Abstract
A 63-year-old white man with a history of schizophrenia plus polysubstance and alcohol abuse was seen by his primary care physician during a routine visit, at which time he was found to have a serum sodium concentration of 113 mmol/L. The patient was contacted by phone and advised to return to Urgent Care for assessment, but he did not respond until 7 days later, at which time his serum sodium concentration was 106 mmol/L. He reported that he felt fine the day before but that he started feeling very lethargic that morning and had trouble “keeping his eyes open.” The patient was noted to be somnolent and confused. Table 1 summarizes the patient's laboratory data on admission. View this table: Table 1. Patient's laboratory results at time of admission. The patient admitted to having drunk one-half to 1 bottle of beer on the day of admission—only beer and no more than 2 beers. He later admitted, however, to a higher beer consumption of up to 12 bottles a day. He did not recall whether he had breakfast on the morning of admission, and his nutritional history was inconsistent. His severe hyponatremia and history of excessive consumption of beer, a poor source of sodium and protein, coupled with his poor intake of food was consistent with the diagnosis of beer potomania. The patient was treated with 500 mL of normal saline (300 Osm/L). The patient's serum sodium value increased to 116 mmol/L but then increased rapidly to 126 mmol/L over a 12-h period. The rapid overcorrection of sodium (10 mmol/L in the first 12 h) increased the risk of osmotic demyelination because complications have been noted if the serum sodium change is >0.55 mmol · L−1 · h−1 (>10 mmol/L in 24 h and >18 mmol/L in 48 h). The goal of the management of hyponatremia should be a sodium increase …
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