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34. General Description of Lung Irritant Gases

35. Methods of dispersion

36. Mode of action of lung irritant gases

37. Morbid anatomy of lung irritant gases

38. General symptoms and signs of lung irritant poisoning

39. Physical signs in lung irritant poisoning

40. Prognosis of lung irritant cases

41. Treatment of lung irritant cases

42. Protection against lung irritant gases

43. After-effects of poisoning by lung irritant gases

44. Invalidism after lung irritant poisoning

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34. General description of lung irritant gases.

The chief members of this group are Chlorine, Chloropicrin, Phosgene, and Di-Phosgene. Chlorine and phosgene are true gases under normal conditions of temperature and pressure, while chloropicrin and di-phosgene are liquids of comparatively high boiling points - a quality which renders them somewhat persistent.

Chlorine was the gas first used by the Germans in the Great War. On release from the cylinder, bomb, etc., it forms a greenish-yellow cloud with a pronounced smell of bleaching powder. It is highly irritant to the mucous membranes of the upper respiratory passages, and a marked feature of its action is the violent and paroxysmal cough which it induces and which persists even after the cessation of exposure. It is of much lower toxicity than phosgene or di-phosgene.

Chloropicrin (P.S.) is a yellow liquid boiling at 1120C. (233.60F.) its smell resembles that of chlorine. Chloropicrin is the most irritant member of the group, causing more sensory irritation of the respiratory passages than chlorine. It is also cumulative in its action, and frequent exposures to small doses of this gas may gradually lead to a greatly increased susceptibility with a liability to attacks of nocturnal asthma. It is also a strong lachrymator.

Phosgene (C.G.) is the most important member of the group, and the most toxic. It is a liquid which boils at 8.20 C. (46.80 F.) with the evolution of a colourless gas. Although the least immediately irritant of the group, phosgene gas is readily detectable even in concentrations which are harmless to the lungs, by its characteristic smell of musty hay.

Di-phosgene is an oily liquid boiling at 1280 C. (262.40 F.), and smelling like phosgene. Apart from its more pronounced lachrymatory power, the symptoms produced by this gas are practically identical with those caused by phosgene.

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35. Methods of dispersion.

With the exception of chlorine, these asphyxiant gases may be dispersed by any type of projectile in ordinary use - shell, aircraft bomb, mortar bomb or Livens drum. In addition, both chlorine and phosgene may be dispersed from cylinders which may be mounted in fixed positions or carried on moving vehicles; in the case of phosgene the emission of the gas is hastened, in cold weather, by mixture with chlorine.

By whatever means these chemical agents are distributed, the resultant gas clouds are carried downwind, and their action on unprotected personnel in the path of the cloud is only limited by the period of their exposure in the cloud, whereas on personnel who have respirators available the effective exposure is only the brief time occupied in adjusting the respirator.

Nevertheless, it must be borne in mind that the sudden release of a heavy cloud of lung irritant gas in enclosed areas or in close proximity to personnel is fraught with danger even to men supplied with (but not wearing) respirators, since the intense spasm induced by a single breath of a heavy concentration of the gas may interfere with their adjusting them quickly.

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36. Mode of action of lung irritant gases.

All lung irritant gases cause essentially the same type of pathological effect, this being most pronounced on the alveoli of the lungs and on the smaller bronchial tubes, and the great danger to be feared is the onset of acute pulmonary oedema. The rate of onset and the degree of oedema depend on the particular gas and on its concentration, and also, to a lesser degree, on the duration of the exposure.

These gases are also quite effective lachrymators, especially chloropicrin and di-phosgene; but they are far less powerful in this respect than the true lachrymators.

Their relative toxicity varies, except in the case of phosgene and di-phosgene, where it is approximately the same. In lethal concentrations it is found that chloropicrin is about four times, and phosgene practically ten times, more toxic than chlorine, and while chlorine and chloropicrin cause more damage to the lining membranes of the respiratory passages, phosgene is more effective in the production of pulmonary oedema.

There is, however, little essential difference between the actions of the various members; the treatment and the prognosis for all alike depend on the extent of the lesions produced in the lungs. The extent of these lesions varies as much with the concentration of the gas as with its particular nature, and they are to be determined by a consideration of the clinical features rather than by reference to the exact nature of the toxic substances.

As a type of the group, the morbid anatomy and the signs and symptoms of phosgene gas poisoning will now be described; differences due to poisoning by other gases of the group will be considered as they arise.

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37. Morbid anatomy of lung irritant gases. (See Appendix III, plate i.)

The essential lesions are pulmonary oedema, rupture of the pulmonary alveoli and concentration of the blood, with increased viscosity and a tendency to thrombosis.

The earlier that death ensues, the greater is the degree of pulmonary oedema found at post-mortem examination. (Oedema may be fully established within two hours of gassing, when the lungs are found to be small or normal in size, heavy and completely waterlogged and with no sign of emphysema.

When death occurs later on the first day the lungs are voluminous, heavily oedematous and congested with blood, while aerated patches of emphysema, especially at the edges of the lungs, alternate with patches of collapse. On section, frothy serous fluid mingled with blood drips from the lung tissue, and petechial haemorrhages may be visible on surface of the lungs. The pleural cavity almost invariably contains a quantity of serous, perhaps blood-stained effusion which may vary in amount from two to twenty ounces.

In the case of deaths occurring on the second or third day evidence of aeration of the lungs is present, especially in the lower lobes, and serous fluid does not drip so freely from the cut surface. With later deaths this dripping of serous fluids has ceased, and commencing bronchopneumonia and pleurisy may indicate that secondary bacterial infection has set in.

The greater aeration of the lungs of cases dying on the second and third days, taken in conjunction with the clinical history of the severe cases that survive, makes it evident that the oedema fluid is rapidly absorbed from the lungs from the second day onwards.

In severe cases the haemoglobin percentages may rise as high as 140 with a corresponding rise in the red cell count. Associated with this concentration is the occurrence of thrombosis in the pulmonary blood vessels, and also, to a variable extent, in those of other organs of the body.

Phosgene has relatively little effect on the upper air passages, but in chlorine and chloropicrin poisoning the bronchial tubes, and even the trachea, may show serious damage. The epithelial lining may be severely affected and desquamation may take place; the liability to blockage of these channels is therefore great, and the paroxysms of violent coughing, so typical of chlorine and chloropicrin poisoning, tend to induce a disruptive emphysema which is much more marked in these cases than in phosgene poisoning. Subcutaneous emphysema was rarely seen in the Great War except after gassing by chlorine.

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38. General symptoms and signs of lung irritant poisoning.

Casualties from poisoning by pulmonary irritants may be classified, according to their modes of onset, into two chief groups-: Acute, with violent onset, and Acute, with insidious onset.

(a) Acute with violent onset.

Exposure to an atmosphere containing phosgene causes immediate sensory irritation of the respiratory passages accompanied by smarting and watering of the eyes. This irritation of the respiratory passages causes catching of the breath, coughing and a sensation of tightness and constriction and pain in the chest. After the initial check, the breathing continues, but is gasping in character and interrupted by violent fits of coughing. After getting out of the poisonous atmosphere the respiration remains rapid and shallow, any attempt to draw a deep breath giving rise to painful discomfort and provoking a fit of coughing. Nausea, retching, and vomiting are prominent features in the early stages of poisoning. There is slight or profuse expectoration. Headache, and a sense of fatigue in all the limbs, often prostrate the patient.

As oedema develops in the lungs, the breathing becomes rapid and panting, but of a characteristically shallow type, unlike the deep ventilation of a healthy man after running, and more resembling the fast respiration of a child with broncho-pneumonia. The ears lips and progressively the entire face assume a cyanotic, bluish-red tint which may deepen to the intense violet of fullest cyanosis, and there may be visible distension of the superficial veins of the face, neck or chest - especially in persons gassed with pure chlorine. In phosgene poisoning this full cyanosis is often omitted, and the patient passes rapidly into a state of circulatory collapse, with a feeble, flickering pulse of over 120, a cold clammy skin, and a leaden hue in the face, in which only the lips and tips of the ears reveal the asphyxial cyanosis that underlies the failure of the man to win his fight for life. While in the stage of cyanosis, whether "blue" or "grey," the patient is always restless and very apprehensive of the seriousness of his condition. The expression is anxious and distressed, with the eyeballs staring and the lids half closed. At this stage casualties can be divided into three types :

(a) The milder case, with reddish flush in the face, with some hurry of respiration, and with pain in the chest and epigastrium which is increased by coughing.

(b) The severe case with "blue" cyanosed face, distended neck veins, and full, strong pulse of 100 (see Appendix III, plate ii).

(c) The severely collapsed case, with leaden "grey" cyanosis of the face, and rapid, thready pulse (see Appendix III, plate iii).

The milder case is often drowsy and soon falls into a sleep from which he wakes refreshed. Coughing upon a deep breath, occasional vomiting after food or drink and a slight sense of rawness in the throat together with general debility, may persist for a few days, after which the patient becomes convalescent. During the early days of convalescence there is often a considerable slowing of the pulse from vagus action, which may bring it down to about 50 or even 45 in the minute. Such early bradycardia is often seen also in recovery from severe poisoning; it has no serious import, but is rather a sign that the patient is beginning to convalesce.

Cases of severer cyanosis, if the depth of the reddish-blue colour is well maintained and the pulse does not exceed 100, tend to recover in two or three days, and their recovery is generally similar to that of the milder cases. Provided that the circulation and the activity of the respiratory centre can be maintained, the oedematous fluid in the lungs is soon absorbed, most of it vanishing by the fourth or fifth day. At any time however, particularly if subjected to much physical effort, those cases may rapidly pass into the most dangerous condition of "grey" cyanosis and collapse. The pulse becomes rapid, thready and irregular. The patient, though obviously weaker, becomes more restless and slightly wandering in mind, or semi-comatose.

Even the worst of the "grey" cases may recover with proper treatment, but the mortality among them is always distressingly high. Recovery from this state of depressed circulation may be succeeded by severe and even fatal broncho-pneumonia. When this infective complication develops, the sputum becomes purulent and the temperature rises. Death usually follows rapidly. If the case lasts into the third week after gassing, he may justly be expected to survive the acute infection.

In 81 per cent. of deaths due to poisoning by phosgene and chlorine the death occurred within 24 hours.

(b) Acute cases with insidious onset.

Cases have been frequently reported in which men who have been exposed to gas have been able to carry on their work for an hour or two with only trivial discomfort, and even to march from their trenches to their billets, and then have become rapidly worse, and passed into a condition of collapse with progressive oedema of the lungs that may prove rapidly fatal. In such cases the ingestion of a heavy meal seems sometimes to have had a prejudicial effect. At other times men who have passed through a gas attack and have subsequently complained of only slight cough, nausea, and tightness of the chest whilst resting in the trenches, have collapsed and even died abruptly some hours later on attempting to perform some vigorous muscular effort. A minor degree of the same effect is sometimes shown when men who have been slightly gassed find on trying to walk down from the trenches that they get unusually "done in" and breathless, and are obliged to rest frequently. In these cases the deficiency of oxygen, the result probably of pulmonary oedema already existing, has not been felt until muscular exertion increased the need for oxygen.

This delay in the onset of serious symptoms is a striking feature in poisoning by the lung irritant gases, especially phosgene and di-phosgene. It is not so evident in cases of poisoning by chlorine or chloropicrin when the violent paroxysms of coughing, the painful dyspnoea, and the vomiting convey the impression that the case is seriously ill from the start.

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39. Physical signs in lung irritant poisoning.

The percussion note may remain resonant over the chest, notwithstanding the existence of pulmonary oedema. The breath sounds are weakened, especially over the back; they may also be harsh in character, but never tubular. Fine rales are heard, chiefly in the axillary region and at the back and sides of the chest, while rhonchi may be noted occasionally.

In the early acute stage the physical signs give little indication of the gravity of the case or the extent of the damage to the lungs. The colour, the pulse and the character of the respiration are the chief guides to prognosis. With the development of inflammatory complications and rising temperature the physical signs become those of pleurisy, bronchitis or broncho-pneumonia.

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40. Prognosis of lung irritant cases.

Cases of the "blue" type which react favourably to the administration of oxygen usually do well, and if the circulation and the activity of the respiratory centre can be maintained the oedematous fluid in the lungs is absorbed within four or five days.

In the "grey" type, when cardiac weakness is increasing, the prognosis is bad; if recovery takes place it is often succeeded by a bronchopneumonia which usually proves fatal. If, however, a case lasts into the third week after gassing, it might justly be expected to survive the acute infection.

In the Great War broncho-pneumonia was found to be more frequent and more serious in men who had been suffering from bronchitis previous to gassing; similarly, men with pre-existing emphysema or lung disease were handicapped in their struggle against pulmonary oedema since the margin available for respiration was correspondingly less.

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41. Treatment of lung irritant cases.

Cases of all degrees of severity may be met with, and it may be difficult at times to decide whether or not a man has really been gassed. The history of the case must be taken into account. The benefit of the doubt should be given to the patient in all cases, and any man showing any feature of lung irritant poisoning should be rested for 24 hours for observation. It should be borne in mind that a delayed action may be exhibited by some pulmonary irritants, notably phosgene and the nitrous gases; but if no objective symptoms have arisen after the lapse of 48 hours the patient can be returned to duty with little delay.

(a) Treatment in the acute stage. - The essentials of treatment for acute poisoning by any pulmonary irritant gas are rest, warmth, venesection and oxygen. It is necessary to think of the lungs choked by an inflammatory oedema which, none the less, may be absorbed in three or four days if the circulation can be maintained for so long.

(1) Rest. - The importance of rest cannot be exaggerated; in the earlier stages undue muscular exertion may lead to an aggravation of the symptoms, while in the later stages, when the oxygen supply of the body is interfered with by pulmonary oedema, any attempt to perform muscular work may have disastrous consequences.

All cases should, if possible, be evacuated lying down, and their collars, belts and braces eased so as not to impede breathing. If this is not possible even the lightest walking cases should be given every assistance and should be relieved of all equipment so that they may avoid physical effort as much as possible. As with every type of gas casualty, the patients' contaminated clothing should be removed on reaching the treatment centre. Those who show definite symptoms should not be allowed to leave their beds or stretchers for any purpose whatever.

(2) Warmth. - This helps to combat shock, and also to diminish the oxygen consumption that is entailed by the muscular movements of shivering; attention should therefore be directed to this point when the patients' clothing is removed.

(3) Venesection.- Deep cyanosis with venous engorgement is an indication for venesection, since this may relieve the right heart which has begun to dilate owing to lack of oxygen and obstruction of the pulmonary circulation. As much as 15-20 ounces (400 c.c.) of blood should be withdrawn from a vein by a large-bore needle. Relief of headache and dyspnoea often results, but if cyanosis still continues oxygen must he administered.

Venesection is contraindicated in cases showing a leaden grey colour with circulatory failure, very low blood pressure and a small, rapid or impalpable pulse.

Experiments carried out on animals late in the Great War indicated that when venesection was combined with the intravenous infusion of isotonic salt solution still better survival results might be expected. There was no evidence that the infusion, when performed some time after venesection, led to an increase of lung oedema. Although this combined treatment was not applied to human casualties, it is possible that the method may prove a useful means of treating cases with pulmonary oedema when the haemoglobin estimation shows an unduly high concentration of the blood.

(4) Oxygen. - Oxygen should always be given to casualties with serious pulmonary oedema, that is, to those with intense blue cyanosis or grey pallor. The aim should be to tide the patients over the critical period of the first two or three days, and for this purpose oxygen should be. administered continuously by means of some special apparatus, such as a B.L.B. or Haldane's mask, an oxygen tent or a nasal catheter, that will ensure a suitable mixture with air. (See Appendix ll.)

The oxygen need not be warmed, and a sufficient current of it should be used (from two to ten litres a minute) to ensure a change in the patient's colour from livid blue or grey to a pink tint. This treatment must be maintained, day and night if necessary, with a progressive lessening of the oxygen supply, until the patient does not lapse into a cyanosis when the oxygen is withdrawn.

If the supply permits, oxygen should also be given to the milder cases of oedema in order to prevent their lapsing into a more serious state of asphyxia.

The experience of the Great War showed that no patient in whom it was possible to restore a pink colour by the proper use of oxygen died from simple pulmonary oedema.

(b) General treatment.

Serious cases are best treated in a well-lit and well-ventilated ward, protected from chill. The diet should be fluid and sparingly given in the acute stage, but bland drinks should be allowed freely.

Expectoration should be encouraged by some postural device; vomiting is helpful in emptying the lungs, and often occurs spontaneously, but it is liable to produce exhaustion, and it should not be induced by powerful drugs such as apomorphine or ipecacuanha. Raising the foot of the bed or stretcher three or four feet for a few minutes at a time, with the idea of draining fluid from the chest, is sometimes effective in helping free expectoration.

Expectorants should not be given to severe cases during the first two or three days for fear of increasing the tendency to cough and so augmenting the damage in the lungs. In mild cases, or when the acute symptoms have abated in the severe cases, ordinary expectorant mixtures containing ammonium carbonate and vinum ipecacuanha may be given with advantage and are helpful in checking the possible development of infective bronchitis.

No drugs were found to be of any special value in the Great War. Atropine did not prove effective in checking oedema or in relieving bronchial spasm, while morphia is dangerous and should only be used in small doses 1/6 gr.), to control extreme restlessness. The relief of asphyxia is the best means of relieving the headache and the best cardiac stimulant is oxygen.

If pulmonary complications develop (such as infective bronchitis, broncho-pneumonia, etc.) the patient should, if possible, be treated in a separate ward; otherwise, he should be separated by at least six feet from his nearest neighbour.

(c) Treatment in convalescent stage.

No case should be moved, for purpose of convalescence, until definite cyanosis or severe symptoms have disappeared; it is also very important that a note of the special symptoms attending the acute illness should be forwarded with each case in order that subsequent treatment may be rightly controlled.

The milder casualties are likely to recover after a short rest; those who have passed through a stage of severe cyanosis, however, or who have suffered from a complicating broncho-pneumonia require a prolonged period of convalescence.

All except the more severe cases should be got up from bed as soon as possible; slight bronchitis or gastric disturbances, which usually are only temporary, do not contra-indicate this, but cases of abnormally rapid or slow pulses should be rested a little longer.

A system of carefully graduated exercises, with full opportunities for lying down and resting in the intervals, should be instituted; the response to exercise of each individual, however, must be carefully studied, and exhaustion must be rigidly guarded against, as symptoms of effort syndrome may develop and add weeks or months to the period of convalescence.

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42. Protection against lung irritant gases.

The protection afforded by the respirator is complete. Moreover, all the members of the group are obvious to the senses in concentrations that can be breathed without serious danger. It follows, therefore, that unless an enemy can exploit an asphyxiant cloud in a concentration that is effective before personnel have time to adjust their respirator, casualties from gases of this group should be infrequent.

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43. After-effects of poisoning by lung irritant gases.

Apart from infective broncho-pneumonia, which usually appears towards the end of a week and which may, in severe cases, develop the usual septic complications, the sequelae of poisoning by the lung irritant gases are, contrary to popular belief, much less grave than was anticipated in the Great War. The great majority of cases were restored to good health; some, however, continued to show inability for severe muscular effort or even for moderate exercise, associated with tachycardia and a rapid shallow type of breathing. Recurring frontal headache, generally worse after exercise, and epigastric pain of a temporary nature were frequent, and, while pain in the chest was variable, the presence of a mild bronchitis was found in an appreciable proportion of cases.

In the Great War two important, though not common, sequelae which tended to prolong invalidism were effort syndrome and nocturnal "asthma."

Effort syndrome, with praecordial pain, a sense of exhaustion, dyspnoea and persistent tachycardia after exercise, but with no evidence of organic heart disease, was the commonest and most: persistent after-effect. A small proportion proved intractable, and there was evidence to show that this invalidism was increased if the men were pressed to physical effort too early and too fast at the beginning of convalescence.

Nocturnal asthma, which differed from the ordinary asthma of civil life, took the form of spasmodic attacks, lasting from three to 30 minutes, with shallow and rapid, but not difficult, respirations and with no abnormal physical signs in the chest during the attack. The pulse might be slow and full, or rapid and almost impalpable, and both the haemoglobin percentage and the red cells were increased.

Both disabilities almost always yield in time to a slowly progressive routine of graduated exercise, coupled with careful supervision and feeding, and firm reassurance to dispel neurasthenic factors.

Patients who have passed through a phase of infective bronchopneumonia should always be considered as a group apart.

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44. Invalidism after lung irritant poisoning.

The after-histories of selected groups of cases were followed out in detail during the war, and the records of the Ministry of Pensions were analysed up to 1920 in order to produce the evidence related in the Official History of the War. Subsequent experience has revealed nothing to alter the conclusions then reached. It was evident that men who had suffered from the most severe cyanosis with acute pulmonary oedema could recover rapidly and completely. Many such went back to full military duty after a convalescent period of from three to four months. Others, as described above, suffered from neurasthenic features of exhaustion or from temporary loss of wind and endurance. But a small proportion did develop permanent disability, with progressive dyspnoea, recurrent bronchitis and a radiographic picture of scattered fibrosis and emphysema in the lungs. Since it was proved that a man could recover completely from the effects of the chemical irritant, it is probable that these rare examples of chronic invalidism were due to slow fibrosis caused by the secondary complications of broncho-pneumonia.

As regards tuberculosis, a general survey of the situation in the Great War was made, and it soon became evident that, in spite of what was being written in certain countries, there was, as would seem logical, no ascertainable connection between gassing and tuberculosis. On the other hand, as would be expected, it is unquestionable that gas aggravated any pre-existing tuberculous condition.

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