A compartment syndrome is a serious and sometimes catastrophic entity that can lead to irreversible local and systemic damage.1 It typically results from increased interstitial pressure in a closed and confined space that leads to inadequate perfusion and impaired function of the tissues contained within that space. Locally, a compartment syndrome may lead to loss of function, contractures, rhabdomyolysis, infection, and amputation. This can be followed by systemic complications such as renal failure, sepsis, and possibly death.2 Common causes of a compartment syndrome include circumferential burns, constrictive dressings, crush injuries, electrical injuries, exercise, external compression of a limb, external trauma to the extremity, open or closed fractures, reperfusion after a vascular insult, snakebites, and tight fitting casts or splints (Table 74-1).1–20
The difficulty in diagnosing a compartment syndrome is that the physical examination is a poor indicator of the degree of microcirculatory compromise.3 The diagnosis requires a high level of suspicion on the part of the Emergency Physician. Refer to Chapter 74 regarding the complete details of a compartment syndrome. Maintaining a low threshold for performing a fasciotomy can be the safest course for the patient. The prognosis is more favorable if a fasciotomy is performed soon after the onset of symptoms. If delayed, there may be little or no benefit to performing a fasciotomy.
The anatomy of a compartment syndrome is variable, as it can occur in any enclosed muscle group. Any muscle tissue that is confined in space by fascia, skin, or any external forces (e.g., casting material) is a potential site for the development of a compartment syndrome. The muscles, nerves, and vasculature within the affected muscle group are all potentially compromised by a prolonged ischemic state followed by swelling. A basic knowledge of the anatomy of commonly affected compartments is necessary to successfully and safely perform a fasciotomy.
The initial imbalance of a compartment syndrome occurs between the volume and pressure within the myofascial compartment. The arterial inflow and venous outflow diminish as either intracompartmental volume or pressure increases. The blood begins to be shunted via capillaries into the muscle tissue. This compensatory shunting of blood further disturbs the volume–pressure balance, resulting in impaired tissue oxygenation.
Skeletal muscles, major nerves, and major blood vessels of the extremities are contained within a noncompliant connective tissue membrane known as the investing or deep fascia. Connective tissue septa from the investing fascia to the bones of the extremities form compartments within the extremity. Each fascial compartment has a relatively constant range of pressure within it in which perfusion is maintained.3 Under normal circumstances, the compartment pressure is ≤10 to 12 mmHg. Any of the previously mentioned insults may set off a cascade of events. This includes edema, hemorrhage, and/or external compression. The pressure within the compartment begins to rise. A critical pressure is reached within the compartment and perfusion is impaired. This results in altered ...