This is a case of beer potomania, which is a very specific case of hypotonic hyponatremia. Humans need solute in order to produce urine. These solutes are predominantly sodium, potassium and urea, along with others.
Beer contains little to no sodium or potassium. Drinking only 50 beers daily for weeks causes solute loss, on top of vitamin deficiency and poor nutrition.
Slowly as sodium is depleted, more volume from beer is accumulated in the body.
Beer contains water, alcohol and carbohydrates, the latter which induces an insulin response in the body to prevent muscle catabolism.
Muscle catabolism could count as protein that would produce urea, but because of insulin response, it doesn’t happen, further exacerbating solute loss.
The accumulation of water in the body and depletion of solute leads to chronic hyponatremia. This is because the kidneys need solute exchange in the process of urine production. If these solutes are absent, minimal urine is produced, and the urine that is produced is maximally dilute (eg low specific gravity) Neurologic sequelae from low sodium presence in blood include seizures and is an emergency.
In this patient, it wasn’t clear whether he was suffering withdrawal syndrome, chronic hyponatremia, or both. In the case as it happened, the hospital ran out of medicines for the SE because it was so frequent, and needed to borrow twice from neighboring hospitals.
Osmotic demyelination syndrome appears to have a higher risk in patients who have more electrolyte abnormalities and metabolic derangements. Please see references for more information.
These cases are patients who I, or my colleagues have seen. They are de-identified and many instances have been presented in more depth in an academic setting. These videos are not individual medical advice and are for general educational purposes only. I do not give medical advice over the internet, see your own physician in person for that.
Additional radiology images provided by Radiopaedia and Wellcome Collection
References: An experimental study of the etiology of rum fits and delirium tremens. Q J Stud Alcohol. 1955;16(1):1.  Sites of alcohol and volatile anaesthetic action on GABA(A) and glycine receptors. Nature. 1997;389(6649):385.  Chronic ethanol administration alters gamma-aminobutyric acid, pentobarbital and ethanol-mediated 36Cl- uptake in cerebral cortical synaptoneurosomes. J Pharmacol Exp Ther. 1988;246(1):158.  Electrolyte disturbances in beer drinkers. A specific “hypo-osmolality syndrome”. Lancet. 1975;2(7928):245.  “Beer potomania” in non-beer drinkers: effect of low dietary solute intake. Am J Kidney Dis. 1998;31(6):1028.  Lancet. 2002;359(9310):942.  NMDA receptors: role in ethanol withdrawal seizures. Ann N Y Acad Sci. 1992 Jun 28;654:52-60.  Central pontine myelinolysis induced by hypophosphatemia following Wernicke’s encephalopathy. Neurol Sci (2003) 24:407–410
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