Cases reported "Alcoholism"

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1/16. Rapid diagnosis of alcoholic ketoacidosis by proton NMR.

    In alcoholic patients, metabolic acidosis can be related to lactate acidosis associated with sepsis or thiamine deficiency, ketoacidosis, methanol or ethylene glycol poisoning. High resolution proton nuclear magnetic resonance (NMR) can be used to detect abnormal organic acid metabolites in urine or serum from patients with various metabolic disorders. In the present case, a 26-year-old patient was admitted for a coma associated with severe metabolic acidosis. Alcoholic ketoacidosis (AKA) was identified by urine proton NMR. Her metabolic disorders rapidly improved. Persisting associated neurological alteration was related to extrapontine myelinolysis as shown by imaging cerebral NMR.
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2/16. Alcoholic ketoacidosis in a pregnant woman.

    A case of alcoholic ketoacidosis in a 23-year-old chronic alcoholic, gravada V, para IV, is reported. Symptoms were constant, severe, nonradiating pain with crampy exacerbations, anorexia, nausea and vomiting. The patient had a tender and irritable full-term uterus. She was treated inhospital with vigorous fluid therapy and 5% dextrose in normal saline, sodium bicarbonate, glucose and insulin and showed improvement overnight. Alcoholic ketoacidosis has not been reported in pregnant women. Metabolic derangements combine to produce ketoacidosis more readily in the pregnant alcoholic. Differentiation of alcoholic ketoacidosis and diabetic ketoacidosis is important since treatment varies. For alcoholic ketoacidosis, treatment is vigorous rehydration with dextrose-saline while diabetic ketoacidosis usually requires multiple therapeutic modalities.
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3/16. Major ketogenesis and the absence of an osmolar gap in an atypical case of alcoholic ketoacidosis.

    A new case of alcoholic ketoacidosis (AKA) is presented because of unusual clinical and biochemical features. Although it shares some similarities with typical cases of AKA, it appears as unique because of predominantly neurological, rather than abdominal symptoms, major ketogenesis with normal ketone body ratio, the presence of large amounts of propanediol and the absence of an osmolar gap.
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4/16. Reversible blindness associated with alcoholic ketoacidosis.

    PURPOSE: To report a case of reversible blindness associated with severe alcoholic ketoacidosis. DESIGN: Observational case report. methods: A 44-year-old male presented with gradual bilateral blindness that developed within a 24-hour period. He suffered from ethanol-induced severe ketoacidosis and shock and was resuscitated with epinephrine and sodium bicarbonate. RESULTS: The treatment of acidosis led to a rapid resolution of the patient's blindness. CONCLUSIONS: It is important to understand the role of severe acidosis as the sole causative factor of reversible bilateral blindness.
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5/16. ketosis and cardiac failure: common signs of a single condition.

    The metabolic effects of chronic alcohol abuse can induce a broad spectrum of disorders. We describe the case of an initially unidentified alcoholic, poorly nourished woman who presented with ketoacidosis. She developed severe cardiac failure, which did not respond to classical treatment. The administration of intravenous thiamine resulted in an impressive recovery of cardiac function. Laboratory examinations confirmed the diagnosis of alcoholic ketoacidosis and cardiac beriberi. The clinical entity and treatment of these two uncommon disorders are discussed. If recognized early both diseases (and their combination) are fully reversible.
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6/16. Alcoholic ketoacidosis associated with multiple complications: report of 3 cases.

    We report 3 patients with alcoholic ketoacidosis (AKA). All had a history of excessive intake and abrupt termination of alcohol. They showed tachypnea, tachycardia, abdominal tenderness, and epigastralgia. Metabolic acidosis with an increased anion gap, decreased PaCO2 and ketonemia were present. One patient whose ratio of 3-hydroxybutyric acid to acetoacetic acid was 4.0 was associated with diabetic ketoacidosis. All patients were successfully hydrated with electrolyte, glucose and thiamine. Complications such as liver dysfunction, lactic acidosis, acute pancreatitis, Wernicke's encephalopathy, rhabdomyolysis and heart failure were present. attention should be paid to multiple complications in the treatment of AKA.
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7/16. Rapid onset of quetiapine-induced diabetic ketoacidosis in an elderly patient: a case report.

    New onset diabetes mellitus (DM) and diabetic ketoacidosis (DKA) among patients using atypical antipsychotics is of clinical importance [1,2,5,7-10]. Recently, atypical antipsychotics have been more widely used in the treatment of behavioral and psychological symptoms with dementia (BPSD) than conventional neuroleptics because of a reduced tendency for movement disorders and psychomotor retardation. We report a case of reversible DKA and new-onset DM that developed in a demented patient who was treated with quetiapine for 14 days.
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8/16. Alcoholic ketoacidosis: a case report.

    A 43-year-old alcoholic presented in coma with ketoacidosis, after three days of nausea and feeling generally unwell, which had been preceded by a prolonged three-week period of heavy alcohol consumption with poor dietary intake. The acidosis responded rapidly to intravenous dextrose. This is the first Scottish report of a case of alcoholic ketoacidosis.
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9/16. The urine anion gap: the critical clue to resolve a diagnostic dilemma in a patient with ketoacidosis.

    Usually, ketoacidosis presents few if any diagnostic or therapeutic problems; in this article, we report a case where ketoacidosis was clinically occult and biochemically obscure. The patient presented with acute pancreatitis associated with a modest antecedent alcohol intake. Metabolic acidosis with a normal anion gap (10 meq/L) was observed together with moderate hyperglycemia and a 2 (but not 4 ) test for serum ketones. None of the usual causes of metabolic acidosis with a normal anion gap was identified nor was there an obvious explanation for a reduction in unmeasured anion gap (e.g., hypoalbuminemia, dysproteinemia, or the presence of abnormal halides). Despite the initial normal anion gap, ketoacidosis was suspected clinically and this was confirmed by the elevated serum B-hydroxybutyrate of 8 mmol/L. We deduced that the serum unmeasured anions, which should have been increased by at least 8 meq/L, were being underestimated because of the effect of hypertriglyceridemia on the serum chloride determination. When the serum chloride was reestimated by a method not influenced by hyperlipidemia, the value was 102 mmol/L not 112 mmol/L and, when reevaluated, the anion gap was indeed appropriately elevated. In addition, the urine anion gap (Na K - Cl) was 103 meq/L in the absence of renal disease. This indicated that the expected large quantity of urinary ammonium must have been masked by an even greater quantity of unmeasured anion; in this case proven by direct measurement to be B-hydroxybutyrate. Finally, metabolism of the alcohol ingested, which yields hepatic NADH, could explain, in part, the modest hyperglycemia and the absence of a 4 test for serum ketones.(ABSTRACT TRUNCATED AT 250 WORDS)
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10/16. Osmolal gap in alcoholic ketoacidosis.

    Severe metabolic acidosis in the setting of alcoholism raises diagnostic and therapeutic problems [Levinsky 1994]. Alcoholic ketoacidosis and toxic alcohol ingestion can be difficult to distinguish on initial presentation [Litovitz 1986]. A high osmolal gap associated with increased anion gap acidosis is said to be indicative of toxic alcohol poisoning though this is not at all specific [Salem and Mujais 1992]. Invasive therapeutic manoeuvers as for toxic alcohol poisoning have been recommended empirically before toxicological confirmation when very high osmolarity gaps are reached. Herein, we report two cases of high anion gap metabolic acidosis with very high osmolal gap due to alcoholic ketoacidosis without any evidence of toxic alcohol ingestion.
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