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Michael C Campbell - One of the best experts on this subject based on the ideXlab platform.
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hyponatremia and central pontine myelinolysis as a result of beer Potomania a case report
The Primary Care Companion To The Journal of Clinical Psychiatry, 2010Co-Authors: Michael C CampbellAbstract:To the Editor: Inpatients treated for alcohol dependence in both psychiatric and traditional hospital settings often demonstrate laboratory abnormalities with varying degrees of significance. Hyponatremia is a common electrolyte abnormality. Beer Potomania is an uncommon cause of hyponatremia that is traditionally thought to occur from a combination of chronic ingestion of hypotonic alcohol solutions (ie, beer), combined with protein malnutrition, that cannot be accounted for by other causes.1–3 Hyponatremia in beer drinkers covers a wide spectrum of clinical significance from completely benign to potentially deadly.1–10 A case of severe hyponatremia due to beer Potomania and the neurologic sequelae of central pontine myelinolysis (CPM) is reported along with a discussion of the clinical significance. Case report. Mr A, a 33-year-old white man, was transferred in 2006 from the associated primary medical facility to the psychiatric addiction unit (dual diagnosis unit [DDU]) for treatment of alcohol dependence. He had been briefly admitted to the medical service for acute neurologic symptoms that consisted of dysarthria, dyspraxia, vertigo, and confusion. During his medical hospitalization, it was discovered that the patient had been hospitalized approximately 10 days previously due to unresponsiveness. Transfer records revealed that the patient was found unconscious by a friend and on emergent workup found to have a serum sodium level of 95 mmol/L. He was treated with intravenous fluids, after which his serum sodium level was corrected per standard of care guidelines of less than or equal to 10–12 mmol/L in the first 24 hours and less than or equal to 18 mmol/L in the first 48 hours. During this previous hospitalization, the patient responded well to the treatment and was discharged without symptoms on day 5. Five days after his discharge, Mr A began to experience increasing neurologic symptoms, as previously described, ultimately leading to a traumatic fall down a hill while walking. The patient had at this time a past medical history of chronic hyponatremia, alcohol dependence including prior detoxification admissions, alcoholic hepatitis, and withdrawal seizures. His admission to our facility revealed a serum sodium level of 132 mmol/L, a serum potassium level of 3.2 mmol/L, a blood urea nitrogen level of 1 mmol/dL, and a serum creatinine level of 0.5 mmol/dL. Serum calcium, magnesium, and phosphate levels were within normal limits. Serum levels of the following components were as follows: albumin 2.9 mg/dL, aspartate aminotransferase 84 IU/L, alanine aminotransferase 86 IU/L, alkaline phosphatase 227 IU/L, and γ-glutamyltransferase 741 IU/L. Report from the previous hospitalization revealed a serum sodium level of 95 mmol/L, and after a negative computed tomography scan was obtained, magnetic resonance imaging (MRI) was ordered for suspicion of CPM secondary to the recent severe hyponatremia. The MRI confirmed an abnormal signal intensity in the central pons suggestive of CPM. His treatment in the hospital, in the DDU, and posthospitalization consisted of significant physical and occupational therapy. Regardless, residual movement and speech deficits were present several months after the second hospitalization. This case displays several unique points in the interaction between the treatment of mental and medical illnesses, particularly substance use disorders (SUDs). It can be convenient to overlook an adequate medical evaluation in the treatment of SUDs with laboratory testing consisting of only a urine drug screen and blood alcohol level. Due to the ever-growing demand for medical services and various other factors, patients presenting for inpatient SUDs may be given minimal laboratory evaluation. Hyponatremia, especially in chronic hypotonic alcohol drinkers, is just one serious adverse condition that can occur in SUDs.11 First described in 1971,4 beer Potomania has been reported in the literature approximately 23 times.1–10 It is a condition along the same spectrum as psychogenic polydipsia. The consumption of large amounts of hypotonic solution, whether water or beer, can lead to the dilution of serum sodium. Generally, hyponatremia is asymptomatic until serum levels fall below 125 mmol/L.11 Hyponatremia can result in nausea, vomiting, imbalance, seizures, and, in severe cases, coma and death.11 The patient described had a history of chronic hyponatremia, most likely due to his chronic alcohol consumption that began when he was a young teenager. He also had a history of withdrawal seizures and alcohol-induced cirrhosis requiring daily lactulose to maintain a serum ammonia level within normal limits. The exact duration or amount of alcohol that was consumed was unknown in this case, as the patient was discovered unresponsive by a friend. A blood alcohol level from his initial hospitalization was not available. However, transfer records from the emergency medical service personnel described a scene in which the patient's residence was surrounded outside by “trash bags full of beer cans.” Additionally, the record described a scene in which they had to “wade” through empty beer cans to attend to the patient. In this extreme case, the danger of developing CPM was very high regardless of the conservativeness of treatment. An extensive literature search revealed this to be the fifth case report of CPM as a direct result of beer Potomania.4,8–10 As has been shown in other cases of severe hyponatremia, even the most conservative or slower-than-guideline corrections of sodium have resulted in CPM.12 This case would also lend support to the supposition that guidelines for severe hyponatremia should be much more conservative, as proposed by Sanghvi et al.10 The management recommendations propose, among others, a maximum serum increase of 10 mmol/L in the first 24 hours and a maximum of 18 mmol/L in the first 48 hours. The distinction emphasizes 10 mmol/L as the maximum rate of change and that correction of sodium resolves spontaneously without the use of hypertonic or isotonic fluids. Dilution was also recommended if serum sodium rose faster than the concrete goals. This case highlights that a patient's medical and psychiatric disease processes do not operate in a vacuum. Recognizing SUDs in the primary care setting and pursuing psychiatric consultation along with appropriate testing are paramount to the patient's overall health. Conversely, those treating SUDs in the psychiatric setting must be attuned to the deceptive nature of underlying health issues that may result in a population with chronic health conditions masked by the resiliency of youth.
Ardeshir Khosraviani - One of the best experts on this subject based on the ideXlab platform.
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beer Potomania an unusual cause of hyponatremia
The Permanente Journal, 2015Co-Authors: Dean A Kujubu, Ardeshir KhosravianiAbstract:The first case of severe hyponatremia, since referred to as beer Potomania, in a heavy beer drinker patient was reported in 1972. Electrolyte abnormalities are common findings in patients with a history of heavy alcohol use. Excessive consumption of beer in particular, which has a low solute content (sodium concentration, 1.8 mEq/L and potassium concentration, 7.2 mEq/L), to the exclusion of other solute intake may result in severe hyponatremia. We report a case of severe hyponatremia that occurred in a patient who, owing to his underlying colon cancer, was drinking beer and ingesting little other food. His hyponatremia improved with increased solute intake and, upon correction of his serum sodium, he had no subsequent neurologic sequelae.
Parvinder S Khurana - One of the best experts on this subject based on the ideXlab platform.
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beer Potomania a challenging case of hyponatremia
Journal of Endocrinology and Metabolism, 2016Co-Authors: Hind Rafei, Raza Yunus, Parvinder S KhuranaAbstract: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. J Endocrinol Metab. 2016;6(4):123-126 doi: http://dx.doi.org/10.14740/jem350e
Allen I Arieff - One of the best experts on this subject based on the ideXlab platform.
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hyponatremic encephalopathy is central pontine myelinolysis a component
The American Journal of Medicine, 1992Co-Authors: R D Tien, Allen I Arieff, W Kucharczyk, Andrze J Wasik, John KucharczykAbstract:Abstract 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.
R D Tien - One of the best experts on this subject based on the ideXlab platform.
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hyponatremic encephalopathy is central pontine myelinolysis a component
The American Journal of Medicine, 1992Co-Authors: R D Tien, Allen I Arieff, W Kucharczyk, Andrze J Wasik, John KucharczykAbstract:Abstract 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.