No abstract

Abstract. The Tokyo subway sarin attack was the second documented incident of nerve gas poisoning in Japan. Prior to the Tokyo subway sarin attack, there had never been such a large-scale disaster caused by nerve gas in peacetime history. This article provides details related to how the community emergency medical services (EMS) system responded from the viewpoint of disaster management, the problems encountered, and how they were addressed. The authors' assessment was that if EMTs, under Japanese law, had been allowed to maintain an airway with a n endotracheal tube or use a laryngeal mask airway without physician oversight, more patients might have been saved during this chemical exposure disaster. Given current legal restrictions, advanced airway control at the scene will require that doctors become more actively involved in out-of-hospital treatment. Other recommendations are: 1) that integration and cooperation of concerned organizations be established through disaster drills; 2) that poison information centers act as regional mediators of all toxicologic information; 3) that a reaI-time, multidirectional communication system be established; 4) that multiple channels of communication be available for disaster care; 5) that public organizations have access to mobile decontamination facilities; and 6) that respiratory protection and chemical-resistant suits with gloves and boots be available for out-of-hospital providers during chemical disasters. HE TOKYO subway sarin attack was the sec-T ond documented incident of nerve gas poisoning in Japan. The first mass public exposure t o sarin (methyl phosphonofluoridic acid l-methylethyl ester) gas occurred in the city of Matsumoto in June 1994.' From a worldwide historical perspective, the Tokyo subway sarin attack represents the largest disaster caused by nerve gas in peacetime history. Until these episodes, a terrorist attack with chemical warfare agents in a public setting was incomprehensible. Indeed, the Japanese believed that the Tokyo subway system was the safest transportation system in the world. As a result of this attack, many problems were encountered and the Japanese have been forced to radically alter their approach to disaster management.We previously published a preliminary report on the Tokyo subway sarin attack.2 The current article provides further detail related to how the community emergency medical services (EMS) system responded from the viewpoint of disaster management, the problems encountered, and how they were addressed. Companion articles address the hospital response3 and the national and international responses4 related to this event. NATIONAL AND REGIONAL EMS SYSTEMIn Japan, disaster planning is based on the "fundamental law of disaster management." This law

Abstract. The Tokyo subway sarin attack was the second documented incident of nerve gas poisoning in Japan. The authors report how St. Luke's Hospital dealt with this disaster from the viewpoint of disaster management. Recommendations derived from the experience include the following: Each hospital in Japan should prepare an emergent decontamination area and have available chemical-resistant suits and masks. Ventilation in the ED and main treatment areas should be well planned at the time a hospital is designed. Hospital disaster planning must include guidance in mass casualties, an emergency staff callup system, and a n efficient emergency medical chart system. Hospitals should establish a n information network during routine practice so that it can be called upon at the time of a disaster. The long-term effects of sarin should be monitored, with such investigation ideally organized and integrated by the Japanese government. Key words: sarin; disaster medicine; chemical warfare agents; emergency medical services; EMS; international medicine. ACADEMIC EMERGENCY MEDICINE 1998; 5:618-624 HE TOKYO subway sarin attack was the sec-1 ond documented incident of sarin (methyl phosphonofluoridic acid 1-methylethyl ester) nerve gas poisoning in Japan, the first episode having occurred in the city of Matsumoto in June 1994.' St. Luke's International Hospital was a major receiving hospital for the Tokyo subway sarin attack. Although St. Luke's Hospital had a disaster plan and disaster drills were carried out regularly, the disaster plan was mainly aimed at responding to fires and earthquakes. After Japan experienced the great Hanshin earthquake in January 1995, every hospital reconsidered its existing disaster plan.2 At the time of the Tokyo subway sarin attack, St.Luke's Hospital was in the process of revising its disaster planning.We have published a preliminary report on the Tokyo subway sarin a t t a~k .~ That article contained little description of the hospital resource deployment that occurred during the sarin attack disaster. In this article we address the St. Luke's Hospital disaster management response, problems encountered, and how the hospital addressed these problems. Companion articles focus oh the community emergency response4 and the national and international responses6 to this disaster.

Expression of group IIA secretory phospholipase A 2 (sPLA 2 -IIA) is documented in the cerebral cortex (CTX) after ischemia, suggesting that sPLA 2 -IIA is associated with neurodegeneration. However, how sPLA 2 -IIA is involved in the neurodegeneration remains obscure. To clarify the pathologic role of sPLA 2 -IIA, we examined its neurotoxicity in rats that had the middle cerebral artery occluded and in primary cultures of cortical neurons. After occlusion, sPLA 2 activity was increased in the CTX. An sPLA 2 inhibitor, indoxam, significantly ameliorated not only the elevated activity of the sPLA 2 but also the neurodegeneration in the CTX. The neuroprotective effect of indoxam was observed even when it was administered after occlusion. In primary cultures, sPLA 2 -IIA caused marked neuronal cell death. Morphologic and ultrastructural characteristics of neuronal cell death by sPLA 2 -IIA were apoptotic, as evidenced by condensed chromatin and fragmented DNA. Before apoptosis, sPLA 2 -IIA liberated arachidonic acid (AA) and generated prostaglandin D 2 (PGD 2 ), an AA metabolite, from neurons. Indoxam significantly suppressed not only AA release, but also PGD 2 generation. Indoxam prevented neurons from sPLA 2 -IIA-induced neuronal cell death. The neuroprotective effect of indoxam was observed even when it was administered after sPLA 2 -IIA treatment. Furthermore, a cyclooxygenase-2 inhibitor significantly prevented neurons from sPLA 2 -IIA-induced PGD 2 generation and neuronal cell death. In conclusion, sPLA 2 -IIA induces neuronal cell death via apoptosis, which might be associated with AA metabolites, especially PGD 2 . Furthermore, sPLA 2 contributes to neurodegeneration in the ischemic brain, highlighting the therapeutic potential of sPLA 2 -IIA inhibitors for stroke.