In the morning rush hour on March 20, 1995 a group of terrorists placed containers of the nerve gas sarin in five carriages on three of Tokyo's ten underground railway lines. The Tokyo Underground comprises 230 km of track and transports many million people daily.
The sarin containers were put in carriages that were all expected to arrive in one Central Tokyo station at approximately the same time. Very soon the Tokyo Emergency Control Centre staff realised that something serious had occurred, for within 15 minutes they received a great number of alarms from fifteen underground stations. Initially a fire or explosion was suspected, but the victimsí symptomatology quite soon indicated a nerve agent. This was verified within a few hours by police chemical experts.
Quite soon there were injured people at fifteen underground stations. They had been exposed to sarin either in the carriages or on the platforms. They reported a strong smell of a solvent (which turned out to be acetonitrile) and intense eye irritation. Soon people also experienced breathing difficulties and muscle weakness and many lost consciousness. Sarin spread from carriage to carriage since these were in communication with each other. Only one person died while still in the carriage: all the other exposed victims managed to get out or were exposed to sarin on the platform.
The sarin concentration could not have been very high in any of the carriages except very locally, which is why symptoms appeared slowly in most cases. Although symptoms normally appear very quickly after sarin exposure there may be a delay of several minutes between exposure and the development of severe symptoms. Several people managed to get out into fresh air before losing consciousness.
Approximately thirty minutes after the first alarm, first aid stations were set up in the street outside the underground stations or in nearby temples. As well as ambulance personnel (including paramedics) medical teams of doctors and nurses also took part in the rescue work. No advanced medical treatment was given on site, only life saving procedures. Ambulance and medical personnel triaged patients for transport to hospitals.
At 08.35 the first patient was transported by ambulance to St Luke¥s International Hospital, arriving at 08.40. In all, 550 persons were transported by ambulance to hospital. Only a few were transported in mini buses provided by the fire brigade. The rest made their way to hospital on foot or in private cars to hospitals or private outpatient clinics.
In all 5-6,000 persons were exposed. 3,227 went to hospital of whom 493 were admitted to 41 of Tokyo's many hospitals. Only 17 developed severe symptoms requiring intensive care. In all twelve people died from the sarin exposure. During the first 24 hours ten persons died, nine at the accident site and one just after arrival at hospital. Two persons died several weeks later from complications of the hypoxic brain damage suffered during the acute phase. Several other people have permanent brain damage.
Most patients arriving at hospital had rather mild symptoms and could leave the hospital after examination and possible treatment, while most who were admitted could be discharged 24 to 48 hours after the accident.
On the third day only a few patients were still in the intensive care unit. Blood samples from the severely injured contained sarin metabolites and a pronounced decrease in plasma cholinesterase activity.
The symptomatology of the exposed victims was typical for nerve gas exposure, i. e. a result of over-stimulation of those nerves that have acetylcholine as transmitter substance. Symptoms of the nicotinic effect dominated, with pallor, tachycardia, hypertension, muscle fasciculation and muscular weakness, while muscarinic effects, e.g. sweating, secretions, bradycardia, were less pronounced. In the severe cases there were also seizures. The predominant symptom which led to the suspicion of a nerve agent as the toxic substance was the pronounced miosis with pin-point pupils.
Initially only symptomatic therapy was given, but in those cases with advanced bradycardia atropine was of course administered. Seizures were treated with diazepam. After nerve gas was verified as being the toxic agent, pralidoxime (a choline esterase activator) was also given at some hospitals as well as atropine. In the severe cases very high doses of atropine were given (up to 10 mg per hour) during the first 24 hours. At those hospitals where pralidoxime was given much lower doses of atropine were used (2.5-9 mg per 24 hours).
Some patients with cardio-pulmonary arrest soon after arrival to hospital were resuscitated and treated with antidotes, recovering completely after a few days¥ hospitalisation.
Informed of the Tokyo incident largely by telephone from Tokyo colleagues, physicians in Matsumoto faxed information on the experience they had gained from a sarin attack on June 27 June, 1994 (see below).
They gave information about the most important symptoms and advice on treatment measures. The results from a current study were also sent.
At 11.00 the police announced via TV that it was sarin that had been put in the underground carriages. This was the primary source of information for most hospitals/clinics (even though sarin was already suspected and treatment started accordingly at an early stage). Few hospitals had available documentation on the treatment of sarin poisoning. About half the hospitals had experience of treating patients poisoned by organophosphate pesticides (sarin is an organophosphate). The antidote pralidoxime was unavailable at many hospitals. Fewer than 50 per cent of the hospitals sought information on sarin poisoning from the Japan Poison Information Centre (JPIC). The Centreís telephone lines were constantly blocked for many hours after the accident.
Of the ambulance personnel taking care of injured people at the accident site. 135 developed symptoms of sarin poisoning and 33 of these required hospitalisation. The ambulance personnel worked without any specific protective clothing. Policemen also developed symptoms and so did hospital staff (doctors and nurses). Several of the hospital staff were treated with atropine and one doctor was even treated with pralidoxime. None of the secondarily exposed hospital staff had decreased plasma cholinesterase activity.
In June 1994, i.e. nine months before the Tokyo attack, the same terrorist group had spread sarin in the city of Matsumoto, approximately 150 km west of Tokyo. Seven persons died and just over 300 were exposed to sarin. Fifty-six required hospitalisation. Also in this accident, both fire personnel and hospital staff were exposed to sarin while taking care of victims.
Experience and conclusions
It is of great value for the Emergency Control Centre to get an overview of the accident site from live pictures via TV from helicopters filming at the site.
Having doctors at an alarm centre makes it easier to optimise the use of ambulance staff. In an unexpected event, it is important for the fire service or the police to have rapid access to analysts, thus permitting identification of any toxic agent that might be involved in an accident. Sarin (and other nerve agents) rapidly penetrates intact skin. Even small amounts of a nerve agent in ”pure” form can cause severe poisoning. Dispersal of sarin as an aerosol seems to increased the number of severely poisoned and killed only by a few percentage units compared to its evaporation from liquid form.
Very many people ñ those with relatively mild symptoms - can be expected to make their own way to hospitals on foot or by car after exposure to chemicals or chemical warfare agents.
All personnel (including hospital and ambulance personnel) taking part in activities at the accident site must have adequate personal protective clothing. Personnel at medical facilities must have access to personal protective clothing (including respirators) if they are expected to take care of victims exposed to chemicals or chemical warfare agents and not properly decontaminated.
People exposed to chemicals or chemical warfare agents must be undressed and, where appropriate, decontaminated before being allowed to enter hospital. It is important to evaluate an incident and to spread this information to others.
The mass media (radio, TV) are important information sources for hospitals/treatment facilities in major accidents. Via mass media important information on e.g. a possible toxic agent may be disseminated.
It is important for medical personnel to have access to treatment guidelines for the most common toxic agents that might be involved in an accident and for those toxic agents where specific (antidote) treatment is available.
In major accidents, requests for information from central bodies (such as the poisons information centre) should be centralised within every hospital or region so as to limit the number of calls ? telephone lines are often blocked in a mass casualty situation.
The general public should get information as soon as possible from the mass media, so that the need to call the poisons information or other authorities for advice will be minimised.
Pronounced miosis with pin-point pupils is an early and predominant sign in nerve agent poisoning. Miosis is present in mild and severe cases. Nicotinic symptoms (e.g. pallor, tachycardia, hypertension, muscle fasciculation, muscle weakness) seem to dominate symptomatology (miosis excepted), while muscarinic symptoms (e.g. sweating, secretions, bronchospasm, bradycardia) are more prominent in severe cases.
Estimation of plasma cholinesterase activity is mainly of diagnostic value and does not guide the need for antidote treatment. This should be based solely on symptomatology. Pronounced symptoms may be present despite normal plasma cholinesterase activity. In severe poisoning, plasma cholinesterase activity may be decreased for several weeks even though severe symptoms have disappeared already after 24 hours. In spite of very severe poisoning, plasma cholinesterase activity may be normalised within a few hours with adequate treatment. Cholinesterase activity in the red blood cells is however affected for several weeks.
Treatment with an oxime for reactivation of the inactivated enzyme in sarin poisoning is important. It diminishes the need for atropine and shortens the poisoning course considerably. (Oximes belong to a group of substances that has the power to reactivate acetylcholin esterase when it has been inactivated by a nerve agent. Oximes of interest are pralidoxime, obidoxime and HI6). The inactivated enzyme acetylcholin esterase ages quickly after exposure to the nerve agent soman. It cannot be reactivated by the oxime pralidoxime (or obidoxime), but probably by HI6.
In most cases of sarin poisoning the need for ventilatory support and intensive care is only 24?48 hours provided treatment with antidotes (atropine and an oxime) is given. Even patients with severe signs of poisoning will recover completely within a few days provided adequate supportive therapy and antidote therapy is started early. In spite of initial severe symptoms of poisoning, antidote therapy is not required for more than one or two days. In spite of adequate systemic atropinization, miosis is not always affected. Pupil size should not be used as guideline for proper atropinization. If it, there is a great risk of atropine poisoning with for example hallucinations. Topical treatment with atropine eye drops eliminates blurred vision and eye pain, but in return accommodation deteriorates. The eyes should be examined by a specialist in all cases of poisoning with nerve agents (and other cholinergics) with advanced miosis. This is because of the risk of traumatic glaucoma and retina detachment.
KAMEDO reports (Summaries) (Copies may be obtained from KAMEDO, National Board of Health and Welfare, S-106 30 Stockholm, Sweden) KAMEDO Report No 71 The Terrorist Attack with Sarin in Tokyo, March 20, 1995 Per Kulling