DEFORMITY

AROUND KNEE
Presented by Dr Amitabh Das
Deformity around knee
 Genu valgum or ‘Knock knee’
 Genu varum or ‘Bowleg’
 Genu recurvatum or ‘hyperextented knee’
 Triple deformities
 Flexion deformity
 How to assess genu varum
 Patient sits at the edge of the couch with both
legs extended.
 In neutral position of the limb, hold the ankles
from behind.
 Try to approximate both malleoli so that they just
touch each other.
 Normally, they touch before the inner surfaces of
the knees come together, rather, there should
be on an average 0.5 cm gap between the
medial surface of the knees.
 If the gap is more(In 10-16 age group <4 cm in
female & <5 cm in male is regarded as normal)
deformity is genu varum.
 For unilateral varus, the distance between the
centre of the medial surface of medial condyle
& central plumb line of the body is measured.

How to assess genu valgum
 Patient sits at the edge of the couch with both
legs extended.
 In neutral position of the limb, hold the ankles
from behind.
 Try to approximate both knee so that they just
touch each other.
 Normally, both knee & malleoli should touch but in
knock knee, there is a gap between both
malleoli(In 10-16 age group, <8 cm in female &
<4 cm in male is regarded as normal) & the gap
is measured.
 For unilateral valgus, the deviation medial
malleolusfrom central plumb line of the body is
measured.


How to assess genu valgum
 Ifthe medial surface of the two knees touch
each other before the medial malleoli can
come together, the deformity is genu
valgum.
 For unilateral valgus, the deviation medial
malleolusfrom central plumb line of the
body is measured.
How to assess genu valgum
Q – angle:-

This is an angle (normal-6 degrees) between,

-a line joining ASIS with centre of
the patella

-the line of the patellar ligament



If there is knock knee this angle

is increased
How to assess the pathology in
lower femur or upper tibia
 Ask the patient to sit
in squatting
position. If
deformity
completely
disappears, the
total fault lies in
the lower femur. Standing position showing genu varum

 If it disappears
partially or does
not disappear, the
fault will be in both
components

In squatting position genu varum partially disappeared

 Definition:-



Genu varum or bow leg is a lateral
curvature of the leg which involves either the
tibia, the femur or both

A minor degree of deformity is very
common & may be regarded as normal in a
child of 3 years of age or less.
 PHYSIOLOGIC GENU VARUM
 Invast majority of
cases genu varum
corrects by itself
with growth.
 Mostly bilateral &
symmetrical
 Normal knee alignment
10-15 degrees of
varus, which
progresses to neutral
alignment at about
18 months of age.
 PHYSIOLOGIC GENU VARUM

 The appearance of
genu varum
frequently is
exacerbated or
accentuated by
concurrent internal
tibial torsion.
 An angle that measures
<15 degrees is an
indication of tibial
torsion.
 PHYSIOLOGIC GENU VARUM
 Most report that persistence of genu varum
beyond 2 yrs of age is abnormal, however,
spontaneous correction of physiologic
genu varumwill occasionally be delayed
until 30 months of age.
 Even pronounced physiologic genu varum
> 30 degrees can correct with continuing
growth.
 Over correction to excessive genu valgum is
maximal at 4 yrs of age, & valgus
angulation averages 8 degrees.
 EVALUATION
 Observe  Deviation of leg axis
the alignment
of the leg component outwards is called
to the thigh valgus & inward is
component. called varus
 Normally mid inguinal
point, centre of
patella & mid ankle
joint are in one line,
& if prolonged it
should pass through
second web.

 EVALUATION
 Anexcessive amount of bowing is often more
apparent than real from internal rotation
of the legs as occurs with persistent fetal
ante-version of the femoral necks or from
obliquity of the tibial epiphysis.
 TREATMENT
 Periodic observation, examination & follow
up.


 Education & reassurance of the parents.


 Corrects with growth after 3 years of age &
required no treatment.

 Definition:-



Genu valgum or knock knees,is the
medial curvature, such that when the knees
are touching, the ankles are separated.

A minor degree of deformity is very
common & may be regarded as normal in a
child of 3 years of age or less.

 PHYSIOLOGIC GENU VALGUM
 Morley (1957) found that between the age of
3-3 ½ years of children having knock knee of
5 cm or more as measured by the distance
between medial malleoli with the extended
knees just touching each other.
 The laxity of medial collateral present in young
children accentuates the deformity when the
child is standing.

 PHYSIOLOGIC GENU VALGUM
 Indetermining the true angles
of the weight bearing knee joint
it is necessary to take a frontal
radiograph of both complete
lower extremities standing so
that the continuation of the
tibialaxis can be followed up
to & through the centre of

femoral head.
 Unilateral genu valgum or severe bilateral genu
valgum, where inter-malleolar distance
exceeds 10cm, should be examined radio
logically to determine whether there is any
disturbance of epiphyseal growth

 TREATMENT
 Periodic observation, examination & follow
up.
 Education & reassurance of the parents.
 Physiologic genu valgumresolves
spontaneously by the age of 7-8 years
without treatment.
 In rare cases of uncorrected physiologic
genu valgum > 20 degrees or more than 10
cm separation between malleoli,
epiphysiodesis & osteotomy may be
indicated.
 Supra-condylar osteotomy of femur or
merely tibial osteotomy is done depending
upon maximum deformity.

 BLOUNT`S DISEASE
 Tibia vara is most frequent non-physiologic
cause of genu varum in children &
adolescents.
 It is considered to be a developmental
condition, which affects posteromedial
aspect of the proximal medial tibial physis,
resulting in a progressive varus deformity.
 Afro-Caribbean with h/o early walking are usually
affected.
 TYPES
 Early onset :-
 - It is difficult to
diagnose in its early
form until 2 yrs of age,
when x-ray changes
shows epiphysis is
sloping & may be
fragmented on the
medial side, & is
accompanied by a
characteristic beak
like curving of medial
metaphysis.

 TYPES
 Late onset :-
 -Complete
metaphyseal arrest,
can occur by the
age of 6.
 -Angular
deformity &
tibialshortening is
seen.

 PATHOLOGY
 Biopsy of the lesions reveals disorganized
physeal cartilage with abnormally large
group of capillaries, densely packed
hypertrophic chondrocytes, & island of
almost acellular fibrous tissue.
 Both fibrovascular & cartilagenous
reparative tissue can be found at the
physeal-metaphyseal junction .
 RADIOLOGY
 Langenskjold (1975) divided radiographic
changes into various age group:-

-Up to 3 years, there is irregularity of
metaphyseal edge.

-Up to 6 years epiphyseal plate is widened
& fragmented.

-Up to 10 years medial plate is growing
inwards & downwards into metaphysis.

-At the age of 12 years medial tongue of
cartilage divides off & finally unites with tibia
metaphysis on medial side, leaving lateral
component still open.
 TREATMENT
 Brace is useful in correcting mild deformity in
patients younger than 3 yrs.
 Early valgus osteotomy before 4 yr with mono
lateral plate or circular external fixation is
done.
 Lateral epiphysiodesis for adolescent with
significant growth remaining.
 Interposing an inert material such as fat has been
described by Langenskjold.
 However, osteotomy is frequently indicated to
prevent a secondary pressure phenomenon on
the joint cartilage & balancing of the knee with
growth & in severe cases repeated
osteotomymay be necessary.
 SKELETAL FLOUROSIS
 Consumption of high intake of endemic fluoride
in the drinking water from birth can cause genu
varum or genu valgum.

 The toxic-effects of fluoride were severe and
more complex and the incidence of metabolic
bone disease (rickets,osteoporosis) & bony leg
deformities (genu valgum, genu varum,bowing,
rotational & wind-swept) was greater (>90%) in
children with calcium deficiency as compared to
<25% in children with adequate calcium who
largely had the osteosclerotic form of skeletal
fluorosis with minimal secondary
hyperparathyroidism.

 SKELETAL FLOUROSIS
 Drinking water supply with fluoride <0.5 ppm
and improvement of calcium nutrition
provide protection against the toxic effects
of fluoride and are recommended as the cost
effective and practical public health
measures for the prevention and control of
endemic fluorosis
 RICKETS

Definition:- It is a metabolic disease of
childhood & is characterized by defective
mineralization of bone matrix at growth
plates.

The organic matrix of bone, fails to
mineralize due to interference with
calcification mechanism.

 pathophysiology
 Defective vitamin D metabolism leads to
lowering of serum1,2-dihydroxyvitamin D
(OH)2 D (calcitrol), which in turn causes
intestinal malabsorption of calcium.
 The normal calcium homoeostatic mechanisms
initially defined the serum level of calcium
so that urinary excretion is reduced.
 The serum calcium falls despite the reduction
in excretion & this stimulates the
parathyroid glands to produce parathyroid
hormone (PTH) which tends to normalize
serum calcium at the expense of reducing
serum phosphate.Therefore
hypophosphataemia may be marked.
 AETIOLOGY
 Poor vitamin D & calcium intake.
 Lack of exposure to sunlight.
 Impaired renal function e.g. glomerular
failure or renal osteodystrophy.
 Defective vitamin D absorption such as in
coeliac diseaese or biliary obstruction.
 PATHOLOGY
 The bone of the skeleton are soft & porotic, &
bend from the body weight or other external
cause.
 Epiphyseal line of the long bones forms a
wide irregular band & metaphysis is broad &
irregular from excessive proliferation of the
cells of epiphyseal line.

The cartilage in the proliferating zone is
hyperplastic, but instead of the normal
palisade arrangement of the cells, the
proliferating cells are arranged more
haphazardly. Extent of zone is increased.
 PATHOLOGY
 In the zone of calcified cartilage the deposit
of calcium salts in the intercellular matrix is
greatly deficient or even absent.
 In zone of ossification the bone deposited by
the osteogenic cells from the diaphysis is
poor in quality, deficient in calcium & of
patchy distribution. Bone resorption may be
increased & replaced by fibrous tissue.
 In the metaphysis the bony trabeculae are
weakened by lack of calcium, the continued
strain stimulates connective tissue
hyperplasia so that the extremity of bone
appears mis-shapen & unmodelled
 DEFORMITIES
 Enlargement of long
bones give rise to
swelling at the bone
ends, prominent at
the costochondral
junctions, & at the
lower end of tibia.
 The tibia gets bowed,
assuming the knee a
valgus attitude or
both valgus or
varusattitude (wind
sweep deformity).


 CLINICAL FEATURES
 Bone pain, so marked that patient awake at night
 Proximal muscle weakness
 Pigeon chest
 Large head with broadened forehead, open
frontanelles & craniotabes.
 Harrison’s sulci
 Rickety rosary
 Pectus excavatum
 Protrubent abdomen
 Delayed dentition
 Wind sweep defomity


 RADIOLOGICAL APPEARANCES
 Epiphysis:-

-Delayed
appearance of
epiphysis and
widening of epiphseal
plate, it lacks a bony
cortical margin &
appears indistinct.

-There may be
epiphyseal separation

 RADIOLOGICAL APPEARANCES
 Metaphysis:-
 -Splayed out giving
Champagne glass
appearance ( widening and
cupping of the distal ends
of long bones) also called as
trumpeting.
 -Zone of calcification
instead of forming a well
defined area, is irregular &
of low density.
 -Its end appears
arranged in longitudinal
rows (fraying or streaking)

 RADIOLOGICAL APPEARANCES
 Diaphysis:-
 -There is generalized
decalcification of bones
resulting in increased
radioluency between the
diaphysis & epiphysis
 -Space between
diaphysis and epiphysis is
increased.
 - Deformity and bowing
of the ends of long bones.
 - Decreased density of
cortex ( rarefraction
trabecular pattern is
course)

 LABORATOY FINDINGS
 calcium level is normal or deceased (due to
compensatory hyperparathyroidism)


 serum phosphorous is low.


 
 Alkaline phosphates is normal.


 Urinary calcium is low


 
 Serum 25 – hydroxycholecalciferol is
decreased

 TREATMENT

Prevention:-
 -Adequate exposure of sunlight & consumption
of food rich in vitamin D like milk,cheese
etc.
 -Daily requirement of vitamin D is10 mcg

(400 I.U.)
 Active treatment :-
 -oral or parental administration of vitamin D
 In active stage 15,000 mcg (60,0000 I.U)
 In milder cases 50-150 mcg (2000-6000 I. U)
 Adequate intake of calcium is ensured

It takes 2 -4 weeks for x- ray healing
 DEFORMITY CORRECTION
 Correction by splinting:

This method is used where deformity is
slight & disease still active.
 Correction by osteotomy:

Before surgery, management of
metabolic defect with vitamin D, phosphorus
& calcium should be carried out for several
month.

Traumatic deformity of knee


 Distal femoral physeal fracture




 Proximal tibial physeal fracture
 Distal femoral physeal
injuries
 It account for 6-9 % of all physeal injuries
(SALTER-HARRIS TYPE).






 Angular deformity following distal femoral
physeal injury accounts 18% - 51%
 Angular deformity in distal
femoral physeal injury
 Progressive angulation
after of distal femoral
epiphysis is usually
caused by
 -asymmetric growth
from either trauma to
the physis at the initial
injury, (Salter-Harris
Type I or II)
 -physeal offset with
bony bar formation after
healing, (Salter-Harris
Type III or IV)



Angular deformity in physeal
injury
 Risk of angular
disturbance is highest
in patient with
significant growth
remaining.
 If the separationis a
Salter-Harris Type II
injury, the physis distal
to the triangular
metaphyseal fragment
usually is spared.
 The localized area of
growth inhibition
occurs in that portion
of the physis not
protected by the
physeal fragment
 TREATMENT
 If a localised area of premature arrest
constitutes < 25% - 50% of the total area of
the physis & if at least 2 year of growth
remain, excision of the bony bridge
recommended.

-Kasser recommends that simultaneous
corrective osteotomy should be performed
when angular deformity exceeds 20 degrees.


 Physeal resection about the distal femur has

a high rate of failure, & one should consider
epiphysiodesis in adolescents.
 TREATMENT
 Hemiepiphysiodesis may be considered in
maturing adolescents with progressive varus
or valgus angulation associated with a
central bony bridge with some remaining
growth medially or laterally.

 If patient is approaching skeletal maturity,
corrective osteotomy (open wedge) is
preferred treatment.
 Angular deformities in
proximal tibial physeal injury
 Incontrast to distal femoral physeal injury
proximal tibial physeal injury is rare, as it
has got a intrinsic anatomic stability.
 On lateral aspect, it is butressed by u/e of
fibula.
 Anteriorly, the tubercle projects down from
the epiphysis to overhang the adjacent
metaphysis.
 Angular deformities in
proximal tibial physeal injury
 Similar to distal femoral
physeal injury, injuries to
proximal tibial epiphysis
may cause shortening or
angulation from
subsequent growth
inhibition.
 -This can occur in all
four types of Salter-Harris
injuries.
 -The amount of
angulation depends on the
proximity of the area of
growth arrest to the
periphery of the physis &
the year left for growth
after injury

 TREATMENT
 If the area of growth arrest is localized to less
than a third of the total area of the physis &
at least two years of growth remain,
resection of the bony bridge may be
attemted.
 Alternatively, epiphysiodesis or stapling of
the side of the physis opposite a peripheral
bar may stop progression of the deformity.
 Existing deformity at the time of surgery may
require proximal tibial osteotomy.
 If there is significant valgus deformity an open
- wedge osteotomy can be done.
 DEFORMITY OF KNEE IN
OSTEOARTHRITIS
 Osteoarthritis(OA) is characterized by
degenerative changes in the articular margin
of diarthrodial joints & subsequent new
bone formation at the articular margins.
 AETIOLOGY
 Age:- loss of mechanical resistance of ageing
cartilage, due to a defect in stabilizing
components of the matrix.
 Sex:- Female are more affected than male.
 Occupation:- manual labourer, factory
workers are more affected due to
continueing using their joints even after
muscular exhaustion.
 Obesity:- failure of subchondral bone to
deform with an impact load, leading to
increased load, leading to increase cartilage
damage.
 AETIOLOGY
 Metabolic factors:- Diabetes &
hyperuricaemia has been found associated
with OA.
 Mechanical factors:- mechanical stress, such
as single impact stress, gross anatomical
damage, subtle mechanical dearrangement,
joint hypermobility etc found to be
associated with OA.
 Development factors:- CDH, Perthes’s
disease, SCFE found to be associated with
OA.
 AETIOLOGY
 Genetic influences:-OA often affects multiple
members of the same family, suggesting that
there is hereditary susceptibility to this
condition. A number of studies have shown
that there is a greater prevalence of the
disease between siblings and especially
identical twins, indicating a hereditary
basis.
 PATHOLOGY
 The primary lesion consists of degeneration of
hyaline cartilage.
 The cartilage easily & rapidly eroded until the
bone matrix is exposed.
 First areas of bone are exposed in a patchy
fashion.
 The perichondrium & the cartilage round the
periphery of the joint are stimulated into
activity, & as a result, the non articular areas of
bones are elevated above the remainder of the
substance known as ‘lipping’.
 In addition, irregular outgrowth appears in this
area, at first cartiliginous but eventually ossified
to form osteophytes.


 PATHOLOGY
 There is synovitis with fibrosis involving the
capsule & sub synovial connective tissue.
 Synovial membrane & capsule are involved in
later stages, & are the site of inflammation &
adhesions.
 The synovial tags or polypi are insinuated into
the joint, & when very exuberant insinuated
into the joint, & when very exuberant the
process is called “lipoma arborescens”.
 Occasionally, cartilage formation occurs in this
tags & they are then liable to be broken off into
the joint, forming loose bodies.
 PATHOLOGY
 The exposed bone ends of the articular
surface are subjected to considerable
friction; in consequences the bone
trabeculae in the immediate neighborhood
fracture & repair & the marrow spaces are
obliterated.
 The change involves only a thin layer abutting
the joint, & when the surface of this layer
gradually becomes more & more smooth &
polished due to continue rubbing, the
process is known as eburnation.
 CLINICAL FEATURES
 Low grade aching & stiffness experienced
after rest, due to inflammation of synovial
membrane, resulting joint effusion &
dissappear after some movements.
 Pain due to reflex muscle spasm occurs to
protect the joint from unnecessary
movement.
 As the disease progress, there is hyperaemia
& venous stasis in the bony surface,
producing continuous pain & is not relieved
by rest or exercises, crepitus may be felt.
 With muscle spasm & capsular contracture
angular deformities become established
result in varus or valgus deformities of
knee.

 RADIOLOGIC CLASSIFICATION OF
OSTEOARTHRITIS

Weight bearing x-rays are taken,


 GRADE DESCRIPTION


 KNEES


0 Normal

 1 Doubtful narrowing of joint space & possible osteophytic lipping

 2 Definite osteophytes & possible narrowing of joint space

3 Moderate osteophytes, definite narrowing of joint space, sclerosis &
 possible deformity of bone ends
 4 Large osteophytes, marked narrowing of joint space, severe sclerosis

& definite deformity of bone ends. Sub chondral cysts may be present
 TREATMENT
 CONSERVATIVE:-

-NSAID’s

-Regular exercises

-Weight control


 OPERATIVE:-

-Arthrodesis~giving pain relief & stability
but no mobility.

-Osteotomy~giving pain relief, stability &
maintaining mobility.

-Arthroplasty~TKR giving pain relief,
stability & mobility.

-Joint debridement & drilling.

-Joint surface allografting.
 GENU RECURVATUM
 Congenital deformity of knee or genu
recurvatum is a rare condition since the
time of its first description by Chatelain & is
characterized by hyperextension of the
knee.
 types
 There are three types:-
 -Traumatic developmental type:-
 most common & is due to malposition in
utero, legs may be caught by the chin or axilla
with the knees extended & uterine compression
may prevent them from assuming the usual flexed
position.

-A primary embryonic defect:-

usually accompanied by other defects,
such as hare lip, cardiac defect, spina bifida, CDH
etc.

-Contracture:-

of the quadriceps extensors muscle
dragging the knee into a deformed position.

 CLINICAL FEATURES
 Knee fixed in hyperextension with varying
degree of subluxation or dislocation
forwards of the tibia on femoral condyles.
 Skin over the anterior aspect of of joint shows
several transverse creases.
 Patella is small or absent.
 On posterior aspect both femoral condyles &
hamstrings (as tense cords) are palpable.
 There may be wind sweep deformity.
 TREATMENT
 Proximal tibia related to distal femur, but
knee is markedly hyperextended:-

-In this type treatment starts at birth or
thereafter.

-Plaster cast is applied, flexing the knee as
much correction as possible.

-Repeated at 2-3 days intervals until
flexion beyond 90 degrees is obtained.

-Thereafter a bivalved cast is used for
flexion & extension exercises twice a day at
30 minutes interval for 3 months.
 TREATMENT
 Proximal tibia dislocated forwards in relation
to distal femur:-

-Manipulation & casting is done, but if
redution is not accomplised, then surgical
intervention is indicated e.g.

-Osteotomy

-Triple tenodesis
 Triple deformity of knee
 Is described as in
flexed position of
the knee, the tibia
subluxates
posteriorly &
laterally & also
rotates laterally
over the femoral
condyle. Gradually
leg also goes in
valgus.

Thus though it has
been identified as
triple subluxation,
actually it is a
“quadruple deformity
complex.
 PATHO DYNAMICS
 The flexed attitude of the knee joint is a
protective position & position of rest.
 Therefore in any painful condition there is early
tendency of spasm of the hamstrings.
 This position allows enough of posterior space in
knee joint for collection of blood or exudates.
 The posterior capsule starts contracting with this
flexed attitude.
 This allow further mechanical benefit to
hamstrings, specially the biceps & iliotibial
band, which now became the main flexors of
joint.
 PATHO DYNAMICS
 While lying down patient tries to keep the hip
in external rotation, till the outer part of
the knee rest on a support or couch.
 In this position gravity assisted contraction of
the IT-band helps in outer subluxation of
the tibiofibular component.
 Taking further advantages, the IT-band &
bicep femoris contracts further & therefore
fibulotibial component rotates laterally.
 Above deforming forces pull the leg outwards,
i.e. in valgus.
 CAUSES

Main causes are:-

 Tuberculosis


 Rheumatoid arthritis


 Postural contracture
 Triple DEFORMITY IN
TUBERCULOSIS
 Tuberculosis of knee is second in frequency of
hip joint.

Two anatomical points to be noted are
large extent of synovial membrane, & the
marked vascularity due to late junction of the
femoral & tibial epiphyses. Much growth of
the leg takes place in this region.
 PATHOLOGICAL ANATOMY
 The disease may begin
either in bone, usually in
the femoral or tibial
epiphysis or in the
patella or synovial
membrane, later being
the most frequent site.
 -The synovial membrane
is thickened, grey &
translucent, & in places
gelatinous or even caseous.
 -Fluid is present in
varying amount, &
adhesions form so that the
outlying synovial pockets
become loculated.

 PATHOLOGICAL ANATOMY
 -Granulations spread
under & over the cartilage,
which, being eroded by
pressure & friction, may
become detached, leaving
the bone exposed.
 -At the same time,
softening & stretching of
the ligaments tend to
produce subluxation of the
tibia, which slips backwards
& rotates laterally(triple
deformity).
 -Inflammation takes
place leading to thickeing
of the joint, so called
spindle-shaped tumor,
known as ‘white swelling’
is formed

 CLINICAL FEATURES
 Pain associated with night cries.
 Swelling of the joint due to
synovial thickening & presence
of fluid.
 Limping
 Muscular atrophy & spasm
 Shortening in early stage cause
lengthening by stimulating
growth locally, but in more
destructive lesion shortening
is the rule.
 TREATMENT
 Conservative treatment:-

-skin traction

-Thomas splint with knee flexion piece
applied, which allows the pull to be made in
the line of deformity, & as treatment
progresses, it can be adjusted daily until full
extension is obtained.

-Care must be taken to avoid backward
rotational displacement of tibia & is achieved
by reverse dynamic sling.

-AKT should be started
 TREATMENT
 Operative treatment:-

-Extra-articular abscess should be drain out

-Synovectomy, in those whose knees
remain warm & swollen after conservative
treatment.

-Arthrodesis,where there is marked
destruction of joint.
TRIPLE DEFORMITY IN RHEUMATOID
ARTHRITIS
 DEFINATION:-


It is a systemic disease of young and
middle aged adults characterized by
proliferation and destructive changes in
synovial membrane, periarticular
structure, skeletal muscle & perineural
sheaths . Eventually the joint are fused and
ankylosed . It is widespread vasculitis of
 PATHOLOGY
The earliest changes is swelling and

congestion of synovial membrane & the

underlying connective tissue, which becomes
infiltrated with lymphocytes, plasma cells &
macrophages.
Effusion of the synovial fluid into joint space

takes place during active phase of the

disease.
Hypertrophy of synovial membrane occurs
 PATHOLOGY
Later fibrous adhesion takes place between

the layers of pannus across the joint space

and fibrous ankylosis may occur.
Microscopically the subcutaneous nodules

shows central area of fibrinoid necrosis

consisting of swollen & fragmented collagen
fibers fibrinous exudates & cellular debris ,
surrounded by palisade of radially, arranged
proliferating mononuclear cells.
 CLINICAL FEATURES
 Multiple joints pain
 Morning stiffness
 Knee joint is tender & swollen
 As disease progress there is limitation of joint
movement.
 Flexion deformity accommodate the swollen &
proliferating tissues with reduction in pain.
 With further progress there is more loss of
cartilage & subchondral bone with
subluxation of joints.
 RADIOLOGIC FINDINGS
 Juxta articular
osteoporosis
 Erosion of joint
margin
 Joint space is
decreased
 Subchondral erosion
& cyst formation
 Fibrous & bony
ankylosis in later
stage

 TREATMENT
 CONSERVATIVE:-

-NSAID’S

-DMARD’S

-Splints & braces

-Physical therapy
 OPERATIVE:-

-Arthroscopic synovectomy

-Open synovectomy

-Proximal tibial osteotomy

-Arthrodesis

-Total joint arthroplasty

 HEMOPHILIC ARTHRITIS


 HEMOPHILIA:-

-Definition:- It is characterized by a
bleeding diasthesis due to the defect in the
clotting mechanism of blood
 PATHOGENESIS
 Repeated hemorrhages into joint produce
synovial hyperplasia, haemosiderin
deposition & fibrous scarring.
 Increased intra-articular pressure due to
haemarthrosis produce intra-articular
adhesion result reduction of joint cavity &
limitation of movements.
 Restriction of motion will reduce the
circulation of nutrients in articular cartilage
& lead to progressive articular cartilage
breakdown.

 CLINICAL FEATURES

The common orthopedic manifestation are,
 Hemorrhages into joint:- there is sudden
attack of haemarthosis in joint following
minimal trauma, the bleeding occurs not
only inside the synovial cavity of joint
but also there is intra-osseous
hemorrhages from subchondral bone.
 Pain & gross deformity at knee
 Loss of movements

 CLINICAL FEATURES
 Fixed flexion
contracture at knee
 Valgus & external
rotation
deformities are
seen
 In late stages the
deformity increases
with posterior
sub-luxation of
tibia & lateral shift
of tibia on the
femur

 RADIOLOGIC FINDINGS
 Early Stage:-

- distended synovium

- no para articular
 skeletal deformity.
 Intermediate stage:-
 -persistent boggy
swelling

- osteoporosis
 -sub-chondral cyst
 -squaring of patella
 -inter-condylar notch
 is widened



 RADIOLOGIC FINDINGS
 Late stage:-
 -Osteoporosis
 -Epiphyseal overgrowth

-Subchondralbone
collapse
 -Cyst formation
with marginal
osteophyte
 formation
 -posterior sub-luxation
of tibia & lateral shift
of tibia on the femur



 POLIOMYELITIS
 Poliomyelitis was recognized as a clinical
entity in the first half of the nineteenth
century.

It is an acute infectious disease occurring
sporadically or in epidemics & is caused by
polio virus.
 treatment

This varies according to stages:-

Acute Stage:- correcting factor deficiency by
-whole blood

-FFP

-Cryoprecipitate

-joint aspiration & R-J Bandage

-immobilization with splint

Late Cases :- prolonged immobilization with

-caliper or splint

-trial aspiration.

-Reversed dynamic traction

Surgical Method:-
-Fresh Frozen Plasma And Blood
-Tranfusion
-Synovectomy
-Supracondylar osteotomy for severe
flexion contracture
-Arthrodesis
-lengthening or release contractures
-Joint replacement
 PATHOGENESIS
 Poliovirus once established in the CNS, has
special affinity for the anterior horn cells of
the spinal cord & for certain nuclei in the
brain stem.
 The early visible changes is chromatolysis of
the Nissl substance in the cytoplasm of the
nerve cell.
 This is followed by inflammatory infiltrations
of polymorphonuclear & mononuclear cells
at first in the perivascular regions & then
diffusely in the grey matter.
 There is destruction of nerve cells in the
anterior horn, peripheral nerve degenerates
& muscle supplied by it atrophy.
 PATHOGENESIS
 Tendons atrophy from disuse & lose their
normal glistening appearance.
 Considerable degree of osteoporosis is found
in bone.
 Joint capsules & ligaments when not
protected by healthy muscles become
stretched, the joint became unduly mobile
& may dislocate.

 Deformity of knee joint
 Inacute & early recovery stages of
poliomyelitis passive movement is limited by
pain & muscle spasm, due to the contraction
of hamstrings which limits SLR to 30
degrees.
 The spasm can be aggravated by nerve tests,
e.g. Lasegue & Kernig

Limitation increased
Limitation of SLR by dorsiflexionof foot
(Lasegue test)
 Deformity of knee joint
 Due to limitation of movements at knee due
to pain there is gradually contracture of the
muscles, commonest is iliotibial band &
flexion deformity at knee persists.
 It may also result from paralyzed quadriceps
in the presence of stronger hamstrings.
 Paralysed quadriceps also can cause genu
valgum & genu recurvatum
 treatment
 Flexion deformity:-
 Wedge plasters
 Rest of the limb in Thomas splint
 Reversed dynamic traction
 Division of IT Band
 Tendon lengthening

Knock knee
 Osteotomy

Genu recurvatum
 Proximal tibial osteotomy with transfer of
hamstrings to patella.
 Arthrodesis

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