Dose-Dependent Pulmonary Injury Following Nitrogen Dioxide Inhalation From Kinepak™ Detonation.

BACKGROUND: Nitrogen dioxide (NO2) is a pulmonary irritant produced as a byproduct of bacterial anaerobic metabolism of organic materials, and is also produced as a byproduct of explosive detonations. Significant NO2 exposure results in free-radical-induced pulmonary injury that may be delayed up to 3-30 h after exposure and can progress to acute respiratory distress syndrome (ARDS) and death. Here we present a case series of 3 patients with dose-dependent pulmonary injury consistent with NO2 inhalation following exposure to fumes from detonation of an ammonium nitrate/nitromethane (ANNM) explosive device. CASE REPORTS: Three individuals presented to the emergency department over the course of 16 h, beginning approximately 16 h after exposure to fumes from an ANNM explosive device. Patient 1, with the most significant exposure, developed ARDS necessitating intubation and mechanical ventilation. Patient 2 exhibited hypoxia and findings concerning for diffuse airway inflammation, but ultimately required only supplemental oxygen. Patient 3, with the least exposure, had imaging abnormalities but required no intervention. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Respiratory distress is a common presenting complaint to the emergency department. Because of the delayed presentation and the potential for progressive worsening of symptoms associated with NO2 exposure, it is important that emergency physicians be aware of the multiple potential means of exposure and consider this diagnosis in the proper clinical context. Patients with suspicion of NO2-related lung injury should undergo more extended observation than their initial clinical presentation may suggest.

Complete clinical course of envenomation by Protobothrops mangshanensis: delayed coagulopathy and response to Trimeresurus albolabris antivenom.

INTRODUCTION: Protobothrops mangshanensis, the Mangshan pit viper, is a rare pit viper native to the area surrounding Mount Mang in China's Hunan province. Toxicity from envenomation is not well characterized. CASE DETAILS: A 33-year-old male presented to an emergency department (ED) after being bitten on the forearm by his P. mangshanensis. He complained of mild swelling and pain at the bite site. He was admitted for observation and toxicology consultation. Following initially normal coagulation studies including platelets, prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen and D-dimer, fibrinogen decreased to 121 mg/dL and D-dimer concurrently rose to 377 ng/mL over 24 h. On hospital day 2 fibrinogen stabilized at 109 mg/dL and he was discharged with outpatient laboratory monitoring. Three days later, he returned with bruising to the contralateral arm. Fibrinogen was undetectable (<40 mg/dL) and PT was 14.6 s. He declined admission but returned 2 d later with bruising to the nose. Bloodwork revealed immeasurably prolonged PT, aPTT, and thrombin time, but he eloped. Late that evening he returned and was treated with three vials of Green pit viper (Trimeresurus albolabris) antivenom. Within 24 h coagulopathy improved markedly; at five days, coagulation abnormalities resolved. DISCUSSION: Mangshan pit viper envenomations may cause isolated hemotoxicity, despite molecular studies suggesting additional neurotoxicity and myotoxicity. T. albolabris antivenom appears effective in treating the resultant coagulopathy. CONCLUSION: We report the natural history of envenomation by the Mangshan pit viper. A delayed coagulopathy, apparently fibrinolytic in nature, is unaccompanied by local tissue destruction and responsive to Green pit viper antivenom.