Alcoholic ketoacidosis aka is a common reason for investigation and admission of alcohol dependent patients in uk emergency departments. Although well described in international emergency medicine literature, uk emergency physicians rarely make the diagnosis of aka. There is increasing evidence that rather than being benign and self limiting, aka may be a significant cause of mortality in patients with alcohol dependence. This literature review discusses the history, characterisation, pathophysiology, diagnosis, and management of aka. keywords: emergency department, alcoholic ketoacidosis, alcohol alcoholic ketoacidosis aka , also termed alcoholic ketosis or alcoholic acidosis, is rarely diagnosed in uk emergency departments eds.

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The clinical features nausea, intractable vomiting, and abdominal pain overlap with a number of conditions that manifest as acute crises in alcohol dependent patients. However, recent forensic studies suggest that the untreated metabolic disturbance may be associated with sudden death in patients with severe alcoholism. This review will examine the characterisation, pathophysiology, diagnosis and management of aka within the ed. A literature search was carried out on medline via pubmed and ovid 1966 x02010 2004 , embase 1980 x02010 2004 , and cinahl 1980 x02010 2004 using the search strategy: and limit to human.

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The majority of papers detected by this search focus primarily on diabetes mellitus and its complications, and were excluded. All remaining papers were retrieved and the reference lists hand searched for any additional information sources. In 1940, dillon et al 1 described a series of nine patients who had episodes of severe ketoacidosis in the absence of diabetes mellitus, all of whom had evidence of prolonged excessive alcohol consumption. It was not until 1970 that jenkins et al 2 described a further three non x02010 diabetic patients with a history of chronic heavy alcohol misuse and recurrent episodes of ketoacidosis.

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This group also proposed a possible underlying mechanism for this metabolic disturbance, naming it alcoholic ketoacidosis. And fulop et al were subsequently reported, with remarkably consistent features. 3 ,4 ,5 all patients presented with a history of prolonged heavy alcohol misuse, preceding a bout of particularly excessive intake, which had been terminated several days earlier by nausea, severe vomiting, and abdominal pain. In 1974, cooperman's series of seven ketoacidotic alcoholic patients all displayed diffuse epigastric tenderness on palpation. 4 in contrast to patients with diabetic ketoacidosis, the patients were usually alert and lucid despite the severity of the acidosis and marked ketonaemia. When altered mental status occurred, this was clearly attributable to other causes. Laboratory results included absent blood alcohol with normal or low blood glucose level, no glycosuria, and a variably severe metabolic acidosis with a raised anion gap.

This acidosis appeared to result from the accumulation in plasma of lactate and ketone bodies including beta x02010 hydroxybutyrate bohb and acetoacetate acac. 3 cooperman et al found that near patient testing for ketone bodies using nitroprusside test acetest, ketostix produced a low to moderate result in these patients. 4 the nitroprusside reaction is most sensitive to acetoacetate, less so to acetone, and not at all to bohb. 5 bohb may therefore be considerably elevated without significant ketonaemia being detected in this standard way. This study also confirmed the elevated ketone levels and an association with an increased bohb:acac previously noted by levy et al.

4 many patients with aka were found to have extremely elevated concentrations of plasma free fatty acids, with mean levels much higher than reported in patients with diabetic ketoacidosis. 3 ,4 patients also had markedly raised cortisol and growth hormone, and relatively low plasma insulin levels. Patients improved rapidly within 12 x02005 hours with intravenous glucose and large amounts of intravenous saline, usually without insulin although small amounts of bicarbonate were sometimes used. Larger studies by fulop and hoberman 5 and wrenn et al 6 24 and 74 patients, respectively clarified the underlying acid base disturbance.

Although many patients had a significant ketosis with high plasma bohb levels 5.2 x02013 14.2 x02005 mmol/l , severe acidaemia was uncommon. It appeared that concurrent disease processes, including extracellular fluid depletion, alcohol withdrawal, pain, sepsis, and severe liver disease, resulted in mixed acid base disturbances in individual patients. 6 the resultant blood ph was dependent on the final balance of these factors table 1 x200b 1 . table 1 x02003 metabolic factors affecting acid base balance in aka wrenn et al 6 studied the clinical presentation in detail. Nausea, vomiting, and abdominal pain were by far the most commonly observed complaints.

Despite the frequency of abdominal symptoms, objective findings other than tenderness were infrequent. Abdominal distension, decreased bowel sounds, ascites, or rebound tenderness occurred rarely and only in the presence of other demonstrable intra x02010 abdominal pathology such as pancreatitis, severe hepatitis, and sepsis or pneumonia. Both wrenn et al 6 and fulop and hoberman 5 found evidence of alcoholic hepatitis to be common, with frequent elevations in serum transaminase activities and bilirubin.

Wrenn et al found altered mental status in 15 x025 of patients, attributable in all but one case to hypoglycaemia, severe alcohol intoxication, or infection. In up to 10 x025 of sudden unexpected deaths in patients with chronic alcoholism, the immediate cause and mechanism of death are unclear even after scene investigation, necropsy, and standard toxicology screen. 7 alcohol is commonly low or absent, and fatty liver is frequently the only pathological abnormality detected. Severe derangements of potassium and/or magnesium may be implicated in the sudden deaths of some alcoholic patients, but not all. 7 ,8 ,9 ,10 in the study from kadis et al of 30 cases of sudden death in patients with chronic alcoholism, 11 bohb levels were 10 times higher than in alcoholic patients in whom another cause of death was found p x03c 0.05.

Denmark noted elevated bohb levels in these unexplained deaths and hypothesised that alcohol ketosis may have caused fatal hypoglycaemia. 7 thomsen et al theorised that the acidosis itself caused metabolic disruption of vital functions and death, proposing the term ketoalcoholic death. 8 thomsen subsequently reported ketoalcoholic deaths in 7 x025 of sudden deaths in alcoholic patients in a prospective series. 9 similarly, pounder et al detected very high levels of total ketone bodies, suggesting profound aka, in 10 x025 of sudden unexplained deaths in alcoholic patients. 12 aka may itself be a cause of sudden death in alcoholic patients through a direct toxic effect or other unknown mechanism.

Ethanol is a toxin, the majority of which is oxidised in the liver to acetaldehyde. There are three oxidative pathways: the cytosolic alcohol dehydrogenase pathway, the microsomal ethanol oxidising system, and the peroxisomal catalase pathway. The alcohol dehydrogenase reaction is the principal oxidative pathway and involves the reduction of nad to nadh fig 1 x200b 1. Acetaldehyde is then further oxidised in hepatic mitochondria to acetic acid, which then forms acetyl coenzyme a acetyl coa. 13 in liver tissue exposed to alcohol, this mitochondrial nadh accumulates, increasing the nadh/nad ratio, and interfering with mitochondrial metabolic activity. This raised nadh/nad ratio is thought to be pivotal in the development of ketoacidosis and lactic acidosis as described below.