory distress.
Treatment and prognosis
Cats with myasthenia gravis can be treated with the
long-acting cholinesterase inhibitor, pyridostigmine
bromide, at a dosage of 0.5–3.0 mg/kg orally
divided two or three times daily. However,
immunosuppressive therapy is often more effective than
treatment with anticholinesterase drugs. In comparison
with dogs, cats are less prone to develop exacerbation
of muscle weakness and are more resistant to the side-
effects of high doses of glucocorticoids79. Prednisolone
is administered at a dose of 2–4 mg/kg divided twice
333
daily for a minimum of 2 weeks, reducing to alternate
day therapy once remission is achieved. Thymectomy
should be considered for cats with thymoma or those
that respond poorly to medical therapy. The prognosis
may be better for myasthenia gravis in cats than
dogs, probably because of the lower incidence
of megaesophagus and aspiration pneumonia in
cats80. The acute fulminating form carries a grave
prognosis.
ORGANOPHOSPHATE AND CARBAMATE
TOXICITY
Cats are particularly susceptible to the toxic effects of
organophosphates and, to a lesser extent, carbamates.
Nevertheless, most poisoning has been associated
with carbamate compounds. Toxicity is generally the
result of accidental exposure, the inadvertent use of
products intended for dogs, or an overzealous
regimen of control for external and internal parasites.
Organophosphates and carbamates exert their effects
by reducing acetylcholinesterase activity throughout
central and peripheral receptors. Diagnosis is based
on the history of exposure to organophophates,
clinical findings, and decreased serum cholinesterase
activity.
Accumulation of excess acetylcholine results in a
variety of clinical signs associated with overstimu-
lation of muscarinic, nicotinic, and central
cholinergic receptors. The neuromuscular signs
include muscle weakness, muscle tremors, neck
ventroflexion, and stiff gait, and are produced by
overstimulation of the nicotinic receptors.
Muscarinic (salivation, diarrhea, miosis) and central
cholinergic signs (seizures, anxiety) are usually seen
within minutes to hours of exposure, but nicotinic
signs may occasionally appear in isolation in cats
treated with the product for several weeks. This
delayed form of neurotoxicity represents a diagnostic
challenge. It can occur after prolonged exposure to
organophosphate compounds; sometimes it is seen
days or weeks after even minimal exposure. The
clinical signs may mimic those of myasthenia gravis
but the signs worsen after edrophonium chloride
administration.
Mildly affected cats recover with symptomatic
therapy. In known cases of acute organophosphate
intoxication, atropine and the cholinesterase
reactivator, pralidoxime (diluted to 20 mg/ml and
given at a dose of 20–50 mg/kg slowly IV over 2
minutes at least), should be administered81.
Pralidoxime may alleviate nicotinic signs but is only
effective if given within 24 hours of exposure and is
usually only required for 24–36 hours. It is
334
contraindicated for carbamate intoxication. Atropine
is effective at a dosage of 0.2 mg/kg for relief of
muscarinic signs. Muscle tremors can be alleviated
using diphenhydramine (2–4 mg/kg orally every
8 hours) and seizures can usually be controlled with
diazepam (0.5–1.5 mg/kg IV).
SNAKE BITE AND TICK PARALYSIS
Clinical signs of weakness and paralysis result from
the effects of neurotoxic components of certain
snake venoms (Elapidae) and tick saliva on the
neuromuscular junction. There is also a significant
elevation of CK following snake envenomation. In the
USA the wood ticks, Dermacentor variabilis and
Dermacentor andersoni, are most often incriminated,
whereas in Australia, Ixodes holocyclus is usually the
cause. There may be a history of a venomous
snakebite or exposure to ticks.
(1) Dr GD Shelton, Comparative Neuromuscular
Laboratory, Basic Science Building, Room 1107,
University of California, San Diego, La Jolla, CA
92093-0612, USA. Tel: (858) 534 1537.
(2) Dr KG Braund, Peripheral Nerve Laboratory,
1476 Lakeview Ridge, Dadeville, AL 36853,
USA. Tel: (256) 825 2624, Fax: (603) 676 2383.
(3) Dr C Hahn, Neuromuscular Disease Laboratory,
Royal (Dick) School of Veterinary Studies, The
University of Edinburgh, Easter Bush, Midlothian,
EH25, UK. Tel: (131) 650 6236, Fax: (131) 650
6588, Email: vetneurolab@ed.ac.uk.

CHAPTER 13
MISCELLANEOUS
ORTHOPEDIC DISORDERS
METABOLIC BONE DISEASES
AND DISORDERS OF CALCIUM
METABOLISM
Calcium is vital for animal life and is present in various
sites in the body, including body fluids and structural
parts of the cell. However, 99% is present as a major
component of the skeleton. Cats in the wild state
obtain calcium and phosphorus by eating the whole
body of their prey. Whole rats and mice contain
approximately 2% calcium as a proportion of
dry matter. Growing kittens have lower absolute
requirements for calcium and phosphorus than
puppies and can also tolerate a calcium:phosphorus
ratio as low as 0.65:1 with no apparent ill effects. The
calcium requirement for kittens is 0.5–2.0 g/400 kcal,
which is more than twice that of the adult cat.
Bone metabolism and mineral homeostasis are
regulated primarily by the calciotropic hormones
(parathyroid hormone [PTH], calcitonin, and vitamin
D or calcitrol) under the influence of dietary calcium
and phosphorus. A number of other hormones and
dietary constituents have a lesser effect on bone growth
and remodeling. Hormones either target bone cells
specifically or have a more generalized influence on cell
function in multiple tissue types. A metabolic bone
disease occurs when there is a disruption in the natural
turnover of bone, with an imbalance between osteoid
production, mineralization, and bone resorption. This
may have significant consequences for skeletal
integrity, by increasing the risk of fracture as a result
of minor trauma and reducing the rate of bone
healing. Bone pain in the absence of fractures is a
frequent feature of metabolic bone disease in humans
and there is no reason to suppose that this does not
occur in cats as well.
Developmental orthopedic disease, such as
osteochondrosis, commonly seen in young, growing,
large-breed dogs, is not recognized as a clinical
problem in cats. In large-breed dogs these conditions
335
may be associated with hypercalcitonism as a result of
excessive consumption of calcium in the diet. It is
likely that the skeleton is protected from these
disorders because of the cat’s smaller stature and
slower growth rate, as with small breeds of dog. When
orthopedic disease does occur during development it
is usually the result of a metabolic disorder, in
which the cat has been fed a wholly inappropriate
diet, or it is related to a genetic disorder, such as
osteochondrodysplasia.
PRIMARY HYPERPARATHYROIDISM
Primary hyperparathyroidism is a rare endocrine disorder
in cats. Probable primary hyperparathyroidism has been
described in a cat with polyostotic lesions1. Lesions
involve particularly the axial skeleton, including the
cranial vault, mandible, and sternebrae. The appendicular
skeleton was involved to a lesser extent. Cervical and
thoracic intervertebral and diarthrodial joints had
collapsed. Bone lesions appear to be uncommon,
however, and have not been described in other cats with
primary hyperparathyroidism2.
RENAL SECONDARY HYPERPARATHYROIDISM
Cause and pathogenesis
Renal secondary hyperparathyroidism (RSH) is a
common complication of chronic renal failure. In a
recent study, 84% of all cats with chronic renal failure
had elevated plasma PTH concentrations on first
presentation3.
Hyperphosphatemia occurs as a consequence of
reduced renal phosphorus excretion in cats with renal
dysfunction. Reciprocal hypocalcemia, coupled with
impaired renal vitamin D metabolism associated
with reduced renal mass, leads to secondary
hyperparathyroidism. Additionally, in chronic cases,
there is a tendency for the parathyroid glands to
function autonomously in spite of restoration of
normal blood calcium (tertiary hyperparathyroidism).
336

Hyperphosphatemia predisposes to metastatic and subtle osteopenia and there is no predilection

calcification of soft tissues, including the kidneys, thus
further compromising renal function and completing
a vicious circle.
Persistent elevation of PTH has widespread
adverse effects on glucose and lipid metabolism,
neurologic function, and the immune system. This has
led to the suggestion that PTH should be regarded as
a uremic toxin4. In addition, PTH has well established
adverse effects on the skeleton. In humans this
includes painful and debilitating bone disease5. In one
study histologic evidence of osteopenia was found in
the majority of cats with advanced renal failure
examined at postmortem6.
Clinical signs
Clinical signs relate primarily to the underlying renal
disease. Rubber jaw, seen classically in the dog
with juvenile nephropathy, has not been reported.
Lesions described in a 5-month-old cat with
glomerulonephritis included marked osteolysis in the
mandible and calvarium with more severe changes in
the appendicular skeleton. Histologically there was a
massive substitution of bone by fibroconnective
tissue7. Clinical signs of bone disease in cats with
renal disease usually represent a more generalized
for the skull. Bone pain on palpation can be elicited
in some cats with chronic renal failure and there may
be more covert pathology, such as an increased risk
of fracture and delayed union. Cutaneous metastatic
calcification is an unusual manifestation of renal
hyperparathyroidism that has recently been reported
in a 10-year-old cat8. The cat presented with
multiple nodular calcifications of the footpads and
interdigital spaces. Recognition of these secondary
phenomena is likely to increase as the life expectancy
of cats continues to rise.
Diagnosis
The majority of cats with chronic renal failure can be
assumed to have RSH and a degree of osteopenia.
A case of suspected RSH has been reported in a cat with
chronic renal insufficiency and radiographic evidence of
spinal and femoral osteopenia9. Osteopenia may not be
readily apparent radiographically, because loss of
30–50% of bone mass must occur before it is detectable
as decreased bone opacity (300)10,11.
Clinically significant skeletal effects are most likely
to be seen in those cases with long-standing and
severe renal disease. All cats with evidence of bone
pain, delayed healing, or pathologic fracture should

300

B
300 Osteopenia in a cat with chronic renal failure.
A Ventrodorsal radiograph of the pelvis showing suspected
pathologic fracture of the femur.
B Lateral radiograph of the pelvis and proximal femur.

A
 Miscellaneous orthopedic disorders
be screened for renal disease by performing urea,
creatinine, and blood phosphate assays. Elevation
of plasma phosphate and PTH are significantly
correlated, whereas measurement of ionized calcium is
unhelpful since significant hypocalcemia is only seen
in cats with end-stage renal failure.
Treatment and prognosis
Treatment is palliative and the prognosis is
determined by the severity of the renal disease.
A commercially prepared phosphate and protein-
restricted diet should be fed to all cats with chronic
renal failure and is an effective means of normalizing
plasma PTH in cats with RSH12.
HYPERTHYROID-RELATED
HYPERPARATHYROIDISM
Hyperthyroidism is now recognized as the
commonest feline endocrine disease. Excessive
circulating concentrations of thyroid hormone have
widespread metabolic actions that include effects on
the skeletal system.
Cause and pathogenesis
In a recent study, 77% of untreated hyperthyroid cats
had a degree of hyperparathyroidism, with decreased
blood ionized calcium and increased plasma phosphate
concentrations13. The hyperparathyroidism appears to
be secondary to the changes in blood calcium and
phosphate. The underlying reasons for the abnormalities
in mineral homeostasis are not fully understood,
although thyroid hormones have powerful direct effects
on bone. In hyperthyroid humans, increased bone
resorption leads to osteopenia and an increased risk of
pathologic fracture. It is possible that bone resorption
induces hyperphosphatemia, with the reciprocal
hypocalcemia driving secondary hyperparathyroidism in
a similar way to chronic renal failure. High plasma
phosphate concentrations may also predispose to soft
tissue metastatic calcification, which will compromise
renal function.
Clinical signs
The clinical signs relate primarily to the underlying
thyroid disease. Osteopenia has been recognized in
cats with hyperthyroid-related hyperparathyroidism
and will have consequences for skeletal integrity.
There may be evidence of bone pain in some cats and
there may be more covert signs, such as an increased
risk of fracture and delayed bone healing. Pathologic
fracture of the femur has been reported in a geriatric
cat with suspected senile osteopenia and a previous
history of hyperthyroidism9.
337
Diagnosis
The majority of cats with hyperthyroidism can
be assumed to have excessive circulating levels of
parathyroid hormone with secondary osteopenia.
This is unlikely to be sufficiently severe to be
detectable radiographically unless the condition has
remained untreated for a prolonged period. All
geriatric cats with evidence of either bone pain,
delayed bone healing, or pathologic fracture, and
compatible clinical signs, should be screened for
hyperthyroidism.
Treatment and prognosis
Treatment for hyperthyroidism has been well described
elsewhere. Phosphate-restricted diets may be of benefit
in the short term for cats with overt signs of bone
disease. The prognosis is predicated by the underlying
disease.
NUTRITIONAL SECONDARY
HYPERPARATHYROIDISM
Nutritional secondary hyperparathyroidism (NSH) is
also referred to as juvenile osteoporosis, nutritional
osteoporosis, or all-meat syndrome. Historically this
disease was reported occasionally in kittens before the
widespread feeding of manufactured pet foods. It is
possible that there may be a resurgence of the condition
with the modern trend towards feeding organic, natural,
or vegetarian foods to pets. Adult cats have lower
absolute demands for calcium and greater reserves of
calcium than kittens, so they are rarely affected.
Cause and pathogenesis
Traditionally the disease is caused by feeding a diet
composed primarily of meat and offal with no bones;
this diet is relatively high in phosphorus and low in
calcium. In the only contemporary case series there
were six cats14. Three of the cats were fed an all-meat
diet, one cat was fed a vegetarian diet, and two cats
were fed a meat and rice diet. The common feature of
all the diets was a severe deficiency of calcium and a
moderate deficiency of phosphorus, resulting in an
unfavorable calcium to phosphorus ratio (0.061:1 to
0.12:1). All the cats were less than 7 months old and
were not allowed outdoors, which prevented them
from supplementing their diet by hunting.
Transient hypocalcemia, owing to low calcium
intake, stimulates the release of PTH from the
parathyroid glands and ionized calcium levels are
restored. If calcium deficiency is sufficiently severe,
ionized blood calcium may remain low. Formation of
bone occurs normally but is outstripped by accelerated
bone resorption under the influence of PTH.
338

Increased PTH also promotes renal reabsorption of
calcium and excretion of phosphorus and renal
synthesis of active vitamin D (calcitrol). Calcitrol, in
concert with PTH, stimulates further bone resorption.
Clinical signs
Affected cats show lameness and pain, which may be
severe. Bony deformity occurs due to pathologic
fractures and joint deformity is seen due to ligament
and tendon laxity. The hindlimbs tend to be more
severely affected than the forelimbs and paresis or
paraplegia may result from spinal cord compression
following vertebral fracture. Four of the six cats in the
aforementioned series also showed neurologic signs,
including seizures, tetanic spasms, and muscle tremors
and fasciculations consistent with hypocalcemia14.
Diagnosis
Radiographs of the skeleton show a generalized loss
of radiopacity and thinning of the cortices of the
long bones with sparing of the physes (301). The
metaphyses appear broader than normal and there may
be regions of relative radiopacity in the metaphyses
adjacent to the growth plates where there is preferential
mineralization. In severely affected cases there will be
folding fractures of the long bones and compression
fractures of the vertebrae. Bony protuberances, such as
the olecranon and the calcaneus, become curved as a
result of weight-bearing forces. Blood testing is not
normally necessary for diagnosis but, if performed, may
show normal to reduced ionized calcium, increased
PTH, normal to increased phosphorus and normal to
increased calcitrol14,15. These biochemical changes are
more marked in severely affected cases but once the cat
is fed a balanced diet they are all reversed rapidly.
Treatment and prognosis
Treatment is by provision of a commercially prepared,
balanced diet formulated for young cats. Cage rest
is vital in the early stages to prevent further injury.
Calcium gluconate should be given intravenously only
to cats with clinical signs of hypocalcemia. There is a
high risk of vertebral fracture in cats presenting with
tetanic muscle contractions. Symptomatic therapy with
nonsteroidal anti-inflammatory drugs (NSAIDs) may be
necessary for a few days to control pain.
Conventional fracture treatment is not possible
because of the fragility of the bones and poor bone
quality for the placement of implants. Early surgical
intervention is inadvisable and coaptation with bandages,

301

A B C
301 Nutritional secondary hyperparathyroidism.
A Ventrodorsal radiograph of the pelvis of a lion cub fed an all-meat diet. Note the thin bone cortices, the pathologic
‘folding’ fractures of the femur, and the pelvic deformity. (Radiograph courtesy of Dr Dan Cantwell.)
B Lateral radiograph of the pelvis and hindlimbs of the lion cub in A. (Radiograph courtesy of Dr Dan Cantwell.)
C Lateral radiograph of the pelvis of a domestic cat fed an all-meat diet. (Radiograph courtesy of Davies Veterinary
Specialists.)
 Miscellaneous orthopedic disorders
339

splints, or casts is contraindicated. Surgical correction of
skeletal deformities should be postponed until the
skeleton has become adequately mineralized. Medical
treatment with glucocorticoids or calcitrol is also
contraindicated. The response to treatment is rapid and
follow-up radiographs obtained after 3 weeks on
a balanced diet should show adequate mineralization
of the skeleton. Osteogenesis imperfecta should be
suspected if skeletal mineralization has not occurred
within 3 weeks. The prognosis is generally good,
although there is likely to be residual deformity and
growth retardation. The prognosis for cats with vertebral
fracture and severe neurologic dysfunction is poor.
HYPERVITAMINOSIS A
Cause and pathogenesis
Hypervitaminosis A is a metabolic disorder caused by
a chronic excessive intake of vitamin A (retinol).
Vitamin A stimulates osteoblastic activity and plays a
role in skeletal growth. The condition has become
rare since the widespread feeding of commercially
prepared pet foods.
Disease usually results from the consumption of
a diet consisting principally of raw liver. Vitamin A
is thermolabile and is largely destroyed by cooking.
Excess vitamin A cannot be excreted and accumulates
in body fat. Kittens are rarely affected; most cases
are the result of accumulation and occur between 2 and
9 years of age. Affected cats have usually been
consuming liver regularly for at least 12 months at the
time of presentation. Chronic toxicity causes decreased
osteoblastic and increased osteoclastic activity.
Microfractures occur at the site of attachment of
ligaments, tendons, and the joint capsule of diarthrodial
joints, leading to dystrophic calcification of the axial
and appendicular skeleton. The chronic form of the
disease was originally described as ‘feline deforming
cervical spondylosis’ because extensive confluent
exostoses of the cervicothoracic vertebrae are the most
frequent pathologic finding16. The osseous lesions are
always accompanied by lipid infiltration of the liver,
which may predispose to secondary disease17.
Clinical signs
Affected kittens show reduced longitudinal growth of
the appendicular skeleton, with flaring of the metaphyses
and osteopenia. The clinical signs in the more common
chronic cases relate mainly to ankylosis of the
cervicothoracic vertebrae. In one of the few recent
reports of the disease, however, there was ankylosis of the
stifles and hips with no spinal involvement18. Signs
include anorexia, weight loss, depression, hyperesthesia,
constipation, joint pain and lameness, and an unkempt
hair coat as a result of decreased grooming. In advanced
cases the neck becomes rigid due to ankylosis of the
cervical vertebrae and there is forelimb lameness and pain
owing to nerve root compression19,20. Affected kittens
are stunted and have limb deformity.
Diagnosis
Radiography shows exostoses affecting the cervical
vertebrae, the sternebrae, and the periarticular regions
of the long bones, particularly the distal humerus and
proximal ulna (302). The ribs may also be affected in
advanced cases. Plasma concentrations of vitamin
A are increased to >16.67 µmol/l (500 µg/dl) in 80%
of clinical cases21, but measurement of this is not
essential for diagnosis.

302

A B
302 Hypervitaminosis A.
A Lateral view of the cervical spine of a cat fed an all-liver diet. There are extensive confluent exostoses of the
cervicothoracic spine. (Radiograph courtesy of Davies Veterinary Specialists.)
B Lateral view of the elbow joint of a cat fed an all-liver diet. (Radiograph courtesy of Malcolm McKee.)
340
Treatment and prognosis
Treatment is by removal of the source of vitamin A
from the diet and substitution in the short term with a
home-made low vitamin A diet. This should contain
lean meat and a source of carbohydrate but exclude
organ meat (heart, liver, and kidneys), eggs, and milk.
It may be difficult to persuade some cats to eat
anything else apart from liver. In the long term
a commercially prepared balanced diet can be fed.
The pathology is irreversible, although clinical
improvement is usually seen within 4 weeks. Limited
remodeling of the osseous changes occurs with time
following dietary correction. Glucocorticoids are
contraindicated and will slow the reduction in plasma
vitamin A concentration. Symptomatic therapy with
NSAIDs may be used to control pain.
RICKETS
Nutritional rickets or hypovitaminosis D is an
extremely rare metabolic bone disease of the young
growing kitten. The term is sometimes erroneously
used as a synonym for NSH. The disease is now so
rare that there are no recent clinical descriptions in
naturally affected cats.
Cause and pathogenesis
Rickets is a disorder of growing bones that occurs when
normal mineralization is prevented by lack of calcitrol
(1, 25-dihydroxycholecalciferol) activity. Cats, in com-
mon with dogs, do not synthesize vitamin D in their
skin when irradiated with ultraviolet B light. Vitamin D
(cholecalciferol) is obtained from the diet and is then
metabolized in the liver before being converted to the
active form (calcitrol) in the proximal kidney tubules.
Lack of vitamin D may be associated with low dietary
intake or secondary to gastrointestinal malabsorptive
syndromes. Hereditary nonnutritional types of vitamin
D-dependent rickets also occur, in which there is either
a deficiency in renal hydroxylation to calcitrol, which is
the active form (type 1 rickets), or there is target organ
resistance to calcitrol (type 2 rickets)22–24.
Hypovitaminosis D impairs gastrointestinal
absorption of calcium leading to secondary
hyperparathyroidism. In growing kittens, there is
defective mineralization of the newly formed organic
matrix of the skeleton. Osteomalacia is the adult
equivalent of hypovitaminosis D and primarily affects
bone remodeling, so that unmineralized matrix
accumulates in all parts of the skeleton.
Clinical signs
The clinical signs are similar to those of NSH, with the
additional findings of bony swellings proximal to the
carpi and tarsi, lateral bowing of the antebrachia, and
muscle weakness.
Diagnosis
Radiographs show generalized loss of radiopacity and
skeletal deformity. In kittens, additional changes
include grossly thickened radiolucent physes
and characteristic mushrooming or cupping of the
enlarged metaphyses. The diagnosis of nutritional
rickets can be confirmed by the demonstration of
reduced circulating levels of the storage form
of vitamin D (25-hydroxycholecalciferol) in the
blood.
Treatment and prognosis
Treatment of nutritional rickets is by substitution of a
commercially prepared feline diet and cage rest in the
early stages. Oversupplementation with vitamin D is
contraindicated. The prognosis is good, although there
may be residual skeletal deformity. Improvement is rapid
and follow-up radiographs taken after 3 weeks should
show nearly normal skeletal mineralization. Failure to
improve should prompt consideration of underlying
renal pathology, an inborn error of vitamin D absorption
or metabolism, or target organ resistance.
Type 1 rickets responds to administration of
physiologic doses of the active form of vitamin D. Type
2 rickets shows a variable response to administration of
supraphysiologic doses of active vitamin D.
OSTEOPETROSIS
Osteopetrosis is a term used to describe a rare group of
genetic diseases in humans characterized by abnormal
hardening of bone due to defective osteoclastic
resorption of immature bone. A similar syndrome has
been reported in adult cats in which there is a generalized
increase in bone density, without alteration in bone
shape. In the cat the disorder is poorly understood but
appears to be acquired and is probably more correctly
known as generalized or diffuse osteosclerosis25.
Radiographically there is a diffuse increase in
medullary opacity with a marbled, densely homogenous
appearance to the long bones and vertebrae. There is
marked endosteal thickening of the diaphyses of long
bones and dense subchondral bone with loss of the
normal trabecular architecture. Usually the osseous
abnormalities are detected incidentally in cats
radiographed for other reasons.
Similar bone lesions have been described in neonate
cats, where they were induced experimentally by
inoculation of FeLV. The lesions probably developed
because of infection of hemopoietic precursor cells,
from which osteoclasts arise26.
 Miscellaneous orthopedic disorders
Osteosclerosis may cause nonregenerative
anemia if the medullary canal is totally
compromised 25,27 and in one cat there was
inspiratory stertor and epiphora owing to
obliteration of the nasal turbinates and nasolacrimal
duct28. In adult cats the etiology and significance of
the osseous lesions has not been established but
most cases have been associated with concurrent
disease, including lymphoblastic leukemia, systemic
lupus erythematosus, lymphoma, C-cell tumor,
myeloproliferative disorders, chronic renal failure,
and fibrosarcoma25,28.
OSTEOGENESIS IMPERFECTA
Osteogenesis imperfecta, also known as brittle bone
disease, is a very rare inherited bone disease. It is
characterized by bone fragility, in which abnormal
bone matrix and secondary osteopenia are associated
with an increased susceptibility to fracture. The main
significance of the condition is as a differential
diagnosis for NSH.
Radiographically there is generalized osteopenia
with thin diaphyseal cortices and multiple fractures in
various stages of union. Fractured bone forms callus
normally and heals, resulting in malunion. A typical
presentation would be a kitten fed on a balanced
diet with multiple fractures, apparently occurring
spontaneously or as a result of minimal trauma. More
common causes of osteopenia, such as NSH and RSH,
should be ruled out first. Definitive diagnosis can be
achieved by laboratory culture of fibroblasts obtained
from a skin biopsy.
HYPERTROPHIC OSTEOPATHY
Hypertrophic osteopathy is also known as
hypertrophic pulmonary osteoarthropathy or Marie’s
disease. It is an extremely rare bone disease
characterized by periosteal new bone formation as a
secondary manifestation of a primary disease process.
The pathogenesis is not fully understood, but
vascular congestion of the distal extremities
secondary to the underlying disease process is
thought to play a major role in the new bone
formation in dogs and humans. The five reported
cases in cats have all been associated with
neoplasia29–33. Two of these were secondary to
bronchiolar carcinoma and there are single reports in
association with benign thymoma, renal papillary
adenoma, and adrenocortical carcinoma. Neurogenic
and humorally mediated mechanisms have been
proposed as causes of the circulatory disturbance.
Clinically there is bilaterally symmetrical soft tissue
swelling affecting the distal portions of the limbs; this
341
may progress proximally to affect all of the bones of
the limb. Clinical signs related to the painful and
swollen distal extremities often precede those arising
from the primary lesion. Affected cats are usually
depressed and reluctant to move around. Radiographs
of the distal limbs show an irregularly marginated
periosteal reaction. Radiographic and/or
ultrasonographic examination of the thorax and
abdomen may be required to reveal the primary
lesion. The prognosis is determined by the primary
lesion and is generally poor. Partial regression and
remodeling of the bony changes occurs following
successful removal of the primary lesion29.
SPONTANEOUS FEMORAL CAPITAL PHYSEAL
FRACTURES
Separation of the femoral capital physis from the femoral
neck in skeletally immature cats is commonly seen as a
result of trauma (see Chapter 9). Less commonly,
separation of the capital physis occurs in heavier
neutered male cats over 12 months of age in the absence
of trauma34. Lameness may have a variable duration of
onset associated with progressive femoral neck osteolysis
and pathologic fracture.
Cause and pathogenesis
Metaphyseal bone necrosis has been produced
experimentally in cats by the intravenous inoculation of
feline herpesvirus35. However, no inclusion bodies
typical of herpes virus have been found in cells of
material removed at the time of surgery.
The high incidence in neutered male cats between
12 and 24 months of age suggests an association
with delayed physeal closure seen after neutering
(see Chapter 1). It seems likely that slipped femoral
capital epiphysis, spontaneous femoral capital physeal
fracture, femoral capital physeal dysplasia syndrome36,37,
and proximal femoral metaphyseal osteopathy38 merely
represent different manifestations and etiopathologic
interpretations of the same condition.
Clinical signs
Typically, affected cats have prodromal hindlimb
lameness, which suddenly worsens when pathologic
fracture occurs. Pain can be elicited on manipulation of
the hip joint although this may be mild until fracture
occurs. Over half the cases eventually show bilateral
disease in which the main clinical sign is stiffness and
reluctance to jump rather than an obvious limp.
Diagnosis
Radiographs of the pelvis show loss of bone within the
femoral neck and, in some cases, an obvious fracture,
342
although there is usually minimal displacement at the
fracture site (303).
Treatment and prognosis
Internal fixation of the capital femoral physis is usually
precluded by the degree of femoral neck resorption.
Total hip replacement is the preferred treatment option
although femoral head and neck ostectomy will
produce satisfactory results. Femoral head and neck
ostectomy may be performed on both hips
simultaneously in bilaterally affected cases.
OSTEOCHONDRODYSPLASIA
Osteochondrodysplasias or metaphyseal chon-
drodysplasias are a group of abnormalities that result
from defects in endochondral bone formation with
variable skeletal and systemic involvement. A number
of dog breeds, such as the Dachshund, have
osteochondrodysplastic features and selecting for this
disorder has created a new breed of cat, the
Munchkin. Potential problems in the Munchkin are
likely to be similar to those in the equivalent dog
breeds, such as intervertebral disc disease and angular
limb deformity. Osteochondrodysplasia has been
303
303 Spontaneous femoral capital physeal fracture.
Ventrodorsal radiograph of the pelvis showing bilateral
femoral neck necrosis and pathologic fracture.
reported as an inherited disease in the Scottish Fold
cat (see Chapter 7)39. There is also a report of
two unrelated kittens with signs similar to nonnutri-
tional vitamin D-dependent rickets that were
diagnosed as having metaphyseal chondrodysplasia40.
Affected Scottish Fold kittens develop progressive
severe hindlimb lameness and a broad-based,
inflexible tail. Radiographic changes of metaphyseal
chondrodysplasia include widening of the physes
(304) and exostoses around the tarsal and metatarsal
joints. The exostoses become palpable clinically and
eventually lead to ankylosis of the joints.
NEOPLASTIC DISORDERS OF BONE
The skeletal system is not a common site for either
primary or secondary neoplasia, with an incidence of
3.1–4.9/100,000 cats41,42. The majority of bone
tumors are malignant. Osteosarcoma (OSA) is the
commonest tumor type, followed by fibrosarcoma and
chondrosarcoma. Other primary tumors such as
liposarcoma, anaplastic or undifferentiated sarcoma,
giant cell tumor, multiple myeloma, plasma cell tumor,
and lymphoma are rarely observed and thus their true
incidence is unknown.
304
A B
304 Osteochondrodysplasia in a kitten (metaphyseal
chondrodysplasia). (Radiographs courtesy of Malcolm
McKee.)
A Craniocaudal radiograph of the distal radius and ulna
showing the abnormal appearance of the physes.
B Mediolateral radiograph of the stifle joint.
 Miscellaneous orthopedic disorders
PRIMARY MALIGNANT TUMORS OF BONE
Osteosarcoma
Primary malignant bone tumors occur much less
commonly in the cat than the dog, representing less
than 1% of all malignancies. OSA accounts for 70–80%
of all feline primary bone tumors43,44. Extraskeletal
OSA has been reported in the cat; it arises from soft
tissue and, accordingly, is not classed as a primary
tumor of bone.
Cause and pathogenesis
The etiology of OSA is not fully understood. Genetic
predispositions exist in dogs with OSA and are the
subject of current investigation, but the situation in cats
is unknown. The risk of tumor development may be
increased at the site of prior local radiation treatment
and at the site of previous fracture or orthopedic
intervention45,46. In the two reported cases
that occurred following previous fracture, the tumor
developed 6 months and 15 months after the
intramedullary pinning of a femoral fracture. The
majority of OSAs are of medullary or endosteal origin.
Parosteal or juxtacortical OSA is a variant, which
develops from the periosteum and thus is found on the
outer cortex of the bone. Parosteal OSA has been
reported in axial and appendicular sites47 and is seen
more commonly in the cat than in the dog. OSA in the
cat is less aggressive than its canine counterpart,
growing more slowly and metastasizing later. There are
no pain fibers in the endosteum, so medullary OSA may
be subclinical until there is cortical destruction and
invasion into the periosteum and surrounding soft
tissues.
Clinical signs
OSA occurs in older cats, between 9 and 12 years of
age. This is in contrast to the dog, where the age
distribution is bimodal, with rare exceptions48. The
hindlimbs are affected more than the forelimbs in
the cat. The predilection sites for appendicular OSA
are distal femur, proximal tibia, and proximal
humerus, although the tumors are not necessarily
metaphyseal in location. Axial OSA originates most
commonly in the skull and pelvis, but has also been
reported in the ribs and vertebrae49,50. Clinical signs
include progressive lameness, pain, and local
swelling. Neoplasia of the vertebrae usually causes
neurologic dysfunction due to spinal cord
compression (see Chapter 11). Lameness may
sometimes be acute, following a minor traumatic
incident, or peracute, if there is pathologic fracture
with no antecedent signs.
343
Diagnosis
The radiographic features of OSA are variable.
The classical picture is that of an aggressive,
poorly delineated, monostotic lesion with a
mixed pattern of destructive and productive bony
change, cortical destruction, and extension into the
soft tissues (305). Lesions of the long bones
are, however, often predominantly lytic in nature and
a solitary osteolytic lesion of a long bone in an older
cat would carry a high index of suspicion for OSA.
The main radiographic differential diagnoses for
OSA are osteomyelitis (bacterial or fungal) and, in
the case of very lytic lesions, bone cysts. Fungal
osteomyelitis is seen mainly in specific geographic areas
but there are sporadic reports in many parts of the
world. It has been suggested that if the radiographic
findings are equivocal, then radiographs should be
repeated at a later date. In this situation it is preferable
either to submit the radiographs to an experienced
radiologist for interpretation or to proceed with
immediate biopsy, since any delay will increase the risk of
metastasis if the lesion is malignant.
Diagnosis should be confirmed by bone biopsy,
either using a full surgical approach or a Jamshidi
needle. The authors prefer the use of the Jamshidi
needle core biopsy instrument. When a minimum of
at least two samples are taken (one central and one in
the transition zone), the accuracy of diagnosing a
known OSA by an experienced pathologist is
probably in the order of 90%. The use of the Jamshidi
305
A B
305 Otseosarcoma. (Radiographs courtesy of Malcolm
McKee.)
A Lateral radiograph of the scapulohumeral joint showing
pathologic fracture of the proximal humerus.
B Ventrodorsal radiograph showing local recurrence and
pulmonary metastasis following amputation.
344

needle is described in Chapter 2. Diagnostic accuracy
can be improved by verifying correct tissue sampling
on a postoperative radiograph of the biopsy site.
A pathology report of reactive bone does not
constitute a diagnosis and further confirmatory
studies are needed. There is no evidence that
performing a biopsy increases the metastatic rate.
Treatment and prognosis
Metastasis of feline OSA is less frequent than its canine
counterpart, but thoracic radiographs should always be
obtained prior to surgery. Both lateral views should be
taken to maximize the detection of metastases,
preferably with the lungs inflated under general
anesthesia; more than one person should review the
radiographs. The treatment of choice for OSA of the
appendicular skeleton is amputation, which has
relatively good results compared with the dog. In one
study of a relatively small number of cases the median
survival time for cats with appendicular OSA treated by
amputation was 64 months and the median survival
time for cats with axial OSA was 5.5 months49. The
mean survival time in a more recent and larger series of
cases was 11.8 months for appendicular OSA treated
by excisional biopsy or amputation and 6.07 months
for cats with axial OSA51. The reason for the difference
in the survival times for appendicular OSA between
these two studies is not clear.
Adjunctive chemotherapy is not normally given
for appendicular OSA because of the success of
surgery alone. OSA of the axial skeleton carries a
less favorable prognosis because the site of the
tumor usually precludes complete surgical removal.
Aggressive excision and adjunctive chemotherapy,
using carboplatin and/or doxorubicin, are likely to
provide the best prognosis for these tumors.
Cisplatin must not be used for adjunctive
chemotherapy in cats because of its toxicity.
been reported43,54, but complete resection, usually
by amputation for tumors of the long bones, is
generally associated with a good prognosis55.
Giant cell tumor
Giant cell tumors of bone are considered rare in all
domestic animals, although they seem to be more
commonly diagnosed in the cat than in the dog.
Giant cells may be found in both neoplastic and
nonneoplastic bone lesions, therefore diagnosis of
neoplasia is based on a combination of the clinical,
radiographic, and histologic features.
The radiographic characteristic of giant cell
tumors is typically an expansile, multiloculated
appearance, causing significant osteolysis of the long
bone diaphysis. They can be confused with bone
cysts or any expanding nonosteogenic tumor.
Treatment by resection of the diseased bone or by
amputation has been successful56,57.
Other sarcomas
Other mesenchymal tumors, such as fibrosarcoma,
hemangiosarcoma, rhabdomyosarcoma, liposarcoma,
and anaplastic sarcoma, occur sporadically.
Fibrosarcomas may arise from soft tissue or bone
and account for up to 12% of all feline neoplasms.
The primary cause in young cats is feline sarcoma
virus (FeSV) and these neoplasms are usually
multicentric, poorly differentiated, and highly
306

Chondrosarcoma
Chondrosarcoma may be indistinguishable clinically
and radiographically from other primary bone
tumors (306). The tumor occurs in both long
bones and flat bones but reported numbers in the
cat are too small to make valid conclusions about
site predisposition52. Presenting signs are similar to
those of OSA; they include pain and lameness
associated with the presence of a mass, which may
have been present for many months. There is one
report of forelimb paralysis secondary to a
chondrosarcoma that was compressing the brachial
plexus53. The growth rate of chondrosarcoma is 306 Chondrosarcoma. Mediolateral radiograph of the
generally slow initially. Pulmonary metastasis has stifle showing chondrosarcoma of the proximal tibia.
 Miscellaneous orthopedic disorders
malignant. Solitary fibrosarcomas are typically less
invasive, occur in geriatric cats, and have no
relationship to FeSV. Fibrosarcomas of bone arise
from medullary or periosteal connective tissue. The
radiographic appearance is predominantly osteolytic
with minimal reactive response; transarticular
involvement has been reported58. Fibrosarcoma
should be considered in the differential diagnosis
of any osteolytic lesion in cats of all ages. Well
differentiated tumors usually do not metastasize and
complete resection of diseased bone, usually by
amputation, may be curative. There are reports of
resection of fibrosarcoma involving the pelvis and
scapula by total hemipelvectomy59 and partial
scapulectomy60,61, respectively.
The metastatic potential and, therefore, the
prognosis with other sarcomas is variable.
Hemangiosarcoma and anaplastic sarcoma may be
more aggressive than osteosarcoma. Limb
amputation is usually the treatment of choice for all
mesenchymal tumors of the long bones, although this
may not be curative. Recurrence at the surgical site
and pulmonary metastasis occurred within 4.5
months in a recent report of a rhabdomyosarcoma
treated by amputation62. It should be noted that not
all bone sarcomas are primary bone tumors.
A thorough search should always be made for other
tumor deposits, since a proportion will be metastases
from mesenchymal tumors of soft tissue origin or
from another skeletal site.
Round cell tumors
Round cell tumors that commonly affect bone are
plasmacytoma, multiple myeloma, and lymphoma.
Multiple myeloma is a plasma cell neoplasm that has
its origin in bone marrow. Plasmacytoma is a plasma
cell tumor arising from tissue other than bone
marrow. Round cell tumors of the skeleton are
uncommon in comparison with the sarcomas. Clinical
signs relating specifically to skeletal involvement are
not common but are seen most often with multiple
myeloma.
Multiple myeloma
Multiple myeloma usually affects middle-aged cats
and there is a male predisposition63. Clinical signs
related to bone involvement include lameness, bone
pain, neurologic dysfunction, and pathologic fracture
due to the osteolytic effect of the neoplastic cells.
Other clinical signs associated with the tumor include
lethargy, inappetence, polyuria, polydipsia, and
neurologic deficits. Laboratory findings include
anemia, thrombocytopenia, and elevated globulin
345
with a monoclonal gammopathy seen on serum
protein electrophoresis. Bence Jones protein may
be present in the urine. Osteolytic lesions, which
can affect any part of the skeleton, are seen on
radiographs; the distal extremities are the commonest
sites, in contrast to the dog. Histopathologic
confirmation can be made from a bone biopsy.
Treatment is by chemotherapy, although euthanasia is
indicated where lesions are widespread or extensive.
Plasmacytoma
Solitary plasmacytomas occasionally affect either the
axial or appendicular skeleton. Where a long bone is
affected, wide surgical excision, usually by amputation,
may be curative. Where this is not possible, radiation
therapy may be considered as an alternative since these
tumors are radiosensitive.
Lymphoma
Lymphoma occasionally presents with skeletal
involvement typically, in the vertebrae of young cats.
A thorough search should be made for tumors in other
sites, since lymphoma is seldom solitary. Local excision
or radiotherapy may be appropriate, but combination
chemotherapy is advisable, even in the absence of overt
disease elsewhere.
SECONDARY MALIGNANT TUMORS OF BONE
Locally invasive tumors
A number of soft tissue tumors have a propensity to
invade bone locally, causing varying degrees of osteolysis
and periosteal reaction. The most common of these
is squamous cell carcinoma. Sarcomas, especially
fibrosarcomas, anaplastic sarcomas, rhabdomyosarcoma,
and synovial cell sarcomas arising in soft tissue adjacent
to bone, often also behave in this way.
Squamous cell carcinoma of the gingiva is
frequently associated with a marked bony reaction of
the mandible or maxilla that may be mistaken
for osteosarcoma radiographically. Primary digital
squamous cell carcinoma arises from the epithelium of
the nail bed and invades the phalanx by direct
extension. Treatment by digital amputation carries
a good prognosis. The majority of feline digital
carcinomas, however, are metastatic with a primary
pulmonary origin.
Metastatic tumors
Some tumors have a predilection for metastasis to
bone, most notably primary pulmonary malignancies.
Hematogenous metastasis of primary pulmonary
malignancies to the distal limbs and digits has been
the subject of a number of case reports64–66. In the
346

only large series of cases, 36 cats were identified with
digital metastases originating from a bronchogenic
carcinoma (307)67. The mean age was 12.7 years
with no breed or sex predilection. The 19 cats for
which full records were available all presented with
the primary complaint of lameness. None of the cats
had respiratory signs, despite the presence of
radiographically detectable pulmonary carcinoma.
The prognosis was poor with a mean survival time of
58 days from initial presentation. Amputation or
biopsy of an affected digit may be required for
diagnosis but does little to alter the clinical course
because of the development of multiple lesions and
progression of the primary pulmonary tumor.
Digital metastasis of pulmonary carcinoma has not
been reported in the dog and is uncommon in
humans. It has been suggested that the vascularity of
the feline footpads required to facilitate heat loss may
predispose to this pattern of metastasis in the cat. It is
important to differentiate metastatic digital pulmonary
carcinoma from primary digital squamous cell
carcinoma. In comparison with metastatic carcinoma,
primary digital neoplasia is rare, is unlikely to be
multiple, and does not usually show pulmonary

307

A B

C
307 Pulmonary bronchogenic carcinoma in a cat and metastasis to
the digits.
A Photograph showing swelling and ulceration of digits.
B Dorsoplantar radiograph showing an osteolytic lesion in the
third phalanx of an affected digit.
C Lateral radiograph of the thorax showing a pulmonary
bronchogenic carcinoma in the caudal lung field.
 Miscellaneous orthopedic disorders
metastasis at the time of initial presentation. All
geriatric cats presented with multiple digital swellings
should have thoracic radiography to rule out a primary
pulmonary neoplasm.
The majority of feline mammary tumors exhibit
malignant behavior, with frequent early metastasis to
the regional lymph nodes and lungs. However,
skeletal metastases were found in only 4% of cases in
one large study of cats with metastatic mammary
adenocarcinoma. In contrast to the dog, the distal
portions of the limbs were more likely to be affected,
particularly the talus68.
BENIGN TUMORS OF BONE
Benign bone tumors are occasionally reported in the
cat, the commonest of which is the osteoma.
Ossifying fibroma, chondroma, and osteochondroma
have been reported less frequently. Osteoma and
ossifying fibroma are similar histologically and have
not been adequately differentiated in the veterinary
literature.
Osteoma
Osteoma occurs as a solitary bony outgrowth with a
sessile base that typically arises on the surface of an
intramembranous bone. The tumor grows slowly
and the underlying cortex remains intact or
remodels with the base of the lesion. Treatment by
surgical excision from the surface of the bone carries
a good prognosis.
Ossifying fibroma
Ossifying fibroma is a tumor-like growth of fibro-
osseous tissue that replaces alveolar or cortical bone in
308
308 Lateral radiograph of the skull showing an ossifying
fibroma arising from the mandible. (Radiograph courtesy
of Malcolm McKee.)
347
the mandible or maxilla (308). Resection of the
affected portion of the jaw is necessary to prevent
local recurrence.
Osteochondroma
An osteochondroma is a solitary cartilage-capped
exostosis that arises from the surface of any bone
formed by endochondral ossification. The lesion is
thought to originate as a result of an abnormality in
the underlying periosteum. Osteochondromas are
rare in cats. The presenting complaint is usually
lameness and the typical radiographic appearance
is of a single bony outgrowth affecting the
appendicular skeleton and consisting of well
demarcated and well organized new bone. Solitary
osteochondromas have no clinical significance
unless there is pressure on adjacent structures.
Affected cats are typically middle-aged and the
Burmese is overrepresented69. The commonest site
is the distal humerus. Surgical excision carries a
good prognosis, although there is a tendency for
local recurrence. Differentiation from the multiple
form of the disease by radiographic evaluation of
the skeleton and FeLV testing is advisable prior to
surgical excision.
Osteochondromatosis
Osteochondromatosis is also know as multiple
cartilaginous exostoses (MCE). It is a polyostotic
disease with the same histologic features as solitary
osteochondroma. The literature on MCE is
confusing because of the numerous synonyms for the
disorder. In humans, dogs, and horses it is an
inherited disease that develops in the immature
skeleton and is considered to be a type of skeletal
dysplasia rather than a true neoplasm. A similar
disease occurs in cats but, in contrast to other
species, the masses first appear after skeletal maturity,
they undergo progressive enlargement, and they
often increase in number until functional impairment
necessitates euthanasia. The mean age of 10 cases
reported in the literature was 2.5 years and all cats
that were checked for the presence of FeLV tested
positive69.
Clinical signs occur due to impingement of the
exostoses on normal anatomic structures. The skull,
scapula, pelvis, ribs, and vertebrae are preferentially
affected. Lesions in the limbs may produce obvious
swelling and pain, and lameness may be present.
Vertebral lesions cause paresis or paralysis if they
impinge on the spinal cord.
Lesions appear radiographically as multiple eccentric
protuberances of cancellous bone that merge into the
348

substance of the parent bone. In long-standing cases
the lesions may take on a more aggressive appearance
and malignant transformation to chondrosarcoma or
OSA may occur (309). Survey radiographs of the
skeleton will reveal the true extent of the disease.
Biopsy of lesions is required for definitive diagnosis
prior to treatment. Cats with MCE should be
considered to be FeLV-positive until proven otherwise.
Treatment by surgical resection may provide temporary
relief, but is palliative at best, because of the tendency
for local recurrence and new lesion development at
other sites.
NEOPLASIA-LIKE DISORDERS OF BONE
Benign bone cyst
Bone cysts are very rare, benign, fluid-filled structures
of unknown etiology. They are most commonly
monostotic but may occasionally be polyostotic. The
cysts are lined with a thin layer of fibrous connective
tissue and filled with serous fluid. Bone cysts are
usually located in the metaphyseal region at the distal
end of long bones, sparing the growth plates and
epiphyses. They are frequently asymptomatic unless
they are large or cause pathologic fracture. Large cysts
may cause local swelling and pain and the adjacent
joint may have a reduced range of motion.
Radiography shows a multilocular radiolucent lesion
with expansion and thinning of the overlying cortical
bone and little periosteal new bone proliferation. In
kittens the cyst may become more diaphyseal as the
bone lengthens. Treatment is not necessary if the cysts
are subclinical, and spontaneous resolution occurs in
some cases. Surgical curettage and autogenous bone
grafting is curative.
Aneurysmal bone cyst
An aneurysmal bone cyst is a benign, vascular lesion
of unknown etiology that results in considerable
local bone destruction. In one study, three cats each
had a solitary lesion arising from the axial skeleton
(sacrum, caudal vertebrae, and pelvis)43. Two of the
cats were 2 years old and the other was geriatric.
Clinical signs, that had been present for between 4
and 18 months, included swelling over the cysts and
tenderness on palpation. Radiography revealed a
large expansile lesion with minimal soap bubble-like
trabecular septation surrounded by a thin rim of
mineralized soft tissue or bone. Treatment by

309

A B C
309 Osteochondromatosis.
A Ventrodorsal radiograph of the pelvis showing an ossified mass attached to the pubis (arrow). The mass was surgically
resected.
B Lateral radiograph of the thorax of the cat in A showing an ossified mass projecting ventrally from the mid-thoracic
vertebrae (arrow).
C Ventrodorsal radiograph of the pelvis of the cat in A and B 1 year later. There are now multiple ossified masses arising
from the pubis and ischium. Biospy revealed malignant transformation to OSA.
 Miscellaneous orthopedic disorders
349

curettage and bone grafting, en bloc resection, or cats and lesions were present in the skull in one case.
amputation may be successful, depending on the Pathologic fractures occurred in two cats. Diagnosis
location of the lesion. is made by bone biopsy or identification of the
organism in the draining lymph nodes or in the
Fibrous dysplasia bloodstream.
Fibrous dysplasia is a rare developmental abnormality Itraconazole is currently the drug of choice for
of bone characterized by the formation of fibro- treatment of histoplasmosis. Studies in cats have
osseous cystic lesions. There is confusion in the shown significant variability in the absorption of the
veterinary literature where the terms fibrous dysplasia, drug and the oral solution is more consistently
aneurysmal bone cyst, and benign bone cyst are absorbed than the capsules72. The response to
sometimes used synonymously. The lesion has been treatment is monitored clinically and radiographically.
reported in two cats; one in the mandible and the The drug is administered at 5–10 mg/kg divided
other in the distal ulna, with signs of trismus and twice daily for at least 3–6 months or until complete
lameness respectively43. Radiographically the affected resolution of the infection.
bone had a marked homogenous increase in
radiopacity. The lesion in the ulna showed thinning of CONGENITAL DEFECTS
the cortices and irregular periosteal new bone Congenital defects of the musculoskeletal system, the
formation. The lesions were resected from both cats spinal cord, and peripheral nerves are occasionally seen
and there was no recurrence 4 years later. in the cat. Many defects occur as breed-specific
syndromes but some disorders are seen sporadically
INFECTIONS OF BONE affecting nonpedigree cats. The most important defects
Inflammation of periosteum, cortical bone, and are shown in Table 30 and, if clinically significant, are
medullary cavity is known as osteomyelitis. Most discussed in the relevant sections of the book.
cases are caused by bacterial infection, which is
discussed in Chapter 3. Infection of the intervertebral
discs with secondary involvement of adjacent
vertebral bodies is termed discospondylitis and is
discussed in Chapter 11. Fungal osteomyelitis is
occasionally encountered and is most commonly
caused by Histoplasma capsulatum.
310
HISTOPLASMOSIS
Histoplasma capsulatum is a soil-borne fungal
organism found in the southeastern and mid-western
regions of North America. Although disease is most
prevalent in these areas, there are sporadic reports of
fungal osteomyelitis in other parts of the world.
Osteomyelitis associated with histoplasmosis has been
reported in cats of various ages70,71. Cases typically
presented with lameness, soft tissue swelling, and pain
on palpation of the affected bone. Draining tracts over
the osseous lesions were present in two cats. Systemic
signs including anorexia, pyrexia, weight loss,
lethargy, and chorioretinitis were present in some
cases. The organism is contracted by inhalation of the
fungal spores, but respiratory signs were absent.
Radiographic features included multifocal
irregular areas of osteolysis and endosteal new bone
formation around the metaphyses of affected long
bones. The appendicular skeleton was most
commonly affected, especially adjacent to the carpus 310 Forepaw of a cat with polydactyly. The cat had
and tarsus. More than one bone was affected in some supernumerary digits on all four limbs.
350
TABLE 30 CONGENITAL DEFECTS.73–75
Condition
Achondroplasia
Craniofacial deformity
Fibrodysplasia ossificans
progressiva
Forelimb underdevelopment
Hereditary myopathy
Hip dysplasia
Hyperchylomicronemia
Hyperoxaluria
Lysosomal storage diseases
Myasthenia gravis
Myotonia
Nemaline myopathy
Distal axonopathy
Patellar luxation
Polydactyly (310)
Radial hemimelia or agenesis
Radioulnar synostosis
Sacrocaudal dysgenesis
Skeletal abnormalities
Spina bifida
Tail kink
Vertebral anomalies
X-linked muscular dystrophy
Breed Comments
Shortened limbs at birth, muscle weakness and atrophy,
usually fatal by 4 months of age
Burmese Known by breeders as ‘head deformity’, usually severe and
stillborn or die soon after birth
Progressively stiff gait, multiple mineralized
radiopacities in affected musculature
Scottish Fold Forelimbs are short, hindlimbs are long, known as kangaroo
kittens, females only
Devon Rex Generalized and progressive weakness and neck ventroflexion
from 3 weeks of age onwards
Maine coon 18% of Maine coon cats but any breed may be affected
Low lipoprotein lipase activity. Compression of peripheral
nerves by lipid granulomas.
Unexplained axonopathy. Renal failure due to deposition of
oxalate crystals usually causes death before 1 year of age
Siamese, Korat Many different types, other breeds and domestic shorthair
cats may be affected, from 6–9 weeks of age
Abyssinian, Somali Congenital deficiency of acetylcholine receptors in
postsynaptic membrane
Domestic shorthair Kittens with hereditary myotonia have widespread
and longhair muscle hypertrophy and an awkward stiff gait
Stilted gait, reluctant to walk from 6–18 months of age
Birman Loss of myelinated fibers, paraparesis develops at 6–10 weeks
of age
Devon Rex, Abyssinian Usually medial and bilateral
Extra digits may be just the first digit on the hindlimbs or
may be multiple extra digits on all limbs. Inherited as an
autosomal dominant trait with variable expressivity
Absence of the radius, frequently bilateral
Bilateral elbow malformation
Manx Malformation of sacrocaudal vertebrae, may be any breed
Scottish Fold Abnormalities of the tail and distal extremities, especially the
hocks, shortening of the caudal vertebrae, overgrown claws
Manx Hindlimb ataxia and fecal and urinary incontinence, may be
no tail
Kink usually near the end of the tail
Hemivertebrae, block, transitional, and butterfly vertebrae
may be associated with spinal cord compression
Siamese, domestic Stilted gait, bunny hopping, from 6–9 weeks of age
shorthair

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In: WO Brinker, DL Piermattei, GL Flo (eds.)
Handbook of Small Animal Orthopedics and
Fracture Management, 3rd edn. WB Saunders,
Philadelphia, pp. 288–320.
28. McLaughlin RM. (1995) Traumatic joint
luxations in small animals. Veterinary Clinics of
North America, 25: 1175–96.
29. McLaughlin RM. (1998) Arthrodesis. In:
WO Brinker, ML Olmstead, G Sumner-Smith
et al. (eds.) Manual of Internal Fixation in Small
Animals, 2nd edn. Springer-Verlag, Berlin,
pp. 247–54.
30. Moak PC, Lewis DD, Roe SC et al. (2000)
Arthrodesis of the elbow in three cats. Veterinary
and Comparative Orthopaedics and
Traumatology, 13: 149–53.
PART 3: RADIUS AND ULNA
1. Montgomery R. (2002) Miscellaneous
orthopedic disease. In: D Slatter (ed.) Textbook of
Small Animal Surgery, 3rd edn. WB Saunders,
Philadelphia, pp. 2251–60.
2. Swalley J. (1978) Agenesis of the radius in a
kitten. Feline Practice, 8: 25.
3. Harari J. (2002) Treatments for feline long bone
fractures. Veterinary Clinics of North America:
Small Animal Practice, 32: 927–47.
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4. Schrader SC. (1994) Orthopedic surgery. In:
RG Sherding (ed.) The Cat – Diseases and Clinical
Management, 2nd edn. Churchill Livingstone,
New York, pp. 1649–709.
5. Milton JL, Horne RD, Goldstein GM. (1980)
Cross-pinning: a simple technique for treatment
of certain metaphyseal and physeal fractures of
the long bones. Journal of the American Animal
Hospital Association, 16: 891–906.
6. Prieur WD. (1989) Management of growth plate
injuries in puppies and kittens. Journal of Small
Animal Practice, 30: 631–8.
7. Piermattei DL, Flo GL. (1997) Fractures of the
radius and ulna. In: WO Brinker, DL Piermattei,
GL Flo (eds.) Handbook of Small Animal
Orthopedics and Fracture Repair, 3rd edn.
WB Saunders, Philadelphia, pp. 321–43.
8. Harari J, Seguin B, Bebchuck T et al. (1996)
Closed repair of tibial and radial fractures with
external skeletal fixation. Compendium on
Continuing Education, 18: 651–64.
9. McLaughlin RM, Roush JK. (1999) Principles
of external skeletal fixation. Veterinary Medicine,
94(1): 53–63.
10. McLaughlin RM, Roush JK. (1999) Repairing
fractures with bone plate and screw fixation.
Veterinary Medicine, 94(1): 64–73.
11. Piermattei DL. (1992) An Atlas of Approaches
to the Bones of the Dog and Cat, 3rd edn.
WB Saunders, Philadelphia.
12. Sardinas JC, Montavon PM. (1997) Use of a
medial bone plate for repair of radius and ulna
fractures in dogs and cats: a report of 22 cases.
Veterinary Surgery, 26: 108–13.
13. Bruse S, Dee J, Prieur WD. (1989) Internal
fixation with a veterinary cuttable plate in small
animals. Veterinary and Comparative
Orthopaedics and Traumatology, 1: 40–6.
14. Gentry SJ, Taylor RA, Dee JF. (1993) The use of
veterinary cuttable plates: 21 cases. Journal of the
American Animal Hospital Association, 29: 455–9.
15. McLaughlin RM, Cockshutt J, Kuzma AB.
(1992) Veterinary cuttable plates for the
treatment of comminuted long bone fractures in
cats. Veterinary and Comparative Orthopaedics
and Traumatology, 5: 22–5.
16. Roush JK, McLaughlin RM. (1998) Principles of
applying pin and wire fixation. Veterinary
Medicine, 93(12): 1075–80.
17. McLaughlin RM. (1995) Traumatic
joint luxations in small animals.
Veterinary Clinics of North America,
25: 1175–96.
368
18. Schwarz PD, Schrader SC. (1984) Ulnar fracture
and dislocation of the proximal radial epiphysis
(Monteggia lesion) in the dog and cat: a review of
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PART 4: CARPAL, METACARPAL, AND
PHALANGEAL INJURIES
1. Piermattei DL, Flo GL. (1997) Fractures
of the carpus, metacarpus, and phalanges.
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Orthopedics and Fracture Repair, 3rd edn.
WB Saunders, Philadelphia, pp. 344–89.
2. Schrader SC. (1994) Orthopedic surgery.
In: RG Sherding (ed.) The Cat – Diseases
and Clinical Management, 2nd edn.
Churchill Livingstone, New York, pp. 1649–709.
3. Piermattei DL. (1993) An Atlas of Approaches to
the Bones of the Dog and Cat, 3rd edn.
WB Saunders, Philadelphia.
4. Lewis DD. (1995) Management of
penetrating joint injuries. Veterinary Clinics
of North America: Small Animal Practice,
25: 1197–223.
5. Harari J, Sequin B, Bebchuk T et al.
(1996) Closed repair of tibial and radial
fractures with external skeletal fixation.
Compendium on Continuing Education,
18: 651–64.
6. Sanchez JR, Swaim SF, Nusbaum KE et al.
(1988) Effects of chlorhexidine
diacetate and povidone–iodine on wound healing
in dogs. Veterinary Surgery, 17: 291–5.
7. Whitelock RG, Dyce J, Houlton JEF. (1999)
Metacarpal fractures associated with pancarpal
arthrodesis in dogs. Veterinary Surgery,
28: 25–30.
8. Swaim SF, Pope ER. (1988) Early management
of limb degloving injuries. Seminars in
Veterinary Medicine and Surgery (Small
Animal), 3: 274.
9. Early TD, Dee JF. (1990) Trauma to the carpus,
tarsus, and phalanges of dogs and cats.
Veterinary Clinics of North America: Small
Animal Practice, 10: 771–747.
10. Miller A, Carmichael S, Anderson TJ et al.
(1990) Luxation of the radial carpal bone in
four dogs. Journal of Small Animal Practice,
31: 148–54.
11. Pritcher GDC. (1996) Luxation of the radial
carpal bone in a cat. Journal of Small Animal
Practice, 37: 292–5.
12. Voss K, Geyer H, Montavon PM. (2004)
Anetbrachiocarpal luxation in a cat. Veterinary
and Comparative Orthopaedics and
Traumatology, 16: 266–70.
13. Haburjak JJ, Lenehan TM, Davidson CD et al.
(2003) Treatment of carpometacarpal and
middle carpal joint hyperextension injuries with
partial carpal arthrodesis using a cross pin
technique: 21 cases. Veterinary and Comparative
Orthopaedics and Traumatology, 16: 105–11.
14. McLaughlin RM. (1995) Traumatic joint
luxations in small animals. Veterinary Clinics of
North America, 25: 1175–96.
15. McLaughlin RM. (1998) Arthrodesis. In:
WO Brinker, ML Olmstead, G Sumner-Smith
et al. (eds.) Manual of Internal Fixation in Small
Animals, 2nd edn. Springer-Verlag, Berlin,
pp. 247–54.
16. Simpson D, Goldsmid S. (1994) Pancarpal
arthrodesis in a cat: a case report and anatomical
study. Veterinary and Comparative Orthopaedics
and Traumatology, 7: 45–50.
17. Bruse S, Dee J, Prieur WD. (1989) Internal
fixation with a veterinary cuttable plate in small
animals. Veterinary and Comparative
Orthopaedics and Traumatology, 1: 40–6.
18. Gentry SJ, Taylor RA, Dee JF. (1993) The use
of veterinary cuttable plates: 21 cases. Journal of
the American Animal Hospital Association,
29: 455–9.
19. Weigel JP. (1993) Amputations. In: D Slatter
(ed.) Textbook of Small Animal Surgery, 2nd edn.
WB Saunders, Philadelphia, pp. 1901–10.
20. Willer RL, Johnson KA, et al. (1990) Partial
carpal arthrodesis for third degree carpal sprains:
a review of 45 carpi. Veterinary Surgery,
19: 334–40.
21. Basher A. (1994) Foot injuries in dogs and cats.
Compendium on Continuing Education,
16: 1159–76.
22. Swaim SF. (1997) Wounds on limbs. In: SF
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Wound Management, 2nd edn. Williams and
Wilkins, Baltimore, pp. 362–70.
23. Patronek GJ. (2001) Assessment of claims of
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with onychectomy in cats. Journal of the American
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24. Patroneck GJ, Beck AM, Glickman LT. (1997)
Dynamics of the dog and cat populations in a
community. Journal of the American Veterinary
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25. Lin HC, Benson GJ, Thurmon JC et al. (1993)
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26. Martinez SA, Hauptman J, Walshaw R. (1993)
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27. Mison MB, Bohart GH, Walshaw R et al. (2002)
Use of carbon dioxide laser for onychectomy in
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28. Schenck CT. (1994) The use of surgical glue
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29. Tobia KS. (1994) Feline onychectomy
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30. Hampel NL, Johnson RG, Pijanowski GJ.
(1991) Effects of isobutyle-2-cyanoacryalte
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31. Benson GJ, Wheaton LG, Thurmon JC et al.
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Effects of analgesics. Veterinary Surgery,
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32. Carroll GL, Howe LB, Slater MR et al. (1998)
Evaluation of analgesia provided by postoperative
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33. Romans CW, Gordon WJ, Robinson DA
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34. Franks JN, Boothe HW, Taylor L et al. (2000)
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37. Jankowski AJ, Brwon DC, Ducal J et al.
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38. Leonard CA, Tillson M. (2001) Feline lameness.
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39. Romans CW, Conzemius MG, Horstman CL
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40. Bennett M, Houpt KA, Erb HN. (1988) Effects
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41. Landsberg GM. (1991) Feline scratching and
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42. Morgan M, Houpt KA. (1989) Feline behavior
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44. Rife JN. (1998) Deep digital flexor
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FRACTURES AND DISORDERS OF
THE HINDLIMB
PART 1: PELVIS
1. Hill FA. (1977) Survey of bone fractures in
the cat. Journal of Small Animal Practice,
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2. Kolata RJ. (1980) Trauma in dogs and cats:
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3. Verstrate FJM, Lambrechts NE. (1992)
Diagnosis of soft tissue injuries associated with
pelvic fractures. Compendium on Continuing
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4. Whitney WO, Mehlhaff CJ. (1987)
370
High-rise syndrome in cats. Journal of the
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191: 1399–403.
5. Bennett D. (1975) Orthopaedic disease affecting
the pelvic region of the cat. Journal of Small
Animal Practice, 16: 723–38.
6. Bookbinder PF, Flanders JA. (1992)
Characteristics of pelvic fractures in the cat.
Veterinary and Comparative Orthopaedics and
Traumatology, 5: 122–7.
7. Bohmer E. (1985) Breckefrakturen und
Luxationen bie der katze in den jahren
1975–1982. Inaugural-Dissertation, Ludwig-
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8. Anderson A, Coughlan AR. (1997)
Sacral fractures in dogs and cats:
a classification scheme and review of
51 cases. Journal of Small Animal Practice,
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9. Muir P. (1988) Rectal perforation associated
with pelvic fracture in a cat. Veterinary Record,
142: 371–2.
10. Jacobson A, Schrader SC. (1987) Peripheral
nerve injury associated with fracture or
fracture–dislocation of the pelvis in dogs and
cats: 34 cases (1978–1982). Journal of the
American Veterinary Medical Association,
190: 569–72.
11. Lanz OI. (2002) Lumbosacral and pelvic
injuries. Veterinary Clinics of North America:
Small Animal Practice, 32: 949–62.
12. Matthiesen DT, Scavelli TD, Whitney
WO. (1991) Subtotal colectomy for the
treatment of obstipation secondary to pelvic
fracture malunion in cats. Veterinary Surgery,
20: 113–17.
13. Payne J. (1993) Selecting a method for
managing pelvic fractures in dogs and cats.
Veterinary Medicine, 88: 969–73.
14. Schrader SC. (1992) Pelvic ostectomy as
a treatment for obstipation in cats with
acquired stenosis of the pelvic canal: six
cases (1978–1989). Journal of the
American Veterinary Medical Association,
200: 208–13.
15. Burgar M, Forterre F, Brunnberg L. (2004)
Surgical anatomy of the feline sacroiliac joint for
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Veterinary and Comparative Orthopaedics and
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16. Smith CW. (1994) Feline orthopedics. Feline
Practice, 22: 16–27.
17. Piermattei DL, Flo GL. (1997) Fractures of the
pelvis. In: WO Brinker, DL Piermattei, GL Flo
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and Fracture Repair, 3rd edn. WB Saunders,
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18. Piermattei DL. (1992) An Atlas of Approaches to
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19. Montovon PM, Boudrieau RJ, Hohn RB.
(1985) Ventrolateral approach for repair of
sacroiliac fracture–dislocation in the dog and
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20. Kaderly RE. (1991) Stabilization of bilateral
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a single transsacral screw. Veterinary Surgery,
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21. Raffan PJ, Joly CL, Timm PG et al. (2002)
A tension band technique for stabilisation of
sacroiliac separations in cats. Journal of Small
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22. Tomlinson JL, Cook JL, Payne JT et al. (1999)
Closed reduction and lag screw fixation of
sacroliliac luxations and fractures. Veterinary
Surgery, 28: 188–93.
23. Ablin LW, Gambardella PC. (1991) Orthopedics
of the feline hip. Compendium on Continuing
Education, 13:1379–86.
24. Berzon JL, Howard PE, Covell SJ et al. (1980)
A retrospective study of the efficacy of femoral
head and neck excisions in 94 dogs and cats.
Veterinary Surgery, 9: 88–92.
25. Lewis DD, Stubbs WP, Neuwirth L et al. (1997)
Results of screw/wire/polymethylmethacrylate
composite fixation for acetabular fracture
repair in 14 dogs. Veterinary Surgery,
26: 223–34.
26. McKee WM, Wong WT. (1994) Symphyseal
distraction-ostectomy using an ulnar autograft
for the treatment of pelvic canal stenosis in three
cats. Veterinary Record, 134: 132–5.
27. McLaughlin RM, Kuzma A. (1991) Surgical
management of collapsed pelvis in a jaguar.
Journal of the American Veterinary Medical
Association, 198: 1789–91.
28. Straw RC, Withrow SJ, Powers BE.
(1992) Partial or total hemipelvectomy in
the management of sarcomas in nine
dogs and two cats. Veterinary Surgery,
21: 183–8.
29. Ferguson J. (1996) Triple pelvic ostectomy for
treatment of pelvic canal stenosis in a cat.
Journal of Small Animal Practice, 37: 495–8.
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PART 2: COXOFEMORAL JOINT
1. Schrader SC. (1994) Orthopedic surgery. In: RG
Sherding (ed.) The Cat – Diseases and Clinical
Management, 2nd edn. Churchill Livingstone,
New York, pp. 1649–709.
2. Ablin LW, Gambardella PC. (1991) Orthopedics
of the feline hip. Compendium on Continuing
Education, 13: 1379–86.
3. Fox SM. (1991) Coxofemoral luxation in dogs.
Compendium on Continuing Education,
13: 381–8.
4. Ehmer EE. (1934) Special casts for the
treatment of pelvic and femoral fractures
and coxofemoral luxations. North American
Veterinary, 15: 31–5.
5. DeVita J. (1952) A method of pinning for
chronic dislocation of the hip joint. Proceedings
of the 89th Annual Meeting of the American
Veterinary Medical Association, pp. 191–2.
6. Wildgoose WH. (1983) Hip dislocation and the
use of the DeVita pin in the cat Journal of Small
Animal Practice, 24: 261–8.
7. Basher AWP, Walter MC, Newton CD. (1986)
Coxofemoral luxation in the dog and cat.
Veterinary Surgery, 15: 356–62.
8. Piermattei DL. (1992) An Atlas of Approaches to
the Bones of the Dog and Cat, 3rd edn. WB
Saunders, Philadelphia, pp. 230–5.
9. Allen SW, Chambers JN. (1986) Extracapsular
suture stabilization of canine coxofemoral luxation.
Compendium on Continuing Education,
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10. Braden TD, Johnson ME. (1988) Technique and
indications of a prosthetic capsule for repair of
recurrent and chronic coxofemoral luxations.
Veterinary and Comparative Orthopaedics and
Traumatology, 1: 26–9.
11. Johnson ME, Braden TD. (1987)
A retrospective study of prosthetic capsule
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12. Piermattei DL. (1992) An Atlas of Approaches to
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13. Bennet D, Duff SR. (1980) Transarticular pinning
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Journal of Small Animal Practice, 21: 373–9.
14. Hunt CA, Henry WB. (1985) Transarticular
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16. Lubbe AM, Verstraete FJM. (1990) Fascia lata
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17. Mehl NB. (1988) A new method of surgical
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18. Meij BP, Hazewinkel AW, Nap RC. (1992)
Results of extra-articular stabilisation following
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19. Hammer DL. (1980) Recurrent coxofemoral
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177: 1018–20.
20. Berzon JL, Howard PE, Covell SJ et al. (1980)
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head and neck excisions in 94 dogs and cats.
Veterinary Surgery, 9: 88–92.
21. Gendreau C, Cawley AJ. (1977) Excision of the
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22. Hayes MH, Wilson GP, Burt JK. (1979) Feline
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23. Patsikas MN, Papazoglou LG, Komninou A et al.
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24. Robin KL, Haan JJ, Ackerman N. (1994) Hip
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25. Holt E. (1978) Hip dysplasia in a cat. Journal of
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26. Keller GG, Reed AL, Lattimer JC et al.
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27. Koeppel E, Ebner J. (1990) Die
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PART 3: FEMORAL AND PATELLAR FRACTURES
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femur and patella. In: WO Brinker, DL
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Repair of femoral capital physeal injuries in
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Orthopaedics and Traumatology,
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5. Jeffrey ND. (1989) Internal fixation of femoral
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6. Fischer H, Norton J, Kobluk LN et al. (2004)
Surgical reduction and stabilization for repair of
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7. Daily WR. (1978) Femoral head and neck
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8. Bennett D. (1994) In: EA Chandler,
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Feline capital physeal dysplasia syndrome.
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10. Queen J, Bennett D, Carmichael S et al. (1998)
Femoral neck metaphyseal osteopathy in the cat.
Veterinary Record, 142: 159–62.
11. Piermattei DL. (1992) An Atlas of Approaches
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12. Harari J. (2002) Treatments for feline long bone
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13. McLaughlin RM. (1999) Internal fixation:
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14. Roush JK, McLaughlin RM. (1998) Principles of
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15. Newman ME, Milton JL. (1989) Closed
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16. Palmer RH, Aron DN, Purinton PT. (1988)
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17. Dallman MJ, Martin RA et al. (1990) Rotational
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18. Gibson KL, van Ee RT. (1991) Stack pinning of
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19. Tarr RR, Wiss DA. (1896) The mechanics
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20. Vassuer PB, Paul HA, Crumley L. (1984)
Evaluation of fixation devices for prevention
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canine femoral shaft: an in vitro study.
American Journal of Veterinary Research,
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21. McLaughlin RM, Roush JK. (1999) Repairing
fractures with bone plate and screw fixation.
Veterinary Medicine, 94(1): 64–73.
22. McLaughlin RM, Cockshutt J, Kuzma AB.
(1992) Veterinary cuttable plates for the
treatment of comminuted long bone fractures in
cats. Veterinary and Comparative Orthopaedics
and Traumatology, 5: 22–5.
23. McLaughlin RM, Roush JK. (1998) Autogenous
cancellous and cortico-cancellous bone grafting.
Veterinary Medicine, 93(12): 1071–4.
24. Reems MR, Beale BS, Hulse DA. (2003)
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7. Johnson ME. (1986) Feline patellar luxation:
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8. Smith GK, Langenbach A, Green PA et al.
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PART 5: TIBIAL AND FIBULAR FRACTURES
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12. Salter RB, Harris WR. (1963) Injuries involving
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14. Prieur WD. (1989) Management of growth plate
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15. Whitney WO, Schrader SG. (1987) Dynamic
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16. Newman ME, Milton JL. (1989) Closed
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18. McLaughlin RM, Roush JK. (1999) Principles of
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19. McLaughlin RM. (1999) Internal fixation pins,
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20. Payne J, McLaughlin R, Silverman E. (2005)
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22. McLaughlin RM, Roush JK. (1999) Repairing
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PART 6: TARSAL,METATARSAL, AND
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23. Doverspike M, Vasseur PB. (1991) Clinical
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FRACTURES AND DISORDERS OF
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7. Shields Henney LH, Galburt RB, Boudrieau
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390
APPENDIX
MANUFACTURERS
3M Animal Care Products, St Paul, MN, USA
Anchor Products Co., Addison, IL, USA
Biomet, Warsaw, IN, USA
Bioscience Ltd., Tampere, Finland
DMS Laboratories, Flemington, NJ, USA
Dow Corning, Midland, MI, USA
ESPE Dental Medizin, Seefeld, Germany;
Knutsford, UK
Ethicon, Piscataway, NJ, USA; Livingstone, UK
Hofmann s.r.l, Monza, Italy
Howmedica International, Rutherford, NJ, USA
IMEX Veterinary Inc., Longview, TX, USA
Innovative Animal Products LLC., Rochester,
MN, USA
Johnson & Johnson, New Brunswick, NJ, USA
Jorgensen Laboratories, Loveland, CO, USA
Kirschner Medical Corp., Marlow, OK, USA
LB Caulk Co., Milford, DE, USA
Luxar Corp., Bothwell, WA, USA
Millpledge, Retford, UK
Novafil, Davis, & Geck, Danbury, CT, USA
Nutramax Laboratories Inc., Edgewood, MD, USA
Nycomed, Oxford, UK
Nyegaard, Oslo, Norway
Pentron Clinical Technologies LLC., Wallingford,
CT, USA
Resco (Tecla Co. Inc.), Walled Lake, MI, USA
Rotec Medizintechnik, Weisendorf, Germany
Securos Veterinary Orthopedics Inc., Charlton,
MA, USA
Soft Paws, Three Rivers, CA, USA
Synthes Inc., Paoli, PA, USA; Welwyn Garden City,
UK; 4500 Solothurn, Switzerland
Tripoint Medical (McArthur Medical Sales Inc.),
Veterinary Instrumentation, Sheffield, UK
Veterinary Orthopedic Implants Inc., South
Burlington, VT, USA
Veterinary Transplant Services Inc., Kent,
WA, USA
Zimmer Inc., Warsaw, IN, USA
 391

INDEX

Note: page references in bold refer angiomatosis, vertebral 319–20 arthroplasty, excision (continued)
to main discussion of a topic, antebrachiocarpal joint 145 shoulder joint 113
standard text other discussion; those arthrodesis 153 arthroscopy 89
in italic refer to tables or boxed text luxation 150–1 arthrotomy, stifle joint 216, 235
antibiotics articular fracture
abdominal injuries 25, 167 bacterial meningomyelitis 314–15 complications 86
Abyssinian cat 218, 332, 350 discospondylitis 315–16 treatment 77, 84–6
acepromazine 38, 38 infected nonunion 84 see also named joints
acetabular fracture176–80 Lyme disease 97 aseptic preparation 58, 59, 68
acetabulum 13 mandibular fracture 262 aspirin 93, 93
Achilles tendon, see calcanean open fracture 33 atlantoaxial articulation, subluxation
(Achilles) tendon osteomyelitis 41 318
achondroplasia 350 postoperative 39 atropine 38, 333–4
acromegaly 91 prophylactic 58 autoantibodies 98, 101
acromion process 10, 11, 108–9 septic arthritis 95–6 avulsion injuries 17, 44
acrylic external skeletal fixators shearing injuries 147, 251 brachial plexus 326–7
71–2, 139 antifungal agent 314 calcanean (Achilles) tendon 106,
Actinomyces spp. 40, 315 antinuclear antibody (ANA) titer 98, 254
activity, postoperative 39 101 cruciate ligament 235
adhesives, cyanoacrylate 160–1, AO Vet fracture classification system femoral head 192–3
162–3 45 tendon 105–6, 254
agenesis, radius 136, 350 appetite stimulants 28 tibial tubercle 233–5
all-meat syndrome 337–8 aquatic therapy 39
alloantibodies 27 arrhythmia 26 back splint 299–300
alpha 2 agonist 38 arthritis bacterial arthritis 21, 94–6
aminoglycoside 33, 41 immune-mediated 87, 96, 97, bacterial L-form 96
amoxicillin 96, 262 97–101 Bacteroides spp. 40, 314
ampicillin 262 infective 17, 21, 94–6, 94–7 Balinese cat 320
amputation synovial fluid analysis 21 bandages 29–30, 29, 30–1
digit 156–7, 259 traumatic 90 effect on joint motion/weight
forelimb 165–6 see also osteoarthritis bearing 29
hindlimb 259–60 arthrodesis 86 onychectomy wound 161
analgesia 35–7 carpal joint 52, 140, 144, 148, Robert Jones 29, 30, 30, 31, 33,
onychectomy 36, 161 152–4 228
postoperative 39 elbow joint 134–5 soft padded 30–1, 30
preoperative/preemptive 35–7, shoulder 113–14 behavior, after onychectomy 164
58 steps 86 benzodiazepine 38, 38, 334
regional 36–7 stifle joint 231–2 biceps brachii muscle 166
spinal disorders 294 talocrural joint 255–6 biceps femoris muscle 172, 177,
analgesic drugs 35–7, 35 tarsal joint 249, 250, 252, 255–9 198, 199
anal tone 304 arthrodesis wire 51 biopsy
anatomy 10–13 arthrography, contrast 89 bone 23
anconeal process 132 arthroplasty, excision muscle and nerve 24
anemia 27 femoral head and neck 177–8, synovial membrane 90, 101
aneurysmal bone cyst 348–9 191, 193, 195 Birman cat 323, 350
392
bite wound 17, 332, 334
causing septic arthritis 94–6
bladder, manual emptying 305
bladder function 283, 284, 305, 306
blood donor 27, 28
blood substitute 28
blood supply, bone 14
blood test 24, 286
blood transfusion 27–8
blood typing 27
blood volume, estimation 27
bobtail cat 317
body weight 18
bone biopsy 23
bone cement 72, 179, 180, 301
bone cyst 348–9
bone graft 80–1
autogenous graft collection 80–1
complications 81
delayed and nonunion fracture 84
indications 80
pelvic malunion fracture 181, 182
placement 81
stifle arthrodesis 232
bone growth 14–16
bone healing 47–9
delayed, see delayed/nonunion
fractures
bone marrow aspiration 308
bone metabolism 335
bone plate fixation
acetabular fracture 179
elbow arthrodesis 135
femoral fracture
diaphyseal 201–5
distal 212, 213
humeral diaphyseal fracture
122–4
ilial fracture 174, 175
nonunion fracture 83, 84
radial fracture
diaphyseal 139–40
distal 140
scapular fracture 109, 110
shoulder arthrodesis 114
tarsal arthrodesis 259
tibial fracture
diaphyseal 240, 241
proximal 237
vertebral fracture 302
bone plate 49, 52–4, 74, 75–8
application technique 76–8
biological healing/lengthening
52, 205
bridging (buttress) 76, 124,
204–5
‘compression’ 76
customizing 52
dynamic compression (DCP) 52,
75, 76, 201–2
function 76
bone plate (continued) carpal joint (continued)
mini plate 53 arthrodesis 52, 140, 144, 148,
reconstruction 52, 212 152–4
stacking 53, 54, 203, 204 combined fracture/luxation 145
tubular 53 fracture 146–7
veterinary cuttable (VCP) 53–4, hyperextension injuries 152
108 luxation 148–51
bone screws 52, 53, 54–5, 74–5 normal anatomy 145
application technique 76–8 range of motion 10
drill bit/tap selection 55, 55 shearing injuries 147–8
Herbert 214 synoviocentesis 20
lag 74–5 carpal varus 16
plate 74, 75 carpometacarpal joint
position 75 arthrodesis 153–4
Borrelia burgdorferi 97 luxation 151–2, 154–5
brachial artery 12, 166 carprofen 35
thromboembolism 324–5 castration, growth plate closure 16,
brachial plexus, avulsion 326–7 341
brachiocephalicus muscle 166 cast 29–30, 30, 59, 60–1
brachycephalic conformation 277 application 60
bradycardia 38 care 61
brain edema 277–8 effect on joint motion/weight-
breathing pattern 26 bearing 29
breed predisposition 18 cauda equina
congenital defect 350 injuries 304, 306
hip dysplasia 191 malformation 317–18
myasthenia gravis 332, 350 cauda equina syndrome 312–13
open mouth locking 277 caudal vertebrae 306
osteochrondrodysplasia 342 cefazolin 58, 147, 251, 262
patellar luxation 218 cefotaxime 314
bridging (buttress) plating 76, 124, ceftazidime 314
204–5 cephalexin 96
bridging osteosynthesis 49 cephalic vein 166
brisement forcée 275 cephalosporin 33, 147, 251
bronchogenic carcinoma 346 cerclage wire 51, 64–7
bullet fragments, removal 34 full 65
Bunnell–Meyer suture 104, 110, hemicerclage 65, 176
248 humeral diaphyseal fracture
bupivacaine 36, 36, 161 118–19
buprenorphine 35, 36, 38 loop 66
Burmese cat 331, 350 patellar fracture 216, 217
butorphanol 26, 35, 38, 93, 161 tightening 65–7
twist 66–7
calcanean (Achilles) tendon cerebrospinal fluid (CSF) 280
avulsion 106, 254 analysis 291–2, 308, 309, 315
tendinopathy 106 collection procedure 292
calcanean tendon (common) ceroid lipofuscinosis 319
avulsion/severance 106, 254 cervical spine, exostosis 339
laceration 252–3 chemotherapy 308
calcaneus, fracture 245–6 chlorhexidine gluconate 34, 58,
calcitriol 338 147, 163, 251
calcium 335, 337–8 chondroitin sulfate 94
calcium gluconate 338 chondrosarcoma 307, 344
calcium to phosphorus ratio 335, chronic renal failure 335–6
337 clavicle 10, 11
calcivirus arthritis 17, 96–7 clavulanate 262
carbamate toxicity 325, 333–4 claws
carbon dioxide laser 160 capping 165
cardiomyopathy, hypertrophic 324–5 regrowth after onychectomy 161
carpal flexion bandage 152 removal see onychectomy
carpal joint 145 trimming 164

clindamycin 33, 41, 96, 147, 251,
262, 313, 332
Clostridium spp. 40, 328
collateral ligament 13
injuries 225–7
prosthetic 151, 248
colloid solutions 26–7
comminuted fracture 44
distal femoral articular surface
214
femoral diaphysis 202–5
fragment stabilization 80
humerus 124, 125, 126, 127
mandible 265–6
olecranon process 142
plate application 77
repair options 65
tibial diaphysis 238, 239
comparative anatomy 9–13
computed tomography (CT) 22–3,
292, 294
concomitant injuries 25, 167
concurrent injuries 25, 167
congenital defects 316–18, 349, 350
see also named disorders
conservative treatment 9
acetabular fracture 176–7
coxofemoral luxation 185
cruciate ligament injuries 223
femoral head fracture 193
femoral neck fracture 195
mandibular fracture 262
palatine fracture 272–3
patellar fracture 216
patellar luxation 219
pelvic fracture 168
proximal tibial fracture 233
sacroiliac injury 169
spinal disorders 294–5
spinal injuries 298, 299
conus medullaris 280
coracoid process 10, 11
cosequin 93, 94
coxa vara 218
coxofemoral joint
luxation 184–91
normal anatomy 184
cranial draw sign 19, 223
craniofacial deformity 350
creatine kinase (CK), serum level
328, 329, 331, 332
crepitus, joint 90
crossed extensor reflex 283
cross-matching 27
cross-pin fixation 64
femoral fracture
distal 210
distal growth plate 209
radial fracture 137, 140, 141
distal 140, 141
proximal 137
Index
cross-pin fixation (continued)
supracondylar humeral fracture
126
cruciate ligament injuries 13, 17,
208–9, 222–7
caudal 225, 230
cranial 17, 103, 222–5, 230, 235
cryptococcosis 313–14
Cryptococcus spp. 97, 313, 314
cryptoheptadine 28
crystalloid solution 26, 27
cutaneous trunci (panniculus) reflex
282, 283
cyanoacrylate tissue adhesive 160–1,
162–3
cyclophosphamide 101, 308
cysts
bone 348–9
subchondral 89, 91
synovial 102
cytotoxic drug 101, 326
decision-making (fracture treatment)
45–7
declawing see onychectomy
decompression
skull fracture 278
spinal cord 294–5, 304, 306
deep digital flexor tenectomy 164–5
deep pain perception 283–4, 297,
304
deformities, limb 16, 136
degenerative joint disease (DJD),
definition 87
degloving injuries see shearing
injuries
delayed/nonunion fracture 73, 74,
82–4
cause 83
diagnosis 83–4
treatment 84
dental malocclusion 262, 271
dental restorative 268–9
Dermacentor spp. 334
dermoid cyst, spinal 320
developmental anomalies, radial
hemimelia/agenesis 136, 350
developmental orthopedic disease
335
DeVita (ischioilial) pin 186
Devon Rex cat 218, 329, 350
dexamethasone 298
diabetic polyneuropathy 325
diagnostic tools 19–24
diaphyseal fractures, repair options
65
diazepam 28, 38, 38, 334
digital flexor tendon, severance 104
digits
amputation 156–7, 259
metastatic tumor 346
393
digits (continued)
squamous cell carcinoma 345
diphenhydramine 334
discospondylitis 315–16, 349
distal axonopathy 323
dog
comparative anatomy 9–13
developmental orthopedic disease
335
dietary protein 28
open mouth locking 277
spinal disease 284, 299
synovial sarcoma 102
domestic longhair cat 350
domestic shorthair cat 218, 350
dorsal laminectomy 294
doxorubicin 308
doxycycline 97
drill, power 50
bit selection 55, 55
dynamic compression plate (DCP)
52, 75, 76
femoral fracture 201–2, 205
humeral fracture 123
limited contact (LC-DCP) 52,
201–2, 205
dynamic intramedullary (Rush)
pinning 63, 126, 127, 210–11,
212, 214, 242
humeral fracture 120
edrophonium chloride 333
Ehmer sling 30, 32, 185–6, 187, 191
elbow joint
anatomy 12
arthrodesis 134–5
ligament injury 105
luxation 130–4
range of motion 10
synoviocentesis 20
electrical stimulation 84
electrocautery 34
electromyogram (EMG) 294
Ellis pin 55
enrofloxacin 314
enteral feeding 28
enthesiophyte 91, 92
epidural analgesia 36–7, 36
erythromycin 96
Escherichia coli 40, 58, 315
esophagostomy tube feeding 29
examination 17–19
physical 18
neurologic 281–6, 297
orthopedic 18–19
rectal 168
trauma patient 25–6
exercises, passive motion 86
exostosis 339
multiple cartilaginous
(osteochondromatosis) 347–8
394
extensor carpi radialis reflex 282, femoral fracture, diaphyseal fusion podoplasty 155, 259
283 (continued) Fusobacterium spp. 40, 314
external coaptation 29–30, 29, oblique 202
59–62 transverse 202, 203 gabapentin 36
distal femoral fracture 208 distal 208–14 gait
elbow luxation 132 condylar/trochlear 212–14 analysis 10, 22
femoral diaphyseal fracture 198 growth plate 209–11 observation 18
humeral fracture 118 supracondylar 211–12 gastrostomy tube feeding 29
radial fracture 138, 140 greater trochanter 197 gender 18
spinal injuries 299–300 head 192–5 gentamycin 96
tibial diaphyseal fracture 238 iatrogenic neuropathy 327–8 genu recurvatum 330
external fixation 29–30 neck 195–6 giant cell tumor 344
femoral fracture postoperative care 215 gingiva, squamous cell carcinoma
diaphyseal 200, 201, 206–8 proximal growth plate 193–5 345
distal 211–12, 214 femoral head gingivitis 270
humeral fracture excision arthroplasty 177–8, 191, glenohumeral ligament
diaphyseal 120–2 193 imbrication 112
supracondylar 126, 127 necrosis (Legg–Calvé–Perthes prosthetic replacement 112, 113
mandibular fracture 265–6 disease) 13 glenoid fracture 110
radial fracture 138–9, 140–1 femorofabellar ligament 224 glenoid tubercle fracture 110
tibial fracture fentanyl 35 globulin, serum 100
distal 243 epidural 36, 36 glucocorticoids 313
metaphyseal 239–40 transdermal patch 37, 161 head trauma 278
proximal 236, 237 fiberglass casting material 60 immune-mediated arthritis 101
external skeletal fixator 46, 55–6, fibrocartilaginous embolism 315 myasthenia gravis 333
67–74 fibrodysplasia ossificans progressiva osteoarthritis 93, 94
acrylic 71–2, 139 329, 350 septic arthritis 96
application 29–30, 68–70, 236 fibroma, ossifying 347 glucosamine 94
circular/ring 56, 72–3, 240, 241 fibrosarcoma 344–5 gluteal muscle 172
complications 73–4, 73 fibrotic myopathy 330 deep 177, 178
frame configuration 68, 69 fibrous dysplasia 349 middle 172, 174, 177
frame stiffness 68 figure-of-eight skewer technique 63 D-glycerate dehydrogenase 322
linear system 67–8 flexor (withdrawal) reflex 282, 283, glycopyrrolate 38
removal 82 284–5 glycosaminoglycan, polysulfated 94
transarticular (TESF) 56, 86, fluconazole 314 gracilis muscle 260
105, 133–4, 135 fluid therapy 26–7 greater trochanter
flunixin meglumine 93 fracture 197
fabella 224 fluoroquinolone 33, 41, 96 transposition 187
fabellar–patellar suture 219 fluoroscopy 22 growth, bone 14–16
fabellar–tibial antirotational suture food growth plate fractures
219 contamination with salinomycin classification 43
fascia lata 189–90, 198 325 distal femur 209–11
feline immunodeficiency virus (FIV) see also nutrition humeral head 115–16
24, 98, 99, 314, 316 forceps, bone holding 50 proximal femur 193–4
feline infectious peritonitis (FIP) 98, forelimb proximal tibia 233, 235–6
309 amputation 165–6 growth plate 15–16
feline leukemia virus (FeLV) 24, 98, reflex 282, 283 closure 15, 15, 16, 341
99, 306–7, 314, 316, 347 shearing injuries 147–8 gunshot wound 34
feline sarcoma virus (FeSV) 344–5 underdevelopment 350
feline syncytia forming virus (FeSFV) see also named parts of the forelimb hanging-limb technique 58–9, 68
99 fracture callus 48 hard palate, fracture 263, 271–3
feline synovial sarcoma 101–2 fracture classification 43–5 Hartmann’s solution 26
femoral artery 260 fracture configurations 44, 45–6 Haversian system, remodeling 47,
femoral capital epiphysis, blood fracture gap 48–9 48
supply 13 fracture healing head trauma 277–8
femoral capital physeal fracture, bridging osteosynthesis 49 heart failure 324–5
spontaneous 341–2 direct 48–9 hemaglobin-based oxygen carrying
femoral fracture indirect 47–8 (HBOC) solution 28
complications 215, 330–1 fracture hematoma 26 hematoma, fracture 26
diaphyseal 198–208 fracture reduction 58–9 hemicerclage wire 65, 176
comminuted 202–5 fungal arthritis 97 hemilaminectomy 294–5, 304, 311

hemipelvectomy 260
hemorrhage 26, 161
Herbert bone screw 214
‘high rise’ syndrome 271–2
Himalayan cat 330
hindlimb 9
amputation 259–60
reflex 282, 283, 285
shearing injuries 250–2
see also named parts of the
hindlimb
hip joint
anatomy 13
dysplasia 17, 88, 191, 350
range of motion 10
replacement 57, 191, 193, 195
synoviocentesis 20
Histoplasma capsulatum 97, 349
histoplasmosis 349
history taking 18
hock joint, see tarsus
Horner’s syndrome 327
humerus
anatomy 11, 12
bone graft collection 81
forelimb amputation 166
fracture 11
causes and signs 115
combined
supracondylar/condylar 128–30
condylar 126–8
diaphyseal 117–25
postoperative care 130
proximal 115–17
supracondylar 11, 126, 127
osteomyelitis 40
supracondylar foramen 11, 12,
117, 126
hyaluronic acid 21, 22
hydrocephalus 309
hydromyelia 319
hydromorphone 35
hydrotherapy 39
hyperchylomicronemia 323, 350
hyperextension injuries, carpus 152
hyperglycemia 278
hyperoxaluria 322–3, 350
hyperparathyroidism
hyperthyroid-related 337
nutritional secondary 180, 181,
337–9
primary 335
renal secondary 335–6
hyperphosphatemia 335–6
hyperthyroidism 333, 337
hypervitaminosis A 102, 320,
339–40
hypokalemia 331
myopathy 331–2
hypovitaminosis D 340
hypovolemic shock 26
Index
iliacus muscle 172
iliofemoral suture, extraarticular
190–1
iliolumbar vessel 172, 174
ilium
bone graft collection 81
fracture 173–6
Ilizarov, GA 72
imaging
advanced techniques 22–3
fluoroscopy 22
scintigraphy 22, 41, 84
sonography 22, 89
see also radiography
imbrication
shoulder joint/glenohumeral
ligament 112
stifle joint capsule 219–20
IMEX-SK System, mini 69
immune-mediated disease 17, 87,
96, 97, 97–101
laboratory tests 21, 90, 98
immunosuppression 101, 316
implants 51–7
removal 82
see also named implants
infection
after onychectomy 162–3
bone 84, 349
wound 40, 94, 95, 332
see also osteomyelitis
infectious myopathy 332
infraspinatus muscle 10
instruments 50
interarcade fixation 268–9
interdental fixation 266–7
interfragmentary wires 269–70
interlocking nail (ILN) 57,
78–80
complications 80
femoral fracture 208
humeral fracture 124, 125
insertion 78–80
removal 80
intertrochanteric fracture 198
intervertebral disc 13
disease 309–12
intracranial pressure 277–8
intramedullary (Steinmann) pin 51,
62–3, 62–3, 77–8
closed 236, 239
distal tibial fracture 242
femoral fracture
diaphyseal 199–200, 201
distal 210
humeral fracture
diaphyseal 11, 118–20
supracondylar 126, 127
insertion 62–3, 77–8
radial fracture 140
shoulder stabilization 112
395
intramedullary (Steinmann) pin
(continued)
tibial fracture
diaphyseal 238–40
proximal 236, 237
ulnar diaphyseal fracture 144
see also dynamic intramedullary
(Rush) pinning
intubation
mandibular fracture 262
pharyngostomy 262, 263
iohexol 89
ischemic neuromyopathy 324–5
ischial fracture 167, 180
ischiatic/sciatic neuropathy 327
ischioilial (DeVita) pin 186
isoniazid 97
itraconazole 314, 349
Ixodes holocyclus 334
Jamshidi bone marrow biopsy needle
23
joint disease
classification 87
investigations 88–90, 101
joints
arthrodesis (fusion) 86
fracture 22, 77, 84–6
lavage 94, 95
range of motion 10, 10
see also named joints
joint space 89
junctionopathies 322, 323, 332–4
ketamine 28, 38, 38
ketoprofen 35, 93
Kirschner–Ehmer (KE) fixator
system 67–8
Kirschner wire 51, 63–4
articular fracture 86
calcanean fracture 246
femoral fracture
distal 210
greater trochanter 197
head 192, 193–5
neck 195–6
humeral fracture
diaphyseal 120
proximal 115–17
ilial fracture 176
maxillofacial fracture 271–3
patellar fracture 216, 217
radial fracture 137
sacroiliac joint
fracture/dislocation 170, 171
scapular neck fracture 109–10
shoulder arthrodesis 114
stifle arthrodesis 231–2
styloid process fracture 144
tibial fracture 234
kittens, septic arthritis 95
396
Klebsiella spp. 40
Korat cat 350
laboratory tests, joint disease 90
lag screw fixation
acetabular fracture 179
distal femoral fracture 212, 213
distal radius 140
elbow arthrodesis 135
greater trochanter 197
ilial fracture 176
proximal tibial fracture 237
sacroiliac joint fracture/luxation
170, 171, 172
shoulder arthrodesis 114
lag screw 74–5
percutaneous placement 173
lameness
after onychectomy 164
differential diagnosis 17, 17
osteoarthritis 91
septic arthritis 95
laminectomy 294–5, 304, 306
laser, carbon dioxide 160
lavage
joint 94, 95
wound 34, 147, 251
Legg–Calvé–Perthes disease 13
Ligament–bone suture technique
234
ligaments 13, 104–6
carpal ligament injuries 147
collateral ligament injuries 225–7,
230, 247, 248
cruciate ligament injuries 13, 17,
103, 222–5, 230, 235
functions 104
healing 104
repair 105
limb deformities 16, 136
limb load forces 10
liver, in diet 339
L plate 237
luxation 17
carpal joint 148–51
coxofemoral joint 184–91
elbow joint 130–4
patella 218–22
radial head 136, 137
sacroiliac joint 169–73
shoulder joint 111–13
stifle joint 228–31
talocalcaneal joint 249–50
talocrural joint 247–9
temporomandibular joint 268,
273–5
Lyme disease 97
lymphoma 326, 345
spinal 306–8
lysosomal storage diseases 318–19,
323, 350
magnetic resonance imaging (MRI)
22–3, 294
Maine coon cat 191, 329, 350
malformations
patella 103
spinal 316–18, 350
malleolar fracture 243
malnutrition 28
malunion
femoral diaphysis fracture 198
pelvic fracture 180–3
mammary tumor 347
mandibular fracture 261–71
body 264–70
complications 271
postoperative care 270–1
principles of repair 262
ramus 270
symphyseal 262–4
mandibulectomy 270
manipulations, specific 19
mannitol 277–8
Manx cat 306, 317, 350
Marie’s disease 341
Maroteaux–Lamy disease 319
Mason metasplint 30, 32, 61
matrix supplements 94
maxillary–mandibular fixation 268–9
maxillofacial fracture 271–3
maxillofacial mini plate 53
medetomidine 35, 36, 38
median nerve 12
megaesophagus 332
meloxicam 35, 93–4, 93, 191
meningioma 307
meningomyelitis 309, 314–15
meniscus
calcification 103, 223
tear 223
metabolic disease 318–19
bone 335–42
metacarpus 145
fracture/luxation 154–5
metaphyseal fracture 77
metasplint 30, 32, 61
metatarsal bone 244
fracture/luxation 259
methimazole 333
methylprednisolone sodium
succinate (MPSS) 278, 298, 315,
323
metronidazole 33, 41, 96, 262
midazolam 28, 38, 38
Miniature Interface pin 71
mini IMEX-SK System 69
mini plate 53
distal femoral fracture 212
femoral trochlear fracture 214
ilial fracture 174
maxillofacial 53
proximal tibial fracture 237
mini plate (continued)
scapular fracture 109, 110
Monteggia fracture 143
morphine 38
epidural 36, 36
motor neuron disease, adult onset
323
mouth
inability to open 275
open locking 277
mucin clot test 22
mucopolysaccharidosis 318–19
mucopolysaccharidosis VI
(Maroteaux–Lamy disease) 91,
319
multiple cartilaginous exostoses
(MCE/osteochondromatosis)
347–8
Munchkin cat 342
muscle atrophy 19
muscle biopsy 24
muscle tendon unit (MTU), injury
104
muscular dystrophies 329, 350
muzzle, tape 264–5, 274
myasthenia gravis 321, 332–4, 350
mycoplasmas, septic arthritis 96
myelography 286–91, 298, 308,
310–11, 313
myeloma, multiple 345
myelopathy, degenerative 318
myocarditis 26
myopathies 322, 323, 328–32
acquired 329–32
clinical signs 323
Devon Rex cat 329
hereditary 328–9, 350
nemaline (rod) 328–9, 350
paraneoplastic 332
myositis ossificans 331
myotatic reflex 282, 283, 284
myotonia 329, 350
nail trimmer, guillotine-type 158,
159
nasal bone, fracture 271–3
nasogastric tube feeding 29
neck ventroflexion 321, 323
nemaline (rod) myopathy 328–9,
350
neoplasia 17, 18, 342–8
benign 347–8
chondrosarcoma 344
feline synovial sarcoma 101–2
fibrosarcoma 344–5
giant cell tumor 344
hypertrophic osteopathy 341
neuropathies 326
osteosarcoma 343–4
paraneoplastic myopathy 332
round cell tumor 345

neoplasia (continued)
secondary/metastatic 102, 345–7
spinal 306–9
Neospora caninum 313, 332
neosporosis 313, 332
nerve biopsy 24
neurocranium, fracture 277–8
neurologic deficit, pelvic fracture
169
neurologic examination 281–6, 297
neuromuscular disease
causes 322
classification 322
clinical signs 321, 323
diagnosis 321
junctionopathies 332–4
myopathies 328–32
neuropathies 322–8
neuropathies 322–8, 322, 323
diabetic 325
iatrogenic 327–8
idiopathic 323–4
toxic 325–6
traumatic 326–7
neutering, growth plate closure 16,
341
Niemann–Pick disease
(sphingomyelinosis) 319, 323
90/90 flexion splint 30, 32–3, 215
nonsteroidal anti-inflammatory drug
(NSAIDs) 35, 36, 191, 294, 338
osteoarthritis 93–4, 93
nonunion fracture 73, 74, 82–4
causes 83
diagnosis 83–4
treatment 84
see also malunion
Norberg angle 191
nuchal ligament 13
nuclear scintigraphy 22, 41, 84
nutraceutical 93, 94
nutrition 28–9
all-meat diet 180, 337–8
calcium 335
mandibular/maxillofacial injuries
269, 270–1
rickets 340
vitamin A excess 102, 320, 339–40
nutritional secondary
hyperparathyroidism 337–9
olecranon process
fracture 142
ostectomy 133
onychectomy (declawing) 157
alternatives to 164–5
analgesia 36, 161
complications 161–4
humane issues 157
surgical technique 157–60
wound management 160–1, 163
Index
397
open fracture palatine fracture 263, 271–3
classification 44–5 palmar splint 146, 147, 150, 153
initial treatment 33–4 palmigrade stance 163
open mouth locking 277 pancarpal arthrodesis 140, 144, 148,
opioids 35, 36 152–4
epidural 36, 36 panniculus (cutaneous trunci) reflex
oral cavity injuries 262 282, 283
organophosphate toxicity 325, pantarsal arthrodesis 258–9
333–4 paraneoplastic myopathy 332
orthopedic wire 51, 51 paraparesis 307
Ortolani sign 19 paratenon 104
ossifying fibroma 347 parathyroid hormone (PTH) 335,
ossifying myositis 331 336, 337–8
ostectomy parenteral feeding 28
femoral head and neck 178 passive motion exercises 215
greater trochanter 187 Pasteurella spp. 40
olecranon process 133 Pasteurella multocida 94, 332
pelvic 182–3 patella
tibia/femur in stifle arthrodesis fracture 215–17
231–2 luxation 17, 218–22, 350
zygomatic arch 277 malformation 103
osteoarthritis 17, 86, 90–4 patellar reflex 282, 283
causes and pathogenesis 91, 209 patellectomy 216
classification 90 pedigree cats 18, 310
clinical signs 91 see also breed predisposition and
coxofemoral joint 88, 191 named breeds
defined 87, 90 pelvectomy, partial 182–3
diagnosis 21, 92–3 pelvic canal, narrowing 180, 181,
incidence 90–1 182
treatment 93–4 pelvis
osteochondrodysplasia 103, 341 fracture 167–9
osteochondroma 102, 347 acetabular 176–80
osteochondromatosis 347–8 ilial 173–6
osteochrondritis dissecans 103 ischial 180
osteogenesis 80 malunion 180–3
osteogenesis imperfecta 339, 341 pubis 180, 181
osteoinduction 80 sacroiliac joint 169–73
osteoma 347 normal anatomy 167
osteomalacia 340 osteoarthritis 88
osteomyelitis 39–42, 95, 316, 349 osteochondromatosis 348
causes 39–40, 349 osteopenia 336
diagnosis 40–1 penicillins 33, 328
prevention 41, 73 Pennington locking-loop suture
treatment and prognosis 41–2 104, 105
osteopathy, hypertrophic 341 pentosan polysulfate 94
osteopenia 49, 336, 337 perianal reflex 282, 283
osteopetrosis 340–1 periosteal proliferative polyarthritis
osteophytes 89, 91, 95 (PPP) 17, 99, 101
radiographic appearance 92 diagnosis 100
osteosarcoma 307, 343–4 treatment 101
osteosclerosis, diffuse (osteopetrosis) Persian cat 277
340–1 phalanges
overweight cat 18, 222 amputation 156–7, 259
oxygen therapy 26 fracture/luxation 155–7,
oxymorphone 35, 36, 36 259
metastatic tumor 346
packed cell volume (PCV) 26, 27 phosphorus, dietary 335, 337–8
pain physical therapy
assessment 35 acetabular fracture 178
control, see analgesia pelvic fracture 168
perception 283–4, 297, 304 spinal disorders 296
398
physis
closure 14, 15, 15, 16
injuries 16, 43, 105–6
see also growth plate
plantigrade stance 252, 325
plasmacytoma 345
plate-rod fixation 77–8, 124
femoral diaphyseal fracture 205
PMS see polyarthritis/meningitis
syndrome
podoplasty, fusion 155, 259
polyarthritis
chronic progressive (erosive
immune-mediated) 99
idiopathic 98–9
periosteal proliferative (PPP) 17,
99, 100, 101
polyarthritis/meningitis syndrome
(PMS) 98
polydactyly 349, 350
polydioxanone (PDS) 214
polyglycolide 214
polylactide 214
polymethylmethacrylate (PMMA)
72, 179, 180, 301
polymyopathy, idiopathic 332
popliteal sesamoid bone 13
postoperative care 38–9
femoral fracture 215
humeral fracture 130
mandibular fracture 270–1
patellar fracture 216
pelvic fracture 169
postural reaction 282–3
potassium, serum level 331–2
potassium gluconate 332
povidone–iodine 34, 58
pralidoxime 333–4
prednisolone 93, 94, 101, 308, 333
preoperative care
analgesia 35–7, 58
aseptic preparation 58, 59, 68
blood tests 24
sedation 38
pressure platform analysis 10, 22
prostheses
collateral ligament 151, 248
coxofemoral joint 186–7
hip joint 57, 191, 193, 195
medial glenohumeral ligament
112, 113
protein, dietary requirement 28
Proteus spp. 40
protozoal myopathy 332
pseudoarthrosis 178
Pseudomonas spp. 40
pubic symphysiotomy 181, 182
pubis
fracture 180
osteochondromatosis 347
pulmonary edema 27
pyridostigmine bromide 333
quadriceps muscle 216, 260
contracture 330–1
radial head, luxation 136, 137
radial nerve
injury in onychectomy 162
paralysis 327
radiography 19
delayed/nonunion fracture 83–4
immune-mediated arthritis 100
joint disease 88–9
mandibular fracture 261
osteomyelitis 40
postoperative 39
preoperative 58
septic arthritis 95
spinal 286, 297–8
radiohumeral joint, luxation 143
radiotherapy 308
radioulnar joint, luxation 143
radioulnar synostosis 350
radius
diaphyseal fracture 138–40
distal fracture 140–1
growth plate 16
hemimelia/agenesis 136, 350
proximal fracture 137–8
reconstruction plate 52, 212
rectal examination 168
reflexes 282–3, 282, 284–5
rehabilitation 39, 86, 296
renal secondary hyperparathyroidism
335–6
respiration 26
resuscitation 26–8
retractor 50, 170, 174
revascularization, fracture site 84
rheumatoid arthritis 100, 101
rheumatoid factor 101
rhomboideus muscle 165
rickets 340
rifampicin 97
Ringer’s solution 34
Robert Jones bandage 29, 30, 30,
31, 33, 143, 228
Rush pinning, see dynamic
intramedullary (Rush) pinning
sacral fracture 304–6
sacrocaudal hypoplasia/dysgenesis
317–18, 350
sacrocaudal luxation/fracture 304–6
sacroiliac fracture 169–73
sacrotuberous ligament 13
salinomycin 325
Salter–Harris fracture 16, 43
distal femur 209–11
humeral head 115–16
proximal femur 193–4
Salter–Harris fracture (continued)
proximal tibia 233, 235–6
saphenous vein 260
sarcoma
chondrosarcoma 307, 344
feline synovial 101–2
fibrosarcoma 344–5
locally-invasive 345
osteosarcoma 307, 343–4
sarcoma virus, feline (FeSV) 344–5
sartorius muscle 13, 198, 260
scapula
dorsal displacement 111
fracture 107–10
acromion process 108–9
body and spine 107–8
glenoid and supraglenoid
tubercle 110
neck 109–10
removal in forelimb amputation
165–6
scapulohumeral joint 10–11
Schiff–Sherrington phenomenon
285
sciatic nerve 168, 174, 179, 199
traumatic injury 327–8
scintigraphy 22, 41, 84
Scottish Fold cat 103, 257, 342,
350
screw-wire-polymethylmethacrylate
(PMMA) composite fixation 179,
180
Secur-U External Fixator Clamp 68
sedation 38
blood donor 28
trauma 26
sedative drugs 38, 38
semitendinosus muscle, fibrotic
myopathy 330
serratus ventralis muscle 111
sesamoid bones
popliteal 13
supinator muscle origin 12
Sharpey’s fibers 104
shearing (degloving) injuries
forelimb 147–8
hindlimb 250–2
principles of management 250–1
shock, hypovolemic 26
shorthair cat, domestic 218, 350
shoulder joint
anatomy 10–12
arthrodesis 113–14
luxations 111–13
range of motion 10
synoviocentesis 20
Siamese cat 310, 319, 323, 329, 350
signalment 18
size of cats 9
SLE see systemic lupus
erythematosus

sling 29–30, 29, 31–2
effect on joint motion/weight
bearing 29
Ehmer 30, 32, 185–6, 187, 191
internal in sacrocaudal injury
305–6
Velpeau 31–2, 107, 109–113,
118, 132
snake bite 334
soft tissue mineralization
periarticular 89, 92
skeletal muscle 331
soft tissue reconstruction
elbow joint 133
patellar luxation 219–20
shoulder joint 112
Somali cat 332, 350
sonography 22, 89
sphincter tone 282, 283, 304
sphingomyelinosis (Niemann–Pick
disease) 319, 323
Spica splint 30, 31, 33, 109, 111,
112, 114, 132, 133–5
spina bifida 317–18, 318, 350
spinal cord
anatomy 13, 280
decompression 294–5, 304, 306
functional regions 281–2
spinal cord lesions
diagnostic tests 286–94
differential diagnosis 285–6, 287
localization 281–5
neoplasia 306–9
treatment 294–6
spinal injuries 296–304
biomechanics and classification
296, 297
clinical signs 297
diagnosis 297–8
sacral/sacrocaudal 304–6
treatment and prognosis 298–304
spinal reflex 282–3
spinal stapling 303–4
spine
anatomy 13, 279–80
congenital anomalies 316–18, 350
flexibility 13
intervertebral disc disorders
309–12
see also spinal
splint, 90/90 flexion 30, 32–3, 215
splints 29, 29–33, 59, 61–2
application 61
care 62
effect on joint motion/weight
bearing 29
metasplint 33
palmar 146, 147, 150, 153
Spica 30, 31, 33, 109, 111, 112,
114, 132, 133–5
spinal injuries 299–300
Index
399
splints (continued) synovial osteochondromatosis 102
spoon 154, 259 synoviocentesis 20, 94
spondylosis deformans 312 syringomyelia 319
spontaneous fracture, femoral capital systemic lupus erythematosus (SLE)
physis 341–2 98
spoon splint 154, 259 diagnosis 98, 101
sprains 90, 104 treatment 101
squamous cell carcinoma 345
stance tachycardia 26
palmigrade 163 tail
plantigrade 325 amputation 306
Staphylococcus spp. 40, 58, 94 disorders 306
Steinmann pin, see intramedullary paralysis 305, 306
(Steinmann) pin tail kink 306, 350
stifle joint 218–22 talocalcaneal joint, luxation 249–50
anatomy 13 talocrural joint 244
arthrodesis 231–2 arthrodesis 255–6
arthrotomy 216, 235 luxation 13, 247–9
collateral ligament injury 225–7 tap, selection 55, 55
cruciate ligament injury 13, 17, tape muzzle 264–5, 274
208–9, 222–5 tape stirrups 60, 61
luxation 228–31 tarsocrural joint 243, 244
meniscal calcification 103, 223 tarsus
osteomyelitis 40 anatomy 13, 244–5
patella arthrodesis 255–9
fracture 215–17 fracture 245–7
luxation 17, 218–22, 350 immobilization 252, 253
malformation 103 ligament injury 105
quadriceps muscle contracture luxation 247–50
330–1 range of motion 10
range of motion 10 shearing injuries 250–2
synoviocentesis 20 synoviocentesis 20
stomatitis 270 teeth
stool softener 169 injuries 262
Stout multiple loop wiring 267 interarcade bonding 268–9
strains 104–106 wiring in mandibular fracture
Streptococcus spp. 40, 94 266–7
Streptococcus canis 315 temporomandibular joint (TMJ)
streptomycin 97 ankylosis 275–6
styloid process fracture 144 fracture 276–7
subarachnoid cyst, spinal 319 luxation 268, 273–5
subchondral bone plate 88–9 tendinopathy 104, 106
subchondral cyst 89, 91 tendon 104–6
subluxation, atlantoaxial articulation avulsion injuries 105–6, 254
318 displacement 106
sulcoplasty 220 function 104
supraglenoid tubercle fracture 110 healing 104
suprascapular nerve 108, 109, 113 repair 104–5
suture tendon stretch (myotatic) reflex 282,
hip luxation 190–1 283
patellar luxation 219 tenectomy, deep digital flexor
tendon injuries 104–5 tendon 164–5
synovial cyst 102 Tensilon test 333
synovial effusion 19 tension band wire fixation 64
synovial fluid acetabular fracture 179, 180
analysis 21–2, 21, 92–3 calcanean fracture 245–6
bacterial arthritis 95 greater trochanter 197
cytology 21–2, 21, 101 humeral fracture 115
immune-mediated arthritis 100, patellar fracture 216–17
101 proximal tibia fracture 234
synovial membrane, biopsy 90, 101 radial fracture 140, 141
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tension band wire fixation transfixation pin (continued) wire (continued)
(continued) full pin 67 gauge and diameter 51
sacroiliac luxation 173 half pin 67 orthopedic 51, 51
scapular fracture 108–9, 110 loosening 73 see also cerclage wire; Kirschner
shoulder arthrodesis 114 negative profile thread 55 wire; tension band wire
stifle arthrodesis 232 positive profile thread 55, 56, 67 wound dressing 148, 252
tetanus, local 328 size 55, 56, 56 wound
tetracycline 96 transfusion, blood 27–8 bacterial myositis 332
tetraparesis 307 trapezius muscle, rupture 111 bite 17, 94–6, 332
‘T’-fracture trauma patient 25 debridement 34
distal femur 212 history taking 18 infection 40, 332
distal humerus 128–30 physical examination 25–6 initial management 33–4
thermoregulation 39 triceps brachii muscle 12 lavage 34, 147, 251
thoracic injuries 25, 167 triceps tendinopathy 106 onychectomy 160–1, 163
thoracodorsal nerve 165 triceps tendon 166 septic arthritis 94–6
three-loop pulley suture 104, 105 Trilam nail 51 shearing injuries 147, 148, 250–2
thromboembolism, arterial 324–5 trochlear notch fracture 142–3
thymectomy 333 trochlear wedge recession 220 xylazine 35, 38, 38
thymoma 332, 333, 341 trochleoplasty 220–1
thyroid hormones 333, 337 tuber calcis, tendon injuries 252–3 ‘Y’-fracture, see ‘T’-fracture
tibia tubercular arthritis 97
diaphyseal fracture 238–42 tumors see neoplasia zygomatic arch
distal and malleolar fractures tylosin 96 fracture 273
242–3 partial ostectomy 277
osteomyelitis 40 ulna
proximal fracture 233–8 distal physis 16
tibial compression test 19, 223 exostoses in hypervitaminosis A
tibial plateau fracture 235–6 339
tibial tubercle, avulsion fracture fracture 137, 141–4
233–5 osteomyelitis 40
tibial tuberosity, transposition 221–2 ulnar nerve 12
tick paralysis 334 ultrasonography 22, 89
tissue necrosis undernutrition 28
external fixation 73 ungual crest, removal 158, 159
onychectomy 163 urethral sphincter tone 283, 304
TMJ see temporomandibular joint urinary function 283, 305, 306
toggle rod fixation, coxofemoral
luxation 188–9 vaccination, calcivirus 96
tolfenamic acid 93 vastus lateralis muscle 13, 177, 178,
total hip replacement 57, 191, 193, 198, 199
195 Velpeau sling 31–2
tourniquet 156, 162 application 32
toxicities 325–6, 333–4 indications 107, 109, 110, 111,
Toxoplasma spp. 314 112, 113, 118, 132
Toxoplasma gondii 313, 332 ventral neck flexion 321, 323
toxoplasmosis 313, 332 vertebrae
T plates 237 anatomy 279–80
traction 58–9 angiomatosis 319–320
transarticular external skeletal fixator fracture/luxation 296–304
(TESF) 56, 86 veterinary cuttable plate (VCP)
elbow joint 134, 135 53–4, 107
hinged 56 vincristine 308, 326
ligament repair 105 viscosupplement 94
transarticular pinning vitamin A, excess 102, 320, 339–40
coxofemoral joint 188 vitamin D 335
elbow joint 133–4 deficiency 340
shoulder joint 112
stifle joint 228–9 weight bearing, effects of external
transdermal fentanyl patch 37 coaptation 29
transfixation pin 55–6, 67 wire 51
acrylic fixator 71 arthodesis 51