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Emergency And Acute Medicine – Rhabdomyolysis
Rhabdomyolysis is a potentially life-threatening condition characterized by the abnormal systemic release of skeletal muscle cell contents—including creatine phosphokinase (CPK), myoglobin, potassium, phosphate, and urate—into the bloodstream. It results from trauma, toxins, infections, metabolic disturbances, medications, inherited muscle disorders, or extreme exertion. Major complications include acute renal failure (15–50% in adults and about 5% in children), life-threatening hyperkalemia, hypocalcemia, metabolic acidosis, hypovolemia from fluid sequestration into damaged muscle, compartment syndrome (particularly in crush injuries), hepatic dysfunction, and disseminated intravascular coagulation (DIC). Approximately 26,000 cases occur annually in the United States, and disaster situations may produce large numbers of renal failure cases.
The underlying pathophysiology begins with disruption of the sarcolemma, which normally maintains low intracellular calcium levels. Membrane injury allows calcium influx, activating calcium-dependent proteases that destroy muscle fibers. Ischemia and inflammatory mediators further exacerbate damage. Intracellular components such as myoglobin, potassium, phosphate, lactate, and CPK are released into the circulation. Myoglobin contributes to renal injury through direct tubular toxicity in acidic urine, precipitation with proteins causing tubular obstruction, and renal vasoconstriction worsened by hypovolemia. Potassium release may lead to fatal arrhythmias, while calcium binds to phosphate in injured muscle, resulting in systemic hypocalcemia.
The cause is often obvious but not always. Trauma and crush injury are the most common overall causes. Other etiologies include strenuous exertion (such as marathon running or seizures), prolonged immobilization, ischemia from shock or thrombosis, surgery with hypotension, temperature extremes, and massive blood transfusion. Drugs and toxins—such as alcohol, cocaine, amphetamines, opioids, carbon monoxide, and certain medications including statins and antipsychotics—are frequent contributors. Metabolic abnormalities, infections (viral, bacterial, parasitic), inherited myopathies, and autoimmune muscle disorders may also be responsible. In children, viral myositis is a common nontraumatic cause.
Clinical presentation varies widely depending on the underlying cause. Classic symptoms include muscle pain, weakness, and dark “tea-colored” urine, although muscle pain is present in only about half of patients. Decreased urine output may occur. Physical findings can include hypovolemia with tachycardia and hypotension, altered mental status, hypo- or hyperthermia, and signs of compartment syndrome. In children, physical findings may be minimal, and the condition should be suspected in the setting of viral illness with muscle symptoms.
Diagnosis relies primarily on laboratory evaluation, as history and examination may be nonspecific. A serum CPK level greater than 1,000 U/L is considered diagnostic, and levels above 15,000 U/L are associated with a higher risk of renal failure. Urine dipstick testing may show heme positivity without red blood cells, suggesting myoglobinuria; however, myoglobin clears rapidly, and the dipstick may be negative despite significant disease. Electrolytes must be closely monitored, especially potassium, calcium, phosphate, bicarbonate, BUN, and creatinine. An ECG should be obtained early to detect hyperkalemia-related changes. Imaging studies are generally not required for diagnosis but may be used to evaluate complications.
Management centers on early and aggressive intravenous fluid resuscitation to prevent renal failure. In trauma or crush injuries, isotonic saline should be started as early as possible. In the emergency department, adults typically receive 1–1.5 liters per hour, and children receive 10–20 mL/kg per hour, aiming for a urine output of 200–300 mL per hour (3–5 mL/kg per hour in children). Total daily fluid requirements may reach 10–12 liters in severe cases. Urine alkalinization with sodium bicarbonate to maintain a urine pH greater than 6.5 is often recommended, particularly in crush injuries, though evidence is mixed. Hyperkalemia must be treated promptly with standard therapies such as insulin with dextrose and beta-agonists; calcium should be reserved for severe cases with ECG changes. Hypocalcemia should be treated only if symptomatic. Hemodialysis is indicated for refractory hyperkalemia, severe acidosis, fluid overload, or persistent anuria. Compartment syndrome requires urgent surgical evaluation and possible fasciotomy.
All but the most trivial elevations in CPK should prompt hospital admission because complications are unpredictable. Intensive care admission is indicated for severe electrolyte disturbances, very high CPK levels, renal failure, or significant comorbid illness. Prognosis is excellent in patients who do not develop renal failure but worsens significantly when renal failure occurs. Early recognition and aggressive hydration remain the most important interventions to reduce morbidity and mortality.
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