Toxicology Experience Report Med. Toxicol. Adverse Drug Exp. 4: 219-227 (1989) oI I 3-5244/89/0005-02 I9/S04.50/0 © ADIS Press Limited All rights reserved. Three Fatal Sodium Azide Poisonings* Wendy Klein-Schwartz,l Richard L. Gorman, 1 Gary M. Oderda,l Brian P. Massaro, 2 Thomas L. Kurt 3 and James C. Garriott 4 I Maryland Poison Center, University of Maryland School of Pharmacy and School of Medicine, Baltimore, Maryland, USA 2 Frederick Memorial Hospital, Frederick, Maryland, USA 3 North Central Texas Poison Center, Parkland Memorial Hospital, Dallas, Texas, USA 4 Office of the Medical Examiner, San Antonio, Texas, USA Summary We report 3 cases and review the published literature on sodium azide ingestion. A 38-year-old man intentionally ingested 2 tablespoonsful of sodium azide in water and developed seizures. coma. hypotension and fatal ventricular arrhythmias within 2 hours. A 33-year-old male ingested an unknown quantity of sodium azide. In the emergency department he was unconscious and underwent immediate intubation and gastric lavage. Nitrite therapy was instituted without improvement. He remained acidotic despite bicarb­ onate therapy and developed hypotension which was unresponsive to pressor agents. He died approximately 8 hours after admission despite resuscitative efforts. A 52-year-old male ingested 1.5 to 2g of sodium azide and survived for 40 hours. Nitrite therapy was ineffective. The role of sodium nitrite in treating sodium azide toxicity by producing methaemo­ globin which complexes with azide is discussed. Sodium azide is a highly toxic chemical which ported previously. In 2 of the fatal cases the amount is lethal in small amounts. It is used both in the ingested was estimated to be 10 to 20g (Abrams et explosive industry to prepare heavy metal azides al. 1987; Albertson et al. 1986). Clinical manifes­ for shell detonators and as a common preservative tations include neurological, cardiovascular and in laboratory reagents. Sodium azide is a direct va­ pulmonary toxicity. We report 3 additional fatal sodilator and was used to treat hypertension in the intentional ingestions of sodium azide. 1950s. Sodium azide interferes with mitochondrial phosphorylation and inhibits cytochrome oxidase Case Reports and other oxidative enzymes. 13 cases of sodium azide ingestion, including 4 deaths, have been re- Case I A 38-year-old man intentionally ingested 2 tablespoonsful of sodium azide diluted in water * Presented in part at the annual meeting of the American Association of Poison Control Centers, Santa Fe, New Mexico, (55g, estimated based on density). In the ambul­ September 28, 1986. ance 30 minutes after ingestion he had a heart rate Fatal Azide Poisonings 220 of 80 beats per minute, blood pressure of 110/ ation revealed a pIa_sma bicarbonate concentration 80mm Hg, respiratory rate of 30 per minute. The of 8 mmol/L as the only abnormality with normal patient had a generalised tonic clonic seizure and complete blood count, prothrombin time, partial his level of consciousness progressively deterio­ thromboplastin time and other electrolytes. Sali­ rated. On arrival in the emergency department I cylate level was 4.1 mg/dl (0.30 mmol/L), but blood hour after ingestion, he was comatose and unres­ and urine were negative for common toxins. The ponsive with heart rate of 160 beats per minute, methaemoglobin level approximately I hour after blood pressure of 130/80mm Hg, respiratory rate administration of sodium nitrite was below 0.5 g/ of 20 per minute. Naloxone was administered dl (within normal physiological range). without response. He was immediately intubated, On admission to the intensive care unit, the placed on 100% oxygen and gastric lavage per­ patient was comatose with corneal reflexes present. formed. 20 minutes after arrival in the emergency The pupils remained fixed and dilated. Lungs were department he developed ventricular fibrillation clear and he was breathing spontaneously on 100% and hypotension (blood pressure of 84/50mm Hg). oxygen by nasal cannula. Arterial blood gases re­ He was unresponsive to resuscitative efforts in­ vealed pH = 7.34, pC02 = 11.4mm Hg, p02 = cluding intravenous dopamine and was pro­ I 52mm Hg, base excess = -18. His neurological nounced dead 1.5 hours after ingestion. and cardiovascular condition deteriorated rapidly and he became unresponsive to pain with loss of Case 2 corneal and deep tendon reflexes. At 3 hours after A 33-year-old male coworker of case I inten­ admission, his blood pressure dropped to 80/ tionally ingested an unknown quantity of sodium 40mm Hg and dopamine was started. He remained azide approximately 2 months later. He told his profoundly hypotensive (60/30mm Hg) and oli­ wife of the ingestion and then collapsed. En route guric despite increasing doses of dopamine. Pre­ to the emergency department he became uncon­ mature ventricular contractions developed which scious with muscle rigidity, a heart rate of 120 beats responded to lignocaine (lidocaine). Acidosis (pH per minute, blood pressure of 90/60mm Hg and = 7.2) persisted despite continued administration respiratory rate of 20 per minute. On arrival, he of sodium bicarbonate. At 5 hours after admission was unconscious and diaphoretic. His pupils were he developed respiratory depression and was placed fixed and dilated. Lungs were clear. Cardiac exam­ on a ventilator; lungs remained clear. Eight hours ination was remarkable only for tachycardia. after admission he became bradycardic (30 beats/ Muscles were flaccid with fasciculations. Electro­ min) which briefly responded to atropine and sod­ cardiogram showed sinus tachycardia with non­ ium bicarbonate. He became profoundly brady­ specific T -wave changes, and a chest x-ray was un­ cardic I minute later and did not respond to ad­ remarkable. The patient was immediately intubated ditional atropine or adrenaline (epinephrine), and and started on 100% oxygen. Orogastric lavage was he was pronounced dead shortly thereafter. performed which recovered a large amount of flaky white material. Later, nasogastric tube drainage was Case 3 grossly bloody. Intravenous therapy was initiated A 52-year-old white man ingested between 1.2 with Ringers lactate and the patient received 300 and 2g of sodium azide in a suicide attempt. The mmol of sodium bicarbonate. Nitrite therapy to in­ man held a doctorate in pharmacology and was un­ duce methaemoglobinaemia was initiated with the der severe psychological stress at the time of the cyanide antidote kit: amyl nitrite (0.3ml) by in­ ingestion. He had access to sodium azide at his halation for 15 seconds, followed by 300mg of sod­ place of employment in the hospital. On arrival in ium nitrite intravenously. The patient also re­ the emergency department about 3 hours post­ ceived 12.5g of sodium thiosulphate. No ingestion he was alert and oriented, moving all ex­ improvement was noted. Initial laboratory evalu- tremities and ambulating well. 10 minutes after ar- Fatal Azide Poisonings 221 rival he experienced a generalised tonic clonic treatments with the cyanide antidote kit with 5- seizure which was controlled with intravenous di­ minute infusions of 300mg sodium nitrite followed azepam. by 3-minute infusions of 12.5g of sodium thiosul­ He was admitted to a medical intensive care unit phate. An autopsy showed bilateral pulmonary with a diagnosis of acute sodium azide ingestion. oedema and congestion, brain swelling and ery­ His condition upon admission was described as thema of the gastric lining but no other cause of flaccid with no response to deep pain. Pupils were death. The conclusion of the medical examiner was 3mm and unreactive. He was intubated, a venous that the death was a result of acute intoxication line was placed into a central vein and an indwell­ with sodium azide. ing urethral catheter was placed. Initial laboratory The maximum methaemoglobin level was 16.1 % evaluation revealed a plasma bicarbonate concen­ which was obtained 1 hour after the second treat­ tration of 8 mmol/L with normal prothrombin ment. The methaemoglobin level ranged from 9 to time, partial thromboplastin time and other elec­ 14% for the other courses of therapy. trolytes. After consultation with the Poison Center, treatment with the cyanide antidote kit (sodium Discussion nitrite and sodium thiosulphate) was initiated. Plasma cyanide ion concentration obtained at this Sodium azide is a neutral, stable, white crystal­ time was 1.6 mg/L; the minimum toxic concentra­ line solid which is hydrolysed in aqueous solutions tion is 0.5 mgfL and the lethal concentration is 2.0 to release hydrazoic acid (Reinhardt & Brittelli mg/L. The blood and urine were negative for com­ 1981). It is rapidly absorbed from the gastrointes­ mon toxic substances. The contents of the vial from tinal tract, skin and respiratory tract. Sodium azide which he ingested the powder were analysed and is highly toxic, with an LDso of 27 mg/kg in mice were negative for cyanide. The vial was not ana­ (Christensen & Luginbyhl 1974). Toxicity results lysed for sodium azide. During the first 12 hours, from inhalation of the gas (hydrazoic acid) or sodium nitrite 300mg and sodium thiosulphate ingestion of the sodium salt. Ingestion produces 12.5g were administered intravenously 3 times. neurological, cardiovascular and pulmonary tox­ Seven hours after admission, the patient was de­ icity. Neurological symptoms include headache, scribed as responsive to pain, making purposeful restlessness, faintness, muscle weakness, hypo- or movements and responding to commands. Plasma areflexia, convulsions, coma and respiratory fail­ cyanide ion concentration 12 and 18 hours after ure. The cardiovascular effects include profound admission were 1.7 mg/L and 0.6 mg/L, respec­ hypotension and tachycardia. tively. 24 hours after admission the patient was re­ The severity of the poisoning is dose dependent. sponsive and 'mouthed' around his endotracheal Table I summarises 13 previously reported cases tube that he had taken sodium azide and was aware and the 3 cases reported herein.