School of Medicine and Health Sciences Poster Presentations

Title

Beer Potomania: A Challenging Case of Hyponatremia

Poster Number

181

Document Type

Poster

Publication Date

3-2016

Abstract

Beer potomania is a syndrome of hyponatremia associated with excessive beer drinking. Little or no salt content of beer, and suppression of protein breakdown by the carbohydrate and alcohol content of beer, result in marked reduction in the solute load to the kidney. This leads to impaired water clearance and a dilutional hyponatremia. Beer potomania is difficult to recognize especially in the presence of other factors commonly affecting sodium excretion.

A 66 year-old man with history of alcoholism and alcoholic cardiomyopathy presented to the emergency room with tremors of his upper and lower extremities. History dated back to 6 days prior to presentation when he developed tremors of all four extremities, and was unable to walk. He had a significant history of alcohol consumption, usually drinking 4 to 5 cans of beer per night for the past 34 years. In addition, he had consumed a fifth of a vodka bottle the day before presentation. He had a pattern of often skipping meals though was compliant with both his diuretics medications: furosemide 40 mg once daily and spironolactone 25 mg daily. He was not on any antipsychotic or antidepressant drugs. His history was negative for seizures, confusion or somnolence. He denied diarrhea, vomiting, cold intolerance, shortness of breath, swelling, or excessive water intake. On physical exam, he was euvolemic with no JVD, lower extremity edema or pulmonary crackles. Neurological exam revealed resting tremors of both his hands. Labs were remarkable for plasma sodium of 122, BNP of 474, serum osmolality of 268, urine osmolality of 223, and urine sodium of 20. Patient was assessed to have severe euvolemic hypotonic hyponatremia. The combination of euvolemic hyponatremia with history of excessive beer drinking made beer potomania very likely. His urine osmolality and urine sodium, however were higher than expected in beer potomania. These could be explained by the two diuretics that the patient was taking. Furthermore, patient’s poor nutritional intake added to the severity of his hyponatremia. History, physical exam and lab testing excluded SIADH and hypothyroidism. Patient was managed with fluid restriction, appropriate nutritional and sodium intake and withholding of his diuretics. Plasma sodium slowly corrected to 130 over the course of 3 days.

This case illustrates the condition beer potomania, an infrequent cause of hyponatremia. Findings in hyponatremia do not always point in one direction, especially with the concomitant use of diuretics. Understanding of pathophysiology can be useful in interpreting lab results. Recognition of beer potomania as a separate entity of hyponatremia is critical. Management should be tailored for this specific etiology, as if unrecognized can lead to serious neurologic sequelae and even death. Patient education and alcohol related counseling, is essential to prevent recurrence.

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Presented at: GW Research Days 2016

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Beer Potomania: A Challenging Case of Hyponatremia

Beer potomania is a syndrome of hyponatremia associated with excessive beer drinking. Little or no salt content of beer, and suppression of protein breakdown by the carbohydrate and alcohol content of beer, result in marked reduction in the solute load to the kidney. This leads to impaired water clearance and a dilutional hyponatremia. Beer potomania is difficult to recognize especially in the presence of other factors commonly affecting sodium excretion.

A 66 year-old man with history of alcoholism and alcoholic cardiomyopathy presented to the emergency room with tremors of his upper and lower extremities. History dated back to 6 days prior to presentation when he developed tremors of all four extremities, and was unable to walk. He had a significant history of alcohol consumption, usually drinking 4 to 5 cans of beer per night for the past 34 years. In addition, he had consumed a fifth of a vodka bottle the day before presentation. He had a pattern of often skipping meals though was compliant with both his diuretics medications: furosemide 40 mg once daily and spironolactone 25 mg daily. He was not on any antipsychotic or antidepressant drugs. His history was negative for seizures, confusion or somnolence. He denied diarrhea, vomiting, cold intolerance, shortness of breath, swelling, or excessive water intake. On physical exam, he was euvolemic with no JVD, lower extremity edema or pulmonary crackles. Neurological exam revealed resting tremors of both his hands. Labs were remarkable for plasma sodium of 122, BNP of 474, serum osmolality of 268, urine osmolality of 223, and urine sodium of 20. Patient was assessed to have severe euvolemic hypotonic hyponatremia. The combination of euvolemic hyponatremia with history of excessive beer drinking made beer potomania very likely. His urine osmolality and urine sodium, however were higher than expected in beer potomania. These could be explained by the two diuretics that the patient was taking. Furthermore, patient’s poor nutritional intake added to the severity of his hyponatremia. History, physical exam and lab testing excluded SIADH and hypothyroidism. Patient was managed with fluid restriction, appropriate nutritional and sodium intake and withholding of his diuretics. Plasma sodium slowly corrected to 130 over the course of 3 days.

This case illustrates the condition beer potomania, an infrequent cause of hyponatremia. Findings in hyponatremia do not always point in one direction, especially with the concomitant use of diuretics. Understanding of pathophysiology can be useful in interpreting lab results. Recognition of beer potomania as a separate entity of hyponatremia is critical. Management should be tailored for this specific etiology, as if unrecognized can lead to serious neurologic sequelae and even death. Patient education and alcohol related counseling, is essential to prevent recurrence.