What is beer potomania?

Beer Potomania: Definition and Clinical Syndrome

Beer potomania is a syndrome of severe hyponatremia caused by excessive beer consumption combined with poor dietary solute intake, resulting in impaired free water excretion. 1

Pathophysiology

The critical mechanism involves two key factors that create a perfect storm for dilutional hyponatremia:

• Beer has extremely low solute content (typically <100 mOsm/L), which creates a fundamental problem for renal water excretion 1
• The minimal solute intake combined with the hypoosmolality of beer leads to the kidney's inability to excrete sufficient free water to match the large volume of hyposmolar beer ingested 2
• Alcohol suppresses proteolysis, further reducing solute delivery to the kidney 3
• The reduced solute delivery to the kidney eventually causes dilutional hyponatremia secondary to impaired clearance of excess fluid 3

Clinical Presentation

Patients typically present with a characteristic pattern:

• History of binge beer drinking with poor dietary intake 2
• Mental status changes, seizures, fatigue, dizziness, and muscular weakness 2, 3
• Severe hyponatremia (often <120 mmol/L, sometimes as low as 111 mmol/L) 2, 4
• Concurrent electrolyte abnormalities including hypokalemia and hypomagnesemia 4
• Very dilute urine despite severe hyponatremia 2

Critical Management Principles

Immediate Actions

Discontinue alcohol immediately and initiate cautious sodium correction, with maximum increases of 4-6 mmol/L per day. 1

Correction Rate Limitations

• Beer potomania patients are at extremely high risk for osmotic demyelination syndrome (ODS) during correction 1
• Correction rates should be strictly limited to 4-6 mmol/L per day 1
• Even rates previously considered "safe" (up to 10 mmol/L per 24 hours) have resulted in central pontine myelinolysis in beer potomania patients 5

Fluid Management Strategy

• For severe symptoms, administer isotonic saline cautiously with sodium monitoring every 2 hours initially 1
• A critical pitfall: Initial normal saline administration can cause massive diuresis (up to 3,500 mL in 6 hours), leading to dangerously rapid sodium correction 4
• If overcorrection occurs, immediately administer 5% dextrose and vasopressin to prevent further sodium rise 4

Concurrent Electrolyte Management

Correct hypokalemia and hypomagnesemia aggressively, as these impair vasopressin responsiveness and perpetuate polyuria. 1, 4

• Severe hypokalemia (<2.0 mmol/L) and hypomagnesemia can render vasopressin ineffective in controlling diuresis 4
• Restoration of potassium and magnesium levels is essential before vasopressin can adequately control urine output 4

Key Clinical Pitfall

The most dangerous aspect of beer potomania is the paradoxical response to treatment: patients respond quickly to sodium-containing IV fluids, but this rapid response creates the risk of overcorrection 2. The syndrome has unique pathophysiology where simply stopping beer intake and providing normal diet can correct the electrolyte imbalance, making aggressive IV correction potentially more harmful than beneficial unless life-threatening neurological complications are present 5.