Review Article

Intrinsic Contracture of the Hand:

Diagnosis and Management

Abstract
Rick Tosti, MD Intrinsic contracture of the hand may result from trauma, spasticity,
Joseph J. Thoder, MD ischemia, rheumatologic disorders, or iatrogenic causes. In severe
cases, the hand assumes a posture with hyperflexed
Asif M. Ilyas, MD
metacarpophalangeal joints and hyperextended proximal
interphalangeal joints as the contracted interossei and lumbrical
muscles deform the natural cascade of the fingers. Considerable
disability may result because weakness in grip strength, difficulty
with grasping larger objects, and troubles with maintenance of
hygiene commonly encumber patients. Generally, the diagnosis is
made via history and physical examination, but adjunctive imaging,
rheumatologic testing, and electromyography may aid in
determining the underlying cause or assessing the severity.
Nonsurgical management may be appropriate in mild cases and
consists of occupational therapy, orthoses, and botulinum toxin
injections. The options for surgical management are diverse and
dictated by the cause and severity of contracture.

I ntrinsic contracture of the hand is

From the Department of
Orthopaedic Surgery, Temple
University, Philadelphia, PA (Dr. Tosti
and Dr. Thoder), and the
Department of Orthopaedic Surgery,
the Rothman Institute, Philadelphia
(Dr. Ilyas).
Dr. Ilyas or an immediate family
member serves as a paid consultant
to Integra LifeSciences. Neither of
the following authors nor any
immediate family member has
received anything of value from or
has stock or stock options held in a
commercial company or institution
related directly or indirectly to the
subject of this article: Dr. Tosti and
Dr. Thoder.
J Am Acad Orthop Surg 2013;21:
581-591
http://dx.doi.org/10.5435/
JAAOS-21-10-581
Copyright 2013 by the American
Academy of Orthopaedic Surgeons.
a condition in which adherent, fi-
brotic, or contracted interosseous
and lumbrical muscles result in an
imbalance of the viscoelastic forces
about the extensor mechanism and
cause stiffness, deformity, and/or dis-
location of the fingers. Although a
spectrum of severity exists, severe
cases deform the finger into a pos-
ture in which the metacarpophalan-
geal (MCP) joint is flexed while the
proximal interphalangeal (PIP) joint
is extended. Additionally, dislocation
of the MCP joint may occur in rheu-
matoid patients with concurrent syn-
ovitis.
In mild cases, the patient may per-
ceive a feeling of weakness or tight-
ness when attempting to grasp a
large object because the contracture
hinders PIP joint flexion while the
MCP joint is extended. Synonymous
terms used to describe the same
pathomechanics are intrinsic plus
hand or hyper-intrinsic hand. Intrin-
sic tightness describes a less severe
process in which PIP joint flexion de-
ficiency is still passively correctable.
While observing a greater fre-
quency of intrinsic hand deformities
following World War II, Bunnell ex-
panded on the first description of in-
trinsic hand contracture presented by
Finochietto in 1920.1,2 In the early
descriptions, intrinsic contracture
was thought to occur from ischemia.
However, subsequent observations
have identified a variety of etiologies
that additionally include trauma, in-
fection, burns, injection injuries,
compartment syndrome, stroke and
cerebral palsy, rheumatoid arthritis
(RA), lumbrical plus finger, and pain
syndromes.1-8 Importantly, patients
with intrinsic contracture of the
hand may experience disability and
frustration from the resultant defor-

October 2013, Vol 21, No 10 581

Intrinsic Contracture of the Hand: Diagnosis and Management

Figure 1

Illustration of finger extensor mechanism anatomy. A, Lateral view. B, Dorsal view. DIP = distal interphalangeal joint,
MCP = metacarpophalangeal joint, ORL = oblique retinacular ligament, PIP = proximal interphalangeal joint,
TRL = transverse retinacular ligament. (Adapted with permission from Coons MS, Green SM: Boutonniere deformity.
Hand Clin 1995;11:387-402.)

mity, loss of grasp and pinch
strength, and impaired dexterity. The
severity of disability is dependent on
the etiology, duration, and integrity
of the joints of the affected fingers.4
Anatomy
The intrinsic muscles are defined as
those having an origin and insertion
within the hand; muscles of the the-
nar and hypothenar compartments,
interossei, and lumbricals are in-
cluded in this category. Four dorsal
interossei and three volar interossei
have been identified. The first dorsal
interosseous inserts onto the index
finger, the second and third dorsal
interossei insert onto the middle fin-
ger, and the fourth inserts onto the
ring finger. The volar interossei insert
onto the index, ring, and small fin-
gers. The first and second lumbrical
muscles originate from the radial
side of the flexor digitorum profun-
dus (FDP) tendons and insert onto
the dorsal expansion as the radial
lateral band. The third and fourth
lumbricals are often bipennate, hav-
ing origins from the middle and ring
finger profundus tendons and from
the ring and small finger profundus
tendons, respectively.9
Considerable individual variability
exists regarding the intrinsic muscles.
Classic teaching is that all of the dor-
sal interossei except the third have two
heads and all of the volar interossei
have one head. However, single or mul-
tiple heads of the interosseous and lum-
brical muscles may alternatively exist,
and the insertion sites may also be
found variably at the base of the prox-
imal phalanx, dorsal aponeurosis,
and/or volar plate.10,11
The extensor mechanism (Figure 1)
is a plexus of tendons that balances
and extends the phalanges. The ex-
tensor digitorum communis origi-
nates in the forearm, divides into
four tendons, and continues distally
beyond the MCP joint. The extensor
indicis proprius and extensor digiti
minimi usually course parallel and
ulnar to the index and small finger
communis tendons, respectively. At-
taching to each tendon at the MCP
joint are the sagittal bands, which in-
sert onto the volar plate at the proxi-
mal phalanx. As the extensor tendon
courses distally to the PIP joint, it di-
vides into one central slip and two
lateral slips. The central slip inserts
onto the middle phalanx; the lateral
slips join with the tendons of the in-
terosseous and lumbrical muscles to
form the conjoined lateral tendons
(ie, lateral bands). The lateral bands
finally cross the distal interphalan-

582 Journal of the American Academy of Orthopaedic Surgeons


geal (DIP) joint to insert as the termi-
nal tendon on the distal phalanx.9
Accessory soft-tissue structures ad-
ditionally balance the extensor
mechanism. On the dorsal expansion
of the proximal phalanx, the in-
terosseous tendons give slips dorsally
just distal to the sagittal bands,
which are known as the transverse
and oblique fibers. Moreover, the lat-
eral bands are balanced by the trian-
gular ligament and the transverse ret-
inacular ligament, which prevent
excessive volar and dorsal sublux-
ation, respectively. Finally, the
oblique retinacular ligaments origi-
nate from the volar flexor sheath
subjacent to the PIP joint and spiral
dorsolaterally to insert onto the ter-
minal tendon. The spiral-oblique
course produces tension on the liga-
ment when the PIP joint extends and
supplies a synergistic extension force
to the DIP joint that contributes up
to 31% of its passive resistance to
flexion.12
Biomechanics
Extension of the digit occurs as the
result of tension generated along the
sagittal bands, central slip, and ter-
minal tendon to extend to the MCP,
PIP, and DIP joints, respectively.
However, the strength and versatility
of the hand is dependent on the bal-
ance of the intrinsic muscles with the
long flexors and extensors. The in-
trinsic muscles account for approxi-
mately 53% of grip strength and
85% of pinch strength.13 In general,
these muscles produce MCP joint
flexion and interphalangeal joint ex-
tension, which occurs because the
tendons of lumbricals and interosse-
ous muscles course volar to the axis
of rotation of the MCP joints but
dorsal to the axis of rotation of the
interphalangeal joints (Figure 2).
However, one exception to this rule
occurs when the MCP joint is hyper-
October 2013, Vol 21, No 10
Rick Tosti, MD, et al
Figure 2
Illustration of the balance of viscoelastic forces about the extensor
mechanism (lateral view). Generally, the intrinsic tendons pass volar to the
axis of rotation of the metacarpophalangeal (MCP) joints but dorsal to that of
the interphalangeal joints. Thus, the intrinsic tendons flex the MCP joints and
extend the interphalangeal joints. The extrinsic extensors can extend the
MCP and interphalangeal joints. The extrinsic flexors flexor digitorum
superficialis (FDS) and flexor digitorum profundus (FDP) flex the
interphalangeal joints. E = extrinsic tendons, I = intrinsic tendons. The single
dots represent the axes of flexion-extension at each joint. The double dots
represent the areas of action of the corresponding tendons at each joint.
(Adapted with permission from Kaplan EB: Anatomy, injuries and treatment of
the extensor apparatus of the hand and digits. Clin Orthop 1959;13:24-41.)
extended; then, the dorsal interosse- multaneously. In the absence of func-
ous tendon drifts in line with the axis tioning intrinsics, the interphalangeal
of rotation and is capable of produc- joints flex before the MCP joint,
ing an extension moment.14 which produces a hook fist. As a re-
During the functional range of mo- sult, the radius of curvature of the
tion (ROM) at the finger joints, the fingers becomes too narrow to ac-
intrinsics contribute to motion via quire larger cylindrical objects into
their attachments to the dorsal hood. the palm.
Flexion of the MCP joints is initiated
by the attachments of the transverse
fibers, and extension of the interpha- Etiology
langeal joints is facilitated by the at-
tachments of the oblique fibers more Intrinsic contracture may result from
distally. Additionally, the volar in- adhesions, contractures, displace-
terossei adduct the digits toward the ment, or spasticity of the muscula-
middle finger, while the dorsal in- ture from a variety of causes.
terossei abduct them. The little finger
is abducted by the extensor digiti Trauma
quinti and abductor digiti quinti.9 Fractures of the phalanges, metacar-
Without the intrinsic muscles, pals, and distal radius may predis-
grasp of a cylindrical object (ie, inte- pose the patient to intrinsic tightness
grated finger flexion) would not be primarily from edema and immobili-
possible.15 When the fingers grasp zation, which lead to adhesions and
around a large sphere, the FDP flexes fibrosis of the tendons and muscle
the DIP joint, the flexor digitorum bellies.3-5 Similar consequences may
superficialis flexes the PIP joint, and be observed from indirect traumatic
the intrinsics flex the MCP joint si- events such as burns, infected
583
Intrinsic Contracture of the Hand: Diagnosis and Management

Figure 3 mally along with the origin of the

lumbrical. As the lumbrical origin re-
tracts, tension is generated along the
distal insertion. When the patient at-
tempts to make a fist, the PIP joint
“paradoxically extends” instead of
flexing, as the FDP pulls harder on
the lumbrical tendon attaching to the
extensor mechanism4,18,19 (Figure 4).

Spasticity
Upper motor neuron disease produc-
ing upper extremity spasticity is a
heterogeneous collection of clinical
scenarios caused most commonly by
cerebral palsy, stroke, tetraplegia, or
traumatic brain injuries.4,6,20 Intrinsic
Illustrations showing progressive intrinsic contracture (red). A, Normal range
of the proximal interphalangeal (PIP) joint when the metacarpophalangeal contracture of the hand may present
(MCP) joint is extended and the intrinsics are stretched. Panels B and C along with associated contractures
depict a mildly contracted intrinsic muscle. B, The MCP joint is extended, the of the upper extremity, including
contracted intrinsic is stretched, and the PIP joint cannot flex. C, The MCP adduction/internal rotation of the
joint is flexed, the contracted intrinsic is relaxed, and PIP joint flexion is
possible. D, A severely contracted intrinsic muscle. The MCP joint is driven shoulder or flexion of the elbow,
into flexion, and the PIP joint is driven into extension. wrist, or fingers. Intrinsic tightness is
often uncovered after surgical proce-
dures that exclusively correct the ex-
trinsic flexion contractures of the
wounds, injection injuries, crush in- which would restrict PIP joint ROM hand.6
juries, or any surgical procedure in regardless of MCP position.5
which prolonged immobilization or Congenital
excessive edema have occurred.3 Ischemia
Mild cases present as a restricted In the upper extremities of pediatric
Compartment syndrome of the hand patients with arthrogrypotic syn-
ROM of the PIP joint when the MCP
and vascular injuries cause contrac- dromes, congenital joint contractures
is extended. Progressive contracture
tures through ischemia, which results usually present as internally rotated
drives the PIP joint into hyperexten-
in partially or completely function- shoulders, extended elbows, flexed
sion, which causes the terminal ten-
less fibrotic muscle tissue.1-5,16,17 Tight wrists, and flexed MCP joints. Al-
don to slacken but the FDP tendon
bandages and tight casts are prevent- though the contractures have a mul-
to tighten (Figure 3). Swan neck de-
formity occurs when the DIP joint able causes of ischemia and were the tifactorial etiology that includes soft-
falls into flexion as a net result of most common etiology seen during tissue and joint capsule contracture,
these forces.4 Chronic swan neck the original descriptions of this intrinsic tightness may also be pres-
posturing may also lead to attenua- disorder.1-3 In addition, case reports ent.21 In persons diagnosed with vari-
tion of the PIP joint volar plate or of intrinsic contracture have de- able forms of distal arthrogryposis
capsular contraction about the col- scribed ischemic mechanisms related (eg, Freedman-Sheldon syndrome),
lateral ligaments of the PIP or MCP to physical restraints, compression the hand assumes a rheumatoid pos-
joints. during intoxication, and crush inju- ture with flexed and ulnarly deviated
Additionally, trauma about the prox- ries.16,17 MCP joints22 (Figure 5).
imal phalanx may cause intrinsic tight-
ness via displacement of the lateral Lumbrical Plus Finger Rheumatoid Arthritis
bands. As the fracture callus enlarges, A rupture of the profundus tendon, a Intrinsic contracture in the hand of a
a mass effect stretches the lateral bands lax FDP tendon graft, or a distal fin- rheumatoid patient may result from
and tenses them.4 Adhesions may gertip amputation may cause the adhesions, muscle spasm from local
also form within the lateral bands, profundus tendon to retract proxi- inflammation, or contracture from

584 Journal of the American Academy of Orthopaedic Surgeons


decreased movement.4,5,7 In a recent
study, Akhavani et al23 suggested that
tissue hypoxia may be primarily re-
sponsible for intrinsic tightening and
MCP joint deformation. Although
the mechanism of ulnar deviation in
the rheumatoid hand is multifacto-
rial, intrinsic contracture in the pres-
ence of instability is contributory.4,7,23
Synovitis within the MCP joint
causes instability, the capsule and
collateral ligaments weaken, and the
proximal phalanges subluxate vol-
arly or ulnarly. In the absence of syn-
ovitis, the MCP joint remains stable.
Diagnosis and Evaluation
Evaluation begins with a focused his-
tory that identifies the level of dys-
function, etiology, and duration of
symptoms. Depending on the sever-
ity, patients may report deformity,
loss of grip strength, or difficulty
with grasping large cylindrical ob-
jects. Inspection of a hand with an
advanced intrinsic contracture might
also reveal a swan neck deformity.
Other postural features may include
an adducted thumb, an exaggerated
carpal arch, or decreased interdigital
spaces. Rheumatoid patients may
present with shortened or ulnarly de-
viated digits.
Passive and active motion of all
joints should be assessed to distin-
guish joint from muscle contracture.
The intrinsic tightness test, devel-
oped by Bunnell, is performed first
by passively extending the MCP joint
and measuring the degree of passive
PIP flexion. This maneuver stretches
the intrinsic muscles, and difficulty
in PIP flexion indicates intrinsic
tightness. The second part of the test
examines PIP flexion with the MCP
joint positioned in flexion, which re-
laxes the intrinsics. Increased flexion
of the PIP joint should then be ob-
served in isolated intrinsic contrac-
ture1 (Figure 6). The radial and ulnar
October 2013, Vol 21, No 10
Figure 4
Illustration of a lumbrical plus
finger. When the flexor digitorum
profundus (FDP) is lax or lacerated
distal to the lumbrical origin (red)
(A), intrinsic tightness can occur
when making a composite fist (B).
The FDP tendon retracts proximally
along with the lumbrical origin,
which pulls on the extensor
mechanism, causing paradoxical
extension of the PIP joint (arrows).
intrinsics can further be evaluated by
performing the Bunnell intrinsic
tightness test with the MCP joint in
radial or ulnar deviation. For exam-
ple, placing the MCP joint into ra-
dial deviation during the test would
further tighten the ulnar-side intrin-
sic tendons.
Although intrinsic tightness is a
clinical diagnosis, several adjunctive
tests may yield useful information.
PA, oblique, and lateral radiographs
of the hand should be evaluated for
the presence of bony deformity or
joint instability. Rheumatologic labo-
ratory testing may also establish an
etiology in patients with insidious
symptoms. In spastic patients, the
addition of a brachial plexus nerve
block before the intrinsic tightness
test can assist the examiner in dis-
cerning increased muscle tone from
Rick Tosti, MD, et al
Figure 5
Clinical photograph of an adult
patient with a hereditary form of
distal arthrogryposis. Note the
adducted, flexed, and ulnarly
deviated metacarpophalangeal
joints. Grasping large objects was
difficult for the patient, but she
managed her condition in her
profession as a seamstress
because it mostly required grasping
small items.
fixed contractures.24 If the informa-
tion obtained from physical exami-
nation is still not sufficient, some
surgeons supplement it with dynamic
electromyography (EMG) to evalu-
ate the level of volitional control.24
However, the use of dynamic EMG is
limited by the availability of testing
centers; it is also not universally con-
sidered to yield information that
would influence surgical decision
making.25,26
Management
Nonsurgical
Prevention of contracture should be
mentioned as the first nonsurgical
strategy for the general orthopaedist.
Following trauma to the hand, pa-
tients should be instructed on limb
elevation and early digital motion
exercises because persistent edema
585
Intrinsic Contracture of the Hand: Diagnosis and Management

Figure 6 pletely lost function and hinder good

hygiene practices, salvage options in-
clude a proximal tenotomy or ulnar
neurectomy. It is worth noting that
intrinsic contracture may also be
found with extrinsic contracture,
joint contracture, joint instability, or
joint destruction, which would addi-
tionally need to be addressed at the
time of surgery.

Distal Intrinsic Release

For mild cases, resection of the ulnar
and/or radial lateral bands can im-
prove PIP joint ROM. Generally, the
Clinical photographs of the intrinsic tightness test. A, The metacarpopha-
langeal (MCP) joint is held extended while the degree of proximal interpha-
resection begins on the side judged to
langeal (PIP) joint motion is measured (arrow). B, The MCP joint is flexed, be tighter by the intrinsic tightness
and the degree of PIP motion is again examined (arrow). With intrinsic con- test. The contralateral side can then
tracture, PIP joint motion is restricted while the MCP joint is extended and is be resected if satisfactory motion is
improved when the MCP joint is flexed.
not achieved. The dorsal expansion
can be approached through a single
leads to serum protein deposition spastic etiologies, this time may be midline dorsal incision or a double
and subsequent scar tissue forma- longer because neurologic recovery mid axial incision. The oblique fibers
tion.5 If intrinsic contracture has not may continue for 12 months follow- are identified in the distal third of
been prevented, mild cases may re- ing a stroke and for 18 months fol- the proximal phalanx, and increas-
spond to several nonsurgical modali- lowing a traumatic brain injury.24,29 ing amounts of tissue are re-
ties. Hand therapy protocols may be- sected4,7,8,28,30 (Figure 7). The amount
gin with edema reduction via elastic Surgical of oblique fiber resection necessary
pressure wrapping or compression varies by individual, but it is deter-
A variety of procedures may be se-
gloves. Manual stretching of the in- mined by the degree of PIP flexion
lected to manage intrinsic contrac- during repeated intrasurgical intrin-
trinsics is performed by passive ab-
ture; choice is dictated by the etiol- sic tightness tests. A recent biome-
duction or by placing the MCP joints
into extension and flexing the inter- ogy, severity, duration of symptoms, chanical study by Espiritu et al30 re-
phalangeal joints.27 Progressive static and the joints involved. Contractures ported that to produce significant
splints are custom fit to hold the affecting the PIP joint alone may be changes in PIP flexion, the index and
MCP joints in extension, and stretch- correctable with only a distal intrin- middle fingers require approximately
ing can be performed by PIP joint ac- sic release. However, a chronic con- a 59% and 65% resection of the
tive and passive hook exercises. Flex- tracture with swan neck deformity oblique fibers, respectively, while the
ible swan neck deformities may be requires the surgeon to impart stabil- ring and small fingers require 26%
treated with a figure-of-8 splint or a ity to the lax, hyperextended PIP and 33%, respectively.
silver ring splint, which prevents PIP joint, which may be achieved by a
joint hyperextension yet allows full lateral band tenodesis, translocation, Radial Lateral Band Resection
flexion.27,28 For spastic patients, opti- or mobilization. Contractures affect- A lumbrical plus finger results from
mizing antispastic medication or in- ing both the PIP and MCP joints tightness of the lumbrical, which
jecting botulinum toxin can improve must be addressed by relaxing the arises from the radial side of the FDP
symptoms.6,24 tendons more proximally. tendon. To correct the paradoxical
In general, nonsurgical therapies If some function is still present, the extension, the radial lateral band is
should be continued until progress is muscles need only to be weakened, transected at the origin in the palm,
no longer observed. A trial of 3 which may be achieved by fractional as detailed in the proximal intrinsic
months is often warranted for most lengthening or interosseous muscle release, or at the insertion on the
etiologies before surgical interven- slide. For situations in which ne- dorsal apparatus, as described by the
tion is considered. For patients with crotic or spastic muscles have com- distal intrinsic release.4,18,19

586 Journal of the American Academy of Orthopaedic Surgeons

 Rick Tosti, MD, et al

Intrinsic Tenodesis Figure 7

With an intrinsic contracture result-
ing in a swan neck deformity,
chronic hyperextension of the PIP
joint causes the volar plate to attenu-
ate and the collaterals to tighten in a
shortened position; a distal intrinsic
release will not correct the defor-
mity.4 A dorsal capsulectomy and
collateral release may be required to
address the joint contracture, and the
tighter intrinsic tendon is released
distally as described above. As de-
scribed by Littler,31 the contralateral
intrinsic tendon is rerouted under the
Cleland ligament at the level of the
PIP joint to serve as a restraint
against recurrent hyperextension de-
formity. The dorsal apparatus is ex-
Illustration of distal intrinsic release. The oblique fibers of the dorsal
posed by a dorsal midline incision, apparatus are resected from distal to proximal until the proximal
and the intrinsic tendon is tenoto- interphalangeal flexion is adequate. The resection begins with the tighter
mized at the proximal third of the intrinsic and may progress to both if necessary.
proximal phalanx. The lateral band
is dissected from the central slip and
Figure 8
triangular ligament and then passed
volar to the Cleland ligament. The
tendon is then secured to the proxi-
mal phalanx with a bone tunnel, but-
ton, or suture anchor4,7 (Figure 8).

Lateral Band Translocation

A modified technique for lateral
band tenodesis, described by Zan-
colli,32 was developed because of
concerns that the Cleland ligament
was not strong enough to hold the
lateral bands in a volar position. The
lateral bands are translocated volarly
beneath a pulley formed by the
flexor tendon sheath (Figure 9). To
date, the choice between these proce-
dures is based on surgeon preference
because no comparative studies exist.
The technique begins with a mid-
lateral incision on the radial side of
the digit. The lateral band is dis-
sected from the midshaft of the prox-
imal phalanx to the midshaft of the
middle phalanx, and its attachments
to the central slip and transverse reti-
nacular ligament are released. Note-
worthy is that the lateral band is not
Illustration of lateral band tenodesis. The lateral band is dissected along its
length and tenotomized at the proximal end. It is then rerouted volar to the
Cleland ligament.
transected at either end. The Cleland 5 years for patients affected by cere-
ligament is then divided, and the bral palsy.
volar plate and fibrous flexor sheath
are identified. A dorsally based, 1-cm Lateral Band Mobilization
flap of the flexor sheath is raised, the With a rigid swan neck deformity,
lateral band is translocated volarly adhesions may form within the lat-
into the flap, and the flap is closed eral bands, long extensors, and joint
back into anatomic position. Tonkin capsule, thereby limiting PIP motion
et al33 reported good correction of regardless of the MCP joint position.
hyperextension deformity in 30 fin- Thus, both intrinsic and extrinsic
gers that were predominantly af- tightness are present. In such cases,
fected by RA. Contrarily, de Bruin restoration of motion can be
et al34 reported a disappointing 40% achieved via extensor tenolysis, dor-
rate of swan neck recurrence within sal capsulectomy, and lateral band

October 2013, Vol 21, No 10 587

Intrinsic Contracture of the Hand: Diagnosis and Management
Figure 9
Illustration of lateral band translocation. The lateral band is mobilized at both
ends, translocated below the axis of motion, and maintained by a pulley
formed by the flexor tendon sheath.
mobilization. If articular destruction
is present, then the procedures are
performed with an interposition ar-
throplasty.
Through a single dorsal incision,
both lateral bands are released from
their attachments to the central slip
and the triangular ligament. The lat-
eral bands naturally fall volar to the
axis of motion at the PIP joint and
create a flexion moment because
their dorsal constraints have been re-
leased.7,28 Retrospective studies by
Gainor and Hummel35 and Kiefhaber
and Strickland36 reported an increase
in the total arc of motion at the PIP
joint; the arc of motion was also
noted to have shifted to be centered
over a more flexed position, which
allowed greater tip-to-tip pinch and
grasp postoperatively.
Crossed Intrinsic Transfer
As an adjunctive procedure to MCP
joint reconstructive surgery, the
crossed intrinsic transfer was de-
signed to correct ulnar drift22,28,37,38
(Figure 10). Currently, the operation
of choice for advanced rheumatoid
MCP joint destruction is the Silastic
interposition arthroplasty. In addi-
tion to securing the implant, soft-
tissue balancing such as release of
the ulnar intrinsics, release of the
palmar plate, and realignment of the
extensor tendon must be performed
588
to optimize postoperative function.
Some surgeons additionally employ
the crossed intrinsic transfer for ad-
ditional balance and reinforcement
of the attenuated radial side.
From a dorsal exposure, the ulnar
interosseous tendons of the index,
middle, and ring fingers are cut and
dissected proximally to their muscle
bellies. The tendons are then re-
routed and secured to the radial sides
of the adjacent ulnar digits. The ten-
dons may be fixed by suture to the
radial collateral ligament or through
a drill hole into the proximal pha-
lanx. The tendons of the flexor digiti
quinti and the abductor digit quinti
are only transected.4,28
Some debate exists regarding the
merits of this procedure. A prospective,
randomized trial by Pereira and
Belcher37 found no advantage in subjec-
tive functional scores, ROM, or grip
strength measurements in patients who
did or did not receive a crossed intrin-
sic transfer with Silastic arthroplasty
for RA. However, their study group in-
cluded only 43 subjects, and follow-up
ranged from 7 to 50 months. More re-
cently, Trail et al38 retrospectively re-
viewed 404 operations over 17 years
and found that crossed intrinsic
transfer was associated with in-
creased survivorship of the implant
and fewer revision procedures.
Journal of the American Academy of Orthopaedic Surgeons
Figure 10
Illustration of crossed intrinsic
transfer. The ulnar interosseous
tendons are transferred to the
adjacent radial digit (arrows), which
simultaneously relaxes a deforming
force and provides a corrective
force.
Proximal Interosseous
Muscle Slide
If some residual function of the in-
trinsic muscles exists from an ische-
mic or spastic mechanism, then the
intrinsics may only need to be weak-
ened to improve function or defor-
mity. The metacarpal shafts are ap-
proached by a dorsal transverse
incision or two longitudinal inci-
sions. The periosteal origins of the
dorsal and volar interossei are ele-
vated from both sides of their respec-
tive metacarpals. If MCP joint exten-
sion of the index finger cannot be
achieved after stripping the second
metacarpal, then the first dorsal in-
terosseous attachment to the thumb
metacarpal may be released. Follow-
ing the release, the MCP joints are
splinted in full extension, which al-
lows the origin to heal in a more dis-
tal position4,25 (Figure 11).
 Rick Tosti, MD, et al

Interosseous Tendon Figure 11

Fractional Lengthening
As an alternative to proximal in-
terosseous muscle slide, fractional
lengthening is indicated for contrac-
ture with volitional control. The
volar interosseous tendons are
lengthened by a transverse palmar
incision. While protecting the neuro-
vascular structures, the tendinous
portion of the myotendinous junc-
tion is obliquely incised, leaving the
muscular portion intact.24,25 Frac-
tional lengthening may be technically
challenging because of the depth of
the volar interossei and the short my- Illustration of proximal interosseous muscle slide. The interosseous origin is
otendinous junction of the intrinsics elevated; generally, both origins of the interosseous muscles are stripped
from the sides of the metacarpals. The ulnar side of the thumb metacarpal
themselves limiting the amount of may also be stripped to release the first dorsal interosseous muscle if
lengthening. necessary. Postoperatively, the fingers are splinted in extension, allowing the
muscle to heal more distally.
Proximal Intrinsic Release
As a salvage procedure for con- Figure 12
tracted, nonfunctional intrinsics,
proximal tenotomy addresses the
fixed flexion of the MCP joint and
extension of the PIP joint. Most
commonly, this procedure is indi-
cated to improve a patient’s hygiene
practices as a result of necrotic or
spastic etiologies, especially when se-
rial physical examinations or dy-
namic EMG indicates that volitional
control is not present. Multiple joints
may be addressed through a single
dorsal transverse incision. The radial
and ulnar interosseous tendons are
identified and transected proximal to
the MCP joint4,14,24 (Figure 12).

Ulnar Neurectomy
For spastic patients in whom voli-
tional control is absent, surgical de-
nervation paralyzes the intrinsics and
allows easier hygiene care.24,25,29 This
procedure cannot be performed in
isolation if muscle-tendon unit con-
tractures or joint contractures are
present. Moreover, ulnar neurectomy
can be performed concurrently with
other soft-tissue releases to prevent
recurrence. The amount of deformity
correction that can be achieved by
Illustration of proximal intrinsic release. The intrinsic tendons are transected
at the proximal origin, usually bilaterally. Release of both metacarpophalan-
geal and proximal interphalangeal joint contractures may be achieved by te-
notomy at this level.
ulnar neurectomy can be estimated branch paralyzes the interossei, the
by a preoperative ulnar nerve block. ring and small finger lumbricals, the
The motor branch of the ulnar adductor pollicis, and the deep head
nerve is approached through the of the flexor pollicis brevis. The lum-
Guyon canal and identified as it bricals of the index and the middle
courses deep to the sensory branch fingers are not paralyzed by the ul-
around the hook of the hamate. Ex- nar neurectomy, but fortunately they
cising a segment of the deep motor provide only a small contribution to

October 2013, Vol 21, No 10 589

Intrinsic Contracture of the Hand: Diagnosis and Management
the flexion moment at the MCP
joint.5,39
Summary
A variety of mechanisms and associ-
ated pathologies complicate the man-
agement of intrinsic contracture of
the hand. Traumatic, ischemic, spas-
tic, congenital, or rheumatoid etiolo-
gies may be causative. Mild intrinsic
tightness may present as only limited
PIP flexion with an extended MCP
joint and can be treated with hand
therapy or distal release. Severe dis-
ease may cause intrinsic plus postur-
ing or swan neck deformity, and the
surgeon must address the pathome-
chanics to restore function. Non-
functioning intrinsics may be com-
pletely released or denervated to
assist interdigital hygiene.
References
Evidence-based Medicine: Levels of
evidence are described in the table of
contents. In this article, references
20, 23, and 33-37 are level III stud-
ies. References 16, 17, 22, and 38
are level IV studies. The remaining
references are level V expert opinion.
References printed in bold type are
those published within the past 5
years.
1. Bunnell S, Doherty EW, Curtis RM:
Ischemic contracture, local, in the hand.
Plast Reconstr Surg (1946) 1948;3(4):
424-433.
2. Finochietto R: Retraccion de Volkmann
de Los Musculos Intrinsicos de las
Manos. Bol Trab Soc Cir Buenos Aires
1920;4:31-37.
3. Harris C Jr, Riordan DC: Intrinsic
contracture in the hand and its surgical
treatment. J Bone Joint Surg Am 1954;
36(1):10-20.
4. Smith RJ: Non-ischemic contractures of
the intrinsic muscles of the hand. J Bone
Joint Surg Am 1971;53(7):1313-1331.
5. Paksima N, Besh BR: Intrinsic
contractures of the hand. Hand Clin
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6. Tafti MA, Cramer SC, Gupta R:
Orthopaedic management of the upper
extremity of stroke patients. J Am Acad
Orthop Surg 2008;16(8):462-470.
7. Boyer MI, Gelberman RH: Operative
correction of swan-neck and boutonniere
deformities in the rheumatoid hand.
J Am Acad Orthop Surg 1999;7(2):92-
100.
8. Patterson RW, Li Z, Smith BP, Smith
TL, Koman LA: Complex regional pain
syndrome of the upper extremity. J Hand
Surg Am 2011;36(9):1553-1562.
9. Smith RJ: Balance and kinetics of the
fingers under normal and pathological
conditions. Clin Orthop Relat Res 1974;
104:92-111.
10. Eladoumikdachi F, Valkov PL, Thomas
J, Netscher DT: Anatomy of the intrinsic
hand muscles revisited: Part I. Interossei.
Plast Reconstr Surg 2002;110(5):1211-
1224.
11. Eladoumikdachi F, Valkov PL, Thomas
J, Netscher DT: Anatomy of the intrinsic
hand muscles revisited: Part II.
Lumbricals. Plast Reconstr Surg 2002;
110(5):1225-1231.
12. Ueba H, Moradi N, Erne HC, Gardner
TR, Strauch RJ: An anatomic and
biomechanical study of the oblique
retinacular ligament and its role in finger
extension. J Hand Surg Am 2011;36(12):
1959-1964.
13. Kozin SH, Porter S, Clark P, Thoder JJ:
The contribution of the intrinsic muscles
to grip and pinch strength. J Hand Surg
Am 1999;24(1):64-72.
14. Eyler DL, Markee JE: The anatomy and
function of the intrinsic musculature of
the fingers. J Bone Joint Surg Am 1954;
36(1):1-9.
15. Brand PW, Brandsma JW: Paralysis of
the intrinsic muscles of the fingers.
J Hand Surg Br 1989;14;2(2):361-366.
16. McLardy-Smith P, Burge PD, Watson
NA: Ischaemic contracture of the
intrinsic muscles of the hands: A hazard
of physical restraint. J Hand Surg Br
1986;11(1):65-67.
17. Spinner M, Aiache A, Silver L, Barsky
AJ: Impending ischemic contracture of
the hand: Early diagnosis and
management. Plast Reconstr Surg 1972;
50(4):341-349.
18. Parkes A: The “lumbrical plus” finger.
J Bone Joint Surg Br 1971;53(2):236-
239.
19. Lilly SI, Messer TM: Complications after
treatment of flexor tendon injuries. J Am
Acad Orthop Surg 2006;14(7):387-396.
20. McCarthy CK, House JH, Van Heest A,
Kawiecki JA, Dahl A, Hanson D:
Intrinsic balancing in reconstruction of
Journal of the American Academy of Orthopaedic Surgeons
the tetraplegic hand. J Hand Surg Am
1997;22(4):596-604.
21. Bevan WP, Hall JG, Bamshad M, Staheli
LT, Jaffe KM, Song K: Arthrogryposis
multiplex congenita (amyoplasia): An
orthopaedic perspective. J Pediatr
Orthop 2007;27(5):594-600.
22. Kalliainen LK, Drake DB, Edgerton MT,
Grzeskiewicz JL, Morgan RF: Surgical
management of the hand in Freeman-
Sheldon syndrome. Ann Plast Surg 2003;
50(5):456-462.
23. Akhavani MA, Paleolog EM, Kang N:
Muscle hypoxia in rheumatoid hands:
Does it play a role in ulnar drift? J Hand
Surg Am 2011;36(4):677-685.
24. Keenan MA, Matzon JL: Upper
extremity dysfunction after stroke or
brain injury, in Wolfe SW, Hotchkiss
RN, Pederson WC, Kozin SH, eds:
Green’s Operative Hand Surgery, ed 6.
Philadelphia, PA, Churchill Livingstone,
2011, vol 2, pp 1184-1205.
25. Carlson MG: Cerebral palsy, in Wolfe
SW, Hotchkiss RN, Pederson WC, Kozin
SH, eds: Green’s Operative Hand
Surgery, ed 6. Philadelphia, PA,
Churchill Livingstone, 2011, vol 2,
pp 1167-1170.
26. Manske PR, Strecker WB: Cerebral
palsy, brain injury, stroke: Spastic
disorders of the upper extremity, in
Peimer CA, ed: Surgery of the Hand and
Upper Extremity. New York, NY,
McGraw-Hill, 1996, vol 2, pp 1517-
1538.
27. Seu M, Pasqualetto M: Hand therapy for
dysfunction of the intrinsic muscles.
Hand Clin 2012;28(1):87-100.
28. Feldon P, Terrono AL, Nalebuff EA,
Millender LH: Rheumatoid arthritis and
other connective tissue diseases, in Wolfe
SW, Hotchkiss RN, Pederson WC, Kozin
SH, eds: Green’s Operative Hand
Surgery, ed 6. Philadelphia, PA,
Churchill Livingstone, 2011, vol 2,
pp 2041-2052.
29. Keenan MA: Management of the spastic
upper extremity in the neurologically
impaired adult. Clin Orthop Relat Res
1988;233:116-125.
30. Espiritu MT, Kuxhaus L, Kaufmann RA,
Li ZM, Goitz RJ: Quantifying the effect
of the distal intrinsic release procedure
on proximal interphalangeal joint
flexion: A cadaveric study. J Hand Surg
Am 2005;30(5):1032-1038.
31. Littler JW: The finger extensor
mechanism. Surg Clin North Am 1967;
47(2):415-432.
32. Zancolli E: Structural and Dynamic
Bases of Hand Surgery, ed 2.
Philadelphia, PA, JB Lippincott, 1979.
33. Tonkin MA, Hughes J, Smith KL: Lateral

band translocation for swan-neck
deformity. J Hand Surg Am 1992;17(2):
260-267.
34. de Bruin M, van Vliet DC, Smeulders
MJ, Kreulen M: Long-term results of
lateral band translocation for the
correction of swan neck deformity in
cerebral palsy. J Pediatr Orthop 2010;
30(1):67-70.
35. Gainor BJ, Hummel GL: Correction of
rheumatoid swan-neck deformity by
lateral band mobilization. J Hand Surg
Am 1985;10(3):370-376.
October 2013, Vol 21, No 10
36. Kiefhaber TR, Strickland JW: Soft tissue
reconstruction for rheumatoid swan-
neck and boutonniere deformities: Long-
term results. J Hand Surg Am 1993;
18(6):984-989.
37. Pereira JA, Belcher HJ: A comparison of
metacarpophalangeal joint Silastic
arthroplasty with or without crossed
intrinsic transfer. J Hand Surg Br 2001;
26(3):229-234.
38. Trail IA, Martin JA, Nuttall D, Stanley
JK: Seventeen-year survivorship analysis
Rick Tosti, MD, et al
of Silastic metacarpophalangeal joint
replacement. J Bone Joint Surg Br 2004;
86(7):1002-1006.
39. Buford WL Jr, Koh S, Andersen CR, Vie-
gas SF: Analysis of intrinsic-extrinsic
muscle function through interactive
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591
 Review Article

Objective Structured Clinical

Examinations: A Guide to
Development and Implementation
in Orthopaedic Residency

Abstract
Donna Phillips, MD Objective Structured Clinical Examinations (OSCEs) have been
Joseph D. Zuckerman, MD used extensively in medical schools and residency programs to
evaluate various skills, including the six core competencies outlined
Eric J. Strauss, MD
by the Accreditation Council for Graduate Medical Education
Kenneth A. Egol, MD (ACGME). Orthopaedic surgery residency programs will be
required by the ACGME to assess residents on core competencies
in the Milestone Project. Thus, it is important that evaluations be
made in a consistent, objective manner. Orthopaedic residency
programs can also use simulation models in the examination to
accurately and objectively assess residents’ skills as they progress
through training. The use of these models will become essential as
resident work hours are decreased and opportunities to observe
skills become more limited. In addition to providing a method to
assess competency, OSCEs are a valuable tool for residents to
develop and practice important clinical skills. Here, we describe a
method for developing a successful OSCE for use in orthopaedic
surgical resident training.

S ince 1975, Objective Structured

From Bellevue Hospital Center
(Dr. Phillips) and the Department of
Orthopaedic Surgery, NYU Hospital
for Joint Diseases, New York, NY
(Dr. Zuckerman, Dr. Strauss, and
Dr. Egol).
J Am Acad Orthop Surg 2013;21:
592-600
http://dx.doi.org/10.5435/
JAAOS-21-10-592
Copyright 2013 by the American
Academy of Orthopaedic Surgeons.
Clinical Examinations (OSCEs)
have been used extensively in medi-
cal schools to evaluate students’
knowledge and communication
skills.1 OSCEs are used for medical
licensing examinations, as well.
The OSCE consists of 5 to 12 sta-
tions in which the learner is asked to
interact with a standardized patient
(SP) or standardized healthcare pro-
fessional (SHP) within a specified pe-
riod of time, completing each station
sequentially. The stations represent a
specific simulated scenario that is
commonly encountered in the prac-
tice of medicine or surgery, with spe-
cific challenges that simulate a real
interaction incorporated into the sta-
tion. Feedback about resident perfor-
mance is given in writing, via indi-
vidual verbal feedback, or in group
debriefing sessions. Objective assess-
ments and feedback make OSCEs an
excellent method of evaluating the
core competencies in a simulated en-
vironment.
In 1999, the Accreditation Council
on Graduate Medical Education
(ACGME) identified six core compe-
tencies that residency programs are
required to teach: interpersonal and
communication skills, professional-
ism, patient care, systems-based
practice, practice-based learning and
improvement, and medical knowl-
edge.2 Faculty members evaluate resi-
dents on these core competencies us-

592 Journal of the American Academy of Orthopaedic Surgeons

 Donna Phillips, MD, et al

ing global evaluations, which will
soon be used to report on residents’
skills in these areas as part of the
ACGME Educational Milestone
Project.2 Although the ACGME has
accepted observation as a method of
assessing professionalism and inter-
personal communication skills, it is
challenging for faculty to consis-
tently observe residents during busy
clinics and as they evaluate and care
for emergency patients. The residents
may present cases to the attending,
but the entire patient interaction is
rarely observed. Therefore, interac-
tions between residents and patients
may be inferred from the presenta-
tion on rounds rather than actual ob-
servations.3,4 In addition, restricted
resident work hours limit opportuni-
ties to observe residents’ interactions
with patients and healthcare profes-
sionals. Therefore, faculty may not
be able to give an accurate assess-
ment of communication skills and
professionalism across the residency
group.
The OSCE, which has been recog-
nized by the ACGME as a valuable
tool for evaluating residents,2 also
provides a means for residents to
practice skills in a simulated environ-
ment. The examination can be used
to identify strengths and weaknesses
in individual learners and to identify
and correct deficiencies in the curric-
ulum. A wide variety of clinical skills
can be evaluated using the OSCEs.
The examination is a tool that pro-
vides residents with an opportunity
to practice interactions in a safe envi-
ronment and receive feedback on
their performance before they inter-
act with patients or staff in their pro-
fessional practice. The OSCE also
provides a means to assess residents’
skills objectively, and it provides the
residency program with information
about the weaknesses and strengths
of individual learners and the group
as a whole.
Patient satisfaction is now linked
to reimbursement; thus, there has
been added emphasis on ensuring
that residents and faculty are profes-
sional and communicate effectively
to enhance the patient’s experience
with the medical profession.5 OSCEs
can be used to assess isolated skills
(eg, communication) or simulate a
complete encounter. Clinical skills
that can be evaluated include taking
a history, performing a physical ex-
amination, making a diagnosis, edu-
cating the patient, and enlisting the
patient’s collaboration in the next
steps of his or her care. Each of these
skills can be practiced and evaluated
independently using the OSCE. For
example, a diagnosis may be pro-
vided and the resident may be asked
to educate the patient and assess
whether he or she understood the in-
formation provided; or the resident
may be required to manage a diffi-
cult encounter using good communi-
cation skills. Other skills can be in-
corporated into the stations as well,
including teamwork, patient safety
issues, interactions with a patient
who has limited English proficiency,6
culturally competent care,7-9 and
making a moral decision.
What residents are taught may not
be the same as what they learn.10
OSCEs can be used to determine
what residents are learning and in-
corporating into their practice. These
examinations can be designed to test
medical knowledge and the ability to
apply that knowledge to patient care.
Thus, all the core competencies can
be practiced and assessed using
OSCEs.
In most training programs, the
teaching faculty participates in a for-
mal core curriculum of orthopaedic
knowledge. Informally, faculty mem-
bers teach residents in clinical prac-
tice. Communication and profession-
alism need to be taught with the
same formal rigor as medical knowl-
edge throughout residency train-
ing.11,12 OSCEs can provide valuable
information about residents who
may not have mastered the expected
skills. Coaching can then be used to
help these residents correct deficien-
cies before there is a problem or pa-
tient complaint. Moreover, the OSCE
can be used to identify a hidden cur-
riculum in which faculty members
impart information, attitudes, and
behaviors that they may not even be
aware of.10,13 Faculty development is
an integral part of a successful cur-
riculum that is taught and tested
with OSCEs.14
Orthopaedic departments can de-
velop OSCEs specifically designed to
test professionalism, ethical decision-
making, and the ability to manage
difficult conversations with good
communication skills. Prior to taking
the OSCEs, residents learn about
communication skills and profes-

Dr. Phillips or an immediate family member is a member of a speakers’ bureau or has made paid presentations on behalf of Human
Genome Sciences/GlaxoSmithKline and has stock or stock options held in Johnson & Johnson, Pfizer, and Medtronic. Dr. Zuckerman
or an immediate family member has received royalties from Exactech; has stock or stock options held in Hip Innovation Technology
and NeoStem; has received nonincome support (such as equipment or services), commercially derived honoraria, or other non-
research–related funding (such as paid travel) from OrthoNet; and serves as a board member, owner, officer, or committee member
of the American Orthopaedic Association, the Musculoskeletal Transplant Foundation, and the Orthopaedic Research and Education
Foundation. Dr. Strauss or an immediate family member has received research or institutional support from Omeros and Dynasplint
Systems. Dr. Egol or an immediate family member has received royalties from and serves as a paid consultant to Exactech and has
received research or institutional support from Synthes, the Orthopaedic Research and Education Foundation, the Orthopaedic
Trauma Association, and OMeGA Medical Grants Association.

October 2013, Vol 21, No 10 593

Objective Structured Clinical Examinations: A Guide to Development and Implementation in Orthopaedic Residency
sionalism via the American Academy
of Orthopaedic Surgeons communi-
cation skills workshop15 and a series
of interactive conferences on manag-
ing difficult conversations in medi-
cine.16 Residents must be taught the
skills tested by the OSCE before the
skills are assessed. The results of the
examinations can be used to rein-
force the commitment to improving
professionalism and interpersonal
and communication skills on a
department-wide level. The faculty
needs to be informed of the findings
to enhance resident education in the
clinical setting. Here, we describe a
process for developing and imple-
menting a useful, reproducible OSCE
for use in the education and assess-
ment of orthopaedic surgery resi-
dents.
Development of an OSCE
Three main components comprise
the development and implementation
of a successful OSCE. First, a team is
assembled to select the core compe-
tencies to be tested and develop the
OSCE stations, including the scenar-
ios and the assessment tool to be
used. Second, implementation of the
OSCE includes recruiting and train-
ing actors to serve as the SPs or SHPs
and developing the logistics of ad-
ministering the examination. Third,
once the OSCE is completed, analy-
sis of the results is performed.
Strengths and deficiencies in the edu-
cational program are identified, and
necessary changes can be made to
the curriculum.
Assemble a Team to
Develop the Examination
OSCE development and implementa-
tion is a team effort. The team
should consist of at least one ortho-
paedic faculty member with an inter-
est in curriculum development and
resident education. Medical school
594
faculty members with a background
in education and experience in devel-
oping and implementing OSCEs are
integral to examination develop-
ment. Simulation center faculty can
be instrumental in structuring and
facilitating the OSCE to give the
most information to the participants
and the department. A project coor-
dinator with the ability to organize
and implement the OSCE is essential.
Determine the Core
Competencies to Test
The team determines which compe-
tencies will be tested. Assessment of
patient care, professionalism, and in-
terpersonal and communication
skills competencies via an OSCE is
considered most desirable.1 The pa-
tient care competency, which in-
cludes interview skills, decision-
making, and performing a physical
examination,17,18 can be readily as-
sessed with the OSCE, but other
skills, such as performing medical
procedures, can be tested as well if
access to simulation models is avail-
able. Other core competencies can
also be evaluated, including medical
knowledge, practice-based learning
and improvement, and systems-
based practice. The stations can be
made more interesting and challeng-
ing by adding details to the scenario,
such as interacting with a patient
with limited English language skills,6
working with a translator, under-
standing cultural differences,7-9 and
modifying treatment plans to accom-
modate those differences.
Faculty evaluations, 360° evalua-
tions, and even patient or staff com-
plaints about individual residents or
the group of residents can serve as
guides on areas that need to be prac-
ticed and evaluated in the OSCE. De-
partments that have a core curricu-
lum that teaches communication
skills or professionalism may assess
the integration of these skills in the
Journal of the American Academy of Orthopaedic Surgeons
residents’ clinical practice by using
an OSCE. For example, if there is a
perceived weakness in intraprofes-
sional respect, then an OSCE station
can be developed to test this aspect
of professionalism. Faculty members
may identify difficulty in evaluating
residents through observation, and
want to confirm that the residents
are meeting expectations in an
OSCE.
OSCE Station Development
The stations are developed and
guided based on previously deter-
mined resident educational needs.
The scenarios are written using ex-
amples from actual faculty or resi-
dent experiences to make the charac-
ter of the SP or SHP seem real and
aid the actor in assuming the as-
signed role. A length of time is speci-
fied for the stations. The SP or SHP
requires adequate time between sta-
tions to complete the checklist and
provide the learner with verbal feed-
back. A sample five-station OSCE
that assesses communication skills
and professionalism is shown in Ta-
ble 1. For example, in Table 1, deliv-
ering bad news involves telling a
young woman that she has a torn an-
terior cruciate ligament (ACL) that
can be reconstructed surgically. The
challenge for the resident is to recog-
nize that this is bad news for this pa-
tient and modify communication to
address the emotions of the SP. Cases
from a pool of scenarios used in
other clinical departments can be
adapted for orthopaedic residents or
developed from actual faculty or res-
ident experiences.
A standardized format is developed
for the OSCE station description to
assist in making modifications and
sharing cases. The first page of the
description is an overview that in-
cludes the objectives of the station
and the logistics, including props,
materials needed, and personnel. The

Table 1
Objective Structured Clinical Examination Station Examples
Station
Number Case
1 Obtaining informed
consent
2 Giving a sign out
(physician at risk)
3 Disclosing medical
error
4 Test results (deliver-
ing bad news)
5 Interaction with a
nurse on the ortho-
paedic floor
second page lists resident instruc-
tions that state the role of the resi-
dent, the name of the person they are
interacting with, the reason for the
encounter, and the tasks to perform
in the allotted time. The resident in-
struction sheet will be posted on the
station door and in the room for
quick reference. The instructions
need to be clear and concise. For ex-
ample, at one station, the resident
may be given the task of speaking
with a nurse on the phone. The resi-
dent needs to ensure that preopera-
tive medication is administered in a
timely fashion to prevent a subse-
October 2013, Vol 21, No 10
Description
The patient is an older Jewish man with hip To obtain informed consent, six elements are
arthritis. The resident must obtain informed
consent before the patient’s surgery. The
patient is very preoccupied with the day of
the week he would be discharged and had
difficulty following the discussion.
The resident encountered a standard third-
year resident who was taking a sign out
before the resident went home for the
night. The on-call resident was clinically
depressed and abusing alcohol.
The resident is asked to talk to the father of To tell the father what happened in the oper-
a teenage girl who has just undergone
posterior spinal fusion for scoliosis. The girl an error or tell the father that the plan was
is a preprofessional dancer, and the father
was told that the shortest fusion possible
would be done. During the case, the fellow
was noted to have gone further into the
lumbar spine than planned.
The intern is given the task of telling a
young woman that she has a complete an-
terior cruciate ligament tear confirmed on a cial resources. The resident is evaluated on
recent MRI.
The resident learns that his or her patient
has not reached the operating room hold-
ing area because the nurse was delayed in
administering the preoperative medication.
The resident’s task is to phone the nurse,
form a partnership with the nurse to ensure
that the patient receives the medication,
and understand the nurse’s viewpoint.
quent delay in transporting the pa-
tient to the operating room. Details
such as the telephone number to call,
the names of the patient and the
nurse, the surgical case, and the rea-
son that a delay may result in cancel-
lation of the case are included in the
resident instructions; this is the only
portion of the description that the
resident has access to before begin-
ning the encounter.
The orthopaedic faculty member
on the team is responsible for writing
an in-depth, detailed description of
the scenario. The scenario is then re-
viewed by the rest of the OSCE team
Donna Phillips, MD, et al
Challenge
addressed: clinical issues; pros and cons of
options; uncertainties of decision; assess-
ment of patient understanding; exploration
of preferences; and understanding and re-
sponse to the request for discharge before
Friday afternoon.
To recognize a physician at risk, make sure
that the resident is safe for the night, that
he or she is competent to take call, and that
a plan is created for obtaining support for
the resident.
ating room and make a decision to disclose
purposely changed intraoperatively. To man-
age a difficult conversation with an angry,
upset father.
To recognize that this may be bad news for a
working mother with little support or finan-
the ability to collaborate with the patient
about treatment options after exploring the
social situation and appropriately respond-
ing to her distress about her diagnosis.
To collaborate with other professionals, put-
ting the patient’s needs first.
and modifications are made as
needed to ensure that the case is ac-
curate and realistic. Extensive back-
ground information is included to
enrich the encounter. The SP scenar-
ios include a description of the char-
acter, the orthopaedic issue, social
history, family history, medical his-
tory, and the medical encounter. The
scenarios include character responses
based on the resident’s approach to
the challenge presented. The SHP
scenarios have similar detail, includ-
ing support systems; medical and
mental health history; and social his-
tory if depression, stress, or sub-
595
Objective Structured Clinical Examinations: A Guide to Development and Implementation in Orthopaedic Residency
stance abuse are part of the scenario.
Sufficient detail must be included to
make the character well developed.
In the allotted time, the resident
will not obtain all the background
information, but some of the infor-
mation may be shared during the en-
counter. For example, in the case of
the woman with the ACL tear, the
diagnosis is bad news because she is
a single mother who works in a fab-
ric store and will not be able to take
time off from work. She does not
have insurance and she is dependent
on her salary to support her son. Her
support system is limited and she
does not have backup care for her
child if she has surgery. On the other
hand, she is unable to adequately do
her job with her knee pain and insta-
bility. The challenge for the resident
is to obtain enough of the informa-
tion to understand her emotional re-
action to the news and collaborate
with her on managing her injury.
Without understanding the social sit-
uation, the resident may assume that
an ACL tear is easy to brace or re-
construct and that the SP should be
able to return to excellent function.
If the resident makes empathetic
statements, the SP shares more infor-
mation to help the resident under-
stand her dilemma and collaborate
on a plan of care. If the resident ig-
nores her show of emotion or is dis-
missive, the SP becomes less willing
to discuss her social situation.
The team selects an assessment
tool to score the skills tested in the
OSCE. Many checklists are available
and have been used extensively and
validated.19-22 Selection of the check-
list will be determined in part by the
skills that are being tested. Specific
checklists on interview skills23,24 can
be combined with other checklists.17
It is important to have a rating scale
for communication skills and profes-
sionalism. In general, a “yes” or
“no” checklist is used to assess phys-
ical examination skills,17 but commu-
596
nication skills checklists use a range
of scores. Checklists can be generic
and used for all OSCEs, or they can
be case specific.25 In general, commu-
nication skills can be assessed across
all stations,26 whereas other core
competencies are assessed with case-
specific stations. Analysis of the
scores will depend on the checklist
selected and the competencies as-
sessed.
Implementation of the
OSCE
Recruiting and Training
Actors
Often, the medical school can recom-
mend a group of actors who have ex-
perience portraying SPs and/or SHPs.
Other sources include acting schools,
local theaters, or networks of profes-
sional actors that are found in most
cities. Alternatively, students or
adults of varying ages who are not
professional actors but are interested
in teaching resident skills can be ade-
quately trained to portray convinc-
ing patients or healthcare profession-
als.
The OSCE development team will
recruit and train the actors in their
characters and in the use of the
checklist assessment tool. The writ-
ten scenario is reviewed by the actor
ahead of time and read through with
the training group at the first session.
Modifications are made as needed,
and all of the actors’ questions an-
swered. The assessment checklist is
reviewed to ensure that the items are
clear to the SP or SHP. The station is
then practiced repeatedly with differ-
ent faculty playing the role of the
learner. After each role-play, the de-
velopment team, SP, and SHP com-
plete the selected checklist, and an-
swers are compared for consistency.
Each actor will require 3 to 6 hours
of formal training. The amount of
training will be determined by the
Journal of the American Academy of Orthopaedic Surgeons
actor’s previous experience and abil-
ity to consistently use the checklist.
The actors are extensively trained to
portray the character as designed
and respond in different ways based
on how the resident manages the
conversation. Videos of similar en-
counters used in other departments
at the medical school can be shown
in the training session to give the ac-
tor a framework to learn the charac-
ter. The training is continued until
the actors are comfortable with the
characters and are capable of using
the checklist consistently.
Logistics
Once the actors are selected and
trained, the team must work out the
logistics of implementing the OSCE.
The time required for each station
will depend in part on the complex-
ity of the issues and the core compe-
tencies being evaluated. Each station
needs to be the same length of time,
ranging from 10 to 20 minutes. The
SPs and SHPs will need time between
stations to complete the checklist
and give immediate verbal feedback.
The timing is determined when the
stations are developed and con-
firmed during the training sessions.
The checklists completed at the end
of each station can be done electroni-
cally for rapid data retrieval or man-
ually, with the data entered at a later
time.
Costumes (eg, scrubs, ethnic
clothes) to be worn by the actors are
made available before beginning the
OSCE. Other props such as knee
models, radiographs, canes, and tis-
sues are made available and/or are
placed in the rooms. Many facilities
have simulation centers that are de-
signed for OSCEs and are equipped
with a video recording device in each
room and digital checklists. How-
ever, clinic examination rooms can
also be used, with video recorders
used to document the encounter.

Figure 1
Photograph demonstrating the monitoring of an objective structured clinical
examination.
The residents must have protected
time to complete the OSCE. The
number of stations, the amount of
time required to complete the check-
lists, and whether or not the SP and
SHP provide verbal feedback will de-
termine the amount of time required
for a group of residents to complete
the examination. A minimum of 2
hours is typically required, but more
time may be needed based on the
complexity of the OSCE. Residents
may substitute the OSCE for sched-
uled academic time or participate af-
ter work hours. It should be clear
that the OSCE is part of residency
education and is not optional.
Make-up sessions need to be sched-
uled to accommodate vacations,
emergencies, and even an actor’s ill-
ness during a session.
OSCEs can be developed and im-
plemented relatively inexpensively.27
The greatest cost associated with de-
veloping and implementing an OSCE
is faculty time commitment, which is
difficult to quantify. Other costs in-
clude administration and data analy-
sis. Actors are paid an hourly fee for
October 2013, Vol 21, No 10
training sessions and the OSCE ses-
sion. Departments should budget ap-
proximately $150 per resident, ex-
cluding faculty time and facility fees.
Administering the OSCE
Before the OSCE begins, the resi-
dents meet with the faculty member
on the development team and the
project coordinator, who introduce
the plan for the session. The resi-
dents are informed of the length of
each station and the time between
stations. Instructions for the resident
are written ahead of time and posted
on the door of the station to be
looked at before entering. A second
copy is available in the room for
quick reference. Multiple stations
will be in progress simultaneously.
Each resident stands outside the door
of the room and reads the instruc-
tions when the program coordinator
announces the beginning of the sta-
tion. A warning is given two minutes
before the end of the session. The
end of the session is announced, and
all stations end promptly.
Donna Phillips, MD, et al
The OSCE stations described in
Table 1 are 10 minutes long. The ex-
amination was administered in a
large space with video recording ca-
pability that was specifically de-
signed for OSCEs (Figures 1 and 2).
Groups of six or seven residents par-
ticipated in the same session so that
one or two residents were at a “rest”
station at all times. A blueprint of
the schedule was given to the resi-
dents at the beginning of the session.
The resident instruction sheet was on
the door of each station and in each
room for quick reference. The SP or
SHP was given 5 minutes between
each station to complete an online
checklist after each encounter. No
verbal feedback was given for this
OSCE. In two stations (informed
consent and disclosing surgical er-
ror), there was a short post-
encounter questionnaire for the resi-
dents to complete with questions
that reflected their moral decisions
about how they managed the conver-
sation. A short debriefing was facili-
tated by a faculty member after each
OSCE session. The residents com-
pleted a questionnaire about their
OSCE experience that included eval-
uations of each scenario and general
questions about their attitudes about
OSCEs (Table 2).
Results Analysis
The results of the OSCE are used for
resident feedback and education and
to evaluate the program curriculum.
Immediate feedback can have a pow-
erful effect on resident learning. The
SP or SHP can provide verbal feed-
back, with attention paid to specific
items on the checklist or general im-
pressions of the encounter that the
resident may not be aware of during
the interaction (eg, tone of voice,
mannerism, appearance, body lan-
guage) that was not captured in a
checklist.
597
Objective Structured Clinical Examinations: A Guide to Development and Implementation in Orthopaedic Residency
Figure 2
Photograph of a scene in which an orthopaedic resident interacts with a
standardized health professional, who is portraying a depressed resident on
call as part of a resident objective structured clinical examination station.
The checklist data are analyzed.
Each resident is given a score for the
domains tested, and the score is com-
pared with that of the resident’s
peers. A global score is provided and
may have marked value for resident
in terms of feedback.28,29 The scores
provide a quantitative assessment of
the checklist items and the relative
strengths of each resident.
Residents should have access to
their videos for independent review.
In addition, it is useful for residents
to review clips of videos in small
groups with one or two faculty mem-
bers who are familiar with OSCE
feedback. This is particularly true
when interpersonal and communica-
tion skills and professionalism are
being evaluated. When evaluated in
an OSCE, medical knowledge, pa-
tient care, and physical examinations
typically are more obviously correct
or incorrect to the learner than are
interpersonal and communication
skills. The resident should evaluate
his or her own performance before
598
the group feedback session as part of
his or her education and to fulfill the
competency of practice-based learn-
ing and improvement. Residents will
be exposed to other approaches to
managing difficult conversations by
seeing videos of their peers. The
group sessions are facilitated by fac-
ulty members who are trained in
providing feedback in order to en-
courage open discussion of what was
useful and what skills need improve-
ment. Feedback is an integral part of
the OSCE educational experience,
providing residents with strategies
for managing patient interactions
and implementing these strategies in
clinical situations. Video review in
small groups allows the residents to
critique their peers and them-
selves—a key to professionalism and
lifelong learning. Details not cap-
tured in the checklist (eg, standing
during the encounter, tone of voice,
not responding to clues given by the
SP or SHP, personal appearance, pos-
ture) are obvious when viewed on
Journal of the American Academy of Orthopaedic Surgeons
Table 2
Post-Objective Structured
Clinical Examination
Questionnaire
Statements
OSCEs are an important part of my
training.
My clinical training prepared me for the
OSCE.
OSCEs are an effective means of dem-
onstrating my clinical skills.
My performance on this OSCE accu-
rately reflects my performance in clini-
cal practice.
These OSCE cases are similar to ac-
tual encounters.
The immediate feedback that I received
was very useful.
It will be useful to get summary feed-
back on the OSCE compared to my
peers.
After feedback, I will develop a plan to
improve my clinical skills.
I will incorporate what I learned from
this OSCE into my clinical practice.
Effective patient education and counsel-
ing ensures that patients will follow
through on their treatment plan.
It is likely I will miss that a patient does
not understand the treatment plan.
Responses
Strongly disagree
Moderately disagree
Moderately agree
Strongly agree
OSCE = Objective Structured Clinical
Examination
the video. The faculty member is
able to openly discuss behaviors that
may be learned by the residents in
the hidden curriculum and reinforce
expectations.
Residents with consistently low
scores may require coaching in pa-
tient interactions in clinical practice.
The OSCE videos are an excellent
way to demonstrate behaviors that
residents may be unaware of. Gaps
in communication skills cannot be
ignored or denied when viewed on
the video. At the same time, effective
communication skills can be rein-

forced and shared with peers.
Discussion of OSCE results and
core competencies can occur during
faculty retreats to familiarize faculty
members with specific strengths and
weaknesses identified using the
OSCE. Expectations for the residents
are made clear to the faculty. Faculty
members are then encouraged to as-
sess these skills in the clinical setting
during actual encounters. Similarly,
if the faculty identifies a specific
problem area in the residents’ perfor-
mances, this area can be incorpo-
rated into the curriculum. Involving
the faculty in the OSCE results anal-
ysis will provide a unified approach
to resident education, allowing iden-
tification of skills that require close
observation by faculty and providing
an opportunity for resident coach-
ing. Positive feedback can be based
on actual accomplishments in the
core competency areas and rein-
forced. Weaknesses in performance
across the residency group suggest
the need for programmatic changes
in curriculum; follow-up OSCEs will
determine whether the residents’ per-
formance has changed over time.
The post-OSCE questionnaire re-
sponses are reviewed to provide feed-
back to the OSCE development team
(Table 2). Residents are asked
whether their training prepared them
to take the examination, if the sta-
tions were realistic and the immedi-
ate feedback was useful, and if the
OSCE was a useful method of dem-
onstrating educational experience.
The OSCE is an important part of
resident education.30 It is a valuable
learning tool that can help residents
use what they learned in their prac-
tices. Their feedback is used for de-
velopment of future OSCEs.
Summary
The ACGME requires that faculty
members evaluate residents on core
October 2013, Vol 21, No 10
competencies; the OSCE is an objec-
tive way to perform such an evalua-
tion. OSCEs provide residents with
feedback and an assessment of their
strengths and weaknesses in writing,
via verbal feedback, and by review-
ing video of their own performance
and that of their peers. Soon, the
ACGME will institute milestones for
reporting resident evaluations, with
the focus on specific developmental
skills within the six core competen-
cies. The accuracy of these evalua-
tions depends on ample observation
by faculty. However, limited work
hours make consistent evaluation of
residents’ performance challenging.
Using OSCEs to assess the skills ex-
pected of residents at all levels can
help address this challenge; the ex-
amination is also invaluable for de-
veloping compassionate and compe-
tent orthopaedic surgeons, allows for
the identification of deficiencies in
the residency program curriculum,
and may help to improve patient sat-
isfaction and outcomes.
Acknowledgments
We would like to acknowledge the
assistance of Sondra Zabar, MD, in
the development and implementation
of the OSCE. We are grateful for the
generous support from Drs. Susan
and Norman Scott through the Scott
Communications in Orthopaedic
Residency Education grant.
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Neil P. Sheth, MD
Charles L. Nelson, MD
Wayne G. Paprosky, MD
From the Department of
Orthopaedic Surgery, University of
Pennsylvania, Philadelphia, PA
(Dr. Sheth and Dr. Nelson), and
Midwest Orthopaedics, Rush
University Medical Center, Chicago,
IL (Dr. Paprosky).
Dr. Sheth or an immediate family
member serves as a paid consultant
to Zimmer. Dr. Nelson or an
immediate family member serves as
a paid consultant to Cadence
Pharmaceuticals, Greatbatch
Medical, and Zimmer and serves as
a board member, owner, officer, or
committee member of the J. Robert
Gladden Orthopaedic Society.
Dr. Paprosky or an immediate family
member has received royalties from
Wright Medical Technology and
Zimmer, is a member of a speakers’
bureau or has made paid
presentations on behalf of Zimmer,
serves as a paid consultant to
Biomet and Zimmer, and serves as
a board member, owner, officer, or
committee member of The Hip
Society.
J Am Acad Orthop Surg 2013;21:
601-612
http://dx.doi.org/10.5435/
JAAOS-21-10-601
Copyright 2013 by the American
Academy of Orthopaedic Surgeons.
October 2013, Vol 21, No 10
Review Article
Femoral Bone Loss in Revision
Total Hip Arthroplasty: Evaluation
and Management
Abstract
Primary total hip arthroplasty (THA) is one of the most effective
procedures for managing end-stage hip arthritis. The burden of
revision THA procedures is expected to increase along with the
rise in number of primary THAs. The major indications for revision
THA include instability, aseptic loosening, infection, osteolysis,
wear-related complications, periprosthetic fracture, component
malposition, and catastrophic implant fracture. Each of these
conditions may be associated with mild or advanced bone loss.
Careful patient evaluation and bone loss classification guide
preoperative planning and overall patient care. Historically,
uncemented fixation has provided the best results, but cemented
fixation is required in some cases.
T he aging of the population and
the consideration of younger pa-
tients for primary total hip arthro-
amination, and radiographs. Key ele-
ments of the history include the loca-
tion, character, timing, and duration
plasty (THA) has resulted in increas- of pain as well as provocative factors
ing numbers of these procedures and associated symptoms.
being performed annually. The revi- In all cases of painful hip replace-
sion burden is expected to increase, ment, laboratory tests should be
as well. The major indications for done, including serum erythrocyte
femoral revision include aseptic loos-
sedimentation rate (normal, <20
ening, infection, instability, osteoly- mg/dL) and C-reactive protein level
sis, periprosthetic fracture, compo- (normal, <10 mg/dL). In most cases,
nent malposition, and catastrophic patients with elevated serum inflam-
implant failure.
matory markers should undergo pre-
Femoral revision is often compli- operative hip aspiration. Synovial
cated by bone loss or the poor integ-
fluid obtained from the hip aspira-
rity of the remaining bone stock. We
tion should be sent for cell count
offer an approach by which to evalu-
analysis, including differential, and
ate candidates for femoral revision
anaerobic and aerobic cultures. A
and define methods by which to as-
white blood cell count of 2,500 to
sess and manage femoral bone loss
3,000 and a differential of >60%
encountered during revision surgery.
segmented neutrophils is considered
suspicious for infection, unless the
Preoperative Evaluation aspiration is performed in the imme-
diate postoperative period.1,2
Preoperative evaluation begins with In the setting of loose femoral
a comprehensive history, physical ex- components—most commonly loose
601
Femoral Bone Loss in Revision Total Hip Arthroplasty: Evaluation and Management
Table 1
American Academy of
Orthopaedic Surgeons Femoral
Bone Loss Classification8
Type Description
I Segmental defect
II Cavitary defect
III Combined segmental and
cavitary defect
IV Femoral malalignment
(rotational or angular)
V Femoral stenosis
VI Femoral discontinuity
cemented stems—the proximal femur
often remodels into varus and retro-
version (ie, proximal femoral remod-
eling). Recognizing the potential for
such remodeling preoperatively mini-
mizes the risk of cortical perforation,
intraoperative fracture, and under-
sizing of the implant. Extended tro-
chanteric osteotomy (ETO) is often
useful at the time of revision, partic-
ularly in the setting of significant
varus remodeling, a well-fixed unce-
mented implant, or a long column of
cement below the stem.3
Plain radiographs often underesti-
mate bone loss. CT is occasionally a
useful adjunct for further defining
the severity of femoral bone loss.4
We recommend the use of CT for
any cases that require further delin-
eation of the bone loss pattern and
any degree of femoral deformity that
may influence the plan for femoral
reconstruction.
Preoperative Planning
Surgical Approach
The surgical approach for revision
surgery is based on surgeon experi-
ence and utility of the planned recon-
struction. Selection of surgical ap-
proach is also influenced by
additional exposure (ie, osteotomy),
602
degree and location of bone deficits,
presence of distorted anatomy (eg,
heterotopic ossification), and patient
factors (eg, high risk of instability).
The posterolateral approach is most
commonly used. It affords excellent
acetabular and femoral exposure;
however, it is associated with higher
postoperative instability.
The locations and configurations
of femoral osteotomy vary consider-
ably. Standard single plane, trochan-
teric slide, Wagner, and extended tro-
chanteric are types of osteotomy
performed about the greater tro-
chanter.5
The ETO, which is most com-
monly used in the setting of revision
THA, facilitates acetabular exposure
and femoral component removal.6
The results of ETO in femoral revi-
sion THA have been favorable. Pa-
prosky and Sporer6 evaluated 122 re-
vision THAs performed with the use
of an ETO and reported a 98%
union rate of the osteotomized frag-
ment at a mean 2.6-year follow-up.
Femoral Component
Removal
During preoperative planning, it is
important to identify key osseous
and functional structures that are at
risk during implant removal. In addi-
tion, the surgeon must have at the
ready implants that would allow re-
construction in the event that greater
bone loss than anticipated is discov-
ered intraoperatively.
To facilitate stem removal, the fol-
lowing instruments should be on
hand: manufacturer-specific explant
tools, flexible osteotomes, trephines,
high-speed burrs (eg, pencil tip, car-
bide tip, metal cutting wheel), ultra-
sonic cement removal instruments,
and universal extraction tools that
allow attachment to the stem or ta-
per. The decision to remove a well-
fixed implant must be made care-
fully.7
Journal of the American Academy of Orthopaedic Surgeons
Femoral Bone Loss
Classifications
The American Academy of Ortho-
paedic Surgeons introduced a femo-
ral bone loss classification based on
the presence of segmental, cavitary,
or combined defects8,9 (Table 1). This
classification is simple in its organi-
zation; however, it is not quantitative
and its practical application is lim-
ited. We find the Paprosky classifica-
tion to be the most useful for de-
scribing femoral bone loss.9-11
The Paprosky classification is
based on the location of femoral
bone loss (metaphyseal or diaphy-
seal), degree of remaining support of
the proximal femur (ie, degree of
cancellous bone loss), and the
amount of isthmus remaining for di-
aphyseal fixation (Table 2). These
three variables allow for objective as-
sessment of bone loss and provide re-
constructive options based on the
pattern of femoral bone loss.9,10
With type I femoral bone loss, the
proximal metaphyseal bone is main-
tained, and proximal femoral remod-
eling typically is not exhibited. Type
I defects can be managed with stan-
dard length cemented or uncemented
implants. We prefer to manage type I
defects with a standard length exten-
sively porous-coated implant9,10 (Fig-
ure 1).
Type II femoral defects are the
most common type. These demon-
strate absent metaphyseal bone loss
with an intact diaphysis. Slight prox-
imal varus femoral remodeling is
common. Excellent results have been
reported using extensively porous-
coated femoral implants9,10 (Figure
2).
Type III defects are subclassified as
either type IIIA or IIIB. Both type III
defects exhibit metadiaphyseal bone
loss with significant proximal femo-
ral remodeling. Type IIIA defects
have ≥4 cm of isthmus remaining for
 Neil P. Sheth, MD, et al

Table 2
Paprosky Classification of Femoral Bone Loss9
Proximal Proximal Reconstruction
Type Definition Metaphysis Diaphysis Remodeling Options

I Minimal proximal meta- Intact Intact None Uncemented fixation; proximal

physeal bone loss fitting (ie, S-ROM [DePuy]) or
extensively porous-coated
stem
II Moderate to severe Absent Intact Slight Extensively porous-coated stem
proximal metaphyseal
bone loss
IIIA Severe proximal meta- Absent ≥4 cm Significant Extensively porous-coated stem
physeal bone loss with of isthmus if <19 mm in diameter. If ≥19
diaphysis intact for mm in diameter, then modular
some distance tapered stem.
IIIB Severe proximal meta- Absent <4 cm Significant Modular tapered stem
physeal bone loss with of isthmus
diaphysis intact for
some distance
IV Complete loss of meta- Absent Absent Slight Allograft prosthetic composite,
physeal and diaphy- cemented stem, or impaction
seal bone grafting plus cemented stem

distal fixation (Figure 3), whereas

Figure 1
type IIIB defects have <4 cm remain-
ing9,10 (Figure 4). Treatment options for
type III defects include extensively
porous-coated cylindrical stems, corun-
dumized tapered stems with splines (eg,
circumferential fluted projections
around the tapered stem that confer ro-
tational stability of the implant), and
cemented stems with impaction bone
grafting. Our preference is to manage
type IIIA defects with an extensively
porous-coated stem and type IIIB de-
fects with a modular tapered stem with
antirotational splines. In general, these
tapered stems can obtain predictable
fixation with only 1 to 2 cm of diaphy-
seal bone contact.
Type IV defects exhibit complete
loss of the isthmus with little proxi-
mal femoral remodeling9,10 (Figure
5). Biologic fixation is unlikely, and
reconstruction typically requires the
use of an allograft prosthetic com- A, Illustration of a Paprosky type I femoral defect. Preoperative (B) and
posite (APC), a long cemented stem, postoperative (C) AP radiographs of a patient treated with an extensively
porous-coated stem at the time of two-stage reimplantation to manage
impaction grafting with a long ce- periprosthetic infection and Paprosky type I bone loss. (Panel A courtesy of
mented femoral component, or prox- DePuy, Warsaw, IN.)
imal femoral replacement.

October 2013, Vol 21, No 10 603

Femoral Bone Loss in Revision Total Hip Arthroplasty: Evaluation and Management

Figure 2
Clinical Results by
Reconstruction Method
The goals of femoral component re-
vision are to achieve rotational and
axial component stability while re-
storing hip biomechanics. Cemented
femoral revisions have demonstrated
failure rates as high as 19%, com-
pared with 4% to 6% with unce-
mented revisions, which rely on 4 to
6 cm of diaphyseal fixation.12,13
When possible, uncemented biologic
fixation is the preferred method of
reconstruction (Table 3); however, it
may be necessary to use cemented
fixation (Table 4).

Uncemented Revision
Proximally Porous-coated
A, Illustration of Paprosky type II femoral defect. Preoperative (B) and Femoral Components
postoperative (C) AP radiographs of a patient treated with an extensively Proximally porous-coated uncemented
porous-coated femoral stem to manage a loose cemented stem and stems can be used for revision THA in
Paprosky type II bone loss. (Panel A courtesy of DePuy, Warsaw, IN.)
cases of minimal proximal metaphys-

Figure 3

A, Illustration of a Paprosky type IIIA femoral defect. B, Preoperative AP radiograph of a Paprosky type IIIA defect with
>4 cm of isthmus remaining for diaphyseal fixation. C and D, Postoperative AP radiographs of a patient treated with a
size 20 modular tapered stem to manage an aseptically loose cemented femoral component. An extensively porous-
coated stem was not chosen because of the large diameter needed for femoral reconstruction. (Panel A courtesy of
DePuy, Warsaw, IN.)

604 Journal of the American Academy of Orthopaedic Surgeons

 Neil P. Sheth, MD, et al

eal bone loss (ie, Paprosky type I).29 sleeve into which a slotted diaphy- cisely milled to match the proximal
In the setting of proximal bone loss, seal segment is inserted. This design sleeve and accommodates fluted di-
multiple reports have indicated diffi- allows for the metaphysis to be pre- aphyseal stems of differing lengths
culty in obtaining stable proximal
Figure 4
metaphyseal fixation. Berry et al14
assessed 375 femoral revisions per-
formed using proximally porous-
coated femoral components. At
8-year follow-up, the mean survivor-
ship was only 52%, using aseptic
loosening as an end point. Poor sur-
vivorship was directly correlated
with the degree of preoperative bone
loss and poor integrity of the remain-
ing proximal metaphyseal cancellous
bone.

Proximally Modular
Femoral Components
The inherent difficulty in achieving
adequate initial implant stability
with a monoblock proximally coated
stem during femoral revision has re-
sulted in increased enthusiasm for A, Illustration of a Paprosky type IIIB femoral defect. B, Preoperative AP
the use of proximally modular femo- radiograph demonstrating a loose cemented femoral stem with Paprosky
ral components such as the S-ROM type IIIB bone loss. C, AP radiograph following implantation of a modular
tapered stem with <4 cm of isthmus remaining for diaphyseal fixation. (Panel
prosthesis (DePuy). These implants A courtesy of DePuy, Warsaw, IN.)
consist of a press-fit metaphyseal

Figure 5

A, Illustration of a Paprosky type IV femoral defect. B, Preoperative AP radiograph demonstrating Paprosky type IV
bone loss secondary to periprosthetic infection. C and D, Postoperative AP radiographs following reimplantation with
an allograft-prosthesis construct to manage the bone loss. (Panel A courtesy of DePuy, Warsaw, IN.)

October 2013, Vol 21, No 10 605

Femoral Bone Loss in Revision Total Hip Arthroplasty: Evaluation and Management

Table 3
Results of Uncemented Reconstruction by Type of Bone Loss

Study No. of Hips Stem Type

Berry et al14 375 Proximal metaphyseal fitting

Cameron15 320 Proximal modular (S-ROM [DePuy])

Weeden and Paprosky16 170 Extensively porous-coated

Sporer and Paprosky17 51 Extensively porous-coated

Park et al18 62 Modular tapered

Garbuz et al19 Modular tapered stem, 31. Extensively Modular tapered vs extensively porous-coated
porous-coated stem (Solution [DePuy]),
189.

Richards et al20 Modular tapered stem, 103. Extensively Modular tapered vs extensively porous-coated
porous-coated stem, 114.
Grünig et al21 38 Nonmodular tapered

Isacson et al22 43 Nonmodular tapered

N/A = not applicable

a
Paprosky classification unless otherwise noted.
b
Class I, partial or complete cortical loss above the level of the lesser trochanter; class II, partial or complete cortical loss above a point
10 cm below the lesser trochanter; class III, partial or complete cortical loss >10 cm below the lesser trochanter.
c
Class I, bone below the lesser trochanter is intact, and generally, a primary stem can be used; class II, subtrochanteric bone is damaged
significantly and requires the use of a long stem; class III, >70 mm of the proximal femur is completely missing, which requires the use of a
structural allograft.
d
Different Paprosky classification: type 1, minimal metaphyseal and diaphyseal loss; type 2A, absent calcar below the intertrochanteric line;
type 2B, absent anterolateral metaphyseal bone; type 2C, absent calcar and posteromedial bone; type 3A, B, and C, same as type 2A, B, and
C but with diaphyseal extension.

and configurations. Proximal modu-
larity also addresses proximal femo-
ral retroversion by allowing version
to be dialed in separately. Unlike
proximally coated nonmodular com-
ponents, the results of femoral revi-
sions with these prostheses have been
favorable.
Cameron15 reported on 320 revi-
sions performed with S-ROM stems
(109 short, 211 long). At a mean
follow-up of 7 years (range, 2 to 12
years), there were no reported revi-
sions for aseptic loosening in the
short stem group and only 3 in the
long stem group (1.4%). Subsidence
was >5 mm in only two hips (0.6%),
and there were no cases of distal os-
teolysis. The author concluded that
proximally coated, proximally mod-
ular stems can be used successfully in
the setting of femoral revision.
Extensively Porous-coated
Femoral Stems
Extensively porous-coated stems have
been the workhorse for femoral revision
THA. In general, 6-inch stems are suf-
ficient for most type II and IIIA femo-
ral defects. However, when using lon-
ger, bowed stems (eg, 8 in, 10 in), it is
important to ensure adequate hip sta-
bility because suboptimal stem antever-
sion may be dictated as a consequence
of the femoral bow.
Weeden and Paprosky16 evaluated
170 revisions over a mean of 14.2
years. The femoral defects were clas-
sified as type I (11%), type II (30%),
type IIIA (48%), and type IIIB
(11%). The overall mechanical fail-
ure rate, that is, the percentage of
stems that required revision surgery
or were radiographically unstable,
was 4.1%. Eighty-two percent of
hips had radiographic evidence of
bone ingrowth, and 14% had stable
fibrous fixation. Four percent were
unstable radiographically. There was
a high rate of failure (21%) with
worsening bone loss (type IIIB), and

606 Journal of the American Academy of Orthopaedic Surgeons

 Neil P. Sheth, MD, et al

Table 3 (continued)
Results of Uncemented Reconstruction by Type of Bone Loss
Mean Clinical
Bone Loss Classificationa Follow-up Re-revision Rate (%) Survivorship

Minimal, 49; class I, 60; class II, 218; 4.7 y 16 52% at 8 y. Worse preoperative
class III, 38;b periprosthetic fractures, 10 bone loss correlated with
poorer survivorship.
Class I, 109; classes II and III, 211c 7y Class I, none; class II and III, N/A
1.4
Type I, 18; type II, 51; type IIIA, 82; type 14.2 y Overall failure rate, 4.1. Failure N/A
IIIB, 19 rate with type IIIB bone loss,
21.
Type IIIA, 17; type IIIB, 26 (15 with ≤19 4.2 y Type IIIA, none; type IIIB (≤19 N/A
mm canal diameter, 11 with >19 mm ca- mm canal diameter), 6.7; type
nal diameter); type IV, 8 IIIB (>19 mm canal diameter),
27.3; type IV, 25
Type IIIA, 37; type IIIB, 19 4.2 y None N/A
Modular group: type I, 4; type II, 5; type Modular, 37 mo; non- Quality of life measures better N/A
IIIA, 29; type IIIB, 58; type IV, 7. Non- modular, 49 mo with modular tapered stems
modular group: type I, 1; type II, 15;
type IIIA, 60; type IIIB, 31; type IV, 4.
Modular group: types IIIB and IV, 65. Non- 23 mo for each Quality of life measures better N/A
modular group: types IIIB and IV, 35. with modular tapered stems
Type 1, 1; type 2A, 6; type 2B, 6; type 2C, 47 mo 7.5, to manage stem subsi- N/A
5; type 3A/B/C, 9d dence (3 of 40)
— 25 mo 18.6, due to subsidence and N/A
instability

N/A = not applicable

a
Paprosky classification unless otherwise noted.
b
Class I, partial or complete cortical loss above the level of the lesser trochanter; class II, partial or complete cortical loss above a point
10 cm below the lesser trochanter; class III, partial or complete cortical loss >10 cm below the lesser trochanter.
c
Class I, bone below the lesser trochanter is intact, and generally, a primary stem can be used; class II, subtrochanteric bone is damaged
significantly and requires the use of a long stem; class III, >70 mm of the proximal femur is completely missing, which requires the use of a
structural allograft.
d
Different Paprosky classification: type 1, minimal metaphyseal and diaphyseal loss; type 2A, absent calcar below the intertrochanteric line;
type 2B, absent anterolateral metaphyseal bone; type 2C, absent calcar and posteromedial bone; type 3A, B, and C, same as type 2A, B, and
C but with diaphyseal extension.

the intraoperative fracture rate with
stem insertion was 8.8%.
The limitations of extensively
porous-coated stems in the setting of
femoral revision were identified by
Sporer and Paprosky17 in a study of
51 patients with type III or IV femo-
ral bone defects. No failures were re-
ported in the 17 femurs with type
IIIA defects. One failure was re-
ported in the 15 patients with type
IIIB defects and femoral canals <19
mm in diameter (6.7%), and an 18%
rate of mechanical failure (ie, revi-
sion for aseptic loosening or radio-
graphic evidence of instability) was
reported in patients with type IIIB
defects and femoral canals >19 mm
in diameter (2 of 11). Additionally,
three of eight patients with type IV
defects treated with extensively
porous-coated stems experienced
mechanical failure. These authors
recommended use of a modular ta-
pered stem or impaction bone graft-
ing in type IIIB defects with canals
>19 mm in diameter and in type IV
defects.
Tapered Stems
Enthusiasm for tapered stems has
grown in the past decade, and they
arguably have become the new
workhorse for femoral revision sur-
gery in the setting of advanced bone
loss. Tapered stems can be nonmod-
ular or modular. Final seating of
these devices is sometimes difficult to
predict during bone preparation.
Modular designs allow more predict-
able restoration of length, offset, and
version. However, concerns exist re-
lated to stem fracture at the Morse
taper with these designs.
Modular Tapered Stems
Modular tapered revision femoral
components have been successfully
used in the reconstruction of femurs
with moderate to severe proximal
bone loss. Park et al18 followed 62

October 2013, Vol 21, No 10 607

Femoral Bone Loss in Revision Total Hip Arthroplasty: Evaluation and Management

Table 4
Results of Cemented Reconstruction by Type of Bone Loss

Study No. of Hips Type of Reconstruction Stem Type

Ornstein et al23 1,305 Cemented impaction grafting Polished cemented

Blackley et al24 63 Cemented APC Cemented

Safir et al25 50 Cemented APC Cemented

Babis et al26 57 Cemented APC Cemented

Malkani et al28 50 Cemented Proximal femoral replacement

Haentjens et al27 16 Cemented Proximal femoral replacement

APC = allograft prosthesis composite, N/A = not applicable

a
Paprosky classification unless otherwise noted.
b
AAOS classification of femoral bone loss: level I, bone loss up to the level of the lesser trochanter; level II, bone loss up to 10 cm distal to
the lesser trochanter; level III, bone loss distal to 10 cm below the lesser trochanter (this also depicts loss of host-prosthesis contact with the
need for structural bone graft).

Figure 6 in this cohort required revision due

A, Preoperative AP radiograph demonstrating femoral bone loss secondary
to osteolysis. B, Postoperative AP radiograph following treatment with
impaction grafting.
femoral revisions using a fluted mod-
ular tapered component for a mean
of 4.2 years (range, 2 to 7.8 years).
Thirty-seven (60%) were classified as
Paprosky type IIIA, and 19 (31%)
were type IIIB. None of the patients
to mechanical failure at final follow-
up.
In similarly designed studies, Gar-
buz et al19 and Richards et al20 com-
pared the results of tapered, fluted,
modular titanium femoral compo-
nents with cylindrical nonmodular
cobalt chrome stems in revision ar-
throplasty. Both studies reported su-
perior results with the modular ta-
pered components. Richards et al20
found that although the modular ta-
pered cohort had worse preoperative
bone defects (65% Paprosky types
IIIB and IV femurs versus 35% in the
nonmodular group), they had better
clinical outcome scores (ie, Western
Ontario and McMaster Universities
Osteoarthritis Index, Oxford Hip
Score, satisfaction), fewer intraoper-
ative fractures, and better restoration
of the proximal femoral host bone.
Overall, modular tapered femoral
components have shown excellent
promise in short- to midterm studies
for revision THA in patients with
substantial proximal bone loss.
These stem designs are widely used
in revision THA, and longer-term

608 Journal of the American Academy of Orthopaedic Surgeons

 Neil P. Sheth, MD, et al

Table 4 (continued)
Results of Cemented Reconstruction by Type of Bone Loss
Clinical Follow-up in
Bone Loss Classificationa Years Re-revision Rate (%) Survivorship

— Range, 5–18 5.4 94% for women and 94.7% for

men at 15 y
Level II and III bone lossb Mean, 11 27 (graft resorption in 13 of 48 77% at final follow-up
hips)
— Mean, 16.2 14 N/A
Type IV, 55 Mean, 12 33 69% at 10 y. Survivorship de-
creased with worse bone loss
(ie, type IV).
Type IV, 33 Mean, 11.1 32 64% at 12 y
Not reported Mean, 5 Not reported N/A

APC = allograft prosthesis composite, N/A = not applicable

a
Paprosky classification unless otherwise noted.
b
AAOS classification of femoral bone loss: level I, bone loss up to the level of the lesser trochanter; level II, bone loss up to 10 cm distal to
the lesser trochanter; level III, bone loss distal to 10 cm below the lesser trochanter (this also depicts loss of host-prosthesis contact with the
need for structural bone graft).

studies are needed to determine their
efficacy.
Nonmodular Tapered Stems
Elimination of the modular junction
in femoral component revision de-
creases the risk of stem fracture, fret-
ting corrosion, metallosis, and resul-
tant osteolysis. However, the lack of
modularity makes proper component
position and restoration of hip bio-
mechanics more difficult. Grünig
et al21 evaluated 38 revisions per-
formed with one particular nonmod-
ular tapered stem. At a mean
follow-up of 47 months, 3 (8%) of
38 hips required revision for stem
subsidence, and an additional 16
stems had subsided <1 cm by
3-month follow-up. This early subsi-
dence did not appear to affect clini-
cal outcome, and the authors recom-
mended protected early weight
bearing.
Isacson et al22 reported results us-
ing the same type stem in 43 hips. At
a mean follow-up of 25 months, 22
of 23 patients (96%) showed abun-
dant new bone formation. However,
5 of 42 patients (12%) had subsi-
dence >20 mm, and 22 (52%) had
subsidence <5 mm. There were nine
dislocations, of which eight required
re-revision to manage instability.
Cemented Revision
Impaction Grafting
Impaction grafting is performed in
an attempt to restore bone stock in
young or active patients with severe
proximal bone loss (ie, Paprosky
type IIIB or IV defects). The old stem
is extracted, and the canal is dé-
brided of all previous cement, neo-
cortex, and fibrous tissue or en-
dosteal membrane. Deficient cortices
are reinforced as necessary with any
combination of wire mesh, strut al-
lograft, and cerclage wires. A plug is
placed distally, and morcellized can-
cellous allograft is tightly packed
into the canal using cannulated
tamps and broaches over a guide
rod. The revision stem (typically a
polished tapered stem) is then ce-
mented into the reconstituted femur.
Initial reports on impaction graft-
ing described variable outcomes.
Centers with significant experience
with this technique reported very
good short- and intermediate-term
results; however, many other centers
reported high rates of femoral com-
ponent subsidence as well as intraop-
erative or early postoperative femo-
ral fracture. Some recent studies have
demonstrated satisfactory long-term
results with a high level of construct
survivorship.
Ornstein et al23 evaluated 1,188 re-
visions performed with impaction
grafting using a polished Exeter stem
(Stryker). The original cohort con-
sisted of 1,305 revisions. Clinical
and radiographic follow-up ranged
from 5 to 18 years. Only 70 cases re-
quired re-revision (5.9%). The survi-
vorship at 15 years was 94.0% for
women and 94.7% for men, using
any reason for revision as an end
point. Survivorship at 15 years was
99.1% for aseptic loosening, 98.6%
for infection, 99% for subsidence,
and 98.7% for fracture. Overall,
long-term results of impaction graft-
ing are encouraging, but proper pa-
tient selection is required, and the
procedure is labor intensive, requir-
ing adequate surgeon experience
(Figure 6).
Allograft Prosthetic Composite
The use of an APC should be consid-
ered in the setting of severe circum-
ferential femoral bone loss. With this

October 2013, Vol 21, No 10 609

Femoral Bone Loss in Revision Total Hip Arthroplasty: Evaluation and Management
technique, the deficient proximal fe-
mur is osteotomized and removed. A
long-stem prosthesis then is ce-
mented into the bulk proximal femo-
ral allograft, and this APC is mated
to the host bone while the distal part
of the stem is press-fit or cemented
into the host femoral canal. Stable
fixation between the APC and host is
enhanced by press-fitting the distal
stem and by creating a step cut at the
APC-host interface, thereby increas-
ing the surface area for creeping sub-
stitution. Cerclage wires are also
used to enhance junctional stability.
Advantages of reconstruction with
an APC over a proximal femoral
prosthesis include the ability to re-
store bone stock in young patients
and the ability to reattach host soft
tissues. One disadvantage is the po-
tential for disease transmission. The
risk of viral transmission with fresh-
frozen, unprocessed allograft is ap-
proximately 1 in 500,000 (range,
440,000 to 600,000).30 There is also
a risk of secondary bacterial infec-
tion. Other disadvantages include
difficulty obtaining the appropriate
allograft, the risk of nonunion or
graft resorption, and greater techni-
cal demands.31
Several studies, most from the or-
thopaedic oncology literature, have
reported encouraging results with
the use of this technique in revision
THA, although most demonstrate
short-term clinical follow-up. Black-
ley et al24 reported on 63 consecutive
revisions using an APC construct.
With a mean follow-up of 11 years
(range, 9 years 4 months to 15
years), the success rate was 77% for
the 45 patients who were alive at the
latest follow-up. The nonunion rate
was 6% at the host-allograft junc-
tion, and all patients required treat-
ment with autograft. Allograft re-
sorption was seen in 27% of patients
who were followed for at least 9
years. Four of the 63 hips dislocated,
and 2 of these required acetabular
610
revision. Five hips developed deep in-
fection, all of which required reoper-
ation. There were only three cases of
aseptic loosening, and all occurred at
the implant-cement interface. The
average time to loosening was more
than 10 years.
Safir et al25 recently published a
retrospective study with an average
clinical and radiographic follow-up
of 16.2 years (range, 15 to 22 years).
They reported the results of 50 hips
out of an original cohort of 93.
Seven APC constructs were revised
for any reason. The authors con-
cluded that proximal femoral al-
lograft in revision THA is a durable
option for most patients with severe
femoral bone loss.
Babis et al26 evaluated the use of APC
in the setting of complex revision THA
for severe proximal femoral bone loss.
A total of 57 hips was available at a
mean follow-up of 12 years (range, 8
to 20 years). APC survivorship at 10
years was 69%, with 19 hips (33.3%)
requiring revision at a mean follow-up
of 44.5 months (range, 11 to 153
months). Survivorship was significantly
affected by the degree of preoperative
bone loss (ie, Paprosky type IV) (P =
0.019), the number of previous hip sur-
geries exceeding two (P = 0.047), and
the length of the APC graft (P = 0.005).
Satisfactory results were seen with the
use of APC to manage severe proximal
bone loss in revision THA.
Megaprosthesis (Proximal
Femoral Replacement)
The use of proximal femoral–replac-
ing prostheses (ie, megaprostheses)
has substantial disadvantages and
should be limited to elderly and low-
demand patients with massive bone
loss for whom the alternative is re-
section arthroplasty. Disadvantages
include problems with fixation and
early loosening,11,32,33 instability sec-
ondary to inadequate soft-tissue at-
tachment,27,34 severe stress shielding
Journal of the American Academy of Orthopaedic Surgeons
and late fatigue fracture, limb-length
discrepancy, sciatic nerve palsy, and
cost.35,36 Additionally, further loss of
bone stock makes subsequent revi-
sion more challenging. The one ad-
vantage is that implantation can be
done quickly, which makes this an
attractive reconstructive option for
elderly patients in poor health.
Few reports describe the use of
megaprostheses in the setting of fem-
oral revision THA. Malkani et al28
published long-term results using a
proximal femoral replacement for non-
neoplastic disorders. Thirty-three of 50
hips were revised to address femoral
bone loss. The mean clinical follow-up
was 11.1 years (range, 5.1 to 18.8
years). Overall survivorship was 64%
at 12 years. Sixteen components in 12
patients required revision for any rea-
son (32%). Eleven hips dislocated
(22%), 4 of which required re-revision.
Additionally, 27% of patients had
moderate to severe pain, and 48% of
patients had a severe limp or were un-
able to walk. Harris Hip scores im-
proved from 46 points preoperatively
to 76 points at latest follow-up.
Haentjens et al27 evaluated 16 pa-
tients treated with proximal femoral
replacement for salvage of a failed
THA. At a mean follow-up of 5
years (range, 2 to 11 years), all pa-
tients reported pain relief, but all pa-
tients also required an assistive de-
vice for ambulation. Four patients
sustained an intraoperative fracture,
seven had a dislocation, and two had
deep infection. Given the high rate of
complications and limited postopera-
tive function provided by the mega-
prostheses, revision with this type of
construct should be considered only
as a salvage procedure.
Summary
Management of femoral bone loss
during revision THA begins with
proper preoperative evaluation. In

patients who require femoral compo-
nent revision, bone loss should be
classified to help determine an ap-
propriate prosthesis and fixation
strategy. For Paprosky types I, II,
and IIIA bone loss, cylindrical fully
porous-coated uncemented femoral
components have been associated
with predictable long-term fixation.
In our experience, type IIIB defects
are generally best managed with
modular tapered fluted stems; how-
ever, some centers have had good
long-term results with impaction
bone grafting. APC and megapros-
theses should be considered part of
the armamentarium for managing
type IV femoral bone loss.
References
Evidence-based Medicine: Levels of
evidence are described in the table of
contents. In this article, references 2,
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Reference 3 is level V expert opinion.
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years.
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(295):172-178.
11. Aribindi R, Barba M, Solomon MI, Arp
P, Paprosky W: Bypass fixation. Orthop
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13. Pellicci PM, Wilson PD Jr, Sledge CB,
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516.
14. Berry DJ, Harmsen WS, Ilstrup D,
Lewallen DG, Cabanela ME: Survivor-
ship of uncemented proximally porous-
coated femoral components. Clin
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15. Cameron HU: The long-term success of
modular proximal fixation stems in revi-
sion total hip arthroplasty. J Arthro-
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16. Weeden SH, Paprosky WG: Minimal
11-year follow-up of extensively porous-
coated stems in femoral revision total hip
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suppl 1):134-137.
17. Sporer SM, Paprosky WG: Revision total
hip arthroplasty: The limits of fully
coated stems. Clin Orthop Relat Res
2003;(417):203-209.
18. Park YS, Moon YW, Lim SJ: Revision
total hip arthroplasty using a fluted and
tapered modular distal fixation stem
with and without extended trochanteric
osteotomy. J Arthroplasty 2007;22(7):
993-999.
19. Garbuz DS, Toms A, Masri BA, Duncan
CP: Improved outcome in femoral revi-
sion arthroplasty with tapered fluted
modular titanium stems. Clin Orthop
Relat Res 2006;453:199-202.
Neil P. Sheth, MD, et al
20. Richards CJ, Duncan CP, Masri BA,
Garbuz DS: Femoral revision hip arthro-
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signs. Clin Orthop Relat Res 2010;
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21. Grünig R, Morscher E, Ochsner PE:
Three-to 7-year results with the unce-
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187-197.
22. Isacson J, Stark A, Wallensten R: The
Wagner revision prosthesis consistently
restores femoral bone structure. Int
Orthop 2000;24(3):139-142.
23. Ornstein E, Linder L, Ranstam J, Lewold
S, Eisler T, Torper M: Femoral impac-
tion bone grafting with the Exeter stem:
The Swedish experience. Survivorship
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between 1989 and 2002. J Bone Joint
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24. Blackley HR, Davis AM, Hutchison CR,
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Am 2001;83(3):346-354.
25. Safir O, Kellett CF, Flint M, Backstein
D, Gross AE: Revision of the deficient
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467(1):206-212.
26. Babis GC, Sakellariou VI, O’Connor MI,
Hanssen AD, Sim FH: Proximal femoral
allograft-prosthesis composites in revi-
sion hip replacement: A 12-year
follow-up study. J Bone Joint Surg Br
2010;92(3):349-355.
27. Haentjens P, De Boeck H, Opdecam P:
Proximal femoral replacement prosthesis
for salvage of failed hip arthroplasty:
Complications in a 2-11 year follow-up
study in 19 elderly patients. Acta Orthop
Scand 1996;67(1):37-42.
28. Malkani AL, Settecerri JJ, Sim FH, Chao
EY, Wallrichs SL: Long-term results of
proximal femoral replacement for non-
neoplastic disorders. J Bone Joint Surg
Br 1995;77(3):351-356.
29. Meding JB, Ritter MA, Keating EM,
Faris PM: Clinical and radiographic eval-
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following revision total hip arthroplasty.
J Arthroplasty 1994;9(4):399-408.
30. Tomford W: Current concepts review:
Transmission of disease through trans-
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J Bone Joint Surg Am 1995;77(11):1742-
1754.
31. Chandler H, Clark J, Murphy S, et al:
Reconstruction of major segmental loss
of the proximal femur in revision total
hip arthroplasty. Clin Orthop Relat Res
1994;(298):67-74.
32. Morris HG, Capanna R, Del Ben M,
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Femoral Bone Loss in Revision Total Hip Arthroplasty: Evaluation and Management

Campanacci D: Prosthetic reconstruction
of the proximal femur after resection for
bone tumors. J Arthroplasty 1995;10(3):
293-299.
33. Sim FH, Chao EY: Hip salvage by proxi-
mal femoral replacement. J Bone Joint
Surg Am 1981;63(8):1228-1239.
34. Malkani AL, Sim FH, Chao EY:
Custom-made segmental femoral re-
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1993;24(4):727-733.
35. Clarke HD, Berry DJ, Sim FH: Salvage
of failed femoral megaprostheses with
allograft prosthesis composites. Clin
Orthop Relat Res 1998;(356):222-229.
36. Renard AJ, Veth RP, Schreuder HW,
Schraffordt Koops H, van Horn J, Keller
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Surg 1998;117(3):125-131.

612 Journal of the American Academy of Orthopaedic Surgeons


Bradley R. Kuzel, MD
Steven Grindel, MD
Rick Papandrea, MD
Dean Ziegler, MD
From Essentia Health, Duluth, MN
(Dr. Kuzel), the Medical College of
Wisconsin, Milwaukee, WI
(Dr. Grindel), the Orthopaedic
Associates of Wisconsin, Waukesha,
WI (Dr. Papandrea), and Blount
Orthopaedic Clinic, Milwaukee
(Dr. Ziegler).
Dr. Grindel or an immediate family
member serves as a board member,
owner, officer, or committee member
of the American Society for Surgery
of the Hand, the Wisconsin
Orthopaedic Society, and the
Milwaukee Orthopaedic Society.
Dr. Papandrea or an immediate
family member is a member of a
speakers’ bureau or has made paid
presentations on behalf of and
serves as a paid consultant to
Acumed and Exactech. Dr. Ziegler
or an immediate family member
serves as a paid consultant to
DePuy. Neither Dr. Kuzel nor any
immediate family member has
received anything of value from or
has stock or stock options held in a
commercial company or institution
related directly or indirectly to the
subject of this article.
J Am Acad Orthop Surg 2013;21:
613-623
http://dx.doi.org/10.5435/
JAAOS-21-10-613
Copyright 2013 by the American
Academy of Orthopaedic Surgeons.
October 2013, Vol 21, No 10
Review Article
Fatty Infiltration and Rotator Cuff
Atrophy
Abstract
Moderate to severe fatty infiltration and rotator cuff atrophy are
commonly associated with poor clinical outcomes and failed rotator
cuff repair. Numerous animal and human studies have attempted to
elucidate the etiology of fatty infiltration and rotator cuff atrophy.
Mechanical detachment of the tendon in rotator cuff tears is
primarily responsible. Suprascapular nerve injury may also play a
role. CT, MRI, and ultrasonography are used to evaluate severity.
The Goutallier staging system is most commonly used to evaluate
fatty infiltration, and rotator cuff atrophy is measured using multiple
techniques. The presence and severity of fatty infiltration have
been associated with increasing age, tear size, degree of tendon
retraction, number of tendons involved (ie, massive tears),
suprascapular neuropathy, and traumatic tears. Fatty infiltration is
irreversible and progressive if left untreated. Slight reversal of
muscle atrophy has been noted after repair in some studies. Novel
therapies are currently being evaluated that may eventually allow
clinicians to alter the natural history and improve patient outcomes.
G outallier et al1 introduced the
concept of fatty degeneration of
the rotator cuff in 1989. They de-
fatty infiltration are undoubtedly
part of the same process, they have
been found to be independent predic-
vised a staging system and noted that tors of outcome.10
degeneration of the rotator cuff mus- Poor interobserver correlation ex-
cles was associated with rotator cuff ists between orthopaedic surgeons
tears (RCTs). Numerous natural his- when determining the degree of atro-
tory and outcomes studies published phy and fatty infiltration.14-16 Al-
since then have noted progressively though the Goutallier staging system
higher re-tear rates and poorer func- is the most commonly used, many
tional outcomes in patients with pre- modifications have been developed.
operative fatty infiltration and rota- The description of rotator cuff atro-
tor cuff atrophy.2-12 phy also varies.3,5,17
The terms fatty degeneration, fatty It is important to understand the
infiltration, fatty change, and even original Goutallier staging system
fatty atrophy are often used inter- and its variations in order to apply
changeably. Using histologic analysis them in clinical practice and to effec-
in an ovine model, Meyer et al13 tively review the literature. Greater
noted infiltration of adipose cells, understanding of the etiology of fatty
not muscle fiber degeneration. Cur- infiltration and rotator cuff atrophy
rently, the term fatty infiltration is may ultimately lead to an improved
the most commonly used descriptor. understanding of management algo-
Although rotator cuff atrophy and rithms, outcomes, and prognosis.
613
Fatty Infiltration and Rotator Cuff Atrophy

Figure 1 tator cuff muscle (ie, infraspinatus).

CT, histologic analysis, and electron
microscopy were used to evaluate the
effect of tendon detachment over the
course of 40 weeks, after which the
effects of tendon repair were moni-
tored for 35 weeks. Detachment did
not alter vascular perfusion of the
tendon or the composition of indi-
vidual muscle fibers. It did, however,
lead to increased muscle atrophy,
Superior axial photographs of a normal intact supraspinatus muscle (A) and inter- and intrafascicular fat content,
of a large retracted supraspinatus tear with muscle atrophy, fibrosis, and fatty and connective tissue content. These
infiltration (B) in a cadaver specimen. Note shortening of the muscle fibers
and the increased pennation angle in panel B. (Adapted with permission from
changes progressed over time, even
Tomioka T, Minagawa H, Kijima H, et al: Sarcomere length of torn rotator cuff after repair of the rotator cuff at 40
muscle. J Shoulder Elbow Surg 2009;18[6]:955-959.) weeks. The severity of these findings
was associated with the amount of
retraction. The degree of muscle at-
Figure 2
rophy improved slightly 12 weeks af-
ter repair, but the amount of fatty in-
filtration did not.
Nerve injury has also been implicated
in the development of rotator muscle
atrophy and fatty infiltration. Re-
tracted tears of the supraspinatus may
increase tension on the suprascapular
nerve (SSN) at the suprascapular
notch.20 Traction on the nerve can
also occur at the scapular spine in
combined supraspinatus/infraspin-
atus tears21 (Figure 2). Mallon et al22
found slowed SSN conduction veloc-
ity in patients with massive RCTs.
A, Illustration of suprascapular nerve (SSN) traction injury at the base of the
Vad et al23 reported a 28% rate of
scapular spine due to medial and inferior retraction of a massive
posterosuperior rotator cuff tear. B, Illustration of relief of traction on the SSN peripheral neuropathy in the axillary
following repair of the rotator cuff tear. nerve and SSN associated with full-
thickness RCTs and atrophy. Other
studies have shown nerve recovery
denervation likely play a role in the after repair of massive RCTs.21
Pathophysiology development of muscle atrophy and Rowshan et al24 found a decrease
fatty infiltration. Mechanical un- in muscle mass and cross-sectional
The etiology of fatty infiltration and area and an increase in fat content 6
loading of the muscle has been
rotator cuff atrophy is complex and weeks after tenotomy of rabbit sub-
shown to increase the pennation an-
not fully understood. Along with in- gle of muscle fibers13 (Figure 1). In- scapularis muscles. Rabbits subjected
creased connective tissue content and terstitial fat and fibrous tissue fills in to transection of the subscapular
fibrosis, both atrophy and fatty infil- the spaces between reoriented muscle nerve showed similar patterns of fat
tration decrease the elasticity and vi- fibers following musculotendinous accumulation, both temporally and
ability of the rotator cuff and impair retraction. The muscle fibers them- spatially (Figure 3). Histologic analy-
healing.9,18,19 Investigations are un- selves do not degenerate.13 sis showed wallerian degeneration, ax-
derway to discover the causative cel- Using a sheep model, Gerber et al18 onal demyelination, and myelin debris
lular and molecular processes. studied the effect of muscle detach- formation of the subscapular nerve in
Both mechanical unloading and ment on the composition of one ro- the tenotomy and nerve transection

614 Journal of the American Academy of Orthopaedic Surgeons

 Bradley R. Kuzel, MD, et al

Figure 3 Figure 4

Clinical photograph of infraspinatus

atrophy noted on physical
examination.

may be evaluated subjectively or can

Photomicrographs of cross-sectional rabbit subscapularis muscle stained with be quantified with a dynamometer.
hematoxylin-eosin (original magnification ×200). Control (A), complete Patients with massive RCTs and se-
tenotomy (B), and subscapularis nerve transection (C) at 2 weeks. Control
(D), complete tenotomy (E), and nerve transection (F) at 6 weeks. vere stage 3 or 4 fatty infiltration of
(Reproduced with permission from Gupta R, Lee TQ: Contributions of the the infraspinatus and teres minor
different rabbit models to our understanding of rotator cuff pathology. J may exhibit decreased or absent ex-
Shoulder Elbow Surg 2007;16[5 suppl]:S149-S157.) ternal rotation strength as well as a
positive external rotation lag sign
groups. Rabbits that underwent partial rophy should follow the standard (infraspinatus) and a hornblower
tenotomy had minimal change in mus- principles used for the evaluation of sign (teres minor)29 (Figure 5). Per-
cle mass and fat content. shoulder pathology. The history sons with massive anterosuperior
Kim et al25 evaluated the effect of should contain a thorough discus- cuff tears and severe atrophy and
tenotomy and neurotomy on rodent ro- fatty infiltration exhibit weak or ab-
sion of the patient’s shoulder pain
tator cuff muscles. Histologic analysis sent findings on the belly press, lum-
and function, as well as the effect of
showed adipocytes, intramuscular fat bar lift-off, and bear hug tests.30-32
that pain on work and activities of
globules, and intramyocellular fat drop- Injections of the glenohumeral
daily living. The patient’s perceived
lets in both groups. Those authors joint, subacromial space, acromio-
level of shoulder function can be as-
noted that adipogenic and myogenic clavicular joint, suprascapular notch,
sessed using the Simple Shoulder
transcription factors were upregulated and biceps tendon may be of diag-
Test, the Constant-Murley score, or nostic and therapeutic benefit.33 Pa-
and that histologic changes increased
the American Shoulder and Elbow tients with suspected suprascapular
over time. Rodents with both tenotomy
Surgeons (ASES) shoulder score or neuropathy can be evaluated using
and neurotomy had the most severe
an equivalent.28 electromyography (EMG) and nerve
findings.
In patients with suspected or conduction velocity (NCV) studies.
Overviews of the current knowl-
known rotator cuff atrophy and fatty The SSN must be specifically re-
edge of cellular- and molecular-level
processes related to atrophy and infiltration, a standard shoulder quested because it is not always rou-
fatty infiltration can be found else- physical examination should be per- tinely tested. It is important to note
where.26,27 formed with special emphasis on a that overall sensitivity and specificity
few key elements. Patients with se- of EMG-NCV studies can be quite
vere rotator cuff disease often exhibit variable.34
Clinical Evaluation atrophy of the supraspinatus and/or
infraspinatus muscles on visual sur- Imaging
History and Physical face examination (Figure 4). Mild to Standard shoulder radiographs
Examination moderate atrophy of the supraspina- should be evaluated. Narrowing of
Clinical evaluation of patients with tus can be masked by the overlying the acromiohumeral interval has
rotator cuff fatty infiltration and at- trapezius. Supraspinatus weakness been associated with increasing rota-

October 2013, Vol 21, No 10 615

Fatty Infiltration and Rotator Cuff Atrophy

tor cuff atrophy and fatty infiltra-
tion, and it is most pronounced with
infraspinatus involvement.35
In the initial iteration of the
Goutallier staging system, axial CT
was used to evaluate the supraspina-
tus, subscapularis, and infraspinatus
muscles.1,2 The supraspinatus was eval-
uated on the axial image with the most
muscle surface area (approximately 5
mm above the humeral head) (Figure
Figure 5
6). The subscapularis and infraspina-
tus were evaluated superiorly at the
level of the tip of the coracoid and in-
feriorly at the level of the lower gleno-
humeral joint. The muscles were then
assigned a stage (Table 1). The sub-
scapularis and infraspinatus values
were averaged individually. The mean
value of all rotator cuff muscles to-
gether was then averaged to create a
global fatty degeneration index
(GFDI).1,2
Fuchs et al36 modified the Goutal-
lier staging system, using magnetic
resonance arthrography to assess
fatty infiltration (Table 2). All mus-
cles were evaluated on the most lat-
eral parasagittal image on which the
scapular spine was in contact with
the scapular body (Figure 7). Inter-
observer agreement improved in the
evaluation of MRI and CT studies,
although correlation was poor be-
tween MRI and CT.36 Differences be-
tween the MRI and CT findings were
likely related to the difficulty of dis-
tinguishing fibrous tissue from fat on
CT scans and the variability in the
image plane used between the two
techniques.
Rotator cuff atrophy has generally
been evaluated using either an occu-
pation ratio as described by
Thomazeau et al4 or the tangent sign
introduced by Zanetti et al.17 The oc-
cupation ratio was defined as the
surface area supraspinatus muscle/
surface area supraspinatus fossa4
(Figure 8) (Table 3). The tangent sign
is negative if the supraspinatus
crosses a line between the superior
aspect of the coracoid and the supe-

Table 1
Goutallier Staging System for Grading Fatty Infiltration Based on CT1
Stage Rotator Cuff Fat Content

0 Normal muscle with no fatty streak

Clinical photograph of a patient
with a positive hornblower sign.
When asked to bring both hands to
her mouth, the patient was unable
to do so on the affected (ie, right)
side without abducting her right
arm.
1 Some fatty streaks in the muscle
2 Fatty infiltration is present, but more muscle exists than fat
3 Equal amounts of fat and muscle
4 More fat than muscle
Adapted from Omid R, Lee B: Tendon transfers for irreparable rotator cuff tears. J Am Acad
Orthop Surg 2013;21(8):492-501.

Figure 6

A, Axial CT scan demonstrating Goutallier stage 2 fatty infiltration of the supraspinatus muscle (SS). B, Superior axial
cut demonstrating stage 1 fatty infiltration of the subscapularis (Sub) and infraspinatus (asterisk) muscles. C, Inferior
axial cut demonstrating stage 2 fatty infiltration of the subscapularis and infraspinatus muscles. Note the black fatty
streaks (arrows) within the muscle. (Adapted with permission from Goutallier D, Postel JM, Gleyze P, Leguilloux P, Van
Driessche S: Influence of cuff muscle fatty degeneration on anatomic and functional outcomes after simple suture of
full-thickness tears. J Shoulder Elbow Surg 2003;12[6]:550-554.)

616 Journal of the American Academy of Orthopaedic Surgeons

 Bradley R. Kuzel, MD, et al

rior border of the scapular spine.
MRI evaluation is performed using
the most lateral image where the
scapular spine is in contact with the
body of the scapula17 (Figure 9). The
grading system for rotator cuff atro-
phy proposed by Warner et al5 in-
cludes the subscapularis as well as
the supraspinatus (Figure 10).
Williams et al37 studied 87 CT scans
to determine the best plane for evalu-
ating fatty infiltration of the supraspi-
natus on CT. Using both the Goutallier
and Fuchs staging systems, they found
the axial plane to be superior to the
sagittal and coronal planes. Moreover,
they found grade 3 fatty infiltration of
the supraspinatus to be directly corre-
lated with a positive tangent sign (P <
0.0001).
Rotator cuff atrophy and fatty in-
filtration have also been evaluated
using ultrasonography. Benefits of
ultrasonography include affordabil-
ity, ease of use, dynamic evaluation
of the rotator cuff, and patient bene-
fits (eg, affordability, comfort, ability
of the patient to view the study in
real time). Drawbacks include avail-
ability and dependence on technician
skill.15,38,39 Khoury et al15 evaluated
45 shoulders in 39 patients and de-
termined occupation ratios with
both MRI and ultrasonography. The
correlation with MRI evaluation was
0.90. Fatty infiltration was also eval-
uated using ultrasonography. On ul-
trasonography, it was possible to dif-
ferentiate between mild and severe
fatty infiltration by grading echoge-
nicity as mild or marked and to de-
termine the status of the muscle pen-
nation pattern (ie, normal, effaced,
or absent). However, it is difficult to
distinguish moderate from severe
fatty infiltration using ultrasonogra-
phy.15
Concerns about current grading
systems include lack of agreement
among clinicians and variability in
Table 2
Fuchs System of Grading Fatty Infiltration on MRI36
Grade
Goutallier stages 0 and 1 (minimal)
Goutallier stage 2 (moderate)
Goutallier stages 3 and 4 (severe)
images assessed. Given the spatial
variation in fatty infiltration, single
sagittal oblique images may not pro-
vide an accurate assessment of the
whole rotator cuff musculature.
Clinical studies performed after rota-
tor cuff repair must be interpreted
with caution. Lateralization of the
supraspinatus muscle may falsely in-
crease the occupation ratio and will
change the portion of the muscle
evaluated for fatty infiltration.
Recent investigations have called
into question the reproducibility of
the techniques used to assess rotator
cuff atrophy and fatty infiltration. In
an MRI study in which multiple
findings were evaluated by 10
fellowship-trained orthopaedic sur-
geons who specialize in the shoulder,
Rotator Cuff Fat Content
No fat to minimal fat
More muscle than fat
Equal amounts fat and muscle or more fat
than muscle

Figure 7

T1-weighted sagittal oblique magnetic resonance images of the shoulder demonstrating the Fuchs method of
determining fatty infiltration of muscle. A, Normal rotator cuff musculature in a healthy young person. B, Severe
Goutallier (G) stage 3/4 fatty infiltration of the supraspinatus (SS), subscapularis (Sub), and infraspinatus (IS) muscles
in an elderly patient. The teres minor (TM) demonstrates moderate Goutallier stage 2 fatty infiltration. C, Severe
Goutallier stage 3/4 fatty infiltration of the external rotators of the IS and TM, stage 3 infiltration of the IS, and stage 2
fatty infiltration of the Sub and SS muscles in a middle-aged patient.

October 2013, Vol 21, No 10 617

Fatty Infiltration and Rotator Cuff Atrophy
Figure 8
Illustration of the elements involved
in the Thomazeau method of
calculating the occupation ratio
based on a sagittal oblique view.
S1 = surface of the supraspinatus
muscle, S2 = entire supraspinatus
fossa
Spencer et al14 reported interobserver
agreement of 0.36 with the Goutal-
lier grading system. Interobserver
agreement for the tangent sign was
0.59.
Oh et al16 evaluated both CT scans
and magnetic resonance images of 75
shoulders using both the Goutallier
and the Fuchs classifications. Two
musculoskeletal radiologists and
three fellowship-trained orthopaedic
surgeons who specialize in the shoul-
der were noted to have slightly better
interobserver agreement on MRI (in-
terclass correlation coefficient [ICC],
0.6 to 0.72) than on CT (ICC, 0.43
to 0.6). No difference was noted be-
tween the Goutallier and Fuchs grad-
ing systems. Interobserver agreement
was significantly better among radi-
ologists (ICC, 0.58 to 0.78) than or-
thopaedic surgeons (ICC, 0.32 to
0.68).
Several applications are being in-
vestigated in an effort to make the
evaluation of rotator cuff atrophy
and fatty infiltration more objective
and clinically practical. For example,
618
Table 3
Thomazeau Grading System of Rotator Cuff Atrophy4
Grade Atrophy Status
I Normal/slight
II Moderate
III Severe
Figure 9
Coronal magnetic resonance image
of a shoulder demonstrating a
negative (almost positive) tangent
sign (black line). IS = infraspinatus
muscle, SS = suprascapular
muscle, Sub = subscapularis
muscle, TM = teres minor
multidetector CT has been used to
determine occupation ratios using Y
views of the supraspinatus fossa.
High intra- and interobserver corre-
lation was found between multide-
tector CT and T1- and T2-weighted
MRI (range, 0.89 to 0.98; P <
0.001).40 Proton magnetic resonance
spectroscopy programs have been de-
veloped to quantify the fat content of
muscle.41 The technology that gains
the greatest acceptance and wide-
spread use must be easy to use, inex-
pensive, and readily available.
Natural History
In general, the natural history of
fatty infiltration is one of progres-
Journal of the American Academy of Orthopaedic Surgeons
Occupation Ratio
0.6–1.0
0.4–0.6
<0.4
sion. In a retrospective review of
1,688 shoulder MRI and CT studies,
Melis et al12 found moderate supra-
spinatus fatty infiltration (Goutallier
stage 2) an average of 3 years after on-
set of shoulder symptoms (traumatic
tears, P = 0.04). Onset of moderate
fatty infiltration was noted earlier in
traumatic RCTs than in chronic tears
(34.8 mo [P = 0.04] and 54.1 mo [P =
0.003], respectively). Severe infiltration
was noted an average of 57.7 months
after traumatic tears (P = 0.04) and
83.9 months after chronic progressive
tears (P = 0.003). Patients had a pos-
itive tangent sign indicating severe at-
rophy at an average of 4.5 years after
symptom onset (P = 0.001). Fatty in-
filtration of the supraspinatus was as-
sociated with increasing patient age,
delay between symptom onset and di-
agnosis, and the number of tendons in-
volved. Degree of muscle atrophy was
influenced by fatty infiltration, the
number of tendons involved, delay be-
tween symptom onset and diagnosis,
and patient age. The authors of the
study concluded that rotator cuff repair
should be performed before Goutallier
stage 2 fatty infiltration or the develop-
ment of a positive tangent sign.
Maman et al42 retrospectively eval-
uated 59 shoulders in patients who
were diagnosed with RCT on MRI
evaluation and who elected to un-
dergo nonsurgical treatment. Partial-
thickness tears did not exhibit atro-
phy, and only one had fatty
infiltration. Fatty infiltration was
present or advanced in 70% of pa-
tients whose tear size increased dur-
 Bradley R. Kuzel, MD, et al

Figure 10

Illustration of the Warner method of evaluating rotator cuff atrophy based on T1-weighted sagittal oblique magnetic
resonance images.5 The grade is determined by the amount of muscle above or below a line drawn from the edge of
the coracoid to the tip of the scapular spine. The Zanetti tangent line extends from the superior aspect of the coracoid
to the superior border of the scapular spine.

ing the course of the study (P =
0.0089). By contrast, 24% of shoul-
ders without new fatty infiltration or
advancement of existing fatty infil-
tration developed progressive tears
(P = 0.0089). In addition, the in-
crease in overall tear size was signifi-
cantly larger for patients with fatty
infiltration than for those without in-
filtration (P = 0.0089). The authors
also noted that 17% of tears pro-
gressed in patients aged ≤60 years
compared with 54% in patients
older than 60 years (P = 0.007). The
authors concluded that factors asso-
ciated with progressive RCT include
age >60 years, full-thickness tears,
and fatty infiltration.
Kim et al43 used ultrasonography
to evaluate both shoulders in 262 pa-
tients and noted that tear length and
width were significantly greater in
shoulders with fatty degeneration (P
< 0.0001). The location of the su-
praspinatus tears was more impor-
tant than tear size or retraction in
the degree of fatty degeneration. The
odds of having fatty degeneration de-
creased significantly the farther the
tear was from the biceps tendon. The
anterior region of the supraspinatus
insertion near the biceps tendon is
the site of attachment of the rotator
cable, and the authors speculated
that it is under greater load than
other portions of the muscle. In-
fraspinatus fatty degeneration was
more closely associated with tear size
and retraction.
Melis et al35 reported on the natu-
ral history of fatty infiltration of the
infraspinatus. They noted that in-
fraspinatus fatty infiltration in-
creased significantly in the presence
of infraspinatus tendon tear and
when multiple tendons were torn (P
< 0.0005). Likewise, they noted
worse fatty infiltration with increas-
ing age (P < 0.0005). Other studies
have shown that the infraspinatus
can develop fatty infiltration even
when it is not torn.44 This finding
has been noted in patients with large
anterosuperior tears.1,44 It may be at-
tributed to a traction injury of the
SSN caused by retraction of the an-
terosuperior cuff. It is also possible
that tears of the infraspinatus have
been mistaken as tears of the su-
praspinatus. Mochizuki et al45 noted
the insertion of the infraspinatus to
be far more anterior than previously
thought. Infraspinatus degeneration
is speculated to upset the anterior-
posterior glenohumeral force couple
and to lead to proximal humeral mi-
gration and further degradation of
the supraspinatus.35 Goutallier et al1
noted that infraspinatus lesions were
associated with poorer functional
outcomes and external rotation.
The natural history of massive
RCTs is paradoxical. Zingg et al46
retrospectively evaluated the natural
history of fatty infiltration in 19
shoulders with massive RCTs at an
average of 48 months after diagno-
sis. They noted a significant increase
in tear size (P = 0.003) and glenohu-
meral arthritis (P = 0.014) as well as
decreased acromiohumeral distance
(P = 0.005). Fatty infiltration in-
creased by approximately one stage
in all three muscles (P = 0.001). Even
so, patients maintained satisfactory
shoulder function (ie, mean Constant
score of 83). Four of eight tears,
however, became irreparable (ie,
acromiohumeral distance <7 mm and
Goutallier stage 3 or greater).

October 2013, Vol 21, No 10 619

Fatty Infiltration and Rotator Cuff Atrophy
Outcomes
Outcomes diminish as rotator cuff
atrophy and fatty infiltration
worsen. Using preoperative CT scans
as well as follow-up CT scans and
magnetic resonance images obtained
an average of 3 years after repair,
Goutallier et al6 evaluated 220 open
RCTs repaired with sutures through
bone tunnels. GFDI values were tab-
ulated for each shoulder before sur-
gery and at follow-up. The overall
re-tear rate was 36% (P < 0.001). All
shoulders with a GFDI ≥2 exhibited
evidence of recurrent tear (P <
0.001). A GFDI <0.5 was required
for a re-tear rate <25%. Constant
scores improved from 46 to 70 in the
group of patients with recurrent tear
and from 46 to 78 in the patients
with intact repairs (P < 0.0001). A
higher preoperative GFDI was asso-
ciated with a lower postoperative
Constant score (P < 0.001).
Fuchs et al7 evaluated 32 one-
tendon open rotator cuff repairs pre-
operatively and at an average of 38
months after repair. They noted a
13% re-tear rate, all of which were
distinctly smaller than the original
tear. The average Constant score im-
proved from 63.9% preoperatively
to 94.5% postoperatively (P <
0.0001). Muscular atrophy did not
decrease significantly after tendon re-
pair. Fatty infiltration of the su-
praspinatus and infraspinatus in-
creased significantly despite repair (P
< 0.0053 and P < 0.003, respec-
tively). Rotator cuff atrophy was sig-
nificantly worse in patients with re-
tears than in those with intact repairs
(P < 0.049).
In a study published in 2009,
Goutallier et al11 retrospectively eval-
uated patients with a GFDI ≤2 with
intact repairs 1 year after surgery
and at an average of 9 years after
surgery. They found functional out-
comes to be related to GFDI at base-
620
line and last follow-up. Constant
scores improved significantly for 2
years after surgery and then re-
mained stable, with an average final
Constant score of 77 (range, P <
0.0001 to 0.0002). In general, pa-
tients with a GFDI ≤2 had excellent
results and intact rotator cuff re-
pairs. These results were maintained
over time.
Gladstone et al10 evaluated 38 open
and arthroscopic rotator cuff repairs
with MRI studies obtained before re-
pair and 1 year after surgery. Rotator
cuff atrophy and fatty degeneration,
specifically of the infraspinatus, had a
negative effect on functional assess-
ment scores, strength, and the integrity
of the rotator cuff repair. Using a re-
gression analysis model, fatty infiltra-
tion and rotator cuff atrophy of the in-
fraspinatus were found to be the only
preoperative variables that predicted
poorer ASES and Constant scores.
There was no relation between the
quality of the rotator cuff muscles and
patient pain levels. Both fatty infiltra-
tion and atrophy progressed during the
study, even in successful repairs. Re-
ruptured rotator cuffs developed a
greater degree of fatty infiltration and
atrophy than did successful repairs.
Based on the results of this study, Glad-
stone et al10 agreed with the prior
suggestion that there might be a so-
called point of no return when the
muscles are irreversibly damaged.
Liem et al47 retrospectively evalu-
ated 53 consecutive patients who un-
derwent arthroscopic repair of iso-
lated supraspinatus tears. They
obtained MRI studies on all patients
at an average of 26.4 months post-
operatively and noted a re-tear rate
of 25%. Constant scores improved
dramatically regardless of integrity
of the rotator cuff. Preoperative
stage 2 fatty infiltration was a posi-
tive predictor of recurrent tear, and
older age was associated with re-tear.
In patients with intact repairs, fatty
infiltration and atrophy did not
Journal of the American Academy of Orthopaedic Surgeons
progress. In those with recurrent
tear, fatty infiltration and atrophy
worsened significantly; these patients
had inferior functional results.
Gerber et al3 studied 29 patients
who had undergone open repair to
manage massive RCT and noted a
34% re-tear rate. Re-tears were more
likely in patients with traumatic
RCTs (P < 0.05). Supraspinatus atro-
phy was mildly reversed after repair.
Infraspinatus atrophy worsened even
after successful repairs. Fatty infiltra-
tion was not reversible but pro-
gressed less in patients with intact re-
pairs. As found in other studies, the
Constant score improved signifi-
cantly even in patients with re-tears,
from 49% to 85% (P = 0.0024).
Range of motion improved and pain
decreased.
Warner et al5 evaluated the open
repair of combined subscapularis
and supraspinatus (anterosuperior)
tears and noted significantly worse
Constant scores in patients with se-
vere fatty infiltration and atrophy.
The average postoperative Constant
score was 79 for patients with stage
1 fatty infiltration compared with 31
in patients with stage 4 fatty infiltra-
tion (P < 0.05).
Arthroscopic repair of massive
RCTs has demonstrated promising
results. Burkhart et al48 evaluated 22
patients with massive RCTs with
Goutallier stage 3 and 4 fatty infil-
tration of the infraspinatus. At an
average of 39.3 months after surgery,
they noted significant improvement
in range of motion; strength; Univer-
sity of California, Los Angeles
(UCLA) score; and Constant score.
Of patients with Goutallier stage 3
or 4 fatty infiltration, those with
50% to 75% fatty infiltration had
significantly better results than did
those with >75% fatty infiltration.
Burkhart et al48 speculated that their
improved outcomes were associated
with patient selection, tear recogni-
tion, and surgical technique.

Future Directions
At best, current interventions (eg,
successful rotator cuff repair) can
halt the progression of fatty infiltra-
tion. They cannot reverse it. Al-
though rotator cuff atrophy may im-
prove, the musculature will not fully
return to normal. Most rotator cuff
basic science studies have focused on
tendon-to-bone healing. Consistently
successful repairs cannot be expected
if the rotator cuff muscle itself is un-
healthy. Our knowledge of the
pathophysiology of rotator cuff atro-
phy and fatty infiltration is improv-
ing. Investigations into the cellular
and molecular pathogenesis of these
conditions offer the hope of creating
new management techniques that
will halt or reverse the progression of
fatty infiltration and rotator cuff at-
rophy.26,27
Gerber et al19 evaluated indirect
improvement of the local environ-
ment by studying the effect of slow
continuous traction on torn retracted
rotator cuff muscles in sheep. They
postulated that tension created when
repairing chronic retracted RCTs in
one-stage procedures is harmful to
the muscle, whereas slow continuous
traction would allow normalization
of the muscle architecture. They
elongated the infraspinatus musculo-
tendinous unit 1 mm per day and
noted partial reversal of atrophy and
normalization of the rotator cuff
muscle architecture histologically.
Fatty infiltration did not progress in
sheep managed with traction, and at-
rophy decreased to 78% of the mus-
cle square area of the contralateral
side (P = 0.0001). In sheep in which
traction failed, fatty infiltration in-
creased, but not to a statistically sig-
nificant degree (P = 0.144).
In a study published 2 years later,
Gerber et al49 evaluated the effect of
anabolic steroids on fatty infiltration
and atrophy in rabbits with chronic
October 2013, Vol 21, No 10
RCTs. They noted that nandrolone
decanoate administered either locally
or systemically inhibited the develop-
ment of fatty infiltration and par-
tially preserved muscle function.
Our understanding of gene expres-
sion patterns and complex molecular
pathways continues to evolve. Ulti-
mately, the goal is to find ways to
prevent the differentiation of mesen-
chymal stem cells into adipose cells.
Investigators hope to determine ways
to slow or halt the progression of fi-
brosis that often occurs after injury
and restore the ability of the muscle
to regain normal architecture.26,27
Summary
Increased fatty infiltration and rota-
tor cuff atrophy are associated with
increased re-tear rates as well as
poorer functional outcomes follow-
ing rotator cuff repair. Most studies
indicate that fatty infiltration does
not decrease after successful repair. It
increases, however, in patients with
failed repair. In some studies, atro-
phy has been shown to improve only
partially after successful repair. Risk
factors for progression of fatty infil-
tration include size and location of
the tear, degree of retraction, age,
and time from onset of symptoms to
diagnosis. Infraspinatus fatty infiltra-
tion predicts a poorer prognosis and
functional outcome following rota-
tor cuff repair. This is most likely
due to disruption of the anterior-
posterior glenohumeral force couple.
Management options are wide-
ranging. There are currently no
evidence-based guidelines for the
treatment of patients with fatty infil-
tration and rotator cuff atrophy. Un-
derstanding the degree of pain and
functional deficits in the context of
the patient’s everyday life is essential
to developing a treatment plan.
Historically, interobserver correla-
tion among orthopaedic surgeons
Bradley R. Kuzel, MD, et al
has been poor. In addition, signifi-
cant variation exists in the tech-
niques used to determine Goutallier
stage and degree of muscle atrophy.
Outcome studies must be read care-
fully to understand the technique
used. Our understanding of fatty in-
filtration and rotator cuff atrophy
will improve as methods of evalua-
tion become more objective and in-
clude analysis of the involved muscle
as a whole and the entire rotator cuff
as a functional unit.
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623

Richard L. Uhl, MD
Andrew James Rosenbaum, MD
Cory Czajka, MD
Michael Mulligan, MD
Christopher King, MD
From the Division of Orthopaedic
Surgery (Dr. Uhl, Dr. Rosenbaum,
Dr. Czajka, and Dr. Mulligan) and
the Department of Emergency
Medicine (Dr. King), Albany Medical
Center, Albany, NY.
Dr. Uhl or an immediate family
member is a member of a speakers’
bureau or has made paid
presentations on behalf of Auxilium
and has received nonincome
support (such as equipment or
services), commercially derived
honoraria, or other non–research-
related funding (such as paid travel)
from ConMed Linvatec, Stryker, and
Synthes. None of the following
authors or any immediate family
member has received anything of
value from or has stock or stock
options held in a commercial
company or institution related
directly or indirectly to the subject of
this article: Dr. Rosenbaum,
Dr. Czajka, Dr. Mulligan, and
Dr. King.
J Am Acad Orthop Surg 2013;21:
624-631
http://dx.doi.org/10.5435/
JAAOS-21-10-624
Copyright 2013 by the American
Academy of Orthopaedic Surgeons.
624
Review Article
Minor Traumatic Brain Injury: A
Primer for the Orthopaedic
Surgeon
Abstract
Minor traumatic brain injury (mTBI) is a major public health
problem. The Centers for Disease Control and Prevention and the
National Center for Injury Prevention and Control label it a “silent
epidemic.” Subtle signs and symptoms of mTBI, including
headache, fatigue, and memory loss, are often seen in conjunction
with musculoskeletal trauma. Although sometimes evident
immediately, mTBI may not manifest until patients return to work
and their personal lives. In the patient with acute concurrent mTBI,
skeletal management must be based on either a period of
observation to rule out evolving neurologic symptoms or, when
warranted, the recommendations of a neurosurgeon. Such input is
particularly important when mTBI is associated with a prolonged
loss of consciousness or posttraumatic amnesia. In the outpatient
setting, when concern for mTBI exists weeks after an injury,
familiarity with and referral to locally available mTBI specialists and
programs can facilitate proper care. Armed with this knowledge, the
orthopaedic surgeon has an opportunity to positively influence
outcomes and help provide crucial care that extends beyond the
management of musculoskeletal injuries.
mTBI have residual symptoms that
Background sometimes lead to compromised
function and can last a year or more
In the United States, approximately
1.4 million people suffer a traumatic after the original injury.1,8,9 The ex-
brain injury (TBI) annually.1 Of tent of this problem has led the Cen-
these, 75% sustain a minor TBI ters for Disease Control and Preven-
tion and the National Center for
(mTBI). Multiple definitions for
mTBI exist, but it is probably best Injury Prevention and Control to de-
described as a head injury that re- clare mTBI a major public health is-
sults in a transient change in mental sue and a silent epidemic; these orga-
status.1,2 nizations recommend that research
Despite the connotation of the efforts to reduce disability after
term minor, significant postinjury mTBI become a national priority.10
cognitive, emotional, behavioral, Falls and motor vehicle accidents
physical, and psychosocial problems are responsible for most cases of
are a relatively common cause of dis- mTBI and are a common cause of or-
ability and stress for patients with thopaedic injuries, as well.11 As such,
mTBI and their families.3-7 Fifteen a large number of patients with mus-
percent to 25% of those who sustain culoskeletal trauma may also have
Journal of the American Academy of Orthopaedic Surgeons

Table 1
Signs and Symptoms of Minor
Traumatic Brain Injury
Observed signs
Appears dazed
Confused about events
Repeats questions
Answers questions slowly
Amnesia for events before and/or
after the injury
Loss of consciousness
Behavioral or personality changes
Forgetfulness
Sleeping more or less than usual
Difficulty falling asleep
Physical symptoms
Headaches
Nausea or vomiting
Dizziness
Balance problems
Feeling tired
Blurry vision
Sensitivity to light and noise
Numbness or tingling
Cognitive symptoms
Difficulty concentrating
Difficulty thinking clearly
Difficulty remembering
Feeling sluggish and slow
Emotional symptoms
Irritability
Sadness
More emotional than usual
Nervous
sustained TBIs.12,13 Orthopaedic sur-
geons are in a position to evaluate
for and recognize mTBI, which is not
necessarily the result of high-energy
trauma. Often, mTBI goes undiag-
nosed initially because symptoms do
not appear until the patient resumes
everyday life. These patients may
present for routine orthopaedic care
following an accident, and they or
their family members may express
concern regarding the unexpected
cognitive sequelae associated with
mTBI. Therefore, the orthopaedic
October 2013, Vol 21, No 10
surgeon must be equipped to identify
mTBI and also facilitate proper care
that could have greater long-term ef-
fects on patient outcomes than mus-
culoskeletal care.
Case Study
A 54-year-old man was seen 3 weeks
after undergoing open reduction and
internal fixation for a bimalleolar
ankle fracture-dislocation. The in-
jury occurred when he fell 10 ft from
a ladder at his home. The fracture
was healing well, but the patient re-
ported significant ongoing symp-
toms, including headaches, dizziness,
difficulty concentrating, and de-
pressed mood. He experienced a
traumatic loss of consciousness for
several minutes after the fall but a
CT scan of the head, which was ob-
tained as part of the trauma evalua-
tion, was negative. He was con-
cerned about being able to return to
work after his extremity injury
healed.
This case depicts an all too com-
mon scenario in which the orthopae-
dic surgeon is the first, and possibly
only, healthcare provider to learn of
a patient’s cognitive symptoms fol-
lowing a presumed isolated ortho-
paedic injury.
Definitions
The terms head injury and TBI are
frequently, but incorrectly, used in-
terchangeably. Head injury is defined
as clinically evident trauma above
the clavicles, including lacerations,
ecchymosis, and abrasions. TBI im-
plies impairment of the brain’s func-
tion, which can occur even in the ab-
sence of visible head injury.1 Specific
signs of TBI include confusion, an al-
tered level of consciousness, focal
neurologic deficits, and more subtle
findings identifiable only on neurop-
sychological examinations (Table 1).
Richard L. Uhl, MD, et al
The orthopaedic surgeon must be fa-
miliar with these signs and symp-
toms and appreciate that these
findings are not always evident im-
mediately. Often, symptoms develop
insidiously and go unrecognized un-
til outpatient follow-up.
In a clinical context, the terms con-
cussion and mTBI are often used
synonymously. Although they are
conceptually similar, mTBI more ac-
curately pertains to the pathologic
state of the brain after a concussive
event.14 The American Academy of
Neurology has classified concussions
into three grades.15 In grades 1 and
2, no loss of consciousness occurs;
however, altered mental status is
present for <15 minutes (grade 1) or
>15 minutes (grade 2). Grade 3 con-
cussions involve any loss of con-
sciousness.
In the literature pertaining to mTBI,
a consensus definition does not exist,
and the precise criteria for diagnosis is
a topic of debate.5,16-18 Historically,
the criteria have included a loss of
consciousness for <30 minutes, am-
nesia for <24 hours, or peri-injury
confusion/disorientation in a patient
with a Glasgow Coma Scale (GCS)
score of 13 to 1516-19 (Table 2). How-
ever, patients with a persistent GCS
score of 13 are currently excluded
from the category of mTBI because
this score is more commonly associ-
ated with intracranial lesions found
on CT, the need for neurosurgical in-
tervention, and adverse long-term se-
quelae.1 Generally, these patients are
now classified as having moderate
TBI. Patients with severe TBI are
those who have structural brain ab-
normalities that result in permanent
neurologic dysfunction or death.
Pathophysiology
In all types of TBI, the brain is sub-
ject to linear forces (acceleration/
deceleration), rotational forces, or
625
Minor Traumatic Brain Injury: A Primer for the Orthopaedic Surgeon
both. Because the type and severity
of these forces vary with each pa-
tient, a wide variety of resulting inju-
ries are seen. Animal models and hu-
man studies that used novel imaging
techniques (eg, magnetic resonance
spectroscopy, single photon emission
CT) suggest that mTBI results in a
complex cascade of neurometabolic
changes.20-22 Abnormalities in the
brain, including unchecked ionic
shifts, indiscriminant release of neu-
rotransmitters, impaired axonal me-
tabolism, and alteration in cellular
glucose metabolism, likely result in a
metabolic energy crisis that may per-
sist for long periods. In addition, ul-
trastructural axonal shearing injuries
may also influence the pathophysiol-
ogy of mTBI.23
Implications of Minor
Traumatic Brain Injury
Symptoms such as headache, fatigue,
dizziness, anxiety, impaired cognition,
and memory deficits may affect more
than 58% of patients 1 month after in-
jury and 25% of patients at 1 year.24
When symptoms last for >3 months, a
patient is said to have postconcussion
syndrome (PCS), a disorder that can be
associated with substantial financial,
social, and emotional challenges. Ap-
proximately 20% of patients with PCS
are unemployed at 1 year postinjury,
and medical costs for treating a patient
with mTBI and PCS may surpass
$85,000 annually.18,25
The literature suggests that ap-
proximately 80% of patients who
have sustained an mTBI can be safely
discharged from the emergency de-
partment (ED) and will fully recover,
particularly in the setting of a nega-
tive head CT and a return to the pa-
tient’s baseline mental status.24,26
However, these patients must be
counseled at discharge regarding
postconcussive symptoms and leave
with written instructions and refer-
626
rals for follow-up in the event that Table 2
any of the previously described
Glasgow Coma Scalea
symptoms develop. The distribution
of patient education materials fol- Category Points
lowing mTBI has been validated as Eye opening
an effective means of counseling; Eyes open spontaneously 4
these materials describe mTBI- Eyes open to verbal com- 3
associated symptoms and coping mand
strategies and have resulted in a de- Eyes open only with painful 2
crease in patient-reported anxiety stimuli
and fewer reports of ongoing prob- No eye opening 1
lems at 3 months following injury.27 Verbal response
Recovery following mTBI is ad- Oriented and converses 5
versely affected by the presence of Disoriented and converses 4
concurrent extra-cranial injuries.28,29 Inappropriate words 3
In a study by Jackson et al,28 patients Incomprehensible sounds 2
with multisystem trauma and mTBI No verbal response 1
were almost twice as likely than Motor response
those with multisystem trauma alone Obeys verbal commands 6
to have persistent cognitive impair- Localizes pain 5
ment and to report symptoms of de- Withdraws from pain 4
pression, anxiety, and posttraumatic Flexor posturing 3
stress disorder. Extremity trauma im- Extensor posturing 2
pedes short- and long-term recovery No motor response 1
more than do nonmusculoskeletal in-
juries.29 Additionally, patients who a
The total score is the sum of each of the
present with mTBI and lower ex- three categories. Brain injury severity is
classified based on total scores: <9, se-
tremity injuries are three times more vere; 9 to 12, moderate; and ≥13, minor.
likely to experience cognitive and be-
havioral difficulties at 1 year postin-
proper specialist evaluation and
jury than are those who sustain iso-
treatment, and provide patients and
lated lower extremity trauma.30 This
their families with the resources
is a significant issue for the ortho-
needed to combat the adverse cogni-
paedic surgeon because up to 50%
tive sequelae that are often associ-
of patients with musculoskeletal in-
ated with mTBI.
juries have been found to have con-
current mTBI.30
Orthopaedic surgeons must recog- Evaluation and
nize that many patients with muscu- Management of Minor
loskeletal injuries will also have Traumatic Brain Injury
mTBI, which may result in greater
morbidity than that associated with Minor traumatic brain injury is pre-
isolated musculoskeletal injuries. Or- dominantly a clinical diagnosis.31 How-
thopaedic surgeons can have a dra- ever, when mTBI is suspected, addi-
matic effect on the overall health and tional testing and evaluation methods
well-being of patients who present may help to determine the presence and
with these injuries if a high index of severity of mTBI (Figure 1). Examples
suspicion for mTBI is maintained of these methods include the Graded
and appropriate referral is provided. Symptom Scale Checklist, Acute Con-
It is of paramount importance to cussion Evaluation, Immediate Postcon-
look beyond the skeletal injuries, rec- cussion Assessment and Cognitive Test-
ognize minor head trauma, facilitate ing, King-Devick test, and Military
Journal of the American Academy of Orthopaedic Surgeons
 Richard L. Uhl, MD, et al

Figure 1

The Acute Concussion Evaluation is an assessment tool for minor traumatic brain injury (mTBI) that provides the
clinician with an evidence-based approach for evaluation and diagnosis of mTBI. This tool aids the practitioner in
developing a follow-up action plan.24 (Reproduced with permission from the Centers for Disease Control and Preven-
tion: Acute Concussion Evaluation [ACE]. Available at: http://www.cdc.gov/concussion/headsup/pdf/ACE-a.pdf.
Accessed July 12, 2013.)

October 2013, Vol 21, No 10 627

Minor Traumatic Brain Injury: A Primer for the Orthopaedic Surgeon
Acute Concussion Evaluation.31-34
The Centers for Disease Control and
Prevention’s concussion website
(www.cdc.gov/concussion) is a valu-
able resource for clinicians and pa-
tients who wish to know more about
mTBI; it provides various fact sheets,
screening tools, and online seminars
free of charge.31
Noncontrast CT of the head is
considered the standard of care with
regard to imaging for diagnosis of
mTBI. However, neuroimaging is of-
ten of minimal utility because 85%
of patients with mTBI show no pa-
thology on initial CT.1 Additionally,
imaging rarely changes neurologic
management, with only 1% of pa-
tients with suspected mTBI requiring
neurosurgical intervention.1,35 How-
ever, the absence of pathology on CT
does not imply a clinically insignifi-
cant injury; the risk of persistent cog-
nitive and emotional impairment fol-
lowing mTBI remains even with
normal findings on imaging.10,11
Cognitive rehabilitation therapy
(CRT) is becomingly an increasingly
important component of treatment
in patients with persistent symptoms
following mTBI and is one focus of
current research.36 In a 2011 Insti-
tute of Medicine report, the Commit-
tee on Cognitive Rehabilitation
Therapy for Traumatic Brain Injury
supported the use of CRT for pa-
tients with behavioral and cognitive
deficits due to TBI.37 However, the
committee also acknowledged that,
based on current evidence, no defini-
tive conclusion could be made re-
garding the efficacy of CRT in man-
aging the sequelae of mTBI.
CRT uses a goal-oriented approach
to management of mTBI and at-
tempts to restore a person’s ability to
process information and perform
cognitive tasks. This is accomplished
by retraining previously learned
skills, teaching compensatory strate-
gies, and making environmental
modifications to the person’s domes-
628
tic and work settings.38 CRT may in-
volve a wide variety of providers
across multiple disciplines, including
nursing, rehabilitation medicine,
sports medicine, neurology, physical
therapy, speech pathology, occupa-
tional therapy, and psychiatry. CRT
can be administered in various set-
tings, including hospitals, patients’
homes and workplaces, and commu-
nity care centers.
Referral of a patient to a cognitive
rehabilitation specialist can be made
by any healthcare provider and is in-
dicated when a patient is symptom-
atic following mTBI, as in the patient
described in the case study. A person
who is trained to assess mTBI (eg,
physician, nurse, nurse practitioner,
physician assistant) performs the ini-
tial evaluation, which should be
done within 30 days of referral. If a
significant impairment is identified,
further treatment by providers with
expertise in managing mTBI is gener-
ally indicated. The website for the
Society for Cognitive Rehabilitation
is an excellent resource for patients
with mTBI, their families, and physi-
cians because it provides information
on CRT and mTBI support groups.39
Patients and healthcare providers
can contact the society through its
website for assistance with finding a
cognitive rehabilitation specialist.
Orthopaedic Approach to
Minor Traumatic Brain
Injury
Patients with musculoskeletal inju-
ries and concomitant mTBI are sus-
ceptible to second-impact syndrome,
which can have devastating conse-
quences, including rapid-onset cere-
bral edema, worsening neurologic
deficit, and physiologic instability. It
is also associated with a rate of mor-
tality approaching 50%.18 Second-
impact syndrome is traditionally
thought of in the context of a person
Journal of the American Academy of Orthopaedic Surgeons
who sustains a second concussion
before symptoms of an earlier con-
cussion have resolved, thus com-
pounding the initial injury. However,
this condition is also caused by the
systemic inflammatory response that
occurs after trauma or a major oper-
ation. Orthopaedic procedures are
notoriously implicated, with in-
tramedullary instrumentation specifi-
cally linked to a systemic inflamma-
tory response that can cause a
second-impact event.40
Damage-control orthopaedics is an
effective means of preventing second-
impact syndrome in critically injured
and physiologically unstable pa-
tients.41 However, the use of damage-
control orthopaedics should also be
considered for treatment of stable
patients with mTBI because they too
are vulnerable to second-impact syn-
drome. Richards et al42 found that
reamed nailing was associated with a
moderate risk factor for development
of cognitive impairment at 1 year
following initial injury in patients
with negative findings on intracra-
nial imaging and Injury Severity
Scores >15.
At our institution, an urban aca-
demic trauma center, patients who
present with a GCS score of ≤13 fol-
lowing blunt trauma are first evalu-
ated by ED and trauma service phy-
sicians, with strict adherence to
Advanced Trauma Life Support
guidelines. These teams also deter-
mine the need for intracranial imag-
ing and neurosurgical consultation.
Members of the orthopaedic surgery
team are taught to assess each pa-
tient for the presence of mTBI be-
cause patients initially thought to
have an isolated musculoskeletal in-
jury may have an associated mTBI.
We have developed an algorithm to
assist orthopaedic residents and at-
tending physicians with clinical deci-
sion making in the setting of concern
for mTBI (Figure 2). This algorithm
can be used to determine whether a
 Richard L. Uhl, MD, et al

Figure 2

The Albany Medical Center Division of Orthopaedic Surgery algorithm for the management of minor traumatic brain
injury (mTBI) in the setting of presumed isolated musculoskeletal trauma.

patient can be safely discharged
home after a minor injury and inter-
vention (eg, cast application for a
distal radius fracture) or if a more
formal workup is required either pre-
operatively or before discharge. This
workup also addresses the need for
neurosurgical consultation; we do
not order intracranial imaging with-
out first seeking a neurosurgery con-
sult (Table 3). The indications for
neurosurgical consultation are part
of a modified version of the guide-
lines for management of mTBI in
adults developed by the Centers for
Disease Control and Prevention and
the American College of Emergency
Physicians.26 In the setting of mTBI,
we defer to the neurosurgeon for
preoperative clearance; we specifi-
cally ask for guidance on whether
damage-control orthopaedics should
be initiated to minimize the risk of a
second-impact syndrome. In patients
with an orthopaedic injury that is
neither limb- nor life-threatening and
a possible mTBI that does not re-
quire a neurosurgical evaluation, we
routinely observe the patient for up
to 4 hours before proceeding to the

October 2013, Vol 21, No 10 629

Minor Traumatic Brain Injury: A Primer for the Orthopaedic Surgeon
Table 3
Indications for Neurosurgical
Consultation in the Setting of
Presumed Isolated
Musculoskeletal Trauma
Loss of consciousness for >5 min or
posttraumatic amnesia and one or
more of the following:
Headache
Vomiting
Age >60 y
Drug or alcohol intoxication
Short-term memory deficit
Posttraumatic seizure
Physical evidence of trauma above
the clavicle
Glasgow Coma Scale score <15
Focal neurologic deficit
Coagulopathy
operating room or discharging the
patient, whichever is indicated. This
protocol is also based on the practice
guideline developed by the Centers
for Disease Control and Prevention
and the American College of Emer-
gency Surgeons. It is intended to
avoid any potential worsening of
neurologic status. Prior to discharge,
we routinely discuss with the patient
the signs and symptoms of mTBI, re-
fer the patient to www.cdc.gov/
concussion, and recommend a
follow-up visit with a primary care
physician for evaluation and moni-
toring of symptoms.
The manifestations of mTBI may de-
velop insidiously or initially go unrec-
ognized until orthopaedic outpatient
follow-up, as depicted in the case study.
In such instances, the orthopaedic sur-
geon must be familiar with physicians
and other specialists in the community
who can evaluate for and manage
mTBI, to facilitate appropriate referral
and follow-up for patients with mTBI.
If concern for intracranial hemorrhage
or a more severe TBI exists at any time
during orthopaedic outpatient follow-
up, emergent transfer to an ED is crit-
630
ical because such symptoms (eg, severe,
persistent, worsening headache; altered
level of consciousness; focal neurologic
symptoms) require neuroimaging and
further evaluation.
Summary
mTBI is now recognized as an impor-
tant public health problem. It is asso-
ciated with potentially severe cogni-
tive, behavioral, social, and physical
dysfunction, leading to unemploy-
ment and significant disability. Of-
ten, mTBI is a clinical diagnosis, and
neuroimaging is typically of limited
utility.
Orthopaedic surgeons can play a
crucial role in the diagnosis of this
condition because they are com-
monly the only physicians who pro-
vide long-term care for patients after
trauma. Consequently, it is impor-
tant for orthopaedic surgeons to be
adept at detecting the signs and
symptoms of mTBI. In addition to
caring for musculoskeletal injuries,
these healthcare providers can iden-
tify potentially subtle indications of
mTBI and ensure that patients are
appropriately referred to those with
expertise in managing this condition.
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Cognitive Rehabilitation Therapy for
Traumatic Brain Injury: Evaluating the
Evidence. Washington, DC, National
Academy, 2011.
38. Tsaousides T, Gordon WA: Cognitive
rehabilitation following traumatic brain
injury: Assessment to treatment. Mt
Sinai J Med 2009;76(2):173-181.
39. The Society for Cognitive Rehabilitation:
Practical innovation in cognitive
rehabilitation therapy. Available at:
www.societyforcognitiverehab.org.
Accessed July 11, 2013.
40. Pape HC, Grimme K, Van Griensven M,
et al: Impact of intramedullary
instrumentation versus damage control
for femoral fractures on
immunoinflammatory parameters:
Prospective randomized analysis by the
EPOFF Study Group. J Trauma 2003;
55(1):7-13.
41. Giannoudis PV, Giannoudi M, Stavlas P:
Damage control orthopaedics: Lessons
learned. Injury 2009;40(suppl 4):S47-
S52.
42. Richards JE, Guillamondegui OD,
Archer KR, Jackson JC, Ely EW,
Obremskey WT: The association of
reamed intramedullary nailing and long-
term cognitive impairment. J Orthop
Trauma 2011;25(12):707-713.
631
 Review Article

Septic Arthritis of the Neonatal

Hip: Acute Management and Late
Reconstruction

Julie Balch Samora, MD, PhD
Kevin Klingele, MD
Abstract
Septic arthritis of the hip in neonates is rare but can have
devastating consequences. Presenting signs and symptoms may
differ from those encountered in older children, which may result in
diagnostic challenge or delay. Many risk factors predispose
neonates to septic arthritis, including the presence of transphyseal
vessels and invasive procedures. Bacterial infection of the joint
occurs via hematogenous invasion, extension from an adjacent
site, or direct inoculation. A strong correlation exists between
younger age at presentation and severity of residual hip deformity.
Diagnosis is based on clinical examination, laboratory markers, and
ultrasound evaluation. Early management includes parenteral
antibiotics and surgical drainage. Late-stage management options
include femoral and pelvic osteotomies, trochanteric arthroplasty,
arthrodesis, pelvic support procedures, and nonsurgical measures.
Early diagnosis and management continues to be the most
important prognostic factor for a favorable outcome in the neonate
with septic arthritis.

I n neonates, septic arthritis (SA) of

From the Department of
Orthopaedics, The Ohio State
University (Dr. Samora), and the
Department of Orthopedics,
Nationwide Children’s Hospital
(Dr. Klingele), Columbus, OH.
Neither of the following authors nor
any immediate family member has
received anything of value from or
has stock or stock options held in a
commercial company or institution
related directly or indirectly to the
subject of this article: Dr. Samora
and Dr. Klingele.
J Am Acad Orthop Surg 2013;21:
632-641
http://dx.doi.org/10.5435/
JAAOS-21-10-632
Copyright 2013 by the American
Academy of Orthopaedic Surgeons.
the hip is rare and often difficult
to diagnose. Because of the paucity
of signs and symptoms, diagnosis of
SA in newborns is more challenging
than it is in older children. The true
incidence of SA in children younger
than age 3 months is unknown. In a
South African population, it has
been reported to be 1 in 20,000.1 A
retrospective study of patients at US
military hospitals reported the inci-
dence of SA in infants aged up to 1
year to be 3.1 to 12.5 per 100,000.2
In India, the incidence is as high as 1
in 1,500 newborns, but this study
also included patients with osteomy-
elitis.3
Failure to recognize SA results in a
high social and economic burden4
and can have devastating conse-
quences for the patient. Delayed di-
agnosis leads to worse outcomes.5
Furthermore, a strong correlation
exists between the severity of resid-
ual hip deformity and age at
presentation.6-8 Therefore, the goal is
early detection and management to
preserve hip function and prevent
painful hip deformity.
Anatomy and
Pathophysiology
SA most commonly affects the hip
joint in children younger than age 2
years.9-12 Bacterial infection of the
hip joint can occur via hematoge-
nous invasion of the synovium from
a distant site, direct extension from
an adjacent infected bone, or direct
introduction of bacteria.13 Neonates

632 Journal of the American Academy of Orthopaedic Surgeons


Figure 1
Illustrations comparing the blood supply of a neonate (A) with that of a
toddler (B). Note the presence of transphyseal vessels in the neonate. These
vessels allow for direct blood flow into the joint via the metaphysis into the
epiphysis and resorb by age 18 months.
are thought to be at increased risk of
SA of the hip in part because trans-
physeal vessels allow direct blood
flow into the joint via the metaphysis
and into the epiphysis, allowing
transfer of bacteria from the arterial
vessels into the joint11 (Figure 1). The
metaphysis of the proximal femur is
intracapsular, particularly in neo-
nates, further potentiating a contin-
uum of infection between joint and
bone. There is potential for osteone-
crosis and rapid destruction of the
osseous architecture in the aftermath
of SA in immature children (up to
age 18 months). These vessels typi-
cally resorb by approximately 18
months of age.14
The products of white blood cell
(WBC) breakdown, including lytic
enzymes, interleukin-1, and bacterial
toxins that develop during SA, can
rapidly destroy the hyaline cartilage
of the femoral head and acetabulum
and may even damage the proximal
femoral epiphysis, physis, metaphy-
sis, and the triradiate cartilage.15,16
Sustained elevated intracapsular
pressure and occlusion and stretch-
October 2013, Vol 21, No 10
Julie Balch Samora, MD, PhD, and Kevin Klingele, MD
ing of the vascular supply can result
in ischemia of the femoral head.13
Many risk factors predispose neo-
nates to SA. Invasive procedures
such as umbilical catheterization, ve-
nous catheterization, heel puncture,
and perinatal asphyxia can result in
transient bacteremia, which may
eventually lead to deep infec-
tion.2,11,17,18 Patients treated in the
Neonatal Intensive Care Unit
(NICU) commonly have multiple po-
tential portals for entry of bacteria
into the bloodstream, including in-
dwelling lines, repeated laboratory
draws, and thin skin that may be in-
jured easily.
Prematurity is another known risk
factor for SA in the setting of bacter-
emia. Preterm infants are relatively
immunocompromised because they
have low levels of passively trans-
ferred maternal immunoglobulins
and immaturity of all immune mech-
anisms.3,17,19 These infants have poor
humoral response to infection, as ev-
idenced by limited neutrophil re-
sponse, low complement activity,
and poor function of T cells and
macrophages.3 Breech presentation
also has been found to be a predis-
posing factor for the development of
a septic hip in the first year of life.2
It should be noted, however, that
there is a distinct difference between
the neonate in the NICU who is pre-
disposed to multifocal musculoskele-
tal infection with nosocomial organ-
isms, such as methicillin-resistant
Staphylococcus aureus and Candida
albicans (due to frequent use of in-
strumentation and lines/catheters),
and the neonate who leaves the hos-
pital and is returned to medical at-
tention when he or she is found to
have limited range of motion (ROM)
and swelling in the extremity. The
second group is exposed to entero-
bacteriaceae and group B Streptococ-
cus during transvaginal delivery,
which leads to eventual infection.
These are two divergent clinical sce-
narios that should be understood by
pediatric healthcare providers.
Clinical Presentation
SA of the hip in neonates differs from
that in older children. There may be a
history of preceding trauma, catheter-
ization, or infection. The physical ex-
amination is difficult because neonates
may not demonstrate suspicious
findings.13 They may present with an-
orexia, irritability, lethargy, and/or an
unwillingness to move the affected
limb.11,20 Limitation of movement
(64%) and local swelling (60%)
were found to be the most common
presentation in an international
study of neonatal SA and osteomyeli-
tis.3 Edema of the buttock or leg, lo-
cal hip tenderness, and a slight differ-
ence in resting position or ROM in
the affected hip may be identified.11,21
These patients are often afebrile.21
Septicemia may or may not produce
fever or a toxic appearance.13 WBC
counts and other laboratory values
are frequently unreliable,21 and the
633
Septic Arthritis of the Neonatal Hip: Acute Management and Late Reconstruction
Table 1
Differential Diagnoses for Septic
Arthritis of the Hip in the
Neonate
Developmental dysplasia of the hip
Transient synovitis of the hip
Osteomyelitis of the proximal femur/
pelvis
Henoch-Schönlein purpura
Pyomyositis of the surrounding muscu-
lature
Traumatic synovitis
Fracture
Intra-abdominal pathology
Sacral agenesis
Superficial cellulitis
Superficial abscess
Psoas abscess
Pyogenic sacroiliitis
Acute leukemia
Various rheumatologic disorders
Nonspecific arthritides
Proximal focal femoral deficiency
Acute rheumatic fever
differential diagnosis for neonatal SA
of the hip is broad11 (Table 1).
Evaluation and Predictive
Algorithms
Multiple clinical factors must be con-
sidered for diagnosis of SA of the
hip, including patient history, physi-
cal examination, and laboratory and
radiographic studies. At a minimum,
serologic tests should include a WBC
count with differential, erythrocyte
sedimentation rate (ESR), C-reactive
protein (CRP) level, and blood cul-
tures.
A clinical prediction algorithm has
been developed to distinguish SA
from transient synovitis in children
(mean age, 5 to 6 years) using four
independent multivariate predictors.
These include fever, elevated ESR, re-
fusal to bear weight, and an in-
creased serum WBC count.22 If all
634
four factors are present, the proba-
bility of having SA is 99.6%. If no
predictors are present, the probabil-
ity of having SA is <0.2%. In an-
other study, children aged 1 to 12
years with an ESR <25 mm/h or CRP
level <1.0 mg/dL had an 85% or
87% probability of not having SA,
respectively.23 These algorithms,
however, cannot be readily applied
to the neonate because the clinical
presentation is not comparable and
inflammatory markers are unreliable
indicators. For example, when infec-
tion is present, neonates may demon-
strate thermoregulatory dysfunction,
resulting in hypothermia rather than
fever.21 In addition, leukopenia
rather than leukocytosis may be
more suggestive of infection in the
neonate.
CRP is an acute-phase protein pro-
duced in the liver and is an indicator
of inflammation, infection, and tis-
sue necrosis.24 The CRP level rises as
soon as 6 to 8 hours after injury or
infection.25 An elevated CRP level is
a strong independent risk factor that
can aid in diagnosis of SA of the hip
in patients with an average age of
5.5 years.26 The CRP level is best
used as a negative predictor; if values
are <1.0 mg/dL, there is an 87%
probability that the patient does not
have SA.23 In neonates, when CRP
level is used in conjunction with
interleukin-6, it has a 90% negative
predictive value to rule out acute in-
fection.27 However, CRP remains an
inconsistently reliable marker in neo-
nates because newborns do not al-
ways mount an inflammatory re-
sponse.
Aspiration and inspection of intra-
capsular fluid is the standard of care
for definitive determination of SA.28
Bacterial growth results in an influx
of inflammatory cells such as poly-
morphonuclear leukocytes (PMNs),
leading to an increase in cell count
within the joint fluid.29 Fluid should
be sent for Gram stain, cell count
Journal of the American Academy of Orthopaedic Surgeons
with differential, aerobic and anaer-
obic cultures, and fungal cultures. If
there is sufficient fluid, it is also im-
perative to inoculate the specimen in
an aerobic blood culture bottle to
improve the recovery rate of the bac-
teria in culture. SA is traditionally
defined by a positive synovial fluid
Gram stain or culture or a syno-
vial fluid WBC count of >50,000
cells/mm3 with >75% PMNs.19,22,30
More recently, the recommended
WBC criteria is >30,000 cells/mm3.23
Others argue that if there are >5,000
WBCs/mm3 with >90% PMNs, the
joint is considered infected.21
Historically, the incidence of posi-
tive synovial fluid cultures in chil-
dren diagnosed with SA has ranged
from 30% to 90%5,30-33 Although
some investigators found that 70%
of synovial fluid aspirate cultures
were negative in children aged 1
month to 16 years (average age, 4.8
years) who had clinical findings of
SA,19 others found that cultures were
negative in most patients (aged 1 to
15 years) with septic hips.34 A recent
study reported that, in children aged
3 days to 14 years (mean age, 5 years
and 3 months), only 42% of aspi-
rates in clinically diagnosed septic
hips were positive.35 At our institu-
tion, only 57% of joint aspirate cul-
tures were positive in infants
younger than age 3 months with SA
of the hip.
S aureus is the most common in-
fecting organism, but other organ-
isms include group B Streptococcus,
Streptococcus pneumoniae, Kleb-
siella pneumoniae, Proteus mirabilis,
and gram-negative rods.3,7,11,18,36 Al-
though Kingella kingae, a slow-
growing, aerobic, fastidious, gram-
negative coccobacillus, has been
found to cause SA and osteomyelitis
in infants aged approximately 1
year,37 it has never been reported in
children younger than age 6
months.5,38

Imaging
Several imaging modalities can be
used to assess the neonatal hip, in-
cluding plain radiography, ultra-
sonography, bone scintigraphy, and
MRI, none of which is without
shortcomings. Plain radiographs of
the pelvis are often normal but can
demonstrate capsular swelling, wid-
ening of the joint space, subluxation
or dislocation, radiolucency in the
proximal femoral metaphysis, or
periosteal elevation of the upper end
of the femur.21 Radiography may
suggest developmental dysplasia of
the hip; therefore, practitioners
should have a low threshold for ob-
taining additional imaging studies,
such as ultrasonography (Figure 2).
Isotopic bone scanning has not been
found to be reliable in neonates.39
MRI is useful for detecting fluid in
the hip as well as adjacent osteomy-
elitis, but it is expensive and requires
sedation or general anesthesia in ne-
onates.40
Ultrasonography has several ad-
vantages over bone scintigraphy and
MRI; it is rapid, painless, noninva-
sive, portable, and relatively inex-
pensive.28,34,41 Hip effusion can be de-
tected by performing an ultrasound
along the axis of the femoral neck,
with the hip in external rotation to
best assess intra-articular fluid. The
amount of effusion is defined by the
width of the joint in millimeters. A
difference of >5 mm compared with
the contralateral side is considered
an indication for aspiration because
the larger measurement represents an
additional 5 mL of fluid in the hip
joint.42 Ultrasonography has been
shown to safely confirm or exclude
effusion in children and may also be
used to identify periosteal elevation,
cortical erosion, or a subperiosteal
collection.43 The reported sensitivity
and specificity of ultrasonography
for diagnosis of pediatric septic hip
October 2013, Vol 21, No 10
Julie Balch Samora, MD, PhD, and Kevin Klingele, MD
Figure 2
AP radiograph of the pelvis
demonstrating a right hip
dislocation that may be consistent
with developmental hip dysplasia in
a neonate.
arthritis are 86.4% and 89.7%, re-
spectively, with a positive predictive
value of 87.9%.43 In a study of 80
ultrasound examinations in children
aged 1 to 15 years, the false-negative
rate was 2.5%.44 After effusion is de-
tected, aspiration of the hip should
be performed.44
Ultrasonography is also beneficial
for differentiating SA from develop-
mental hip dysplasia. Often, radio-
graphs of the neonatal abdomen or
pelvis reveal what appears to be a
dislocated hip. An ultrasound can be
obtained to evaluate for the presence
of a femoral ossific nucleus and may
reveal the absence of a femoral
epiphysis in a patient with long-
standing SA (Figure 3).
Other joints should be assessed for
involvement; thus, clinicians should
have a low threshold for ultrasono-
graphic evaluation of the surround-
ing joints.3 Because osteomyelitis in
neonates can lead to epiphyseal in-
sult or SA in up to 76% of patients,20
it has been suggested that an ultra-
sound of the hips be obtained in chil-
dren with documented osteomyelitis
or SA of another joint.29,45 We recom-
mend ultrasonographic evaluation of
the contralateral hip in infants with
hip SA and evaluation of both hips
in neonates with any documented
bone/joint infection.
Figure 3
Ultrasound of the right hip in the
same patient shown in Figure 2.
The findings are abnormal,
demonstrating a partially absent
proximal femoral epiphysis that is
consistent with previous septic
arthritis rather than classic
developmental dysplasia of the hip.
Management
After specimens have been obtained
for culture, antibiotic therapy is usu-
ally determined in consultation with
infectious disease specialists who
may recommend empiric antibiotic
therapy based on the most likely
causative organism given the age and
exposure history of the neonate. Pa-
renteral administration is the ac-
cepted treatment in neonates because
these patients are prone to general-
ized sepsis, have less consistent oral
antibiotic absorption, and have a less
predictable serologic response to
treatment.14 The empiric antibiotic
regimen in infants (age, 1 to 3
months) is combined treatment with
vancomycin and gentamicin. A 15
mg/kg dose of vancomycin is admin-
istered intravenously every 6 to 8
hours, with a target trough of 15 to
20 mcg/ml. Creatinine level and tar-
get trough must be monitored every
2 to 3 days. A 2 mg/kg dose of gen-
tamicin is administered intrave-
635
Septic Arthritis of the Neonatal Hip: Acute Management and Late Reconstruction
Table 2
Radiographic Classification of
Hip Deformity51
Type Description
I Absent or minimal femoral
head changes
II Deformity of the femoral
head with an intact growth
plate (type A) or premature
fusion of the growth plate
(type B)
III Pseudarthrosis of the femo-
ral neck
IV Complete destruction of the
proximal femoral epiphysis
with a stable (type A) or
unstable (type B) neck
segment
V The most severe form of de-
formity, with complete loss/
destruction of the femoral
head and neck to the inter-
trochanteric line with dislo-
cation of the hip
nously every 8 hours for full-term in-
fants. If the patient is aged <29
weeks, a 4 mg/kg dose of gentamicin
should be administered every 36
hours. If the patient is aged ≥29
weeks, the same dosage should be
administered every 24 hours. These
recommendations vary markedly by
institution based on the local micro-
biology and epidemiology.45
Irrigation and débridement must
be urgently performed not only to
clear the joint of bacteria, associated
enzymes, and degradation materials
that can destroy the articular carti-
lage, but also to reduce intra-
articular pressure and decrease epi-
physeal ischemia. This can be done
in an open fashion via an anterior
approach, providing direct access to
the joint and avoiding the ascending
branch of the medial circumflex ar-
tery.6,11 After an arthrotomy is per-
formed, a drain is placed and irriga-
tion is performed to allow continued
drainage of the joint postoperatively.
A partial capsulectomy also can be
performed, but complications of
636
overly generous capsulectomy in-
clude persistent wound drainage of
synovial fluid and hip subluxation,
which may require the use of a spica
cast or abduction bracing. Continu-
ous lavage and drainage has previ-
ously been proposed, but this option
has been associated with technical
problems, including drain dislodge-
ment and clogging.34 The physician
should maintain suspicion for coex-
isting osteomyelitis, which may war-
rant drilling of the proximal metaph-
ysis. Some authors have advocated
using a Pavlik or spica cast after sur-
gery to prevent instability, although
others believe it is wise to begin pas-
sive ROM exercises immediately af-
ter surgery.11
Givon et al34 contend that serial as-
pirations of the hip are safe and effi-
cacious, prevent scarring and the
need for general anesthesia, and re-
sult in faster return to normal activ-
ity. These recommendations are
based on the authors’ findings in a
study of 28 children aged 1 to 15
years with SA of the hip who under-
went serial hip aspirations. The hips
healed completely after a mean 3.6
aspirations. Four patients required
subsequent arthrotomy. Follow-up
was 6.1 years (range, 2 to 12 years),
with no immediate or late complica-
tions reported. Gait and ROM were
normal in all patients, and there was
no evidence of limb-length discrep-
ancy.
Journeau et al35 treated 43 pediat-
ric hips with SA with needle
aspiration/irrigation with or without
fluoroscopic guidance. The patients’
mean age was 5 years (age range, 3
days to 14 years). The authors re-
ported a favorable outcome in 38
hips, with 5 patients requiring open
arthrotomy. Follow-up ranged from
1 to 78 months (mean, 16 months).
Only one permanent complication
was reported—moderate impinge-
ment of the joint space—which de-
veloped at 5 months after needle
Journal of the American Academy of Orthopaedic Surgeons
aspiration/irrigation. According to
the authors, the complication did not
lead to functional impairment.
Outcomes and
Classification
Early diagnosis and urgent manage-
ment with surgery and appropriate
antibiotic therapy are expected to re-
sult in good outcomes in most neo-
nates with SA. Failure or delayed di-
agnosis can lead to well-known
neonatal hip sequelae, including de-
creased motion, limp, osteonecrosis,
destruction of the capital epiphysis,
limb-length discrepancy, subluxation
or dislocation of the hip, growth ar-
rest at the epiphyseal plate, femoral
osteomyelitis, fibrous union at the
hip joint and progressive ankylosis,
destruction of the hip joint, and life-
long hip deformity and gait
disturbance.6,8,11,46-49 Young age corre-
lates with more severe outcomes.6-8,18
Prematurity has a high correlation
with subsequent severe deformity of
the hip.7 More virulent organisms
(eg, S aureus) resistant to methicillin,
cephalosporin, and vancomycin, and
delayed diagnosis, also portend infe-
rior outcomes.6,7,46 In a long-term
study (>40 years) of 28 patients (32
affected hips) with SA during child-
hood, Betz et al50 found that painful
hips occurred in 47% of patients
who had SA when they were younger
than age 3 months at disease onset,
with 42% reporting poor Harris hip
scores.
Hunka et al51 developed a radio-
graphic classification system based
on a study of 10 patients with dis-
ease onset at age ≤18 months (with
an exception of 1 patient), with type
I representing mild changes and type
V representing the most severe defor-
mities (Table 2). Choi et al7 modified
this system after review of 34 pa-
tients with onset of infection before
12 months of age, and subsequent
 Julie Balch Samora, MD, PhD, and Kevin Klingele, MD

Table 3 iodesis of a portion of the capital

7
femoral physis and/or greater tro-
Modified Radiographic Classification of Hip Deformity
chanteric apophysis also has been
Type Description performed and may produce good
I Proximal femoral ossification results in an almost normal hip. Delay of ossi- results.7
fication is followed by relatively rapid and complete reossification. Type IB In type III hips, the femoral neck is
is the same as type IA, but with mild coxa magna. malaligned and may result in pseud-
II The epiphysis, physis, and metaphysis are involved, resulting in coxa breva arthrosis (type IIIB). Management re-
(type IIA) or progressive coxa vara or valga (type IIB). These hips have a lies on varus or valgus realignment
delay in ossification, flattening and irregularity of the femoral head, and
coxa magna. The femoral neck is short and wide, and there is relative of the proximal femur with bone
overgrowth of the greater trochanter because of premature closure of the grafting, if needed. Contralateral epi-
capital physis. There may be considerable limb-length discrepancy. physiodesis is often required because
III Deformity is secondary to injury of the femoral neck, resulting in either an- of anticipated limb-length inequality;
gular deformity with severe anteversion or retroversion (type IIIA) or
derotational correction also may be
pseudarthrosis (type IIIB). Deformity may be secondary to osteomyelitis of
the femoral neck. needed.
IV Severe deformity with a persistent stable remnant of the femoral neck (type In type IV hips, the absence of the
IVA) or complete loss of the femoral head and neck with no articulation of femoral head and neck may cause a
the hip (type IVB). Radiographic findings include severe limb-length dis- loss of hip stability (Figure 5). Pre-
crepancy, acetabular dysplasia, premature closure of the triradiate carti-
vention of hip pistoning may require
lage, and marked proximal migration of the femur.
either an open reduction of the re-
maining proximal femur, a greater
trochanteric arthroplasty, pelvic sup-
treatment algorithms52,53 based on for idiopathic osteonecrosis or Legg-
port procedures, or hip arthrodesis.
this system have been reported (Ta- Calvé-Perthes disease. Abduction
Trochanteric arthroplasty substitutes
ble 3, Figure 4). The authors found casting or bracing may be the treat- the cartilage of the trochanteric
the prevalence of hip sequelae to be ment of choice, but these methods apophysis for the absent femoral
as follows: 15%, type I; 32%, type can necessitate >12 months of head in the acetabulum; this proce-
II; 15%, type III; and 38%, type IV.7 weight-bearing protection.7,54 Future dure is accompanied by a distal
management options may include the transfer of the abductor musculature
use of epiphyseal drilling, antiresorp- (Figure 5, B). The technique, origi-
Reconstructive Options
tive agents, or even receptor activa- nally described by Colonna,57 has
Management of residual bony defor- tor of nuclear factor-κ B ligand inhi- shown better results with the addi-
mity postinfection remains contro- bition, as has been suggested for tion of a combined subtrochanteric
versial and must be individualized.8 femoral deformity due to other varus osteotomy and pelvic osteot-
Many management options are causes.55,56 omy to obtain sufficient coverage,
available and should be chosen based Various options can be used for stability, and containment.7,54
on the patient’s mobility, functional management of type II hips, which In a long-term study of outcomes
level, need for hip stability, the pres- may have epiphyseal, physeal, and in five hips treated with a trochan-
ence of pain, and expectations. Care- metaphyseal involvement. Type IIA teric arthroplasty and a proximal
ful assessment of hip anatomy, in- hips have femoral head deformity femoral varus osteotomy in patients
cluding the quality of the femoral and coxa breva. Nonsurgical man- with a mean age of 30 months,
head and whether it is subluxated or agement using a Pavlik harness, ab- Dobbs et al54 reported good results,
dislocated, will help the clinician de- duction brace, or Petrie cast may be with stable, painless, and functional
fine a treatment strategy. all that is required for the patient hips; improved gait; and less severe
On the basis of the radiographic with a type IIA hip. Bracing must be limb-length discrepancy. However,
classification of hips by Choi et al,7 continued until reossification is suffi- another study reported two fair and
radiographic findings in type I hips cient to allow weight bearing.7 Some three poor results in five patients
are relatively normal with and with- patients may require one of several who had trochanterplasties.6 The age
out evidence of osteonecrosis (types pelvic osteotomy options. Type IIB at which any of these procedures
IA and IB, respectively). These pa- hips have a valgus or varus femoral should be performed remains some-
tients are treated on a case-by-case neck that requires a proximal femo- what controversial but should be
basis, with protocols similar to those ral redirectional osteotomy. Epiphys- considered for patients aged <6 to 8

October 2013, Vol 21, No 10 637

Septic Arthritis of the Neonatal Hip: Acute Management and Late Reconstruction

Figure 4 Figure 5

A, AP radiograph of the pelvis

Illustration demonstrating the radiographic hip classification developed by demonstrating type IVA bilateral hip
Choi et al.7 Type I represents mild deformity and type IV represents severe deformity in a boy aged 2 years
deformity. (Reproduced with permission from Choi IH, Pizzutillo PD, Bowen and 7 months. B, Intraoperative AP
JR, et al: Sequelae and reconstruction after septic arthritis of the hip in in- arthrogram of the hip following
fants. J Bone Joint Surg Am 1990;72[8]:1150-1165.) trochanteric arthroplasty with
subtrochanteric femoral varus
osteotomy and distal transfer of the
abductor musculature to the lateral
years, even as temporizing proce- the mechanical axis of the limb (Fig- aspect of the femur. Concomitant
dures. Patients should be old enough ure 6). Remodeling may result in loss pelvic osteotomy was not
to follow therapy instructions and of correction in younger patients. performed.
young enough to allow for remodel- Outcomes can be classified as satis-
ing.7 factory or unsatisfactory based on
Pelvic support osteotomy is becom- criteria proposed by Hunka et al.51 cedures were unsatisfactory.18 In a
ing more popular for management of Satisfactory results include a stable long-term study (mean, 31.5 years),
severe hip deformity.58 Instability, joint, arc of flexion >70°, <20° of Wopperer et al8 evaluated the func-
limb-length discrepancy, and abduc- flexion contracture, a pain-free hip, tional capacity and radiographic ap-
tor weakness can all be addressed and the ability to perform activities pearance of 8 patients (9 hips) af-
with this procedure, which involves a of daily living. Several authors have fected by infantile septic hip arthritis.
proximal abduction femoral osteot- found that, in patients with unstable No surgical intervention was per-
omy for support and a more distal and severely damaged proximal fe- formed. Three patients had high iliac
lengthening osteotomy that realigns murs, outcomes of late salvage pro- dislocations with no pain and almost

638 Journal of the American Academy of Orthopaedic Surgeons

 Julie Balch Samora, MD, PhD, and Kevin Klingele, MD

Figure 6

AP radiographs demonstrating Ilizarov hip reconstruction for late sequelae. A, Femoral lengthening was performed,
with pins inserted into the pelvis to prevent proximal migration of the femur. Completion of distraction (B) and final
standing AP radiograph (C) obtained 2 years postoperatively. (Reproduced with permission from Rozbruch SR, Paley
D, Bhave A, Herzenberg JE: Ilizarov hip reconstruction for the late sequelae of infantile hip infection. J Bone Joint Surg
Am 2005;87[5]:1007-1018.)

Figure 7
AP radiograph of the pelvis
demonstrating type IVA deformity of
the left hip in a 10-year-old girl.
The patient was treated
nonsurgically because she was
pain free and had adequate range
of motion to perform daily activities.
normal motion. Three patients had
type IV hips with Trendelenburg
gaits and one had a marked limb-
length discrepancy, but they were all
pain free with near-normal ROM
(Figure 7). Two of these patients had
reductions for dislocated hips and
were severely debilitated by joint de-
formity and pain.
All patients must be followed clini-
cally until skeletal maturity. Bone
growth should be documented, with
scanograms obtained as necessary to
establish ideal timing for epiphys-
iodeses, if indicated. Although these
are general recommendations based
on types of hip sequelae, any treat-
ment performed at late stage must be
individualized.
Summary
SA of the hip in the neonatal popula-
tion is difficult to diagnose. Given
the devastating consequences of
missed SA, expedient and accurate
diagnosis is crucial. Physicians must
use multiple clinical factors, includ-
ing the history, physical examina-
tion, laboratory studies, and imag-
ing, to aid in diagnosis. No simple,
highly sensitive and specific test
or algorithm exists to determine
whether a neonate has a septic hip. A

October 2013, Vol 21, No 10 639

Septic Arthritis of the Neonatal Hip: Acute Management and Late Reconstruction

high index of suspicion must be
maintained, and a diligent search for
underlying infection is of paramount
8.
importance. The most significant
prognostic factor for a favorable out-
come in patients with neonatal SA is
9.
early diagnosis and treatment. Re-
constructive options for late sequelae
should be individualized based on
10.
degree of involvement, hip stability,
and patient expectations.
reconstruction after septic arthritis of the
hip in infants. J Bone Joint Surg Am
1990;72(8):1150-1165.
Wopperer JM, White JJ, Gillespie R,
Obletz BE: Long-term follow-up of
infantile hip sepsis. J Pediatr Orthop
1988;8(3):322-325.
Buxton RA, Moran M: Septic arthritis of
the hip in the infant and young child.
Curr Orthop 2003;17:458-464.
Frederiksen B, Christiansen P, Knudsen
FU: Acute osteomyelitis and septic
arthritis in the neonate, risk factors and
outcome. Eur J Pediatr 1993;152(7):
577-580.
Am 1999;81(12):1662-1670.
23. Levine MJ, McGuire KJ, McGowan KL,
Flynn JM: Assessment of the test
characteristics of C-reactive protein for
septic arthritis in children. J Pediatr
Orthop 2003;23(3):373-377.
24. Pepys MB: C-reactive protein fifty years
on. Lancet 1981;1(8221):653-657.
25. Peltola H, Vahvanen V, Aalto K: Fever,
C-reactive protein, and erythrocyte
sedimentation rate in monitoring
recovery from septic arthritis: A
preliminary study. J Pediatr Orthop
1984;4(2):170-174.

References
Evidence-based Medicine: Levels of
evidence are described in the table of
contents. In this article, references 1
and 25-27 are level I studies.
References 5-7, 22, 28, 30, 31, 34,
and 41 are level II studies. References
2-4, 8, 10, 19, 23, 32, 35-37, 40, 43-
48, 50-52, 54, and 58 are level III
studies. References 15, 18, 21, 38, 39,
42, and 49 are level IV studies.
References 9, 11-14, 17, 20, 24, 29,
53, and 57 are level V expert opinion.
References printed in bold type are
11. Nade S: Acute septic arthritis in infancy
and childhood. J Bone Joint Surg Br
1983;65(3):234-241.
12. Jackson MA, Nelson JD: Etiology and
medical management of acute
suppurative bone and joint infections in
pediatric patients. J Pediatr Orthop
1982;2(3):313-323.
13. Chung SM, Pollis RE: Diagnostic pitfalls
in septic arthritis of the hip in infants
and children. Clin Pediatr (Phila) 1975;
14(8):758-761, passim.
14. Wong M: Osteomyelitis and septic
arthritis. Sem Neonatal 1996;1:161-168.
15. Wientroub S, Lloyd-Roberts GC, Fraser
M: The prognostic significance of the
triradiate cartilage in suppurative
arthritis of the hip in infancy and early
childhood. J Bone Joint Surg Br 1981;
26. Caird MS, Flynn JM, Leung YL,
Millman JE, D’Italia JG, Dormans JP:
Factors distinguishing septic arthritis
from transient synovitis of the hip in
children: A prospective study. J Bone
Joint Surg Am 2006;88(6):1251-1257.
27. Laborada G, Rego M, Jain A, et al:
Diagnostic value of cytokines and
C-reactive protein in the first 24 hours of
neonatal sepsis. Am J Perinatol 2003;
20(8):491-501.
28. Zawin JK, Hoffer FA, Rand FF, Teele
RL: Joint effusion in children with an
irritable hip: US diagnosis and aspira-
tion. Radiology 1993;187(2):459-463.
29. Sucato DJ, Schwend RM, Gillespie R:
Septic arthritis of the hip in children.
J Am Acad Orthop Surg 1997;5(5):249-
260.

those published within the past 5
years.
1. Nunn TR, Cheung WY, Rollinson PD: A
prospective study of pyogenic sepsis of
the hip in childhood. J Bone Joint Surg
Br 2007;89(1):100-106.
2. Cieslak TJ, Rajnik M: Fetal breech
presentation predisposes to subsequent
development of septic arthritis of the hip.
Pediatr Infect Dis J 2005;24(7):650-652.
3. Narang A, Mukhopadhyay K, Kumar P,
Bhakoo ON: Bone and joint infection in
neonates. Indian J Pediatr 1998;65(3):
461-464.
4. Forlin E, Milani C: Sequelae of septic
arthritis of the hip in children: A new
classification and a review of 41 hips.
J Pediatr Orthop 2008;28(5):524-528.
5. Wilson NI, Di Paola M: Acute septic
arthritis in infancy and childhood: 10
years’ experience. J Bone Joint Surg Br
1986;68(4):584-587.
6. Fabry G, Meire E: Septic arthritis of the
hip in children: Poor results after late
and inadequate treatment. J Pediatr
Orthop 1983;3(4):461-466.
7. Choi IH, Pizzutillo PD, Bowen JR,
Dragann R, Malhis T: Sequelae and
63(2):190-193.
16. McGuire-Goldring MB, Meats JE, Wood
DD, Ihrie EJ, Ebsworth NM, Russell
RG: In vitro activation of human
chondrocytes and synoviocytes by a
human interleukin-1-like factor. Arthritis
Rheum 1984;27(6):654-662.
17. Morrissy RT: Bone and joint infection in
the neonate. Pediatr Ann 1989;18(1):33-
34, 36-38, 40-44.
18. Little DG, Barrett IR: Septic arthritis of
the hip in infancy. Aust N Z J Surg 1993;
63(2):116-119.
19. Lyon RM, Evanich JD: Culture-negative
septic arthritis in children. J Pediatr
Orthop 1999;19(5):655-659.
20. McCarthy JJ, Dormans JP, Kozin SH,
Pizzutillo PD: Musculoskeletal infections
in children: Basic treatment principles
and recent advancements. Instr Course
Lect 2005;54:515-528.
21. Vidigal EC, Jácomo AD: Early diagnosis
of septic arthritis of the hip in neonates.
Int Orthop 1994;18(3):189-192.
22. Kocher MS, Zurakowski D, Kasser JR:
Differentiating between septic arthritis
and transient synovitis of the hip in
children: An evidence-based clinical
prediction algorithm. J Bone Joint Surg
30. Bennett OM, Namnyak SS: Acute septic
arthritis of the hip joint in infancy and
childhood. Clin Orthop Relat Res 1992;
281:123-132.
31. Fink CW, Nelson JD: Septic arthritis and
osteomyelitis in children. Clin Rheum
Dis 1986;12(2):423-435.
32. Welkon CJ, Long SS, Fisher MC,
Alburger PD: Pyogenic arthritis in
infants and children: A review of 95
cases. Pediatr Infect Dis 1986;5(6):669-
676.
33. Molteni RA: The differential diagnosis of
benign and septic joint disease in
children: Clinical, radiologic, laboratory,
and joint fluid analysis, based on 37
children with septic arthritis and 97 with
benign aseptic arthritis. Clin Pediatr
(Phila) 1978;17(1):19-23.
34. Givon U, Liberman B, Schindler A,
Blankstein A, Ganel A: Treatment of
septic arthritis of the hip joint by
repeated ultrasound-guided aspirations.
J Pediatr Orthop 2004;24(3):266-270.
35. Journeau P, Wein F, Popkov D, Philippe
R, Haumont T, Lascombes P: Hip septic
arthritis in children: Assessment of
treatment using needle aspiration/
irrigation. Orthop Traumatol Surg Res
2011;97(3):308-313.

640 Journal of the American Academy of Orthopaedic Surgeons


36. Wang CH, Huang FY: Septic arthritis in
early infancy. Zhonghua Min Guo Xiao
Er Ke Yi Xue Hui Za Zhi 1990;31(2):
69-75.
37. Lundy DW, Kehl DK: Increasing
prevalence of Kingella kingae in
osteoarticular infections in young
children. J Pediatr Orthop 1998;18(2):
262-267.
38. Goutzmanis JJ, Gonis G, Gilbert GL:
Kingella kingae infection in children: Ten
cases and a review of the literature.
Pediatr Infect Dis J 1991;10(9):677-683.
39. Ash JM, Gilday DL: The futility of bone
scanning in neonatal osteomyelitis:
Concise communication. J Nucl Med
1980;21(5):417-420.
40. Lee SK, Suh KJ, Kim YW, et al: Septic
arthritis versus transient synovitis at MR
imaging: Preliminary assessment with
signal intensity alterations in bone
marrow. Radiology 1999;211(2):459-
465.
41. Zieger MM, Dörr U, Schulz RD:
Ultrasonography of hip joint effusions.
Skeletal Radiol 1987;16(8):607-611.
42. Moss SG, Schweitzer ME, Jacobson JA,
et al: Hip joint fluid: Detection and
distribution at MR imaging and US with
cadaveric correlation. Radiology 1998;
208(1):43-48.
43. Zamzam MM: The role of ultrasound in
differentiating septic arthritis from
transient synovitis of the hip in children.
J Pediatr Orthop B 2006;15(6):418-422.
44. Gordon JE, Huang M, Dobbs M,
October 2013, Vol 21, No 10
Julie Balch Samora, MD, PhD, and Kevin Klingele, MD
Luhmann SJ, Szymanski DA,
Schoenecker PL: Causes of false-negative
ultrasound scans in the diagnosis of
septic arthritis of the hip in children.
J Pediatr Orthop 2002;22(3):312-316.
45. Kabak S, Halici M, Akcakus M, Cetin
N, Narin N: Septic arthritis in patients
followed-up in neonatal intensive care
unit. Pediatr Int 2002;44(6):652-657.
46. Lunseth PA, Heiple KG: Prognosis in
septic arthritis of the hip in children.
Clin Orthop Relat Res 1979;(139):81-
85.
47. Wang CL, Wang SM, Yang YJ, Tsai CH,
Liu CC: Septic arthritis in children:
Relationship of causative pathogens,
complications, and outcome. J Microbiol
Immunol Infect 2003;36(1):41-46.
48. Chen CE, Ko JY, Li CC, Wang CJ: Acute
septic arthritis of the hip in children.
Arch Orthop Trauma Surg 2001;121(9):
521-526.
49. Hoffman AI, Murphy TP: Septic arteritis
causing iliac artery rupture and
aneurysmal transformation of the distal
aorta after iliac artery stent placement.
J Vasc Interv Radiol 1997;8(2):215-219.
50. Betz RR, Cooperman DR, Wopperer JM,
et al: Late sequelae of septic arthritis of
the hip in infancy and childhood.
J Pediatr Orthop 1990;10(3):365-372.
51. Hunka L, Said SE, MacKenzie DA,
Rogala EJ, Cruess RL: Classification and
surgical management of the severe
sequelae of septic hips in children. Clin
Orthop Relat Res 1982;(171):30-36.
52. Choi IH, Shin YW, Chung CY, Cho TJ,
Yoo WJ, Lee DY: Surgical treatment of
the severe sequelae of infantile septic
arthritis of the hip. Clin Orthop Relat
Res 2005;(434):102-109.
53. Choi IH, Yoo WJ, Cho TJ, Chung CY:
Operative reconstruction for septic
arthritis of the hip. Orthop Clin North
Am 2006;37(2):173-183, vi.
54. Dobbs MB, Sheridan JJ, Gordon JE,
Corley CL, Szymanski DA, Schoenecker
PL: Septic arthritis of the hip in infancy:
Long-term follow-up. J Pediatr Orthop
2003;23(2):162-168.
55. Kim HK, Randall TS, Bian H, Jenkins J,
Garces A, Bauss F: Ibandronate for
prevention of femoral head deformity
after ischemic necrosis of the capital
femoral epiphysis in immature pigs.
J Bone Joint Surg Am 2005;87(3):550-
557.
56. Kim HK, Morgan-Bagley S, Kostenuik P:
RANKL inhibition: A novel strategy to
decrease femoral head deformity after
ischemic osteonecrosis. J Bone Miner Res
2006;21(12):1946-1954.
57. Colonna P: A new type of reconstruction
operation for old ununited fractures of
the neck to the femur. J Bone Joint Surg
Am 1935;17:110-122.
58. Rozbruch SR, Paley D, Bhave A,
Herzenberg JE: Ilizarov hip
reconstruction for the late sequelae of
infantile hip infection. J Bone Joint Surg
Am 2005;87(5):1007-1018.
641

Michael J. O’Brien, MD
Topics from the frontiers of basic
research presented by the
Orthopaedic Research Society.
From the Department of
Orthopaedics, Tulane University
School of Medicine, New Orleans,
LA.
Dr. O’Brien or an immediate family
member has received research or
institutional support from DePuy and
Mitek, and has received nonincome
support (such as equipment or
services), commercially derived
honoraria, or other non-
research–related funding (such as
paid travel) from DePuy, Mitek, and
Smith & Nephew.
J Am Acad Orthop Surg 2013;21:
642-643
http://dx.doi.org/10.5435/
JAAOS-21-10-642
Copyright 2013 by the American
Academy of Orthopaedic Surgeons.
642
On the Horizon From the ORS
Update on Biologics in the Treatment of
Rotator Cuff Disease
Rotator cuff disease is the most
common condition affecting the
shoulder, causing significant pain
and functional impairment in the
adult population. Improvements in
arthroscopic instrumentation and
suture anchor technology have al-
lowed the development of stronger
constructs with multiple suture
configurations, allowing repair of
large and massive tears through
minimally invasive means. How-
ever, although repair instrumenta-
tion and techniques have improved,
healing rates have not. A high fail-
ure rate remains for large and mas-
sive rotator cuff tears. The next
frontier in the management of rota-
tor cuff disease is biologic augmen-
tation to facilitate healing follow-
ing repair.
The biology of the patient and
the tendon remains a notable factor
in rotator cuff healing. Repair ef-
forts are negatively affected by de-
creased vascularity with normal ag-
ing, increased collagen fragility,
muscle atrophy, and fatty infiltra-
tion of the chronically torn tendon.
Surgical techniques to enhance the
biology of the repair site and im-
prove mechanical stability should
be used whenever possible. Recog-
nizing the tear pattern and per-
forming an anatomic, tension-free
repair provides the best chance for
success. Microfracture of the heal-
ing bed of the greater tuberosity1
and the use of vented suture an-
chors allow marrow contents from
the humerus to bathe the repair site
and facilitate healing. These surgi-
cal techniques can be used by the
surgeon during any repair and may
improve rotator cuff healing rates
for large and massive tears.
Journal of the American Academy of Orthopaedic Surgeons
The use of medications in the
postoperative period may facilitate
tendon healing to bone. Matrix
metalloproteinases (MMPs) play a
role in the pathophysiology of rota-
tor cuff disease. Doxycycline has
anticatabolic effects and blocks the
destructive action of MMPs. Bedi
et al2 demonstrated that adminis-
tration of oral doxycycline reduced
MMP activity and enhanced heal-
ing at the enthesis following rotator
cuff repair in a rat model. Doxycy-
cline has the added benefit of pro-
tecting against infection with Pro-
pionibacterium acnes, which may
inhibit healing of the rotator cuff.
Chechik et al3 showed that atorva-
statin had a beneficial effect on the
repaired rotator cuff, increasing the
biomechanical strength of the re-
pair through a cyclooxygenase-2–
dependent mechanism.
Platelet-rich plasma (PRP) may be
a safe adjuvant to rotator cuff re-
pair; however, current studies have
reported mixed results and have
not shown improvement in healing
rates or functional outcomes.
Hoppe et al4 recently showed that
platelet-released growth factors
heighten tenocyte proliferation and
promote synthesis of the extracellu-
lar matrix to enhance healing of ro-
tator cuff tendon in a laboratory
culture medium. More clinical
studies are necessary to determine
the efficacy of PRP injections for
rotator cuff disease.
Several papers presented at the
2013 Annual Meeting of the Amer-
ican Academy of Orthopaedic Sur-
geons demonstrated the use of bio-
logics to facilitate healing in animal
models. Angeline et al5 showed that
low vitamin D levels negatively af-

fect early healing at the rotator cuff
repair site in a rat model. Morikawa
et al6 presented that deficiency of
SOD1, an antioxidant enzyme, in-
duced degeneration and reduction of
mechanical properties in the rotator
cuff tendon. Biologic augmentation
has shown success in the knee, as
well. Strauss et al7 showed that intra-
articular injection of growth hor-
mone demonstrated improvement in
the gross and histologic appearance
of repair tissue in the treatment of
focal articular cartilage lesions, and
Figueroa et al8 reported that the ad-
dition of mesenchymal stem cells and
a collagen scaffold aided in regenera-
tion of the anterior cruciate liga-
ment. The addition of these biologics
may be on the horizon in surgical re-
pair in the shoulder.
Gulotta and colleagues9,10 have
shown in several studies that mesen-
chymal stem cells can augment rota-
tor cuff healing in a rat model. Oh
et al11 won the Neer Award for their
2013 paper on the use of adipose-
derived stem cells (ADSCs). The au-
thors injected ADSCs into the rota-
tor cuff repair site in a rabbit model
with simulated chronic subscapularis
tears. The tendon-repair group with
ADSCs demonstrated better healing
compared with controls, superior
muscle action potentials, higher load
to failure in biomechanical testing,
and less fatty degeneration by histo-
logic examination. The authors con-
October 2013, Vol 21, No 10
cluded that the local administration
of ADSCs might improve tendon
healing and decrease muscle atrophy
and fatty degeneration following ro-
tator cuff repair.
Studies such as these pave the way
for the future use of biologics in or-
thopaedic surgery. Continued re-
search and advancements in biologic
augmentation will likely improve
healing rates and patient outcomes
following rotator cuff repair.
References
1. Milano G, Saccomanno MF, Careri S,
Taccardo G, De Vitis R, Fabbriciani C:
Efficacy of marrow-stimulating
technique in arthroscopic rotator cuff
repair: A prospective randomized study.
Arthroscopy 2013;29(5):802-810.
2. Bedi A, Fox AJ, Kovacevic D, Deng XH,
Warren RF, Rodeo SA: Doxycycline-
mediated inhibition of matrix
metalloproteinases improves healing
after rotator cuff repair. Am J Sports
Med 2010;38(2):308-317.
3. Chechik O, Dolkart O, Alhajajra FY,
Gigi R, Mozes G, Maman E: Paper No.
310. Atorvastatin increases the biome-
chanical strength of the repaired rotator
cuff by the cyclooxygenase-2 mechanism.
AAOS Annual Meeting Proceedings.
CD-ROM. Rosemont, IL, American
Academy of Orthopaedic Surgeons,
2013, pp 774-775.
4. Hoppe S, Alini M, Benneker LM, Milz S,
Boileau P, Zumstein MA: Tenocytes of
chronic rotator cuff tendon tears can be
stimulated by platelet-released growth
factors. J Shoulder Elbow Surg 2013;
22(3):340-349.
5. Angeline ME, Ma SY, Garrido CP, et al:
Paper No. 304. The effect of vitamin D
On the Horizon From the ORS
deficiency on rotator cuff healing in a rat
model. AAOS Annual Meeting Proceed-
ings. CD-ROM. Rosemont, IL, American
Academy of Orthopaedic Surgeons,
2013, p 771.
6. Morikawa D, Itoigawa Y, Nojiri H,
et al: Paper No. 305. The contribution of
oxidative stress on degeneration of rota-
tor cuff enthesis. AAOS Annual Meeting
Proceedings. CD-ROM. Rosemont, IL,
American Academy of Orthopaedic Sur-
geons, 2013, pp 771-772.
7. Strauss E, Joshi BB, Daher RJ, Dunn AR,
Jazrawi LM: Paper No. 183. Can intra-
articular growth hormone improve re-
pair tissue quality after marrow stimula-
tion techniques? AAOS Annual Meeting
Proceedings. CD-ROM. Rosemont, IL,
American Academy of Orthopaedic Sur-
geons, 2013, p 933.
8. Figueroa D, Espinosa M, Calvo R, et al:
Paper No. 365. Anterior cruciate liga-
ment regeneration using mesenchymal
stem cells and collagen type I scaffold in
a rabbit model. AAOS Annual Meeting
Proceedings. CD-ROM. Rosemont, IL,
American Academy of Orthopaedic Sur-
geons, 2013, p 959.
9. Gulotta LV, Kovacevic D, Montgomery
S, Ehteshami JR, Packer JD, Rodeo SA:
Stem cells genetically modified with the
developmental gene MT1-MMP improve
regeneration of the supraspinatus
tendon-to-bone insertion site. Am J
Sports Med 2010;38(7):1429-1437.
10. Gulotta LV, Kovacevic D, Packer JD,
Deng XH, Rodeo SA: Bone marrow-
derived mesenchymal stem cells
transduced with scleraxis improve
rotator cuff healing in a rat model. Am J
Sports Med 2011;39(6):1282-1289.
11. Oh JH, Chung SW, Kim SH, et al: Poster
No. P293. Effect of adipose-derived stem
cell for improvement of fatty degenera-
tion and rotator cuff healing in rabbit
model. AAOS Annual Meeting Proceed-
ings. CD-ROM. Rosemont, IL, American
Academy of Orthopaedic Surgeons,
2013, pp 812-813.
643

Mary F. Barbe, PhD
Sean Gallagher, PhD, CPE
Steven N. Popoff, PhD
Topics from the frontiers of basic
research presented by the
Orthopaedic Research Society.
From the Department of Anatomy
and Cell Biology, Temple University
School of Medicine, Philadelphia, PA
(Dr. Barbe and Dr. Popoff), and the
Department of Industrial and
Systems Engineering, Auburn
University, Auburn, AL
(Dr. Gallagher).
None of the following authors or any
immediate family member has
received anything of value from or
has stock or stock options held in a
commercial company or institution
related directly or indirectly to the
subject of this article: Dr. Barbe,
Dr. Gallagher, and Dr. Popoff.
J Am Acad Orthop Surg 2013;21:
644-646
http://dx.doi.org/10.5435/
JAAOS-21-10-644
Copyright 2013 by the American
Academy of Orthopaedic Surgeons.
644
On the Horizon From the ORS
Serum Biomarkers as Predictors of
Stage of Work-related Musculoskeletal
Disorders
Musculoskeletal disorders (MSDs)
are a leading worldwide cause of
long-term pain and physical dis-
ability,1 with diagnoses including ten-
dinopathies, nerve compression syn-
dromes, and muscular and joint
disorders.2,3 Studies in people with up-
per extremity work-related MSDs
(WMSDs) find evidence of inflamma-
tion, fibrosis, and degeneration in se-
rum and musculotendinous tissues,
although the timing of each is
unknown.4-7 Serum biomarkers that
might aid in pinpointing the stage
of these disorders are being investi-
gated.
Several risk factors have been
identified, including forceful exer-
tions, repetitive motion, and non-
neutral body postures. A recent sys-
tematic review showed a consistent
pattern of force-repetition interac-
tion for musculoskeletal disorder
risk, with low-force repetitive tasks
demonstrating a modest increase in
MSD risk, whereas high-force re-
petitive tasks result in rapid escala-
tion in MSD risk, which is indica-
tive of tissue fatigue failure.8
We have developed a rat model of
voluntary reaching and handle-
pulling for food reward,9 in which
reach rates and force levels were
determined from epidemiologic
studies. One goal of our laboratory
is to identify biomarkers for moni-
toring disease progression of
WMSDs and appropriate targeting
of treatments. We recently exam-
ined whether serum inflammatory
cytokines exhibit force × repetition
interaction responses using this rat
model.10 Serum tumor necrosis fac-
tor–α (TNF-α) shows a significant
Journal of the American Academy of Orthopaedic Surgeons
force × repetition interaction (P =
0.0003) with task performance
(Figure 1, A). No increases in
TNF-α were seen in low-force
groups, but high increases were ob-
served in rats performing high-
repetition, high-force tasks.11-13
These results indicate that serum
TNF-α follows the fatigue-failure
theory during acute phases of ≤3
months. TNF-α and related cyto-
kines may provide the best gauge of
overall acute tissue damage result-
ing from repetitive, forceful exer-
tions and may be the best biomark-
ers of this phase of WMSDs.
The timing of the inflammatory ver-
sus fibrotic responses with WMSDs is
also of clinical interest. Studies have
detected serum biomarkers of inflam-
mation in patients with upper extrem-
ity WMSDs of short duration (≤3
months), including TNF-α,4-6 again
suggesting a role for inflammatory cy-
tokines early in the course of upper
extremity WMSDs. However, studies
examining tissues from patients with
upper extremity WMSDs during sur-
gical intervention show increased tis-
sue fibrogenic proteins and fibrotic
histopathology, which is indicative of
deranged extracellular matrix pro-
duction and degeneration in tissues
by this time point.7
Therefore, we extended our rat
studies to examine the effects of
performing a high-repetition, low-
force task for 24 weeks. Serum
TNF-α levels increased early after
training but declined by week 18
(Figure 1, B). In contrast, serum
interleukin-10 (IL-10), an anti-
inflammatory cytokine, increased
steadily until week 18. This may be
 On the Horizon From the ORS

Figure 1 Our results indicate that most serum

inflammatory cytokines, including
TNF-α, demonstrate force-repetition
interactions. These findings support the
use of key pro-inflammatory cytokines
as biomarkers of acute tissue damage
and the fatigue failure hypothesis as a
mechanism underlying WMSDs. We
have also observed significantly in-
creased serum and tissue CTGF levels
that correlated with tissue fibrosis. Ad-
ditional studies are underway to deter-
mine whether elevated CTGF is an es-
sential mediator of fibrotic events. If so,
one could envision CTGF as a poten-
tial therapeutic target to prevent fibro-
sis and reduced function and as a se-
rum biomarker of tissue fibrogenic
changes occurring with WMSDs.

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