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Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e

Chapter 278: Compartment Syndrome Paul R. Haller

Content Update

November 2, 2016

Added significant additional content on EXERTIONAL COMPARTMENT SYNDROME.

INTRODUCTION

Compartment syndrome occurs when increased pressure within a limited space compromises the circulationand function of the tissues within that space. It was first described in 1881 by Richard Van Volkmann, aGerman physician who noted that paralysis and contractures were the late sequelae of an interruption of theblood supply to the muscles in the forearm. In 1924, it was shown that the result could be prevented byprompt surgical decompression of the compartment.

Today, a high degree of clinical suspicion, coupled with timely surgery, can be used to save function of themuscles and nerves that are at risk of permanent damage from elevated compartment pressures.

ANATOMY

The borders of a confined space are o�en made up of bone or tissue that o�ers minimal capacity to stretch.Any increase in volume within that compartment results in an elevated intracompartmental pressure. In thelower extremity, the most common site is at the level of the tibia and fibula, where 40% of compartmentsyndromes occur. The lower leg has four compartments: anterior, lateral, superficial posterior, and deepposterior (Figure 278–1). (Also see Figure 271–1 in chapter 275, Leg Injuries.)

FIGURE 278–1.

The four compartments of the lower leg.

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The upper leg has three compartments: anterior, posterior, and medial. Due to the larger size of thesecompartments and their interconnectivity, they are less predisposed to elevated tissue pressures. The footand buttock region of the leg also have a lower incidence of compartment syndrome.

In the upper extremity, the forearm has three compartments: flexor, extensor, and mobile wad (Figures 278–2and 278–3). These are the high- risk areas in the arm. The hand (Figure 278–4) or upper arm (Figure 278–5) isless likely to develop a compartment syndrome.

FIGURE 278–2.

Forearm compartments.

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FIGURE 278–3.

Forearm compartments: transverse sections through the right forearm at various levels.

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FIGURE 278–4.

Hand compartments: transverse section through the right hand.

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FIGURE 278–5.

The biceps-brachialis (anterior) and triceps (posterior) compartments of the right arm.

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PATHOPHYSIOLOGY

Muscle death and nerve damage in the setting of compartment syndrome are caused by prolonged elevationof tissue pressures. This can result from external forces, such as a cast or tight dressing, which compress acompartment. It can also result from an increase in the volume of a compartment that exceeds the limits ofthe surrounding fascia's ability to stretch. This may be the result of hemorrhage into a compartment oredema caused by reperfusion injury (Table 278-1). In e�ect, any mechanism that increases the volume ofblood or tissue within the compartment has the potential to cause a compartment syndrome. Tissueperfusion is determined by the di�erence between the arterial blood pressure and the pressure of the venous

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return. As tissue pressure increases within a compartment, the normal gradient between arterial and venouspressure decreases.

Table 278–1

Causes of Compartment Syndrome

Orthopedic Tibial fractures

Forearm fractures

Vascular Ischemic-reperfusion injury

Hemorrhage

Iatrogenic Vascular puncture in anticoagulated patients

IV/intra-arterial drug injection

Constrictive casts

So� tissue injury Prolonged limb compression

Crush injury

Burns

Hematologic Hemophilia

Adverse e�ects of anticoagulants (warfarin)

The normal pressure within a compartment is <10 mm Hg. Anoxia and muscle death occurs with prolongedelevated pressure. Pressures up to 20 mm Hg can be tolerated without significant damage. The exact level ofpressure elevation that causes cell death is unclear and may be related to the length of time that the pressureremains high. Tissue pressures exceeding 30 to 50 mm Hg have traditionally been thought to be toxic if le�

untreated for several hours.1 However, the di�erence between the diastolic pressure and the measured

tissue pressure may be a better determinant of potential for irreversible muscle damage.2 This "deltapressure" is the diastolic blood pressure minus the intracompartmental pressure, and the critical level has

been found to range between 10 and 35 mm Hg.3The delta pressure that is most commonly used to diagnose

acute compartment syndrome is 30 mm Hg.4 Using the delta pressure as a threshold for surgical interventionmay help avoid unnecessary fasciotomies and can correctly classify patients with pressures su�icient tocause tissue compromise. In one study, none of the patients with a delta pressure >30 mm Hg su�eredclinically significant complications related to acute compartment syndrome when fasciotomy was withheld,although such clinical parameters may not be su�iciently sensitive to exclude all sequelae that may result

from a compartment syndrome.4 For example, a hypotensive patient may be less able to tolerate the samedegree of pressure elevation when compared to a normotensive patient.

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Some tissues are more sensitive to the ischemic injury produced by elevated compartment pressures. Boneis relatively resistant to this ischemia. The muscles and nerves in the compartment are most susceptible topermanent damage. Short periods of elevated pressures may cause reversible damage, whereas longerperiods lead to permanent deficits (see Table 278-2).

Table 278–2

Tissue Survival of Ischemia

Muscle Nerve

3–4 Hours Reversible change 2 Hours Loss of nerve conduction

6 Hours Variable damage 4 Hours Neurapraxia

8 Hours Irreversible damage 8 Hours Irreversible damage

CLINICAL FEATURES

HISTORY

Compartment syndrome may occur with or without known trauma. For example, patients with hemophilia orrhabdomyolysis can develop compartment syndrome without direct trauma, and crush injury or tibialfracture can result in compartment syndrome to the a�ected extremity. In the post-trauma setting,symptoms usually develop within a few hours of the injury. The awake patient may initially complain ofsevere pain in the a�ected compartment; pain o�en may be refractory to opioids. The pain is due to elevatedtissue pressures within a compartment. Thus the pain worsens when the muscle groups in that compartmentare passively or actively stretched.

PHYSICAL EXAMINATION

This pain and the aggravation of pain by passive stretching of muscles in the compartment in question arethe most sensitive (and o�en the only) clinical findings before the onset of ischemic dysfunction in thenerves and muscles.

When nerve conduction is a�ected, the patient will note numbness or dysesthesia in the sensory distributionof the nerve traversing that compartment. Motor nerve function may also be a�ected. Because tissuepressures do not become higher than arterial pressures, the distal pulse in the extremity will remain normaland there will not be a change in the color or warmth of the extremity. Squeezing or palpation of the musclegroups in the compartments will exacerbate pain. Firmness or fullness in the a�ected compartment is o�endetected.

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DIAGNOSIS

In the appropriate clinical setting, these exam findings alone may be su�icient to make the diagnosis andpropel the patient in a timely fashion to the operating room for surgical treatment. At times, directmeasurement of the tissue pressures in the compartment should be performed to help calculate the deltapressure, confirm the diagnosis, and determine patient disposition.

COMPARTMENT PRESSURE MEASUREMENT

Several commercial devices are available for measuring intracompartmental pressures. A Stryker Kit® is onesuch system. The kit consists of a saline-filled syringe, a manometer, and a needle with a side port. Connectthe manometer between the syringe and the needle. Insert the needle into the compartment. Inject a fewdrops of saline to ensure that there are no air pockets and that the needle is not inserted into a tendon. Thegauge gives the pressure reading in mm Hg. Check pressures twice in each compartment. Also checkadjacent compartment pressures. Because pressures are highest near the injured area, obtain themeasurements within 5 cm of a fracture site. Figure 278–1 demonstrates appropriate sites for pressuremeasurements in the lower leg, whereas Figure 278–6 shows sites for the forearm. The hands and feet havemany compartments within them, all too numerous and small to easily measure. If compartment syndromeis suspected in these sites, some specialists opt for surgical intervention without documentation of elevatedpressures.

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FIGURE 278–6.

A. Forearm extensor compartment. B. Forearm flexor compartments. C. Mobile wad compartment.

The measurement of compartment pressures may be helpful in certain settings. The patient may beobtunded, making clinical evaluation with suspected compartment syndrome di�icult. Patients who are togo to the operating room for other procedures will be di�icult to monitor clinically while under anesthesia.

It is not necessary to measure compartment pressures in a clinically obvious compartment syndrome.

LABORATORY TESTING

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Laboratory testing is of no benefit in the setting of compartment syndrome. At times, the serum creatinephosphokinase may be elevated, as may myoglobin levels. Urinalysis may reveal myoglobinuria.Hemophiliacs or patients with clotting disorders need assay of coagulation parameters and factor levels.

TREATMENT

The initial medical management of these patients includes supplemental oxygen, if needed, and bloodpressure support in the hypotensive patient. Immediately remove restrictive casts or dressings. This alonecan markedly reduce tissue pressures. Place the a�ected limbs at the level of the heart; elevation higher thanthe heart increases the arteriovenous pressure gradient.

Hemophiliacs should have replacement of factor levels (see chapter 235, Hemophilias & von WillebrandDisease), and patients on anticoagulants should have reversal or factor replacement (see chapter 239,Thrombotics and Antithrombotics).

Surgical fasciotomy reduces intracompartmental pressure. Long incisions are necessary to release pressurein the a�ected compartment and simultaneously incise adjacent compartments. Tissue edema within thecompartment will typically cause the muscle to bulge from the incision sites. The wounds should be initiallyle� open and a second look procedure for debridement and possible closure scheduled for 48 to 72 hoursa�er the initial intervention. Ideally, definitive wound closure is obtained within 7 to 10 days. This mayrequire skin gra�ing.

A contraindication to fasciotomy is a missed timely diagnosis of compartment syndrome. Tissue pressuresthat have been elevated for 24 to 48 hours may have already caused permanent dysfunction and opening thecompartments at this time may be futile.

DISEASE COMPLICATIONS

When fasciotomy is performed in a timely fashion, it can prevent death of the muscle within thatcompartment and the nerves that travel through it. When delayed, permanent neuropathy may occur, as canmuscle death. Functional impairment is unlikely when compartment syndrome is diagnosed and treatedwithin 6 hours of its onset.

DISPOSITION AND FOLLOW-UP

Admit all patients with compartment syndrome to the operating room or appropriate inpatient unit for serialobservation and re-examination.

EXERTIONAL COMPARTMENT SYNDROME

Brit Long, MD and Alex Koyfman, MD

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INTRODUCTION

Acute compartment syndrome is commonly due to fracture or acute trauma; however, it can be caused byseveral other conditions, including overexertion. Mavor in 1956 first described chronic compartment

syndrome due to exertion in young athletes.5 This condition can be debilitating to patients, and it is

commonly misdiagnosed.5-8 

This condition most commonly a�ects young endurance athletes due to overexertion. Athletes a�ectedinclude runners, gymnasts, soccer players, lacrosse players, and hockey players, with men and women

equally a�ected.6-10 The prevalence is unknown, as many individuals su�ering from the condition do not

seek medical attention.7 Over 30% of patients with chronic lower leg pain may have elevated compartment

pressures.8  Increased pressures occur in 28% of patients with recurrent, exercise-induced pain.9 The anterior

compartment of the lower leg is most commonly a�ected.6,10-12 However, this condition a�ects many other

populations and can include compartments in the foot, thigh, forearm (gymnasts and climbers), and hand.13-

15

PATHOPHYSIOLOGY

Compartment syndrome due to exertion is associated with several mechanisms, including inability to clear

metabolic waste products due to decreased vascular flow.5-7 Exercise leads to increased vascular flow,

causing muscular expansion and increased pressure.16-18 This pressure elevation reduces blood flow withinthe specific compartment, causing ischemia. Patients a�ected by this condition may have reduced capillary

flow at baseline.19,20 Fascial defects are also common, as 20% to 60% of those with exertional compartmentsyndrome su�er from a fascial hernia near the intramuscular septum between the anterior and lateral

compartments of the lower extremity.7-9,21,22

CLINICAL FEATURES

The patient with lower leg pain has an extensive di�erential, with many benign pathologies, though somemay be life or limb-threatening. This di�erential is demonstrated in (Table 278-3).

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Table 278-3

Di�erential Diagnosis

Di�erential for Lower Leg Pain

- Medial tibial stress syndrome (or shin splints)

- Venous vascular disease: deep venous thrombosis, phlegmasia alba dolens, phlegmasia cerulea dolens

- Arterial vascular disease: thrombus, embolus, popliteal artery entrapment, dissection

- Neurogenic claudication

- Lumbar radiculopathy and other conditions causing cord compression (malignancy, abscess, fracture)

- Peripheral nerve entrapment or injury

- Myopathy

- Periostitis

- Bone tumor

- Stress fracture of the tibia or fibula

- Tendinopathy

Most patients with exertional compartment syndrome are athletes, who typically describe graduallyworsening pain with exertion in a specific anatomical region. The pain can be characterized as aching,

squeezing, cramping, or sharp, o�en with a specific time of onset during exercise.7,11,17,21,23 Symptoms areo�en bilateral and usually stop with rest. In the setting of severe ischemia, paresthesias and weakness can

occur. Symptoms and examination findings are dependent on the specific compartment a�ected.24-

26 Several findings increase likelihood of exertional compartment syndrome in the anterior compartment ofthe lower leg: pain induced by athletic activity only, pain limited to the anterior compartment of the lowerleg, pain requiring the athlete to cease activity, and tenderness to palpation only in the involved

compartment.9

Examination is commonly normal if the patient is resting.6,7,9 If the patient has recently exercised, theinvolved compartment may be tender to palpation. Weakness or absent pulses on examination suggest latestage disease, acute compartment syndrome, or another condition such as claudication or vascular

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disease.6,7,17,21,24 As opposed to exertional compartment syndrome, stress fractures and medial tibial stresssyndrome have localized bony tenderness, with minimal so� tissue tenderness. They also have pain at restand with first impact.

EVALUATION

Acute compartment syndrome should be di�erentiated from the exertional form.  Acute compartmentsyndrome presents with pain that does not resolve, pain out of proportion to examination, pain with passive

stretching, paresthesias, and decreased or absent distal pulses in the involved extremity.6-8,23,24-26 Pain thatresolves could be exertional; however, if pain does not abate a�er exercise, acute compartment syndrome

should be assumed.14,27 Any objective neurologic finding, specifically weakness in the a�ected distribution,is concerning.

DIAGNOSIS

LABORATORY STUDIES

Laboratory studies do not provide definitive diagnosis. Serum creatinine kinase (CK) level will be elevated in

the setting of rhabdomyolysis, and acidosis and myoglobinuria may be found.24,28

COMPARTMENT MEASUREMENTS

Consider consulting an orthopedic surgeon for further evaluation and management. Diagnosis relies onhistory and physical examination, though compartment pressures are a vital adjunct to the diagnosis of

acute compartment syndrome. Failure to diagnose may result in permanent deformity and dysfunction.6-8

For patients with exertional compartment syndrome where the pain has resolved but the provider is

considering the diagnosis, compartment pressure measurement is needed for definitive diagnosis.6-

9,12,24 Measurement technique and timing recommendations di�er among experts, though criteria includestimed measurements: preexercise pressure > 15 mm Hg, 1 minute postexercise pressure > 30 mm Hg, and 5

minute postexercise pressure > 20 mm Hg.6-9,29,30 These criteria are associated with a 5% false positive

rate.10

IMAGING

Near infrared spectroscopy and magnetic resonance imaging (MRI) can be used for diagnosis, but theseshould not be obtained on an emergent basis. Both imaging tests display suboptimal capabilities, with

inadequate sensitivity and specificty.31

MANAGEMENT

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Chronic exertional compartment syndrome management includes rest with exclusion of inciting activity.

Non-steroidal medications, orthotics, stretching, and ice are adjuncts.10,11,14,28 If symptoms resolve, theathlete can gradually return to full activity over several weeks. However, conservative treatment is o�en

ine�ective.6-9 If compartment syndrome is confirmed by pressure measurement, surgical interventionincluding subcutaneous fasciotomy may be needed, with success rates of 80% to 90%. Patients withinvolvement of the deep posterior compartments or those with diabetes have decreased success rates and

o�en require fasciectomy.25,32-34

Acute on chronic compartment syndrome requires emergent orthopedic surgery consultation withconsideration of fasciotomy. 

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