Favorable Gastrointestinal Outcome in Severe Systemic Toxicity after Concentrated Acetic Acid Poisoning (Case Report)

Objectives: Concentrated acetic acid ingestion results in upper gastrointestinal tract caustic injuries and systemic effects. We present a case with early development of hemolysis, acute renal failure, hyperthrombotic condition but without significant caustic gastrointestinal sequelae. Case report: A 48-year old women was admitted to the hospital with a history of concentrated acetic acid ingestion about an hour and a half before in a suicidal attempt. She had no medical history. The first sign of the poisoning was massive haematemesis occurring at home. The patient presented with BP 100/70 mm Hg, HR 105/min, ECG with flattened T waves, leucocytosis, normal BUN and creatinine, bilirubin rise: total 81 g/l, dir 53g/l, indirect 28 g/l, and AST 126 U/l, fibrin-degradation products more than 2030 ng/ml (ref range 250 ng/ ml), prolonged activated partial thromboplastin time 51 sec (22 sec) and urine sample with hae-maturia. Physical examination revealed epigastric pain, metrorrhagia, and anuria at admission. Toxicological analysis did not reveal ingestion of other toxins or medications. Diagnostic oesophagogastroduodenoscopy performed on the second day of admission showed oesophagitis and gastritis corrosive gr IIa and IIb (Kikendall), echotomography revealed enlarged kidneys. Because of anuria with increased urea nitrogen 15.6 mmol/l and creatinine up to 823 micromol/ l (normal 130 micromol/l) the patient underwent 10 periods of hemodialysis with heparin 5000 IE in the first and the following with 500 IE due to the intensive hematemesis after each one. Echo color-doppler-investigation showed phlebothrombosis illeofemoralis l.sin. Conservative treatment included parenteral proton pump inhibitor, antacids, broad-spectrum antibiotics, methylprednisolone, fresh frozen plasma and blood substitution, heparin during dialysis, low molecular heparin, total parenteral nutrition. The patient was discharged after 30 days stay at the hospital with regulated hypertension but no upper gastrointestinal complications on control oesophagogastroduodenoscopy and regular diuresis, degradation products, electrolytes and blood count. She was advised to take antihypertensive therapy and anticoagulant therapy until controlled. Conclusion: Glacial acetic acid poisoning with marked systemic complications usually causes severe GI lesions. The favorable GI outcome in our patient with severe hemolysis and renal failure may indicate an individual response to the toxin and may indicate a pos