Gerard II 
MEDICAL aspects of chemical warfare 
By 
Dr. Pc, Gerard 
Professor of Physiology, University of Chicago 
x • ••' . I have been assign- 
ed the duty of skipping lightly over the whole field of the med- 
ical aspects of gas warfare; which means, I hope, that almost 
everything I say this morning will bo taken up in somewhat more 
detail by subsequent speakers. Perhaps the most useful thing I 
can do is to compare the several gases and emphasize the diff- 
erences in the various problems they raise, rather than to go into 
detail about any one. 
May I start by reading two quotations, to get ourselves in- 
to the proper atmosphere of this subject. The first is from 
Col, Waitt's book "Gas larfare". He says; 
"The adoption of chemicals as weapons was as logical as it 
was inevitable in a world war in which all the principal combat- 
ants were nations highly developed in science, ‘Then the German 
advance was halted after the Battle of the Marne in 1911, both 
sides firmly entrenched themselves, A dead-lock oxistod| neith- 
er side could gain any material advantage. Machine guns had in- 
creased firepower to such an extent that only by a mass superior- 
ity in manpower could ground be captured. The attack had failed, 
and mobility for both the Germans and the Allies had been lost. 
” It became apparent that the issue could be determined 
only by exhaustion, and the odds were that the Germans, complete- 
ly surrounded, would bo exhausted first. The Gormans recognized 
the situation and tried to find some agency to reach the enemy 
behind his sandbags and down in his dugouts. They looked for 
something which would rob the defender of the superiority which 
the machine guns and rifles fired from behind entrenchments had 
given him. Thus chemical warfare was born. The gas particles 
that could shoot around corners and into holes wore given the 
job of driving the defender out of the dugouts into which steel 
particles had driven him, and from which artillery shells had 
failed to blast him." 
Ho goes on then to describe the first gas attack, 
“The weather was perfect, a glorious spring day. During 
the morning there had been somewhat more than the daily artill- 
ery shelling of Yprcs, but it was not unusual, and by noon time 
it had stopped. During the early port of the afternoon every- 
thing was quiet. Suddenly at five o’clock (British Time) the 
calm of the spring afternoon was shattered as a vicious bombard- Gerard XX 
nent of Ypres was started by the heavy guns. For the first ten 
minutes the German light batteries were silent and no shell fell 
in the forward trenches, which were about four miles north of 
Ypres. Nothing must disturb the quiet air here. As the bombard- 
ment began, the men in the forward positions hoard a hissing sound 
coming from the Gorman trenches. At first two greenish-yellow 
•louds appeared on each side of Langenmarck, which was in poss- 
ession of the French. Then these merged and a heavy cloud almost 
like a wall, nearly five miles in length, stretched itself along 
the German trenches from Stoenstraat to a point a half a mile west 
of Pcolcappelle. This wall-like cloud was perhaps as high as a 
man's head at first, but gradually it became higher as it moved 
slowly to the Allied trenches. Observers who saw it from a dis- 
tance said it had the appearance of a mist 'such as is seen over 
water meadows on a frosty night.1 The wind was light that after- 
noon, only four or five miles per hour. Gradually the cloud borne 
by the wind swept over the Allied linos, bringing horror, confusion 
and death into the ranks of some fifteen thousand men. The time 
consumed by emission of the gas was only fifteen minutes, but the 
poisonous clouds of chlorine hung over the Allied trenches for a 
much longer tine and swept back into the rear areas for several 
miles, gradually becoming weaker• 
"The French Colonials had the worst of it, for the cylinders 
were all emplaced in front of then. Only a part of the third brigade 
on the extreme left oi the Canadian Division was in the main path 
of tho gas, but the cloud s’.aing in to the roar of the Canadians and 
moved back with the wind. 
"Tho Allies were entirely unprepared for such an attack. 
They had information through military intelligence that a gas attack 
was coming, but they didn’t believe it. A few days earlier a desert- 
er captured near Langennarck had told tho French that the Germans 
intended to use 'tubes of asphyxiating gas placed in batteries of 
twenty tubes for every forty motors along the front of the XXVI 
Corps (French).' The prisoner even had in his possession a cotton 
pad which ho said was to be dipped in chemicals to counteract the 
effect of the gas. The Royal Flying Corps was ordered to observe 
the German linos, to see if any special apparatus could bo dis- 
covered, but they found nothing suspicious, and no further steps 
were taken. It was not until French Colored troops without their 
officers began drifting upon tho roads through tho British area 
that it was realized that the greenish-yellow cloud was the gas 
against which they had boon warned. It is sometimes difficult to 
convince a military man of the possibilities of new and untried 
methods." I am still quoting Colonel Haiti!, 
’’The Casualties wore about 5,000| a largo number of deaths 
occurred on the ground, and besides these there were many deaths 
in the hospitals.” Gerard II 
I now turn from the picture of the gas attack to an eye wit- 
ness account of the consequences. This is taken from an article 
by Dr. G, W, Norris, "Some Medical Impressions of the War." 
"A field hospital full of freshly and badly gassed men is, 
in the estimation of all who have had an opportunity of seeing it, 
the most horrible and ghastly sight of the war. Even the man ?.fho 
has received multiple and severe wounds, when he has been splinted, 
put to bed and given his morphine, is relatively comfortable3 but 
to see a hundred or more men, hale and hearty a few hours before, 
slowly strangling to death from pulmonary edema with gradually in- 
creasing dyspnoea, cyanosis and pallor, making futile efforts to 
expectorate and to assist their breathing by voluntary effort and 
muscular contortions, until exhausted they pass from semi-delirium 
into stupor, collapse and death, is a never-to-be-forgotten sight, 
a sight which makes one clench one's teeth and curse the Hun who 
started this dastardly infamy. This is phosgene’ But can nothing 
be done? Yes I The cyanotic cases are promptly bled, one pint, 
sometimes two. The ward looks like a shambles because in hurrying 
from bed to bed, twenty to thirty in a row, the spurting blood has 
left its trace upon bed and floor and linen. Meanwhile oxygen is 
being administered to greedy mouths while hands are loath to loose 
the bag when their five minutes of respite are over, for never are 
there enough bags for all, and the precious gas we must not waste, 
for it has been no small task to bring those great iron tanks up 
to the front. Opium we dare not use, for it checks an oft life- 
saving cough. But the gray cases, what of them? Lying about with 
a clammy skin, too weak to move or even care. Some venturous 
spirits say that one should bleed and then transfuse, but most that 
we should not meedle," 
That is the last war• Such effects are not likely to be seen, 
in the civilian area3 certainly, nor are the same treatments recom- 
mended| but, as Dr, Serf.or has already emphasized, there are certain 
very obvious morals to be drawn from these experiences by physicians 
today, and I should like to reiterate some of them. He spoke of the 
great importance of supporting morale. I agree that unquestionably 
the most important service physicians can render in a gas raid or a 
supposititious gas raid will be in supporting morale. Perhaps the 
best way to start on this problem is to counteract these ugly pic- 
tures I have just recalled by some cold figures. 
Slide 1 is a summary of the American Expeditionary Force 
casualties and deaths in V'orld War I. As you see, about two-thirds 
of all casualties were due 'to gunshot" or like mechanical injury and 
about one-third were due to gas. Now, of those Casualties, most'.idjsaths 
were hospital- deaths,- -The actual numbers do not interest us particu- 
larly*' but note'that although one-third of all thes-'casual ties 
casualties, only one-tenth of the deaths were gas death’s. Gas certain- 
ly did not produce anything like its proportional amount of deaths, -The 
actual percentage of gassed individuals dying, from all sorts of Gerard II 
gases and under all conditions, was somewhat under two percent. 
Slide 2 gives the material in somewhat greater detail, for each of 
the gases. Note that the average hospitalization is about six 
weeks after gassing with either mustard or phosgene. 
Thus gas in itself is not so terribly bad, medically consid- 
ered. It may disable a large number of individuals and it may have 
extremely valuable military harassing or other purposes; but, in 
terras of the clear facts, as we will see, gas is not so horrible. 
There is no basis for the almost morbid fear of gas and of the 
whole subject, which most lay people and oven some medically train- 
ed people have. 
Actually, even the deadly war gases are not very deadly 
agents as compared with many of the substances used routinely by 
the medical profession. They are not extremely toxic chemicals. 
In the case of phosgene, for example, the exact amount of gas whith 
is necessary to kill is not precisely known, but it may be assumed 
it is of the order of one milligram per kilo body weight. You con- 
tinuously use drugs in practice that would kill in far smaller 
doses. 
Slide 3 gives some data on toxicitios and concentrations. 
Some of this material has already been referred to. It is based 
largely on Prentiss, Concentration is expressed in ounces per thous- 
and cubic feet or milligrams per liter; and minimal doses are stated 
for a detectable odor, for irritation after ten minutes exposure, 
or for lethal action after the same exposure, I call your attention 
to the law that toxic effect is proportional to the time of exposure 
multiplied by the concentration of the gas. In those gases, of 
course, the amount that actually gets into the body increases with 
the time during which the gas is being breathed; so that with a 
thirty minute exposure, approximately one-third the indicated con- 
centration for ten minutes would have a like effect. 
Tho slide shows: the vesicant group — mustard. Lewisite, and 
cthyIdichlorarsine; tho lung irritant group — chlorine, phosgene, 
and chiorpierin; the stonutant group — diphenylaminochlorarsino and 
diphenylchlor arsine; and tho lacrimant group — chiora«etophenone 
and brombenzylcyanidc. You will notice that certain of those gases 
are particularly mischovious. The concentration which will produce 
irritation is actually less, in tho case of the vesicants, than 
the amount which can be detected by odor. In other words, one can 
be seriously exposed to mustard or Le?d.sito or ethyldichlorarsinc 
and not be warned by smell of tho exposure. 
The lethal coneentra.tions arc rather interesting. Lewisite 
and mustard are about tho same, lethal in lowest concentrations; 
phosgene is almost tho same order; the others are definitely less 
toxic. Chlorine is relatively a non-toxic gas; and you will note Gerard II 
that the irritant gases, because of their extremely low concentra- 
tions which suffice to produce irritation, arc less dangerous. 
The indicated concentrations for irritation can, in fact, probably 
be tolerated for loss than ton minutes. 
The duty, then, of the physician, which you will wish to 
impress especially upon the physicians whom you train, is mainly 
to support morale, to avoid panic in case of a gas attack or of an 
attack which is misjudged by the populace to be a gas attatk. The 
physician will have little opportunity to exercise any prophylac- 
tic maneuvers. He will ordinarily not bo called upon, as you al- 
ready know, to be responsible for decontamination or even cleansing. 
HOv-will, however, be responsible for the appropriate treatment of 
gas casualties, and that involves, of course, a correct differen- 
tial diagnosis. You have already seen lists of references and guides 
that you may consult and. recommend, I have a few references in 
slides 5, and 65 and some comments on those may help you to de- 
cide on their usefulness. Jacobs’ book is essentially chemical. 
Prentiss’ is a little out of date, but is a comprehensive treatment 
of the whole subject of gas, mainly from the chemical point of vio?;, 
but including also a discussion of tactics and a little on the med- 
ical side, Sartori treats gas almost entirely from the chemical 
side, Voddcr's book, ’’Medical Aspects of Chemical Warfare,” is un- 
fortunately rather out of date, but still has a groat deal of val- 
uable information in it and is a full sized treatment of just what 
the title indicates. Wachtel gives some account of the history and 
results of research in Germany curing' the last war. The next two 
references I most emphatically commend to your attention. "The 
treatment of Gas Casualties,” available from the Superintendont of 
Documents, Washington, D. C., at ton cents. (I believe the latest 
edition of tho.t is November 27, 1942, which you have), is vory use- 
ful as a concise source of information on this subject. Even more 
readable and informative is the British, ’’Manual on Chemical War- 
fare,” published in this country by Chemical Publishing Company. 
For a concise, lucid and highly interesting account of the medical 
aspects of gas warfare I think you can hardljr do bettor. Finally, 
the volume by Waitt is a good treatment for the layman and easy 
reading — as you can toll from the quotation I read from it. 
So much then for such general introductory comments. We 
must pass on to a more particular consideration of the medical as- 
pects. The speakers to follow will consider with you, in order, 
the lung irritant group, with emphasis on phosgene; then the ves- 
icant group, covering mustard, the now nitrogen mustards, and Lewisite 
and the other arsenicals. Later speakers will take up the sternuta- 
tors and lacrimators, the systemic poisons, the treatment of burns, 
and so on. 
The systemic poison gases will probably not corao into much 
practical uso; but you are familiar with them. Cyanide, monoxide, 
perhaps hydrogen sulphide, and arsine are the ones most likely to 
need attention. And harassing agonts vrould hardly be dropped on a Gerard II 
civilian population* The lung irritant group constitute a real dan- 
ger, and the persistant vesicants are likely to need most attention. 
To varying degrees — based on present knowledge, time, and person- 
al methods — I believe the speakers will take up these gases from 
the medical point of view under the heads of: essential mechanism 
of action, physiological pathology, signs and symptoms, prognosis, 
treatment (probably in some detail), and late effects* 
The action of all those gases, to sum them up collectively 
(and they are called gases and arc breathed, although some are sol- 
ids), centers more or less upon the lungs* All of them except the 
systemic poisons produce lung damage, whatever else they do. All 
of them, except the vesicants (which reach the skin even with the 
head protected by a mask) enter the body through the lungs* It 
will perhaps be specially useful to compare the respiratory system 
actions of these different gases* 
The systemic poisons exert little such action. Hydrogen 
sulphide does produce some irritation of the respiratory tree; 
arsine a negligible amount; the others none* The mouth is essen- 
tially a mere portal of entry, and the effects are produced after 
absorption, mostly on the respiratory and other centers of the cen- 
tral nervous system. Dr, Farmer will take them up in a body to- 
morrow* The other groups do act on the respiratory system. Slide 
7 is a simple diagram indicating the positions of action in the res- 
piratory system, of those different types of gases. The position 
of the label shows whether the gas acts high up or low down in the 
respiratory troo. Ammonia and. the irritant gases act mostly right 
in the nose and mouth; mustard on the trachea and bronchial system 
particularly; chlorine acts thuro and also in the alveoli; phosgene 
and its related compounds act hardly at all on the upper respiratory 
passages, but produce violent damage in the terminal tubes and al- 
veoli of the lungs. There is a progressive descent of action from 
the harassing, through tho vesicant, to the lung irritant group. 
Turning now more particularly to tho vesicants, you oro well 
aware that those gases arc called vesicants not because they act 
only upon the body surface, to produce vesication, but because they 
are the only ones of the gases which do act on the skin. All the 
vesicants also do other things. Besides tho skin, the eyes are in- 
jured and even smaller exposure may do more serious damage to them. 
They are also respiratory irritants, acting on tho pulmonary system, 
and in addition they are systemic poisons, I shall not go into tho 
systemic action, but mention that mustard, the N mustards, and Lewis- 
ite produce narked changes in the bone marrow and the lymphatic 
system; and, of course, the arsenic group, Lewisite and so on, pro- 
duce all sequelae or concomrnitants of arseni* poisoning as well. 
A characteristic of this group is latency of onset; from 
exposure to symptoms there is always an interval. In the *ase of 
liquid splashes of Lewisite or mustard, that interval may bo rather Gerard II 
short| in fact splashes of liquid Lewisite in the eye will produce 
serious symptoms within perhaps two to five minutes. But there is 
no immediate effect even here and, in the case of vapors, the lat- 
ency of eye symptoms may be a couple of hours and of skin symptoms 
six to twelve hours• Then the pathology and symptoms progressive- 
ly increase until a maximum is reached usually within one or two 
days. Because of the delayed action, one common error is made by 
the uninitiated person who has not had the mask drill that 
Dr, Senior emphasized. He is exposed to Lewisite, let us say, 
and puts on his gas mask. Everything goes nicely for a few minutes, 
but then ho begins to have burning of the nose and eyes and decides, 
very naturally, that his gas mask has stopped working; so ho takes 
it off. Of course, the gas mask is working, but the effect of the 
initial brief exposure was delayed. 
The further discussion of this group must bo restricted to 
mustard, itself, as the type vesicant. One of the striking early 
symptoms after gassing, appearing in an hour or two, is hoarseness. 
It may be noticed ovon before conjunctival symptoms in those ex- 
posed, The reason for the hoarseness is obvious from the pathology. 
Slide 8 shows the larynx of a dog exposed to mustard vapor; and I 
think you can soo that the tissues are puffy and. inf lammed. Slide 
9 is a photomicrograph of a cross section of the trachea of a mouse 
one day after exposure to mustard. It shows strikingly the severe 
damage done to the respiratory passages by the gas. The epithelium 
is gone, except in patches, and a tremendous exudate and inflamma- 
tion extends through the mucosa even into tho cartilagenous rings 
of tho trachea. 
Slide 10 illustrates an exceptional aspect of mustard action 
but brings out the fact that the damage to the tissues is deep, 
penetrating and severe; and can lead to senrring. This is tho 
trachea of a dog a month after gassing with mustard, Tho dog had 
recovered, but with a stenotic scar in tho upper trachea follow- 
ing actual necrosis of the tracheal wall. Such a scar is rare ex- 
cept on the skin under certain conditions or in tho eyo; but its 
occurance in the regions of action of the vesicants in the respir- 
atory tract indicates that the gas oats deeply and may do permanent 
damage there. 
Slide 11 shov/s that mustard is essentially inactive on the 
lung parenchyma. It is a section of a mouse lung one day after ex- 
posure to mustard. You can see slight bronchial irritation, and a 
very slight injection of tho alveolar vessels, a pneumonitis; but 
this clears up without edema or destruction. There are no immediate 
lung symptoms v/ith mustard, rather more with Lewisite and with the 
nitrogen mustards, as you will hoar later on. 
Slide 12 shows, however, that there arc important respiratory 
aspects of the vesicants. Although tho lungs themselves are not 
directly damaged by the gas, gas injury to the upper passages often 
leads to aspiration of food and the like, as seen here, and so to Gerard II 
aspiration pneumonia. Slide 13 shows grossly an abscessed pneumon- 
ia in the lungs of a dog five days after exposure to mustard; and 
slide 14 shows the severe histopathology. Broncho-pneumonia is an 
important sequel of mustard gassing; in fact, it is the main cause 
of death after mustard. The ether mustard actions produce casual- 
ties in troops or civilians for weeks or even months and they nay, 
uncommonly, have permanent consequences in blindness or skin scars; 
but the mortality and long invalidism result from attion on the 
respiratory system. 
The vesicant action of these gases is to be considered later 
in detail,,but a few slides now will servo to illustrate the skin 
lesions. Slide 15 shows a typical mustard burn on the abdomen of a 
man, resulting from contact, through clothing, with contaminated 
rags. Tho clear fluid bleb and marginal erythema are characteris- 
tic. Slide 16 shows mustard blisters on the fingers, and slide 17 
Lewisite blisters for comparison. In these the blister fluid is 
cloudy and the edges sharp with little rod flare. Slide IS shows 
a mild mustard burn of the face, an erythema outlining tho position 
of a gas mask. This officer was sprayed with mustard from a plane, 
in a field test with mask and protective clothing. But in the hot 
weather perspiration carried some mustard under the mask edges - 
with the result you see. 
Tho treatment of mustard burns, after cleansing, is that of 
other burns or open skin wounds; as tho treatment of mustard pneu- 
monia is that of any broncho-pnounonia. Because of danger of 
pneumonia, caro against cross infection is important. Tho British 
recommend, under conditions whoro it is possible, as in civilian 
hospitals, that mustard casualties be treated as contagious disease 
Ceases and kept in isolation. Further consideration of treatment I 
leave to later speakers. 
May I say ono last word, however, about lato effects. Accord- 
ing to careful studies on casualties after the last war, there seems 
no justification for the prevalent belief in permanent effects of 
gas. Mustard cases nay retain an injurious scar, such as you saw in 
the dog’s trachea; perhaps an increased tendency to bronchitis; if 
pneumonia occurred in nay leave the usual damage; and, of course, 
typical skin and eye lesions nay be left, although most heal. There 
is no indication of an increased tendency to tuberculosis, although 
it is possible that tuberculous lesions may be activated by gassing. 
Many soldiers after the last war seemed to suffer permanent effects 
from mustard, such as photophobia and night cough. Most of these 
co.ses could rather regularly be cleared up without medical inter- 
ference by "eye exercises’1 or deep breathing routines, and so seen 
to have been essentially psychiatric, with conversion symptoms. The 
handling is a psychiatric rather than a clinical problem. 
Parsing next to tho respiratory irritants, I shall consider Gerard II 
primarily phosgene and diphosgeno, which has an identical action 
although its different physical properties have important tactical 
consequences. (For example, there is an impossible discrepancy 
between American figures for deaths from phosgene, 2% of the cas- 
ualties, and the German figures, S‘0/o. Perhaps the Germans used more 
diphosgene which was less effective in building up high vapor con- 
centrations. ) By comparison, chlorpicrin and chlorine are more 
irritating and less toxic. Phosgene, if I may guess, would be as 
apt to appear over the Chicago area as any gas. It would cone 
on a cold, still, clear winter night, when it night build up to 
an effective vapor concentration over a considerable area. 
Phosgene breaks up over a matter of seconds or minutes on 
contact with aqueous media. It must, then, act promptly in the 
lungs after being inhaled, or the damage must be done by the acid 
liberated by its decomposition, .although we are told that hydro- 
chloric acid, perhaps liberated intracol3.ulo.rly, causes injury, 
I doubt whether acid is very important, What the exact chemical 
mechanism of action is, although of profound academic interest and 
perhaps of importance in'developing better means of handling cases, 
is of no consequence to the physician faced with a case of phosgene 
poisoning. The pathology and physiology of its action is important. 
As a result of chemical damage produced in the lung endothelium by 
phosgene there is an increase in permeability to blood plasma. 
Whole plasma leaks out through these now permeable membranes under 
the hydrostatic pressure in the pulmonary vessels, and edema sets 
in promptly. 
That is a particularly unfortunate combination of local con- 
ditions. Not only is fluid being lost from the blood, resulting 
in henocontration to a degree of increased viscosity and decreased 
blood volume which may seriously interfere with circulation through 
the body, but also the fluid that loaves the blood remains in the 
lungs where, like a pneumonia or any other type of pulmonary trans- 
udation, it interferes with the gas exchange through tho alveolar 
membranes. Consequently, stasis anoxia and anoxic anoxia sum their 
effects on tho body tissues — which receive less blood carrying 
loss oxygen per unit of blood. 
Slide 19 shows the lungs of a goat exposed some ten or twelve 
hours earlier to phosgene. You can perhaps identify the foamy ex- 
udate, or transudate really, filling the trachea. Dr, Lushbaugh 
expects to autopsy some phosgene animals tomorrow and you will see 
the water-loggod state of tho lungs. Slide 20 represents a very 
typical phosgene lung, from a rabbit, with irregular patches of 
edematous consolidation and of emphysema. 
Slide 21 shows, in contrast with the mustard series, that the 
upper respiratory passages arc little, if at all, injured by phos- Gerard II 
gene. This is the larynx of a cat after a severe phosgene dose* 
All the epithelium is intact, a very slight sub-mucous edema is 
seen, and nothing else. 
Slide 22 shows a section of a monkey’s lung after phosgene. 
The tremendous damage — with emphysematous patches, necrosis and 
congestion, and the whole full of edema fluid spreading out from 
the vessels -- is obvious. 
Slide 23 is of a case of diphosgeno poisoning, with the lungs 
still in situ in the dog. It sho?/s that diphosgeno gives the iden- 
tical effects of phosgene itself| emphysematous blebs appear all 
over a congested and edematous lung. 
The signs following aro rather important because the early 
symptoms are not. An individual may be well along the course of 
developing a pulmonary odoma, even a fatal one, without the physi- 
cian being able to hear much on physical examination of the chest. 
There is perhaps a small increase of breath sounds in the axilla 
or back, and some rales may bo hoard, but even those are not at all 
commensurate with the pathology which has developed. Perhaps the 
most convenient laboratory tost to use in following the course of 
the developing disturbance is the hematocrit. It may fall a little 
in the first four hours but subsequently, in all serious cases, it 
rises and may rise very much indeed — over 50 per cent. Of course, 
by that time there is adequate clinical evidence of what is happen- 
ing to tho patient, A decreased blood oxygen, particularly venous 
oxygen, is obviously indicative of pathologyi and a falling arterial 
pressure is a concommitant finding. 
The phases of phosgene poisoning can perhaps be divided into 
four. First is a phase of acute reflex effects immediately after 
exposure. Those are often mild or absent unless gas is inhaled in 
high concentration, and even then they soon pass off. Some shallow 
rapid respiration, slow heart, constriction of the chest, nausea 
and diarrhoea, ere of importance mainly as evidence as to the actual 
exposure. Then follows the phase of so-called latent period, which 
may last for five, ten or fifteen horn's. The patient may seem, dur- 
ing this interval, quite normal and over his trouble. Yet during 
this period obviously lung edema is developing, When sufficient 
edona is present so that tho gas exchange is interfered with and so 
that tho circulation is embarrassed in one way or another, cyanosis 
begins to sot in. The patient then enters the blue stage (slide 24)• 
His face is blue, nock veins are engorged, blood pressure is lowered, 
respiration is labored, frothy and perhaps bloody sputum may bo 
raised, and the individual begins definitely to struggle for breath. 
It is then that oxygen brings such dramatic relief. If relief is 
not obtained, if tho pathology does not begin to resolve, circula- 
tory failure eventually supervenes. This is the gray stage (slide 
25), It is a typical shock, except that the patient’s face is a Gerard II 
greenish gray due to the concomitant asphyxia. The blood pressure 
drops away and the patient dies. Unhappily, in this typical shock 
condition, there isn't much use in treating the shock, because the 
plasma leak remains. Fluid introduced into the body simply comes 
out again into the lungs and exaggerates the pulmonary problem 
of gas exchange. 
In the blue stage, bleeding is widely recommended. It was 
emphasized in the memorandum I read you from Norris, and is also 
advised in the current war manuals. I doubt that it is as useful 
as is generally believed. 
While I am indulging in personal medical heresies let me 
also express one other bit of skepticism, which may be of very great 
practical import. All present instructions about handling phosgene 
casualties emphsize the need of immediate and absolute rest. This 
does not seem entirely logical to a physiologist. It is perfectly 
true that when fluid has accumulated in the lungs so that gas ex- 
change is interfered with, the oxygen need of the body must be min- 
imized and exercise avoided. But during this early period, of a 
few minutes to a few hours after exposure, if no considerable lung 
edema is present, I can't see that the amount of exercise involved 
in walking from the point of exposure to a proper treatment center 
will do the patient any damage. And it makes an enormous differ- 
ence in the organization of the medical services whether every gas 
case or suspected gas case is to be treated as a stretcher problem 
or is allowed to ambulate for further attention. 
The late effects of phosgene are rarely serious. If the 
patient doesn’t die in a day or so he is likely to recover complete- 
ly , unless he gets a secondary pneumonia with its consequences. 
Slide 26 shows the lungs of a dog sacrificed five days after a 
severe phosgene gassing. As you see, they appear quite normal. 
Asthma at night and D.A.H. (disordered action of the heart) have 
been seen with some frequency, but the medical evidence again seems 
to place these problems in the psychiatric field. 
Finally, may I say a few words on the problem of diagnosis. 
It is well to realize that the doctor faced with a case at a gas 
casualty station has to make three diagnoses| or has to answer three 
questions. The first one is: Was the individual gassed? The answer 
is of importance both medically and tactically. When bertain that 
the patient was gassed, the second question is; Which of the known 
gases was it? But don't forget that there is a third question, 
which the physician particularly should keep in mind: Is this a 
new gas? When symptoms and history are atypical, the alert doctor 
seeing immediate casualties is about as likely to first get evidence 
of a new gas as are the special gas detecting agents or the control 
office. 
There are certain points to keep in mind in making the usual Gerard XX 
differential diagnosis. The history is of especial importance* 
Obvious points are; just when was the exposure| how long was the 
exposure| what were the conditions — was exposure in a closed room 
or outdoors, was there a big explosion or a little one, were the 
eyes open or closed while sleeping, (the eyes being closed during 
exposure may confuse the symptoms), was a gas mask worn, and so on. 
But one of the most important things for the physician to ascertain 
is character of the immediate symptoms* He must note the positive 
ones, which are reported and, by careful inquiry, make sure those 
not reported did not occur. Was there an immediate irritation of 
the eye or wasn't there? It may be a crucial diagnostic point -- 
severe immediate irritation is probably due to one of the harass- 
ing irritant gases and not likely to be serious in the long run# 
The British Medical pamphlet to which I referred you has a 
definite system of differential diagnosis outlined, depending on 
the parts of the body involved. If the skin is attacked you are 
dealing with a vesicant, whatever else there may be. Those are 
then differentiated; reddening without blisters probably excludes 
mustard or Lewisite, it may bo one of the irritant drugs. Mustard 
gives a blister with a red flare and clear fluid, Lewisite a blis- 
ter with little flare and turbid fluid. If the skin is not in- 
volved the next question is: "Arc the eyes involved?" If they are, 
you are dealing again either with one of the vesicants or with a 
lacrimator. If the eye effect was immediate and acute, one of the 
harassing irritant gases was responsible, and there is little to 
worry about. If the effect was delayed, a dangerous vesicant ac- 
tion must be guarded against. If, whether or not the eyes are in- 
volved, there ore no respiratory symptoms all the lung irritant 
gases can be eliminated, (Some lung irritant gases, especially 
chlorpicrin, do produce some eye irritation,) If there is no eye 
irritation and no respiratory symptoms have appeared but the patient 
is sick, the case is one of systemic poisoning. With no eye or skin 
symptoms but with respiratory effects, you are obviously dealing 
with one of the lung irritants. And lot me remind you that harass- 
ing gases act highest in the respiratory tract, vesicants lower, 
and pulmonary irritants most deeply in the lungs-. This general 
scheme of differential diagnosis is a handy one to have in mind. 
One last comment: I think you can be pretty sure that when 
a supposedly gassed individual comes to your attention, the serious- 
ness of the case is likely to be inversely related to the intensity 
of the initial symptoms. The most acute onsets have to do with the 
second order nuisance gases, or to be sheer panic. When irritation 
is intermediate and slowly developing, the vesicant group is in- 
dicated | and when there was little or no initial effect but late 
symptoms begin to appear, suspect the respiratory irritants. The 
whole situation is a bit like that of the ham actor who had to 
climax the great scene in a play, when the villian shot him, by 
clutching his hand over his heart and crying, "My God, I’m shot.” Gerard II 
Since he didn’t manage to get expression into his cry during rehears 
als, a fellow actor put some red ink in the squirt pistol used in 
the actual performance. The play wont on, the climax reached, the 
gun shot, and the uninspired ”My God, I’m shot,” As the ham drew 
his hand away, ho saw the red and exploded vehemently, ’’Jesus 
Christ, I am shot,” Patients who feel that way about their gass- 
ing arc likely to be as easily cured.