“Beer Potomania” – A Syndrome of Severe Hyponatremia with Unique Pathophysiology: Case Studies and Literature Review

Abstract

Beer potomania, a unique syndrome of hyponatremia, was first reported in 1972. It is described as the excessive intake of alcohol, particularly beer, together with poor dietary solute intake that leads to fatigue, dizziness, and muscular weakness. The low solute content of beer, and suppressive effect of alcohol on proteolysis result in reduced solute delivery to the kidney. The presence of inadequate solute in the kidney eventually causes dilutional hyponatremia secondary to reduced clearance of excess fluid from the body. Early detection of hyponatremia due to beer potomania in the hospital is necessary to carefully manage the patient in order to avoid neurological consequences as this syndrome has unique pathophysiology. We are reporting two cases, presenting to the emergency department with severe hyponatremia. After a detailed initial evaluation of the patients and labs for hyponatremia, a diagnosis of beer potomania was established in both cases. Considering the unique pathophysiology of beer potomania syndrome, the patients were closely monitored and treated appropriately to prevent any neurological sequelae.

Magnesium, Calcium, Potassium, Sodium, Phosphorus, Selenium, Zinc, and Chromium Levels in Alcohol Use Disorder: A Review

“…The low content of nutrients in beer and the suppressing effect of alcohol on proteolysis cause secondary dilution hyponatremia, which leads to reduced removal of excess fluid from the body. Progeny includes severe hyponatremia (plasma sodium concentration, <110 mmol/L), hypokalemia, low blood urea nitrogen (indicating low protein intake), and maximum diluted urine (<100 mOsm/kg of water) [ 150 ].…”

Beer Potomania: A View on the Dynamic Process of Developing Hyponatremia

“…The reports of hyponatremic patients described as beer potomania first appeared in the medical literature in the early 1970’s [ 5 - 6 ]. Over the following years, more than thirty five cases have been reported with all of them as individual case reports [ 5 - 26 ]. These patients were hospitalized for symptoms and signs of various neurological impairment, including unconsciousness, seizures, confusion, and agitation.…”

The osmotic demyelination syndrome: the resilience of thalamic neurons is verified with transmission electron microscopy

“…29 In the old and current literature, number of reports of regional CPM and EPM ODS defects showed as consequences of abrupt adjustment of a temporary or chronic deficiency of the homeostatic sodium gradient. Its etiology can be found in a series of diverse afflictions, 30 such as in these exemplary list of clinical studies: alcoholism and/or combined with malnutrition, 1,19,[31][32][33][34][35][36][37][38][39][40] craniofacial and neurosurgeries, 41,42 diarrhea with AIDS, 43 excessive vomitus alone 44 or associated with pregnancy, 45,46 hyper glycemia, 47 pediatric diabetes, 48 diabetes insipidus due to cancer treatments, 49 folate deficiency, and kidney defect, 50 Grave's disease, 51 diuretic unbalance, and heart failure, [52][53][54][55] heat exhausting exercise, 56,57 liver cirrhosis, 58,59 or liver transplantation. 29,60,61 Disorders of sodium and osmotic homeostasis have been found in diverse small mammals.…”