ArticleAnnals of medicine and surgery (2012)2022
Ketoacidosis can Be alcohol in origin: A case report.
Article in Annals of medicine and surgery (2012), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed, 1 citations in OpenAlex.
- Stereotypical diagnostic bias for alcohol-induced ketoacidosis could lead to death: Normal blood sugar levels in SGLT2 blocker-induced severe diabetic ketoacidosis.PCN reports : psychiatry and clinical neurosciences · 2025Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
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Abstract
Background: Alcoholic ketoacidosis (AKA) is a common reversible biochemical pathology arising from hyperketonaemia in patients with a history of chronic alcohol consumption. It is typically fatal when there is a delay in early recognition and management. A further complicating factor is that this condition is frequently confused with diabetic ketoacidosis (DKA). Case presentation: This report presents the case study of an elderly Chinese man with a 40-year history of alcohol consumption. The patient presented with acute shortness of breath, generalised abdominal pain, and vomiting. Blood gas analysis indicated severe high anion gap metabolic acidosis (HAGMA) with elevated serum ketones and modest hyperglycaemia which was initially treated as diabetic ketoacidosis (DKA). A diagnosis of AKA was later made after obtaining a thorough history of his binge drinking. The patient subsequently responded well to thiamine and aggressive fluid resuscitation. This case highlights the importance of a well-documented patient history and in-depth knowledge of ketoacidosis. Discussion: AKA must be suspected in patients with a history of chronic alcohol consumption and dependence. The symptoms are non-specific such as abdominal pain, nausea, vomiting and diarrhoea. The latter two result in malnutrition and starvation subsequently leading to hyperketonaemia, hypovolaemia and HAGMA. AKA should be clearly differentiated from DKA to prevent mismanagement. The mainstay of management of AKA is thiamine, fluid resuscitation and good sugar control to prevent Wernicke's encephalopathy. Conclusion: A precise patient's medical history is crucial to prevent misdiagnosis. A non-diabetic patient with a history of chronic alcohol consumption who presents with severe HAGMA, hyperketonaemia and dysglycaemia should raise a clinical suspicion of AKA. Thiamine and judicious fluid resuscitation as well as electrolytes and malnutrition correction should be promptly initiated in patients with AKA. Good family, social support and rehabilitation programs are crucial to help patients with alcohol abuse.
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