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

Sanghvi, Shalin R.; Kellerman, Paul S.; Nanovic, Lisa

doi:10.1053/j.ajkd.2007.07.015

Cited by 62 publications

(53 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…5 Case reports of ODS with rapid sodium correction in patients with beer potomania have been published. In a literature review done by Sanghvi et al, 6 of 22 patients with beer potomania, 4 (18%) had ODS. Although infusion of hypertonic saline classically has been associated with development of ODS, Karp and Laureno 7 suggest that the rapid correction of hyponatremia may occur even with infusion of normal saline or with fluid restriction alone, resulting in ODS.…”

Section: Discussionmentioning

confidence: 96%

“…Although infusion of hypertonic saline classically has been associated with development of ODS, Karp and Laureno 7 suggest that the rapid correction of hyponatremia may occur even with infusion of normal saline or with fluid restriction alone, resulting in ODS. On the basis of the underlying pathophysiology of beer potomania, Sanghvi et al 6 provided clinical recommendations for the management of these patients (see Sidebar: Management Recommendations for Hyponatremia Caused by Beer Potomania).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Beer Potomania—An Unusual Cause of Hyponatremia

Kujubu

Khosraviani

2015

TPJ

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Beer Potomania—An Unusual Cause of Hyponatremia

Kujubu

Khosraviani

2015

TPJ

View full text Add to dashboard Cite

“…In a review of 22 cases of beer potomania, Sanghvi et al showed that hyposthenuria on admission was not a consistent finding in beer drinkers with hyponatremia. They concluded that recognizing this finding prevents the erroneous dismissal of beer potomania [11]. Figure 1 illustrates the pathophysiology of hyponatremia in this particular patient.…”

Section: Rafei Et Al J Endocrinol Metab 2016;6(4):123-126mentioning

confidence: 94%

“…It is mainly explained by water intake that exceeds excretory capacity [11]. Free water clearance is dependent on solute excretion and urinary diluting capacity [13].…”

Section: Rafei Et Al J Endocrinol Metab 2016;6(4):123-126mentioning

confidence: 99%

Beer Potomania: A Challenging Case of Hyponatremia

2016

View full text Add to dashboard Cite

Beer potomania is a syndrome of hyponatremia associated with excessive beer drinking. Little or no salt content of beer results in marked reduction in the solute load to the kidney. This leads to impaired water clearance and dilutional hyponatremia. A 66-year-old man with history of alcoholism and alcoholic cardiomyopathy presented to the emergency room with tremors of his upper and lower extremities. He had a significant history of alcohol consumption, usually drinking 4 -5 cans of beer per night for the past 34 years. In addition, he had consumed a fifth of a vodka bottle the day before presentation. He had a pattern of often skipping meals though was compliant with both his diuretics medications: furosemide 40 mg once daily and spironolactone 25 mg daily. On physical exam, he was euvolemic. Neurological exam revealed resting tremors of both his hands. Labs were remarkable for plasma sodium of 122, brain natriuretic peptide of 474, serum osmolality of 268, urine osmolality of 223, and urine sodium of 20. Patient was assessed to have moderate euvolemic hypotonic hyponatremia. The combination of euvolemic hyponatremia with history of excessive beer drinking made beer potomania very likely. His urine osmolality and urine sodium, however, were higher than expected in beer potomania. These could be explained by the two diuretics that the patient was taking. Patient was managed with fluid restriction, appropriate nutritional and sodium intake and withholding of his diuretics. Plasma sodium slowly corrected to 130 over the course of 3 days. This case illustrates the condition beer potomania, an infrequent cause of hyponatremia. Findings in hyponatremia do not always point in one direction, especially with the concomitant use of diuretics. Recognition of beer potomania is critical as it is associated with serious neurologic sequelae that should be part of counseling against alcohol abuse.

show abstract

“…The pathogenesis is still to be clearly understood, it is known that rapidly increasing serum osmolality shifts water out of the cells as a response to correct solute imbalance resulting in shrinkage of glial cells that can consequently lead to disruption of the blood-brain barrier allowing inflammatory mediators to enter the central nervous system damaging oligodendrocytes and myelin [4][5][6][7] . Even though ODS has been classically thought to be exclusively secondary to a rapid correction of hyponatremia, it has also been described, even though rarely, in various other situations such as malnutrition, liver transplantation, alcoholism, hypokalemia, hypophosphatemia, AIDS, lithium toxicity, hypoglycemia, and folate deficiency, among others [8][9][10][11][12][13][14][15] . In all cases a growing body of evidence demonstrates that more than sodium per se, the key factor, in ODS pathogenesis, is a rapid change in serum osmoles.…”

Section: Introductionmentioning

confidence: 99%

Osmotic Demyelination Syndrome Occurs Early in The Course of Hyperosmolar Hyperglycemic State.

Das¹,

A.S²,

Mossang³

et al. 2017

IOSR JDMS

View full text Add to dashboard Cite

Osmotic demyelination syndrome (ODS) is a life-threatening demyelinating syndrome. The association of ODS with hyperosmolar hyperglycaemic state (HHS) has been seldom reported. The aim of this study was to show that Osmotic Demyelination Syndrome occurs early in the course of Hyperosmolar I. BackgroundOsmotic demyelination syndrome (ODS) is a life-threatening demyelinating syndrome, which usually occurs in the setting of a rapid correction of severe chronic hyponatremia 1,2 .ODS is a clinical syndrome characterized by altered mental status, quadriparesis, dyspnoea, dysarthria, and dysphagia which all occur characteristically five to seven days after the correction of serum sodium 3 . The pathogenesis is still to be clearly understood, it is known that rapidly increasing serum osmolality shifts water out of the cells as a response to correct solute imbalance resulting in shrinkage of glial cells that can consequently lead to disruption of the blood-brain barrier allowing inflammatory mediators to enter the central nervous system damaging oligodendrocytes and myelin 4-7 . Even though ODS has been classically thought to be exclusively secondary to a rapid correction of hyponatremia, it has also been described, even though rarely, in various other situations such as malnutrition, liver transplantation, alcoholism, hypokalemia, hypophosphatemia, AIDS, lithium toxicity, hypoglycemia, and folate deficiency, among others [8][9][10][11][12][13][14][15] . In all cases a growing body of evidence demonstrates that more than sodium per se, the key factor, in ODS pathogenesis, is a rapid change in serum osmoles. The association of ODS with hyperosmolar hyperglycemic state (HHS) has been seldom reported with less than five cases in the literature [16][17][18][19][20] . Previous cases have been in the clinical scenario of concomitant hypernatremia, chronic hyperglycemia/epilepsy, and after HHS treatment.Herein we present the case of a patient with HHS who presented with ODS early in the course of her illness. A review of previous cases and pathophysiological mechanisms involved in ODS secondary to HHS will be presented and discussed. Case PresentationA 45 year old female with poorly controlled Type2 Diabetes Mellitus came to the emergency room due to loss of consciousness. She was a known case of Type2 Diabetes Mellitus on Tab.Glipizide 5mg and Metformin 500mg for 10years and long acting Isophane Insulin(30:70) for 5years and she was a known Hypertensive on Tab Amlodipine 5mg for 5 years. She had irregular Medication.On Physical examination, her BP was 100/60 mmHg. Heart rate was 140/min and SpO 2 was 90% in Room air. Her BMI was 27.2. Mucus membranes were dry. ECG showed Right Axis Deviation. She had a Glasgow Coma Scale of 3/15 and muscle power was 0/5 in all the limbs and plantars were flexor B/L.There was no neck rigidity. Blood Glucose levels were 600mg%. Plasma and urinary ketones were negetive. ABG analysis showed pH 7.31. HbA1C was 14.1%, Serum Calcium 7.9mg/dL. Serum creatinine was 4.5mg/dL. Her eGFR

show abstract

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

Cited by 62 publications

References 19 publications

Beer Potomania—An Unusual Cause of Hyponatremia

Beer Potomania—An Unusual Cause of Hyponatremia

Beer Potomania: A Challenging Case of Hyponatremia

Osmotic Demyelination Syndrome Occurs Early in The Course of Hyperosmolar Hyperglycemic State.

Contact Info

Product

Resources

About