Chloroform ingestion causing severe gastrointestinal injury, hepatotoxicity and dermatitis confirmed with plasma chloroform concentrations
Autor: | Dushan Jayaweera, Geoffrey K. Isbister, Michael S. Roberts, Latesh Poojara, Chris Cowie, Naren Gunja, James Broska, Shawkat A. K. M. Islam |
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Přispěvatelé: | Jayaweera, Dushan, Islam, Shawat, Gunja, Naren, Cowie, Chris, Broska, James, Poojara, Latesh, Roberts, Michael S, Isbister, Geoffrey K |
Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
Adult hepatotoxicity Abdominal pain Gastrointestinal Diseases Antidotes Aspartate transaminase Toxicology Models Biological 03 medical and health sciences 0302 clinical medicine Liver Function Tests acetylcysteine medicine Ingestion Humans dermatitis Enterocolitis biology medicine.diagnostic_test chloroform enterocolitis business.industry toxicity 030208 emergency & critical care medicine General Medicine Abdominal Pain Acetylcysteine 030104 developmental biology Alanine transaminase Anesthesia Toxicity biology.protein Vomiting Female Chloroform Drug Eruptions medicine.symptom Chemical and Drug Induced Liver Injury Drug Overdose Liver function tests business Respiratory Insufficiency Half-Life |
Zdroj: | Clinical toxicology (Philadelphia, Pa.). 55(2) |
ISSN: | 1556-9519 |
Popis: | Context: Poisoning due to chloroform ingestion is rare. The classic features of acute chloroform toxicity include central nervous system (CNS) and respiratory depression, and delayed hepatotoxicity. Case details: A 30-year-old female ingested 20–30 mL of 99% chloroform solution, which caused rapid loss of consciousness, transient hypotension and severe respiratory depression requiring endotracheal intubation and ventilation. She was alert by 12 h and extubated 16 h post-overdose. At 38-h post-ingestion, her liver function tests started to rise and she was commenced on intravenous acetylcysteine. Her alanine transaminase (1283 U/L), aspartate transaminase (734 U/L) and international normalized ratio (2.3) peaked 67- to 72-h post-ingestion. She also developed severe abdominal pain, vomiting and diarrhoea. An abdominal CT scan was consistent with severe enterocolitis, and an upper gastrointestinal endoscopy showed erosive oesophagitis, severe erosive gastritis and ulceration. She was treated with opioid analgesia, proton pump inhibitors, sucralfate and total parenteral nutrition. Secretions caused a contact dermatitis of her face and back. Nine days post-ingestion she was able to tolerate food. Her liver function tests normalized and the dermatitis resolved. Chloroform was measured using headspace gas chromatograph mass spectrometry, with a peak concentration of 2.00 μg/mL, 4 h 20 min post-ingestion. The concentration-time data fitted a 1-compartment model with elimination half-life 6.5 h. Discussion: In addition to early CNS depression and delayed hepatotoxicity, we report severe gastrointestinal injury and dermatitis with chloroform ingestion. Recovery occurred with good supportive care, acetylcysteine and management of gastrointestinal complications. Refereed/Peer-reviewed |
Databáze: | OpenAIRE |
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