Potomania

Not to be confused with Dipsomania.

Potomania
Other names	Beer potomania, Beer drinker's potomania, Beer drinker's hyponatremia, Frat boy syndrome
Annual beer consumption per capita.
Symptoms	hyponatremia
Risk factors	alcoholism

Potomania (From Greek pōtō "drink (liquor)" + mania) is a specific hypo-osmolality syndrome related to massive consumption of beer, which is poor in solutes and electrolytes. With little food or other sources of electrolytes, consumption of large amounts of beer or other dilute alcoholic beverages leads to electrolyte disturbances, where the body does not have enough nutrients known as electrolytes, namely sodium, potassium, and magnesium. The symptoms of potomania are similar to other causes of hyponatremia and include dizziness, muscular weakness, neurological impairment and seizures, all related to hyponatremia and hypokalaemia. While the symptoms of potomania are similar to other causes of hyponatremia and acute water intoxication, it should be considered an independent clinical entity because of its often chronic nature of onset, pathophysiology, and presentation of symptoms.

Pathophysiology

The normal human kidney, through suppression of anti-diuretic hormone, is able to excrete vast amounts of dilute urine. Healthy adult kidneys are able to excrete over 20 liters of water each day. However, maximum hourly rates rarely exceed 800 to 1,000 mL/hr. The intake of solutes is necessary to excrete free water. Under normal circumstances, this is clinically irrelevant. In the lack of proper solute intake, the amount of free water excretion can be severely limited. Without adequate solute intake, the normal functioning electrolyte gradient that pulls water into urine will be effectively destroyed.

To excrete water the kidney must also excrete solute. Solute presented to the kidney is derived from the diet in the form of electrolytes such as sodium, chloride and potassium. The other main solute is blood urea nitrogen which is created from protein metabolism. The kidney is able to excrete urine with a broad range of osmolalities - roughly 40 to 1200mOsmol/kg. It cannot excrete urine that is more dilute than 40mOsmol/kg. A normal diet provides a renal solute load of approximately 600mOsmol/kg. An individual with a normal diet can therefore excrete up to 15L of water per day (600/40). If a person has a very poor dietary intake of electrolytes and either eats very little protein (and/or inhibits protein metabolism by the intake of carbohydrate) - which is very characteristic of alcoholics - then the renal solute load may fall below a level that is sufficient to clear the volume of water ingested. Although beer has a relatively high osmolality due to the ethanol concentration (standard beer osmolality is roughly 1000mOsmol/kg) it provides little renal solute contribution and is low in sodium. If the dietary/renal solute load is less than the volume of water ingested (in litres divided by 40) then the excess free water will be retained leading to dilutional hyponatremia. For example if the renal solute load is 200 the maximum water able to be excreted per 24 hours is 5L. If the person drinks 6L of beer then 1L per day will be retained as free water.

Any vomiting or GI absorptive problems due to alcohol intoxication can also compound the effect of potomania due to additional electrolyte and acid-base disturbances.

Diagnosis

The diagnosis of potomania requires both clinical and biochemical criteria.

Hypotonic hyponatremia

Dilute urine (< 100mOsmol/kg) although this finding is variable in the few cases described in the medical literature

Clinical evidence of excessive beer (or equivalent alcoholic drinks such as cider) consumption often accompanied by evidence of poor dietary intake.

No alternative diagnosis that is considered more likely.

Treatment

Patient with severe hyponatremia are at risk of cerebral oedema, coma and seizures. International guidelines recommend the use of hypertonic saline to treat profound hyponatremia with severe neurological symptoms. For less severe symptoms restoring a normal diet and restricting alcohol intake reverses the abnormality as there is no underlying physical disease.

The rise in serum sodium due to redistribution alone can be estimated from the following equation.

${\text{Na}}_{\text{final}}={\frac {({\text{Na}}_{\text{serum}}\times {\text{ECF}})+({\text{Na}}_{\text{infusate}}\times V_{\text{infusate}})}{{\text{ECF}}+V_{\text{infusate}}}}$

Where Na_serum is the concentration of the patient's plasma sodium, ECF is an estimate of extracellular water in litres (approximately body weight in kg x 0.2 for males and body weight x 0.17 for females), Na_infusate is the sodium concentration of the IV fluid and V_infusate is the volume of the IV fluid in litres. For a 100kg man with a plasma Na of 105mmol/L given 300mLs of 2.7% saline (462mmol of Na) the final dilution of plasma sodium would only be 110mmol/L.

${\frac {(105\times 20)+(462\times 0.3)}{20+0.3}}=110.3$

This initial 5mmol/L rise is usually sufficient to stabilise the patient's acute neurological deterioration due to cerebral oedema. Note that it is a rise in osmolality that is the treatment aim rather than Na itself - however for simplicity the Na is used as a measure of the osmolality and the osmolar rise will be roughly twice the Na rise. Direct measurement of osmolality would be preferable but the turnaround time in most hospital laboratories is too long to be useful so serum Na is used and therapeutic targets are set against this.

Patients with potomania are a particularly high risk subgroup for the development of osmotic demyelination syndrome (ODS). This is not because of the immediate rise in osmolality due to the hypertonic saline from the redistribution calculated above. Rather the treatment can induce a water diuresis as a secondary phenomena.

However after the initial rise from this mixing of 300mLs of 2.7% saline with the patients blood there is an osmotic load (Na⁺ + Cl^-) of 277mOsmol/kg available to the kidneys. With this load the patient could then potentially produce a water diuresis of up to 7L (277 / 40). This secondary water diuresis (sometimes termed aquaresis) usually happens in the subsequent 24 hours. It is this secondary water diuresis that can cause a very rapid rise in serum osmolality, sometimes greater then 2mmol/L/hr which can lead to ODS. Physicians treating patients at high risk of ODS should both measure plasma Na every 3-4 hours and also the urine output for at least 24 hours. If a brisk diuresis does occur (>2mL urine per kg body weight per hour) prophylactic desmopressin (4mg 8 hourly IV) can be given to limit free water clearance. If the patient does overshoot the recommended rise (10mmol/l in 24 hours and 18mmol/l in 48 hours) bolus 5% dextrose in water can be given to bring the Na level back down to target levels.

See also

• Alcohol (drug)
• Holiday heart syndrome
• Hyponatremia
• Primary polydipsia
• Water intoxication

References

• Hilden, T; Svendsen, T. L. (1975). "Electrolyte Disturbances in Beer Drinkers: a Specific 'Hypo-osmolality Syndrome'". The Lancet. 306 (7928): 245–246. doi:10.1016/S0140-6736(75)90961-7. PMID 49796. S2CID 12873417.)
• Harrow, A. S. (1989). "Beer potomania syndrome in an alcoholic". Virginia Medical. 116 (6): 270–271. PMID 2763635.
• "Beer Potomania". renalfellow.org. 2009-03-12. Retrieved 2025-02-22.
• Berl, T. (2008). "Impact of Solute Intake on Urine Flow and Water Excretion". Journal of the American Society of Nephrology. 19 (6): 1076–1078. doi:10.1681/ASN.2007091042. PMID 18337482.