Beer Potomania Research Articles

Treating Profound Hyponatremia: A Strategy for Controlled Correction

An alcoholic patient presented with profound hyponatremia (serum sodium concentration, 96 mEq/L) caused by the combined effects of a thiazide diuretic, serotonin reuptake inhibitor, beer potomania, and hypovolemia. A computed tomographic scan of the brain was indistinguishable from one obtained 3 weeks earlier when he was normonatremic. Concurrent administration of 3% saline solution and desmopressin controlled the rate of correction to an average of 6 mEq/L daily and resulted in full neurologic recovery without evidence of osmotic demyelination. This case illustrates the value of controlled correction of profound hyponatremia.

Hyponatremia at autopsy: an analysis of etiologic mechanisms and their possible significance

While electrolyte measurements after death may be confounded by a number of variables, vitreous humor sodium tends to remain stable for some time, enabling correlation between ante- and postmortem levels. Review of natural and unnatural causes of reduced vitreous humor sodium levels at autopsy was undertaken to demonstrate the range of diseases that may result in this finding. Natural diseases affecting the vasopressin-renin-angiotensin axis may cause reduction in sodium levels with associated hypovolemia, euvolemia, and hypervolemia. Low sodium measurements may also occur with redistribution of water, and artefactually when there are underlying lipid and protein disorders. Unnatural causes of hyponatremia at autopsy include water intoxication from psychogenic polydipsia, environmental polydipsia, ingestion of dilute infant formulas, beer potomania, endurance exercise, fresh water immersion (including water births) and iatrogenic causes including drug and parenteral fluid administration, and surgical irrigation. A knowledge of the range of conditions that may result in lowered postmortem sodium levels will help to exclude or confirm certain diseases at autopsy. In addition, significant vitreous hyponatremia may be a useful finding to help clarify mechanisms of unnatural deaths.

Beer Potomania: An Unusual Cause of Hyponatremia at High Risk of Complications From Rapid Correction

Beer Potomania: An Unusual Cause of Hyponatremia at High Risk of Complications From Rapid Correction

184: Beer Potomania: A Unique Cause of Hyponatremia at High Risk of Complications from Rapid Correction

184: Beer Potomania: A Unique Cause of Hyponatremia at High Risk of Complications from Rapid Correction

Rapid Correction of Severe Hyponatremia After Computed Tomography With Intravenous Contrast

To the Editor: Overly rapid correction of hyponatremia is a major concern in severely hyponatremic patients because of the potential development of osmotic demyelination. Numerous factors can contribute to overly rapid correction of hyponatremia (Table 1).1Pham P-CT Pham P-MT Miller J et al.Treatment of chronic hyponatremia.Proc UCLA Healthcare. Fall 2002; 6: 32-36Google Scholar We report a case in which a patient developed osmotic diuresis after contrast dye injection that rapidly self-corrected the severe hyponatremia.TABLE 1Potential Causes of Overly Rapid Correction of HyponatremiaAdapted from Proceedings of UCLA HealthCare,1Pham P-CT Pham P-MT Miller J et al.Treatment of chronic hyponatremia.Proc UCLA Healthcare. Fall 2002; 6: 32-36Google Scholar with permission. Unawareness of the recommended rate of correction for hyponatremiaMiscalculationsUnrecognized sources of sodium Exogenous Sodium administration at another site before transfer to the current unitAddition of excess salt to patient's diet by patient's family or facility staff membersEndogenous Potassium supplementation with resultant extracellular sodium shiftExcess free water loss Water deprivation in primary polydipsiaWithdrawal of thiazide diuretics during treatment of hyponatremiaGlucocorticoid replacement in a cortisol-deficient patientRecovery from acute respiratory failureExcessive gastrointestinal, pulmonary, or skin hypotonic fluid lossSevere hyponatremia with subsequent cerebral edema and pituitary infarctionNonelectrolyte osmotic diuresis: urea, glucose, mannitol, contrast dye, total parenteral nutritionIntracellular free water shift SeizuresRhabdomyolysisCorrection of hyperglycemiaPotassium supplementation Open table in a new tab Report of a Case. A 59-year-old woman with diabetes mellitus and hypertension presented with a 1-week history of slow mentation, fatigue, nausea, vomiting, abdominal pain, and subjective left hemiparesthesia. A dietary history revealed that she routinely ate only fruits and cereals and drank only water. Her medications included hydrochlorothiazide, fosinopril, atenolol, metformin, and aspirin. Physical examination revealed dry oral mucosa, slow mentation, and generalized sluggish deep tendon reflexes. On initial evaluation, the serum sodium concentration was 115 mEq/L, and urinary studies revealed an osmolality of 526 mosm/kg, a sodium level of 130 mEq/L, and a chloride level of less than 10 mEq/L. The patient was given two 500-mL boluses of normal saline during the first 12 hours of hospitalization. In the interim, she underwentcomputed tomography of the head and abdomen with intravenous contrast (iohexol). Despite correction of the hypovolemia, the patient had no improvement in her symptoms or serum sodium concentration during the first 24 hours. However, approximately 24 to 26 hours after presentation, she developed progressive polyuria (up to 150-175 mL/h). During the polyuric phase, the urine osmolality ranged from 217 to 393 mosm/kg. During the subsequent few hours, the patient's mentation noticeably improved in association with a spontaneous rapid increase in serum sodium concentration (8 mEq/L over 6 hours). In fact, hypotonic saline had to be administered to halt the rapid self-correction of the hyponatremia. Given the patient's history of poor dietary nutrition, use of hydrochlorothiazide, and current pain and vomiting, we suspected that the hyponatremia resulted from ongoing water intake concurrent with the patient's inability to excrete free water maximally because of a reduced dietary solute load and syndrome of inappropriate secretion of antidiuretic hormone-induced enhanced free water reabsorption.2Fichman MP Vorherr H Kleeman CR Telfer N Diuretic-induced hyponatremia.Ann Intern Med. 1971; 75: 853-863Crossref PubMed Scopus (239) Google Scholar, 3Thaler SM Teitelbaum I Berl T “Beer potomania” in non-beer drinkers: effect of low dietary solute intake.Am J Kidney Dis. 1998; 31: 1028-1031Abstract Full Text Full Text PDF PubMed Scopus (89) Google Scholar Despite saline infusion, the patient's serum sodium concentration remained at 115 mEq/L 12 to 18 hours after presentation, presumably a reflection of the sustained syndrome of inappropriate secretion of antidiuretic hormone caused by her nausea and pain. However, by 24 hours after presentation, the patient had a rapid increase in urinary output as well as serum sodium concentration despite the discontinuation of all intravenous fluids at least 6 hours previously. At that point, the patient possibly had adequate volume reexpansion, reduced proximal tubular reabsorption of salt and water, and resultant increased distal delivery for excretion. In addition, the control of nausea and pain and the volume reexpansion may have inhibited antidiuretic hormone secretion sufficiently to result in the aquaretic phase. However, subsequent urinary electrolyte studies revealed high osmolality (217-393 mosm/kg) relative to serum osmolality (240-264 mosm/kg), which suggested that she had osmotic diuresis, not aquaresis. Further analysis of her urine by ultraviolet spectrophotometry revealed that the predominant source of the urine osmolality during the polyuric phase was the contrast dye iohexol. The findings in this case are important because computed tomography with intravenous contrast is performed routinely for the evaluation of nonspecific complaints in severely hyponatremic patients.

Crash diet potomania

most commonly reported in beer drinkers (beer potomania), since beer contains no protein, very little salt (2-4 mmol/L) and a lot of water. It has also been described in a person who consumed fairly modest amounts of water (4 to 5 L per day) whilst eating an ovolactovegetarian diet which generated a low solute load. These patients are frequently hypokalaemic and often pass sub-maximally dilute urine. In this patient, the thiazide may have contributed to her sub-maximal urine dilution by inhibiting sodium reabsorption in the distal convoluted tubule thereby increasing urine osmolality.

Mechanisms of hyponatraemia in alcohol patients.

Hyponatraemia is commonly reported in chronic alcoholic patients. However, the underlying pathogenetic mechanisms are not well delineated. In the current study, we analysed the possible pathophysiological mechanisms of hyponatraemia in a group of alcoholic patients (n = 127) admitted to our hospital for causes related to alcohol misuse. Hyponatraemia (serum sodium <134 mmol/l) was found in 22 patients (17.3%). The most common cause of hyponatraemia in our cohort was hypovolaemia (12 patients); pseudohyponatraemia was diagnosed in six patients with alcohol-induced severe hypertriglyceridaemia. It is of interest that two patients fulfilled the criteria of the so-called 'beer potomania' syndrome, while in two others, hyponatraemia was due to reset osmostat or to cerebral salt wasting syndrome, not previously described in alcoholic patients. It is concluded that hyponatraemia is a frequently observed electrolyte disorder in hospitalized alcoholic patients and is related to various pathophysiological mechanisms.

Beer drinker's hyponatraemia: a case report

Beer drinker's hyponatraemia, also called beer potomania, is a syndrome of hyponatraemia in patients who consume excessive amounts of beer and have a poor dietary intake. We describe a patient with chronic asymptomatic hyponatraemia due to beer potomania. The pathophysiology of this syndrome, the treatment and prevention are reviewed. (See Expert opnion p. 101.)

SEVERE HYPONATRAEMIA SECONDARY TO BEER POTOMANIA COMPLICATED BY CENTRAL PONTINE MYELINOLYSIS

SUMMARY A case of severe hyponatraemia in a 56‐year‐old male alcohol misuser secondary to beer potomania is presented. In view of severe volume depletion and the patient's inability to drink, normal saline was cautiously infused. Despite initial improvement, he subsequently deteriorated neurologically. Magnetic resonance imaging demonstrated the classical lesion of central pontine myelinolysis (CPM). The rate of correction of plasma sodium was within limits normally considered safe. Beer potomania should be considered as a cause of hyponatraemia in alcohol misusers. Recognition is important as the electrolyte imbalance repairs simply with cessation of alcohol intake and institution of normal diet. Correction of chronic hyponatraemia by infusion of normal or hypertonic saline should not be attempted unless life‐threatening neurological complications supervene. When the balance of risks favours correction, caution should be exercised, as CPM may occur. Although a rate of correction of plasma sodium of up to 10 mM per 24‐hour period has been associated with a low risk of precipitating CPM, this case illustrates that a completely safe rate of correction probably cannot be defined.

“Beer potomania” in non-beer drinkers: Effect of low dietary solute intake

A ovolactovegetarian patient presented with hyponatremia. She had maximally dilute urine and undetectable vasopressin levels. Dietary history revealed very low protein intake but no beer intake. We postulated that the very low intake of solute limited her water excretion and caused the hyponatremia despite only a modest increase in fluid intake. When protein intake was increased in a clinical research center setting, free water excretion increased and serum sodium normalized despite maintaining the water intake at 4 to 5 L daily. We discuss the role of dietary solute in water excretion. Previously described in beer drinkers, the phenomenon can occur in the absence of beer drinking. In this era of weight consciousness, hyponatremia because of low solute intake may be seen with increased frequency. (Am J Kidney Dis 1998 Jun;31(6):1028-31)

Hyponatremic encephalopathy: Is central pontine myelinolysis a component?

purpose: Severe hyponatremia is often associated with permanent brain damage. There has been substantial controversy about whether central pontine myelinolysis (CPM), a rare neurologic disorder of uncertain etiology, can complicate either hyponatremia or its therapy. This study was undertaken to determine how often hyponatremic patients with the clinical diagnosis of CPM actually have the disorder as an integral structural component of their encephalopathy. patients: Analyses were carried out in 20 patients who had severe symptomatic hyponatremia and a presumptive diagnosis of CPM, based on clinical and/or neuroradiologic findings. All had been referred for neuroradiology consultation. The mean age (± SD) was 47 ± 14 years, the lowest serum sodium level was 104 ± 8 mM, and 85% of the patients were female. The etiologies were diverse and included postoperative status, thiazide diuretics, polydipsia, infection, acute renal failure, chronic alcoholism with emesis, and beer potomania. methods: The original and subsequent films of 20 patients were reevaluated retrospectively by two neuroradiologists. The clinical course was also reevaluated, and in eight patients, the postmortem brain findings were reviewed. The diagnosis of CPM was made only on the basis of strict criteria relating to either (1) pathologic findings of CPM on postmortem examination; or (2) computed tomographic scan and/or magnetic resonance imaging findings diagnostic of CPM. results: No pontine lesions were present in 15 of 20 patients in whom the diagnosis of CPM had initially been made. All 15 had extrapontine demyelinating lesions but the pons was normal. Two others had only lateral pontine lesions, so that only three of 20 patients had definite CPM. All but one of the 20 hyponatremic patients had a definite hypoxic event prior to any therapy with intravenous sodium chloride. The involved brain areas included basal ganglia, thalamus, cortical gray matter, and periventricular white matter, areas often affected by hypoxia. Each of the three patients in whom unequivocal findings of CPM were present had long histories of chronic alcoholism and hepatic cirrhosis. conclusions: These results suggest that: (1) Neither hyponatremic encephalopathy nor its therapy is commonly associated with CPM; (2) Patients with chronic alcoholism who also become hyponatremic can develop pontine demyelinating lesions; (3) Most patients with symptomatic hyponatremia who are diagnosed as having CPM in fact have diffuse cerebral demyelinating lesions with a normal pons; (4) The distribution of cerebral demyelinating lesions in patients with hyponatremic encephalopathy is compatible with hypoxic damage.

Beer potomania: An unusual cause of symptomatic hyponatremia

A 43-year-old woman presented to the emergency department with acute agitation, confusion, and tonic seizures. She had a history of drug abuse, most notably beer, which constituted her major dietary intake. The patient's seizures were at first thought to be factitious in association with an acute psychosis; however, her serum sodium concentration was 110 mEq/L and urine sodium was 14 mEq/L. The patient responded to IV hypertonic saline and subsequently recovered completely. Beer potomania, the most likely etiology for this patient's hyponatremia, is a rare disorder in which dietary sodium and protein insufficiency lead to dilutional hyponatremia.

COMA DUE TO WATER INTOXICATION IN BEER DRINKERS

Twelve cases of neurological syndrome due to severe hyponatræmia were investigated. Serum-sodium levels ranged between 120 and 98 meq. per litre. Neurological signs included disorders of consciousness (stage I and II coma) sometimes associated with pyramidal signs or epileptic attacks. In all cases where the electroencephalogram was recorded, it showed diffuse theta and delta waves. Hypokalæmia was frequent. In no case were there signs of intracranial hypertension. Necropsy in three cases, after correction of hyponatræmia, showed no lesions of cerebral œdema, but there were lesions characteristic of alcoholic encephalopathy in two cases. In all twelve cases, a sodium-depletion factor lay at the origin of the hyponatræmia, often associated with a dilution factor. In the seven most severe cases of hyponatræmia there was beer potomania. The importance of this factor in the pathogenesis of hyponatræmia may be explained by sodium deficiency in the diet, the absorption of large quantities of water, and the possible role of inappropriate secretion of antidiuretic hormone in these alcoholic patients. Under adequate treatment the neurological symptoms disappeared in all cases.