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The patient with acute endocrine problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Differential diagnosis:Diabetic ketoacidosis: known history of diabetes.Alcoholic ketoacidosis: usually known history of alcohol abuse (no hyperglycaemia).
Alcohol
Published in S.J. Mulé, Henry Brill, Chemical and Biological Aspects of Drug Dependence, 2019
Increased availability of fatty acids in the liver may also contribute to the hyperketonemia and ke tonuda observed during chronic alcohol consumption in association with fat-containing diets. Increased ketogenesis in the liver has been incriminated.43 This may explain the recently described variety of “alcoholic ketoacidosis.”44
The Decomposed Body and the Unascertained Autopsy
Published in Julian L Burton, Guy Rutty, The Hospital Autopsy, 2010
The individual dying from alcoholic ketoacidosis typically has a history of chronic excess alcohol consumption. There may be a history of binge drinking. The individual typically has a poor diet and has sourced most of their calorific intake from alcohol and so has low glycogen stores in the liver. After a period of abstinence these glycogen stores are rapidly depleted and the liver begins to metabolise fatty acids to ketones. Typically then there is a history of heavy alcohol use, a period of abstinence followed by nausea and vomiting, lethargy, dehydration, confusion and ultimately coma and death. Macroscopic examination of the body often yields few or no positive findings though the liver usually shows profound fatty change. The diagnosis is made on the basis of toxicological examination of vitreous humour, blood and urine (see Table 20.4).
Approach to the patient presenting with metabolic acidosis
Published in Acta Clinica Belgica, 2019
Jill Vanmassenhove, Norbert Lameire
In chronic alcohol abuse, hypoglycemia is common due to malnutrition and a low glycogen storage with impaired gluconeogenesis. Because of the high NADH/NAD+ generated by the alcohol metabolism, there is a preferential conversion of pyruvate to lactate, impeding gluconeogenesis. This also explains why there is mostly more lactate than ketoacid anion accumulation in alcoholic ketoacidosis. Alcoholic ketoacidosis should be suspected in any patient who has a history of chronic alcohol dependency, malnutrition or a recent episode of binge drinking. Patients typically present with non-specific features including nausea, vomiting and generalized abdominal pain. Vomiting and/or diarrhea is common and can lead to hypovolemia and potassium depletion. Signs of shock, including tachycardia and hypotension can be complicated by overlap of alcohol withdrawal. Electrolyte abnormalities are common in this condition and can precipitate fatal cardiac arrhythmias [22].
The logistic organ dysfunction system score predicts the prognosis of patients with alcoholic ketoacidosis
Published in Renal Failure, 2018
Ha Nee Jang, Hee Jung Park, Hyun Seop Cho, Eunjin Bae, Tae Won Lee, Se-Ho Chang, Dong Jun Park
Alcoholic ketoacidosis (AKA) is usually characterized by metabolic acidosis, an increased anion gap, elevated serum ketone levels, and either a normal or low glucose concentration. A typical AKA patient has a history of chronic alcohol abuse, little or no food intake, and recent binge drinking followed by abrupt cessation of alcohol intake [1–6]. The physiological and mechanistic features of the condition are poorly known, but three factors may be in play. First, starvation may induce a decrease in insulin secretion and a rise in glucagon secretion. Second, the ratio of the level of the reduced form of nicotinamide adenine dinucleotide (NADH) to the oxidized form (nicotinamide adenine dinucleotide (NAD+)) may become elevated during alcohol metabolism. Finally, the extracellular fluid volume may be depleted by vomiting and low fluid intake [5–8]. The principal symptoms are nausea, vomiting, and/or abdominal pain [5,6]. Although the symptoms improve upon conservative management (infusion of large amounts of normal saline and glucose solution), AKA is occasionally associated with multiple complications [9,10].
Distinguishing between toxic alcohol ingestion vs alcoholic ketoacidosis: how can we tell the difference?
Published in Clinical Toxicology, 2021
Emily T. Cohen, Mark K. Su, Rana Biary, Robert S. Hoffman
Alcoholic ketoacidosis (AKA) is a metabolic derangement caused by poor nutritional status and an altered oxidation-reduction state in patients with AUD. During starvation, fatty acids undergo beta-oxidation, with resulting ketone and ketone-like byproducts causing both an elevated osmol gap and an elevated AGMA [13,14]. Frequent ethanol consumption produces an excessively reduced biochemical state (nicotinamide adenine dinucleotide, NADH excess) favoring formation of β-hydroxybutyrate over acetoacetate and lactate over pyruvate [9].