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Chapter VII




Here will be found a textbook description largely compiled from information furnished by our Allies when we entered the war, and later. They were also the source of the various circulars of instruction which emanated from the offices of the chief surgeon and the Chemical Warfare Service. The most important of these circulars are printed elsewhere in this volume. This chapter then contains little original with us and is justified only by the fact that the majority of our readers will not have easy access to the authorities responsible for first making of clinical record observations relating to the symptoms and treatment of the various poisonous gases employed during the war.

In the discussion of the symptoms which followed exposure to toxic gases, the classification of these agents according to their physiological action, as given in Chapter III, is employed. The symptoms of carbon monoxide poisoning are also considered, since this gas, though not a combat gas, was responsible for some casualties.

It should be remembered that the character of the symptoms due to any of the combat gases was materially dependent upon the concentration of the gas to which the individual was exposed, whether high, medium, or low, and the period of time during which he was subjected to its action. Exposure to a iow concentration for a prolonged period produced symptoms similar to those from exposure to a high or a medium concentration for a much shorter period.

While it has proved practical and convenient to group the various gases used during the World War, viz, lung irritants, vesicants, etc., this grouping is based on their most important action. That is to say, because, for example, a lung irritant is so classified this does not imply that its sole action is irritation of the lungs. On the contrary, all the toxic gasses employed exerted effects other than their group name implies.



The chief gases classified as lung irritants were phosgene, diphosgene, chlorine, and chloropicrin. Nitrous fumes, while not used for combat purposes, are also included, as they gave rise to a similar train of symptoms, while dichlorethylsulphide (mustard gas) is classed with the vesicant group, it possesses lung irritant properties which call for consideration.

The chief characteristic of gases of this group is the irritation of and damage to the deeper respiratory passages, especially the alveoli of the lungs, which they produce, with resulting inflammatory exudation of fluid, acute pulmonary edema, and frequently death by asphyxia. In addition to their action as lung irritants, some of these gases are effective lacrymators.

While the presence in one patient of symptoms characteristic, not of one but of several gases, was at times confusing, it was usually possible for a medical officer to determine very promptly that intoxication with a gas of lung-irritant group had occurred. On the other hand, to determine which gas of this group was responsible for the symptoms was difficult. Fortunately, this was of little clinical importance.



Certain differences in character and action of the individual gasses of this group will be noted later. The following detailed consideration of the general symptomatology of the group is based largely on the effects actually produced by phosgene and the similar chemical compound, diphosgene, since the majoritv of the casualties in American troops were due to these two substances.

The immediate effect of a lung-irritant gas in high concentration, aside from irritation of the eyes, was suffocation, due seemingly to spasmodic arrest of respiration, which, if the concentration of the gas was very high, often killed almost instantly by respiratory paralysis. These were the so-called fulminating intoxications. Usually, however, as the concentration of the gas was not commonly as high as this, the initial suffocative phase was passed over safely. Other effects from the gas were delayed. The victim even felt comparatively well during the ensuing intermission, though on examination his pulse and respiration usually were found accelerated and his temperature subnormal. Sometimes he complained of headache, substernal and epigastric pain, some irritation of the eyes, slight cough, and a sense of constriction in the chest. Nausea and vomiting were common. The latter effects appeared in from two to six hours. The predominant manifestation then was pulmonary edema. In very light cases only, the patients seemed to escape this edema and showed merely bronchitis. The pulmonary edema was general, or was localized in certain areas of the lungs. Its extent and the rapidity of its development seemed to depend on two factors, the amount of gas inhaled and the efficiency of the heart. The importance of the latter was emphasized by the ill effects due to increased strain incident to muscular exertion and by the disproportionately large number of cases with chronically disordered hearts and lungs that terminated fatally.

As the quantity of fluid which escaped into the alveoli of the lungs increased, symptoms appeared. caused by its presence. The chief were tachycardia, dyspnea, cyanosis, and cough, with the expectoration of frothy serous fluid. Dyspnea was an early sign and a danger signal. The cyanosis was usually accompanied by a peripheral venous engorgement, the so-called "blue" cases, but not infrequently, and especially in the more severe intoxications, the skin was pale and the peripheral veins collapsed, the so-called "gray" cases.

The clinical features of the two types of cases just mentioned were often distinctive. In the first ("blue") group, in which the patients showed definite venous engorgement, there was marked restlessness, the face was congested and deeply cyanosed, the lips and tongue were a full blue color, and frequently there was visible distention of the superficial veins of the face, neck, and chest. The respiration was increased in frequency and at times deeper than normal. Cough might be present and the expectoration of large quantities of thin, frothy, blood-tinged fluid was more common than in the "grav" cases. The pulse was full and strong and the rate about 100 per minute.

Cases in the "gray" group showed an ashen pallor rather than a deep cyanosis, the lips being pale and leaden colored. There was marked tachypnea and shallow respiration. Though the lungs were intensely edematous, there was often little expectoration, but cough was frequent. The pulse was weak and thready and the rate 130 to 140 per minute. The blood pressure was low. Marked collapse was present. Needless to say, the prognosis in this group was far worse than in the former.


In both, the edema first developed in the upper lobes of the lungs and extended downward. It was manifested by fine crepitant r les and relative dullness, but this was sometimes masked by superficial emphysema.

Digestive disturbances were common, notably nausea, vomiting, and anorexia. The spleen was often enlarged and icterus (seemingly a cardiac icterus resulting from passive congestion of the liver) sometimes was observed. Renal disturbances were not important. Albuminuria occasionally occurred, oliguria was common, but prolonged anuria was unusual. Moderate excitation, anxiety, and restlessness were frequently seen, offering a sharp contrast to men gassed with the fumes of dichlorethylsulphide (mustard gas). In some instances patients were semicomatose, with a muttering delirium, but, as a rule, they could be aroused to answer questions. Sometimes the respiration increased, even to 60 and 80 per minute, and was frequently labored and superficial. In many patients the pain became very severe and they moaned continuously. A thin, serous, foaming, blood-tinged expectoration was frequently present, especially after spasms of coughing. This fluid flowed from the mouth and nose until a mushroom-shaped collection of bloody froth formed on the face.

In cases progressing unfavorably, the respiration continued accelerated, the pulse grew more rapid and feeble, sonorous tracheal râles became audible, bloody froth exuded from the mouth, and death occurred. Usually this was in the second half of the first day, more exceptionally on the second or third day.

The danger period in all uncomplicated cases was usually passed by the end of 72 hours, and then followed improvement, with subsidence of the pulmonary edema. This stage was ushered in by the slowing of the pulse, which returned to normal and then fell below normal, to 60, 50, or even 40 beats per minute. The heart, however, remained irritable, and the slightest exertion increased the pulse rate to over 100, prolonged rest then being required to reduce it to normal. The arterial tension remained low for weeks.

As a rule, a patient recovered rapidly after the third day, and at the end of the week was fully convalescent. So rapid and complete might be the reabsorption of the fluid from the lungs that one who, in the acute stage. had showed the usual signs of extensive pulmonary edema, presented hardly any physical signs in the chest eight or nine days after exposure to the gas.

Complete recovery of cases of even moderate severity often required a very considerable time. Convalescent patients occasionally showed for some time a certain amount of digestive disturbance, associated with pain in the epigastrium, which was frequently accentuated after taking food, and loss of appetite. Bronchitis and pain in the chest occurred in a number of such patients. but yielded readily to treatment. Lassitude was common.

Certain patients continued to have precordial pain, dyspnea. exhaustion. and persistent tachycardia after exertion. After a brief period of moderate exercise they looked exhausted and obviously suffered from respiratory distress, while the pulse rate for several minutes remained higher than would have been the case with a normal person.

Other convalescent patients. and they were less common than those just described, had recurrent attacks of spasmodic dyspnea. These attacks might occur, every night, or might be separated by an interval of a week; more than


one sometimes occurred during the same night. During the attack, which lasted from 5 to 30 minutes, the patient sat up in bed, his respiration was shallow and rapid, but not difficult, being very different from that shown in an ordinary asthmatic attack. Slight cyanosis might he present, but usually the color remained normal, and the patient appeared anxious rather than acutely ill. During the attack the pulse was usually slow and full, but might be rapid and almost impalpable.

In the great majority of these gas cases the symptoms ceased completely, and many patients who had been gravely ill were in time returned to full duty in the field. In a certain number of cases recurrent bronchitis and emphysema followed.

The precise cause of the symptoms which occurred during convalescence is obscure. Physical examination of the heart of patients who then exhibited tachycardia and dvspnea after exertion revealed no gross defects. Functional murmurs occurred, but afforded no guide as to the severity of the cases. It was quite apparent, however, that if muscular exercise was begun too early or pushed too far, a definite condition of irritable heart might be established which would persist for a long time. Neurasthenia sometimes entered into the clinical picture and care had to be taken not to let this condition obscure any definite abnormality which might be present.

An exceedingly striking feature in some patients with poisoning by lung irritants was the severe or even fatal symptoms induced by exercise. Some men who were apparently not severely gassed and who presented no notable symptoms would, after slight exertion, such as going to a meal or visiting the toilet, suffer a complete collapse, with dyspnea and cyanosis or even death, unless immediate treatment was instituted.

In cases which did not show an improvement after 72 hours, broncho-pneumonia was generally found to be present. In these cases the temperature increased, reaching 38o to 39o C. An increase in the severity of the cough was noted, and the sputum assumed a more mucoid character. Numerous fine and coarse râles were heard on auscultation, and signs of lung consolidation were often present. Death might occur at any time, with symptoms of increased circulatory and respiratory insufficiency. Frequently a striking improvement was noted in cases which had a very stormy onset and in which the condition had appeared most alarming. Occasionally even the most apparently hopeless cases made excellent recoveries. The pulmonary edema was gradually absorbed, the dyspnea improved, and the signs of interference with the circulation disappeared. The cough, however, frequently persisted for a considerable time. The expectoration changed in character from serous to mucoid or mucopurulent, entirely disappearing after a variable period.

On the other hand, the danger was not always removed after a favorable change had supervened. Secondary bacterial infections might occur to produce bronchopneumonia or, more rarely, lobar pneumonia, which threatened the life of the patient.

In a number of cases seen during the war, which at first gave the impression of being severe intoxications, further observation demonstrated that either physical or psychic shock was actually responsible for the condition. As the patient recovered from the shock the further train of symptoms showed that gassing was unimportant. In many cases shock which followed a severe wound made it difficult to determine the extent of gas absorption.


In the greater number of cases of gas poisoning the inhaled gas was of a low degree of concentration, it usually having been freely diluted by the air. Naturally, the greater the extent to which the offending gas had been diluted the milder were the resulting symptoms. Other factors naturally lessening severity of exposure were improvements in gas protection and additional precautions against inhalation, which were generally taken by officers and men after the serious results of gas poisoning were fully realized by them.

When poisoning occurred as a result of the inhalation of a gas of the lung-irritant group which had been greatly diluted the symptoms were much milder than those just described. The effects lasted for a shorter time, and the irritation of the eyes and upper respiratory tract was less severe. The lungs and bronchi were not affected, and if coughing was occasioned it was superficial and from irritation of the pharynx and larynx. The severe constitutional effects were entirely absent in these cases. Difficulty was experienced at times in differentiating intoxications of this character from conditions simulated by men who took advantage of the pretense of having been gassed to escape the dangers of the battle field. Yet, ascertaining whether a man had been gassed was of the utmost importance, for, as has been previously noted, in certain instances patients whose premonitory symptoms were mild developed most aggravated forms of gas intoxication. The majority of men who had inhaled the combat gases in mild concentration made prompt recovery and were returned to duty in a short time.



In the higher concentrations many of the gases of the lung-irritant group caused mild inflammatory reactions of the skin of exposed parts, especially of the neck and of that portion of the face not covered by the gas masks. The inflammation was never of the severe type caused by gas of the vesicant group. The changes in the color of the skin were due to circulatory disturbance, vasomotor influence, and the altered composition of the blood.


The different gases included in the group under consideration (lung irritants) varied in the extent of their action on the eyes. Mild inflammations of the conjunctiva, with pain and flow of tears, were common, but erosion of the cornea and deeper structures did not occur unless there had been a direct application of the gas in a concentrated form. The eye symptoms were of so little importance in comparison with those involving the circulatory and respiratory systems that they were not often noted.


When the exposure had been to gases in low concentration only, the upper part of the respiratory tract was involved and the symptoms were those of a pharyngitis or laryngitis. Following inhalation of gases in higher concentration, the alveoli of the lungs were most seriously involved. The resulting edema sometimes occurred promptly after the inhalation of the gas, but usually was not noted until a few hours later. The symptoms, described above, were the result of deficient oxygenation of the blood. With the onset of the edema an increase of


lung volume frequently occurred, and this emphysema kept pace with the increasing edema, later disappearing with the absorption of the fluid. Cough and expectoration were variable. When expectoration was present the sputum, on being collected, presented three distinct layers-an upper layer of froth, a middle serous layer, and a bottom layer which adhered to the container when the two upper layers had been decanted. This consisted of a mucilaginous liquid of the consistency of apple jelly, which might be rusty or streaked with blood.

Histological examination of the sputum revealed, during the first and shortest stage (first few hours), more or less modified epithelial formations from the bronchial tubes; during the second stage, in addition, debris from the epithelium of the lungs, leucocytes, and red corpuscles. The sputum in both these stages was noticeably free from pathogenic bacteria, only a small number of ordinary mouth saprophytes being present. Later, however, with the onset of pneumonic complications many organisms were found.

In some fatal cases with extensive edema expectoration did not occur, the patient dying before the edema fluid could pass from the alveoli into the bronchial tubes.

After the second or third day absorption of the fluid was rapid. In cases in which secondary infection set up a bronchopneumonia the symptoms were of this complication. In fatal cases of this character the lung changes frequently could not be differentiated from those occurring in the secondary bronchopneumonia following any of the infectious diseases.


The lung-irritant gases are not believed to exert any direct physiological action on the heart. The disordered action of the heart which followed intoxication with a gas of this class was the result of the pathological changes occur- ring in the lungs and of the changes in the composition of the blood. As the obstacles to the circulation of the blood increased, the additional efforts on the part of the heart resulted in dilatation, first of the right side and later of the entire organ. This increase in size could be readily demonstrated by X-ray observations. The first indications of interference with the circulation of the blood were cyanosis, paleness, blue lips, and signs .of impaired circulation in the extremities. While at first the heart rate was little affected, as the condition of the patient became serious the pulse rate increased and the pulse usually became soft, rapid, and thready; the rhythm was rarely disturbed.

Physical examination of the heart was difficult in severe cases on account of the restlessness of the patient, the dyspnea, and the presence of large sonorous riles in the lungs. When the cardiac sounds could be distinguished, they were distant and uncertain and the respiratory movements had an abnormal influence on the cardiac rhythm. There was no indication of valvular lesions, but by reason of the cardiac insufficiency functional systolic murmurs might be heard. The end of the beat was marked by a rhythmic asystolia. Circulatory disturbances in severe cases were marked by a high degree of cyanosis, darkness of face and extremities, swelling of the jugular vein, enlarged liver, and decrease of the urinary secretion.

The blood pressure was subject to cyclic modification. In the early stages of the intoxication the blood pressure was decreased. Later it remained


low (the usual rule), but in certain exceptional cases the systolic pressure reached 200 mm. Hg. The reasons for these changes are not definitely understood.

Examination of the blood showed less change than might have been anticipated from the results of blood letting when a dark, sticky blood that left the vein slowly and coagulated quickly was obtained. The blood showed neither important chemical changes nor evidence of absorption of the poisonous gas. The hemoglobin retained its facility for absorbing oxygen, but frequently the oxygen content of the blood was below normal. The total volume of blood was considerably decreased on account of the exudation of blood plasma into the lungs as edema. There was no actual change in the number of red corpuscles or in the amount of hemoglobin, consequently a relative increase of these elements existed. The red cells numbered as high as 7,000,000 or 8,000,000 to the cubic millimeter, and the hemoglobin readings ranged as high as 140. The number of leucocytes appeared normal (7,000 to 9,000 per mm.), therefore, in view of the decreased blood plasma, an actual leucopenia must have existed. An important acceleration of blood coagulation occurred.


Nausea and vomiting were often among the first symptoms noted. They probably were more often the result of reflex action from irritation of the throat rather than from the direct effect of the gas on the stomach, although at times the swallowing of poisonous material was responsible. Anorexia, a frequent symptom, was often noticed in the early stages and might be very protracted. Constipation was more frequent than diarrhea, but during the period of convalescence enterocolitis with diarrhea was encountered in some cases.

The liver was enlarged and sensitive. Only rarely was jaundice observed. Enlargement of the spleen was not uncommon.


The nervous system was always involved. From the time of the first sensation of suffocation, immediately following intoxication, the patient seemed completely overcome with fatigue. Among the nervous symptoms noted were headache (marked by crisis when any exertion was undertaken). vertigo, staggering, muscular weakness, disturbance of tendon reflexes, nystagmus, numbness, and even unconsciousness. Mental torpor was characteristic of many cases, while in some severe ones restlessness was marked, with at times a low muttering semidelirium.

In fatal cases consciousness was usually maintained until the end. In patients addicted to the use of alcohol great excitement, delirium, and even hallucinations were not uncommon. The psychic element, which was prominent in many cases, was usually of a depressive nature, and during convalescence the hysterical and neurasthenic complexes were frequently in evidence. Neuritis and neuralgia were not noted as sequelae.


These gases did not appear to have any selective action on the kidneys. In cases where suffocation and cyanosis were marked, there were signs of congestion of the kidneys. In the early stages of the intoxication the amount of urine was generally reduced, and transient albuminuria was not uncommon. In patients who recovered. the urine was usually normal after a few days.



Both the general and local effects exerted an influence on the body temperature. Febrile reactions were always in evidence. In mild cases the temperature reached 380 C. on the first day, but returned to normal by the third. When a complicating infection of the lung occurred the temperature rose to 38o or 39o during the first day, 38o to 40o on the following day, and remained between 39o and 40o for several days.


In certain patients during the early stages of poisoning with the lung- irritant gases, no abnormal auscultatory or percussion signs could be discovered; there was simply an increase of the respiratory rate and an increased fullness of the pulse. In a well-developed case inspection showed labored respiration and cyanosis.

It is noteworthy that such physical signs as were detected at first were most marked over the upper lobes of the lungs. and not at the bases. The percussion note might remain resonant over the chest notwithstanding the existence of marked pulmonary edema. In many cases, however, the note was impaired, especially over the back. Local tympany might be found, resulting from emphysematous areas.

With the onset of the pulmonary edema the signs of this condition were elicited on auscultation-fine crackling râles, harsh and distant breath sounds, and not infrequently pleural friction rubs. As the edema increased resonance became impaired, and breath sounds were lost, being totally replaced by crackling râles or silent areas.

The heart dullness was increased to the right, and on auscultation the heart sounds were weak, especially the pulmonic second sound.

When bronchopneumonia supervened the physical signs were those of that disease.


Phosgene and diphosgene are among the most intense lung irritants known, and are regarded as the most effective war gases of their type. The odor of these gases is perceptible in a concentration of 1 to 1,000,000, and they will cause death in men exposed to a concentration of 1 to 5,000 for 5 minutes, of 1 to 20,000 for 60 minutes, and even of 1 to 1,000,000 if breathed for a considerable length of time. In a dilution of 1 to 50, which it is rarely possible to produce for battle uses, one inhalation will cause death. It was in cases of poisoning by phosgene that the delayed action, mentioned above under the general symptoms, was most apt to occur. Lacrymation usually occurred, but cough was not a prominent symptom. Of the two types of cases, one with the "blue" cyanosis face, the other with the "gray" cyanosis, the gray type was more frequently observed, but many intermediate types were seen. Sometimes a patient who, in the early stages, had shown a congestive cyanosis, with a full pulse, would gradually assume a grayish pallor. the pulse becoming accelerated and weak.

Instances were not infrequently reported in which soldiers who had been exposed to phosgene were able to carry on their work for an hour or two with only trivial discomfort. and even to march from the trenches to their quarters,


then to show marked symptoms of intoxication and to pass into a state of collapse, with progressive edema of the lungs, which in some proved rapidly fatal. In such cases the ingestion of a heavy meal seemed sometimes to have a prejudicial effect. In other instances men who had passed through a gas attack and subsequently complained of only slight cough, nausea, and tightness of the chest while resting in the trenches, collapsed and even died quickly after attempting to perform some vigorous muscular effort several hours later.

A minor degree of the same delayed effect was sometimes seen when men who had been slightly gassed discovered, on trying to walk, that they became unusually tired and breathless, and in consequence were obliged to rest frequently. In these cases the deficiency of oxygen, the probable result of an already existing pulmonary edema, was not felt until muscular exertion in- creased the need for oxygen.

One very striking example of the delayed effect was observed in a patient who was carefully watched after only a brief exposure to a strong concentration of phosgene. The greatest care was taken to prevent any muscular exertion, so that no complicating factor was introduced. The immediate irritant symptoms and coughing that were produced during the exposure soon diminished when the patient was removed to uncontaminated surroundings. An hour and a half later there was no coughing and the patient seemed practically well, the pulse being normal. His condition remained very good until four or five hours after exposure to the gas, when he showed signs of cyanosis about the lips. Coughing then recommenced, with the expectoration of frothy sputum. Soon the face and lips became of a gray, ashen color, though the pulse remained fairly strong. About 4 pints of clear, frothy, yellowish liquid was coughed up in the next 75 minutes, and at the end of this time he died. At no time was there any marked struggle for breath, nor did the patient realize how ill he was.


A much stronger concentration of chlorine is required to cause severe pulmonary edema, or even lacrymation, than is the case with phosgene. In a concentration of 1 to 100,000 chlorine is perceptible, a strength of 1 to 50,000 causes inconvenience, in a dilution of 1 to 1,000 death results after exposure for five minutes.

Chlorine is far more irritant to the respiratory passages than is phosgene. A very marked feature in the early gas attacks, when chlorine alone was used, was the paroxysmal and violent coughing, which not only occurred during the exposure but persisted for a long time afterwards. Emphysematous changes were pronounced and submucous emphysema of the neck and chest occurred in a number of instances. As a general rule these patients exhibited deep cyanosis rather than pallor and collapse, with a fairly full pulse and marked dyspnea. Copious frothy expectorations was common. The gastric symptoms were often marked, vomiting frequently being an early symptom.

Delay in the onset of serious symptoms was not evident in chlorine poisoning. Though exudation of fluid into the lungs perhaps did not start at once, the violent paroxysms of coughing, the pain, the dyspnea, and the repeated attacks of vomiting from the first conveyed the impression that the patient was seriously ill.



This gas occupies a position midway between phosgene and chlorine in respect to its efficacy as a combat gas. To produce severe pulmonary edema chloropicrin must be used in decidedly higher concentrations than phosgene, but it is much more deadly than chlorine. It is a stronger lacrymatory agent than phosgene, though inferior in this respect to the true lacrymators. Pain in the chest and epigastrium, abdominal discomfort, and violent attacks of vomiting were exceptionally marked. Brief exposure to a strong concentration in some instances caused temporary unconsciousness.

Unlike phosgene and chlorine, chloropicrin had a cumulative action. Frequent exposures to small doses of chloropicrin, each of which would have only a trivial effect in itself, would gradually lead to a greatly increased susceptibility to this gas. A man who had acquired this susceptibility was liable to attacks of "asthma" whenever he had been exposed to a trace of chloropicrin in the air. The attacks usually occurred at night and were characterized by the sudden onset of a rapid, shallow type of respiration associated with a feeling of tightness of the chest and a sense of suffocation which caused considerable distress. There was usually a short, dry cough at intervals, which was occasionally followed by the expectoration of a small quantity of tenacious mucus. The attacks lasted for as long as two hours and resembled, though exaggerated, the attacks of nocturnal dyspnea, described as occurring during convalescence from poisioning by lung irritants.


As regards the production of pulmonary edema, nitrous fumes are perhaps somewhat less toxic than chlorine. The great danger of nitrous fumes arose from the fact that in the concentration usually met with there was comparatively little sensory irritation of the eyes or upper respiratory passages, and in consequence a man working in such an atmosphere would not recognize its deadly nature. Air which contains enough nitrous fumes to cause irritation to the nose or air passages must be regarded as very dangerous.

Delay in the onset of acute symptoms was pronounced unless the concentration of the gas was high, when fatal asphyxiation might ensue rapidly. As a rule a quiet period of four to eight hours elapsed after exposure, during which time the patient usually felt quite well and had no hesitation in performing his usual routine tasks, or in eating a hearty meal. After this, symptoms of acute pulmonary edema frequently developed with alarming rapidity, death often ensuing in a few hours.


The gases of the vesicant group exert an intense effect on the skin and eyes, also on the respiratory tract as well when inhaled. The extent of inflammatory reaction produced in the skin varied with the strength of the gas and the duration of the exposure. Skin lesions which followed exposure to these irritants varied from simple erythema to burns of the second or third degree. Conjunctivitis, of varying degree, was the usual type of eye involvement, although keratitis occurred in the more severe cases. All degrees of inflammation might be present in the respiratory tract, from a simple hyperemia to a necrosis of the mucous membrane.



Dichlorethylsulplhide (mustard gas) was the only gas of the vesicant group which was used on a large scale during the war: for this reason, the symptomatology given below is based on observation of the effects of this gas.

The effects of mustard gas were not experienced for several hours after exposure. While it has a characteristic odor. it is toxic in concentrations which can not be detected by the sense of smell. Soldiers might be exposed for several hours, therefore, to mustard gas of sufficient concentration to cause serious results without being aware of the fact. Furthermore, the action on the skin was at first painless. and the presence of the gas could not be detected in this way The effects of mustard gas depend largely upon whether the liquid or vapor was encountered and upon the concentration of the gas in the latter case. Exposures may be roughly grouped into three classes: (1) to liquid; (2) to vapor of high concentration; (3) to vapor of low concentration. The liquid penetrated clothing and leather in a very short time and produced severe blistering. Such cases usually resulted from direct splashes of shell bursts, or from sitting or lying in places covered by the liquid.

Vapors of high concentration penetrated clothing rather quickly and sufficiently to cause general irritation of the skin. Without mask protection, serious lesions of the eyes, throat, and lung resulted.

Vapors of low concentration, with brief exposure, might result in nothing more than insignificant irritation of the moist surfaces of the body or in slight conjunctivitis, but when a long exposure was sustained, the same results were to be expected that were produced by a vapor of high concentration.

British field experimentation showed that severe eve effects, involving incapacitation, might follow exposures of:


The sense of smell became fatigued soon after entering a vapor of low concentration, an(I this, together with indifference to the presence of such area contaminations on the part of inexperienced troops, resulted in many skin and eye casualties. Dichlorethylsulphide, as a general rule, was fired at night so that its odor was apt to be disregarded by many on the following day. The sun was counted on to slowly vaporize the gas during the ensuing days and to produce results.


The effects of mustard gas varied widely according to the concentration, the period of exposure, and the susceptibility of the individual. It was found that many persons had what might be regarded as an immunity against certain concentrations of the gas and could pass through exposure to such concentrations without ill effect . On the other hand, a marked idiosyncrasy to its action was noted in certain individuals.


Occasionally nausea, retching, vomiting, and smarting of the eyes occurred as early as from 20 to 60 minutes after exposure; they were of great value in warning of the presence of the gas. Usually, however, symptoms did not appear until from two to six hours after exposure. Nausea, vomiting, a sense of fatigue, and headache were then noted. The eyes were inflamed and lacrymation, blepharospasm, and photophobia were present. A watery discharge ran from the nose and sneezing was frequent. The face and neck became red, and signs of pharyngitis and bronchitis appeared. The pulse and respiratory rate were increased.

The symptoms mentioned increased in severity, and by the end of 24 hours the face, neck, hands, inner surface of the thighs, genitals, and buttocks were acutely inflamed, vesication frequently being present. One of the most distressing symptoms was pain in the eyes, which might be very severe. The patient was virtually blinded, with tears oozing from between the bulging, edematous eyelids, over his reddened and slightly blistered face, while there was a constant nasal discharge and an occasional harsh, hoarse cough. Widespread and severe inflammation of the mucosa of the upper respiratory tract might be present, and the expectoration was then thick and blood tinged. Practically never did death occur during the first day. During the second day the condition of the patient grew progressively worse. Large blisters formed on the skin surface involved, while the scrotum and penis were swollen and edematous. The bronchitis became fully developed, with abundant expectoration of mucopus in which might be found large necrotic sloughs from the tracheal and bronchial mucous membrane. Cough was severe, and temperature, pulse, and respiration were increased.

After this, bronchopneumonia, the result of secondary infection, frequently developed rapidly, with marked coalescence of the involved areas. The patient was usually delirious, coughed and expectorated frequently, and complained of severe pain; cyanosis was marked. After a varying period he lapsed into unconsciousness and died, or recovery might set in. Death occurred from the end of the second day to as late as the fourth week after exposure.

The description given above is that of a severe case. When lower concentrations were encountered the patient usually escaped with a mild pharyngitis or bronchitis, if the gas was inhaled; the action of the gas was frequently exerted locally on the skin without involvement of the respiratory tract. In the latter case the skin lesions were those described later in this chapter.

Patients who developed severe bronchopneumonia usually died; those not so severely gassed eventually made a good recovery. Signs of improvement might appear at any time during the progress of the illness, and the period of convalescence depended on the severity of the local lesions. Photophobia usually persisted for a long time after the local inflammatory changes had disappeared. The bronchitis, also, was frequently persistent, and complaints of substernal and epigastric pain were made. Residual complaints were frequently of psychic origin. It is very doubtful whether severe sequelae occurred in those recovering from poisoning by dichlorethylsulphide; this subject is considered in a later chapter.

Properly used, well-fitting gas masks generally prevented the inhalation of mustard gas in sufficient quantity to cause pulmonary symptoms, but, of course, had no effect in preventing the skin lesions resulting from contact with the gas.




The cutaneous effects of mustard gas were caused by direct contact with the liquid or by the vapor which, in addition to affecting exposed parts, was diffused through the clothing. The distribution of the consequent injury varied accordingly. Certain areas of the skin, particularly parts where moisture and sebaceous excretions are excessive, were much more sensitive to the irritant action. The hardened skin of the palms of the hands and soles of the feet was much less affected than that of such parts as the crotch and genital organs.

The skin lesions may be classified, according to severity, as follows: 1. Erythema, which usually involved the face, neck, and chest; the axillve and flexure of the elbows; the inner surfaces of the thighs; and the scrotum and penis. This might appear in from 2 to 48 hours, or be delayed, either locally or generally, for several days. This condition resembled the erythema of scarlet fever, but was frequently accompanied with slight swelling and a mild burning sensation and itching. This erythema disappeared in a few days without leaving any trace or passed into the next type. 2. Very superficial blistering over the same areas, either in small vesicles or large blebs, which developed as painless collections of yellow or reddish serum just beneath the epithelium. If the covering was removed, a raw, moist surface was exposed, and secondary infections of these areas led to severe tissue destruction. This was particularly frequent in blisters of the scrotum and penis. The blisters usually appeared on the second day, but there might be an outcrop even as late as the second week after exposure, long after the patient had been carefully cared for and his clothing had been changed. 3. Staining of the skin with a (lark brownish-purple tint, usually in areas that previously had been erythematous. This staining was of no consequence and disappeared in a few weeks with desquamation.

The more severe skin lesions following exposure to mustard gas (that is. the lesions similar to burns of the second or third degree) were always the result of secondary bacterial infection. In some instances these severe lesions ran a protracted course, and a considerable degree of scarring resulted. It was the impression at first that the contents of the skin blisters would cause an erythema of uninvolved skin, but apparently this was disproved later.

An interesting observation made during the war was that men, without exception, who permitted the hair on the head to grow long and who were subjected to mustard-gas exposure had the most severe symptoms. This was due to the fact that this shaggy growth of hair afforded an excellent place for harboring the gas.


Conjunctivitis of sufficient intensity to incapacitate those exposed to mustard gas usually developed in from 2 to 48 hours. When very low concentrations of the gas had been encountered, the resulting conjunctivitis was mild and might develop only after several days had elapsed. In severe cases the patients were temporarily blinded by swelling and spasm of the evelids. In a case of ordinary severity the first symptoms to appear were of a subjective nature and were noticed from two to six hours after exposure. The patient complained of a feeling of pressure on the upper evelids, a feeling like that of


a foreign body in the eve, slight burning and tingling; he avoided light, and had increased tear production. Profuse lacrymation, with pain and headache followed. By the second day the lids had become swollen, the conjunctiva was markedly congested, a mucopurulent discharge was present, which frequently adhered to the edge of the lids, gluing them together and causing scab formation. The cornea at times became steamy, especially in the line of exposure, but actual ulceration was rare.

The conjunctivitis cleared up quickly and usually the injection disappeared in less than a month. But the inflammation was liable to be succeeded by photophobia which, if improperly treated, delayed the patient's return to duty even as long as two or three months. This condition was apt to assume a neurasthenic character and irritation was sometimes maintained, consciously or unconsciously, by frequently rubbing the eyes. In such cases it was found that the ocular conjunctiva opposite the lower lid was red while the conjunctiva above was normal.

Serious eye complications resulted from secondary infections. Even in the very severe cases of uncomplicated mustard gas, conjunctivitis cultures from the eye discharge rarely yielded any organisms other than saprophytes of the conjunctival sac.


The effects of mustard gas on the respiratory tract depended on the concentration of the gas inhaled and the length of time exposure lasted. The nasal mucous membrane was involved to a less degree than the remainder of the tract, but even here a profuse watery section resulted which might later become purulent and contain sloughs. Actual ulceration was rare. In the more severe cases epistaxis was common.

Inflammation and erosion of the posterior pharyngeal wall sometimes was sufficient to interfere with swallowing. Laryngoscopic examination revealed redness and swelling of the mucous membrane and sometimes of the false vocal cords. Edema of the larynx was present, but was never sufficient to necessitate tracheotomy. Ulceration occurred after exposure to high concentrations. Hoarseness was rare, but exposure to low concentrations frequently caused laryngitis and some aphonia, even when the conjunctiva was not involved. Severe pain in the throat, with cough, was often complained of and disturbed the patient's rest at night.

In mild cases the trachea and bronchi were only slightly affected. In severe cases there was an extreme inflammation of the mucous membrane, with extensive necrosis. Death was usually the result of bronchopneumonia caused by secondary bacterial invasion; in extremely severe cases, however, it might be caused by asphyxia due to the blockage of the air passages by large pieces of displaced sloughing membrane. When bronchopneumonia developed, the symptoms were of that disease. The characteristic pulmonary edema of the lung-irritant gases was not present in intoxications with the vesicants.


The early vomiting rarely persisted for more than a day, and the epigastric pain disappeared in a short time. Hematemesis was exceedingly rare. There were no lasting effects in the stomach, and the intestines were never affected.



The blood was unaltered and the heart was unaffected, except by the changes associated with the pulmonary infection. During early convalescence some patients complained of fatigue after exercise and shortness of breath, associated with precordial pain and tachycardia. These symptoms were chiefly due to a nervous debility, and yielded promptly to tonics and graduated exercise under firm discipline. Secondary anemia sometimes was noted after a severe and chronic illness.


Albuminuria was reported in the first 24 hours (in cases of early fatality), but was not found at a later date. Very rarely, acute hemorrhagic nephritis was observed. Pain during micturition and even retention of urine occasionally resulted from the edema and blistering of the penis.


Various bromine compounds, notably benzylbromide, were used for their lacrymatory effect. They were not often used by themselves, but generally with or as preliminary to an attack with lung-irritant gases. The irritant effect of lacrymators on the eyes and upper respiratory tract rendered it extremely difficult for the men affected by them to properly wear their gas masks; thus they were rendered easy victims to the lethal gases which were to follow. The lacrymators were used also in gas chambers for purposes of instruction and to test the fit of gas masks. The lacrymator gases caused acute irritation of the eyes, with profuse lacrymation, thus producing a temporary functional blindness. This did not last long, and after the immediate effects had passed away the man was ready for full duty.


The sternutator or "sneeze" gases, of which diphenylarsine was one of the chief, exerted their action on the nose and pharynx.

The symptoms, and these appeared immediately after inhalation, were sneezing, coughing, sinus and substernal pain, headache, increased flow of saliva, and frequently nausea and vomiting. While these were most disagreeable, they were never of serious import and complete recovery occurred in a few hours.


Carbon monoxide was not used as a combat gas, but during combat activities casualties frequently occurred as the result of inhaling it. Carbon monoxide was generated by the detonation of high explosives, as when considerable firing took place from an improperly ventilated emplacement and also by fires in dugouts. By the detonation of 1 kg. of modern high explosive from 600 to 800 liters of carbon monoxide are evolved. Carbon monoxide is lighter than air; consequently it diffuses rapidly in open spaces, and fatalities in such places are rare. On the other hand, within closed areas, as trenches and dugouts, dangerous concentrations frequently occurred, and these resulted in numerous casualties.

Carbon monoxide, which is odorless and colorless, owes its poisonous action to the fact that it combines with the hemoglobin of the blood to form


a dissociable compound, and thereby takes the place of oxygen. If, therefore, a small proportion of carbon monoxide is present in the air breathed, the hemoglobin in the blood will divide itself between the two gases, the final partition being determined by their relative concentration. The oxygen-carrying properties of the blood are properly diminished as the hemoglobin becomes more and more saturated with carbon monoxide.

Gas masks were useless against this type of gas. Mine-rescue apparatus or similar protective oxygen apparatus afford protection when properly used.

Carbon monoxide causes asphyxiation, with symptoms of vomiting, giddiness, semiparalytic weakness, acceleration of the pulse, shallow, irregular, and jerky respiration; and, finally, dulling of the sensibility, which may pass into complete unconsciousness, with widely dilated insensitive pupils, general functional failure, and death. Mental confusion frequently occurred, and in slight cases only headache was complained of; sometimes this is accompanied with nausea or the patient might appear to be madly intoxicated.

Except with massive doses, when loss of consciousness was rapid, the symptoms developed gradually as the gas was slowly absorbed. The demand for oxygen by the individual was important in determining the rapidity of the poisonous effect. In a man at rest in a concentration of the gas of 1 part in 1,000 it would be about two hours before definite symptoms appeared, and he was not disabled until after a lapse of two and a half hours. Muscular work accelerated symptoms.

The symptoms might remain stationary at any stage, since the degree of saturation of the hemoglobin with carbon monoxide had reached a final point which was determined by the relative concentrations of the carbon monoxide and the oxygen which were simultaneously trying to combine with the hemoglobin.


The successful treatment of gassed patients depended on early recognition of the condition, removal of the patient from the gassed area, determination of the type of gas responsible, and prompt application of the necessary thera- peutic measures. Many who were affected by the lacrymators or sternutators, as well as mild cases of mustard-gas poisoning, were promptly returned to duty, while others required longer or shorter time.

If gas was still present in the area where the patient was first seen, the good fit of his mask was verified, and care was taken to see that it was properly applied. If the mask was broken or did not fit properly, a new one was adjusted. Then, at the earliest possible moment, all gas casualties were evacuated from the contaminated area. Strict orders were in force that no patient affected by the lung-irritant gases be permitted to walk or to indulge in undue exertion of any character. Such patients, as already explained, were always transported. Similar precautions were taken with patients who had inhaled mustard gas, although, as has been noted, the danger from exertion was not so marked in this type of gas poisoning as in poisoning with gases of the lung-irritant group.

When no gas was present in the area at the time the patient was discovered, an ether pearl was administered if he was dyspneic or coughing. This was repeated in 5 minutes, again in 10 minutes, annd thereafter every 15 minutes. until the dressing station was reached. When indlicated, artificial respiration


by the Schaeffer method was practiced. While being conducted to dressing stations patients were kept in the open so far as possible, and later on, the doors of ambulances carrying gassed men remained open.

Oxygen was administered to and venesection performed on patients whose condition so indicated (lung-irritant gases) at first-aid or dressing stations where the necessary facilities were available. From the dressing stations patients were conducted to the triage or collecting station; in some divisions the dressing station also functioned as the triage.

In mild cases of mustard-gas poisoning, however, the patients were conducted to a dressing station where they were bathed and furnished with a change of clothing. They were then transferred to a gas hospital for further treatment.

At the triage, cases of gas poisoning and suspected poisoning were examined by a medical officer, especially skilled in the diagnosis of this condition (usually the division gas medical officer or his assistant), and those not gassed were separated from the gassed patients. A distinction between those affected by the different types of gases was made, and the various patients were transferred to suitable gas hospitals or to hospitals equipped for the care of gas cases.

Upon arrival at a division gas hospital patients were classified according to the type of gas to which they had been exposed and then by the severity of their symptoms. The slightly gassed and doubtful cases of gassing were placed in an observation ward for a few days, at the end of which time they were usually ready for return to duty. The more severe cases were assigned to the proper ward and then were either retained temporarily in the hospital or were evacuated to corps or army gas hospitals located farther to the rear, as determined by their condition.

At all places where the clothing of sufferers from mustard gas was removed, facilities were provided for the immediate degassing by appropriate methods of all articles of wearing apparel. Especial care was taken by all attendants coming in contact with these articles and gloves were always worn.


The first indication was removal from the gassed area. If this was not possible for any reason, a well-fitting gas mask was properly applied. In any event, at the earliest possible moment the patient was transported into uncontaminated atmosphere. While moving such a gas casualty in an ambulance, provision was made for an inflow of air, the windows being left open.

The treatment of poisoning by gases of the lung-irritant group comprised the following measures: (1) Rest, (2) warmth, (3) venesection, (4) oxygen inhalations, (5) cardiac stimulation, (6) fresh air, (7) inhalation of ether, (8) regulation of diet.

Rest.- Rest at all times was essential, and the nearer this approached absolute rest the better. The lack of a sufficient supply of oxygen in the circulating blood, consequent upon the pathological changes in the lungs, was the main factor in the production of the serious symptoms attending this type of gas poisoning. As is well known, the oxygen requirements of the human organism are largely dependent on the amount of work being done by the body muscles. Physical effort of any sort greatly increases the demand for oxygen by the tissues of the body. For these reasons every effort was made to prevent seriously gassed from making any unnecessary exertion.


These patients were always regarded as litter cases and were transported as little as circumstances permitted. Usually the clothing was not removed until they had been admitted to a hospital where they could be retained for treatment. They were not bathed until they had been sufficiently rested. Even in cases progressing favorably, rest in bed was enforced for several days.

Warmth.-Warmth was regarded as important. Cold caused an increased demand for oxygen. Heat was provided by methods similar to those adopted for the treatment of shock.

Venesection.-This was a matter of routine treatment and was performed as early as possible if the patient was at all dyspneic or cyanotic. Even at the first-line dressing stations venesection was performed when indicated. It was frequently necessary to select a large-sized vein and to incise it freely or to excise a portion of the vein wall, as the blood was inspissated, clotted quickly, and flowed with difficulty.

For practicing venesection, two different methods were adopted. Usually from 250 c. c. to 600 c. c. of blood were withdrawn, and if necessary this was repeated in a few hours. The other method involved the removal of about 250 c. c. of blood every three or four hours during the first day. The patient stood the removal of this amount of blood at such intervals without harm. Some observers believed that these repeated withdrawals of a small amount of blood were more efficacious than a single bleeding of a larger quantity. The majority were of the opinion that venesection was contraindicated in patients who were in the ashen-gray type of asphyxiation, although some reports indicate that the results of bleeding proved most gratifying even in this class of patients. Venesection performed later than during the first 18 hours after gassing was not appreciably beneficial.

Oxygen inhalation.-The administration of oxygen to all dyspneic, cyanotic patients was of vital importance. Under its influence the cyanosis often disappeared temporarily, and the respiration was quieted. Oxygen was given by means of a face mask equipped with in-and-out valves in such a manner that the patient received a mixture of about a 40 percent oxygen. The oxygen was administered as continuously as possible up to the point of disappearance of the cyanosis, and was repeated whenever indicated. Rectal, subcutaneous, and intramuscular injections of oxygen were also tried, but were not found advantageous.

Cardiac stimulation.- If the heart action indicated cardiac weakness, stimulants were given. Camphor, sparteine, and caffeine were found beneficial. Digitalis was used by some medical officers, but others objected to its use on account of the slowing of the heart action.

Fresh air.- The desirability of an ample supply of good air has already been mentioned in connection with transportation. For the relief of the substernal pain, especially in inhalation of ether, a few drops of ether held before the patient's nose on a piece of gauze and inhaled by him was found to he satisfactory. Alcohol or spirits of menthol used in the same manner also gave relief.

Sedatives.- Pearls of ether and ipecac, administered every one-fourth hour. were used at the front for their immediate sedative action. Cough was allayed and respirations made more regular. The emetic action of the ipecac unloaded the stomach, lowered arterial tension, and prevented pulmonary congestion.


Camphorated oil, caffeine, and emetine hydrochloride were found beneficial.

Regulation of diet.-The selection of it proper diet for the first 48 hours was very important. Food seemed to stagnate in the stomach, probably on account of the intense passive congestion of this organ, and caused distension, pressure on the diaphragm, and interference with the action of the heart. Deaths were observed which were apparently attributed to this cause, and accounts were numerous of men, gassed in the trenches, who had gone about their duties with no great discomfort only to fall dead at an meal several hours later. For this reason it was considered advisable to limit the diet for the first 48 hours to small amounts of well-diluted milk and then to permit a gradual increase of food. No restrictions were placed on the water intake.

Contraindications.- Opium in any form, atropine, adrenalin, the expectorants, and depressants, such as the coal-tar derivatives, were found to be harmful. Opium and its derivatives tended to check cough and hence to drown the patient in his own secretions. Smoking by gassed patients was prohibited, and convalescents were not permitted to smoke in wards containing acute cases. Digitalis and digitalin retarded heart action. Adrenalin increased pulmonary edema. Morphine should be given only in cases of extreme agitation. Inhalations of ammonia contraindicated because of the toxic action of chloramine which is formed when ammonia combines with chlorine.

Prevention of secondary infections.- In order to prevent the secondary pulmonary infections and complications of gas poisoning, which were so frequently attended with fatal results, care was taken to see that the patient was kept warm in a dust-free, well-ventilated ward and that careful nursing was provided. Especial care was taken to cleanse the mouth and teeth, particularly of unconscious patients. Exposure to cold of patients having bronchopneumonia was avoided.

Convalescence.- In general, gassed patients made rapid recoveries. The chief exceptions to this rule were those who developed secondary infections or those in whom cardiac symptoms appeared. Patients of the latter class often proved a most difficult problem to the medical officers in charge. They required constant observation for some time, especially those who, while usually appearing quite normal, developed severe attacks of dyspnea after physical exercise.

Graduated exercise was started after patients had been out of bed for from three to five days .Such exercise not only proved directly of benefit hut also served as a valuable index of progress toward recovery. The first exercise was a moderate walk of a few hundred yards; and if no signs of breathlessness or undue increase in pulse rate were noted, longer walks were prescribed for each succeeding day. If at any time evidence of dyspnea or tachycardia appeared. all exercises were stopped for a few days and then gradually commenced again.

The most satisfactory treatment for the breathlessness and increased heart action was the routine administration of small amounts of oxygen. Camphor or caffeine, administered hypodermatically, and in severe cases, digitalis. were used with good results in these conditions.


Soldiers who had been exposed to mustard gas were evacuated from the contaminated areas as promptly as circumstances permitted. If signs of


respiratory involvement were present, they were not allowed to walk, but were transported on litters or in ambulances, although the evil effects of exertion were not so marked in cases of this type of gas poisoning as in that where the tung irritants were responsible. In the care of patients with respiratory symptoms. all the precautions previously mentioned in connection with lung irritants were taken and, in addition, the clothing was entirely removed and the men were thoroughly bathed with soap and water at the earliest opportunity, care being taken to prevent chilling. After the bath, clean clothing was supplied. In mustard-gas poisoning it was not permissible to provide undue warmth until the clothing had been removed, as heat favors the diffusion of this gas.

Soldiers who had been exposed to mustard gas, but who showed no signs of pulmonary irritation, were conducted to the nearest station with the proper equipment close to the front lines, where they were thoroughly bathed and given a change of clothing. Bathing and change of clothing were usually accomplished at dressing or sorting stations.

The hair was clipped short. Observation of numerous cases demonstrated that long hair harbored the fumes of mustard gas and was instrumental in affecting the eyes, as well as increasing the irritation of the respiratory tract, besides the effect on the skin already mentioned.


No attempt was made to remove the liquid gas from the body by means of gauze or other swabs before bathing. Such an action would have resulted in spreading the liquid over a wider surface, thus causing additional skin involvement. Efforts were made to find some agent which would neutralize the action of mustard gas on the skin. Alkalies were found to be valueless, and oxydizing agents, such as chloride of lime or potassium permanganate, were useless unless applied within a very short time. Chloride of lime was used both in the dry form and as a paste and, if applied within one or two hours after exposure, gave satisfactory results. The paste, however, could not be allowed to remain on the skin for longer than three or four hours, as it was itself irritant and corrosive. The central laboratory of the American Expeditionary Forces advocated and provided dichloramine-T in 5 percent solution in an oily base. This substance liberates chlorine and was much less irritant than chloride of lime. Like the other oxydizing agents, it was of benefit only to patients who could be treated early. The ideal procedure for the cleansing of the skin proved to be thorough washing with soap and water.

When blisters had formed they were opened with surgical precautions; the fluid was taken up on gauze and not permitted to touch the neighboring skin. Skin erythema was treated with an alkaline dusting powder (talc, magnesium carbonate, zinc oxide) or by oily dressings such as petrolatum or paraffin. An excellent dusting powder, which was in general use, consisted of 200 grams each of calcium carbonate, magnesium carbonate, and zinc oxide, and 400 grains of talcum powder. For desquamated areas, especially the scrotum, zinc oxide ointment was used. Ambrine was found very satisfactory in treating the deeper burns.

When secondary infection had supervened in the burns the following wet antiseptic dressing gave good results: Zinc sulphide, 35; copper sulphide, 10; camphor water, 1,000. This was diluted with 9 volumes of water before use. Boracic acid compresses were also used. These dressings were continued until suppuration had ceased, when mildly antiseptic ointments were used.


Heliotherapy was reported as being of assistance in the disinfection and cicatrization of the more severe burns.

Coal oil or kerosene as an early wash was used extensively in France with good results, this procedure being followed by a hot bath with alkaline soap.

While dichloramine-T prevented to a great extent the development of erythematous areas around the vesicles, it did not prevent the damage already done to the skin. When used as a treatment for gas burns, the affected parts were kept moist with a 1 per cent solution in a 0.5 percent solution of sodium chloride applied on lint.

Dakin solution in mild cases proved very satisfactory. The parts were either washed with the solution or, if possible, were immersed for two to three hours in a solution of a strength of about 0.5 percent hypochlorous acid. If much of the body surface was burned, the solution was used as a bath, and for lesions of the genital organs a sitz bath was employed.

Of the many ointments used, the butyl salicylate ointment contained 20 to 60 percent anhydrous wool fat and 25 percent water proved to be very satisfactory, especially in relieving the troublesome irritations so often present.

The Italian ointment was also used extensively during the latter days of the war. This ointment consisted of the following:

Manganese linoleate..............................................50
Zinc linoleate ........................................500
Linseed oil...................................................500

This ointment, if applied to the skin immediately after contract with mustard gas, prevented the formation of blisters.


The eyes when affected required frequent irrigation with warm boric-acid solution or with 2 percent sodium bicarbonate solution, followed by the instillation of liquid paraffin. Castor oil, while more irritating than paraffin, was often used if the latter was unobtainable. If the cornea was involved, sterilized atropine ointment of 1 percent strength was substituted for the paraffin and repeated sufficiently often to keep the pupils dilated. While some hospitals used a 1 percent solution of cocaine to relieve pain, the general opinion was that cocaine should not be used on account of its harmful effect on the cornea. If the discharge from the eye became mucopurulent, a weak solution of argyrol or protargol was used once a day. When the acute inflammation had subsided a weak solution of zinc sulphate was frequently employed as eyedrops.

The eyes were protected from the light either by darkening the ward or by the use of eye shades. Bandages were not permitted, as they helped to retain the discharges in the eyes. The patients were encouraged to pull the lids apart in order that the discharge might flow freely.


Little could be done for symptoms due to irritation of the respiratory tract beyond controlling the violent coughing. For this purpose morphine was sometimes used, but heroin and dionine were regarded as preferable. Relief for the laryngeal irritation was obtained by the inhalation of steam saturated with menthol or benzoin. In the hospital treatment of patients who had inhaled mustard gas, of principal importance were measures to prevent secondary infection and the ensuing bronchopneumonia. These included care-

aThe more severe burns of the eye, requiring attention by the ophthalmologist, are discussed in Vol. XI, Pt. 11. Sees. III and IV, of this history.


ful nursing; adequate ventilation, obtained by open windows, and ample floor space per patient; ward cleanliness; avoidance of dust; and sufficient warmth.

The treatment of a supervening bronchopneumonia was conducted along the lines indicated for that disease, the patients being removed to a separate ward and cubicled.

Diet.-Patients with respiratory symptoms of mustard-gas poisoning were kept on a light diet on account of the intolerance for food that was usually manifest. The routine diet adopted for phosgene cases appeared to be the safest, namely, milk and water for 48 hours after exposure, then light diet, to which meat and vegetables were added as the patient's condition permitted.


The effects of the lacrymators and sternutators, while most disagreeable, were not severe, and they usually passed off in a few hours.

For the relief of symptoms caused by the eye irritants the best treatment was found to be an eyewash of 14 percent saline solution or 22.5 per cent sodium bicarbonate solution. A 1 percent solution of cocaine was used when necessary to relieve pain.

For nasal irritants a 1 percent cocained vaseline was applied to the nostrils. In case vomiting was a symptom, solution of magnesia was given internally.


As the symptoms caused by the inhalation of carbon monoxide are due to the gradual diminution of the oxygen-carrying power of the blood, it is clear that any increase in the oxygen demand on the body must be avoided. Therefore, absolute rest was one of the important factors in the treatment of carbon monoxide poisoning. The patients were not permitted to walk, but were transported by litter or ambulance. Fresh air was also essential, though not cold air if avoidable. When the patient was removed into an uncontaminated atmosphere the carbon monoxide gradually separated from the hemoglobin of the blood, and the hemoglobin resumed its normal function as an oxygen carrier. The removal of carbon monoxide from its association with the hemoglobin was greatly hastened by the administration of oxygen. It was regarded, therefore, as important to begin the administration of oxygen as soon as possible after the patient had been removed to a gas-free atmosphere. The administration of oxygen was continued from a half hour to an hour, depending on the severity of the symptoms. If the respiration was very shallow the administration of oxygen was often combined with artificial respiration. Collapse was combated by external warmth and friction of the limbs. While in cases of poisoning with the lung irritants the interference with the gaseous exchange between the blood and the air in the lungs, consequent upon the pulmonary edema and the pathological changes in the lung tissue, often persisted for some time and necessitated the administration of oxygen for several days. In carbon monoxide poisoning the structure of the lung tissue was not damaged and oxygen was administered only with the intention of accelerating the discharge of carbon monoxide from the blood. After this had been accomplished there was no need of continuing the oxygen, as the oxygen-carrying power of the blood had become normal again. Any symptoms that persisted were due to the effects produced while the blood was charged with carbon monoxide and were unlikely to be influenced by the further administration of oxygen. Further oxygen administration was required, therefore, only if cyanosis began to develop subsequently as a result of secondary cardiac or respiratory failure.