Alcoholic ketoacidiosis: a cause of sudden death of chronic alcoholics

There have been numerous speculations as to the cause and mechanism of death. Severe metabolic disturbances including high levels of free fatty acids do probably play a major role due to the effect on the Krebs Cycle. However, following senior medical review, given a recent history of drinking alcohol to excess, the diagnosis of AKA was felt more likely.

• There have been numerous speculations as to the cause and mechanism of death.
• Postmortem serum cortisol and urine free cortisol were elevated in all individuals studied, along with decreased postmortem serum free triiodothyronine.
• Glycated hemoglobin was determined in femoral whole femoral blood samples stored in tubes containing ethylenediaminetetraacetic acid by ion-exchange high-performance liquid chromatography (Bio-Rad D-10 Dual Program, Hercules, CA, USA).
• Other electrolyte abnormalities concomitantly present with alcohol abuse and poor oral intake include hypomagnesemia and hypophosphatemia.
• Free fatty acids were quantified in postmortem serum from femoral blood by the enzymatic colorimetric method ‘NEFA-HR(2)’ (Wako Diagnostics, USA) adapted on a Cobas MIRA Plus (Roche Diagnostics, Switzerland).

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• All chronic alcohol misusers attending the ED should receive intravenous B vitamins as recommended by The Royal College of Physicians.23 Strenuous efforts must be made to exclude concomitant pathology.
• If severe hypokalemia is present dextrose containing fluids can be held until potassium levels are normalized.
• Alcoholic ketoacidosis (AKA) is defined by metabolic acidosis and ketosis in a patient with alcohol use.
• If a person is already malnourished due to alcoholism, they may develop alcoholic ketoacidosis.

Other electrolyte abnormalities concomitantly present with alcohol abuse and poor oral intake include hypomagnesemia and hypophosphatemia. Magnesium and phosphate levels should be measured and repleted if the serum levels are found low. Examination should reveal a clear level of consciousness, generalised abdominal tenderness (without peritoneal signs), and tachypnoea. There may be concomitant features of dehydration or early acute alcohol withdrawal. Bedside testing reveals a low or absent breath alcohol, normal blood sugar, metabolic acidosis, and the presence of urinary ketones, although these may sometimes be low or absent.

Pathogenetic mechanisms of hypomagnesemia in alcoholic patients

If your blood glucose level is elevated, your doctor may also perform a hemoglobin A1C (HgA1C) test. This test will provide information about your sugar levels to help determine whether you have diabetes. If you develop any of these symptoms, seek emergency medical attention. They can also reduce the amount of insulin your body produces, leading to the breakdown of fat cells and the production of ketones. Of all deaths that could be traced to alcohol in 2019, the report found that an estimated 1.6 million were from noncommunicable diseases, including 474,000 deaths from cardiovascular diseases and 401,000 from cancer.

• Vitreous sodium concentrations were normal or only slightly decreased, likely reflecting total body sodium depletion, whereas hypochloremia was systematically observed, possibly secondary to prolonged vomiting.
• Although previous series of the scenario of sudden death in association with fatty liver in alcoholics have been published, these are mainly from outside of the UK and are published in languages other than English [9,15,16].

Complicated Acidosis Presentations: When Is Diabetic Ketoacidosis Not Diabetic Ketoacidosis? A Case Series

There are no drugs to be detected and only insignificant levels of alcohol or none at all. IL-10 was measured in postmortem serum from femoral blood by the ELISA technique using a commercially available kit. IL-6 was measured in postmortem serum from femoral blood by the enzyme-linked immunosorbent assay (ELISA) technique using a commercially available kit (R&D System, Inc., Minneapolis, MN, USA). LBP was determined in postmortem serum from femoral blood by chemiluminescent immunometric assay Immulite®2000 (Siemens Medical, Germany). Determination of free triiodothyronine (fT3) in postmortem serum from femoral blood was performed by chemiluminescent microparticle immunoassay (Abbott Architect analyser, Abbott reagents).

BOX 3 MANAGEMENT OF AKA

Larger studies by Fulop and Hoberman5 and Wrenn et al6 (24 and 74 patients, respectively) clarified the underlying acid base disturbance. Although many patients had a significant ketosis with high plasma BOHB levels (5.2–14.2 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​1). The key differential diagnosis to consider, and exclude, in these patients is DKA. Although DKA can also present with a severe metabolic acidosis, with a raised anion gap and the presence of ketones, the history and examination are quite distinct from that of someone presenting with AKA (Table 1).

Results and discussion

In the two cases in which there was toxicology available, alcohol was present at non-fatal or low levels, as shown in previous studies [6,8]. These seven cases represented alcoholic ketoacidosis 0.5% of deaths undergoing coroner’s post mortem. In 2005, 230,000 deaths were referred to Coroners in England and Wales, accounting for 45% of all deaths [19].

• The clinical importance in recognizing AKA from DKA is demonstrated by cases of patients who were treated as DKA and developed severe hypoglycaemia as a result of inappropriate insulin administration [8].
• Denmark on 49 autopsy cases that included chronic alcohol abuse-related deaths.
• In the liver mitochondria, acetaldehyde is oxidized to acetic acid by aldehyde dehydrogenase.
• The entity of alcoholic ketoacidosis, sometimes called alcoholic acidosis in the literature, was first described by Dillon et al. in 1940.

We studied 30 cases of sudden death of chronic alcoholics, for all of which autopsies, histological, alcoholimetric and toxicological tests had been performed, and for which we determined the β-hydroxybutyrate concentration in bodily fluid samples (blood, urine, cerebrospinal fluid and vitreous humour). Alcoholic ketoacidosis (AKA) is a condition that presents with a significant metabolic acidosis in patients with a history of alcohol excess. The diagnosis is often delayed or missed, and this can have potentially fatal consequences. There are a variety of non-specific clinical manifestations that contribute to these diagnostic difficulties. In particular, cases of AKA can be misdiagnosed as diabetic ketoacidosis (DKA).

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