|
Chemical agents were used from 1915 to 1918 during World War I. Their use was catalyzed by the battlefield stalemate of trench warfare and have been used in such conditions ever since.[8] They do not fit well with the tactics of a mobile war. Large-scale releases of chlorine and phosgene in 1915 had considerable effects against unprotected troops and caused large numbers of casualties and deaths. It was these early attacks that probably gave rise to the notion of CBW agents being WMDs. At less than 4%, they had the lowest ratio of dead to wounded of all the arms used during the war,[13] whereas explosive shells had the highest (>15%). Artillery caused 59% of the overall mortality on all sides. Many different chemical agents were tried during the war and usually were delivered by shell fills, but there was difficulty in building high-enough concentrations of agent to be lethal, and continuous development of countermeasures meant that better-trained troops with masks were less affected. Although phosgene could easily be regarded as the most lethal of the agents used, causing untreatable toxic pulmonary edema, mustard, a vesicant disabling agent, probably caused the most injury and removed many from the field of battle (usually temporarily). One feature of the casualties from World War I that is overlooked is the possibility of mixed toxic and physical trauma. The exact figures are not available, but of 546 American soldiers who died after exposure to chemical warfare agents during the period of March to November 1918, 6% also had ballistic injuries.[21] The figures for dead and wounded do not reveal the true extent of the disability caused by exposure to toxic agents, and it is likely that the degree of long-term pathologic effects was high, particularly given the limited postwar medical facilities at that time.
Nerve agents were developed by Germany under conditions of the strictest secrecy during World War II, and although never used in action during that time, they became the major toxic hazard during the Cold War and later. A major nerve agent plant was captured by the Russians and rebuilt in the Soviet Union in 1945, giving the USSR a "mass-destructive" capability long before it possessed nuclear weapons. A lesson for military and civilian anesthetists is that mixed casualties can be expected after the use of toxic agents. It has been known for some time that Soviet commanders saw the use of chemical weapons as part of a normal armamentarium rather than as exceptional weapons.[22]
There is some evidence of the use of biological warfare agents in China by the Japanese, who had a secret unit devoted to their development since the early 1930s. Plague and clostridia were used in tests on prisoners and against civilian populations. The considerable knowledge gathered was passed on to the United States by the head of the section after his capture and formed the basis of an offensive biological warfare development program that was terminated only in 1972 with the signing of the Biological Warfare Treaty.[13] It is now known that a major Soviet biological warfare program began at that time, which led to the use of genetic engineering and other techniques to develop a whole new range of possible agents, including "agents of biological origin" that probably are currently deployed.[15]
There was continued development of nerve and other agents during the Cold War and extensive research into an antidote-based approach to the management of the wounded. The USSR had an extensive program of development of biological weapons and toxins and applied genetic engineering to produce new agents.[15]
The Iran-Iraq War of the 1980s gave rise to the sustained use of chemical agents and the first application of modern medical techniques for the treatment of injuries from chemical weapons ( Table 64-2 ). Extensive investigations by the United Nations established that sulfur mustard and Lewisite, both vesicant agents, had been used together with the nerve agent tabun and the biological agent mycotoxin.[8] [23] Casualties were almost exclusively Iranian and numbered about 27,000. The mortality rate among those affected was less than 1%. This continues the trend observed during World War I of the low mortality rate with chemical weapons and almost certainly reflects the impact of organized medical care for the casualties and techniques of protection. However, an Iraqi attack against an unprotected Kurdish village at Hallabjah in 1989 produced 5000 deaths.
In 1995, the first recorded terrorist use of a chemical warfare agent against a civilian population occurred with the release of the nerve agent isopropyl methylphosphonofluoridate (sarin) in attacks in Matsumoto and Tokyo, Japan, and for the first time, hospital medical teams were brought into direct contact with chemical warfare during the initial and continuing management of the casualties. [24] Unfortunately, because of a lack of experience, there were several casualties among the attending emergency staff, but the number of fatalities was low. The incident brought home a number of lessons for medical responders, including anesthesiologists. The first was that the use of a hitherto military chemical warfare agent was possible by a terrorist group. Second, the incident management underlined all the lessons taught by the HAZMAT system in that secondary casualties occurred among the attending staff because of a lack of control, protection, and decontamination. Third, fatalities that occurred at the release site were essentially caused by a lack of on-site resuscitation. Fourth, the well-documented clinical management of the many thousands of cases that were admitted to hospital provided for the first time a significant clinical database for a population exposed to a nerve agent.[25]
|