Acute Compartment Syndrome Upper Extremity JAAOS REVIEW

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Acute Compartment Syndrome ofthe Upper Extremity

Abstract

Acute compartment syndrome occurs when pressure within a fibro-

osseous 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 andexpeditious surgical treatment are essential to obtain a good

clinical outcome and prevent permanent disability.

Compartment syndrome was firstdescribed in 1881 by Richardvon Volkmann.1 The etiology, patho-

physiology, and management of

compartment syndrome and the as-

sociated complications have been ex-

tensively described. Acute compart-

ment 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 is-

chemia of the tissues within this con-

fined space. In the upper extremity,

the dorsal and volar compartments

of the forearm are the most com-

monly affected. Upper extremity

ACS can lead to devastating loss of

function, including Volkmann ische-

mic contracture, neurologic deficit,

infection, amputation, and death.

A wide range of causes of ACS in

the upper extremity has been re-

ported, 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 compart-

ment syndrome in the upper extrem-

ity.1,2 Compartment syndrome is a

clinical diagnosis, and it can be diffi-

cult to make in certain patient popu-

lations, such as persons who are ob-

tunded and children.2-5 Emergent

surgical treatment is required; themost important determinant of out-

come is early recognition and expedi-

tious surgical intervention.3,5-9 Re-

constructive 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 con-

sists of a flexor (ie, volar) compart-

ment and an extensor (ie, dorsal)

compartment. The forearm is divided

into three compartments: volar, dor-

sal, and lateral (ie, mobile wad) (Fig-

ure 1). The hand has 10 compart-

Mark L. Prasarn, MD

Elizabeth A. Ouellette, MD

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 hasreceived 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 Surg2011;19:

49-58

Copyright 2011 by the American

Academy of Orthopaedic Surgeons.

Review Article

January 2011, Vol 19, No 1 49


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ments: hypothenar, thenar, and

adductor pollicis as well as four dor-

sal interosseous and three volar in-

terosseous17 (Figure 2). The volar

forearm is the most commonly af-

fected compartment in the upper ex-

tremity. Compartment syndrome in

this area typically occurs following

fracture of the distal radius, supra-

condylar humerus, or diaphysis of

the radius or ulna.2,17,18 Any compart-

ment can be affected, however. Digi-

tal fasciotomy is necessary in some

cases19 (Figure 3).

In the upper arm, the medial and

the lateral intermuscular septa sepa-

rate the flexor compartment from

the extensor compartment. The bra-

chial fascia is a dense fibrous sheath

that surrounds the muscles in each of

the two compartments. In the fore-

arm, the stiff interosseous membrane

bridges the distance between the ra-

dius and the ulna. Just anterior to

this membrane lie the flexor digito-

rum profundus, flexor pollicis lon-

gus, and pronator quadratus mus-

cles. Some consider the pronator

quadratus to lie within an additional

compartment of the distal volar fore-

arm, separate from the flexor ten-dons at this level.20 These deep volar

muscles are the most commonly

damaged muscles in forearm com-

partment 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 syn-

dromes of the extensor carpi ulnaris

muscle have been noted in case re-

ports.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 bra-

chial fascia, envelops the compart-

ments and muscles in the forearm.

The compartments of the hand are

divided by the carpal bones, metacar-

pals, and individual investing fascial

layers. Pressures within the carpal tun-

nel 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 in-

volved compartments. The digital fas-

cial compartments are bound by the

Cleland ligament and the Grayson lig-

ament, and elevated pressure may oc-

cur in individual digits (Figure 3).

Compartment syndrome of the hand

typically necessitates carpal tunnel re-

lease and dorsal interosseous compart-

ment releases; however, any compart-

ment 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 mea-

surements.3

Cross section at the junction of the proximal and middle thirds of the forearmdemonstrating 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 carpiulnaris (FCU), as well as the ulnar nerve (UN), ulnar artery (UA), mediannerve (MN), median artery (MA), radial artery (RA), superficial branch of theradial nerve (RN), anterior interosseous artery (AIA), and anteriorinterosseous nerve (AIN). The dorsal and volar compartments are separatedby the interosseous membrane. The dorsal compartment contains the fingerand thumb extensors and the long thumb abductor as well as the posteriorinterosseous artery (PIA), posterior interosseous nerve (PIN), extensor carpiulnaris (ECU), extensor pollicis longus (EPL), and extensor digitorumcommunis (EDC). The mobile wad, which is often considered to be a thirdcompartment, is composed of the extensor carpi radialis brevis and longusmuscles (ECR) and the brachioradialis (BR). (Reproduced with permissionfrom Ouellette EA: Compartment syndromes in obtunded patients. Hand Clin1998;14[3]:431-450.)

Figure 1

Acute Compartment Syndrome of the Upper Extremity

50 Journal of the American Academy of Orthopaedic Surgeons


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Etiology

ACS of the upper extremity is caused

by a myriad of factors, including

fracture, bleeding disorders, constric-

tive dressing and casting, arterial in-

jury, 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, bleed-

ing, edema, purulent material, extra-

neous fluids) or restricts the com-

partment from expanding (eg, burn,

casting, dressing, tourniquet) can

cause ACS.

It is difficult to estimate the true

incidence of compartment syndromeof the upper extremity, but most

cases occur in the setting of fracture.

McQueen et al17 analyzed 164 pa-

tients 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 di-

aphysis 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 in-

jury without fracture was the second

most common cause of injury

(23.2%). Incidence in the forearm

and hand was 5.5% and 0.6%, re-

spectively. Within this subgroup,

10.3% occurred in patients with

bleeding disorders or who were tak-

ing anticoagulants.

Grottkau et al2 reviewed a national

trauma database and found the inci-

dence of pediatric forearm compart-

ment syndrome to be 1%. Ouellette

and Kelly3 reported on 19 patients

with compartment syndrome of the

hand. Most cases were iatrogenic, re-

sulting from complications related to

intravenous or intra-arterial adminis-

tration of drugs. The incidence of

compartment syndrome in unstable

fractures of the distal end of the ra-

dius is substantially higher with con-

comitant 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 de-

creased tissue perfusion. The initial

rise in intracompartmental pressure

causes increased extravascular ve-

nous 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 perfu-

sion and increased interstitial pres-

sure. This increased interstitial pres-

sure in turn causes increased edema

within the compartment, and this

cascade of events repeats itself per-

petually.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 arte-

riovenous gradient and when circula-

tion 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 col-

leagues38,39 prefer to compare intra-

compartmental pressure with mean

arterial pressure, but diastolic blood

pressure is easier to obtain and cal-

culate. Experimental data in a canine

model have shown that terminal ar-

terial pressure is equal to diastolic

blood pressure;40 thus, we use dia-

stolic blood pressure to determine

the critical threshold.

In a canine study, muscle necrosis

occurred when the intracompart-

Cross section at the level of the metacarpal shafts demonstrating the 10compartments of the hand: hypothenar, thenar, and adductor pollicis as wellas four dorsal interosseous and three volar interosseous. (Reproduced withpermission from Ouellette EA: Compartment syndromes in obtundedpatients.Hand Clin1998;14[3]:431-450.)

Figure 2

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



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mental pressure rose to a level 20

mm Hg below diastolic blood pres-

sure.40 Heckman et al41 demonstrated

that irreversible changes to the pe-

ripheral nerves and skeletal muscle

occur following 8 hours of complete

ischemia. Following onset of cellular

anoxia, affected cells begin anaero-

bic metabolism and may die. Devas-

tating loss of function may occur fol-

lowing substantial loss of muscle and

neural tissue in the upper extremity.

Muscle ischemia can lead to release

of myoglobin, which can cause myo-

globinuria, metabolic acidosis, and

hyperkalemia. Renal failure, cardiac

arrhythmia, cardiac failure, and

shock may then ensue. The magni-

tude of these systemic effects is de-

pendent on the duration of ischemia

and the size of the muscle compart-

ments 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 sub-

stantial amount of time has elapsed

following the onset of compartment

syndrome, and outcomes typically

are poor even with expedient fasciot-

omy. Pain out of proportion to in-

jury and pain with passive stretching

of muscles in the involved compart-ment are the earliest indicators of

compartment syndrome.23 Compart-

ment syndrome also should be sus-

pected with tense, swollen compart-

ments. In a series of patients with

compartment syndrome of the hand,

Ouellette and Kelly3 demonstrated

that the most consistent clinical find-

ing was a tense, swollen hand in an

intrinsic minus position (ie, exten-

sion of the metacarpophalangeal

joints and flexion of the intercarpal

joints) (Figure 5).

ACS is typically diagnosed clini-

cally. However, it may be necessary

to measure compartment pressure

(Figure 6). Animal studies demon-

strate that compartment syndrome is

indicated in the presence of a differ-

ence between diastolic blood pres-

sure and the compartment measuring

Table 1

Causes of CompartmentSyndrome of the UpperExtremity3-5,23-35

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 madeon the index finger. This incision is made on the ulnar side of digits 2 through4 and on the radial side of digits 1 and 5. The neurovascular bundles areidentified and retracted volarward, and the fascia between them is cut alongwith the flexor sheath. B and C, Clinical photographs following fasciotomiesof the hand and digits. (Reproduced with permission from Ouellette EA:

Compartment syndromes in obtunded patients. Hand Clin1998;14[3]:431-450.)

Figure 3




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20 mm Hg40 or a difference be-

tween 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 con-

sider a differential between diastolic

pressure and the compartment of

20 mm Hg to be an absolute indica-

tion for emergent fasciotomy. In the

patient with swollen compartments

and nearly normal pressures (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 pe-

diatric patients, Bae et al6 demon-

strated that an increased need for an-algesics was most predictive of

compartment syndrome.

Compartment PressureMeasurement

We typically measure compartment

pressures in patients with equivocal

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

Figure 4

A and B, Photographs demonstrating a tense, swollen hand and forearm.The hand is held in the intrinsic minus position. (Reproduced with permissionfrom Prasarn ML, Ouellette EA, Livingstone A, Giuffrida AY: Acute pediatricupper extremity compartment syndrome in the absence of fracture. J PediatrOrthop2009;29[3]:263-268.)

Figure 5




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examination and in those who can-

not be examined fully. An equivocal

examination is one in which com-

partment syndrome is suspected anduncertainty exists regarding the clini-

cal examination. Measurements are

also often taken in the operating the-

ater to verify which compartment or

compartments are affected and to en-

sure that they are fully decompressed

following fasciotomy. Compartments

that clinically appear to be involved

are tested, and measurements are

taken when the compartment ap-

pears to be the most tense and swol-

len. In the case of associated frac-

ture, the catheter is inserted close to

the fracture site. Otherwise, mea-

surements are taken at the location

that is most accessible to the com-

partment. Typically, a single mea-

surement is taken for each suspected

compartment. When in doubt re-

garding the resulting pressure value,

repeat measurements should be ob-

tained at other sites.

The two most common measure-

ment 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 measure-

ments. In the past, we used an arte-

rial 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 con-

venient and requires no setup. Boody

and Wongworawat43 evaluated three

commonly used modalities for com-

partment pressure measurement and

found an arterial manometer to be

the most accurate method, followed

by the Intra-Compartmental Pressure

Monitor System. They concluded

that the Whitesides manometer lacks

the precision required for clinical

use.

Fasciotomy

The main goals in the management

of ACS of the upper extremity are

expedient release of all fascial and

epimysial envelopes and decompres-

sion of all affected compartments

and nerves. Compartments that are

clearly affected clinically are re-

leased, and those that cannot be ex-

amined adequately are measured

with the Intra-Compartmental Pres-

sure Monitor System or an arterial

manometer. Pressure in the carpaltunnel is measured when involve-

ment of that area is suspected. Pres-

sure measurement 20 mm Hg with

decreased sensation and/or dimin-

ished strength in the thenar muscles

is an indication for open carpal tun-

nel release.

Ronel et al20 described a technique

that allows decompression of the su-

perficial muscles and the deep mus-

cles of the volar forearm as well as

release of the median nerve at possi-

ble 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 de-

scribed approaches to the volar fore-

arm. 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 incor-

porate 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 su-

perficialis is retracted radially to al-

low visualization and opening of the

Algorithm for evaluating and managing suspected compartment syndrome.

Figure 6




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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 com-partment or the mobile wad, a sec-

ond fasciotomy is performed. We use

a dorsal longitudinal incision extend-

ing from 2 cm distal to the lateral

epicondyle of the humerus toward

the midline of the wrist. Deep dissec-

tion is made through the interval be-

tween the extensor digitorum com-

munis and the extensor carpi radialis

brevis. This allows decompression of

the musculature in the dorsal com-

partment and the mobile wad.Release of the volar and dorsal in-

terosseous compartments and the ad-

ductor 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 in-

terosseous muscles is incised. To de-

compress the first volar interosseous

and adductor pollicis muscles, blunt

dissection is performed along the ul-

nar side of the 2nd metacarpalthrough the more radial incision.

The second and third volar interosse-

ous 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 compart-

ments, longitudinal incisions are

made at the junctions of the glabrous

and nonglabrous skin over the radial

side of the 1st metacarpal and the ul-

nar side of the 5th metacarpal.

Compartment syndrome of the up-

per arm is rare. The anterior and the

posterior compartments can be de-

compressed through a single medial

or lateral incision. Maginn and El-

liot44 suggested that the creation of

two separate midline incisions di-

rectly over the anterior and posterior

compartments causes less disruption

Surgical approaches to the volar compartment of the forearm. A, Illustrationdemonstrating the skin incision for the ulnar approach. B, The intervalbetween the flexor carpi ulnaris muscle and the flexor digitorum superficialismuscle is entered. C, After the ulnar nerve and artery are identified andprotected, the fascia over the deep compartment is opened completely.D,Incision for the Henry approach, which is performed through the intervalbetween the flexor carpi radialis and the brachioradialis muscles.(Reproduced with permission from Ouellette EA: Compartment syndromes inobtunded patients. Hand Clin1998;14[3]:431-450.)

Figure 7




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to the perforating septal vessels, re-

sulting in decreased iatrogenic ische-

mia to the muscles and flaps com-

pared with a single medial incision.

In our experience, compartment syn-

drome in the upper extremity is usu-

ally associated with humeral frac-

ture, 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 longitudi-

nal incision over the affected com-

partment to first perform thorough

decompression. We use the same in-

cision for open reduction and inter-

nal fixation of the fractured hu-

merus. If the other compartment is

also involved, a second fasciotomy is

made over it.

Wound Closure

Wounds are typically left open and

initially are covered with sterile wet-

to-dry dressings. The skin should not

be closed acutely following fasciot-

omy. We do not routinely use reten-tion sutures or rubber catheters to

prevent wound edge retraction. In

wounds with exposed tendon, bone,

or neurovascular structures, a bovine

collagen matrix wound dressing (In-

tegra artificial dermis; Integra Life-

Sciences, Plainsboro, NJ) is applied

to prevent desiccation. This can be

grafted over later. The patient is re-

turned to the operating suite after 48

to 72 hours for irrigation and d-

bridement. Delayed primary woundclosure may be done at this time, as

well. In the patient with muscle ne-

crosis, all nonviable muscle is

sharply dbrided. When muscle via-

bility is a concern, repeat dbride-

ment is done every 48 hours. Under-

mining the skin flaps often assists

with tension-free closure. For

wounds that cannot be closed, a

vacuum-assisted wound closure sys-

tem (VAC Therapy System; KCI, San

Antonio, TX) is placed, and split-thickness skin grafting is performed

at a later date. Potential advantages

of a vacuum-assisted closure system

include shorter hospital stays, re-

duced need for skin grafting, and a

lower rate of nosocomial infec-

tion.45,46

Outcomes andComplications

Outcomes following compartment

syndrome are dependent on injury

severity, duration of ischemia, and

preinjury status and comorbidities.

The amount of infarction varies con-

siderably, as do outcomes. Time

from diagnosis to fasciotomy is the

most important predictor of out-

come. 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 af-

ter 8 hours in a canine model.40 Full

recovery with minimal residual dys-

function can be expected with

prompt diagnosis and intervention ofcompartment syndrome of the upper

extremity.3-6,12,13,25,48 Delay beyond 6

to 24 hours may result in Volkmann

ischemic contracture, neurologic def-

icit, infection, amputation, or death.

How late is too late to perform

surgical decompression? In most

cases the exact time of onset of com-

partment syndrome cannot be deter-

mined; thus, it is impossible to deter-

mine its duration. In such instances,

the clinical examination is relied onheavily. Voluntary muscle contrac-

tion 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 func-

tion, the best treatment may involve

supportive care for myoglobinuria

and aggressive splinting to maintain

the arm and hand in a functional po-

sition.37

Ouellette and Kelly

3

noted poor re-sults in 4 of 19 patients with hand

compartment syndrome. All four pa-

tients were obtunded at the time of

onset, and two required amputation.

A high index of suspicion for com-

partment syndrome must be main-

tained 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 syn-

drome of the forearm in 10 patients.

No patient developed Volkmann

contracture, but only two patients

had normal postoperative results. Six

patients who underwent volar fas-

ciotomy required supplemental skin

grafting. The worst results were ob-

served in patients with severe crush

injuries and in another with arterial

injury.

Illustration demonstrating twolongitudinal incisions made overthe 2nd and 4th metacarpals torelease the dorsal and volarinterosseous compartments andthe adductor compartment of thethumb. (Reproduced withpermission from Ouellette EA:Compartment syndromes inobtunded patients. Hand Clin1998;14[3]:431-450.)

Figure 8




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Volkmann Contracture

Irreversible tissue ischemia results in

muscle necrosis within the affected

compartment, which leads to con-

tracture. 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 me-

dian nerve lies in the deeper zone

that is more severely compromised

by ischemia.

Tsuge

15

classified contracture asmild, moderate, and severe. The mild

type involves mild ischemic contrac-

ture primarily of the flexor digito-

rum profundus and no neurologic

deficit. In the moderate type, the

flexor digitorum profundus, flexor

pollicis longus, and pronator teres

are affected, and the flexor digito-

rum superficialis and flexor carpi ul-

naris are affected to a lesser degree.

Intrinsic muscle paralysis and sen-

sory neuropathy of the median and

ulnar nerves are also present. The se-

vere type involves ischemic damage

to all of the flexors in the fore-

arm, variable involvement of the ex-

tensors, and severe neurologic

injury.12,14-16

The main goal in the management

of Volkmann contracture is to re-

store 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. Iso-

lated tendon lengthening is not rec-

ommended because it typically re-

sults in recurrent contracture and

loss of grip strength.12,16 In persons

with mild contracture, the flexor/

pronator slide may be performed to

improve hand position as well as

function of the forearm flexors. Ten-

don transfer may be performed to

improve specific dysfunction in per-

sons with moderate contracture.

Usually this involves use of an exten-sor tendon transfer; however, flexor

tendons can be transferred in the

case of dorsal contracture. Free mus-

cle transfer, typically using the graci-

lis muscle, is necessary to improve

function in persons with severe con-

tracture.12,15,16

Summary

ACS of the upper extremity is a poten-

tially 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 is-

chemia. All affected compartments in

the upper extremity must be recog-

nized, and thorough decompression

must be performed in an expedient

manner. Compartment syndrome is dif-

ficult to diagnose in some cases, partic-

ularly in obtunded patients and young

children. Prompt diagnosis and emer-

gent surgical decompression are essen-

tial to obtain a good clinical outcome

and preventing a catastrophic result.

References

Evidence-based Medicine: Levels of

evidence are described in the table of

contents. In this article, references2-6, 9, 10, 14-20, 28, 31, 42, 46,

and 47 are level IV studies. Refer-

ences 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.

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Compartment syndrome in children and

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3. Ouellette EA, Kelly R: Compartmentsyndromes of the hand. J Bone JointSurg Am1996;78(10):1515-1522.

4. Ouellette EA: Compartment syndromesin obtunded patients.Hand Clin1998;14(3):431-450.

5. Prasarn ML, Ouellette EA, LivingstoneA, Giuffrida AY: Acute pediatric upperextremity compartment syndrome in theabsence of fracture.J Pediatr Orthop2009;29(3):263-268.

6. Bae DS, Kadiyala RK, Waters PM: Acutecompartment syndrome in children:Contemporary diagnosis, treatment, andoutcome.J Pediatr Orthop2001;21(5):

680-688.

7. Mabee JR, Bostwick TL: Patho-physiology and mechanisms ofcompartment syndrome.Orthop Rev1993;22(2):175-181.

8. Matsen FA:Compartmental Syndromes.New York, NY, Grune and Stratton,1980.

9. McQueen MM, Christie J, Court-BrownCM: Acute compartment syndrome intibial diaphyseal fractures.J Bone JointSurg Br1996;78(1):95-98.

10. Bunnell S, Doherty EW, Curtis RM:Ischemic contracture, local, in the hand.Plast Reconstr Surg1948;3:424-433.

11. Dellaero DT, Levin LS: Compartmentsyndrome of the hand: Etiology,diagnosis, and treatment.Am J Orthop(Belle Mead NJ)1996;25(6):404-408.

12. Friedrich JB, Shin AY: Management offorearm compartment syndrome. HandClin 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 OrthopRelat Res1981;(161):252-261.

14. Stevanovic M, Sharpe F: Management ofestablished Volkmanns contracture of

the forearm in children.Hand Clin2006;22(1):99-111.

15. Tsuge K: Treatment of establishedVolkmanns contracture.J Bone JointSurg Am1975;57(7):925-929.

16. Ultee J, Hovius SE: Functional resultsafter treatment of Volkmanns ischemiccontracture: A long-term followup study.Clin Orthop Relat Res2005;(431):42-49.

17. McQueen MM, Gaston P, Court-Brown




10/10

CM: Acute compartment syndrome:

Who is at risk? J Bone Joint Surg Br

2000;82(2):200-203.

18. Elliott KG, Johnstone AJ: Diagnosing

acute compartment syndrome. J Bone

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19. Schnall SB, Vu-Rose T, Holtom PD,

Doyle B, Stevanovic M: Tissue pressuresin pyogenic flexor tenosynovitis of the

finger: Compartment syndrome and its

management.J Bone Joint Surg Br1996;

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20. Ronel DN, Mtui E, Nolan WB III:

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Anatomical analysis of surgical

approaches to the deep space.Plast

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21. Tompkins DG: Exercise myopathy of the

extensor carpi ulnaris muscle: Report of

a case.J Bone Joint Surg Am 1977;59(3):

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22. 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.

23. Whitesides TE, Heckman MM: Acutecompartment syndrome: Update ondiagnosis and treatment.J Am AcadOrthop Surg1996;4(4):209-218.

24. Docker C, Titley OG: A case of forearmcompartment syndrome following a ringavulsion injury.Injury2002;33(3):274-275.

25. Cosker T, Gupta S, Tayton K:Compartment syndrome caused by

suction.Injury2004;35(11):1194-1195.26. Bacal D, Lampman RM, Hogikyan JV,

Wolk SW: Compartment syndrome ofthe arm and disseminated intravascularcoagulation.Am J Orthop (Belle MeadNJ)2001;30(5):422-423.

27. Kleshinski J, Bittar S, Wahlquist M,Ebraheim N, Duggan JM: Review ofcompartment syndrome due to group Astreptococcal infection.Am J Med Sci2008;336(3):265-269.

28. Ramos C, Whyte CM, Harris BH:Nontraumatic compartment syndrome ofthe extremities in children.J Pediatr Surg2006;41(12):e5-e7.

29. Cohen J, Bush S: Case report:Compartment syndrome after asuspected black widow spider bite. AnnEmerg Med2005;45(4):414-416.

30. Roberts RS, Csencsitz TA, Heard CW Jr:Upper extremity compartmentsyndromes following pit viperenvenomation.Clin Orthop Relat Res

1985;(193):184-188.31. Ragland R III, Moukoko D, Ezaki M,

Carter PR, Mills J: Forearmcompartment syndrome in the newborn:Report of 24 cases.J Hand Surg Am2005;30(5):997-1003.

32. Benson LS, Sathy MJ, Port RB: Forearmcompartment syndrome due toautomated injection of computedtomography contrast material. J OrthopTrauma 1996;10(6):433-436.

33. Moen TC, Sarwark JF: Compartmentsyndrome following intraosseousinfusion.Orthopedics2008;31(8):815.

34. Funk L, Grover D, de Silva H:Compartment syndrome of the handfollowing intra-arterial injection ofheroin.J Hand Surg Br1999;24(3):366-367.

35. Ananthanarayan C, Castro C, McKee N,Sakotic G: Compartment syndromefollowing intravenous regionalanesthesia.Can J Anaesth2000;47(11):1094-1098.

36. Hwang RW, de Witte PB, Ring D:Compartment syndrome associated withdistal radial fracture and ipsilateralelbow injury.J Bone Joint Surg Am2009;91(3):642-645.

37. Olson SA, Glasgow RR: Acutecompartment syndrome in lowerextremity musculoskeletal trauma.J AmAcad Orthop Surg2005;13(7):436-444.

38. Heppenstall RB, Scott R, Sapega A, ParkYS, Chance B: A comparative study ofthe tolerance of skeletal muscle toischemia: Tourniquet applicationcompared with acute compartmentsyndrome.J Bone Joint Surg Am1986;68(6):820-828.

39. Heppenstall RB, Sapega AA, Scott R,et al: The compartment syndrome: Anexperimental and clinical study ofmuscular energy metabolism usingphosphorus nuclear magnetic resonance

spectroscopy. Clin Orthop Relat Res1988;(226):138-155.

40. Matava MJ, Whitesides TE Jr, Seiler JGIII, Hewan-Lowe K, Hutton WC:Determination of the compartmentpressure threshold of muscle ischemia ina canine model. J Trauma 1994;37(1):50-58.

41. Heckman MM, Whitesides TE Jr, GreweSR, Judd RL, Miller M, Lawrence JH III:Histologic determination of the ischemicthreshold of muscle in the caninecompartment syndrome model.J OrthopTrauma 1993;7(3):199-210.

42. Yuan PS, Pring ME, Gaynor TP,Mubarak SJ, Newton PO: Compartmentsyndrome following intramedullaryfixation of pediatric forearm fractures.

J Pediatr Orthop2004;24(4):370-375.

43. Boody AR, Wongworawat MD:Accuracy in the measurement ofcompartment pressures: A comparison ofthree commonly used devices. J Bone

Joint Surg Am2005;87(11):2415-2422.44. Maginn P, Elliot D: Upper arm

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

45. Tarkin IS: The versatility of negativepressure wound therapy with reticulatedopen cell foam for soft tissuemanagement after severe musculoskeletaltrauma.J Orthop Trauma 2008;22(10suppl):S146-S151.

46. Yang CC, Chang DS, Webb LX:Vacuum-assisted closure for fasciotomywounds following compartmentsyndrome of the leg. J Surg Orthop Adv2006;15(1):19-23.

47. Hope MJ, McQueen MM: Acutecompartment syndrome in the absence offracture.J Orthop Trauma 2004;18(4):220-224.

48. Vaienti L, Vourtsis S, Urzola V:Compartment syndrome of the forearmfollowing an electromyographicassessment.J Hand Surg Br2005;30(6):656-657.

49. Gelberman RH, Garfin SR,Hergenroeder PT, Mubarak SJ, Menon J:Compartment syndromes of the forearm:Diagnosis and treatment.Clin OrthopRelat Res1981;(161):252-261.



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