To the Editor: Sodium azide (NaN3) is a highly reactive, crystalline solid found in almost every new car as the gas-generating chemical for airbag deployment (1). Similar to hydrogen cyanide, absorption of NaN3 leads to inhibition of cytochrome c oxidase and eventual cell death. In addition to its toxic metabolic effects, NaN3 exposure also leads to significant physiological compromise. We describe a case of transcutaneous NaN3 exposure after a laboratory explosion that led to several days of profound hemodynamic instability. Rapid recognition of NaN3’s physiological effects led us to appropriately manage this patient both intraoperatively and in the intensive care unit. A 33-yr-old male postdoctoral fellow was attempting a chemical reaction using approximately 13 g of NaN3 in a solution of molybdenum sulfate (a transdermal drug delivery enhancer), when an explosion occurred. The patient suffered traumatic amputations of his left hand at the wrist and the fourth and fifth digits of his right hand. Sprayed glass particles and NaN3 produced chemical and thermal burns to his face, chest, arms, and abdomen (Fig. 1). He was washed with water in a laboratory safety shower prior to transport to the emergency department. The patient remained in the emergency department while awaiting transfer to the operating room (OR) for wound debridement and revision amputation of his hand injuries. No chemical decontamination was performed during that time.Figure 1.: Postoperative photograph showing chemical and thermal burns to face, torso, and arms with traumatic amputation of left hand.Upon arrival to the OR, 3 h after the accident, the patient was slightly hypotensive (90s/50s), despite having received 9 L of crystalloid. His estimated blood loss was minimal. After induction of general anesthesia and transtracheal intubation, the patient’s arterial blood pressure declined rapidly to a systolic pressure of 70 mm Hg, despite minimal anesthetic (desflurane 2.5%). He received approximately 2000 μg of phenylephrine over 30 min in 100 μg boluses. The exposure to NaN3 was subsequently communicated to the anesthesia team, and a literature search suggested we should expect severe hypotension. On the basis of this, we stabilized the patient on a phenylephrine infusion (20–40 μg/min) and decreased IV fluids to maintenance levels. After decontamination and revision of his traumatic amputations, we transferred the patient to a local burn center, where he required a continuous phenylephrine infusion for 4 days. Initial pulmonary artery catheter readings revealed a systemic vascular resistance of 475 and a cardiac index of 4.99 L/min/m2, on 80 μg/min of phenylephrine. The patient subsequently recovered completely from his burn and other injuries, and he was discharged on hospital day 28. NaN3 exposure has been described after accidental ingestion by laboratory technicians, intentional poisonings in the workplace, an explosion at a waste facility handling airbags, and an exposure after an airbag deployment (2–4). The toxic dose of NaN3 has been reported to be 700 mg. (5) Our patient was exposed to more than 13 g by inhaled and transdermal routes, and his exposure was potentially enhanced by a molybdenum sulfate solution. The Center for Disease Control and the National Institute for Occupational Safety and Health recommendations for anyone exposed to NaN3 are immediate removal of all clothing in an upwind environment, followed by washing of skin and hair with warm water and soap using moderate friction (6). Quick removal of NaN3 is necessary to limit inhibition of cytochrome c oxidase, as well as to prevent the hemodynamic instability we observed. There is no known antidote. The most important physiological impairment from NaN3 exposure is hypotension. The body converts NaN3 to nitric oxide, leading to vasodilation (5). Analysis of several NaN3 exposures suggests that the time between exposure and the onset of hypotension often predicts outcome. This case offers three important teaching points: First, chemical exposure needs to be communicated to everyone involved with the patient’s care. Anyone touching this patient was potentially being exposed to a toxic and lethal agent. Second, patients exposed to NaN3 need to be decontaminated immediately with soap and water, not delayed for 3 h while awaiting OR time. Third, the rapid availability of information systems in the OR, such as the Internet, made it possible to obtain vital life-saving information quickly, prompting us to aggressively treat his refractory hypotension. Timothy Angelotti, MD, PhD Samuel Mireles, MD Department of Anesthesia Stanford University Medical Center Stanford, California [email protected] Dennis McMahon, MD Department of Surgery Stanford University Medical Center Stanford, California