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Syndrome in Lower Extremity Musculoskeletal Trauma Abstract Acute compartment syndrome is a potentially devastating condition in which the pressure within an osseofascial compartment ris

Syndrome in Lower Extremity Musculoskeletal Trauma

Abstract

Acute compartment syndrome is a potentially devastating condition in which the pressure within an osseofascial compartment rises to a level that decreases the perfusion gradient across tissue capillary beds, leading to cellular anoxia, muscle ischemia, and death A variety of injuries and medical conditions may initiate acute compartment syndrome, including fractures, contusions, bleeding disorders, burns, trauma, postischemic swelling, and gunshot wounds Diagnosis is primarily clinical, supplemented by compartment pressure measurements Certain anesthetic techniques, such as nerve blocks and other forms of regional and epidural anesthesia, reportedly contribute to a delay in diagnosis Basic science data suggest that the ischemic threshold of normal muscle is reached when pressure within the compartment

is elevated to 20 mm Hg below the diastolic pressure or 30 mm Hg below the mean arterial blood pressure On diagnosis of impending

or true compartment syndrome, immediate measures must be taken Complete fasciotomy of all compartments involved is required to reliably normalize compartment pressures and restore perfusion to the affected tissues Recognizing compartment syndromes requires having and maintaining a high index of suspicion, performing serial examinations in patients at risk, and carefully documenting changes over time

The importance of timely diagno-sis and management of compart-ment syndrome was recently empha-sized in a review of the medical-legal aspects of this condition.1McQueen

et al2studied 164 patients (149 men,

15 women) with acute traumatic compartment syndrome The inci-dence of compartment syndrome was 7.3 per 100,000 in men (average age,

30 years) and 0.7 per 100,000 in women (average age, 44 years).2The

most common cause of acute com-partment syndrome in this series was fracture (69%); fracture of the tibial diaphysis was most frequent (36%), followed by distal radius fractures (9.8%) Soft-tissue injury without fracture was the second most com-mon cause (23.2%), with 10% of these occurring in patients taking an-ticoagulants or with a bleeding disor-der The incidence of compartment syndrome associated with high- and

Steven A Olson, MD, and

Robert R Glasgow, MD

Dr Olson is Associate Professor,

Division of Orthopaedic Surgery, Duke

University, Durham, NC Dr Glasgow is

Orthopaedic Surgeon, Division of

Orthopaedic Surgery, Royal Alexander

Hospital, Edmonton, AB, Canada.

None of the following authors or the

departments with which they are

affiliated has received anything of value

from or owns stock in a commercial

company or institution related directly or

indirectly to the subject of this article:

Dr Olson and Dr Glasgow.

Reprint requests: Dr Olson, Duke

University, Box 3389, Durham, NC

27710.

J Am Acad Orthop Surg

2005;13:436-444

Copyright 2005 by the American

Academy of Orthopaedic Surgeons.

low-energy injuries is nearly equal.

The presence of open wounds does

not mean that compartments are

de-compressed; compartment syndrome

is seen after open fractures.2-4

Etiology

A variety of injuries and medical

conditions may initiate acute

com-partment syndrome (Table 1)

Frac-tures; contusions; bleeding

disor-ders; burns; trauma; postischemic

swelling; tight casts, dressings, or

external wrappings; and gunshot

wounds are some of the most

fre-quent causes.2-12 Anatomic

struc-tures, including epimysium, fascia,

and skin, may limit the potential

size of a compartment Therefore,

closure of incisions or defects in

these structures should not be done

acutely when the patient is at risk

for compartment syndrome

Ther-mal injuries, especially

circumferen-tial third-degree burns, can cause an

acute compartment syndrome by

forming inelastic constrictions,

es-chars, and massive edema which, in

combination, result in ischemia to

neurovascular and muscular

struc-tures.2,5,7,13 Circumferential wraps,

such as casting material or cast

pad-ding, can lead to restriction of

com-partment expansion and increased

compartmental pressure.8,13,14

Re-leasing all circumferential dressings,

splitting casts, and cutting casting

material results in a marked decrease

in intracompartmental pressure

Pneumatic antishock garments have been associated with lower ex-tremity compartment syndromes

Templeman et al9reported on a pa-tient who developed bilateral com-partment syndromes in uninjured extremities after wearing a pneu-matic antishock garment However, inflation pressures <50 mm Hg in these garments have been used for long periods of time (eg, 48 hours for pelvic fractures) without adverse se-quelae.9

Traction, ankle joint position, and limb positioning have been shown to affect compartment volume and pressure and to contribute to the formation of compartment syn-dromes.3,8,10,11,13,15,16Traction causes the fascia to tighten and constrict the limb, decreasing the compart-ment volume Shakespeare and Henderson15described compartmen-tal pressure changes during calca-neal traction for tibial fractures

Pressure in the anterior and deep posterior compartments rose

linear-ly with increasing traction, up to 9.1

kg (Figure 1) The pressure did not fall during the time the traction was applied For each increase of 1 kg in longitudinal traction, the compart-ment pressure within the deep pos-terior compartment increased by more than 5%; pressure in the ante-rior compartment increased by <2% Intramuscular pressure is lowest in the anterior compartment with the ankle in the neutral to dorsiflexed position; it is lowest in the deep pos-terior compartment when the ankle

is in the plantarflexed position.13

Longitudinal calcaneal traction tends to dorsiflex the ankle and in-crease the pressure in the deep pos-terior compartment more than in the anterior compartment After cast application, the pressure in both the anterior and deep posterior compart-ments increases three- to seven-fold, depending on the position of the an-kle.13Ankle plantar flexion of 0° to 37° is the most protective position for minimizing the combined risks

of anterior and posterior compart-ment syndromes.13

Table 1

Causes of Compartment Syndrome

Fracture

Soft-tissue trauma without fracture

Intracompartmental bleeding

Tight casts, dressings, or external

wrappings

Thermal injury, burn eschar

Extravasation of intravenous infusion

Venous obstruction

Reperfusion injury following

prolonged ischemia

Penetrating trauma

Figure 1

Change in compartment pressure (percent) with increasing calcaneal pin traction (kg) in patients with tibial shaft fractures (Adapted with permission from

Shakespeare DT, Henderson NJ: Compartmental pressure changes during

calcaneal traction in tibial fractures J Bone Joint Surg Br 1982;64:498-499.)

Compartment syndromes have

been described with prolonged use

of the Lloyd-Davies (lithotomy)

po-sition with flexion, elevation, and

abduction of the well leg during

in-tramedullary nailing of femoral

frac-tures.11,13 The combined effects of

direct compression on the leg,

com-pressive circumferential bindings or

stockings, sequential inflatable

de-vices, and relative elevation of the

limb contribute to increased

partment pressure, decreased

com-partment volume, and decreased

blood flow, leading to the formation

of compartment syndromes.11

Many authors have discussed

ele-vated compartment pressures

asso-ciated with intramedullary nailing

of tibial fractures.4,16-20The etiology

of acute compartment syndrome

as-sociated with intramedullary

fixa-tion is multifactorial: tissue damage

secondary to the injury causes

swell-ing, traction decreases the volume of

the compartments, reaming forces

blood and marrow into the

compart-ments, and limb supports may cause

outflow constriction.16 Moed and

Strom,18using a canine model, found

that pressure changes during

ream-ing were transient, returnream-ing to

base-line or lower after the reamer was

removed from the intramedullary

canal After nail insertion, the

pres-sure remained elevated in the

an-terolateral compartment and was

transiently elevated in the posterior

compartment Mawhinney et al20

showed that peak pressures were

reached after the first two reaming

cycles

Several authors have

recom-mended using an unreamed nail in

tibial fractures with associated

compartment syndrome, or in

pa-tients without compartment

syn-drome who have elevated

compart-ment pressures, in order to minimize

pressure elevation during the

pro-cedure.16-19 Tornetta and French16

reported on anterior compartment

pressures during unreamed tibial

nailing without traction Eight of 20

patients had transient compartment

pressure elevation≥40 mm Hg (max-imum, 58 mm Hg); all pressures returned to below 20 mm Hg by the end of the procedure The authors concluded that patients with a tibial fracture who demonstrate signs and symptoms of an acute compartment syndrome on presentation should undergo a four-compartment fasci-otomy before intramedullary nail-ing, and that pressure elevations during nailing should be minimized

by avoiding prolonged traction

McQueen and Court-Brown4 used continuous compartment pressure monitoring during tibial nailing in a prospective study of 116 patients

Use of reamed versus unreamed nail-ing had no effect on the incidence of compartment syndrome Tibial nail-ing with or without prior canal ream-ing is a safe method of managream-ing tibial shaft fractures at risk for com-partment syndrome Prolonged fixed traction should be avoided to the ex-tent possible

Pathophysiology of Ischemia

The pathophysiologic mechanism that causes compartment syn-dromes is increased tissue pressure and the resulting development of is-chemia, which leads to irreversible muscle damage Cellular anoxia is the final common pathway of all of the varieties of compartment syn-drome However, the interaction be-tween increased compartment pres-sure, blood prespres-sure, and blood flow are incompletely understood It was originally suggested that there was a threshold compartment pressure above which irreversible changes would occur.21More recent evidence indicates that the absolute differ-ence between compartment pressure and blood pressure is the critical variable.21-26 To avoid collapsing of the veins, the pressure inside the veins cannot be less than that of the surrounding tissue.7,27An increase in compartment pressure results in an increase in venous pressure, leading

to a decrease in the arteriovenous gradient.7Change in the local vascu-lar resistance can accommodate for some of the reduction in the arterio-venous gradient; however, this change becomes ineffective with in-creasing tissue pressure Compart-ment syndrome occurs when the lo-cal arteriovenous gradient does not allow sufficient blood flow to meet the metabolic demands of the tis-sue.7Vascular tone, blood pressure, duration of pressure elevation, and metabolic demands of the tissue are important in determining whether a compartment syndrome will oc-cur.7

Muscle ischemia can lead to re-lease of myoglobin from damaged muscle cells During reperfusion, myoglobin is released into the cir-culation with other inflammatory and toxic metabolites Myoglobin-uria, metabolic acidosis, and hyper-kalemia can lead to renal failure, shock, hypothermia, and cardiac arrhythmias and/or failure The de-velopment and extent of these sys-temic effects depends on the sever-ity and duration of compromised tissue perfusion and the size and number of muscle compartments involved.7

By using objective, noninvasive techniques, experimental and clini-cal investigators have determined the changes in muscle blood flow that occur during compartment syn-drome.24Induced compartment syn-dromes in dogs revealed three histo-logic regions of muscle injury.24In skeletal muscle, the central portion

of the muscle becomes ischemic first The surrounding zone of mus-cle tissue then shows evidence of partial ischemic injury with in-creased tissue edema and swelling The peripheral layers of muscle are the last to be affected, often remain-ing normal in incomplete compart-ment syndromes Microangiograms showed an abundance of epimysial vessels with occlusion of central penetrating branches in specimens from severe cases.24

Using autologous plasma infusion

in a canine compartment syndrome

model, Heckman et al21studied the

ischemic threshold of muscle by

in-ducing elevated pressures for 8

hours Irreversible histologic

chang-es, including focal muscle infarction

and fibrosis, were documented in all

compartments subjected to tissue

pressures within 10 mm Hg of

dia-stolic pressure None of the animals

with a difference in perfusion

pres-sure >30 mm Hg from mean arterial

and >20 mm Hg from diastolic

pres-sure demonstrated any evidence of

irreversible changes, although

occa-sional cells underwent myofibrillar

degeneration Mean compartment

pressures of 59 mm Hg with

ade-quate perfusion pressure were

toler-ated for 8 hours without evidence of

infarction The authors concluded

that the ischemic threshold of

skel-etal muscle, beyond which

irrevers-ible tissue damage occurs after 8

hours, is directly related to the

dif-ference between the compartment

and mean arterial or diastolic

pres-sures The critical tissue pressure

differentials were≤30 mm Hg from

mean arterial pressure and≤20 mm

Hg from diastolic blood pressure.21

Matava et al22performed a similar

study in canines and also found that

the threshold for muscle necrosis

was 20 mm Hg less than the

diastol-ic pressure These findings support

the hypothesis that tissue damage is

directly related to absolute

differ-ence between compartment pressure

and blood pressure and that this

dif-ference is a variable that affects not

only microvascular perfusion but

also the onset of tissue damage

Bernot et al25observed that

mus-cle subjected to ischemia before

compartment pressurization had a

lower threshold for metabolic

deteri-oration than did nontraumatized

muscle Hypoxic metabolic changes

occurred in the postischemic limbs

in all compartments with a

perfu-sion pressure (∆P) <40 mm Hg The

metabolic deterioration observed

was more rapid and severe as the∆P

value diminished toward a value of

10 mm Hg Normal limbs did not become metabolically compromised until the ∆P value declined to <30

mm Hg Postischemic muscle is more easily and much more rapidly compromised metabolically by in-creased interstitial pressure than is normal muscle.25

Vollmar et al26 used a skinfold chamber to examine vessel response

to increased pressure in hamsters

Venules exhibited early reduction in size proportional to external pres-sure No similar change was observed

in arterioles This study suggests that impaired venous drainage with cap-illary stasis but without arteriolar constriction is a significant patho-physiologic component in the devel-opment of compartment syndrome

Diagnosis

History and Physical Examination

Critical to recognizing compart-ment syndrome is having and main-taining a high index of suspicion and performing serial examinations in patients at risk to document

chang-es over time.2,5-7,12Patient history is important for determining the me-chanism of injury and whether there are associated risk factors for devel-oping compartment syndrome.6The classic clinical diagnosis

encompass-es the six Ps: pain, prencompass-essure, pulse-lessness, paralysis, paresthesia, and pallor.12

Pain out of proportion to the in-jury, aggravated by passive stretching

of muscle groups in the correspond-ing compartment, is one of the earli-est and most sensitive clinical signs

of compartment syndrome However, pain may be an unreliable indicator and may be absent in an established compartment syndrome.3Pain per-ception may be diminished or absent

in the obtunded patient, thus requir-ing additional diagnostic methods.7

The absence of pain in a compart-ment syndrome is often caused by a superimposed central or peripheral

neural deficit However, McQueen and Court-Brown4reported a patient

in whom a compartment syndrome was diagnosed by increased compart-ment pressures before the onset of signs or symptoms

Pressure or firmness in the com-partment, a direct manifestation of increased intracompartmental pres-sure, is the earliest and may be the only objective finding of early com-partment syndrome Peripheral

puls-es are palpable and, unlpuls-ess a major arterial injury is present, capillary refill is routinely present Only

rare-ly is the compartment pressure ele-vated sufficiently to occlude arterial pressure.7

Paresis is difficult to interpret and may be caused by muscle ischemia, nerve ischemia, guarding secondary

to pain, or a combination of all three True paralysis is a late finding that is caused by prolonged nerve compres-sion or irreversible muscle damage Paresthesia is an early sign of com-partment syndrome that, without treatment, progresses to hypesthesia and anesthesia Sensory symptoms and signs are often the first indica-tion of nerve ischemia.3 Matava et

al22 have shown that peripheral nerve tissue is actually more sensi-tive to an ischemic event than mus-cle, with nerve function ceasing af-ter 75 minutes of total ischemia The duration and degree of pressure elevation leading to irreversible nerve injury secondary to compres-sion is uncertain.22Typically, abnor-mal neurologic findings are

associat-ed with nerves that course through affected compartments The isolated finding of paresthesia is frequently resolved with the release of con-stricting wraps or bandages alone Although frequently listed as one of the “P’s,” pallor is uncommon It oc-curs in the rare circumstance in which arterial inflow is severely di-minished

McQueen et al3reported a mean

of 7 hours from fracture manipula-tion and fixamanipula-tion to the development

of a compartment syndrome in 13

fracture patients undergoing

com-partment pressure monitoring Four

patients had delayed onset of

com-partment syndrome at 14 to 24

hours after fracture manipulation

and fixation.3 However,

compart-ment syndrome occasionally occurs

2 to 4 days after the precipitating

event; therefore, late onset must be

considered.27

Associated conditions can affect

susceptibility to compartment

syn-drome or contribute to missed

diag-nosis The perfusion gradient may

be inadequate in the presence of

systemic hypotension, even with

compartments that are supple to

physical examination Anesthetic

techniques have been reported to

contribute to a delay in diagnosis

Compartment syndromes after

sur-gery done to manage fractures have

been associated with the use of local

nerve blocks, epidural anesthesia,

and other forms of regional

ane-sthesia.28-32 Patients receiving

epi-dural anesthesia have been reported

to be four times as likely to have a

neurologic complication than those

receiving systemic narcotics.32

Epi-dural anesthesia increases local

blood flow secondary to

sympa-thetic blockade, thereby potentially

exacerbating swelling of an injured

extremity.32 The use of local

anes-thetics combined with narcotics

during epidural anesthesia has been

shown to increase the likelihood of

missed compartment syndromes

and is not recommended in the

at-risk patient.31,33

Compartment Pressure

Measurement

Sometimes the clinical picture

may be borderline or the patient

ex-amination may be equivocal,

unreli-able, or unobtainable In such

in-stances, measuring compartment

pressures is recommended to aid the

decision-making process McQueen

and Court-Brown4 reported a

pro-spective clinical series using

con-tinuous compartment monitoring

When a difference between

compart-ment pressure and diastolic blood pressure ≥30 mm Hg was main-tained and compartments were not released, patients had normal mus-cle function at the time of follow-up

Data from preclinical research stud-ies suggest that the ischemic thresh-old of muscle is a perfusion pressure

of at least 20 mm Hg between the compartment pressure and the dia-stolic pressure.21In a fracture at risk, measuring compartment pressures early in the course of treatment can provide a reference point to detect a trend if later compartment pressure measurements are needed

Various methods of measuring compartment pressures have been described.34-39 The two most com-mon techniques are a slit catheter and the side port needle The slit catheter is a low-volume infusion technique.34The measurement cath-eter may be left in situ within the compartment for repeated or contin-uous compartment pressure mea-surements over a period of hours

Side port needles, which were de-veloped to measure multiple

com-partments, have gained widespread popularity Moed and Thorderson35

reported that no statistically signif-icant difference was found between the measurements obtained with the slit catheter and the side port needle However, measurements with a standard 18-gauge needle were

high-er than both the slit cathethigh-er and side port needle by nearly 20 mm

Hg Therefore, a standard 18-gauge needle is less accurate and cannot be recommended Several

commercial-ly available pressure measurement devices are available for determining intracompartmental pressures The location in the compartment from which the measurement is taken is important for accuracy Seiler et al37determined that unin-jured compartments exhibited clin-ically significant intracompartmen-tal pressure measurement variability

in the forearm In their study of 25 patients with closed tibial fracture, Heckman et al23reported a relation-ship between compartmental tissue pressure and the distance from the site of the fracture (Figure 2)

Pres-Figure 2

The mean compartment tissue pressure measurement in a series of tibial shaft fractures The pressures are presented by location relative to the tibial fracture site Data suggest that the highest pressures occur within 5 cm of the fracture (Adapted with permission from Heckman MM, Whitesides TE Jr, Grewe SR, Rooks MD: Compartment pressure in association with closed tibial fractures: The relationship between tissue pressure, compartment, and the distance from the site of the

fracture J Bone Joint Surg Am 1994;76:1285-1292.)

sure was measured at the fracture

site and in 5-cm increments distal

and proximal The highest pressure

recorded was in the deep posterior

or anterior compartment, or both

Eighty-nine percent of

compart-ments had the highest pressure

mea-surement at the fracture site: 5% at

5 cm distal and 2% at 5 cm

proxi-mal The mean difference in pressure

5 cm from the highest level recorded

was 10 mm Hg These data indicate

that pressure measurements should

be performed within all

compart-ments and at multiple sites,

particu-larly within 5 cm of the level of

in-jury.23

Compartment pressure

measure-ment is indicated whenever the

diag-nosis is uncertain in a patient at risk

Several clinical scenarios fall into

this category (Table 2) One of the

most beneficial uses of

compart-ment pressure measurecompart-ment is for

distinguishing an undermedicated

patient from one who is developing

compartment syndrome This

di-lemma can occur when a long-acting

anesthetic block wears off without

appropriate systemic pain

medica-tion In this scenario, the pain can be

severely increased with passive

range of motion, and residual

pares-thesias can remain from a nerve

block It is often helpful to obtain a

baseline set of pressure

measure-ments in at-risk compartmeasure-ments in a

patient who cannot be examined for

an extended period When

subse-quent physical examination findings

are of concern (eg, increased

swell-ing, firmness in the limb), a second

set of compartment pressures can

provide evidence of a trend, in

addi-tion to the actual ∆P value at the

time of pressure measurement

Ob-tunded patients with an increasing

trend in pressure should be

moni-tored closely

At our institution, a ∆P value of

20 mm Hg from measured

compart-ment pressure to diastolic blood

pressure is an absolute indicator for

fasciotomy This approach was

adopted for three reasons (1) Basic

science data suggest that a∆P value

of 20 mm Hg is safe (2) In the inves-tigations of McQueen and Court-Brown,4 fasciotomies were per-formed for a∆P value of 30 mm Hg and did not identify an absolute min-imal∆P threshold (3) In our experi-ence, many patients in the operating room have vasodilatory effects of an-esthesia, leading to transiently low diastolic blood pressure with normo-tensive systolic pressures In the lat-ter situation, a patient with com-partment pressures in the mid 20s with a supple limb may have a∆P value <30 mm Hg with the diastolic blood pressure

Laboratory Tests

Serum creatine phosphokinase, which reflects muscle necrosis, has been used as an indicator of compart-ment syndrome.12 Decompression should result in a downward trend of creatine phosphokinase levels Per-sistently high levels or progression indicates inadequate decompression and ongoing muscle necrosis Myo-globin, a breakdown product of mus-cle cell lysis, is evidenced by myo-globinuria It can be misinterpreted

as hematuria; a definitive diagnosis

is indicated by a positive urine ben-zidine test for occult blood in the ab-sence of red blood cells Myoglobin is toxic to glomeruli of the kidney and leads to renal failure when the com-partment syndrome is not ade-quately treated.12

Treatment

Following the diagnosis of impend-ing or true compartment syndrome, immediate measures are necessary

to ensure that the deleterious se-quelae of compartment syndrome

do not occur First, casts or occlu-sive dressings should be split com-pletely Cast padding or circumfer-ential dressings should be released around their entire circumference

The affected limb should not be elevated higher than the patient’s heart in order to maximize

perfu-sion while minimizing swelling.7

When, despite these steps, the clin-ical diagnosis of compartment syn-drome remains clear, emergent and complete fasciotomy of all compart-ments with elevated pressures is necessary to reliably normalize com-partment pressures and restore per-fusion to the affected tissues The length of skin incision has an effect on fascial decompression in the leg associated with an acute compartment syndrome Some au-thors favor limited incisions, claim-ing low morbidity, while others recommend long incisions, em-phasizing that these are required to decompress affected compartments adequately.40-42 Several instances have been reported in which the skin continued to cause compres-sion after fasciotomy through short incisions.40 Cohen et al40 deter-mined the effect of the length of the skin incision in posttraumatic compartment syndromes of the lower extremity treated with fascial decompression using a two-incis-ion technique The affected com-partments initially were released through 8-cm incisions and the

pres-Table 2 Indications for Compartment Pressure Measurement

One or more symptoms of compartment syndrome with confounding factors (eg, neurologic injury, regional anesthesia,

undermedication)

No symptoms other than increased firmness or swelling in the limb in an awake, alert patient receiving regional anesthesia for postoperative pain control Unreliable or unobtainable examination with firmness or swelling in the injured extremity Prolonged hypotension and a swollen extremity with equivocal firmness Spontaneous increase in pain in the limb after receiving adequate pain control

sures recorded The skin incisions

were enlarged by 2-cm increments

until readings showed no further

de-crease The final length of the

ex-tended incisions averaged 16 cm ± 4

cm Mean final pressure in the

com-partments, which required

exten-sion of the inciexten-sions, was 13 mm Hg,

notably less than pextension

re-cordings Long incisions add little to

morbidity and influence neither the

complication rate nor the late

func-tional result Long incisions also

eliminate the risk of the skin acting

as an unrecognized compartment

envelope, which is especially

impor-tant during the hyperemic period

following decompression of an

is-chemic compartment.40,42

Compartment syndromes can

oc-cur in a variety of locations in the

lower extremity, such as the gluteal

musculature, thigh, lower leg, and

foot Regardless of location, the key

in treatment is to adequately

decom-press the muscles involved In the

gluteal region, a posterior incision

that provides access to the gluteus

maximus and the abductor

muscula-ture is adequate In the thigh, a long

single lateral incision can

adequate-ly decompress the anterior and

pos-terior compartments Occasionally,

a medial adductor incision is

re-quired, as well A one- or

two-incision approach can be used in the

lower leg Generally, a long single

lateral incision is sufficient for a

four-compartment fasciotomy

The one-incision procedure

should be performed through a long

incision based over the anterolateral

calf The extended incision is made

from within 5 cm of either end of the

fibula The basic technique involves

identifying the septum between the

anterior and lateral compartments,

then performing a fasciotomy on

each of these compartments Care

should be taken to avoid injury to

the superficial peroneal nerve

distal-ly Lateral compartment

muscula-ture is then elevated off the

posteri-or intramuscular septum Incision of

this intramuscular septum provides

access to the lateral portion of the superficial posterior compartment

The superficial compartment is mo-bilized posteriorly to give access to the deep posterior compartment in order to perform the fasciotomy

In the two-incision technique, the location of the medial skin incision

is important The bulk of the mus-culature in the superficial posterior compartment is proximal and re-quires a proximal extent to the inci-sion to adequately decompress the region However, the bulk of the deep posterior musculature is

locat-ed in the distal half of the limb Ad-equate decompression requires de-taching the soleus origin from the medial aspect of the tibial shaft

Therefore, to adequately decompress all four compartments through two incisions, long medial and lateral in-cisions are required Foot compart-ment syndrome is typically treated with two longitudinal incisions in the dorsum of the foot, one centered over the fourth metatarsal and one over the space between the first and second metatarsals Adequate de-compression requires release of the fascia of the intrinsic foot muscles attaching to the metatarsals

In their study of secondary clo-sure of the skin following

fascioto-my for acute compartment syn-drome, Wiger et al43noted that tight closures may increase intramuscular pressure to dangerous levels To pvent this, limb swelling must be re-duced before secondary closure Pa-tients were encouraged to perform concentric muscular activity and weight-bearing exercises to assist in reducing elevated intramuscular pressures of the swollen extremities

Active contraction of muscle en-hances lymph flow, and the normal increase of hydrostatic pressure is a powerful edema-reducing mecha-nism At follow-up, there were no signs of ischemic muscular contrac-ture when intramuscular pressure did not exceed 30 mm Hg during sec-ondary closure in a normotensive patient.43

At our institution, the fasciotomy site is typically dressed with a wound vac sponge The patient is re-turned to the operating room 3 to 5 days later to attempt closure When muscle necrosis is a possibility, the patient must return to surgery after

24 to 48 hours for débridement Wound closure should not be at-tempted until all necrotic tissue is débrided Direct closure can be at-tempted when the wound approxi-mates without excess tension When the wound edges will not oppose easily, split-thickness skin graft is indicated

Outcomes and Complications

Sheridan and Matsen44reported the clinical outcome of 44 patients who underwent decompressive fasciot-omy Twenty-two patients were treated with fasciotomy before 12 hours and 22 after 12 hours In the first group, 68% of patients had nor-mal lower extremity function at the time of final follow-up, compared with only 8% in the delayed-treatment group.44

Finkelstein et al45reported on five patients who underwent fasciotomy later than 35 hours after the estab-lished diagnosis of lower extremity compartment syndrome In this ret-rospective review, one patient died

of multisystem organ failure

direct-ly related to complications from the fasciotomy The remaining four pa-tients required amputation

Fitzgerald et al41 reported on long-term sequelae of fasciotomy wounds in 60 patients and demon-strated that the patients frequently had complaints at the fasciotomy site Seventy-seven percent reported decreased sensibility, 7% had teth-ered tendons, and 13% had recur-rent ulcerations within the wound closure area.41 Although a fasciot-omy incision does result in some morbidity to the patient, the mor-bidity of an incompletely released compartment, delayed diagnosis,

or unrecognized compartment

syn-drome is substantially worse

It is not possible to determine the

precise time a compartment

syn-drome begins Therefore, it is not

possible to know how long a

com-partment syndrome has been

estab-lished Anecdotal reports suggest

that performing a fasciotomy in the

setting of a delayed diagnosis can be

harmful to the patient and often

re-sults in amputation

The dilemma is determining how

late a presentation is too late for a

fasciotomy In general, clinical

as-sessment of the limb helps with

decision-making The patient with

clinical evidence of compartment

syndrome who has the ability to

vol-untarily contract muscles within the

compartment has some viable

mus-cle; therefore, fasciotomy is

indicat-ed regardless of the delay

Fascioto-my is not performed when a patient

has clinical evidence of

compart-ment syndrome with a suspected

du-ration≥8 hours, has neither a nerve

injury nor a nerve block that could

potentially alter the clinical

exami-nation, and has no demonstrable

muscle function in any segment of

the involved limb Instead, the limb

is aggressively splinted to maintain

a functional position as the muscle

develops fibrosis and contracture

Supportive care should be given for

the potential risk of myoglobinuria,

which may occur in this scenario

Summary

Acute compartment syndrome is

a potentially devastating condition

associated with musculoskeletal

trauma The final common

path-way is cellular ischemia resulting

from increased tissue pressure

within an osseofascial

compart-ment Compartment syndrome can

occur as a result of many different

causes, such as fractures,

contu-sions, bleeding disorders, burns,

trauma, postischemic swelling, and

gunshot wounds Prompt diagnosis

and treatment are key in limiting

patient morbidity The diagnosis of compartment syndrome is usually made based on clinical factors, such

as pain, pressure, paresthesia, paral-ysis, and pulselessness Adjunctive use of compartment pressure mea-surements is warranted in the ma-jority of patients

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a prospective cohort study (level II study)

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