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ATLAS OF GAS POISONING INTRODUCTION
Out of all the various substances which could be used in gas warfare, only two have been chosen for illustration of their effects in this Atlas. They are Phosgene (COCl2) and Mustard gas or dichloro-di-ethyl sulphide (CH,Cl.CH2)2S.
Phosgene is the chief of the many gases and liquids that are used for their effects as Pulmonary irritants. These pulmonary irritants are inhaled as gases or vapours. They may cause some watering of the eyes, but the chief effect noticed at once is a catching of the breath or a choking sensation so that the chest feels gripped and incapable of free respiration. Coughing and vomiting may follow, and then after some time, varying from a few minutes to several hours, an inflammatory reaction appears in the lungs with the development of an acute oedema that may commence insidiously and yet progress so rapidly as soon to be a menace to life itself.
The alveoli fill with oedema fluid, which then rises into the bronchial tubes and may appear in a most abundant thin, frothy expectoration. Aeration of the blood is seriously interfered with, because the air sacs are either drowned with oedema fluid or burst by the efforts of coughing. Moreover the circulation through the lungs is embarrassed, both by the pressure of the fluid on the capillary vessels and by the local thrombosis that occurs in many places in the smaller lung vessels. The blood is concentrated by the loss of serum so that the count may rise to even eight or nine million red corpuscles to the cu. mm. This change adds to the difficulties of the circulation.
The affected person can no longer get the oxygen he wants, and he either dies from obvious asphyxia with progressive circulatory failure, or he collapses as the result of some muscular effort that suddenly makes a greater call for oxygen and so reveals the deficiency of the supply. Death is the result of this inflammatory oedema of the lung, and it occurs chiefly on the first or second day after exposure to phosgene. A few cases may chance to develop secondary bacterial infections of the lungs and to succumb to a later broncho-pneumonia, but they are relatively rare.
The main clinical features of acute phosgene poisoning may be summarized as follows:
(i) Catching of the breath, choking, and coughing immediately on exposure to the gas.
(ii) Inability to expand the chest in a full breath after removal from the poisoned air.
(iii) Vomiting, hurried shallow respiration, and sometimes coughing with an abundant expectoration, follow. Pain is felt behind the sternum and across the lower part of the chest. Fine rales are heard in the axillae and over the back.
(iv) Cyanosis next appears, in association either with a full venous congestion or with the pallid face of circulatory failure. The development of these dangerous symptoms may occur after many hours' delay, and sometimes, as the result of muscular effort, with unexpected rapidity in an apparently slight case.
(v) Death, which may or may not be preceded by mild delirium or unconsciousness, rarely occurs after the second day.
Mustard gas is known as a vesicant. It may exert its irritant action either as a vapour concentration in the air or by direct contact with the liquid. The liquid or vapour clings to the clothing and slowly exerts its continuously irritant action on the body.
As a rule no irritant effect is felt on exposure, whatever the concentration, but after about two to six hours the skin and mucous membranes begin to react with a progressive inflammation that may result in local necrosis and desquamation of these covering membranes. There is intense conjunctivitis; the skin turns an angry red, and this erythema is soon followed by the skin blistering here and there over the face and body. The passage of the vapour down the respiratory tract may cause such severe injury to the mucous membranes fining the trachea and bronchioles that they are eventually destroyed and sloughed away. Bacterial infection then seizes upon these raw surfaces, and the patient may die from secondary septic broncho-pneumonia.
Death is never the direct result of the action of the poisonous vapour, and there is no initial pulmonary oedema. From the second day onwards through the first and second week severe cases may die, but only as the result of secondary bacterial infection. Mustard gas therefore differs entirely from the lung irritants such as phosgene, which kill directly and speedily by flooding the lungs with oedema fluid.
The main features of poisoning from mustard gas may be resumed as follows--
(i) Delay of the irritant effect for at least two to three hours, and then a comparatively slow development of the various inflammatory reactions.
(ii) Vomiting, and a sense of burning in the eyes, with discomfort in the throat, hoarse cough, and some retro-sternal pain.
(iii) Intense conjunctivitis that temporarily "blinds" the man.
(iv) Reddening of the exposed skin surfaces and of the moist areas in the axffix and groin, followed by blistering, excoriation, and brown staining.
(v) Inflammatory necrosis of the mucous membrane of the trachea and bronchi, with the secondary development of infective bronchitis or septic broncho-pneumonia.
(vi) Death is relatively uncommon : it occurs later than the first day and only as the result of septic complications.
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