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Review Article

Acute Compartment Syndrome of


the Upper Extremity
Abstract
Mark L. Prasarn, MD
Elizabeth A. Ouellette, MD

Acute compartment syndrome occurs when pressure within a fibroosseous space increases to a level that results in a decreased
perfusion gradient across tissue capillary beds. Compartment
syndromes of the hand, forearm, and upper arm can result in
tissue necrosis, which can lead to devastating loss of function. The
etiology of acute compartment syndrome in the upper extremity is
diverse, and a high index of suspicion must be maintained. Pain
out of proportion to injury is the most reliable early symptom of
impending compartment syndrome. Diagnosis is particularly difficult
in obtunded patients and in young children. Early recognition and
expeditious surgical treatment are essential to obtain a good
clinical outcome and prevent permanent disability.

From the Department of


Orthopaedics, University of
Rochester, Rochester, NY
(Dr. Prasarn), and Physicians for
The Hand, Miami, FL (Dr. Ouellette).
Dr. Ouellette or an immediate family
member serves as a paid consultant
to or is an employee of Stryker.
Neither Dr. Prasarn nor any
immediate family member has
received anything of value from or
owns stock in a commercial
company or institution related
directly or indirectly to the subject of
this article.
J Am Acad Orthop Surg 2011;19:
49-58
Copyright 2011 by the American
Academy of Orthopaedic Surgeons.

January 2011, Vol 19, No 1

ompartment syndrome was first


described in 1881 by Richard
von Volkmann.1 The etiology, pathophysiology, and management of
compartment syndrome and the associated complications have been extensively described. Acute compartment syndrome (ACS) occurs with
elevation of interstitial pressure in a
closed fascial compartment, resulting
in microvascular compromise. This
causes the perfusion gradient to fall
below a critical value, leading to ischemia of the tissues within this confined space. In the upper extremity,
the dorsal and volar compartments
of the forearm are the most commonly affected. Upper extremity
ACS can lead to devastating loss of
function, including Volkmann ischemic contracture, neurologic deficit,
infection, amputation, and death.
A wide range of causes of ACS in
the upper extremity has been reported, and a high index of suspicion
must be maintained. Distal radius
fracture in adults and supracondylar
humerus fracture in children are the

most frequent causes of compartment syndrome in the upper extremity.1,2 Compartment syndrome is a
clinical diagnosis, and it can be difficult to make in certain patient populations, such as persons who are obtunded and children.2-5 Emergent
surgical treatment is required; the
most important determinant of outcome is early recognition and expeditious surgical intervention.3,5-9 Reconstructive procedures can be
performed to improve the function
of the affected upper extremity in the
patient with Volkmann contracture;
however, return of normal function
should not be expected.10-16

Anatomy
The upper extremity contains 15
compartments. The upper arm consists of a flexor (ie, volar) compartment and an extensor (ie, dorsal)
compartment. The forearm is divided
into three compartments: volar, dorsal, and lateral (ie, mobile wad) (Figure 1). The hand has 10 compart-

49

Acute Compartment Syndrome of the Upper Extremity

Figure 1

Cross section at the junction of the proximal and middle thirds of the forearm
demonstrating the compartments and the important neurovascular structures.
The volar compartment contains the flexor muscles of the wrist and digits,
including the flexor digitorum superficialis (FDS), flexor carpi radialis (FCR),
flexor pollicis longus (FPL), flexor digitorum profundus (FDP), and flexor carpi
ulnaris (FCU), as well as the ulnar nerve (UN), ulnar artery (UA), median
nerve (MN), median artery (MA), radial artery (RA), superficial branch of the
radial nerve (RN), anterior interosseous artery (AIA), and anterior
interosseous nerve (AIN). The dorsal and volar compartments are separated
by the interosseous membrane. The dorsal compartment contains the finger
and thumb extensors and the long thumb abductor as well as the posterior
interosseous artery (PIA), posterior interosseous nerve (PIN), extensor carpi
ulnaris (ECU), extensor pollicis longus (EPL), and extensor digitorum
communis (EDC). The mobile wad, which is often considered to be a third
compartment, is composed of the extensor carpi radialis brevis and longus
muscles (ECR) and the brachioradialis (BR). (Reproduced with permission
from Ouellette EA: Compartment syndromes in obtunded patients. Hand Clin
1998;14[3]:431-450.)

ments: hypothenar, thenar, and


adductor pollicis as well as four dorsal interosseous and three volar interosseous17 (Figure 2). The volar
forearm is the most commonly affected compartment in the upper extremity. Compartment syndrome in
this area typically occurs following
fracture of the distal radius, supracondylar humerus, or diaphysis of
the radius or ulna.2,17,18 Any compartment can be affected, however. Digi-

50

tal fasciotomy is necessary in some


cases19 (Figure 3).
In the upper arm, the medial and
the lateral intermuscular septa separate the flexor compartment from
the extensor compartment. The brachial fascia is a dense fibrous sheath
that surrounds the muscles in each of
the two compartments. In the forearm, the stiff interosseous membrane
bridges the distance between the radius and the ulna. Just anterior to

this membrane lie the flexor digitorum profundus, flexor pollicis longus, and pronator quadratus muscles. Some consider the pronator
quadratus to lie within an additional
compartment of the distal volar forearm, separate from the flexor tendons at this level.20 These deep volar
muscles are the most commonly
damaged muscles in forearm compartment syndrome. The remaining,
more superficial flexor muscles are
less prone to ischemia than their
deeper counterparts. The finger and
wrist extensors lie on the posterior
aspect of the forearm. Isolated
exercise-induced compartment syndromes of the extensor carpi ulnaris
muscle have been noted in case reports.21,22 The mobile wad, which
consists of the brachioradialis, flexor
carpi radialis longus, and flexor
carpi radialis brevis tendons, is rarely
involved.12 The antebrachial fascia,
which is a continuation of the brachial fascia, envelops the compartments and muscles in the forearm.
The compartments of the hand are
divided by the carpal bones, metacarpals, and individual investing fascial
layers. Pressures within the carpal tunnel may become elevated in cases of
hand or volar forearm compartment
syndrome. Release of the transverse
carpal ligament is often necessary in
addition to release of the other involved compartments. The digital fascial compartments are bound by the
Cleland ligament and the Grayson ligament, and elevated pressure may occur in individual digits (Figure 3).
Compartment syndrome of the hand
typically necessitates carpal tunnel release and dorsal interosseous compartment releases; however, any compartment may be involved and may require
release. The decision regarding the
number and location of incisions
should be based on the clinical findings
and on intraoperative pressure measurements.3

Journal of the American Academy of Orthopaedic Surgeons

Mark L. Prasarn, MD, and Elizabeth A. Ouellette, MD

Etiology
ACS of the upper extremity is caused
by a myriad of factors, including
fracture, bleeding disorders, constrictive dressing and casting, arterial injury, extravasation of intravenous or
intraosseous infusion, and regional
anesthesia3-5,23-35 (Table 1). Anything
that causes increased volume within
the confined fascial space (eg, bleeding, edema, purulent material, extraneous fluids) or restricts the compartment from expanding (eg, burn,
casting, dressing, tourniquet) can
cause ACS.
It is difficult to estimate the true
incidence of compartment syndrome
of the upper extremity, but most
cases occur in the setting of fracture.
McQueen et al17 analyzed 164 patients with traumatic ACS. In 69%
of cases, compartment syndrome was
associated with fracture. The most
frequent fracture types observed
were of the tibial diaphysis (36%),
the distal radius (9.8%), and the diaphysis of the forearm bones (7.9%).
Only 2.5% occurred following hand
fracture, and the incidence was 0.6%
each for elbow fracture-dislocation
and humeral fracture. Soft-tissue injury without fracture was the second
most common cause of injury
(23.2%). Incidence in the forearm
and hand was 5.5% and 0.6%, respectively. Within this subgroup,
10.3% occurred in patients with
bleeding disorders or who were taking anticoagulants.
Grottkau et al2 reviewed a national
trauma database and found the incidence of pediatric forearm compartment syndrome to be 1%. Ouellette
and Kelly3 reported on 19 patients
with compartment syndrome of the
hand. Most cases were iatrogenic, resulting from complications related to
intravenous or intra-arterial administration of drugs. The incidence of
compartment syndrome in unstable
January 2011, Vol 19, No 1

Figure 2

Cross section at the level of the metacarpal shafts demonstrating the 10


compartments of the hand: hypothenar, thenar, and adductor pollicis as well
as four dorsal interosseous and three volar interosseous. (Reproduced with
permission from Ouellette EA: Compartment syndromes in obtunded
patients. Hand Clin 1998;14[3]:431-450.)

fractures of the distal end of the radius is substantially higher with concomitant ipsilateral elbow injury
than with distal radial fracture
alone.36

Pathophysiology
Compartment syndrome is caused by
an elevation of pressure within a
fibro-osseous space resulting in decreased tissue perfusion. The initial
rise in intracompartmental pressure
causes increased extravascular venous pressure. Because of lack of
musculature in the wall media, this
relatively small rise in pressure
causes the venule walls to collapse.
The resulting decrease in hydrostatic
gradient causes reduced local perfusion and increased interstitial pressure. This increased interstitial pressure in turn causes increased edema
within the compartment, and this
cascade of events repeats itself perpetually.12 Vasospasm and shock lead

to decreased arteriolar pressure and


possibly closure of end arterioles,
leading to a further decrease in tissue
perfusion4 (Figure 4).
Ischemia occurs when a critical
threshold is reached in the local arteriovenous gradient and when circulation is compromised to the point that
blood flow is insufficient to meet the
metabolic demands of the tissue.4
This critical variable is represented
by the absolute difference between
compartment pressure and blood
pressure.37 Heppenstall and colleagues38,39 prefer to compare intracompartmental pressure with mean
arterial pressure, but diastolic blood
pressure is easier to obtain and calculate. Experimental data in a canine
model have shown that terminal arterial pressure is equal to diastolic
blood pressure;40 thus, we use diastolic blood pressure to determine
the critical threshold.
In a canine study, muscle necrosis
occurred when the intracompart-

51

Acute Compartment Syndrome of the Upper Extremity

Figure 3

Table 1
Causes of Compartment
Syndrome of the Upper
Extremity3-5,23-35
Fracture
Crush injury
Injection injury
Ring avulsion
Suction injury
Penetrating trauma
Constrictive dressings
Casts
Burns
Infection
Bleeding disorders
Spider bite
Snakebite
Arterial injury
Reperfusion
In utero compression
Extravasation of infusions
Injection of illicit drugs
Regional anesthesia
Prolonged compression

Finger decompression. A, Illustration demonstrating a midaxial incision made


on the index finger. This incision is made on the ulnar side of digits 2 through
4 and on the radial side of digits 1 and 5. The neurovascular bundles are
identified and retracted volarward, and the fascia between them is cut along
with the flexor sheath. B and C, Clinical photographs following fasciotomies
of the hand and digits. (Reproduced with permission from Ouellette EA:
Compartment syndromes in obtunded patients. Hand Clin
1998;14[3]:431-450.)

mental pressure rose to a level 20


mm Hg below diastolic blood pressure.40 Heckman et al41 demonstrated
that irreversible changes to the peripheral nerves and skeletal muscle
occur following 8 hours of complete
ischemia. Following onset of cellular
anoxia, affected cells begin anaerobic metabolism and may die. Devastating loss of function may occur following substantial loss of muscle and
neural tissue in the upper extremity.
Muscle ischemia can lead to release
of myoglobin, which can cause myoglobinuria, metabolic acidosis, and
hyperkalemia. Renal failure, cardiac
arrhythmia, cardiac failure, and
shock may then ensue. The magni-

52

tude of these systemic effects is dependent on the duration of ischemia


and the size of the muscle compartments involved.4

Clinical Evaluation
Historically, the five Ps (pain, pallor,
pulselessness, paralysis, paresthesia)
were taught as the symptoms that
herald compartment syndrome.
Pulselessness is rare, occurring only
after arterial injury. Most of these
symptoms present only after a substantial amount of time has elapsed
following the onset of compartment
syndrome, and outcomes typically

are poor even with expedient fasciotomy. Pain out of proportion to injury and pain with passive stretching
of muscles in the involved compartment are the earliest indicators of
compartment syndrome.23 Compartment syndrome also should be suspected with tense, swollen compartments. In a series of patients with
compartment syndrome of the hand,
Ouellette and Kelly3 demonstrated
that the most consistent clinical finding was a tense, swollen hand in an
intrinsic minus position (ie, extension of the metacarpophalangeal
joints and flexion of the intercarpal
joints) (Figure 5).
ACS is typically diagnosed clinically. However, it may be necessary
to measure compartment pressure
(Figure 6). Animal studies demonstrate that compartment syndrome is
indicated in the presence of a difference between diastolic blood pressure and the compartment measuring

Journal of the American Academy of Orthopaedic Surgeons

Mark L. Prasarn, MD, and Elizabeth A. Ouellette, MD

Figure 4

Algorithm demonstrating the cascade of events in the pathophysiology of compartment syndrome.

Figure 5

A and B, Photographs demonstrating a tense, swollen hand and forearm.


The hand is held in the intrinsic minus position. (Reproduced with permission
from Prasarn ML, Ouellette EA, Livingstone A, Giuffrida AY: Acute pediatric
upper extremity compartment syndrome in the absence of fracture. J Pediatr
Orthop 2009;29[3]:263-268.)

20 mm Hg40 or a difference between mean arterial pressure and the


compartment measuring 30 mm
Hg.41 Fasciotomy is often performed
in patients with absolute pressure
measuring >30 mm Hg.6,42 We consider a differential between diastolic
January 2011, Vol 19, No 1

pressure and the compartment of


20 mm Hg to be an absolute indication for emergent fasciotomy. In the
patient with swollen compartments
and nearly normal pressures (<30
mm Hg absolute pressure), we advocate waiting and performing serial

examinations and pressure measurements. Increasing swelling and rising


pressures warrant decompression
even when the pressure differential is
20 mm Hg. Emergent fasciotomy is
also performed in the setting of a
concerning physical examination and
extremely elevated pressures, even
with a pressure differential of >20
mm Hg. Compartment pressure
should be measured when suspected
in a patient who is uncooperative,
who has an altered mental status, or
whose young age renders the clinical
examination inadequate.3-6,8,23 In pediatric patients, Bae et al6 demonstrated that an increased need for analgesics was most predictive of
compartment syndrome.

Compartment Pressure
Measurement
We typically measure compartment
pressures in patients with equivocal

53

Acute Compartment Syndrome of the Upper Extremity

that the Whitesides manometer lacks


the precision required for clinical
use.

Figure 6

Fasciotomy

Algorithm for evaluating and managing suspected compartment syndrome.

examination and in those who cannot be examined fully. An equivocal


examination is one in which compartment syndrome is suspected and
uncertainty exists regarding the clinical examination. Measurements are
also often taken in the operating theater to verify which compartment or
compartments are affected and to ensure that they are fully decompressed
following fasciotomy. Compartments
that clinically appear to be involved
are tested, and measurements are
taken when the compartment appears to be the most tense and swollen. In the case of associated fracture, the catheter is inserted close to
the fracture site. Otherwise, measurements are taken at the location
that is most accessible to the compartment. Typically, a single measurement is taken for each suspected
compartment. When in doubt regarding the resulting pressure value,
repeat measurements should be ob-

54

tained at other sites.


The two most common measurement techniques involve the use of a
slit catheter or a side port needle.
Straight needles have been shown to
provide less accurate results.43 The
catheter may be left in situ for repeat
or continuous pressure measurements. In the past, we used an arterial line and a pressure transducer
similar to the continuous-infusion
technique described by Matsen,8 but
we did not use the infusion pump.
More recently we have begun using
the Stryker Intra-Compartmental
Pressure Monitor System (Stryker,
Kalamazoo, MI), which is more convenient and requires no setup. Boody
and Wongworawat43 evaluated three
commonly used modalities for compartment pressure measurement and
found an arterial manometer to be
the most accurate method, followed
by the Intra-Compartmental Pressure
Monitor System. They concluded

The main goals in the management


of ACS of the upper extremity are
expedient release of all fascial and
epimysial envelopes and decompression of all affected compartments
and nerves. Compartments that are
clearly affected clinically are released, and those that cannot be examined adequately are measured
with the Intra-Compartmental Pressure Monitor System or an arterial
manometer. Pressure in the carpal
tunnel is measured when involvement of that area is suspected. Pressure measurement 20 mm Hg with
decreased sensation and/or diminished strength in the thenar muscles
is an indication for open carpal tunnel release.
Ronel et al20 described a technique
that allows decompression of the superficial muscles and the deep muscles of the volar forearm as well as
release of the median nerve at possible sites of compression. We use this
approach because it causes the least
amount of iatrogenic injury to the
superficial muscles, arteries, and
nerves compared with other described approaches to the volar forearm. A longitudinal skin incision is
made beginning just radial to the
flexor carpi ulnaris at the wrist. The
incision is extended proximally to
the medial epicondyle, then curved
radially over the antecubital fossa
(Figure 7). Distally, the incision may
be extended to the midline to incorporate open carpal tunnel release.
The lacertus fibrosus and fascia over
the flexor carpi ulnaris are opened.
The flexor carpi ulnaris is retracted
ulnarly, and the flexor digitorum superficialis is retracted radially to allow visualization and opening of the

Journal of the American Academy of Orthopaedic Surgeons

Mark L. Prasarn, MD, and Elizabeth A. Ouellette, MD

fascia over the deep muscles of the


forearm.
Release of the volar compartment
often results in decompression of the
dorsal compartment and the mobile
wad, as well. Should the pressures
remain elevated in the dorsal compartment or the mobile wad, a second fasciotomy is performed. We use
a dorsal longitudinal incision extending from 2 cm distal to the lateral
epicondyle of the humerus toward
the midline of the wrist. Deep dissection is made through the interval between the extensor digitorum communis and the extensor carpi radialis
brevis. This allows decompression of
the musculature in the dorsal compartment and the mobile wad.
Release of the volar and dorsal interosseous compartments and the adductor compartment to the thumb is
begun by making two longitudinal
incisions dorsally over the 2nd and
4th metacarpals (Figure 2 and Figure
8). The fascia over the dorsal interosseous muscles is incised. To decompress the first volar interosseous
and adductor pollicis muscles, blunt
dissection is performed along the ulnar side of the 2nd metacarpal
through the more radial incision.
The second and third volar interosseous compartments are released by
dissecting along the radial aspect of
the 4th and 5th metacarpals through
the more ulnar incision. To release
the thenar and hypothenar compartments, longitudinal incisions are
made at the junctions of the glabrous
and nonglabrous skin over the radial
side of the 1st metacarpal and the ulnar side of the 5th metacarpal.
Compartment syndrome of the upper arm is rare. The anterior and the
posterior compartments can be decompressed through a single medial
or lateral incision. Maginn and Elliot44 suggested that the creation of
two separate midline incisions directly over the anterior and posterior
compartments causes less disruption
January 2011, Vol 19, No 1

Figure 7

Surgical approaches to the volar compartment of the forearm. A, Illustration


demonstrating the skin incision for the ulnar approach. B, The interval
between the flexor carpi ulnaris muscle and the flexor digitorum superficialis
muscle is entered. C, After the ulnar nerve and artery are identified and
protected, the fascia over the deep compartment is opened completely.
D, Incision for the Henry approach, which is performed through the interval
between the flexor carpi radialis and the brachioradialis muscles.
(Reproduced with permission from Ouellette EA: Compartment syndromes in
obtunded patients. Hand Clin 1998;14[3]:431-450.)

55

Acute Compartment Syndrome of the Upper Extremity

Figure 8

Illustration demonstrating two


longitudinal incisions made over
the 2nd and 4th metacarpals to
release the dorsal and volar
interosseous compartments and
the adductor compartment of the
thumb. (Reproduced with
permission from Ouellette EA:
Compartment syndromes in
obtunded patients. Hand Clin
1998;14[3]:431-450.)

to the perforating septal vessels, resulting in decreased iatrogenic ischemia to the muscles and flaps compared with a single medial incision.
In our experience, compartment syndrome in the upper extremity is usually associated with humeral fracture, which requires open reduction
and internal fixation. This cannot be
done through a medial approach. It
is rare that both compartments are
involved. Thus, we make a longitudinal incision over the affected compartment to first perform thorough
decompression. We use the same incision for open reduction and internal fixation of the fractured humerus. If the other compartment is
also involved, a second fasciotomy is
made over it.

56

Wound Closure
Wounds are typically left open and
initially are covered with sterile wetto-dry dressings. The skin should not
be closed acutely following fasciotomy. We do not routinely use retention sutures or rubber catheters to
prevent wound edge retraction. In
wounds with exposed tendon, bone,
or neurovascular structures, a bovine
collagen matrix wound dressing (Integra artificial dermis; Integra LifeSciences, Plainsboro, NJ) is applied
to prevent desiccation. This can be
grafted over later. The patient is returned to the operating suite after 48
to 72 hours for irrigation and dbridement. Delayed primary wound
closure may be done at this time, as
well. In the patient with muscle necrosis, all nonviable muscle is
sharply dbrided. When muscle viability is a concern, repeat dbridement is done every 48 hours. Undermining the skin flaps often assists
with tension-free closure. For
wounds that cannot be closed, a
vacuum-assisted wound closure system (VAC Therapy System; KCI, San
Antonio, TX) is placed, and splitthickness skin grafting is performed
at a later date. Potential advantages
of a vacuum-assisted closure system
include shorter hospital stays, reduced need for skin grafting, and a
lower rate of nosocomial infection.45,46

Outcomes and
Complications
Outcomes following compartment
syndrome are dependent on injury
severity, duration of ischemia, and
preinjury status and comorbidities.
The amount of infarction varies considerably, as do outcomes. Time
from diagnosis to fasciotomy is the
most important predictor of outcome. The critical delay from diag-

nosis to treatment is reported to be 6


to 24 hours.3-6,8,9,23,37,47 Irreversible
damage has been shown to occur after 8 hours in a canine model.40 Full
recovery with minimal residual dysfunction can be expected with
prompt diagnosis and intervention of
compartment syndrome of the upper
extremity.3-6,12,13,25,48 Delay beyond 6
to 24 hours may result in Volkmann
ischemic contracture, neurologic deficit, infection, amputation, or death.
How late is too late to perform
surgical decompression? In most
cases the exact time of onset of compartment syndrome cannot be determined; thus, it is impossible to determine its duration. In such instances,
the clinical examination is relied on
heavily. Voluntary muscle contraction in the setting of compression is
indicative of the existence of viable
muscle, and emergent fasciotomy
should be performed. In the patient
with no demonstrable muscle function, the best treatment may involve
supportive care for myoglobinuria
and aggressive splinting to maintain
the arm and hand in a functional position.37
Ouellette and Kelly3 noted poor results in 4 of 19 patients with hand
compartment syndrome. All four patients were obtunded at the time of
onset, and two required amputation.
A high index of suspicion for compartment syndrome must be maintained in persons who are who are
difficult to examine and who cannot
communicate effectively. Gelberman
et al49 reported the results of surgical
decompression of compartment syndrome of the forearm in 10 patients.
No patient developed Volkmann
contracture, but only two patients
had normal postoperative results. Six
patients who underwent volar fasciotomy required supplemental skin
grafting. The worst results were observed in patients with severe crush
injuries and in another with arterial
injury.

Journal of the American Academy of Orthopaedic Surgeons

Mark L. Prasarn, MD, and Elizabeth A. Ouellette, MD

Volkmann Contracture
Irreversible tissue ischemia results in
muscle necrosis within the affected
compartment, which leads to contracture. In the forearm, the typical
posture that develops includes elbow
flexion, forearm pronation, wrist
flexion, and thumb adduction with
the metacarpophalangeal joints in
extension and the interphalangeal
joints in flexion. The median nerve is
often affected to a greater degree
than the ulnar nerve because the median nerve lies in the deeper zone
that is more severely compromised
by ischemia.
Tsuge15 classified contracture as
mild, moderate, and severe. The mild
type involves mild ischemic contracture primarily of the flexor digitorum profundus and no neurologic
deficit. In the moderate type, the
flexor digitorum profundus, flexor
pollicis longus, and pronator teres
are affected, and the flexor digitorum superficialis and flexor carpi ulnaris are affected to a lesser degree.
Intrinsic muscle paralysis and sensory neuropathy of the median and
ulnar nerves are also present. The severe type involves ischemic damage
to all of the flexors in the forearm, variable involvement of the extensors, and severe neurologic
injury.12,14-16
The main goal in the management
of Volkmann contracture is to restore function; however, normal
function of the upper extremity
should not be expected.10-16 Affected
muscles are exposed, and fibrotic or
necrotic tissue is dbrided. Thorough
neurolysis of the median and ulnar
nerves should be performed as well
as tenolysis of scarred tendons. Isolated tendon lengthening is not recommended because it typically results in recurrent contracture and
loss of grip strength.12,16 In persons
with mild contracture, the flexor/
January 2011, Vol 19, No 1

pronator slide may be performed to


improve hand position as well as
function of the forearm flexors. Tendon transfer may be performed to
improve specific dysfunction in persons with moderate contracture.
Usually this involves use of an extensor tendon transfer; however, flexor
tendons can be transferred in the
case of dorsal contracture. Free muscle transfer, typically using the gracilis muscle, is necessary to improve
function in persons with severe contracture.12,15,16

Summary
ACS of the upper extremity is a potentially devastating condition that can
lead to substantial loss of function.
Compartment syndrome has many
causes, and a high index of suspicion
must be maintained. The final common
pathway is a vicious cycle of increased
tissue pressure with resulting cellular ischemia. All affected compartments in
the upper extremity must be recognized, and thorough decompression
must be performed in an expedient
manner. Compartment syndrome is difficult to diagnose in some cases, particularly in obtunded patients and young
children. Prompt diagnosis and emergent surgical decompression are essential to obtain a good clinical outcome
and preventing a catastrophic result.

Muskellhmungen und Kontracturen.


Centralblatt fr Chirurgie, Leipzig 1881;
8:801-803.
2.

Grottkau BE, Epps HR, Di Scala C:


Compartment syndrome in children and
adolescents. J Pediatr Surg 2005;40(4):
678-682.

3.

Ouellette EA, Kelly R: Compartment


syndromes of the hand. J Bone Joint
Surg Am 1996;78(10):1515-1522.

4.

Ouellette EA: Compartment syndromes


in obtunded patients. Hand Clin 1998;
14(3):431-450.

5.

Prasarn ML, Ouellette EA, Livingstone


A, Giuffrida AY: Acute pediatric upper
extremity compartment syndrome in the
absence of fracture. J Pediatr Orthop
2009;29(3):263-268.

6.

Bae DS, Kadiyala RK, Waters PM: Acute


compartment syndrome in children:
Contemporary diagnosis, treatment, and
outcome. J Pediatr Orthop 2001;21(5):
680-688.

7.

Mabee JR, Bostwick TL: Pathophysiology and mechanisms of


compartment syndrome. Orthop Rev
1993;22(2):175-181.

8.

Matsen FA: Compartmental Syndromes.


New York, NY, Grune and Stratton,
1980.

9.

McQueen MM, Christie J, Court-Brown


CM: Acute compartment syndrome in
tibial diaphyseal fractures. J Bone Joint
Surg Br 1996;78(1):95-98.

10.

Bunnell S, Doherty EW, Curtis RM:


Ischemic contracture, local, in the hand.
Plast Reconstr Surg 1948;3:424-433.

11.

Dellaero DT, Levin LS: Compartment


syndrome of the hand: Etiology,
diagnosis, and treatment. Am J Orthop
(Belle Mead NJ) 1996;25(6):404-408.

12.

Friedrich JB, Shin AY: Management of


forearm compartment syndrome. Hand
Clin 2007;23(2):245-254, vii.

13.

Gelberman RH, Garfin SR,


Hergenroeder PT, Mubarak SJ, Menon J:
Compartment syndromes of the forearm:
Diagnosis and treatment. Clin Orthop
Relat Res 1981;(161):252-261.

14.

Stevanovic M, Sharpe F: Management of


established Volkmanns contracture of
the forearm in children. Hand Clin 2006;
22(1):99-111.

15.

Tsuge K: Treatment of established


Volkmanns contracture. J Bone Joint
Surg Am 1975;57(7):925-929.

16.

Ultee J, Hovius SE: Functional results


after treatment of Volkmanns ischemic
contracture: A long-term followup study.
Clin Orthop Relat Res 2005;(431):4249.

17.

McQueen MM, Gaston P, Court-Brown

References
Evidence-based Medicine: Levels of
evidence are described in the table of
contents. In this article, references
2-6, 9, 10, 14-20, 28, 31, 42, 46,
and 47 are level IV studies. References 11-13, 23, 37, 44, and 45 are
level V expert opinion.
Citation numbers printed in bold
type indicate references published
within the past 5 years.
1.

von Volkmann R: Die ischmischen

57

Acute Compartment Syndrome of the Upper Extremity


CM: Acute compartment syndrome:
Who is at risk? J Bone Joint Surg Br
2000;82(2):200-203.

29.

Cohen J, Bush S: Case report:


Compartment syndrome after a
suspected black widow spider bite. Ann
Emerg Med 2005;45(4):414-416.

spectroscopy. Clin Orthop Relat Res


1988;(226):138-155.
40.

Matava MJ, Whitesides TE Jr, Seiler JG


III, Hewan-Lowe K, Hutton WC:
Determination of the compartment
pressure threshold of muscle ischemia in
a canine model. J Trauma 1994;37(1):
50-58.

41.

Heckman MM, Whitesides TE Jr, Grewe


SR, Judd RL, Miller M, Lawrence JH III:
Histologic determination of the ischemic
threshold of muscle in the canine
compartment syndrome model. J Orthop
Trauma 1993;7(3):199-210.

Benson LS, Sathy MJ, Port RB: Forearm


compartment syndrome due to
automated injection of computed
tomography contrast material. J Orthop
Trauma 1996;10(6):433-436.

42.

Yuan PS, Pring ME, Gaynor TP,


Mubarak SJ, Newton PO: Compartment
syndrome following intramedullary
fixation of pediatric forearm fractures.
J Pediatr Orthop 2004;24(4):370-375.

33.

Moen TC, Sarwark JF: Compartment


syndrome following intraosseous
infusion. Orthopedics 2008;31(8):815.

43.

Schmidt GL, Uroskie JA: Isolated


compartment syndrome of the extensor
carpi ulnaris: A case report. Am J
Orthop (Belle Mead NJ) 2004;33(10):
519-520.

34.

Funk L, Grover D, de Silva H:


Compartment syndrome of the hand
following intra-arterial injection of
heroin. J Hand Surg Br 1999;24(3):366367.

Boody AR, Wongworawat MD:


Accuracy in the measurement of
compartment pressures: A comparison of
three commonly used devices. J Bone
Joint Surg Am 2005;87(11):2415-2422.

44.

Maginn P, Elliot D: Upper arm


fasciotomy: A new approach. J Hand
Surg [Br] 1996;21:59-62.

23.

Whitesides TE, Heckman MM: Acute


compartment syndrome: Update on
diagnosis and treatment. J Am Acad
Orthop Surg 1996;4(4):209-218.

35.

Ananthanarayan C, Castro C, McKee N,


Sakotic G: Compartment syndrome
following intravenous regional
anesthesia. Can J Anaesth 2000;47(11):
1094-1098.

45.

24.

Docker C, Titley OG: A case of forearm


compartment syndrome following a ring
avulsion injury. Injury 2002;33(3):274275.

36.

Hwang RW, de Witte PB, Ring D:


Compartment syndrome associated with
distal radial fracture and ipsilateral
elbow injury. J Bone Joint Surg Am
2009;91(3):642-645.

Tarkin IS: The versatility of negative


pressure wound therapy with reticulated
open cell foam for soft tissue
management after severe musculoskeletal
trauma. J Orthop Trauma 2008;22(10
suppl):S146-S151.

46.

Yang CC, Chang DS, Webb LX:


Vacuum-assisted closure for fasciotomy
wounds following compartment
syndrome of the leg. J Surg Orthop Adv
2006;15(1):19-23.

47.

Hope MJ, McQueen MM: Acute


compartment syndrome in the absence of
fracture. J Orthop Trauma 2004;18(4):
220-224.

48.

Vaienti L, Vourtsis S, Urzola V:


Compartment syndrome of the forearm
following an electromyographic
assessment. J Hand Surg Br 2005;30(6):
656-657.

49.

Gelberman RH, Garfin SR,


Hergenroeder PT, Mubarak SJ, Menon J:
Compartment syndromes of the forearm:
Diagnosis and treatment. Clin Orthop
Relat Res 1981;(161):252-261.

18.

Elliott KG, Johnstone AJ: Diagnosing


acute compartment syndrome. J Bone
Joint Surg Br 2003;85(5):625-632.

30.

19.

Schnall SB, Vu-Rose T, Holtom PD,


Doyle B, Stevanovic M: Tissue pressures
in pyogenic flexor tenosynovitis of the
finger: Compartment syndrome and its
management. J Bone Joint Surg Br 1996;
78(5):793-795.

Roberts RS, Csencsitz TA, Heard CW Jr:


Upper extremity compartment
syndromes following pit viper
envenomation. Clin Orthop Relat Res
1985;(193):184-188.

31.

Ragland R III, Moukoko D, Ezaki M,


Carter PR, Mills J: Forearm
compartment syndrome in the newborn:
Report of 24 cases. J Hand Surg Am
2005;30(5):997-1003.

32.

20.

21.

22.

25.

26.

27.

28.

58

Ronel DN, Mtui E, Nolan WB III:


Forearm compartment syndrome:
Anatomical analysis of surgical
approaches to the deep space. Plast
Reconstr Surg 2004;114(3):697-705.
Tompkins DG: Exercise myopathy of the
extensor carpi ulnaris muscle: Report of
a case. J Bone Joint Surg Am 1977;59(3):
407-408.

Cosker T, Gupta S, Tayton K:


Compartment syndrome caused by
suction. Injury 2004;35(11):1194-1195.
Bacal D, Lampman RM, Hogikyan JV,
Wolk SW: Compartment syndrome of
the arm and disseminated intravascular
coagulation. Am J Orthop (Belle Mead
NJ) 2001;30(5):422-423.
Kleshinski J, Bittar S, Wahlquist M,
Ebraheim N, Duggan JM: Review of
compartment syndrome due to group A
streptococcal infection. Am J Med Sci
2008;336(3):265-269.
Ramos C, Whyte CM, Harris BH:
Nontraumatic compartment syndrome of
the extremities in children. J Pediatr Surg
2006;41(12):e5-e7.

37.

38.

39.

Olson SA, Glasgow RR: Acute


compartment syndrome in lower
extremity musculoskeletal trauma. J Am
Acad Orthop Surg 2005;13(7):436-444.
Heppenstall RB, Scott R, Sapega A, Park
YS, Chance B: A comparative study of
the tolerance of skeletal muscle to
ischemia: Tourniquet application
compared with acute compartment
syndrome. J Bone Joint Surg Am 1986;
68(6):820-828.
Heppenstall RB, Sapega AA, Scott R,
et al: The compartment syndrome: An
experimental and clinical study of
muscular energy metabolism using
phosphorus nuclear magnetic resonance

Journal of the American Academy of Orthopaedic Surgeons