Delayed Pulmonary Edema and Bronchospasm After Accidental Lacrimator Exposure FEDERICO E. VACA, MD, JOHN H. MYERS, MD, MARK LANGDORF, MD, MHPE Clinical manifestations of lacrimator exposure can be immediate or significantly delayed. In both phases, the sequelae can be severe and life-threatening. As personal protection devices, these agents have become readily available to the public in many areas of the country. Emergency physicians should gain a firm understanding of the presenta- tion, management, and disposition of the lacrimator-exposed patient. A case of accidental prolonged lacrimator exposure inducing pulmonary edema and bronchospesm is presented. (Am J Emerg Med 1996;14:402- 405. Copyright © 1996 by W.B. Saunders Company) Lacrimators are a group of chemical agents used for riot control by law enforcement agencies throughout the US. Increasingly, civilians are carrying personal protection de- vices that also contain these chemical agents. We describe the case of a young woman who presented to our emergency department (ED) with delayed-onset pulmonary edema and severe bronchospasm after a prolonged accidental exposure to chloroacetophenone (CN) dispensed from a personal protection device. We will review the most commonly used lacrimating agents and their potential clinical sequelae. Emergency physicians must be aware of the complications resulting from exposure to these agents. CASE REPORT A 24-year-old Vietnamese woman was brought to our ED by paramedics with a chief complaint of chest pain and shortness of breath of 3 hours' duration. The paramedics reported that they found the patient diaphoretic, profoundly orthopneic, and holding her chest. Additionally, she complained of a bitter taste in her mouth. She denied fever, nausea, emesis, hernoptysis, or history of tuberculosis. She had a history of rheumatic heart disease and a St. Jude mitral valve replacement in July 1991. Her medications included warfarin and iron. Initial physical examination found a thin woman in obvious respiratory distress. She was alert and awake, holding her chest, sitting upright with labored respirations, and answered questions appropriately with assistance of a Vietnamese translator. Her blood pressure was 90/60 mm Hg, her pulse rate was 100 beats/min, respiration rate was 20 breaths/rain, and oral temperature was 37.4°C. Her saturation by pulse oximetry was 94% on 4 liters of oxygen via nasal cannula. The pupils were equal and reactive. There was mild epiphoria with scleral and subconjunctival injection bilaterally. No jugular venous distention or carotid bruits were appreciated. Her point of maximal impulse (PMI) was normal with a regular tachycardia and a mechanical S1 click. There was a nonradiating II/VI systolic murmur at the left sternal border, with no audible rub or gallop. The lungs had bilateral rales with mild to moderate expiratory wheezes. The remainder of the physical examination was unremarkable. An electrocardiogram showed sinus tachycardia with right atrial enlargement. The initial arterial blood gas consisted of a pH of 7.39, PCO2 of 33.5, PO2of 75.8, HCO3 of 20.2, and Sat of 95.2% on 4 liters of oxygen. The prothrombin time was 14.7 and partial thromboplastin time PTT was 34.3. A portable chest radiograph was obtained with a preliminary reading of cardiogenic pulmonary edema (Figure 1). The patient was treated aggressively in the ED with diuretics and nitroglycerine. She was also heparinized because, initially, coro- nary thrombosis was highly suspected. A cardiology consultation was obtained. An echocardiogram revealed normal left ventricular size and function with mild mitral and tricuspid regurgitation. The patient improved minimally with the initial interventions. Consulta- tion with our expert chest radiologist was obtained. It was immediately recognized that the chest X-ray showed many charac- teristics of inhalation injury lung edema, including unilaterally worsened edema and increased vascular markings. On further questioning, the patient reported that her roommate, the wife of a security officer, had sprayed what she thought was "room deodorizer" throughout the small apartment 18 hours before the onset of symptoms. She recalled a burning sensation in her eyes as well as tearing. The cannister was obtained and determined to contain chloroacetophenone (CN), a potent lacrima- tor designed to cause eye and upper respiratory inflammation and irritation to deter attackers when sprayed in close proximity. The patient was subsequently admitted to the intensive care unit ICU with a diagnosis of inhalation pneumonitis with delayed noncardiogenic pulmonary edema. At that time, it was believed that the already compromised cardiovascular status of the patient was significantly worsened by the prolonged lacrimator exposure and subsequent lung injury. During her hospital course, her symptoms gradually improved over 2 to 3 days. However, several days after admission, her respiratory status deteriorated and she was noted to have worsening pulmonary edema. The cardiothoracic surgery consultant recommended that the patient undergo mitral valve replacement. The procedure was performed and the patient toler- ated the surgery well. She was discharged without further complica- tions. From the Division of Emergency Medicine, University of California Irvine Medical Center, Orange, CA. Manuscript received April 4, 1995, returned May 15, 1995; revision received July 1,1995, accepted July 17, 1995. Address reprint requests to Dr Vaca, 3545 Caminito El Rincon #235, San Diego, CA92130. Key Words: Lacrimators, pulmonary edema, chloroacetophenone, o-chlorobenzylidenemalononitrile, chloropicrin, capsaicin. Copyright © 1996 by W.B. Saunders Company 0735-6757/96/1404-001755.00/0 402 DISCUSSION Lacrimating agents are solid chemicals dispensed as a fine dust or aerosol spray. They are used by law enforcement agencies for riot control, but are being used with increasing frequency by civilians in small personal protection devices. These devices are commonly referred to as tear gas, mace, and more recently, "pepper spray." Lacrimators create several desired effects that temporarily incapacitate the