PMCCPMCCPMCC

Search tips
Search criteria 

Advanced


 
Formats
Article sections
Authors
Related links
Logo of bmjcrInstructions for authorsCurrent ToCBMJ Case Reports
 
BMJ Case Rep. 2010; 2010: bcr10.2009.2414.
Published online 2010 April 29. doi:  10.1136/bcr.10.2009.2414
PMCID: PMC3047485
Copyright 2010 BMJ Publishing Group Ltd
Reminder of important clinical lesson
Beer potomania: a case report
Nimesh Bhattarai, Poonam Kafle, and Mukta Panda
University of Tennessee, College of Medicine, Internal Medicine, Suite 208, 960 E. Third Street, Chattanooga, TN 37403, USA
Correspondence to Nimesh Bhattarai, nimsbdr/at/gmail.com
Abstract
A syndrome of hyponatraemia associated with excessive beer drinking was first recognised in 1971. This syndrome has been referred to as beer potomania. Dilutional hyponatraemia occurs due to excessive consumption of an exclusive beer diet which is poor in salt and protein. We report a case of beer potomania who improved dramatically with introduction of solute load, with no subsequent neurological sequelae.
Background
A syndrome of hyponatraemia associated with excessive beer drinking was first recognised by Demanet et al in 1971.1 This syndrome has been referred to as beer potomania. Since then more than 20 cases have been reported in the English literature. These patients usually have a history of binge drinking and poor dietary intake. Dilutional hyponatraemia occurs due to excessive consumption of an exclusive beer diet which is poor in salt and protein. The pathophysiology involves impaired free water clearance due to a low solute load.2
A 52-year-old Caucasian man with a history of chronic alcohol abuse presented to the emergency room with a reported change in his mental status for 3–4 days. On the day of presentation the patient was drowsy and lethargic. His fiancé reported decreased oral intake with excessive beer consumption of about 30 beers (12 ounces each) in the past three days. Past medical history included chronic alcohol abuse, chronic obstructive pulmonary disease, hypertension, and peptic ulcer disease with gastrointestinal bleeding in July 2008. On physical examination he was afebrile, blood pressure 123/83 mm Hg, pulse rate 83/min, respiratory rate 21/min, and oxygen saturation 93% on room air. He appeared dishevelled, and did not appear dehydrated. Although drowsy and lethargic, he communicated appropriately when aroused. He had no pupillary abnormalities, and deep tendon reflexes were normal with no focal neurological findings. He had palmar erythema and a few spider angiomas on the chest.
Pertinent laboratory data included haemoglobin 15.1 (14–18 g/dl), haematocrit 43.6 (42–52%), white blood cell count (WBC) 6.9 (4.8–10.8×103 cells/mm3), platelets 143 (130–400×103 cells/mm3), prothrombin time (PT) 13 (11.9–14.9 s), INR 0.96, sodium 107 (136–145 mmol/l), chloride 69 (98–107 mmol/l), potassium 4.0 (3.5–5.1 mmol/l), blood urea nitrogen (BUN) 3 (8.4–25.7 mg/dl), creatinine 0.40 (0.70–1.30 mg/dl), magnesium 1.4 (1.6–2.6 mg/dl), thyroid stimulating hormone (TSH) 0.510 (0.40–4.0 IU/ml), albumin 2.4 (3.5–5.0 g/dl), serum alcohol 268 mg/dl, uric acid 3.1 (3.5–7.2 mg/dl), serum osmolality 284 (270–300 mOsm/kg), urine osmolality 383 (500–800 mOsm), and urine sodium 6 mmol/l. Computed tomography (CT) scan of the head without contrast was negative for acute changes.
Treatment
The patient was admitted to the intensive care unit. He received about 1 litre of normal saline in the emergency room followed by 3% saline. Subsequently he underwent brisk diuresis and started autocorrecting his serum sodium. He received a total of 30 ml 3% saline, which was later changed to D5W to match excessive diuresis of about 6 litres in the first 24 h. His sodium increased by 21mmol/l in the first 24 h (fig 1).
Figure 1
Figure 1
Trend of sodium in the first 48 h after hospitalisation.
Outcome and follow-up
Over the next few days in hospital the patient’s sodium returned to normal and remained stable. His hospital course was complicated by respiratory failure secondary to aspiration pneumonia which required intubation and mechanical ventilation; however, he recovered well enough to be extubated and his mental status also improved and he was able to fully communicate verbally once his respiratory failure resolved.
Hyponatraemia is a common electrolyte abnormality found in up to 15–30% of hospitalised patients.3 Hyponatraemia was found in 17% of 127 chronic alcoholic patients in one study.4 Beer potomania is a well known cause of hyponatraemia. In patients with normal renal function, excessive water ingestion does not result in severe hyponatraemia because of an ability to excrete large amounts of free water.2,5 However in malnourished individuals with no solute or protein intake, as in chronic alcoholics, water intoxication can occur with smaller volumes due to loss of the urea concentrating gradient.6 There are several proposed mechanisms for hyponatraemia other than beer potomania in alcohol abusers. They include hypovolaemia, pseudohyponatraemia (due to alcohol induced severe hypertriglyceridaemia), SIADH (syndrome of inappropriate antidiuretic hormone hypersecretion), congestive heart failure and cerebral salt wasting syndrome.6 Patients with hyponatraemia due to beer potomania have a history of alcohol use and recent binging with beer.2,7
The ability of the kidney to excrete free water is dependent on solute excretion and urinary diluting capacity.7 The maximum urinary diluting capability is 50 mOsm/l. If solute excretion decreases, the ability to excrete free water becomes limited. In patients with beer potomania due to poor intake of diet other than beer, the total osmoles generated is low, impairing maximal water excretion. This results in dilutional hyponatraemia (fig 2), which explains why these patients have brisk diuresis when solute is presented.7 This brisk diuresis can rapidly increase serum sodium concentrations making replacement of this water with electrolyte-free water a challenge.
Figure 2
Figure 2
Flow chart showing mechanism of hyponatraemia in beer potomania.
A similar situation of dilutional hyponatraemia may also be found in exercise induced hyponatraemia. The mechanism in exercise induced hyponatraemia, however, involves a combination of excessive water or hypotonic fluid intake, high concentrations of antidiuretic hormone (ADH), sweat sodium loss and metabolic water production.8
Symptoms can range from vague weakness, fatigue and nausea to lethargy, agitation, confusion and seizures.2,9 Development of symptoms varies and has not been shown to correlate closely with serum sodium concentrations.10 Severe hyponatraemia is a consistent finding in beer potomania. This was shown by Sanghvi et al after review of 22 published cases of beer potomania (mean serum sodium 108 mmol/l).7 Low serum osmolality is a consistent finding2,7 (our patient presented with a serum osmolality of 284 mOsm/kg; however, a significant portion of this was contributed by very high serum alcohol level (corrected osmolality 225 mOsm/kg). Low urine osmolality is not a consistent finding and urine osmolality may be inappropriately high, although the urine sodium is usually low when reported.2 Different mechanisms including suppression of ADH by alcohol and appearance of alcohol in the urine with large volume consumption may mask the hypotonicity of urine.2,11
There is no clear cut consensus on sodium replacement in beer potomania. This should, however, be done judiciously. There is always danger of precipitating osmotic demyelination syndrome (ODS) in chronically hyponatraemic patients by infusing saline load.6 There have been case reports of osmotic demyelination with rapid sodium correction in patients with beer potomania. In a literature review done by Sanghvi et al, four of the 22 patients (18%) with beer potomania had osmotic demyelination.7 Most studies have shown that the risk of osmotic demyelination is low when sodium is corrected by less than 10–12 mEq/24 h.12–14 However, even with slower rates of correction, documented cases of ODS have occurred.15 Although development of ODS has been classically associated with infusion of hypertonic saline, it may occur with infusion of normal saline or with fluid restriction alone.14 Fortunately our patient did not have any complication of osmotic demyelination from his relatively rapid correction. At a recent encounter 1 year later he had no new findings suggestive of neurological deficits.
Learning points
  • Beer potomania is a well known cause of hyponatraemia which can occur in chronic alcoholics, especially if associated with recent binge drinking.
  • Low osmolality state can cause management and sodium replacement to be a challenge due to rapid correction of sodium with introduction of solute.
  • Benefit of hindsight—clinicians must keep this principle in mind while replacing sodium, especially with hypertonic saline, in patients with beer potomania even in severe hyponatraemia.
Footnotes
Competing interests: None.
Patient consent: Patient/guardian consent was obtained for publication.
REFERENCES
1. Demanet JC, Bonnyns M, Bleiberg H, et al. Coma due to water intoxication in beer drinkers. Lancet 1971; 2: 1115–7. [PubMed]
2. Fenves AZ, Thomas S, Knochel JP. Beer potomania: two cases and review of the literature. Clin Nephrol 1996; 45: 61–4. [PubMed]
3. Upadhyay A, Jaber BL, Madias NE. Incidence and prevalence of hyponatremia. Am J Med 2006; 119(7 Suppl 1): S30–5. [PubMed]
4. Liamis GL, Milionis HJ, Rizos EC, et al. Mechanisms of hyponatraemia in alcohol patients. Alcohol Alcoholism 2000; 35: 612–6. [PubMed]
5. Fanestil DD. Hypoosmolar syndromes. : Andreoli T, Grantham JJ, Rector FC Jr, editors. , eds. Disturbances in body fluid osmolality. American Physiological Society, 1977: 267–84.
6. Kelly J, Wassif W, Mitchard J, et al. Severe hyponatraemia secondary to beer potomania complicated by central pontine myelinolysis. Int J Clin Pract 1998; 52: 585–7. [PubMed]
7. Sanghvi SR, Kellerman PS, Nanovic L. Beer potomania: an unusual cause of hyponatremia at high risk of complications from rapid correction. Am J Kidney Dis 2007; 50: 673–80. [PubMed]
8. Rosner MH. Exercise-associated hyponatremia. Seminars in Nephrology 2009; 29: 271–81. [PubMed]
9. Joyce SM, Potter R. Beer potomania: an unusual cause of symptomatic hyponatremia. Ann Emerg Med 1986; 15: 745–7. [PubMed]
10. Arieff AI, Llach F, Massry SG. Neurological manifestations and morbidity of hyponatremia: correlation with brain water and electrolytes. Medicine (Baltimore) 1976; 55: 121–9. [PubMed]
11. Eisenhofer G, Johnson RH. Effect of ethanol ingestion on plasma vasopressin and water balance in humans. Am J Physiol 1982; 242: R522–7. [PubMed]
12. Ellis SJ. Severe hyponatraemia: complications and treatment. QJM 1995; 88: 905–9. [PubMed]
13. Sterns RH, Riggs JE, Schochet SS., Jr Osmotic demyelination syndrome following correction of hyponatremia. N Engl J Med 1986; 314: 1535–42. [PubMed]
14. Karp BI, Laureno R. Pontine and extrapontine myelinolysis: a neurologic disorder following rapid correction of hyponatremia. Medicine (Baltimore) 1993; 72: 359–73. [PubMed]
15. Pradhan S, Jha R, Singh MN, et al. Central pontine myelinolysis following ‘slow’ correction of hyponatremia. Clin Neurol Neurosurg 1995; 97: 340–3. [PubMed]
Articles from BMJ Case Reports are provided here courtesy of
BMJ Group