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Introduction: Alcohol use disorder affects close to 20 million people in the United States. Alcohol causes long term damage in various organs including the muscles resulting in alcoholic myopathy. However, other less common etiologies for acute muscle weakness should be considered in these patients. Case presentation: Our patient is a 25 year-old Hispanic male, who presented with 2 hours of acute lower extremity weakness. He had difficulty walking, clothing, grasping and reported myalgia. He admitted to partying and binge drinking while consuming pizza and burgers the night before. He denied similar episodes in the past or any family history of weakness. His physical exam was remarkable for 2/5 strength in the hip flexors bilaterally, hip and knee extension was 4/5 bilaterally, knee flexion was 4/5 bilaterally. He had hyporeflexia, normal muscle bulk and tone and normal sensation. Diagnostic work up revealed a potassium of 1.9 mmol/L, phosphorus 1.9 mmol/L and CK of 176 IU/L (22-269 IU/L). Due to concern for thyrotoxic periodic paralysis, TSH was checked which was normal at 0.47 MCIU/ml (0.550-4.780 MCIU/ml). He was given 40meq IV potassium by slow infusion, followed by 40meq PO. His potassium improved to 2.4mmol/L after supplementation and there was a rapid recovery in his muscle weakness. Potassium levels were monitored for 24 hours. He had persistently normal potassium levels during his stay. His lower motor strength remained to be a 5/5 throughout the hospitalization. He was discharged with counseling and emphasis on alcohol cessation. Discussion: Beer contains 13 grams of CHO in 1 can. It’s high carbohydrate content can result in an insulin surge producing a rapid intracellular shift of potassium through N-K ATPase channels. This produces hypokalemic periodic paralysis (HPP) in predisposed patients. HPP is an uncommon neuromuscular disorder with 1 in 100,000 cases. It results from mutations in sodium, calcium and potassium channels in the skeletal muscles. It is an autosomal dominant disease and found predominantly in young Asian males. These patients are at risk for fatal cardiac arrhythmias due to their significantly low potassium levels on presentation. They carry the same risk for arrhythmias in the treatment period due to increased risk of over-correction resulting in hyperkalemia. Long term recurrent HPP can result in progressive proximal myopathy and reduced functional mobility that may affect quality of life. These short and long term complications in HPP can only be prevented by avoidance of triggers, in our case avoidance of alcohol consumption. Rapid recognition for close electrolyte monitoring and effective counseling by physicians to establish a clear understanding in patients is imperative for their long term health. (1)Vilarinho S, Siegel M D. Paralysis caused by a large carbohydrate meal. J Postgrad Med 2012;58:60-1 |
