Review Article Acute Compartment Syndrome of the …upload.orthobullets.com/journalclub/free_pdf/21205767_21205767.pdfAcute Compartment Syndrome of ... The mobile wad, which is often

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 decreasedperfusion gradient across tissue capillary beds. Compartmentsyndromes of the hand, forearm, and upper arm can result intissue necrosis, which can lead to devastating loss of function. Theetiology of acute compartment syndrome in the upper extremity isdiverse, and a high index of suspicion must be maintained. Painout of proportion to injury is the most reliable early symptom ofimpending compartment syndrome. Diagnosis is particularly difficultin obtunded patients and in young children. Early recognition andexpeditious surgical treatment are essential to obtain a goodclinical outcome and prevent permanent disability.

Compartment syndrome was firstdescribed in 1881 by Richard

von Volkmann.1 The etiology, patho-physiology, and management ofcompartment syndrome and the as-sociated complications have been ex-tensively described. Acute compart-ment syndrome (ACS) occurs withelevation of interstitial pressure in aclosed fascial compartment, resultingin microvascular compromise. Thiscauses the perfusion gradient to fallbelow a critical value, leading to is-chemia of the tissues within this con-fined space. In the upper extremity,the dorsal and volar compartmentsof the forearm are the most com-monly affected. Upper extremityACS can lead to devastating loss offunction, including Volkmann ische-mic contracture, neurologic deficit,infection, amputation, and death.

A wide range of causes of ACS inthe upper extremity has been re-ported, and a high index of suspicionmust be maintained. Distal radiusfracture in adults and supracondylarhumerus fracture in children are the

most frequent causes of compart-ment syndrome in the upper extrem-ity.1,2 Compartment syndrome is aclinical 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 Emergentsurgical treatment is required; themost important determinant of out-come is early recognition and expedi-tious surgical intervention.3,5-9 Re-constructive procedures can beperformed to improve the functionof the affected upper extremity in thepatient with Volkmann contracture;however, return of normal functionshould not be expected.10-16

Anatomy

The upper extremity contains 15compartments. The upper arm con-sists of a flexor (ie, volar) compart-ment and an extensor (ie, dorsal)compartment. The forearm is dividedinto 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 ofOrthopaedics, University ofRochester, Rochester, NY(Dr. Prasarn), and Physicians forThe Hand, Miami, FL (Dr. Ouellette).

Dr. Ouellette or an immediate familymember serves as a paid consultantto or is an employee of Stryker.Neither Dr. Prasarn nor anyimmediate family member hasreceived anything of value from orowns stock in a commercialcompany or institution relateddirectly or indirectly to the subject ofthis article.

J Am Acad Orthop Surg 2011;19:49-58

Copyright 2011 by the AmericanAcademy of Orthopaedic Surgeons.

Review Article

January 2011, Vol 19, No 1 49

ments: hypothenar, thenar, andadductor pollicis as well as four dor-sal interosseous and three volar in-terosseous17 (Figure 2). The volarforearm is the most commonly af-fected compartment in the upper ex-tremity. Compartment syndrome inthis area typically occurs followingfracture of the distal radius, supra-condylar humerus, or diaphysis ofthe radius or ulna.2,17,18 Any compart-ment can be affected, however. Digi-

tal fasciotomy is necessary in somecases19 (Figure 3).

In the upper arm, the medial andthe lateral intermuscular septa sepa-rate the flexor compartment fromthe extensor compartment. The bra-chial fascia is a dense fibrous sheaththat surrounds the muscles in each ofthe two compartments. In the fore-arm, the stiff interosseous membranebridges 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 pronatorquadratus to lie within an additionalcompartment of the distal volar fore-arm, separate from the flexor ten-dons at this level.20 These deep volarmuscles are the most commonlydamaged muscles in forearm com-partment syndrome. The remaining,more superficial flexor muscles areless prone to ischemia than theirdeeper counterparts. The finger andwrist extensors lie on the posterioraspect of the forearm. Isolatedexercise-induced compartment syn-dromes of the extensor carpi ulnarismuscle have been noted in case re-ports.21,22 The mobile wad, whichconsists of the brachioradialis, flexorcarpi radialis longus, and flexorcarpi radialis brevis tendons, is rarelyinvolved.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 aredivided by the carpal bones, metacar-pals, and individual investing fasciallayers. Pressures within the carpal tun-nel may become elevated in cases ofhand or volar forearm compartmentsyndrome. Release of the transversecarpal ligament is often necessary inaddition to release of the other in-volved compartments. The digital fas-cial compartments are bound by theCleland ligament and the Grayson lig-ament, and elevated pressure may oc-cur in individual digits (Figure 3).Compartment syndrome of the handtypically necessitates carpal tunnel re-lease and dorsal interosseous compart-ment releases; however, any compart-ment may be involved and may requirerelease. The decision regarding thenumber and location of incisionsshould be based on the clinical findingsand 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

Etiology

ACS of the upper extremity is causedby a myriad of factors, includingfracture, bleeding disorders, constric-tive dressing and casting, arterial in-jury, extravasation of intravenous orintraosseous infusion, and regionalanesthesia3-5,23-35 (Table 1). Anythingthat causes increased volume withinthe confined fascial space (eg, bleed-ing, edema, purulent material, extra-neous fluids) or restricts the com-partment from expanding (eg, burn,casting, dressing, tourniquet) cancause ACS.

It is difficult to estimate the trueincidence of compartment syndromeof the upper extremity, but mostcases occur in the setting of fracture.McQueen et al17 analyzed 164 pa-tients with traumatic ACS. In 69%of cases, compartment syndrome wasassociated with fracture. The mostfrequent fracture types observedwere 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 handfracture, and the incidence was 0.6%each for elbow fracture-dislocationand humeral fracture. Soft-tissue in-jury without fracture was the secondmost common cause of injury(23.2%). Incidence in the forearmand hand was 5.5% and 0.6%, re-spectively. Within this subgroup,10.3% occurred in patients withbleeding disorders or who were tak-ing anticoagulants.

Grottkau et al2 reviewed a nationaltrauma database and found the inci-dence of pediatric forearm compart-ment syndrome to be 1%. Ouelletteand Kelly3 reported on 19 patientswith compartment syndrome of thehand. Most cases were iatrogenic, re-sulting from complications related tointravenous or intra-arterial adminis-tration of drugs. The incidence ofcompartment syndrome in unstable

fractures of the distal end of the ra-dius is substantially higher with con-comitant ipsilateral elbow injurythan with distal radial fracturealone.36

Pathophysiology

Compartment syndrome is caused byan elevation of pressure within afibro-osseous space resulting in de-creased tissue perfusion. The initialrise in intracompartmental pressurecauses increased extravascular ve-nous pressure. Because of lack ofmusculature in the wall media, thisrelatively small rise in pressurecauses the venule walls to collapse.The resulting decrease in hydrostaticgradient causes reduced local perfu-sion and increased interstitial pres-sure. This increased interstitial pres-sure in turn causes increased edemawithin the compartment, and thiscascade of events repeats itself per-petually.12 Vasospasm and shock lead

to decreased arteriolar pressure andpossibly closure of end arterioles,leading to a further decrease in tissueperfusion4 (Figure 4).

Ischemia occurs when a criticalthreshold is reached in the local arte-riovenous gradient and when circula-tion is compromised to the point thatblood flow is insufficient to meet themetabolic demands of the tissue.4

This critical variable is representedby the absolute difference betweencompartment pressure and bloodpressure.37 Heppenstall and col-leagues38,39 prefer to compare intra-compartmental pressure with meanarterial pressure, but diastolic bloodpressure is easier to obtain and cal-culate. Experimental data in a caninemodel have shown that terminal ar-terial pressure is equal to diastolicblood pressure;40 thus, we use dia-stolic blood pressure to determinethe critical threshold.

In a canine study, muscle necrosisoccurred 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 Clin 1998;14[3]:431-450.)

Figure 2

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


mental pressure rose to a level 20mm Hg below diastolic blood pres-sure.40 Heckman et al41 demonstratedthat irreversible changes to the pe-ripheral nerves and skeletal muscleoccur following 8 hours of completeischemia. Following onset of cellularanoxia, affected cells begin anaero-bic metabolism and may die. Devas-tating loss of function may occur fol-lowing substantial loss of muscle andneural tissue in the upper extremity.Muscle ischemia can lead to releaseof myoglobin, which can cause myo-globinuria, metabolic acidosis, andhyperkalemia. Renal failure, cardiacarrhythmia, cardiac failure, andshock may then ensue. The magni-

tude of these systemic effects is de-pendent on the duration of ischemiaand 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 thatherald compartment syndrome.Pulselessness is rare, occurring onlyafter arterial injury. Most of thesesymptoms present only after a sub-stantial amount of time has elapsedfollowing the onset of compartmentsyndrome, and outcomes typically

are poor even with expedient fasciot-omy. Pain out of proportion to in-jury and pain with passive stretchingof muscles in the involved compart-ment are the earliest indicators ofcompartment syndrome.23 Compart-ment syndrome also should be sus-pected with tense, swollen compart-ments. In a series of patients withcompartment syndrome of the hand,Ouellette and Kelly3 demonstratedthat the most consistent clinical find-ing was a tense, swollen hand in anintrinsic minus position (ie, exten-sion of the metacarpophalangealjoints and flexion of the intercarpaljoints) (Figure 5).

ACS is typically diagnosed clini-cally. However, it may be necessaryto measure compartment pressure(Figure 6). Animal studies demon-strate that compartment syndrome isindicated 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

FractureCrush injuryInjection injuryRing avulsionSuction injuryPenetrating traumaConstrictive dressingsCastsBurnsInfectionBleeding disordersSpider biteSnakebiteArterial injuryReperfusionIn utero compressionExtravasation of infusionsInjection of illicit drugsRegional anesthesiaProlonged 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



≤20 mm Hg40 or a difference be-tween mean arterial pressure and thecompartment measuring ≤30 mmHg.41 Fasciotomy is often performedin patients with absolute pressuremeasuring >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 thepatient with swollen compartmentsand nearly normal pressures (<30mm Hg absolute pressure), we advo-cate waiting and performing serial

examinations and pressure measure-ments. Increasing swelling and risingpressures warrant decompressioneven when the pressure differential is≤20 mm Hg. Emergent fasciotomy isalso performed in the setting of aconcerning physical examination andextremely elevated pressures, evenwith a pressure differential of >20mm Hg. Compartment pressureshould be measured when suspectedin a patient who is uncooperative,who has an altered mental status, orwhose young age renders the clinicalexamination inadequate.3-6,8,23 In pe-diatric patients, Bae et al6 demon-strated that an increased need for an-algesics was most predictive ofcompartment syndrome.

Compartment PressureMeasurement

We typically measure compartmentpressures 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 PediatrOrthop 2009;29[3]:263-268.)

Figure 5



examination and in those who can-not be examined fully. An equivocalexamination is one in which com-partment syndrome is suspected anduncertainty exists regarding the clini-cal examination. Measurements arealso often taken in the operating the-ater to verify which compartment orcompartments are affected and to en-sure that they are fully decompressedfollowing fasciotomy. Compartmentsthat clinically appear to be involvedare tested, and measurements aretaken 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 tothe fracture site. Otherwise, mea-surements are taken at the locationthat is most accessible to the com-partment. Typically, a single mea-surement is taken for each suspectedcompartment. 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 aslit catheter or a side port needle.Straight needles have been shown toprovide less accurate results.43 Thecatheter may be left in situ for repeator continuous pressure measure-ments. In the past, we used an arte-rial line and a pressure transducersimilar to the continuous-infusiontechnique described by Matsen,8 butwe did not use the infusion pump.More recently we have begun usingthe Stryker Intra-CompartmentalPressure Monitor System (Stryker,Kalamazoo, MI), which is more con-venient and requires no setup. Boodyand Wongworawat43 evaluated threecommonly used modalities for com-partment pressure measurement andfound an arterial manometer to bethe most accurate method, followedby the Intra-Compartmental PressureMonitor System. They concluded

that the Whitesides manometer lacksthe precision required for clinicaluse.

Fasciotomy

The main goals in the managementof ACS of the upper extremity areexpedient release of all fascial andepimysial envelopes and decompres-sion of all affected compartmentsand nerves. Compartments that areclearly affected clinically are re-leased, and those that cannot be ex-amined adequately are measuredwith the Intra-Compartmental Pres-sure Monitor System or an arterialmanometer. Pressure in the carpaltunnel is measured when involve-ment of that area is suspected. Pres-sure measurement ≥20 mm Hg withdecreased sensation and/or dimin-ished strength in the thenar musclesis an indication for open carpal tun-nel release.

Ronel et al20 described a techniquethat allows decompression of the su-perficial muscles and the deep mus-cles of the volar forearm as well asrelease of the median nerve at possi-ble sites of compression. We use thisapproach because it causes the leastamount of iatrogenic injury to thesuperficial muscles, arteries, andnerves compared with other de-scribed approaches to the volar fore-arm. A longitudinal skin incision ismade beginning just radial to theflexor carpi ulnaris at the wrist. Theincision is extended proximally tothe medial epicondyle, then curvedradially over the antecubital fossa(Figure 7). Distally, the incision maybe extended to the midline to incor-porate open carpal tunnel release.The lacertus fibrosus and fascia overthe flexor carpi ulnaris are opened.The flexor carpi ulnaris is retractedulnarly, 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



fascia over the deep muscles of theforearm.

Release of the volar compartmentoften results in decompression of thedorsal compartment and the mobilewad, as well. Should the pressuresremain elevated in the dorsal com-partment or the mobile wad, a sec-ond fasciotomy is performed. We usea dorsal longitudinal incision extend-ing from 2 cm distal to the lateralepicondyle of the humerus towardthe midline of the wrist. Deep dissec-tion is made through the interval be-tween the extensor digitorum com-munis and the extensor carpi radialisbrevis. This allows decompression ofthe 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 isbegun by making two longitudinalincisions dorsally over the 2nd and4th metacarpals (Figure 2 and Figure8). The fascia over the dorsal in-terosseous muscles is incised. To de-compress the first volar interosseousand adductor pollicis muscles, bluntdissection 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 bydissecting along the radial aspect ofthe 4th and 5th metacarpals throughthe more ulnar incision. To releasethe thenar and hypothenar compart-ments, longitudinal incisions aremade at the junctions of the glabrousand nonglabrous skin over the radialside 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 theposterior compartments can be de-compressed through a single medialor lateral incision. Maginn and El-liot44 suggested that the creation oftwo separate midline incisions di-rectly over the anterior and posteriorcompartments 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 Clin 1998;14[3]:431-450.)

Figure 7



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 reductionand internal fixation. This cannot bedone through a medial approach. Itis rare that both compartments areinvolved. Thus, we make a longitudi-nal incision over the affected com-partment to first perform thoroughdecompression. We use the same in-cision for open reduction and inter-nal fixation of the fractured hu-merus. If the other compartment isalso involved, a second fasciotomy ismade over it.

Wound Closure

Wounds are typically left open andinitially are covered with sterile wet-to-dry dressings. The skin should notbe closed acutely following fasciot-omy. We do not routinely use reten-tion sutures or rubber catheters toprevent wound edge retraction. Inwounds with exposed tendon, bone,or neurovascular structures, a bovinecollagen matrix wound dressing (In-tegra artificial dermis; Integra Life-Sciences, Plainsboro, NJ) is appliedto prevent desiccation. This can begrafted over later. The patient is re-turned to the operating suite after 48to 72 hours for irrigation and dé-bridement. Delayed primary woundclosure may be done at this time, aswell. In the patient with muscle ne-crosis, all nonviable muscle issharply débrided. When muscle via-bility is a concern, repeat débride-ment is done every 48 hours. Under-mining the skin flaps often assistswith tension-free closure. Forwounds that cannot be closed, avacuum-assisted wound closure sys-tem (VAC Therapy System; KCI, SanAntonio, TX) is placed, and split-thickness skin grafting is performedat a later date. Potential advantagesof a vacuum-assisted closure systeminclude shorter hospital stays, re-duced need for skin grafting, and alower rate of nosocomial infec-tion.45,46

Outcomes andComplications

Outcomes following compartmentsyndrome are dependent on injuryseverity, duration of ischemia, andpreinjury status and comorbidities.The amount of infarction varies con-siderably, as do outcomes. Timefrom diagnosis to fasciotomy is themost important predictor of out-come. The critical delay from diag-

nosis to treatment is reported to be 6to 24 hours.3-6,8,9,23,37,47 Irreversibledamage has been shown to occur af-ter 8 hours in a canine model.40 Fullrecovery with minimal residual dys-function can be expected withprompt diagnosis and intervention ofcompartment syndrome of the upperextremity.3-6,12,13,25,48 Delay beyond 6to 24 hours may result in Volkmannischemic contracture, neurologic def-icit, infection, amputation, or death.

How late is too late to performsurgical decompression? In mostcases 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 isindicative of the existence of viablemuscle, and emergent fasciotomyshould be performed. In the patientwith no demonstrable muscle func-tion, the best treatment may involvesupportive care for myoglobinuriaand aggressive splinting to maintainthe arm and hand in a functional po-sition.37

Ouellette and Kelly3 noted poor re-sults in 4 of 19 patients with handcompartment syndrome. All four pa-tients were obtunded at the time ofonset, and two required amputation.A high index of suspicion for com-partment syndrome must be main-tained in persons who are who aredifficult to examine and who cannotcommunicate effectively. Gelbermanet al49 reported the results of surgicaldecompression of compartment syn-drome of the forearm in 10 patients.No patient developed Volkmanncontracture, but only two patientshad normal postoperative results. Sixpatients who underwent volar fas-ciotomy required supplemental skingrafting. The worst results were ob-served in patients with severe crushinjuries and in another with arterialinjury.

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



Volkmann Contracture

Irreversible tissue ischemia results inmuscle necrosis within the affectedcompartment, which leads to con-tracture. In the forearm, the typicalposture that develops includes elbowflexion, forearm pronation, wristflexion, and thumb adduction withthe metacarpophalangeal joints inextension and the interphalangealjoints in flexion. The median nerve isoften affected to a greater degreethan the ulnar nerve because the me-dian nerve lies in the deeper zonethat is more severely compromisedby ischemia.

Tsuge15 classified contracture asmild, moderate, and severe. The mildtype involves mild ischemic contrac-ture primarily of the flexor digito-rum profundus and no neurologicdeficit. In the moderate type, theflexor digitorum profundus, flexorpollicis longus, and pronator teresare 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 andulnar nerves are also present. The se-vere type involves ischemic damageto all of the flexors in the fore-arm, variable involvement of the ex-tensors, and severe neurologicinjury.12,14-16

The main goal in the managementof Volkmann contracture is to re-store function; however, normalfunction of the upper extremityshould not be expected.10-16 Affectedmuscles are exposed, and fibrotic ornecrotic tissue is débrided. Thoroughneurolysis of the median and ulnarnerves should be performed as wellas tenolysis of scarred tendons. Iso-lated tendon lengthening is not rec-ommended because it typically re-sults in recurrent contracture andloss of grip strength.12,16 In personswith mild contracture, the flexor/

pronator slide may be performed toimprove hand position as well asfunction of the forearm flexors. Ten-don transfer may be performed toimprove specific dysfunction in per-sons with moderate contracture.Usually this involves use of an exten-sor tendon transfer; however, flexortendons can be transferred in thecase of dorsal contracture. Free mus-cle transfer, typically using the graci-lis muscle, is necessary to improvefunction in persons with severe con-tracture.12,15,16

Summary

ACS of the upper extremity is a poten-tially devastating condition that canlead to substantial loss of function.Compartment syndrome has manycauses, and a high index of suspicionmust be maintained. The final commonpathway is a vicious cycle of increasedtissue pressure with resulting cellular is-chemia. All affected compartments inthe upper extremity must be recog-nized, and thorough decompressionmust be performed in an expedientmanner. Compartment syndrome is dif-ficult to diagnose in some cases, partic-ularly in obtunded patients and youngchildren. Prompt diagnosis and emer-gent surgical decompression are essen-tial to obtain a good clinical outcomeand preventing a catastrophic result.

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