Beer Potamania- A reversible cause of symptomatic severe hyponatremia


A Stevenson, SA Qureshi, S.G.Wijetilleka, K. Yoganathan, S. Wright, S. Ladbrookes, R.Kaushal


We present a 65 year old male brought in following a fall at home.  He had a history of T2DM, COPD and congestive cardiac failure. His drug history included, amongst others, irbesartan and furosemide, although his compliance with medications was low. His plasma sodium on admission was 104 mmol/L (136mmol-146mmol). He had normal potassium of 5.1 mmol/L (3.5-5.1mmol/L) and his renal function was normal. On examination his GCS was 13/15 and he was clinically hypervolaemic. He had was anaemic with a haemoglobin of 122 (NR 132-171) and an MCV of 110 (NR 80-100) with normal liver function tests. He had a history of alcohol abuse consuming around 20 units/day for the past 20 years. His serum osmolality was 232mosm/kg (275-295mosm/kg) with a urine osmolality of 488mosom/kg (50-1200mosm/kg) and a urinary sodium of 13mmol. His random cortisol was 635nmol/L (185-625nmol/L), he had a normal thyroid function (TSH 2.73, free T4 = 12.3pM) and a normal lipid profile (triglycerides 0.87). Chest X-ray revealed an enlarged heart with upper lobe dilation but no obvious consolidation.


The initial impression was this was hyponatraemia secondary to CCF and was initially with fluid restriction & furosemide was initiated. It was decided that given his comorbidities he was a ward-based ceiling of care only. His sodium failed to improve on this regime and in 48 hours his GCS had dropped to 6/15. He also developed a respiratory acidosis, thought to be due to fluid overload, necessitating NIV. Treatment was then commenced with careful infusion of 1.8% hypertonic saline, checking sodium levels every 6 hours. His sodium gradually increased from 106mmol/L to 128mmol/L over 72 hours. With this his GCS improved, along with his respiratory effort, he was able to be taken off NIV and has been medically stable ever since.


Learning Points:


1.     Chronic alcoholic patients are commonly found to be hyponatraemia. In this case one contributory factor was certainly fluid overload secondary to alcoholic cardiomyopathy.

2.     In beer potomania, chronic consumption of beer, which is a hypotonic alcoholic solution, combined with protein malnutrition, can lead to profound hyponatraemia.

3.     This case illustrates how the careful administration of additional solute in the form of 1.8% hypertonic saline can provide gentle correction in serum sodium leading to the patients neurological recovery, but minimizing the risk of overcorrection and central pontine myelinolysis.