Muerte súbita por cetoacidosis alcohólica en etilistas crónicos: reporte de 3 casos / Sudden death by alcoholic ketoacidosis in chronic alcoholics: report of 3 cases

Resumen En Patología Forense es común estudiar cadáveres de individuos con antecedente de alcoholismo crónico, que son encontrados fallecidos y cuyo deceso no fue presenciado; por lo que en gran cantidad de autopsias la determinación de la causa de muerte es compleja. La cetoacidosis alcohólica constituye un síndrome complejo derivado de una alteración del metabolismo en el contexto de un consumo excesivo de alcohol e ingesta calórica insuficiente. Se trata de un diagnóstico diferencial importante como causa de muerte en alcohólicos crónicos que fallecen posterior a un ayuno de algunos días, secundario a molestias abdominales como gastritis inducida por etanol, usualmente asociada a vómitos. Clínicamente estas personas presentan además dolor abdominal, taquicardia y alteraciones respiratorias. El diagnóstico postmortem se confirma mediante la presencia de cuerpos cetónicos, especialmente beta-hidroxibutirato, en sangre, humor vítreo u orina. A continuación se presentan tres casos de muerte súbita por cetoacidosis alcohólica con historia de abuso crónico de bebidas etílicas; se discute su fisiopatología, hallazgos al momento de la autopsia y resultados de exámenes complementarios (análisis toxicológico y estudio histopatológico).

Abstract In the forensic pathology setting, it is frequent to study corpses of individuals that were known to be chronic alcoholics and suffered a sudden death. Therefore, many autopsies are performed, in which determining the cause of death is a complex task. Alcoholic ketoacidosis refers to a complex syndrome derived from a metabolic disarrangement, related to excessive consumption of alcohol and an insufficient caloric intake. It is an important diagnosis that should be considered in sudden deaths of chronic alcoholics with a recent history of fasting, due to abdominal complains such as gastritis induced by alcohol and usually associated with recurrent vomiting. Clinically these patients present with abdominal pain, tachycardia and respiratory anomalies. The diagnosis can be confirmed when elevated ketone bodies, especially beta-hydroxybutyrate, are found in blood, vitreous humour or urine. In this paper we present three cases of sudden death by alcoholic ketoacidosis with a history of chronic abuse of alcohol, discussing it´s pathophysiology, autopsy findings and the results of additional studies (toxicologic screening and histopathology).

The Clinical Manifestations of Patients with Severe Alcoholic Ketoacidosis Treated at a Medical Intensive Care Unit / 결핵및호흡기질환

BACKGROUND: Alcoholic ketoacidosis(AKA) is a metabolic disturbance that is caused by prolonged and excessive alcohol consumption. Though the prognosis is reportedly good, its outcome is unclear in some cases that are combined with multi-organ failure. There are few reports of an analysis of cases admitted to an intensive care unit(ICU) METHOD: Cases of AKA admitted to the ICU over the last 5 years were retrospectively analyzed. Severe AKA was characterized by multi-organ failure that required treatment in an ICU RESULTS: All patients were males with a history of excessive alcohol consumption. Five of them (50%) mainly complained of gastrointestinal symptoms (nausea, vomiting, diarrhea), showing metabolic acidosis with an increased asmolar and anion gap. Rhabdomyolysis with acute renal failure was the most common combined organ failure. Mechanical ventilation was performed in 80%. Six patients died and 4 patients survived. In the surviving patients, the arterial blood gas analysis(ABGA) was normalized within 12 hours after admission. CONCLUSION: In severe AKA patients, rhabdomyolysis with acute renal failure was the most common complication. The mortality rate was high and death from shock occurred within 3 days.

Bilateral Lesion of the Basal Ganglia in Patient with Alcoholic Ketoacidosis : Case Report / 신경정신의학

Alcoholic ketoacidosis is a serious metabolic abnormality that occurs in chronic alcoholics. We report a case of bilateral necrosis in the basal ganglia after alcoholic ketoacidosis in a 42-year-old female chronic alcoholics. Magnetic resonance imaging (MRI) of the patient suggested subacute infarction with subsequent necrosis of the basal ganglia, which matches with the patients neurological manifestations. Repeated alcoholic ketoacidosis in chronic alcoholics could be the cause of subacute infarction following necrotic changes in the basal ganglia.