TY - JOUR
AU - MD, D. G. Greenhalgh,
AB - Abstract Chemical burn injuries commonly occur at the workplace and can be caused by a variety of agents. Sodium azide is a volatile compound used in the industrial setting and it is also a constituent of car airbags. The known toxic effects of sodium azide include hypotension, bradycardia, and headaches. At the cellular level, it inhibits of ATP production by blocking the respiratory oxidation cascade. In the burn literature only one previous report documents a sodium azide hand burn caused by airbag malfunction. We report a case of massive exposure and resultant systemic toxicity from a sodium azide canister explosion. Burn injuries comprise approximately 5% of occupational injuries. Most of these burns are relatively minor and require only outpatient treatment. Data from 1981 report that more than 150,000 occupational burns were evaluated in emergency departments that year. 1 Chemical burns represent only a small fraction of these accidents. The number of chemicals, however, that can cause skin and other tissue damage numbers more than 25,000. 2 To our knowledge, only one case of thermal injury from sodium azide (NaN3) exists in the burn literature. 3 Although highly toxic, this agent has long been employed in the industrial setting. The widespread use of sodium azide came when airbags were popularized in the early 1990s. Sodium azide decomposition is the source of the explosive expansion resulting in the inflation of the airbag. There have been a variety of articles regarding the physiologic effects of sodium azide exposure. Poisoning by inhalation and ingestion has also been described. Patients develop dose-dependent symptoms of hypotension caused by direct vasodilation, myocardial and respiratory failure, lactic acidosis, and coma. 4 At the cellular level sodium azide toxicity is related to inhibition of cytochrome C oxidase. 5 Uncoupling of ATP synthase from the respiratory cascade causes cell death analogous to hydrogen cyanide poisoning. We report a lethal case of chemical and thermal injury from this agent. CASE REPORT A 29 year-old man sustained approximately a 50% TBSA deep second-degree burn to the face, neck, chest, back, arms, and legs after his fork lift truck struck a 50-gallon drum containing an unknown waste product that subsequently exploded. Other injuries included crush injuries to the thighs, and bilateral open and comminuted tibia and fibula fractures. He was orally intubated at the scene and transported to the emergency department, where he received the standard trauma evaluation and resuscitative measures. During his diagnostic workup, he developed bradycardia (heart rate of 50/min) and hypotension (systolic pressure of 60 mmHg). Fluids and inotropic support were initiated with no response. He was rapidly transferred to the Burn Unit for further resuscitation. At this time the patient was hypothermic, hypotensive, and bradycardic. The burns to his face, neck, back, arms, and legs appeared deep second to third degree. His eyebrows were singed, but he did not have soot in his upper airway. He had a right upper lobe collapse on chest radiograph. His initial arterial blood gas showed a pH of 7.13, with a bicarbonate level at 14 mmol/L and a base deficit of 15. Pulmonary artery catheter monitoring revealed a cardiac output of 14 L/min (cardiac index = 9.3), and a decreased peripheral vascular resistance. Diagnostic peritoneal lavage and echocardiogram were performed to look for a cause of his hypotension and profound metabolic acidosis. Diagnostic studies revealed no evidence of cardiac anomalies or intra-abdominal injuries. The patient developed refractory hypotension despite massive fluid resuscitation with more than 32 L of crystalloid and blood products in the first 12 hr. Calculated fluid requirements in the first 24 hr for this patient based on the Parkland formula were 20 L of lactated Ringer's solution. His pH after 6 hr of resuscitation was 7.06 despite aggressive fluid resuscitation, vasopressor infusion, and administration of 35 ampules of sodium bicarbonate. At this time we learned from the industrial plant that the canister might have contained sodium azide. It seemed that the patient had sustained both flame and chemical burns after contact with sodium azide and its products of combustion. Toxicology experts, a poison control center, and a national agency for chemical disasters were contacted. All parties stated that the prognosis was poor after exposure to this agent. The patient's blood pressure increased to 90 to 120/50 to 60 mmHg with high-dose epinephrine infusion, but his acidosis never improved. Approximately 12 hr after admission the patient developed further bradyarrhythmias and subsequent asystole unresponsive to atropine or epinephrine. He was pronounced dead after standard resuscitative efforts failed. His autopsy findings were consistent with massive burn injury. No signs of a major airway injury were found at the postmortem examination. Blood sodium azide concentrations were not obtained during hospitalization or at autopsy because of laboratory limitations. This value however, can be measured with a high performance liquid chromatography assay of the azide derivative in blood. 6 DISCUSSION Chemical burns account for 5 to 16% of burns that require inpatient treatment. 7, 8 In a retrospective study, Sykes 9 showed that young men (average age, 28) are commonly affected and that alkali agents are the predominant causative agent. The most common areas burned in decreasing order are the upper extremities, lower extremities, trunk, and head. A chemical burn can be particularly deleterious, because many agents are known to diffuse through intact skin. 10 NaN3 exists as a colorless or white crystalline powder at room temperature. It can be stored in a solid form, but can also be dissolved in water or ethanol. Although listed in the Material Safety Data Sheets as a stable agent, sodium azide is highly flammable and can explode after exposure to heat, shock, or even friction. It reacts with many metals and thus is usually stored in a nonmetallic, explosion-proof container. 11 Pure decomposition generates N2 gas and metallic sodium. Automobile makers use this explosive reaction for airbag deployment. The airbag contains a mixture of sodium azide, silicon dioxide, and other oxide components. Deceleration of the vehicle activates an electrical circuit that ultimately ignites NaN3. N2 accumulates and fills the bag in 40 milliseconds, while metallic sodium is rendered less toxic by an oxidation reaction with silicon dioxide. Accidental exposures, however, usually involve incomplete decomposition or combination with agents such as hydroxide to form toxic fumes. Clinical experience with treatment of sodium azide intoxication is very limited. In the industrial workplace episodes of diarrhea and mild lowering of blood pressure have been documented after prolonged dermal or inhalation exposure. 12 In fact, this agent has been studied in clinical trials as a treatment for hypertension. No adverse effects were noted at low doses. 11 To our knowledge only one previous report of sodium azide thermal injury exists in the burn literature. Vitello et al 3 described a full-thickness hand burn secondary to airbag malfunction. Their patient's exposure to sodium azide was approximately 70 g (before combustion). No systemic effects were included in their report. Airbag malfunction is, fortunately, a rare event, and the use of airbags has been shown to reduce fatality in car crashes. 13 Our case differed in two major aspects. First, our patient suffered a massive exposure in an industrial accident. Second, his shock state was remarkably more profound than predicted by a 50% TBSA burn. Although sodium azide is flammable, exposure to large doses of this agent can also lead to absorption through the skin and lungs. Its potent effects of vasodilation and cytochrome C enzyme inhibition result in marked hypotension and metabolic acidosis that are unresponsive to aggressive fluid resuscitation, vasopressor treatment, and supplemental bicarbonate administration. Massive exposure combined with thermal injury led to death in this case in 12 hr. We believe that the direct massive vasodilatory effect was the primary cause for his hypotension, with a compensatory increase in cardiac output. The cause of the bradycardia is not understood but might have been related to stress. This inadequate cardiac response, however, amplified the shock state. Persistent hypotension led to tissue hypoperfusion and increased acidosis. In addition to the hypotension, the direct end-organ effect of sodium azide was tissue hypoxia caused by the alteration in cellular respiration. With inhibition of oxygen use, cells were forced to rely on anaerobic pathways, which eventually led to cell necrosis. The combination of severe thermal injury with massive sodium azide exposure was fatal. The extent of shock, combined with irreversible acidemia in this patient, prompted us to investigate sodium azide toxicity. Our literature search revealed that clinical experience with sodium azide intoxication was scant and usually consisted of reports involving small-dose exposure. This is the first case report that documents the severity of cellular and organ toxicity to sodium azide. Although blood pressure could be improved with large-volume fluid resuscitation and massive inotropic support, cellular damage was irreversible. There is no known antidote for sodium azide. Further research to clarify the mechanism of cytochrome C inhibition by sodium azide is warranted and ultimately could prevent fatal outcome from large-dose exposure. REFERENCES 1. Occupational Injury Surveillance—United States. MMWR  1981; 30: 578. PubMed  2. Curreri PW, Asch MJ, Pruitt BA The treatment of chemical burns. J Trauma  1988; 10: 634– 42. Google Scholar CrossRef Search ADS   3. Vitello W, Kim M, Johnson M, Miller S Full-thickness burn to the hand from an automobile airbag. J Burn Care Rehabil  1999; 20: 212– 5. Google Scholar CrossRef Search ADS PubMed  4. Herbold M, Schmitt G, Aderjan R, Pedal I Fatal sodium azide poisoning in a hospital: a preventable accident [in German]. Arch Kriminol  1995; 196: 143– 8. Google Scholar PubMed  5. Bennett MC, Mlady GW, Kwon YH, Rose GM Chronic in-vivo NaN3 Infusion induces selective and stable inhibition of cytochrome C oxidase. J Neurochem  1996; 66: 2606– 11. Google Scholar CrossRef Search ADS PubMed  6. Marquet P, Clement S, Lofti H Analytical findings in a suicide involving sodium azide. J Anal Toxicol  1996; 20: 134– 8. Google Scholar CrossRef Search ADS PubMed  7. Herbert K, Lawrence JC Chemical burns. Burns  1989; 15: 381– 8. Google Scholar CrossRef Search ADS PubMed  8. Ng D, Anastakis D, Douglas LG Work-related burns: a 6-year retrospective study. Burns  1991; 17: 151– 9. Google Scholar CrossRef Search ADS PubMed  9. Sykes RA, Mani MM, Hiebert JM Chemical burns: a retrospective review. J Burn Care Rehabil  1986; 7: 343– 7. Google Scholar CrossRef Search ADS PubMed  10. Doull J, Klaassen CD, Amdur MO editors. Casarett and Doull's toxicology: the basic science of poisons.  2nd ed. New York: McMillan Co; 1980. p. 35– 7. 11. Material safety data sheets.  Genium's Reference Collection, Genium Publishing Corp., Schenectady, NY, 1989. 12. Trout D, Esswein EJ, Hales T, Brown K, Solomon G, Miller M Exposures and health effects: an evaluation of workers at a sodium azide production plant. Am J Ind Med  1996; 30: 343– 50. Google Scholar CrossRef Search ADS PubMed  13. National Institute for Highway Safety Driver fatalities in 1985–1993 cars with airbags. J Trauma  1995; 38: 469– 75. CrossRef Search ADS PubMed  Copyright © 2001 by the American Burn Association
TI - Sodium Azide Burn: A Case Report
JF - Journal of Burn Care & Research
DO - 10.1097/00004630-200105000-00012
DA - 2001-05-01
UR - https://www.deepdyve.com/lp/oxford-university-press/sodium-azide-burn-a-case-report-nAKEKZZlo5
SP - 246
EP - 248
VL - 22
IS - 3
DP - DeepDyve
ER -