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Hyponatremia: Beer Potomania and Overcorrection RENALCONSULT Hyponatremia: Beer Potomania and Overcorrection Recently, we had a patient admitted for Q hyponatremia with a serum sodium level of 117 mEq/L. One of the hospi- talists mentioned “beer poto- mania” in the differential. Not wanting to look dumb, I just agreed. What is beer potoma- nia, and how is it related to low serum sodium? Potomania is the excessive consumption of alcoholic bever- ages; beer potomania is used to refer to a dilutional hyponatremia caused by excessive consumption 1 Source Science / Werner Mike and Carol Credit: of beer. First recognized in 1971, Hyponatremia is generally defined as a serum sodium level of less than 135 this cause of hyponatremia is not mEq/L. When it occurs, water is drawn into the cells, causing the brain to the most common but should be swell (shown at right, in contrast to a normal brain at left). in the differential if the patient is a heavy alcohol imbiber who pres- weakness, and gait disturbance nosed more often? There are a lot ents with encephalopathy and with an average serum sodium of beer bingers out there!” Good low serum sodium. concentration of 108 mEq/L.3 question. Let’s review the patho- When considering this diag- Other abnormal lab results con- physiology of beer potomania. nosis, keep in mind that hypona- sistent with this diagnosis include When patients have poor protein tremia is common among chron- hypokalemia (mean potassium, and solute (food, electrolytes) ic alcoholics and can be due 3 mEq/L) and low blood urea ni- intake, they can experience wa- to conditions such as cirrhosis, trogen and urine sodium levels.2,3 ter intoxication with smaller- congestive heart failure, syndrome Another fairly consistent find- than-usual volumes of fluid. The of inappropriate antidiuretic hor- ing is a recent personal history of kidneys need a certain amount mone (SIADH) secretion, and hy- binge drinking (more than about of solute to facilitate free water povolemia. Less common but still 5 L, or 14 cans of beer, in 24 hours) clearance (the ability to clear ex- belonging in the differential are and/or history of illness (vomit- cess fluid from the body). A lack pseudohyponatremia secondary ing, diarrhea) that predisposed of adequate solute results in a to alcohol-induced severe hyper- the patient to a rapid drop in se- buildup of free water in the vascu- triglyceridemia and cerebral salt rum sodium levels.2 lar system, leading to a dilutional wasting syndrome.2,3 Based on the information hyponatremia.3 Beer potomania usually mani- presented thus far, you may ask, Free water clearance is depen- fests as altered mental status, “Why haven’t I seen this diag- dent on both solute excretion and the ability to dilute urine. Some- Renal Consult is edited by Jane S. Davis, CRNP, DNP, a member of the Clinician Reviews editorial board, who is an NP in the Division of Nephrology at the University of Alabama at one consuming an average diet Birmingham and is the communications chairperson for the National Kidney Foundation’s will excrete 600 to 900 mOsm/d Council of Advanced Practitioners (NKF-CAP); and Kim Zuber, PA-C, MSPS, DFAAPA, who is a PA of solute. This osmolar load in- with Metropolitan Nephrology in Alexandria, Virginia, and Clinton, Maryland; she is also past chair of the NKF-CAP. This month’s responses were authored by Kristina Unterseher, MSN, cludes urea generated from protein FNP, CNN-NP, who practices at Peacehealth St. John Medical Center in Longview, Washington. (10 g of protein produces about clinicianreviews.com SEPTEMBER 2014 • Clinician Reviews 19 RENALCONSULT 50 mOsm of urea), along with later, she was readmitted for The National dietary sodium and potassium. mental status changes, and Kidney The maximum capacity for uri- MRI showed brain swelling. Foundation nary dilution is 50 mOsm/L. In a The neurologist stated this Council of nutritionally sound person, a lot was a result of the initial treat- Advanced Practitioners' of fluid—about 20 L—would be ment for her hyponatremia. (NKF-CAP) required to overwhelm the body’s How is this possible? mission is to capacity for urinary dilution.2 The cause-and-effect relation- serve as an advisory resource for the However, when you don’t eat, ship between rapid correction of NKF, nurse practitioners, physician the body starts to break down tis- chronic hyponatremia and sub- assistants, clinical nurse specialists, and the community in advancing sue to create energy to survive. sequent development of neuro- the care, treatment, and education This catabolism creates 100 to 150 logic problems was discovered of patients with kidney disease and mOsm/d of urea, allowing you in the late 1970s. Central pontine their families. CAP is an advocate to continue to appropriately ex- and extrapontine myelinolysis for professional development, crete a moderate amount of fluid (known as osmotic demyelination research, and health policies that impact the delivery of patient care in spite of poor solute intake ... as syndrome or ODS) is a neurologic and professional practice. For more long as you are not drinking ex- condition that can occur from information on NKF-CAP, visit cessive amounts of water.5 rapid sodium correction. It is di- www.kidney.org/CAP Alcoholics get a moderate agnosed by MRI, which shows hy- amount of their calories via beer perintense lesions on T2-weight- first two to three hours. Do not consumption and do not expe- ed images. Clinical signs include exceed 10 mEq/L in 24 hours or rience this endogenous protein upper motor neuron signs, pseu- 18 mEq/L in 48 hours. Exceeding breakdown or its resultant low dobulbar palsy, spastic quadripa- these limits puts patients at high urea/solute level. With low solute resis, and mental status changes risk for ODS. In fact, even when intake, dramatically lower fluid ranging from mild confusion to staying within these parameters, intake (about 14 cans of beer) will coma.2 there is some risk for overcor- overwhelm the kidneys’ ability Treatment for hyponatremia rection. It is always better to go to clear excess free water in the should be guided by symptom slowly.2,3 body.2 Fortunately, most heavy management.2,3 If a patient is as- In the patient with hyponatre- beer drinkers continue to eat at ymptomatic, a simple and effec- mia due to low solute intake (eg, least modestly, which is sufficient tive strategy is to keep NPO for beer potomania), diuresis can to avoid this rare type of hypona- 24 hours, except for medications. start spontaneously after a period tremia. Chronic alcoholics who Simple food and fluid restriction of food and fluid restriction. It can go on a drinking binge beyond will likely increase the serum so- also be initiated with just a small their normal baseline alcohol dium level because of obligate amount of solute. For example, consumption, or who develop a solute losses and urinary electro- administering an IV antibiotic flulike illness that causes elec- lyte free water loss.2,4 While the with a base solution of 100 mL of trolyte depletion (via diarrhea or first instinct is to feed these pa- normal saline or a “banana bag” vomiting), are at higher risk for tients, as they often appear mal- (an IV solution containing 0.5 to beer potomania. nourished, this can cause a solute 1 L of normal saline with multi- load leading to a too-rapid so- vitamins/minerals that cause the A clinic patient of mine dium correction. After 24 hours, if fluid to be yellow) can produce was recently admitted intake restriction is not effective, several liters of diuresis.2 Once Q to the hospital with use 0.5% normal saline but with you open the floodgate, you can hyponatremia (serum sodium, limited dosing orders, as usual unintentionally cause too-rapid 115 mEq/L). She was treated saline dosing can cause too rapid correction that could lead to ODS. with 2 L of normal saline and a correction.2 In chronic hyponatremic pa- discharged home 48 hours For symptomatic patients tients, low antidiuretic hormone later, at her baseline mental (confusion, seizures, coma), the (ADH) levels are often found; thus status with a serum sodium goal is to initially elevate sodium when a solute is introduced, there level of 132 mEq/L. Two days by 1 to 2 mEq/L per hour for the is little ADH in the system to pro- continued on page 22 >> 20 Clinician Reviews • SEPTEMBER 2014 clinicianreviews.com ® Priority Updates from the Research Literature from the Family Physicians Inquiries Network PURLs Why You Shouldn’t Start b-Blockers Before Surgery A new meta-analysis finds that initiatingb -blockers before surgery increases patients’ risk for death. Anne Mounsey, MD, Jodi M. Roque, MD, Mari Egan, MD PRACTICE CHANGER in the process of being updated, up to 30 days postop. Metoprolol Do not routinely initiate b-block- came from the DECREASE (Dutch was used in five trials, bisoprolol ers in patients undergoing inter- Echocardiographic Cardiac Risk in one trial, atenolol in two trials, mediate- or high-risk noncardiac Evaluation Applying Stress Echo- and propranolol in one trial. The surgery. b-Blockers appear to cardiography) trials. These trials primary endpoint was all-cause increase the 30-day risk for all- have been discredited due to se- mortality within 30 days. cause mortality.1 rious methodologic flaws, includ- A total of 5,264 patients were ing falsified descriptions of how randomly assigned to receive b- STRENGTH OF RECOMMENDATION outcomes were determined and blockers and 5,265 to placebo. A: Based on meta-analysis of fictitious databases.3 There were 162 deaths in the b- nine randomized controlled trials A new meta-analysis conduct- blocker group and 129 deaths in (RCTs).1 ed by Bouri et al1 that excluded the placebo group.
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