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cute Limb Compartment Syndrome:Review

tavros Gourgiotis, MD,* Constantinos Villias, MD,* Stylianos Germanos, MD,†thanasios Foukas, MD,‡ and Marco Pericoli Ridolfini, MD§

Second Surgical Department, 401 General Army Hospital of Athens, Athens, Greece; †Upper GI andeneral Surgery, Leighton Hospital, Crewe, United Kingdom; ‡Wrightington Hospital, Wigan, United

ingdom; and §Department of Surgical Sciences, ‘A. Gemelli’ University Hospital, Rome, Italy

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cute limb compartment syndrome (LCS) is a limb-threateningnd occasionally life-threatening condition caused by bleeding ordema in a closed muscle compartment surrounded by fascia andone, which leads to muscle and nerve ischemia. Well-knownausative factors are acute trauma and reperfusion after treat-ent for acute arterial obstruction. Untreated compartment

yndrome usually leads to muscle necrosis, limb amputation,nd, if severe, in large compartments, renal failure and death.lertness, clinical suspicion of the possibility of LCS, and occa-

ionally intracompartmental pressure (ICP) measurement areequired to avoid a delay in diagnosis or missed diagnosis. Openasciotomy, by incising both skin and fascia, is the most reliableethod for adequate compartment decompression. The tech-

iques of measuring ICP have advantages and disadvantages,hereas the pressure level that mandates fasciotomy is contro-ersial. Increased awareness of the syndrome and the advent ofeasurements of ICP pressure have raised the possibility of

arly diagnosis and treatment. This review reports LCS, includ-ng etiology, pathophysiology, diagnosis, ICP measurement,

anagement, and outcome. (J Surg 64:178-186. © 2007 by thessociation of Program Directors in Surgery.)

EY WORDS: compartment syndrome, intracompartmentalressure, limb, fasciotomy

OMPETENCY: Medical Knowledge

NTRODUCTION

cute limb compartment syndrome (LCS) is a surgical emergencynd is caused by raised pressure within a closed fascial space. In-rease of the intracompartmental pressure (ICP) reduces the cap-llary perfusion below a level necessary for tissue viability.

Hippocrates1 first described the dangers of raised ICP and itsequelae in 400 BC. Volkmann2 recognized LCS in 1881, de-cribing the contracture that is a common sequela. The first

correspondence: Inquiries to Stavros Gourgiotis, MD, PhD, 41 Zakinthinou Street, Papa-ou, Athens, 15669 Greece; fax: 30 210 6525802; e-mail: drsgourgiotis@tiscali.co.uk

Journal of Surgical Education • © 2007 by the Association ofPublished by Elsevier Inc.

78

eported treatment was by Peterson in 1888,3 followed byepson4 who reported that venous obstruction may lead to mus-le changes and demonstrated LCS experimentally in 1926. Sireginald Watson-Jones5 attributed the pathology solely to ar-

erial injury in 1952, whereas Whitesides et al6 and Rorabeck3

emonstrated the current concept that the increased ICP re-uces the microcirculatory perfusion and leads to macrocircu-

atory arterial occlusion.The limbs are enclosed in a deep fascial covering that divides

keletal muscle groups and the neurovascular bundles accom-anying them into different compartments. Because of the un-ielding nature of this fascial envelope, an increase in the ICPay reduce the capillary blood inflow, which eventually leads to

rteriolar compression, followed by muscle and nerve ischemiaith muscle infarction and nerve damage, if decompression isot performed promptly.Limb compartment syndrome typically follows fractures, ar-

erial injuries, extensive venous thrombosis, ischemic reperfu-ion injuries, crush injuries, burns, and prolonged limb compres-ion after intra-arterial drug injection or patient malpositioning onhe operating table. The most important determinant of a poorutcome from LCS after injury is delay in diagnosis.3,7 The com-lications are usually disabling and include infection, contrac-ure, deformity, and amputation. Continuous monitoring ofCP may allow the diagnosis to be made earlier and the com-lications to be minimized.7,8

In this review the etiology, pathophysiology, diagnosis, ICPeasurement, management, and outcome of LCS are dis-

ussed. The literature about acute compartment syndrome ofpper and lower limbs was identified with Medline, and addi-ional cited works not detected in the initial search were ob-ained. Articles reporting on prospective and retrospective com-arisons and case reports were included.

TIOLOGY

imb compartment syndrome may be caused by either an in-

rease in volume within a compartment raising the pressure or

Program Directors in Surgery 1931-7204/07/$30.00doi:10.1016/j.jsurg.2007.03.006

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xternally applied pressure compressing a compartment. Eachimb contains several compartments that are at risk for LCS.he upper arm contains the anterior (the biceps-brachialis mus-

le, and the radial, ulnar, and median nerves) and posterior (thericeps muscle) compartments. The forearm has both a volarnd a dorsal compartment. The volar compartment containshe wrist and finger flexors, whereas the dorsal compartmentolds the wrist and finger extensors. In the thigh, there are

muscle compartments (anterior, posterior, and medial),hereas there are 4 in the calf (anterior, lateral/peroneal, deeposterior, and superficial posterior). The anterior compartmentf the lower leg is most frequently involved in this syndromend contains the tibialis muscles and the extensors of the toes.iagrammatic presentation of forearm, thigh, and calf com-

artments are shown in Figs. 1, 2, and 3, respectively.Causes of LCS are summarized in Table 1.9-11

IGURE 1. (A) Fasciotomy incision in the forearm. (B) Forearm compart-ents (R: radius; U: ulna).

IGURE 2. (A) Thigh compartments. (B) Fasciotomy incision in the thigh

F: femur; 1: lateral intramuscular septum; 2: posterior intramuscular sep-um; 3: medial intramuscular septum).

ournal of Surgical Education • Volume 64/Number 3 • May/June 20

rthopedic Causes (Fracture-Related)

ractures of the tibial shaft, the distal radius, and ulna are theost common orthopedic causes of LCS.3,7,12-14 The inci-

ence of LCS after tibial fractures ranges widely from 1% to9%.7,8,12,14,15 The common belief that open fractures ade-uately decompress the compartments and hence prevent anncrease in pressure is often incorrect. In fact, there is no differ-nce in ICP between open and closed fractures; both types ofractures are likely to develop LCS.8 In the leg the anteriorompartment is most commonly affected, whereas in the fore-rm it is the flexor compartment.7

ascular Causes

oth arterial and venous injuries can give rise to LCS.16 Popli-eal artery and vein injuries, particularly when a concomitantracture occurs, often result in LCS.17,18 If both artery and vein

FIGURE 3. Calf compartments.

ABLE 1. Common Causes of Acute Limb Compartmentyndrome10-12

rthopedic(fracture-related)

Tibial fractureDistal radial and ulna fracturesSupracondylar fracture of the humerusFemoral and calcaneal fractures

ascular Arterial and/or venous injuriesRevascularization proceduresPhlegmasia caerulea dolensIntra-aortic balloon pumpingIsolated limb perfusion

atrogenic Intravenous/intra-arterial drug injectionTourniquetPneumatic anti-shock garmentHemophiliacAnticoagulationExtravasation of fluid after an arthroscopic

procedureProlonged surgery

oft tissue Crush injury without fracturesBurnOedema or intramuscular hematomaDrug or alcohol overuse induced stupor

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re injured, then more than 50% of patients require a fas-iotomy presumably for increased compartment pressures.19

mbolectomy, thrombolysis, and bypass surgery can cause LCSith an incidence that ranges up to 21%.20-22 This condition isnown as a post-ischemic compartment syndrome and is causedy revascularization of the leg after a prolonged period of isch-mia.20 The post-ischemic compartment syndrome is fromeperfusion of the ischemic limb leading to tissue swelling andompartmental hypertension. An iliofemoral thrombosis caus-ng phlegmasia caerulea dolens can produce a compartmentyndrome.23,24

atrogenic Causes

ntravenous or intra-arterial administration of drugs has led tooth forearm and leg LCS.25 The use of a pneumatic anti-shockarment for severe hypotension can lead to LCS.26 Prolongedurgery, especially in the Lloyd-Davies position, occasionallyauses LCS,27,28 which is caused by compression of the arterialnflow causing soft tissue necrosis, as a result of direct pressure.

Excessive anticoagulation with bleeding after major joint re-lacement has led to LCS.29 Spontaneous bleeding in a hemo-hiliac is reported to result in LCS.30 Inadvertent injection ofressurized fluid is associated with perioperative LCS.31

oft-Tissue Causes

welling of the soft tissue without a fracture may occur after airect blow to a muscle compartment or after a crushing injury,specially in patients with a coagulopathy or a known bleedingisorder.13,32 In contusion injury, the continued use of the

nvolved muscles may further increase ICP and increase bleed-ng leading to LCS; this may be the result of even minor inju-ies. Burns can also cause LCS by external compression of theompartment from burn eschar, which increases the ICP.33

The relationship between LCS and drug or alcohol overuse isell documented.25 Intra-arterial injections of barbiturates and

ntravenous diazepam have been known to cause vascular dam-ge, whereas drug addicts may suffer non-traumatic rhabdomy-lysis leading to LCS.34

ATHOPHYSIOLOGY

n 1978, Matsen and Krugmire35 first described the arterio-enous pressure gradient theory, which is the most popularypothesis among the number of theories regarding the impair-ent of the microcirculation that occurs in an LCS. The theory

uggests that ischemia begins when local blood flow cannoteet the metabolic demands of the tissue. Rising ICP increases

he intraluminal venous pressures leading to a reduction in therteriovenous pressure gradient with subsequent diminished orbsent local perfusion. Reduced venous drainage increases in-erstitial tissue pressure, which allows tissue edema to form.ymphatic drainage initially increases, but the growing tissue

dema impedes lymphatic drainage. Eventually, arteriolar com- n

80 Journal o

ression occurs, which leads to muscle and nerve ischemia.ensory changes in the nerve, such as paresthesia and hypesthe-ia, develop after 30 minutes of ischemia. Irreversible nerveamage begins after 12 to 24 hours of total ischemia.36 Irrevers-

ble functional changes start in the muscle after 4 to 8 hours.37

Post-ischemic compartment syndrome38 is a consequence ofbiphasic ischemia-reperfusion injury, in which tissue damage

nitiated in the ischemic phase is continued by the reintroduc-ion of oxygenated blood.39 The ischemia-reperfusion injury isediated by the interaction of oxygen-derived free radicals,

ndothelial factors, and neutrophils.40 Oxygen-derived freeadicals can peroxidate the lipid component of cell membranes,hich leads to enhanced capillary permeability.41

IAGNOSIS

n initial high index of suspicious is required to make theiagnosis. A traditional hallmark element in the history of aatient presenting with LCS is pain disproportionate to the sizef injury, which assumes a conscious and aware patient. Clinicaluspicion should be heightened by the following clinical signsf LCS: pain, paresthesia, paralysis, pallor, and pulselessness.

Pain is different to the pain experienced by the initial trauma,hich is produced by muscle ischemia and is only partially

elieved with the usual analgesics used by surgeons for fractures.herefore, pain out of proportion to that expected with the injury

hould provoke a strong suspicion of LCS.42 An important earlynding suggesting need for referral is pain on passive stretching orcompression of ischemic muscles in the compartment.34

Paresthesia results from a disordered cell membrane functionn nerves running through the affected compartment, which

ay be an early sign of impending nerve ischemia. Anesthesiaill result if the pathology is allowed to proceed. Both pain and

nesthesia can only be assessed if peripheral nerve injury can bexcluded. The end point of paresthesia is paralysis.

Pallor confirms lack of blood supply but is an unreliable sign.ulselessness is common in arterial occlusion but otherwisenly noted at a late stage.43 Absence of pulses is indicative ofirect arterial trauma, or of prolonged delay in making theiagnosis of raised ICP, with ICP rising to reach levels approx-

mating mean arterial pressure, and occluding the main axialrteries. An LCS with an absent arterial pulse and no arterialrauma has a poor prognosis.

Seriously increased levels of creatinine phosphokinase (CPK)ay indicate severe muscle damage, or ischemia. In the absence

f clinical signs, it could indicate an unsuspected LCS. How-ver, for early diagnosis, it is clearly not helpful.

NTRACOMPARTMENTAL PRESSUREEASUREMENT

he measurement of ICP is only necessary when the clinicaligns of compartment syndrome are unclear, in an unconscious-

ess or uncooperative patient, in a young child, or when the

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linical symptoms and signs are equivocal. The normal pressuren the muscle compartments is below 10-12 mm Hg.44

An 18-G needle is attached to an intravenous extension tubend then to a stopcock. Approximately half the tubing is filledith sterile saline, being certain that air is not allowed into the

ubing. A second intravenous extension tube is attached tohe 3-way tap and attached to the blood pressure manometer.he skin should be prepped with an antiseptic solution and

nfiltrated with local anesthesia at the prospective site. Only theubcutaneous tissue should be infiltrated. Intramuscular injec-ion may artificially increase ICP. The needle is placed in theompartment, and the apparatus is kept at the level of the nee-le. The stopcock is then turned so that it is open in the direc-ion of the intravenous tubing on either side of a syringe. Theyringe filled with air is slowly compressed, which causes air toove into extension tubes. As soon as movement occurs in the

uid column, the ICP is read from the manometer. A particularroblem of measuring ICP is to ensure that the correct size ishosen for the measurement. The highest pressure is thought toccur in the deep posterior and the anterior compartment in theeg, and when the catheter is close to a fracture, within 5 cm ofhe fracture line.45

Several techniques are available for ICP determinations, andhose commonly used by surgeons are described below.

The simple needle manometry technique.46

The central venous pressure manometer technique.The wick catheter technique.47

The slit catheter technique.48,49

The side-ported needle technique.50

The fibreoptic transducer.51

The near-infrared spectroscopy (NIRS) is a noninvasivemethod that can measure the levels of muscle hemoglobinand myoglobin.52

The laser doppler flowmetry53 and the 99Tcm-methoxy-isobutyl isonitril (MIBI) scintigraphy.54

he Absolute ICP

ome debate exists in the literature regarding what pressureevel mandates fasciotomy. Some investigators base recommen-ations based on absolute ICP,1,55 whereas others feel the ICP

s meaningful only as it relates to the mean blood pressure oriastolic blood pressure.8,56 However, most recommendationsre based on absolute ICP.

Pressure levels ranging exceeding 30 mm Hg,3,12,57,58 45m Hg,59 and 50 mm Hg60 have been proposed as the critical

evels of pressures above which the viability of the compartments compromised. Experimental studies have shown a big differ-nce between individuals, when correlating absolute pressureevels, clinical signs, nerve function, and oxygen levels in the

uscle tissue.44 The lower level of 30 mm Hg is the mostommonly used by surgeons. It is based on the theory that the

apillary pressure is insufficient to maintain muscle capillary b

ournal of Surgical Education • Volume 64/Number 3 • May/June 20

lood flow when the tissue fluid pressure is greater than 30 mmg, and in this pressure level, fascial compliance decreases

harply.58

he Critical Pressure

hitesides et al56 reported that the level of ICP at which isch-mic compromise of muscle tissue occurs is related to the per-usion pressure. They used a difference between the diastolicressure and the ICP to suggest that a differential pressureithin 10-30 mm Hg of the diastolic pressure is the threshold

or performing a fasciotomy.Mubarak et al47 used an ICP of more than 30 mm Hg as a

asis of performing fasciotomy. They identified that the criticalCP of 30 mm Hg can be present only for a period of 6-8 hoursefore irreversible changes occur.61

Others used the “delta pressure.” It is the diastolic bloodressure minus the ICP, and the most commonly cited deltaressure, which is currently used by surgeons to diagnose LCS,s less than or equal to 30 mm Hg.7,8,36 In a study that appliedhis “delta pressure” for surgical intervention, it was demon-trated that many unnecessary fasciotomies were avoided,hereas patients who had developed an increase in ICP suffi-

ient to cause obvious tissue compromise as observed at theime of fasciotomy were identified correctly.8

Finally, Mars and Hadley62 reported that, by using the meanrterial pressure minus the ICP, greater accuracy can bechieved. They found that a differential pressure of 30 mm Hgr less indicated the need for fasciotomy in children.

he Time Factor

dynamic relationship exists among the blood pressure, theevel of ICP, and the duration of time for which a raised pres-ure is maintained. It is known that the higher the pressure,he faster and greater is the damage, but a lower pressureaintained for a longer period of time may also cause similar

issue damage. Many authors7,14 concluded that cata-trophic clinical results were inevitable if fasciotomies wereelayed for over 12 hours, whereas a full recovery waschieved if decompression was performed within 6 hours ofaking the diagnosis.

ANAGEMENT

he goal of treatment of LCS is to decrease tissue pressure,estore blood flow, and minimize tissue damage and relatedunctional loss. External pressure should be released by remov-ng any cast, splint, or occlusive dressing that may lower theCP. If a cast is bivalved, the ICP may decrease as much as 55%,nd if a cast is completely removed, the pressure may decrease asuch as 85%.62-65 Elevation of the limb is sometimes used by

urgeons as a temporary measure in an attempt to reduce ICP,ut this has no effect and may even increase the pressure in

oth upper and lower limb syndromes.59,66 However, in

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hlegmasia caerulea dolens, early aggressive limb elevation isery important.23

urgery

he treatment of LCS requires expedient fasciotomy. If leftntreated, increased tissue pressure leads to muscle mass dam-ge resulting in myoglobinuria, renal failure, metabolic acido-is, hyperkalemia, and ultimately contracture formation or lossf the limb.64,65 Unfortunately, no definitive way exists tonow when muscle, subject to an established LCS, is still viable,nd when subsequent fasciotomy will prevent additional mus-le necrosis. For this reason, irrespective of the length of timehat susceptible muscle has been subjected to sustained com-artmental hypertension, fasciotomy is advised once an LCSas been identified. According to Mabee,67 absolute indicationsor fasciotomy are (1) clinical signs of LCS, (2) raised tissueressure greater than 30 mm Hg in a patient with the clinicalicture of LCS, and (3) interrupted arterial circulation to anxtremity for greater than 4 hours. Adequate treatment is de-ompression of all 4 compartments.

In the forearm, volar fasciotomy is suggested,3,50 but concur-ent dorsal fasciotomy is also performed by some authors.25,50

ig. 1 shows the fasciotomy incision in the forearm. A completeorearm fasciotomy requires decompression of each nerve anduscle. If the clinical status of the hand remains unclear, the

olar incision should be extended into the palm and the carpalunnel should be released. For hand compartment syndromes,he carpal tunnel is always decompressed.26

In the thigh, all 3 compartments can be decompressed via aateral incision (Fig. 2). To prevent muscle hernia, some au-hors68 favor 2 parallel incisions in the fascia lata, with an in-ervening bridge of at least 4-5 cm. In the lower leg, the fas-iotomy can be performed by a single lateral incision, with orithout fibulectomy, or by a double incision technique, withedial and lateral incisions (Fig. 4).69 The skin incision must

e long enough to ensure that all underlying muscle is decom-ressed. The single incision technique allows adequate exposuref all 4 compartments.70 Fibulectomy should be avoided, espe-ially in patients with complex tibial fractures. The skin incisions made directly over the fibula. A transverse incision is made inhe fascia to identify the intermuscular septum between thenterior and the lateral compartments and to identify the su-erficial peroneal nerve. Longitudinal fasciotomies of the ante-ior, the lateral, and the superficial dorsal compartments arehen performed. The final step is to divide the origins of theoleus from the fibula and then to release the deep posteriorompartment by incising directly behind the fibula.

When the double incision technique is used by a surgeon, theosterior compartments are opened from medially, and the an-erior and lateral compartments from the lateral side. Advan-ages include the possible use of local anesthesia; there is noeed for removal of bone, it is quicker, and it carries less risk of

amage to neurovascular structures, with adequate decompres- c

82 Journal o

ion of the posterior compartment. The disadvantage is that itequires 2 separate incisions.

Pearse and Nanchahal71 recommended 2 incisions for fas-iotomies: the superficial and deep posterior compartments areecompressed through a medial longitudinal incision placed 1o 2 cm posterior to the medial border of the tibia, and thenterior and peroneal compartments are decompressed by aecond longitudinal incision placed 2 cm lateral to the anterioribial border. Schepsis et al72 recommended that, when doing aasciotomy for exertional anterior LCS, a lateral compartmentelease is not necessary, because it increases morbidity andengthens recovery. Patman73 used multiple small skin incisionsor decompression in fasciotomy for vascular causes. Leversedget al74 described endoscopically assisted fasciotomy for treatinghronic exertional compartment syndrome in the lower leg.

The length of the fasciotomy wound, using a double-incisionechnique, was evaluated by Cohen et al.58 A skin incision ofcm in length decreased the mean ICP. Mubarak et al47 used

n incision 15 cm long and found that the skin incision aloneeduced the ICP by 5-9 mm Hg. The skin incision in the leghould be approximately 16 cm because small, subcutaneous,nd closed incisions may not decompress the compartmentsully.

The optimal method of wound closure after fasciotomy isot resolved. Early secondary wound closure after fasciotomyas been advocated for same patients on the third or fourth dayfter operation, but only with concurrent ICP monitoring be-ause closing the wound even on the fourth day can still in-

FIGURE 4. Fasciotomy incisions of the calf.

reases ICP.75 Various techniques and devices have been pro-

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osed to increase the rate of skin closure and reduce the need forkin grafting. These techniques and devices include intracuta-eous skin sutures, skin stretching and mechanical closing de-ices, dynamic skin sutures, vacuum-assisted closure, and shoeace suturing techniques.76-78

After fasciotomy, mortality rates of 11% to 15%, amputa-ion rates of 11% to 21%, and serious morbidity have beeneported.42,64 Bermudez et al79 found that patients who havendergone fasciotomy have poor calf muscle function. In aetrospective study by Heemskerk and Kitslaar,80 poor correla-ion existed between prophylactic versus therapeutic treatmentsnd clinical outcome, or between interval delay in fasciotomynd clinical outcome. Alternatively, Reis and Michaelson81 sug-est that when fasciotomy is delayed for more than 24 hours inatients with lower extremity crush injury suffered increasedorbidity and mortality compared with those treated nonop-

ratively. Other reports note poor results when fasciotomy forCS is delayed.3,82 In a study by Sheridan and Matsen, theomplication rates for early and late fasciotomized extremitiesere 4.5% and 54%, respectively. Almost one half of the laterocedures reported by Sheridan and Matsen went on to am-utation.82 Finklestein et al83 reported that fasciotomies per-ormed after 36 hours from injury were invariably associatedith severe infection, dismal rates of limb salvage, and eveneath.The role of fasciotomy in cases of LCS that have been diag-

osed at a late stage is questionable. Established myoneuraleficits seldom recover after fasciotomy. Finklestein et al83 rec-mmended not performing fasciotomies in patients with estab-ished LCS more than 8 to 10 hours after injury. If performedithin 12 hours of symptoms onset, fasciotomy can preventost ischemic myoneural deficits and most patients can regain

xcellent function.84,85 On the other hand, many patients haveinimal limb dysfunction when fasciotomy has been per-

ormed promptly and to an adequate depth. Lagerstrom et al86

eported that decompressive fasciotomy before the develop-ent of ischemic myoneural deficits prevents the ischemic se-

uelae of acute clinically evident LCS.

ONCLUSIONS

imb compartment syndrome occurs when raised ICP causesissue ischemia. It is a potentially limb-threatening and life-hreatening problem after trauma and vascular injury to theimbs. A high index of clinical suspicion is required to diagnosehis pathologic process. For early detection, it is necessary toducate those taking care of patients at risk, especially in thearly symptoms and signs. Monitoring of ICP should be rou-ine, particularly in patients in whom subjective clinical assess-ent is not available, ie, in unconscious, sedated, and uncoop-

rative patients, and in those with injuries to the lower leg.elay in diagnosis or treatment of LCS can result in significantorbidity for the patient. Full and extensive fasciotomies

hould be performed within 6 hours if the delta pressure re-

ains less than 30 mm Hg and/or clinical symptoms and signs

ournal of Surgical Education • Volume 64/Number 3 • May/June 20

ersist despite conservative measures. Although the morbidityf fasciotomies is significant, it is preferable to the outcome of aissed LCS.

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5. Watson-Jones R. Fractures and Joint Injuries. 4th ed. Ed-inburgh: Livingstone ES; 1952.

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