Pathophysiology
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,...