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. Each muscle or muscle group is enclosed in a compartment bound by relatively rigid walls of bone and fascia. Therefore, this is a closed space environment. The compartments of the lower leg are particularly prone to developing elevated compartment pressures. Compartment syndrome is a bonafide medical emergency that requires rapid intervention.
As many as 45% of all cases of CS are caused by tibial fractures. 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. There have also been reports of bilateral lower extremity CS following prolonged surgery in the lithotomy position with the use of compression stocking devices.
Two types of CS have been identified, acute and chronic. Acute CS typically occurs subsequent to a traumatic event, most commonly fractures. Symptoms worsen acutely, and irreversible nerve injury and muscle necrosis occur within hours. Chronic CS is a recurrent syndrome that occurs with exercise or work. This syndrome is usually observed in competitive or collegiate athletes. Often, it occurs bilaterally, and similar to claudication, the pain it causes may be reproducible at a specific exercise distance or time interval. Symptoms tend to subside within 1 hour of terminating the activity and are minimal during normal daily activities but return when activity is resumed.
CS develops after elevated compartment pressure causes muscle and nerve ischemia. Compartment pressures higher than 30 mm Hg in general require surgical intervention. Untreated, within 6-10 hours, the final result is muscle infarction, tissue necrosis, and nerve injury. For unclear reasons, CS associated with surgical positioning may manifest later, with a mean time to presentation of 15-24 hours or longer postoperatively. 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. This circulating myoglobin results in renal injury. Advanced CS may also result in rhabdomyolysis (muscle breakdown), and rhabdomyolysis can also cause renal failure. Fatalities are usually due to renal failure complicated by sepsis.
Clinical History and Physical:
The traditional 5 P’s (ie, pain, paresthesia, pallor, pulselessness, paralysis) are not clinically reliable and manifest only in the late stages of 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. 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. Comparison of the affected limb to the unaffected limb is useful. Sensory nerves tend to be affected before the motor nerves, and selected nerves may be more susceptible than others in the same compartment. Decreased 2-point discrimination is the most consistent early finding. If objective evidence of a major sensory deficit or loss of peripheral pulse is found, the syndrome is far advanced.
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. The level of these tests will also help determine the level of muscle necrosis and rhabdomyolysis. Renal function studies and a potassium level (elevated in rhabdomyolysis, and can cause fatal arrhythmias) must be measured as well.
Diagnosis and Treatment:
If CS is strongly suspected in the clinical examination, operative decompression is the mainstay of therapy. Although compartment pressure measurements are usually reserved for diagnosing chronic CS, for evaluating comatose patients, or for other conditions in which the clinical examination findings are equivocal, if compartment pressures can be quickly obtained, then it is prudent to confirm the clinical suspicion of acute CS. Many surgeons now use a measured compartment pressure of 30 mm Hg as a cutoff for fasciotomy (surgical compartment release). If CS is diagnosed late, fasciotomy is of little benefit. In fact, fasciotomy is probably contraindicated after the third or fourth day, because severe infection usually develops in the necrotic muscle post fasciotomy. These patients usually require life-saving amputation.In terms of medical therapy, certain measures would be employed that are specific to the underlying cause of the compartment syndrome. For example, if due to a plaster case, releasing one side of the cast or bivalving can reduce compartment pressures by 50-60%. In cases of snake envenomation, antivenom may reverse the condition. Mannitol, a potent diuretic, has been found to reduce compartment pressure and lesson reperfusion injury. Lastly, hyperbaric oxygen has been found to promote vasonconstriction which reduces swelling and edema and improves local blood flow and oxygenation, thus ensuring the survival of marginally viable tissue.
The definitive surgical therapy is emergent fasciotomy with subsequent orthopedic reduction or fracture stabilization and vascular repair, if needed. The goal of decompression is restoration of muscle perfusion within 6 hours. Adequate exposure of the entire anterior and posterior compartments and in particular the peroneal nerve are paramount. IV antibiotics should always be given prior to the procedure. After the initial procedure, the patient is returned to the OR in 1-3 days for additional necrotic muscle debridement.
Treatment for rhabdomyolysis include hydration, good diuresis and close monitoring of kidney function and potassium levels. The rehabilitation protocol depends most on the underlying mechanism of injury. Patients may need skin grafting or traction dermoplasty if the skin defect is large.
Postoperative motor deficits resulting from CS are initially treated with appropriate orthotic devices (eg, a drop foot brace when the anterior compartment of the leg is affected). If function does not return in about 1 year, tendon transfer and other forms of reconstructive surgery may be considered. Volkmann contracture (VC) is the most common residual limb deformity seen with untreated CS. Approximately 1-10% of all cases of CS develop VC.Infection is a serious complication of CS. Most studies show that about 50% of patients having late surgical decompression develop infections and about 50% of these patients go on to have an an amputation. Systemic complications include acute renal failure, sepsis, and acute respiratory distress syndrome (ARDS). Most fatalities are due to prolonged intensive care admissions with sepsis and multisystem organ failure.
Late treatment of acute CS often has disastrous outcomes. Muscles tolerate 4 hours of ischemia well, but by 8 hours, the damage is usually irreversible. If fasciotomy is performed within 25-30 hours following onset of acute CS (not of ischemia per se), the prognosis is good. Little or no return of function can be expected when diagnosis and treatment are delayed. However, despite early and aggressive fasciotomy, nearly 20% of patients may have persistent sensory or motor deficits at 1- year follow-up.
A delay in diagnosis is a potentially devastating medical-legal occurrence. The average malpractice award in suits of this nature exceeds $500,000. Because of the potentially catastrophic nature of this condition clinicians must maintain a high index of suspicion and must consider the diagnosis until proven otherwise.
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