BackgroundThe use of hydroxocobalamin has long been advocated for treating suspected cyanide poisoning after smoke inhalation. Intravenous hydroxocobalamin has however been shown to cause oxalate nephropathy in a single-center study. The impact of hydroxocobalamin on the risk of acute kidney injury (AKI) and survival after smoke inhalation in a multicenter setting remains unexplored.MethodsWe conducted a multicenter retrospective study in 21 intensive care units (ICUs) in France. We included patients admitted to an ICU for smoke inhalation between January 2011 and December 2017. We excluded patients discharged at home alive within 24 h of admission. We assessed the risk of AKI (primary endpoint), severe AKI, major adverse kidney (MAKE) events, and survival (secondary endpoints) after administration of hydroxocobalamin using logistic regression models.ResultsAmong 854 patients screened, 739 patients were included. Three hundred six and 386 (55.2%) patients received hydroxocobalamin. Mortality in ICU was 32.9% (n = 243). Two hundred eighty-eight (39%) patients developed AKI, including 186 (25.2%) who developed severe AKI during the first week. Patients who received hydroxocobalamin were more severe and had higher mortality (38.1% vs 27.2%, p = 0.0022). The adjusted odds ratio (95% confidence interval) of AKI after intravenous hydroxocobalamin was 1.597 (1.055, 2.419) and 1.772 (1.137, 2.762) for severe AKI; intravenous hydroxocobalamin was not associated with survival or MAKE with an adjusted odds ratio (95% confidence interval) of 1.114 (0.691, 1.797) and 0.784 (0.456, 1.349) respectively.ConclusionHydroxocobalamin was associated with an increased risk of AKI and severe AKI but was not associated with survival after smoke inhalation.Trial registrationClinicalTrials.gov, NCT03558646

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Sodium azide poisoning is rare (~50 case reports) but can be quickly fatal. A systematic review reported the fatal dose in humans to be over 10 mg/kg 1 . A 69 year-old female was admitted to our hospital for voluntary sodium azide poisoning. She ingested a massive dose of a soup spoon (15 g) of pure sodium azide powder with intention to commit suicide without any co-intoxication. Within minutes, she felt nauseous and had several vomiting. She was immediately brought to the hospital.At admission, 2 hours after the ingestion, despite the absence of hypotension she had widespread marbles on her knees and an extended recoloration time. She had no signs of cardiac insufficiency. Diaphoresis was noticed. Biology showed a balanced metabolic acidosis with (pH of 7.48, bicarbonate 17,2 mmol/L), high blood lactate (6,6 mmol/L) indicating tissue hypoxia, elevated blood glucose (2,1 g/L), normal hypersensitive troponin. The electrocardiogram (ECG) was normal. The patient was immediately treated with gastric lavage and crystalloids. Hyperlactatemia and acidosis resolved within 12 hours.On the 3rd day after the poisoning the biology showed increased hypersensitive troponine (100 ng/mL, normal < 50 ng/ mL). The ECG showed a ST-segment elevation in leads DI, DII, AVL, AVF, and V4 to V6, with reciprocal ST depression in leads AVR and V1 without any chest pain (figure 1). Contemporary blood lactate increased again (4.3 mmol/L), same as liver transaminases (3 times the normal rate) and CRP (80 mg/L). The transthoracic echocardiography showed a decreased left ventricle ejection fraction (LVEF) at 30% with no dilation. Akinesis was noted in the apex, upper third of the lateral and inferior area. The left ventricle was overall hypokinetic. Medium E/E' ratio of 12.5 pointing out elevated left ventricle filling pressure. The right ventricle and the systolic arterial pulmonary pressure were normal. There was no pericardial effusion.She was immediately transferred for emergency coronary angiography which found no clot or coronary spasm, but a 80% stenosis was noticed in the proximal section of the right coronary artery. No angioplasty was carried out. Nitrates were introduced to improve myocardial perfusion.A cardiac MRI (Magnetic Resonance Imaging) was carried out 3 weeks after the poisoning. It showed a LVEF of 52%, a slight overall hypokinesis, no pathological enhancement, thus no myocarditis or infarct sequelae. Besides it showed a circumferential pericardial effusion of moderate volume (maximum 17 millimeters facing the left ventricle).We concluded to toxic cardiomyopathy caused by sodium azide.

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