A case of survival following high-dose sodium azide poisoning

A case of survival following high-dose sodium azide poisoning

To the Editor:

We would like to report the case of a woman who survived the ingestion of a very large amount of sodium azide.

The patient was a 53-year-old woman who was in the hospital for treatment of her diabetes mellitus. She was provided with a 24-hour urine collection preservative containing 1 g of sodium azide, which she drank in error. She immediately complained of feeling sick and subsequently developed convulsions and required endotracheal intubation. Gastric lavage was carried out and activated charcoal (1 g/kg) was administered approximately 20 minutes after the ingestion. Due to low blood pressure (systolic pressure, 50–60 mmHg) approximately 1.5 hours after the ingestion, dopamine and dobutamine infusion was initiated. Hemodialysis was initiated approximately 4 hours after the ingestion and was continued for 3 hours. Pre-hemodialysis arterial blood gas values were pH, 7.343, P_aO₂, 127.1 torr, P_aCO₂, 14.8 torr, base excess, −16.2, HCO₃⁻, 7.8 mEq/L under mechanical ventilation with F_iO₂ 0.5; post-hemodialysis arterial blood gas values were pH, 7.297, P_aO₂, 217.5 torr, P_aCO₂, 39.3 torr, base excess, −6.9, HCO₃⁻, 18.6 mEq/L. Following the administration of 1 g of methylprednisolone within the same day and plasma exchange with 3200 mL of fresh frozen plasma on the following day, she was transferred to our ICU for further critical care.

Upon arrival, her Glasgow Coma Scale scores were E-4, V-5, and M-6 with a body temperature of 37.6°C, a respiratory rate of 28/min, a blood pressure of 88/44 mmHg, and a heart rate of 110 beats/min (regular) supported with dopamine (4 µg/kg/min) and dobutamine (3 µg/kg/min). Complete blood count revealed a white blood count of 23700/mm³, hemoglobin of 14.7g/dL, hematocrit of 43.2%, and a platelet count of 29.2 × 10⁴/mm³. Blood biochemical examination revealed aspartate aminotransferase 50 IU/L, alanine aminotransferase 30 IU/L, urea 12 mg/dL, creatinine 0.53 mg/dL, sodium 142 mEq/L, potassium 3.1 mEq/L, chloride 100 mEq/L, and lactate 67 mg/dL (normal 5 to 20 mg/dL). A chest x-ray demonstrated clear lungs. Continuous hemodiafiltration (CHDF) was initiated immediately after ICU admission in an attempt to remove sodium azide. Before the sodium azide ingestion, her electrocardiogram (ECG) showed no ST-segment abnormalities. Approximately 40 hrs after ingestion, her ECG showed remarkable ST-segment elevation in all leads except aVR. Transthoracic echocardiography (TTE) showed depressed systolic function in a wide area of left ventricle except for the base. Coronary angiography revealed no significant stenosis. Swan-Ganz catheterization demonstrated a cardiac output of 3.00 L/min, cardiac index of 2.06 L/min/m², and pulmonary capillary wedge pressure of 20 mmHg, indicating Forrester Subset IV. Therefore, intensive circulatory support was initiated with intra-aortic balloon pumping (IABP) along with combined infusion of dopamine (5 µg/kg/min) and olprinone (0.1 µg/kg/min). She was weaned from IABP on the eighth day after ingestion. Mechanical ventilation was terminated on the seventh day, followed by weaning from CHDF on the ninth day after ingestion. Left ventricular contraction was entirely normal with an Ejection Fraction of 63% on TTE on the eleventh day after ingestion. Although ST-segment elevation on ECG had disappeared, T wave inversion in leads I, II, III, aVL, aVF, and V3 to V6 remained even on the eighteenth day after ingestion when she was discharged from the ICU. She did not have any arrhythmias and no organ failure, other than heart failure which was noted during her ICU stay. It was subsequently found that the concentrations of sodium azide on pre-hemodialysis blood and post-hemodialysis blood were 174 ppm and 37 ppm, respectively, which then decreased to 0.3 ppm on admission to the ICU.

While sodium azide is highly toxic, details of its in-vivo kinetics and excretion remain unclear. Following ingestion, effects such as nausea, vomiting, diarrhea, vertigo, dizziness, transient loss of vision and consciousness and hypotension are observed immediately, with hypotension being most frequently noted (1). ECG findings similar to those observed in the present case were reported by Judge et al. (2). According to the analysis by Chang et al., the highest survived dose of ingested sodium azide is 150 mg and the lowest fatal dose is 700 mg (1). Based of this fact, Chang et al. reported that the human lethal dose is 700 mg (10 mg/kg). To our knowledge, our case is the first one to survive an ingestion of sodium azide in an amount exceeding the reported lethal dose.