Lewisite

LEWISITE, a combat chemical agent belonging to the vesicant group, exists in the following three fractions, which are liquid arsenicals: 1) chlorovinyldichloroarsine CHCl:CHAsCl₂; 2) dichlorovinylchloroarsine (CHCl:CH)₂AsCl; 3) trichlorovinylarsine (CHCl:CH)₃As. L. is named after Lewis, who obtained L. in pure form and described it in 1918, although in impure form L. was first obtained in 1904. Of the three fractions, the first is the most active, to which the name L. primarily belongs. It freezes at -13° and at normal pressure boils at 190°. Sp. gr. at 0° is 1.92 and at 20° is 1.885. Vapor pressure is insignificant: 0.087 at 0° and 0.395 at 20°. At this temperature 1 liter of air saturated with L. vapor contains 15.6 mg of it. At 0° 1 liter of air contains approximately 1 mg of L. under saturation conditions. In weak concentrations, L. vapor has a geranium-like odor. Water slowly hydrolyzes L., forming poisonous arsine oxides. Alkalies decompose lewisite with the release of acetylene. Oxidizers convert L. into less toxic pentavalent As compounds. The lethal concentration, according to Vedder, is 0.048 mg per 1 liter (with a 30-minute exposure). The concentration producing a vesicant effect, according to the same author, is 0.334 mg per 1 liter. L. has not been used in war, and therefore its effects on humans have been little studied. In dogs, when exposed to an atmosphere poisoned with L., phenomena of irritation of exposed mucous membranes are observed, first of the eyes, accompanied by tearing and profuse nasal discharge, followed by symptoms of digestive tract damage: profuse salivation, nausea and vomiting. The consequences of poisoning manifest in sharply expressed phenomena of mucous, and later purulent, conjunctivitis and rhinitis. Further, the animals are depressed, have difficulty breathing, and cough. Foamy mucus vomiting is often observed, probably previously swallowed after being secreted from the respiratory tract. In lethal poisonings, many animals die in the first 2 days. In those that survive, symptoms of poisoning from both external mucous membranes and respiratory tracts progress until the 5th day; sharp rales are observed, indicating intense bronchitis. During this time, more animals die. Survival beyond 5 days is a favorable sign. False membranes in the nose disappear, and the phenomena of conjunctivitis and bronchitis regress. Usually, complete recovery occurs between the 7th and 10th days. Other symptoms of poisoning should be noted: a temporary drop in temperature of half a degree during the first hour after poisoning, slowing of the pulse during the first day with some acceleration during the second, increased respiration immediately after poisoning with return to normal on the second day. In fatal cases, slowing of respiration was observed before death. Autopsy of dead animals reveals the formation of abundant false membranes in the nose, larynx and trachea, purulent bronchitis, often the same bronchopneumonia along with filling of the lungs with blood and their edema, emphysema and atelectasis, not always equally sharply expressed. At the same time, stagnation phenomena are observed in the liver, kidneys, and dilation of the right heart. The cause of acute death in dogs that died in the first 30 hours after poisoning, in the vast majority of cases according to Vedder's data, is bronchopneumonia. Thus, the picture of poisoning in general very closely resembles mustard gas poisoning. Similarly, when L. vapor acts on the skin, phenomena similar to the effect of mustard gas vapor are observed, with redness appearing after 4-6 hours, and blister formation after 16-48 hours. Smearing with liquid L. gives a similar but more strongly expressed result compared to mustard gas. Essential differences in the action of both substances are as follows: 1) the latent period with L. is significantly shorter—when using liquid L., burning appears immediately after application; 2) the presence of arsenic causes local painful irritation, much less pronounced with mustard gas, and when absorbed through the skin, L. can also cause a resorptive toxic effect. Experiments on animals showed that the application of 0.02 cm³ per 1 kg of weight (provided it acts on a skin surface area equal to as many square centimeters as the animal's weight in kilograms) causes the death of the latter. Thus, for a person weighing 70 kg, the lethal dose should be the application of 1.4 cm³ of L. to 70 cm² of skin, i.e., to an area smaller than the palm. When applying sublethal doses of L. to animal skin, a deeply penetrating, gradually spreading necrosis of tissues is observed. Subsequently, the process proceeds slowly, and non-necrotized tissues separate through suppuration, with secondary infection of affected areas occurring very easily. In fatal cases of poisoning through the skin, autopsy revealed lesions of the lungs, kidneys, sometimes the liver, duodenum, and heart. In chemical analysis of LUMINAL, arsenic was found in all tissues of the body, most however in places adjacent to the lesion, as well as in the liver, kidneys, and spleen. As a rule, arsenic was also found in the urine. When applying 2 mg of undiluted lewisite to his forearm, Rovida observed after 2 hours 20 minutes the appearance of erythema, which then became hemorrhagic and edematous, with a slight itching sensation. After 18 hours, a blister appeared and after opening it—a scab, which fell off after 26 days. Thus, in humans as well, the effect of L. proved to be stronger than that of mustard gas. For poisoning, the following measures are proposed. When liquid L. acts on the skin—immediate application of substances that hydrolyze L., which, even if it does not protect against local damage by L., will protect by its decomposition from its resorptive action. For this purpose, Vedder recommends a 5% aqueous solution of NaOH, applied as soon as possible after the injury. Due to the irritating properties of this solution, it should then be washed off. To destroy L., oxidizers can also be used, including bleaching powder. Further treatment may consist of excising the affected area, which can be successfully applied up to 12 and 24 hours after the injury. The result may be healing by first intention and in less favorable cases a significant reduction in healing time. When exposed to lewisite vapor, Vedder recommends the application of a paste consisting of ferric oxide hydrate with glycerin. The recipe for preparation is as follows: to a nearly saturated solution of ferric chloride, a strong solution of ammonia is added until a slight odor of the latter remains. The resulting precipitate is allowed to settle in narrow vessels. The upper layer of liquid is removed with a siphon and the vessel is again filled with distilled water, repeating such washing until the wash liquid is freed from chlorides. Such washing may require a week's time. After this, the precipitate of ferric oxide hydrate is dried on a filter, and a thick mass (6 parts) is mixed with pure glycerin (1 part). The resulting ointment is placed in metal tubes, where it is well preserved away from air. The paste is thickly applied to the affected area and then covered with parchment paper, etc. The dressing is renewed after 12 hours.* The same ointment can also be used for liquid lewisite immediately after injury.

A. Likhachev. L UN AS Keith (Keith Lucas, 1871-1916), an outstanding English physiologist. The works of L. were concentrated in the field of research into excitation phenomena, where L. became one of the founders of the direction that seeks to approach the explanation of complex processes of summation and inhibition in the central nervous system from the side of the elementary properties of excitable tissues. According to his concept, at the junction points of individual links of a conducting heterogeneous system of tissues (myoneural connections, synapses), there are areas with imperfect conductivity, in which the impulse spreads with a decrement. Their presence leads to the fact that a series of impulses, each of which falls on the relative refractory phase from the previous impulse and reaches such an area in a weakened state, fades within the latter. Conversely, impulses following one another during the supernormal period of the refractory phase are transmitted through the area. Being an excellent experimenter who conducted precise quantitative accounting of the temporal relationships between individual moments in the development of the impulse, L. substantiated his ideas with great persuasiveness. This, combined with the breadth of his coverage of fundamental problems of excitation, places him among the outstanding modern physiologists, despite the fact that many of his views have undergone a fundamental revision in recent years. L.'s main monograph was published posthumously—"The conduction of the nervous impulse" (London, 1917).