CASE REPORT Abstract Background: Ethylene glycol is a toxic alcohol which is used in brake fluid, antifreeze, coolants, preservatives and chemical solvents. Ethylene glycol poisoning usually results in depression of the central nervous system, renal insufficiency and cardiopulmonary compromise, while laboratory findings include metabolic acidosis, increased anion gap, increased osmolar gap and calcium oxalate crystalluria. Case presentation: A 24-year-old previously healthy person died 13 days after self-ingestion of brake fluid (ethylene glycol). He developed multi-organ failure including acute kidney injury, metabolic acidosis, respiratory failure, myocardial infarction, low Glasgow coma scale, and elevation of liver enzymes. He also developed hypotension for which 3 inotropes were started. He had ST elevation myocardial infarction (STEMI) on day 4 of the poisoning associated with a reduction of ejection fraction of up to 25% with septal anterior wall hypokinesia. He needed intensive care treatment via ventilator and inotropic support. Five cycles of hemodialysis were carried out for acute kidney injury. His autopsy examination revealed sub-endocardial hemorrhages. Discussion: Acute kidney injury and metabolic acidosis are frequently seen following ethylene glycol poisoning from brake fluid ingestion. The cardiotoxic effect of its poisoning could be due to multiple microcalcifications of the myocardium. This clinical report highlights the severity and the sequence of events following ethylene glycol poisoning. Conclusion: STEMI may result following ethylene glycol poisoning in addition to other cardiac effects such as hypotension, tachycardia, myocarditis and ischemic changes in ECG. Key words: Acute Kidney Injury; Brake Fluid; Ethylene glycol; Metabolic Acidosis; Myocardial Infarction Acute Kidney Injury, Myocardial Infarction and Death Following Brake Fluid Poisoning; A Case Report 62 had nausea, faintness and headache. On examination he was afebrile, not dyspneic; blood pressure (BP) was 120/80mmHg; pulse rate was 68 beats/min; bilateral lung fields were clear and findings of abdominal and nervous system were normal. As pure ethanol was not available at the hospital 33.5% arrack was given, 1.8ml/kg (90ml) as a loading dose and 0.2ml/kg/hr (10ml) as the maintenance dose orally. On admission his ECG was normal (Figure 1). Laboratory findings are mentioned in Table 1. Arterial blood gas analysis done on FiO2-40% and Hb-14.7g/dL showed severe metabolic acidosis (pH-6.854, pCO2-9.8mmHg, pO2- 140.6mmHg, HCO3-17mmol/L, base excess (-)32.1mmol/L, SO2-96.1% and PO2/FiO2- 234.4 mmHg) and 8.4% NaHCO3 100ml intravenous (IV) bolus was administered. The following day serum K + and Ca 2+ levels were 6.39mmol/L and 1.78mmol/L respectively, so a soluble insulin/dextrose and IV calcium gluconate were administered. Then around 1700 h (24 hours after the ingestion), the patient developed dyspnea associated with lowering of SpO2 and few bilateral crepitations were heard in both lung fields. As he developed _____________ Brake oil is an automobile transmission fluid composed of mainly ethylene glycol (CH2OH)2, a toxic alcohol used also in antifreeze, coolants, preservatives and chemical solvents (1). Poisoning occurs as a result of intentional ingestion in suicide attempts or accidental ingestion (2). Ethylene glycol poisoning results in the depression of the central nervous system, renal insufficiency and cardiopulmonary compromise; laboratory features include increased anion gap metabolic acidosis, increased osmolar gap and calcium oxalate crystalluria (3). We report a fatal case of brake fluid poisoning complicated with metabolic acidosis, acute kidney injury and ST elevation myocardial infarction (STEMI). A 25-year-old previously healthy married man was admitted to the medical ward at 2115 h following self- ingestion of 250ml brake oil (DOT 3) around 1730 h. He was a non-smoker and non-alcoholic. On admission, the patient INTRODUCTION * Correspondence to: Rathnayaka Mudiyanselage Mithun Kaushika Namal Rathnayaka; MBBS, MA, MSc, Dip.in Toxicology, Dip.in OH&S. Intensive care unit, Provincial General Hospital, Ratnapura, Sri Lanka Tel: 09714337784, E-mail: [email protected]Received 23 April 2017, Accepted 10 June 2017 RATHNAYAKA MUDIYANSELAGE MITHUN KAUSHIKA NAMAL RATHNAYAKA 1,2* , PANWILAHENE ELLAWATTE ANUSHA NISHANTHI RANATHUNGA 3 1 Intensive care unit, Provincial General Hospital, Ratnapura, Sri Lanka 2 Department of Veterinary Pathobiology, Faculty of Veterinary Medicine &Animal Science, University of Peradeniya, Sri Lanka 3 Medical Unit, Provincial General Hospital, Ratnapura, Sri Lanka How to cite this article: Rathnayaka RMMKN, Ranathunga PEAN. Acute Kidney Injury, Myocardial Infarction and Death Following Brake Fluid Poisoning; A Case Report. Asia Pac J Med Toxicol 2017;6:62-6. Ethylene Glycol (Brake Fluid) Poisoning R.M.M.K.N. Rathnayaka et al. CASE REPORT
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CASE REPORT
Abstract
Background: Ethylene glycol is a toxic alcohol which is used in brake fluid, antifreeze, coolants, preservatives and chemical solvents.
Ethylene glycol poisoning usually results in depression of the central nervous system, renal insufficiency and cardiopulmonary
compromise, while laboratory findings include metabolic acidosis, increased anion gap, increased osmolar gap and calcium oxalate
crystalluria.
Case presentation: A 24-year-old previously healthy person died 13 days after self-ingestion of brake fluid (ethylene glycol). He
developed multi-organ failure including acute kidney injury, metabolic acidosis, respiratory failure, myocardial infarction, low
Glasgow coma scale, and elevation of liver enzymes. He also developed hypotension for which 3 inotropes were started. He had ST
elevation myocardial infarction (STEMI) on day 4 of the poisoning associated with a reduction of ejection fraction of up to 25% with
septal anterior wall hypokinesia. He needed intensive care treatment via ventilator and inotropic support. Five cycles of hemodialysis
were carried out for acute kidney injury. His autopsy examination revealed sub-endocardial hemorrhages.
Discussion: Acute kidney injury and metabolic acidosis are frequently seen following ethylene glycol poisoning from brake fluid
ingestion. The cardiotoxic effect of its poisoning could be due to multiple microcalcifications of the myocardium. This clinical report
highlights the severity and the sequence of events following ethylene glycol poisoning.
Conclusion: STEMI may result following ethylene glycol poisoning in addition to other cardiac effects such as hypotension,
tachycardia, myocarditis and ischemic changes in ECG.
1Intensive care unit, Provincial General Hospital, Ratnapura, Sri Lanka 2Department of Veterinary Pathobiology, Faculty of Veterinary Medicine &Animal Science, University of Peradeniya, Sri Lanka 3Medical Unit, Provincial General Hospital, Ratnapura, Sri Lanka
How to cite this article: Rathnayaka RMMKN, Ranathunga PEAN. Acute Kidney Injury, Myocardial Infarction and Death Following Brake Fluid
Poisoning; A Case Report. Asia Pac J Med Toxicol 2017;6:62-6.
Ethylene Glycol (Brake Fluid) Poisoning R.M.M.K.N. Rathnayaka et al.