Acute Compartment Syndrome

Acute extremity pain is a common presentation seen daily in EDs. While most etiologies of extremity pain are benign, the complications of acute compartment syndrome are associated with significant morbidity. Moreover, acute compartment syndrome remains a difficult diagnosis that is often missed on initial presentation. Morbidity results from an increased pressure in an anatomically closed space, progressing to decreased perfusion and rapid tissue destruction.

Case

An obese 55-year-old man with a medical history of coronary artery disease, for which he was on aspirin therapy, presented for evaluation of right shin pain. The patient stated that he completed a 5-km race earlier that morning with his son. Immediately following the race, he experienced increasing right shin pain, which he attempted to initially manage with ice compresses and over-the-counter ibuprofen. He noted that neither the ice compresses nor the ibuprofen relieved his pain and that by 5:00 pm, the pain had worsened to the point where he had difficulty walking, prompting his visit to the ED.

Upon arrival at the ED, the patient was ambulatory but had significant pain at both rest and movement. His vital signs and his oxygen saturation on room air were normal. On physical examination, he had normal sensation to the entire right lower extremity and had equal pulses in both feet. The anterolateral aspect of the shin was exquisitely tender to light touch, and the patient was unable to dorsiflex or plantar flex without extreme pain. On passive dorsiflexion and plantar flexion of his right foot, he had exquisite pain. On palpation, the anterior shin was firm compared to the other muscle beds.

Epidemiology

Acute compartment syndrome—elevation of interstitial pressure in closed fascial compartment—affects 10 times as many men as women, at an average age of 32 years old and with an annual incidence of 7.3 per 100,000 men and 0.7 per 100,000 for women.¹ McQueen et al¹ found that the most common cause of acute compartment syndrome was fracture (69%), followed by soft tissue injury (23%). Younger patients are more likely to develop acute compartment syndrome from trauma because they typically have larger muscle beds with more tissue to become edematous compared to the older, hypotrophic muscles of elderly patients.

Pathophysiology

The fascia surrounds the major muscle groups and neurovascular bundles in the extremities to create distinct compartments. Since the fascia is not a compliant structure, it is typically not able to tolerate increases in volume or pressure in a given compartment. Compartment perfusion pressure is the mean arterial pressure minus the compartment pressure. Normal compartment pressure in adults is between 0 to 8 mm Hg.² When compartment perfusion pressures are below 70 to 80 mm Hg, there is an increased risk of compartment syndrome.

Although the exact pathophysiology of acute compartment syndrome is still debated,³ the most commonly accepted theory is the arteriovenous pressure gradient theory.⁴ In this theory, the rise in intracompartment pressure increases venous pressure, which in turn reduces the arteriovenous pressure gradient, reducing local tissue perfusion. The reduction in tissue perfusion, coupled with a reduction in venous drainage, causes significant tissue edema. This change in vascular pressure also causes a reduction in lymphatic drainage, further increasing pressure in the compartment. Finally, the edematous tissue compresses the arterioles leading to end-organ ischemia.⁵

Initially an absolute threshold compartment pressure was thought to cause irreversible tissue ischemia,⁶ but this theory has slowly lost favor after it was found that hypertension was actually protective in compartment syndrome.⁷ Current thinking is that the difference between the diastolic pressure and the compartment pressure leads to tissue ischemia (ie, acute compartment syndrome delta pressure = diastolic blood pressure [BP] – measured compartment pressure).^6,8

In 1996, McQueen and Court-Brown⁶ prospectively admitted all tibial diaphyseal fractures and continuously monitored their anterior compartment pressure. Using a delta pressure value of less than 30 mm Hg, only three patients were diagnosed with acute compartment syndrome and required fasciotomy. The patients’ absolute compartment pressures were 45 mm Hg, 65 mm Hg, and 75 mm Hg, while the delta pressures were 15 mm Hg, 10 mm Hg, and 15 mm Hg, respectively. Conversely, 53 patients had absolute compartment pressures over 30 mm Hg; 30 patients had pressure over 40 mm Hg; four patients had pressure over 50 mm Hg; and none required fasciotomy. This study highlights that the absolute compartment pressure is not helpful in making the diagnosis, and it is the elevated delta pressure that secures the diagnosis.