Chapter 278: Compartment Syndrome

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

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

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

The upper leg has three compartments: anterior, posterior, and medial. Due to the larger size of these compartments and their interconnectivity, they are less predisposed to elevated tissue pressures. The foot and 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 278–2 and 278–3). These are the high- risk areas in the arm. The hand (Figure 278–4) or upper arm (Figure 278–5) is less likely to develop a compartment syndrome.

Muscle death and nerve damage in the setting of compartment syndrome are caused by prolonged elevation of tissue pressures. This can result from external forces, such as a cast or tight dressing, which compress a compartment. It can also result from an increase in the volume of a compartment that exceeds the limits of the surrounding fascia's ability to stretch. This may be the result of hemorrhage into a compartment or edema caused by reperfusion injury (Table 278-1). In effect, any mechanism that increases the volume of blood or tissue within the compartment has the potential to cause a compartment syndrome. Tissue perfusion is determined by the difference between the arterial blood pressure and the pressure of the venous return. As tissue pressure increases within a compartment, the normal gradient between arterial and venous pressure decreases.

The normal pressure within a compartment is <10 mm Hg. Anoxia and muscle death occurs with prolonged elevated pressure. Pressures up to 20 mm Hg can be tolerated without significant damage. The exact level of pressure elevation that causes cell death is unclear and may be related to the length of time that the pressure remains high. Tissue pressures exceeding 30 to 50 mm Hg have traditionally been thought to be toxic if left untreated for several hours.¹ However, the difference between the diastolic pressure and the measured tissue pressure may be a better determinant of potential for irreversible muscle damage.² This "delta pressure" 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 intervention may help avoid unnecessary fasciotomies and can correctly classify patients with pressures sufficient to cause tissue compromise. In one study, none of the patients with a delta pressure >30 mm Hg suffered clinically significant complications related to acute compartment syndrome when fasciotomy was withheld, although such clinical parameters may not be sufficiently 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 same degree of pressure elevation when compared to a normotensive patient.

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

HISTORY

Compartment syndrome may occur with or without known trauma. For example, patients with hemophilia or rhabdomyolysis can develop compartment syndrome without direct trauma, and crush injury or tibial fracture can result in compartment syndrome to the affected extremity. In the post-trauma setting, symptoms usually develop within a few hours of the injury. The awake patient may initially complain of severe pain in the affected compartment; pain often may be refractory to opioids. The pain is due to elevated tissue pressures within a compartment. Thus the pain worsens when the muscle groups in that compartment are passively or actively stretched.

PHYSICAL EXAMINATION

This pain and the aggravation of pain by passive stretching of muscles in the compartment in question are the most sensitive (and often the only) clinical findings before the onset of ischemic dysfunction in the nerves and muscles.

When nerve conduction is affected, the patient will note numbness or dysesthesia in the sensory distribution of the nerve traversing that compartment. Motor nerve function may also be affected. Because tissue pressures do not become higher than arterial pressures, the distal pulse in the extremity will remain normal and there will not be a change in the color or warmth of the extremity. Squeezing or palpation of the muscle groups in the compartments will exacerbate pain. Firmness or fullness in the affected compartment is often detected.

In the appropriate clinical setting, these exam findings alone may be sufficient to make the diagnosis and propel the patient in a timely fashion to the operating room for surgical treatment. At times, direct measurement of the tissue pressures in the compartment should be performed to help calculate the delta pressure, confirm the diagnosis, and determine patient disposition.

COMPARTMENT PRESSURE MEASUREMENT

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

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

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

LABORATORY TESTING

Laboratory testing is of no benefit in the setting of compartment syndrome. At times, the serum creatine phosphokinase 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.

The initial medical management of these patients includes supplemental oxygen, if needed, and blood pressure support in the hypotensive patient. Immediately remove restrictive casts or dressings. This alone can markedly reduce tissue pressures. Place the affected limbs at the level of the heart; elevation higher than the heart increases the arteriovenous pressure gradient.

Hemophiliacs should have replacement of factor levels (see chapter 235, Hemophilias & von Willebrand Disease), 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 pressure in the affected compartment and simultaneously incise adjacent compartments. Tissue edema within the compartment will typically cause the muscle to bulge from the incision sites. The wounds should be initially left open and a second look procedure for debridement and possible closure scheduled for 48 to 72 hours after the initial intervention. Ideally, definitive wound closure is obtained within 7 to 10 days. This may require skin grafting.

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

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

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

Brit Long, MD and Alex Koyfman, MD

INTRODUCTION

Acute compartment syndrome is commonly due to fracture or acute trauma; however, it can be caused by several 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 affects young endurance athletes due to overexertion. Athletes affected include runners, gymnasts, soccer players, lacrosse players, and hockey players, with men and women equally affected.^6-10 The prevalence is unknown, as many individuals suffering 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 affected.^6,10-12 However, this condition affects 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 within the specific compartment, causing ischemia. Patients affected 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 compartment syndrome suffer 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 differential, with many benign pathologies, though some may be life or limb-threatening. This differential is demonstrated in (Table 278-3).

Most patients with exertional compartment syndrome are athletes, who typically describe gradually worsening pain with exertion in a specific anatomical region. The pain can be characterized as aching, squeezing, cramping, or sharp, often with a specific time of onset during exercise.^{7,11,17,21,23} Symptoms are often 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 affected.^24-26 Several findings increase likelihood of exertional compartment syndrome in the anterior compartment of the lower leg: pain induced by athletic activity only, pain limited to the anterior compartment of the lower leg, 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, the involved compartment may be tender to palpation. Weakness or absent pulses on examination suggest late stage disease, acute compartment syndrome, or another condition such as claudication or vascular disease.^6,7,17,21,24 As opposed to exertional compartment syndrome, stress fractures and medial tibial stress syndrome have localized bony tenderness, with minimal soft tissue tenderness. They also have pain at rest and with first impact.

EVALUATION

Acute compartment syndrome should be differentiated from the exertional form.  Acute compartment syndrome 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 that resolves could be exertional; however, if pain does not abate after exercise, acute compartment syndrome should be assumed.^14,27 Any objective neurologic finding, specifically weakness in the affected 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 on history 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 differ among experts, though criteria includes timed 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 these should not be obtained on an emergent basis. Both imaging tests display suboptimal capabilities, with inadequate sensitivity and specificty.³¹

MANAGEMENT

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, the athlete can gradually return to full activity over several weeks. However, conservative treatment is often ineffective.^6-9 If compartment syndrome is confirmed by pressure measurement, surgical intervention including subcutaneous fasciotomy may be needed, with success rates of 80% to 90%. Patients with involvement of the deep posterior compartments or those with diabetes have decreased success rates and often require fasciectomy.^25,32-34

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