Hyponatremia: Beer Potomania

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Q) Recently, we had a patient admitted for hyponatremia with
a serum sodium level of 117 mEq/L. One of the hospitalists mentioned “beer potomania” in the differential. Not wanting to look dumb, I just agreed. What is beer potomania, and how is it related to low serum sodium?

Potomania is the excessive consumption of alcoholic beverages; beer potomania is used to refer to a dilutional hyponatremia caused by excessive consumption of beer. 1 First recognized in 1971, this cause of hyponatremia is not the most common but should be in the differential if the patient is a heavy alcohol imbiber who presents with encephalopathy and low serum sodium.

When considering this diagnosis, keep in mind that hyponatremia is common among chronic alcoholics and can be due to conditions such as cirrhosis, congestive heart failure, syndrome of inappropriate antidiuretic hormone (SIADH) secretion, and hypovolemia. Less common but still belonging in the differential are pseudohyponatremia secondary to alcohol-induced severe hypertriglyceridemia and cerebral salt wasting syndrome. 2,3

Hyponatremia is generally defined as a serum sodium level of less than 135 mEq/L. When it occurs, water is drawn into the cells, causing the brain to swell (shown at right, in contrast to a normal brain at left).

Beer potomania usually manifests as altered mental status, weakness, and gait disturbance with an average serum sodium concentration of 108 mEq/L. 3 Other abnormal lab results consistent with this diagnosis include hypokalemia (mean potassium, 3 mEq/L) and low blood urea nitrogen and urine sodium levels. 2,3 Another fairly consistent finding is a recent personal history of binge drinking (more than about 5 L, or 14 cans of beer, in 24 hours) and/or history of illness (vomiting, diarrhea) that predisposed the patient to a rapid drop in serum sodium levels. 2

Based on the information presented thus far, you may ask, “Why haven’t I seen this diagnosed more often? There are a lot of beer bingers out there!” Good question. Let’s review the pathophysiology of beer potomania. When patients have poor protein and solute (food, electrolytes) intake, they can experience water intoxication with smaller-than-usual volumes of fluid. The kidneys need a certain amount of solute to facilitate free water clearance (the ability to clear excess fluid from the body). A lack of adequate solute results in a buildup of free water in the vascular system, leading to a dilutional hyponatremia. 3

Free water clearance is dependent on both solute excretion and the ability to dilute urine. Someone consuming an average diet will excrete 600 to 900 mOsm/d of solute. This osmolar load in-cludes urea generated from protein (10 g of protein produces about 50 mOsm of urea), along with dietary sodium and potassium. The maximum capacity for urinary dilution is 50 mOsm/L. In a nutritionally sound person, a lot of fluid—about 20 L—would be required to overwhelm the body’s capacity for urinary dilution. 2

However, when you don’t eat, the body starts to break down tissue to create energy to survive. This catabolism creates 100 to 150 mOsm/d of urea, allowing you to continue to appropriately excrete a moderate amount of fluid in spite of poor solute intake ... as long as you are not drinking excessive amounts of water. 5

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