A 40-year-old man initially presented with a headache and was admitted for hypertensive emergency. He rapidly developed altered mental status, acute kidney injury, fever, and weakness. After 12 days of supportive care, he was transferred to our institution. On arrival, the patient was unable to provide a history but his family reported he had been working, walking, and talking normally two days before his initial presentation. They suspected he drank alcohol frequently.
On exam, he was agitated and bed bound. He had 2+ pitting edema to his thighs and his strength was 2/5 proximally and 3/5 distally. He minimally followed commands and was oriented to self and year. He gazed around the room but did not demonstrate tracking and his speech was often incoherent.
He exhibited progressive weakness and worsening somnolence during his admission. By day 16, he could only move his toes and face, made garbled sounds, and followed no commands. On day 20, he received methylprednisone for neurosarcoidosis vs. progressive myopathy of unknown etiology. The following day, he was surprisingly able to wave in response to greetings and he continued to steadily improve thereafter.
A MRI of the brain showed T1 hyperintensity of globus pallidus bilaterally. Lumbar puncture revealed only a mild pleocytosis. Blood cultures were repeatedly negative. Liver and pulmonary nodule biopsies were not consistent with sarcoidosis. An EMG and NCS showed a sensorimotor peripheral neuropathy axonal type and myopathy, consistent with alcoholic myopathy vs. critical illness myopathy. At discharge on day 36, he was completely oriented, ambulating with use of a walker, and speaking clearly with a slight vocal tremble. He was discharged to a rehabilitation facility with a steroid taper.
Chronic alcoholic myopathy is typified by proximal muscle weakness with minimal pain and affects up to 2% of adults in the Western world, 50% of alcohol misusers, and 60% of hospitalized alcoholics with a greater than 3 year history of heavy alcohol abuse. Our patient likely had an underlying chronic alcoholic myopathy, as he recalled mild muscle weakness and difficulty gripping prior to admission. Elevated creatinine kinase and myoglobinuria are not typically present in chronic alcoholic myopathy. Considering his acute decrease in strength over the course of a few days the patient also suffered an acute alcoholic myopathy. Acute alcoholic myopathy is associated with rhabdomyolysis, acute kidney injury, and elevated creatinine kinase. Due to the patient’s altered mental status and edema it was difficult to determine whether his muscles were painful and swollen, as is typical in acute alcoholic myopathy. His altered mental status was likely multifactorial from alcohol withdrawal and encephalopathy, ICU delirium, and sedating medications early in his hospital stay.
As in our patient, acute alcoholic myopathy is self-limiting and patients recover with supportive care and improvement in renal function. Infectious and inflammatory causes of myopathy should be ruled out when considering a diagnosis of acute alcoholic myopathy. Chronic alcoholic myopathy is likely under-recognized by physicians and is highly prevalent in alcoholic populations.
Patients with chronic alcohol abuse are susceptible to acute and chronic alcoholic myopathies. By diagnosing these myopathies correctly, hospitalists can provide the appropriate care in a timely fashion.