What is the pathophysiology of cocaine-induced rhabdomyolysis (muscle breakdown) and myopathy (muscle disease)?

From the Guidelines

Cocaine-induced myopathy should be managed with immediate cessation of cocaine use and supportive care, including intravenous fluids to prevent kidney damage from myoglobin release, as this approach prioritizes reduction of morbidity, mortality, and improvement of quality of life. The condition typically presents as muscle pain, weakness, and tenderness, often accompanied by elevated creatine kinase levels in the blood, which can confound the diagnosis of other conditions such as myocardial infarction 1. Key aspects of management include:

• Immediate cessation of cocaine use to prevent further muscle damage
• Supportive care with intravenous fluids to maintain hydration and prevent kidney damage from myoglobin release
• Monitoring of renal function and electrolyte imbalances, particularly in severe cases
• Referral to addiction treatment programs to address the underlying substance use disorder Cocaine causes vasoconstriction, reducing blood flow to muscles, while also increasing muscle metabolism and temperature, leading to direct muscle fiber damage, and can trigger rhabdomyolysis, a serious condition where damaged muscle fibers release proteins into the bloodstream that can cause kidney failure 1. Recovery from cocaine-induced myopathy depends on the extent of muscle damage and typically begins within days to weeks after stopping cocaine use, though some patients may experience persistent weakness. Prevention involves complete abstinence from cocaine, emphasizing the importance of addressing the underlying substance use disorder through referral to addiction treatment programs.

From the Research

Cocaine Induced Myopathy

• Cocaine induced myopathy and myotoxicity are described in the literature, with cases presenting with acute sciatic symptoms, paraspinal myositis, and rhabdomyolysis 2, 3, 4, 5.
• The clinical spectrum of drug-induced myopathies is wide, ranging from asymptomatic elevations in serum creatine phosphokinase levels to severe life-threatening rhabdomyolysis 6.
• Cocaine intoxication can cause acute rhabdomyolysis with acute renal failure, severe liver dysfunction, and disseminated intravascular coagulation, with a high mortality rate among patients with this syndrome 3.
• Management of suspected drug-induced myopathy should include immediate discontinuation of the offending agent, as well as supportive care when needed, with earlier diagnosis and drug discontinuation raising the likelihood of resolution and recovery 6.

Clinical Presentation

• Patients with cocaine-induced myopathy may present with severe musculoskeletal pain, renal failure, and elevated serum creatine phosphokinase levels 2, 3, 4, 5.
• Clinical examination may be limited by severe pain, but may reveal focal midline lumbar tenderness, periorbital edema, and soft tissue swelling 2, 4.
• Laboratory tests may show elevated creatine kinase levels, deranged renal function, and abnormal liver function tests 2, 3, 4, 5.

Diagnosis and Treatment

• Diagnosis of cocaine-induced myopathy may involve imaging studies such as MRI, as well as laboratory tests to rule out other causes of myopathy 2.
• Treatment typically involves discontinuation of cocaine use, as well as supportive care such as pain management and renal replacement therapy if necessary 2, 6, 4.
• Corticosteroids such as prednisolone may be used to treat paraspinal myositis, with good clinical response and improvement in renal function and creatine kinase levels 2.