Compartment syndrome is caused by an elevation of pressure within the confines of an osseofascial compartment sufficient to compromise the microvascular blood flow of its contained tissue. If uncorrected, this leads to necrosis of the tissue within a few hours. The syndrome may arise in a host of clinical situations, with the most common being trauma.

Elevated pressure may be triggered by bleeding within the compartment and the accompanying tissue damage associated with the trauma.^1,2 A vicious circle of tissue trauma and inflammatory response, with release of inflammatory mediators that effect leaky capillaries and an outpouring of intravascular fluid to the tissue space (edema), contributes to the pathophysiology.^3,4 This outpouring of fluid occurs within the limited (and poorly yielding) osseofascial compartment space and causes an elevation of the tissue pressure within that space. With progression, this results in heightened capillary afterload at the microcirculatory level, with diminished capillary flow and compromised exchange of O₂ and CO₂ in the tissues. This process is a positive biofeedback loop, resulting in tissue ischemia and necrosis with lysis of cells and spillage of their contents into the interstitium. This causes an elevation of solute load within the space and an increased osmotic pressure. The determining factors for compartment syndrome are the tissue pressure within the compartment and its relationship to the diastolic blood pressure, with the critical threshold of a compartment pressure within 30 mm Hg of the diastolic blood pressure.^5,6,7,8 The relative protection afforded by hypertension (and the relative liability of hypotension) are easily understood by their positive and negative effects, respectively, on the microcirculatory flow in this setting.

This chapter describes compartment syndrome in the leg, but compartment syndrome can occur in other areas as well, including the thigh, the gluteal compartment, and the compartments of the foot, forearm, brachium, and deltoid compartment. The pathophysiologic basis for each is the same as that described for the leg, and the remedy is the same: to decompress the compartment in a timely fashion so as to alleviate the embarrassment to the microcirculation of ischemic tissues.

The first clinical symptom of compartment syndrome is pain. The earliest finding on physical examination is pain on passive stretch of the muscle in the affected compartment. Thus, if the anterior compartment of the leg is affected, pulling the toes into a plantarflexed position will elicit significant tenderness. If the deep posterior compartment is affected, dorsiflexion of the toes will elicit significant tenderness. Typically, the affected compartments have a tight (as opposed to soft and pliable) feel, and tenderness is elicited in the assessment (provided the process has not progressed to the point of blocking the nerves and anaesthetizing the leg). Over time, the pain increases and is less likely to be alleviated by narcotics. Numbness, paresthesias, diminished motor function, and ultimately pulselessness can ensue. Not uncommonly, at least some myonecrosis will have occurred if the syndrome progresses to the point of loss of sensation, with diminished motor function, and diminished pulse.⁹ Alleviation of this situation is imperative and should proceed on an emergent basis with fasciotomy of all affected osseofascial compartments.

The accompanying video shows the technique for a two-incision fasciotomy.

VIDEO 69.1 Technique for Two-Incision Leg Fasciotomy. Lawrence X. Webb, MD; John C.P. Floyd, MD (4 min)