There are two forms of alcoholic muscle disease: (1) an acute, painful myopathy associated with weakness, cramps, swollen and tender muscles, high creatine kinase, and rhabdomyolysis with or without myoglobinuria; and (2) a chronic myopathy that is painless and often unnoticed by the patient, causing proximal weakness and type II fiber atrophy on nerve biopsy. In addition to skeletal muscle involvement, patients may have an associated cardiomyopathy. y
Proposed mechanisms of alcoholic injury have included mitochondrial dysfunction, phosphorus and potassium depletion, and rhabdomyolysis induced by either alcohol-related seizures or limb compression from alcoholic stupor. Alcohol may also act synergistically with nutritional deficiencies to disrupt energy metabolism, although a mitochondrial defect has not been demonstrated. y The acute myopathy may require an additional insult, such as hypokalemia, fasting, seizures, delirium tremens, or prolonged limb compression. In chronic myopathy, type IIb fiber atrophy and fiber size variability are present. y In acute myopathy, necrosis with or without inflammation, regenerating fibers, and type I atrophy are seen pathologically. Women are more susceptible than men to develop this complication due to a 40% lower dose of alcohol required to produce cardiac and skeletal myopathy. y Women may metabolize alcohol more slowly, leading to higher blood levels, possibly due to decreased gastric alcohol dehydrogenase and liver metabolism.
Acute necrotizing myopathy and rhabdomyolysis cause severe painful swelling of one or more muscles with induration of the skin and soft tissues. Creatine kinase levels may be elevated, and myoglobinuria may result in acute renal failure. Acute attacks resolve in days to weeks after abstaining and long-term disability is uncommon unless the patient has repeated attacks.y Chronic myopathy is painless weakness of proximal muscles. A cardiomyopathy, peripheral and autonomic neuropathies, and other complications of alcohol abuse may be concomitantly present in these patients. Other myopathic processes including inflammatory (polymyositis/dermatomyositis), endocrine (thyroid, cortisol), electrolyte disorders (low potassium, phosphorus, calcium, and magnesium), toxins (colchicine), and infectious agents (legionella, mycoplasma, viral) should be considered in this clinical setting.
Martin and colleagues performed muscle biopsies in 151 consecutive inpatient alcoholics. Only half had weakness, and 15 percent had an elevated CK level. A chronic myopathy was observed in 60 percent, and 5 percent had necrosis, suggesting an acute myopathy on muscle biopsy. Clinical evidence of a peripheral neuropathy was suggested in 65 percent, yet half were asymptomatic. y
In the evaluation of these patients, laboratory studies should include CK, aldolase, electrocardiograph, and echocardiogram. In one series of patients, the aldolase level was more commonly elevated than CPK and may be more helpful in the diagnosis.y Rarely, when the diagnosis is in question, a muscle biopsy is warranted. Management includes strict abstinence from alcohol, intravenous saline diuresis to prevent renal failure from myoglobinuria, and thiamine and multivitamin supplementation.
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Alcoholism is something that can't be formed in easy terms. Alcoholism as a whole refers to the circumstance whereby there's an obsession in man to keep ingesting beverages with alcohol content which is injurious to health. The circumstance of alcoholism doesn't let the person addicted have any command over ingestion despite being cognizant of the damaging consequences ensuing from it.