Renal function studies and a potassium level (elevated in rhabdomyolysis, and can cause fatal arrhythmias) must be measured as well. The level of these tests will also help determine the level of muscle necrosis and rhabdomyolysis. Laboratory testing revealing a creatine kinase (CK) of 1000 -5000 U/mL or higher, or the presence of myoglobinuria may alert the physician to the occurrence of CS. If objective evidence of a major sensory deficit or loss of peripheral pulse is found, the syndrome is far advanced. Decreased 2-point discrimination is the most consistent early finding. Sensory nerves tend to be affected before the motor nerves, and selected nerves may be more susceptible than others in the same compartment. Comparison of the affected limb to the unaffected limb is useful. This pain is deep and aching in nature and is worsened by passive stretch of the involved muscles.On physical examination, evidence of trauma and gross deformity should alert the physician to the possibility of a developing CS. Symptomatically, however, there is one symptom that is a clinical tip off to the condition: the patient may experience crescendo pain out of proportion to the original injury. The traditional 5 P’s (ie, pain, paresthesia, pallor, pulselessness, paralysis) are not clinically reliable and manifest only in the late stages of CS. Fatalities are usually due to renal failure complicated by sepsis. Advanced CS may also result in rhabdomyolysis (muscle breakdown), and rhabdomyolysis can also cause renal failure. This circulating myoglobin results in renal injury.
In addition to local morbidity due to muscle necrosis and tissue ischemia, cellular destruction and alterations in muscle cell membranes lead to the release of myoglobin into the circulation. For unclear reasons, CS associated with surgical positioning may manifest later, with a mean time to presentation of 15-24 hours or longer postoperatively. Untreated, within 6-10 hours, the final result is muscle infarction, tissue necrosis, and nerve injury. Compartment pressures higher than 30 mm Hg in general require surgical intervention. Symptoms tend to subside within 1 hour of terminating the activity and are minimal during normal daily activities but return when activity is resumed.ĬS develops after elevated compartment pressure causes muscle and nerve ischemia. Often, it occurs bilaterally, and similar to claudication, the pain it causes may be reproducible at a specific exercise distance or time interval. This syndrome is usually observed in competitive or collegiate athletes. Chronic CS is a recurrent syndrome that occurs with exercise or work. Symptoms worsen acutely, and irreversible nerve injury and muscle necrosis occur within hours. Acute CS typically occurs subsequent to a traumatic event, most commonly fractures. Two types of CS have been identified, acute and chronic. There have also been reports of bilateral lower extremity CS following prolonged surgery in the lithotomy position with the use of compression stocking devices. Other causes include any long bone fracture, vascular injury, burns, compression in the setting of crush injury, penetrating injuries, gastrocnemius muscle tears, deep venous thrombosis, overexertion (such as twisting the calf while running, skiing on moguls, and weightlifting), fluid sequestration, IV drug abuse, snake envenomation, ruptured Bakers Cyst of the knee, and a tight cast or dressing. Compartment syndrome is a bonafide medical emergency that requires rapid intervention.Īs many as 45% of all cases of CS are caused by tibial fractures. The compartments of the lower leg are particularly prone to developing elevated compartment pressures. Therefore, this is a closed space environment. Each muscle or muscle group is enclosed in a compartment bound by relatively rigid walls of bone and fascia. Compartment syndrome (CS) is a condition in which the perfusion pressure of the blood vessels falls below the tissue pressure in a closed anatomic space with subsequent compromise of circulation and function of tissues.
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