Epidemiology

The true incidence of acute compartment syndrome (CS) varies with the inciting event. Almost half of all cases of CS are related to tibia fractures. The incidence of CS with tibia fractures is 1.2% with closed fractures, 6% with open fractures, and as high as 19% with concomitant vascular injury.^1,2 The forearm is the second leading site. CS can occur in any contained compartment.

Pathophysiology

CS is a condition of impaired microcirculatory perfusion related to increased interstitial pressure within a closed compartment. CS begins when increased pressure as a result of increased volume within or external pressure compromises microcirculatory perfusion within that space. Once autoregulatory reductions in the arteriovenous gradient are overwhelmed, interstitial pressure will rise above capillary perfusion pressure (normally between 20 and 30 mm Hg in a normotensive patient for most compartments), and tissue ischemia will occur.³ CS is characterized by a self-propagating cycle of impaired perfusion resulting in ischemia, release of osmotically active particles, and edema, which further increase interstitial pressure and diminished perfusion (Fig. 91.1).

Fig. 91.1 Compartments of the leg.

Presenting Signs and Symptoms

CS should be on the working list of “worst-case” diagnoses for every patient with musculoskeletal pain. CS may result from either externally applied compressive force or internally expanding force, and a suggestive history should be elicited (Box 91.1). Myofascial causes include long-bone fracture, vascular injury, reperfusion after ischemia, burns, prolonged positioning from a drug overdose or operating procedures, compression from tight casts and dressings (including military antishock trousers), overexertion, hemorrhage, injection of fluid into the compartment, massive intravenous fluid infusions, envenomations, hypothyroidism, and rhabdomyolysis. CS has also been reported with deep vein thrombosis and ruptured Baker cysts (see Box 91.1). High-risk patients with an altered sensorium may be unable to provide an appropriate history. CS usually develops hours after the inciting event and rarely more than 48 hours after the inciting event.

Clinicians must remain vigilant and retain a high index of suspicion to avoid missing the diagnosis. Patients with a high mechanism of trauma and an altered sensorium should be examined carefully. The physical examination should focus on evidence of trauma and gross deformity, as well as assessment of neurovascular abnormalities. Comparing one extremity with the unaffected side is often very useful.

Serial examinations are often required.

Acute CS is a clinical diagnosis. The essential clinical feature in a conscious patient is severe pain out of proportion to the injury that is aggravated by active or passive stretching of the muscles of the affected compartment or by palpation of the affected compartment. In early cases, pain is the only abnormality. Increasing pain or pain refractory to analgesics suggests the diagnosis. Severe pain while at rest or without any movement should raise suspicion for acute CS. Increasing need for analgesia or increased analgesic dosing is common. The diagnosis is far more challenging in patients who cannot communicate (i.e., altered mental status).

The natural progression of untreated acute CS is severe pain, decreased sensation, decreased strength, and eventual paralysis of the affected limb. With the exception of pain and paresthesia, the traditional five P’s (pain, paresthesia, pallor, pulselessness, poikilothermia) are misleading and more relevant for arterial injury or occlusion. Patients with severe CS, even those with extensive myonecrosis, may have palpable pulses and preserved capillary refill until late in the course. Pulse deficits should raise suspicion for a vascular injury alone or coexisting with acute CS. Decreased two-point discrimination is consistently the earliest physical abnormality and can help differentiate which compartments are affected. Correlation has also been reported between decreasing vibratory sense (256 cycles per second) and increasing compartment pressure.

Differential Diagnosis and Medical Decision Making

The differential diagnosis includes any disorder that can cause musculoskeletal pain, including fracture, contusions, and hematomas; however, pain from other causes generally diminishes after the inciting event, whereas in acute CS, the pain generally increases even while the patient is at rest. Arterial injury will be manifested as abnormal pulses at the onset. Crush injury shares some overlapping features with CS, but the primary pathophysiology is thought to be direct tissue injury, and fasciotomy is rarely indicated.

The diagnosis cannot be made with radiographic imaging. However, because the differential diagnosis for acute CS includes fracture or dislocation and because the risk for CS increases with fracture, radiographic imaging may be useful. Computed tomography or ultrasound is rarely indicated but may be helpful in establishing the cause of the CS (i.e., fracture, hematoma).

Treatment

Prehospital Management

The affected limb should be placed at the level of the heart. Elevation is contraindicated because it decreases arterial flow, which narrows the arteriovenous pressure gradient and thus worsens ischemia.⁴

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