A 42-year-old man is brought to the emergency department due to weakness. The patient drinks alcohol daily and has been binge drinking for the past 2 days. He also used cocaine the previous night. This morning, the patient stumbled and fell several times while trying to get to the bathroom. He has no other medical problems and takes no medications. Temperature is 37 C (98.6 F), blood pressure is 160/100 mm Hg, pulse is 102/min, and respirations are 18/min. Oxygen saturation is 96% on room air. Physical examination shows mildly dilated pupils. The oropharynx is clear. There is no jugular venous distension. Cardiopulmonary examination is normal. The abdomen is soft and nontender. Bilateral thighs and calves are mildly swollen and tender. Lower extremity muscle strength is decreased, but sensation to touch and vibration is normal. Upper extremity examination shows no abnormalities. Over the next several days, this patient is at greatest risk for which of the following complications of his current condition?
Rhabdomyolysis | |
Etiology | Skeletal muscle lysis/necrosis due to:
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Clinical features |
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Diagnosis |
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Management |
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ALT = alanine aminotransferase; AST = aspartate aminotransferase; RBCs = red blood cells. | |
This patient's clinical features are consistent with drug-induced rhabdomyolysis. Alcohol binges can cause acute alcohol myopathy that predominantly affects the lower extremities, causing pain, weakness, and swelling. It likely occurs via direct toxicity of ethanol and its metabolites, leading to disruption of myocyte membranes. Cocaine abuse further contributes to muscle damage via both vasoconstrictive skeletal muscle ischemia and direct myocyte toxicity.
Up to 50% of patients with rhabdomyolysis will develop acute kidney injury (AKI). During muscle cell lysis, intravascular fluid is shifted into the damaged muscle tissue, and heme-containing myoglobin is released into the bloodstream. The intravascular volume depletion causes an initial prerenal insult, which is followed by a subsequent insult from direct tubular toxicity of heme (pigment nephropathy).
Treatment of rhabdomyolysis involves aggressive volume resuscitation to replace intramuscular and intravascular fluid. Affected muscle groups must be monitored closely because the initial tissue damage and subsequent volume replacement create a risk for acute compartment syndrome.
(Choice B) Rhabdomyolysis leads to metabolic acidosis due to the release of lactic acid from lysed muscle cells. In patients with underlying lung disease, the acidosis may sometimes create a high ventilatory demand that cannot be met, resulting in acute respiratory failure. However, such a complication is rare.
(Choice C) Guillain-Barré syndrome typically presents with symmetric muscle weakness that begins in the lower extremities and can progress to the upper extremities, respiratory muscles, and bulbar muscles of the face. Some level of sensory deficit (eg, touch, vibration) is usually expected.
(Choice D) Methanol ingestion usually presents with nausea, vomiting, and altered consciousness. Vision loss can eventually occur due to retinal damage induced by formic acid (a toxic metabolite of methanol). Swelling and weakness of the lower extremities are not typical.
(Choice E) Some degree of hypovolemic hyponatremia may occur with rhabdomyolysis, but severe hyponatremia is not typical. More common abnormalities include hyperkalemia and hyperphosphatemia, which result from the release of these electrolytes from lysed muscle cells into the bloodstream.
Educational objective:
Alcohol bingeing can lead to acute alcohol myopathy and rhabdomyolysis, especially when combined with cocaine abuse. Patients with rhabdomyolysis are at risk of developing acute kidney injury due to both intravascular volume depletion and pigment-induced nephropathy.