Surviving a Massive Sodium Azide Poisoning with Toxic Cardiomyopathy

Overtchouk, Pavel; Poissy, Julien; Thieffry, Camille; Linke, Jean Christophe; Mathieu, Daniel

doi:10.17987/icfj.v4i0.151

Cited by 2 publications

(9 citation statements)

References 9 publications

(8 reference statements)

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“…The remaining four patients were hospitalized, and three died, of whom two were hypotensive and two had metabolic acidosis. The one surviving patient was particularly notable: a 69 year-old female who ingested ~5 g of NaN 3 , about 20-fold more than the estimated lethal human dose, was not hypotensive but had reduced myocardial contraction with a left ventricular ejection fraction of 30% that returned to normal three weeks later [ 63 ].…”

Section: Resultsmentioning

confidence: 99%

“…Therefore, treatments were largely supportive and in response to symptoms. Gastric lavage, with or without activated charcoal, was used in 13 patients, one of whom died [ 46 , 47 , 50 , 54 , 55 , 63 , 73 ]. The NaN 3 dose in these cases ranged from 0.1 g to 1.38 g, with the outlier being the one patient who survived 15 g [ 63 ].…”

Section: Resultsmentioning

confidence: 99%

“…Of six cases of suicidal ingestion of NaN 3 , two of the patients were found dead (Table 1(B-2) [2,[61][62][63][64][65]). The remaining four patients were hospitalized, and three died, of whom two were hypotensive and two had metabolic acidosis.…”

Section: Suicide In a Non-laboratory Setting: Peer-reviewed Papersmentioning

confidence: 99%

“…The hypotension was presumably secondary to azide conversion to nitric oxide. Fifteen patients presented with metabolic acidosis, likely due to profound hypotension and anaerobic metabolism to compensate for mitochondrial inhibition [2,36,47,49,50,[52][53][54][55][57][58][59][60]63]. In some cases, acidosis was severe enough that sodium bicarbonate was administered [36,50,53,54].…”

Section: Treatmentmentioning

confidence: 99%

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Sodium azide poisoning: a narrative review

Tat

Heskett

Satomi

et al. 2021

Clinical Toxicology

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Context: Sodium azide is a highly toxic chemical. Its production has increased dramatically over the last 30 years due to its widespread use in vehicular airbags, and it is available for purchase online. Thus, accidental exposure to azide or use as a homicidal or suicidal agent could be on the rise, and secondary exposure to medical personnel can occur. No antidote exists for azide poisoning. We conducted a systematic review of azide poisoning to assess recent poisoning reports, exposure scenarios, clinical presentations, and treatment strategies. Methods: We searched both medical and newspaper databases to review the literature between 01/ 01/2000 and 12/31/2020, pairing the controlled vocabulary and keyword terms "sodium azide" or "hydrazoic acid" with terms relating to exposures and outcomes, such as "ingestion," "inhalation," "exposure," "poisoning," and "death." We included all peer-reviewed papers and news articles describing human azide poisoning cases from English and non-English publications that could be identified using English keywords. Data abstracted included the number, age, and gender of cases, mode of exposure, exposure setting, azide dose and route of exposure, symptoms, outcome, and treatment modalities. Results: We identified 663 peer-reviewed papers and 303 newspaper articles. After removing duplicated and non-qualifying sources, 54 publications were reviewed describing 156 cases, yielding an average of 7.8 reported azide poisoning cases per year. This rate is three times higher than in a previous review covering the period of 1927 to 1999. Poisoning occurred most commonly in laboratory workers, during secondary exposure of medical personnel, or from a ripped airbag. Hypotension occurred commonly, in some cases requiring vasopressors and one patient received an intra-aortic ballon pump. Gastric lavage and/or activated charcoal were used for oral azide ingestion, and sodium nitrite, sodium thiosulfate, and/or hydroxocobalamin were used in severely poisoned patients. Conclusions: Recent increases in azide poisoning reports may stem from greater commercial use and availability. Treatment of systemic poisoning may require aggressive hemodynamic support due to profound hypotension. Based on mechanistic considerations, hydroxocobalamin is a rational choice for treating azide poisoning.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Suicide In a Non-laboratory Setting: Peer-reviewed Papersmentioning

confidence: 99%

Section: Treatmentmentioning

confidence: 99%

See 2 more Smart Citations

Sodium azide poisoning: a narrative review

Tat

Heskett

Satomi

et al. 2021

Clinical Toxicology

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“… 1 No known antidote exists and its cardiotoxic effects are poorly described in the literature. 1 , 3 …”

Section: Introductionmentioning

confidence: 99%

A case report of sodium azide-induced myopericarditis

Tarabanis,

Banco,

Keller

et al. 2024

European Heart Journal - Case Reports

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Background Sodium azide exposures are rare but can be lethal as the substance inhibits complex IV in the electron transport chain, blocking adenosine-triphosphate (ATP) synthesis. Sodium azide is mostly used as a propellant in vehicular airbags, but is also used in laboratory, pharmacy and industrial settings. No known antidote exists and its cardiotoxic effects are poorly described in the literature. Case summary We describe the case of a 31-year-old patient with major depressive disorder presenting with altered mental status after ingestion of an unknown amount of sodium azide. Although initially chest pain free, she developed pleuritic chest pain 48 hours post-ingestion. This was accompanied by new diffuse ST elevations on the electrocardiogram and serum troponin elevations concerning for myopericarditis. Treatment was pursued with a 14-day course of colchicine resulting in complete symptom resolution within 4 days of treatment initiation. The patient’s transthoracic echocardiogram was only notable for a preserved left ventricular ejection fraction (LVEF). Discussion Cardiac toxicity after sodium azide ingestion usually occurs days after ingestion and has been previously described in the forms of heart failure with reduced ejection fraction complicated by cardiogenic shock. We describe the first case of sodium azide-induced myopericarditis with a preserved LVEF treated with colchicine. Colchicine is an established treatment for pericarditis, but its inhibition of endocytosis, an ATP-dependent cellular function, could be mechanistically relevant to this case.

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Surviving a Massive Sodium Azide Poisoning with Toxic Cardiomyopathy

Cited by 2 publications

References 9 publications

Sodium azide poisoning: a narrative review

Sodium azide poisoning: a narrative review

A case report of sodium azide-induced myopericarditis

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