Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/30094
Title: Life-threatening barium carbonate poisoning managed with intravenous potassium, continuous veno-venous haemodialysis and endoscopic removal of retained ceramic glazes.
Austin Authors: Jamshidi, Nazila;Dhaliwal, Nina;Hearn, Dean;McCalman, Craig;Wenzel, Ross;Koutsogiannis, Zeff ;Roberts, Darren M
Affiliation: Victorian Poisons Information Centre
Sydney Medical School, University of Sydney, Sydney, Australia
Drug Health Services, Royal Prince Alfred Hospital, Camperdown, Australia
Department of Emergency Medicine, Nepean Hospital, Penrith, Australia
Department of Intensive Care, Lismore Base Hospital, Lismore, Australia
New South Wales Poisons Information Centre, The Children's Hospital Westmead, Westmead, Australia
NSW Health Pathology, Trace Elements Laboratory, Royal North Shore Hospital, St Leonards, Australia
Issue Date: 2022
Date: 2022
Publication information: Clinical Toxicology 2022; 60(8): 974-978
Abstract: Barium poisoning is rare but potentially severe. We describe a case of acute barium carbonate poisoning with cardiac arrest, managed with intravenous potassium, dialysis and endoscopic removal of retained ceramic glazes. A 38-year-old woman presented with vomiting 90 min after ingesting 3 cups of barium and strontium carbonate. Initial bloods noted potassium 2.8 mmol/L and creatinine 53 μmol/L. Electrocardiogram demonstrated prolonged corrected QT interval 585msec. Initial management included intravenous potassium. Four hours post-ingestion she developed proximal muscle weakness in upper limbs with a potassium of 2.2 mmol/L. At 15 h post-ingestion she developed profound muscle weakness, polymorphic ventricular tachycardia and cardiac arrest. Treatment included defibrillation, endotracheal intubation and continuous veno-venous haemodialysis (CVVHD) for metabolic derangement and enhanced elimination of barium. Chest X-ray 17 h post-ingestion demonstrated a large radio-opaque mass in the stomach, thought to be the ceramic glaze. Endoscopy removed the retained material 41 h post-ingestion. She was extubated 58 h post-ingestion and CVVHD was ceased on day 3. Serum creatinine peaked at 348 μmol/L on day 7, but normalised by discharge. Biphasic barium concentrations were noted, notably 94 μmol/L on admission, 195 μmol/L at 16 h, 95 μmol/L at 20 h, and 193 μmol/L at 30 h post-ingestion. In barium poisoning with hypokalaemia, prompt potassium supplementation is required but rebound hyperkalaemia can occur. Endoscopic removal of ceramic glazes may be useful more than 12 h post-ingestion. Consider extracorporeal methods to enhance barium elimination in severe cases.
URI: https://ahro.austin.org.au/austinjspui/handle/1/30094
DOI: 10.1080/15563650.2022.2068424
ORCID: 0000-0002-6049-9654
0000-0001-9101-7577
Journal: Clinical Toxicology (Philadelphia, Pa.)
PubMed URL: 35506754
PubMed URL: https://pubmed.ncbi.nlm.nih.gov/35506754/
Type: Journal Article
Subjects: Barium
endoscopy
hypokalaemia
strontium
toxicity
ventricular tachycardia
Appears in Collections:Journal articles

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