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 (), 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.
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.
- 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.