Clinical meaning
Acute compartment syndrome (ACS) occurs when pressure within a closed fascial compartment rises above capillary perfusion pressure (approximately 25-30 mmHg), compromising blood flow to the muscles and nerves within that compartment and causing progressive ischemic necrosis. The pathophysiology follows a predictable cascade: an inciting event (fracture with hemorrhage, crush injury, reperfusion edema, tight cast, burn eschar) increases the volume within the non-expandable fascial compartment. The unyielding fascia prevents expansion, so intracompartmental pressure rises. When compartment pressure exceeds the perfusion pressure of arterioles and capillaries (delta pressure = diastolic BP minus compartment pressure less than 30 mmHg), microvascular blood flow ceases. Without perfusion, muscle and nerve ischemia begin within 30 minutes: muscles tolerate ischemia for approximately 4-6 hours before irreversible necrosis occurs; nerves develop irreversible damage within 4-8 hours. The ischemic muscle swells further from cellular edema (ATP-dependent sodium-potassium pump failure causes intracellular sodium and water accumulation), creating a self-amplifying cycle of increasing pressure and worsening ischemia. Muscle necrosis releases myoglobin (causing rhabdomyolysis), potassium (causing hyperkalemia and cardiac arrhythmias), and creatine kinase into the circulation. Myoglobin precipitates in the renal tubules, causing acute kidney injury (myoglobinuric renal failure). The anterior compartment of the lower leg (tibial fractures) is the most commonly affected site. Fasciotomy is the definitive surgical treatment: all fascial compartments of the affected extremity are incised longitudinally, releasing the pressure and restoring perfusion. The wounds are left open for 48-72 hours to allow swelling resolution before delayed primary closure or skin grafting. Fasciotomy within 6 hours of symptom onset dramatically improves outcomes; delays beyond 12 hours are associated with high rates of amputation, permanent nerve damage, and Volkmann ischemic contracture.