Clinical toxicology (Philadelphia, Pa.) · 2025
Two fatalities from sodium azide ingestion: delayed enhanced elimination was not effective.
СтатьяКлинический случайНазвание и аннотация: Перевод в очереди
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Husak Nicholas, Sidlak Alexander, Westover Rachael, Haciski Stanislaw, Abesamis Michael
Аннотация
BACKGROUND: Ingestion of sodium azide can lead to severe toxicity, including the development of refractory shock. No antidote has been identified. Enhanced elimination has demonstrated variable outcomes in prior reports.
CASE REPORTS: We present two fatal cases of sodium azide toxicity. The first patient, a 27-year-old man, ingested approximately 5 g of sodium azide and developed hypotension 1 h after ingestion. Orogastric lavage was performed, and vasopressors were started. Hemodialysis was performed 13 h after ingestion. Despite stabilization, he developed recurrent cardiac arrest and died. The second patient, a 19-year-old man, presented 2 h after the intentional ingestion of 40 mL of 5% (2 g) sodium azide. This patient was started on vasopressors and had plasma exchange performed, after which vasopressor requirements were reduced. Shortly after, however, the patient experienced recrudescence of shock and ultimately succumbed to toxicity.
DISCUSSION: Despite aggressive supportive measures, decompensation refractory to supportive measures occurred in both patients. Enhanced elimination techniques were attempted, albeit not immediately, and the delay in initiating hemodialysis and plasma exchange may have limited any potential benefit.
CONCLUSIONS: Enhanced elimination did not appear to alter the course of toxicity in these two patients who ingested at least 2 g of sodium azide.
CASE REPORTS: We present two fatal cases of sodium azide toxicity. The first patient, a 27-year-old man, ingested approximately 5 g of sodium azide and developed hypotension 1 h after ingestion. Orogastric lavage was performed, and vasopressors were started. Hemodialysis was performed 13 h after ingestion. Despite stabilization, he developed recurrent cardiac arrest and died. The second patient, a 19-year-old man, presented 2 h after the intentional ingestion of 40 mL of 5% (2 g) sodium azide. This patient was started on vasopressors and had plasma exchange performed, after which vasopressor requirements were reduced. Shortly after, however, the patient experienced recrudescence of shock and ultimately succumbed to toxicity.
DISCUSSION: Despite aggressive supportive measures, decompensation refractory to supportive measures occurred in both patients. Enhanced elimination techniques were attempted, albeit not immediately, and the delay in initiating hemodialysis and plasma exchange may have limited any potential benefit.
CONCLUSIONS: Enhanced elimination did not appear to alter the course of toxicity in these two patients who ingested at least 2 g of sodium azide.