Beer potomania syndrome: Difference between revisions

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==Background==
==Background==
*Constellation of [[electrolyte abnormalities]] that occur secondary to overconsumption of electrolyte-poor liquid with little other sources of nutrition (e.g. drinking a lot of beer and not eating much)
*Poor overall electrolyte intake limits formation of normal renal urea gradient-->inability to excrete sufficient free water
*Total body sodium may be depleted, yet still may have elevated urinary sodium/[[FENa]] due to dysfunction of water metabolism
*Attention to proper nutrition during acute illness may obviate need for hypertonic saline


==Clinical Features==
*History of chronic alcohol ingestion (in a hypotonic form like beer)
*Protein malnutrition
*[[Seizures]]
*[[Altered Mental Status]]
*[[Weakness]]


The pathophysiology involves the inability to excrete sufficient free water, based on a loss of normal renal urea gradients. Patients may actually be total-body sodium depleted, yet have elevated urinary sodium and fractional sodium excretion due to this disorder of water metabolism. Attention to proper nutrition during the acute illness may obviate the need for potentially hazardous administration of hypertonic saline
==Differential Diagnosis==
{{Ethanol DDX}}


==Evaluation==
===Work-Up===
*Chem 10
*Osmolality
*ADH


==Diagnosis==
===Evaluation===
*Signs, symptoms and laboratory values consistent with water intoxication
**[[Hyponatremia]]
**Hypochloremia
**[[Hypokalemia]]
*No evidence of another cause of hyponatremia (such as [[steroid]]] use, [[diuretic]] use, hyperlipidaemia, etc.)


==Management==
*If seizing or other severe symptoms, bolus [[hypertonic saline]]
*Otherwise, gentle replacement of electrolytes with close attention paid to diet is important


1) a history of chronic alcohol ingestion (in a hypotonic form)2) protein malnutrition3) signs, symptoms and laboratory values consistent with water intoxication, including hyponatraemia, hypochloraemia and, usually, hypokalaemia4) no evidence of another cause of hyponatraemia such as steroid use, diuretic use, hyperlipidaemia, etc. ==Work-Up==
==Disposition==
 
Admit patient with:
 
*[[Seizures]]
Chem 10 ==DDx==
*[[altered mental status]]
 
*Severe [[hyponatremia]]
 
Insert ==Treatment==
 
 
Insert ==Disposition==
 
 
Insert
 


==See Also==
==See Also==
*[[Ethanol toxicity]]


 
==References==
Tox: ETOH Intoxication
<references/>
 
*Va Med. 1989 Jun;116(6):270-1.  Beer potomania syndrome in an alcoholic.  Harrow AS.
Tox: ETOH Withdrawl
 
 
==Source==
 
 
Va Med. 1989 Jun;116(6):270-1.  Beer potomania syndrome in an alcoholic.  Harrow AS.
 

 


[[Category:FEN]]
[[Category:FEN]]
[[Category:Toxicology]]

Latest revision as of 22:10, 18 October 2023

Background

  • Constellation of electrolyte abnormalities that occur secondary to overconsumption of electrolyte-poor liquid with little other sources of nutrition (e.g. drinking a lot of beer and not eating much)
  • Poor overall electrolyte intake limits formation of normal renal urea gradient-->inability to excrete sufficient free water
  • Total body sodium may be depleted, yet still may have elevated urinary sodium/FENa due to dysfunction of water metabolism
  • Attention to proper nutrition during acute illness may obviate need for hypertonic saline

Clinical Features

Differential Diagnosis

Ethanol related disease processes

Evaluation

Work-Up

  • Chem 10
  • Osmolality
  • ADH

Evaluation

  • Signs, symptoms and laboratory values consistent with water intoxication
  • No evidence of another cause of hyponatremia (such as steroid] use, diuretic use, hyperlipidaemia, etc.)

Management

  • If seizing or other severe symptoms, bolus hypertonic saline
  • Otherwise, gentle replacement of electrolytes with close attention paid to diet is important

Disposition

Admit patient with:

See Also

References

  • Va Med. 1989 Jun;116(6):270-1. Beer potomania syndrome in an alcoholic. Harrow AS.