Services Home > Diagnosing Compartment Syndrome
 

Compartment syndrome (CS) occurs when pressure within a closed muscle compartment exceeds the perfusion pressure and results in muscle and nerve ischemia. The cycle of events leading to acute CS begins when tissue pressure exceeds venous pressure and impairs blood outflow. Lack of oxygenated blood and lack of waste product removal result in pain and decreased peripheral sensation secondary to nerve irritation. Late manifestations of CS include the absence of a distal pulse, hypoesthesia, and extremity paresis as the cycle of elevating tissue pressure eventually compromises arterial blood flow. Untreated, the muscles and nerve within the compartment undergo necrosis, and a limb contracture, called a Volkmann contracture (VC), results.

The compartments of the lower leg, foot, and the volar forearm are particularly prone to developing CS. The intrinsic muscle compartments of the hand and, less commonly, the upper arm may also be affected. The most common etiology of an upper extremity CS is a displaced supracondylar humerus fracture. The diagnosis is made on clinical examination when the physician has a high index of suspicion, and operative decompression is the definitive treatment. In the forearm, usually both volar and dorsal compartments are released.

Compartment pressure measurements are usually reserved for diagnosing chronic compartment syndrome (CCS), for evaluating comatose or anesthetized patients, or for situations in which the clinical examination findings are equivocal and the possibility of nonoperative management is likely. Some authors suggest documentation of compartment pressures in all cases, regardless of the clinical examination findings, yet others do not advocate measurement of compartment pressures when the findings on examination are clear and the patient is selected for surgery.

Morbidity and mortality from CS stem from a delay in treatment or diagnosis. After prolonged muscle ischemia, muscle necrosis results in scarring and contracture, named after von Volkmann who described the contracture in 1875. Rhabdomyolysis and subsequent renal failure are among the most severe complications. However, they usually have a self-limited course if treated appropriately.

 

.Treatment of Choice: Decompression

The treatment of choice for CS is early decompression. If the tissue pressure remains elevated in a patient with any other signs or symptoms of a CS, adequate decompressive fasciotomy must be performed as an emergency procedure. The fasciotomy technique is a matter of surgical choice. The goal is salvage of a functional extremity. In no way should the adequacy of decompression be compromised due to concern over cosmesis. It is essential to decompress all tight compartments, and the skin must be considered a potentially significant limiting structure.

If a developing CS is suspected, place the affected limb or limbs at the level of the heart. Elevation is contraindicated, as it decreases arterial flow and narrows the arterial-venous pressure gradient. Releasing one side of a plaster cast can reduce compartment pressure by 30%, bivalving can produce an additional 35% reduction, and complete removal of the cast reduces the pressure by another 15%, for a total decrease of 85% from baseline. Cutting Webril may decrease compartmental pressure by 10-30%. Hence, when CS is identified or suspected, all bandages and casts must be removed. In cases of snake envenomation, administration of antivenom may reverse developing CS.

In the setting of an acute CS, capillary permeability is altered after 3 hours, resulting in postischemia tissue swelling of 30-60%. The role of mannitol in decreasing tissue edema is still under investigation. Ischemia lasting 4 hours leads to significant myoglobinuria, which reaches a maximum about 3 hours after the circulation is restored but persists for as long as 12 hours. IVF administration and potentially bicarbonate may be used to keep urine output at 1-2 mL/kg/h in the face of rhabdomyolysis. Contractures are produced after 12 hours of total ischemia. Relative hypertension and correction of acute anemia may help prevent the development of an impending acute CS. Recent research continues to examine the role of nitric oxide.

 

 

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