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Chapter VI





The purpose of this chapter is to describe the anatomical lesions caused by the poisonous gases as they were actually observed and to present the detailed records of 107 autopsy protocols. The general description of the pathology is based chiefly upon these protocols, although advantage has been taken of experimental data to supplement the description of the skin lesions caused by mustard gas and to consider the possible effect of this agent upon the blood and blood-forming tissues.

Without questioning the fundamental importance of the work done upon animals in establishing the general mode of action of the different gases, it is advisable to point out again the difficulties in applying the knowledge thus gained to the human material.

To begin with, the experimental worker knew the gas that was being used, its concentration, at least approximately, the duration of exposure, and the manner of application, whether by contact or inhalation. The pathologist in the field had to rely upon uncertain evidence in regard to the nature of the gas; in many cases no information of any sort was obtainable. There was always the possibility, too, that the subject had been exposed to more than one kind of gas. As to the concentration and length of exposure, it was only in exceptional cases that even a crude and approximate estimate could be hazarded from the history of the case, as, for instance, where a shell burst at the door of a dugout, and it might be inferred that the inmate had been subjected to a very high concentration for a brief period.

There were other complications which made the interpretation of the cases very difficult. Frequently the soldier was severely injured by the very gas shell which poisoned him, or he may have been gassed as he was lying wounded by another projectile. In either event, the traumatic injuries complicated the picture. For example, it was not possible to distinguish between the terminal pneumonia which is always present in patients dying from infected wounds and the secondary pneumonia consequent upon the gassing.

The most difficult problem of all for the pathologist was to distinguish between the direct effect of the gas and the lesions caused by the secondary or supervening infection of the respiratory tract. Many of the gas casualties occurred during the months of October and November, when the pandemic of influenza was at its height amongst our troops.1 There will be pointed out in detail, later, the extraordinary resemblance between the respiratory lesions in this disease and those caused by certain of the irritant gases, notably mustard gas a resemblance which extends to the finest histological detail and which is of considerable interest. Here will be indicated the possible interpretations which often arose in such a case. Were the lesions due to the gas alone? Had an influenza infection followed upon the injury caused by the gas? Was it certain


at all that the patient had initial gas lesions of the respiratory tract, and could he not simply have acquired an influenza pneumonia while he was in the hospital being treated for skin burns? The last possibility is indicated in some of our cases in which the respiratory complications developed long after the gassing, but is equally possible in some of the more acute cases in which death ensued.

The experimental work upon animals seemed to establish a clear-cut distinction between such gases as have a vesicant or irritant effect upon the skin and upper respiratory passages, and gases of the edema-producing or suffocant type, such as phosgene and diphosgene, whose action is manifest only upon the parenchyma of the lung and which are without obvious effect upon the upper respiratory epithelium. In the majority of the human cases sufficient data are at hand to permit at least of this general differentiation in regard to the type of gas concerned. In individual cases, however, the matter is not so simple. Extensive pulmonary edema, whether as a result of the gas itself or of the succeeding pneumonia (particularly in the influenzal cases), or as a terminal event associated with the failing circulation, was of common occurrence. In the absence of precise clinical data, and of characteristic changes in the skin, eyes, and upper respiratory tract, the diagnosis might remain uncertain. It was particularly difficult to decide in such cases whether the subject might not have been exposed to a suffocant gas in addition to mustard gas.


In the series of 107 completely studied cases only 4 may with probability be ascribed to poisoning with this type of gas (Cases 1, 2, 3, 4). Death occurred in all of these cases in 3 days or less after gassing. In addition 2 other cases are ascribed to phosgene in the records, but in these the evidence in support of the diagnosis seems inconclusive (Cases 78, 104). The first of these (Case 78) died 14 days, the other (Case 104) 72 days, after the alleged exposure to phosgene. The difficulties in interpreting these cases will be evident on reference to the detailed protocols and need not be discussed here.

This material is inadequate for a full consideration of the pathology and especially for a study of the late or residual lesions which, on experimental and clinical grounds, may reasonably be expected to follow the inhalation of gases of the suffocant type. The discussion, therefore, is limited to a brief description of a typical acute case. Through the courtesy of the French G. A. C. the writer of this chapter had the opportunity to witness several autopsies upon French soldiers and to study the large collection of histological preparations in the laboratory of Professor Mayer at the Collége de France, and the following account is based in part upon these experiences, in addition to the records of the series appended and the references in the literature. Reference is made, also, to the observations of Wilder on his series of 50 necropsies of phosgene cases, in which he states:2

All of these patients had passed through the initial suffocative stage of the intoxication and had died one hour or several hours later. Cyanosis was conspicuous in all. In some cases the skin was an ashy gray, in others it was distinctly violaceous. In all cases the blood in the veins was of a deep chocolate color and very thick. The mouth and nose were usually filled and covered with an accumulation of frothy serous fluid. The lungs were greatly distended and very heavy; they completely filled the thoracic cavity and showed definite


imprints of the ribs. The pleural cavities in bodies examined immediately after death contained from 100 c.c. to 1,000 c.c. of a thin serous or serosanguineous exudate. The surfaces of the lungs were mottled with areas of subpleural emphysema. Cut surfaces of the lungs were extremely wet and bloody from edema and passive hyperemia. The trachea and larger bronchi were filled with foamy serous or serosanguineouis fluid, and pressure on the lungs caused this to flow abundantly. The larynx, trachea, and bronchi were moderately hyperemic but presented no edema, erosion, or ecchymosis.

In those cases in which death was delayed for two or three days the edema was less homogeneous, hyperemia was more extensive, particularly at the bases of the lungs, and zones of emphysema occurred at the apices and at the anterior margins. There was also some atelectasis, and if secondary infection had occurred nodules of pulmonic consolidation were in evidence.

Histologically the edematous material seemed to consist of liquid and the debris of epithelial cells. Leucocytes and erythrocytes occurred in late cases only. The cells of the alveolar walls and those of the terminal bronchi appeared swollen and indistinctly outlined, their nuclei staining poorly. Many alveolar capillaries appeared thrombosed and other capillaries were engorged. Still others appeared to be collapsed.


There was a dusky, livid hue to the lips, ears, finger tips, and dependent portions of the body. Thin, blood-stained fluid flowed from the mouth and nostrils, or a mushroom of foam (champignon d' écume) projected from the lips. The opened thorax showed the lungs bulky, meeting in the median line, with very little tendency to collapse when the air was admitted to the chest. They completely filled the pleural cavities, and often showed the imprint of the ribs. The pleural cavities almost always contained several hundred cubic centimeters of blood-tinged serous fluid. The visceral pleura was under great. tension, moist, and dotted with petechial hemorrhages or larger reddish splotches. The color was strikingly variegated, pale pink areas of emphysema alternating with dark red firmer patches or even lobes of atelectasis and hemorrhagic edema. The interlobular septa were wide and translucent from edema. The lung weight was greatly increased, often to 900 or 1,000 grams or even more. It offered a tense, doughy, cushion-like resistance, with a strong tendency to pit on pressure. The lobules were large and clearly defined by the edematous interlobular septa. The trachea and bronchial tree were completely or partially filled with pink fluid and foam and the smaller tubes appeared distended. The mucosa was pink or darker red, velvety, and smooth, and there was no necrosis, ulceration, or membrane formation. The sectioned surface of the parenchyma poured forth fluid and foam in great abundance. The alternation of paler, glistening areas, which under the loop were seen to be composed of distended vesicles, with the dark red collapsed regions, inundated with bloody edema, was very characteristic. Some of the cases showed disruptive emphysema beneath the visceral pleura, the air escaping to the subcutaneous tissue about the neck and shoulders.

The blood was thick and very dark in color, but its coagulability was apparently unchanged. Thromboses have been described in the vessels of the lung and elsewhere but were not present in any of the cases of the series. The right chambers of the heart were usually greatly dilated and full of soft very dark cruor. Petechial hemorrhages were seen in the epicardium, in the sheaths of the great vessels, and in the gastrointestinal mucosa. The remaining organs, apart from very intense venous congestion, showed nothing abnormal.


 No opportunity was presented for study of the central nervous system. Ricker showed that petechial hemorrhages were found in experimentally gassed animals.3


In the early cases the edematous fluid in the alveoli appeared in the sections as a uniform pink staining material or as a granular or shreddy coagulum. (Fig. 2.) There was little or no stainable fibrin. The capillaries were congested and protruded in a tortuous manner into the lumen of the air spaces.

FIG. 2 - Case 2. Lung. Poisoning with phosgene and blue cross gas. Intense alveolar edema, dilatation of atria, stasis of leucocytes in capillaries. Epithelium of small bronchi is intact

The preparations studied showed no clear evidence of thrombus formation, due to agglutination of red blood cells, to ante-mortem fibrin deposition or to the agglomeration of platelets in the pulmonary capillaries. Wilder,2 however, refers to the occurrence of thrombi, and the experimental findings of Dunn 4 upon the impermeability of the pulmonary capillaries to injection of saline and carmine gelatine, and the observations of Meek and Eyster5 upon the agglutination of red corpuscles in vitro when phosgene is bubbled through a suspension, make it seem possible that the obstruction to the pill-


monary circulation was not due merely to stasis but to an actual clumping of the cells under the direct influence of gas. In addition to the intense edema and congestion there was diapedesis of red blood cells, and, in some areas, more extensive alveolar hemorrhage. The alveolar epithelium was exfoliated and in many of the air spaces the capillaries appeared to lie exposed. There was usually an abnormal number of leucocytes in the blood vessels, a few of which emigrated into the alveoli and septal spaces.

Their nuclei were caryorrhectic. The epithelium of the small bronchi might be lifted up by the underlying edema and partly exfoliated. The peri- bronchial, perivascular, and subpleural lymphatics were distended, usually with a granular or partly fibrinous coagulum. In view of the statement and the currently accepted belief, based upon animal experiment, that the epithelium of the upper respiratory passages is uninjured by phosgene and diphosgene, it was rather surprising to find that in three cases of the series the tracheal epithelium

FIG. 3.- Case 2. Large bronchus. The epithelium is in part lost, in part altered, the superficial cells being non-ciliated, and showing hyaline degeneration. There is marked congestion of the capillaries of the submucosa

showed a definite lesion. In two of these cases the superficial cells were hyalinized, the ciliated border was destroyed, and there were signs of nuclear degeneration. (Fig.3.) Ricker has reported similar lesions of the bronchial epithelium in cats exposed to high concentrations of phosgene in the gassing chamber.3 In the third case there were in addition definite erosions, with local inflammatory reaction. Whether these lesions were due to the phosgene or diphosgene alone or, as seems more probable, to the admixture of more irritant gases, such as chloropicrin or diphenylchlorarsine. or whether they were the result of the early bacterial invasion, can not be decided from the study of the very limited material. In one of the cases (Case 3) there had already occurred, after 24 hours, a very massive invasion of streptococci in both trachea and lungs.

In the other viscera lesions were not found which could with any degree of probability be attributed to the gassing. The intense venous congestion found in the gross was evident also, of course, in the sections. Parenchymatous


changes in liver and kidney may he ascribed to the concurrent infection rather than to a direct toxic action of the gas upon these viscera. There has been general agreement, indeed, that absorption of the gas (phosgene) is unlikely, in view of its rapid decomposition in the presence of water.



The pathology of the skin lesions caused by dichlorethysulphide was very throughly studied by Warthin and Weller in this country and by Mayer at the central laboratory of the French medicolegal service at the College de France, Paris. The studies recorded here on the human cases coming to autopsy have been supplemented by the examination of pieces of skin excised at the varying intervals after the application of mustard gas in alcoholic solution of known strength under standard conditions.

The gross changes which followed he application of this substance may be summarized as erythema, followed by vesication and a variable degree of pigmentation. The vesicles were usually superficial; only rarely was the superficial portion of the corium involved. The customary sites for the burns were the face, especially the scalp, the eyelids, nose and lips, neck, axillae, elbows and knees (from lying or kneeling on contaminated ground), the under surface of the penis and the contiguous anterior aspect of the scrotum, the inner surface of the thigh, the buttocks, and the hands and feet. (Pls. II, VII, VIII.)

It is now a familiar fact that after exposure there was a definite latent period which varied from a half hour to six or eight hours or even longer. It was not uncommon for small sudaminal-like vesicles to appear in crops at intervals of days after exposure. In some cases, presumably those exposed to low concentration of the vapor, there was produced a very diffuse, almost scarlatina form erythema, changing in color from a somewhat dusky pink, through purple, to brownish. In other cases the vesicles were surrounded by an erythematous zone, which later became brownish. The duration of the pigmentation was not definitely known and probably varied in different indivituals. Pigment flecks at the site of a small experimental burn were apparent after a year. The contents of the vesicles were usually clear, although the fluid might contain a few filmy fibrin clots. If infection occurred the fluid might become purulent, but ordinarily relatively few leucocytes were found on examination of the fresh fluid. It was frequently reported that a burn over the sacrum had developed into decubital ulcers.

Since deaths usually occurred from the fifth day to the end of the third week after exposure, the pathologist was apt to see only raw surfaces, blebs, ulcers, scars, or pigmentation,. Rather than erythematous lesions. These were also more apt to be in locations subjected to long friction during travel to the hospitals and thus, to a certain extent, the regional distribution of the burns, when tabulated from autopsy reports, differed from that of the lighter burns sustained by those who recovered.

The earlier lesion examined histologically was excised 3 hours and 25 minutes after the application of a 10 percent solution of dichlorethysulphide



Note change in staining of necrotic epidermis and vascular degeneration of nuclei at margin of vesicle.



PLATE VI. CASE 6. MUSTARD GAS, 2 DAYS. LUNG. The distended atria are lined with a hyaline band giving an indistinct fibrin reaction with Gram-Weigert Saffranin stain.



(Gram-Weigert Saffranin stain.)



in absolute alcohol, applied for 5 minutes over an area of 1 mm. in diameter in the skin of the back; at the time of excision there was a slightly elevated area of erythema about 3 mm. in diameter.

The only change noted in the epidermis was a slight thinning with a flattening out of the papillary processes; over the summit of the lesion thev were completely obliterated. Under the high power a few individual cells showed a vacuolated cytoplasm with displacement of the nucleus to the periphery of the cell. There was slight edema of the corium; the sweat glands, hair follicles, and sebaceous glands showed no recognizable injury; the blood vessels, especially the superficial capillaries, were dilated and filled with red cells and a few were surrounded by a loose mantle of lymphoid cells; the lymphatic vessels were distended, containing a fine granular coagulum; the deeper portion of the corium and the subcutaneous tissue showed no injury.

Another lesion was examined after 45 hours, having been produced at the same time, in the same individual; the lesion consisted of a small elevated vesicle filled with clear fluid and surrounded by an area of erythema 4 to 5 mm. in width.

The overlying superficial horny layer was still intact, but the remainder of the epithelium covering the vesicle was entirely necrotic. The contents of the vesicle consisted of interlacing fibrin strands inclosing a homogeneous coagulum loosely infiltrated with polynuclear leucocytes. At the margin of the vesicle the epithelial cells were dissociated for a short distance but rapidly became normal. No mitoses were found and there was no indication of increased proliferative activity. The base of the vesicle was formed by edematous corium which, in its most superficial portion, was devoid of connective tissue nuclei and was loosely infiltrated with round cells and polynuclear leucocytes. These were most densely aggregated about the blood vessels. The deeper connective tissue showed no edema or inflammatory reaction.

The perivascular infiltration extended for a considerable distance beyond the area of the vesicle; the sweat glands and hair follicles in the vicinity of the lesion showed no significant changes.

Although it would appear from a study of this experimental lesion that the vesicle was formed between the epidermis and the superficial corium, a study of numerous other accidental lesions showed that this was by no means always the case; the vesicle may be formed within the epidermis itself by a dissociation of the epithelial cells with the accumulation of fluid between them and their subsequent necrosis. In this way a cleft may be formed, the epidermis and some of the basal cells remaining visible. (Fig. 4.)

Not only might fluid accumulate between the cells, forcing them apart, hut the cells themselves might undergo hydropic changes, so that the cytoplasm would contain a single large vacuole which pushed the nucleus in crescentic form to the periphery of the cell. This type of hydropic degeneration was frequently seen at all stages, especially amongst the less severely injured cells at the periphery of the lesion.

In other cases individual cells, or the entire epidermis, would undergo a hyaline necrosis, the nucleus becoming shrunken and pycnotic and the cytoplasm taking on a dense refractile appearance and staining deeply with eosin. This mummified or hyalinized epidermis, constituting often the cap of the vesicle,


might persist for a long time, showing in a shadowy way the outline of the individual epithelial cells. It might persist until a new growth of epithelium proceeding from the margin of the vesicle had completely undermined it and recovered the base of the vesicle. This was one of the common methods by which regeneration took place. (Fig. 5.) There was no doubt that the sheaths of the hair follicles also played an important part in reinvesting the base of the vesicle or ulcer, although this was even more striking in the lesions experimentally produced in horses

FIG 4.- Case 8. Mustard-gas burn of skin of 2 days' duration. Necrosis of epidermis, with beginning of intra-epidermal vesicle formation

The opportunity was presented to examine histologically experimental lesions produced in the way indicated above in negroes. Although it has been demonstrated by the studies of Marshall, Lynch, and Smith, cited below (see also Chap. XII), that the negro is relatively insusceptible to dichlorethyl-sulphide, the lesion produced by a 10 percent alcoholic solution differed in no respect from the lesions in white individuals. One of the preparations excised after six hours showed very clearly the early edema in the papillary layer of the corium which preceded vesiculation. The tissue was very loose and foamy, and occasionally the entire epidermis was elevated by a granular


FIG. 5.- Case 89. Mustard-gas burn of 20 days’ duration. Regeneration if new epithelium beneath crust if necrotic original epithelium. Hyperemia. Absence of inflammatory reaction.


coagulum. The same type of degeneration of the cytoplasm was found in the connective tissue and endothelial nuclei. There was hyperemia and a moderate inflammatory reaction in which polynuclear leucocytes played the leadingpart. (PWs. III, IV.)

Many of the preparations obtained from autopsy cases showed definite evidence of infection, with the typical inflammatory response. Since these may be regarded as incidental lesions and are in nowise distinctive they need not be considered in detail.

FIG. 6.- Case 18. Mustard-gas burn of 5-6 days' duration. Section through vesicle. Overlying epithelium is necrotic. The contents of the vesicle consist of homogeneous, slightly fibrinous coagulum with moderate numbers of leucocytes. The underlying corium is edematous

The pigmentation which was so striking a feature of the later stages was due to an increased production of melanin pigment by the cells of the rete mucosum and was not to be attributed to the deposition of blood pigment following capillary hemorrhages. The pigment production was often irregular, individual cells being loaded with coarse clumps, while adjacent cells might be wholly pigment free. Moreover, pigment-containing cells could be present in abnormal situations-in the stratum granulosum, for example, or even amongst the cells of the keratin layer. Usually, numerous chlromatophores were seen in the capillary layer of the corium. (Pl. V.)


Where the burn had been a severe one, and the subepithelial tissue had been involved, definite fibroblastic growth was found in the later stages., The leucocytes which, in the early stages, were chiefly polymorphonuclear, and which tended to become fragmented as they approached the surface, gave way to lymphoid cells; but at no stage of the process was the cellular reaction, in uninfected cases, a very intense one.

The vascular lesions throughout appeared to be of minor importance. Thrombosis was exceptional, being found only in very severe burns in which there was a direct necrosis of the corium. These findings, therefore, are not

FIG. 7.- Case 18. Another section, showing condition similar to that seen in Fig. 6

in accord with the view of other observers, who hold that the injury to the blood vessels is an important factor in delaying the repair. The persistence of the injury and the retarded healing appeared to be due, rather, to the continued action of the dichlorethylsulphide.

To summarize briefly the lesions produced in the skin: There was caused a hydropic degeneration, or a hyaline necrosis of epidermal cells, often with the formation of vesicles within the epidermis. There was produced, also, edema of the corium beginning in the loose tissue of the papillae and leading to the separation of the epidermis from the underlying connective tissue and the formation of the vesicle. (Figs. 6 and 7.) There might be


in severe burns a direct necrosis of the superficial portion of the corium. There was an initial hyperemia and a very moderate acute inflammatory reaction in which polynuclears were the predominant element in the early stages. The leucocytes became pycnotic and fragmented as they approached the surface. A severe injury to the small cutaneous vessels was exceptional and thrombi were rarely found.

Regeneration took place by a growth of new epithelium from the margin of the vesicle, as well as from the sheaths of the hair follicles. If the dead epidermis was not artificially removed, it might remain as a protective covering until healing was completed.

There was an active growth of new connective tissue in the superficial layers of the corium where this had been injured. The hyperpigmentation was due to increased melanin production by the cells of the stratum mucosum. It was frequently irregular and atypical.


No material was available for the study of the histopathology of eye lesions in human cases. The subject will be considered in Chapter XV of this volume and in Section IV, "Ophthalmology, American Expeditionary Forces," of Part II, Vol. XI.


It is difficult to describe a typical picture, inasmuch as great variations were encountered in different cases. Appearances depended upon a number of factors--the duration of life after gassing, the concentration of the gas, and the duration of exposure. Most of all did the lesions vary with the character of the secondary infection which invariably followed the original chemical injury. One can not hope, therefore, to depict a graded series of injuries followed by repair. Indeed, the more cases that are studied the more difficult does it become to trace out the direct effects of the poison amidst the havoc wrought by the secondary bacterial invaders, and the more difficult is it to decide whether late changes in the respiratory tract shall be considered as the healing of the chemical injuries or of the infectious lesions.

It is with this reservation, therefore, that the cases are described as they were actually recorded in the case protocols and notes, leaving to the experimental workers the determination of the precise part played by the poison itself and by the bacterial infection in the production of the lesions.


Mustard gas in sufficient concentration produced a complete necrosis of the epithelium of the larynx, trachea, and bronchi. It was the rule for the smallest bronchi to be less severely injured, but yet there were many exceptions to this, and in some cases the necrosis extended into the smallest bronchi, infundibula, and, perhaps, although this was more difficult to determine, to the alveolar epithelium itself. The usual gross picture in the early cases was that of a diphtheritic inflammation, with the formation of a false membrane, which began at the epiglottis, or even in the pharynx. and extended more or less continuously to the small bronchi. (Figs. 8 to 11, PI. I.) The membrane often was firm and tenacious and lined the upper air passages, forming a cast more or less


adherent, or there might be small adherent raised patches covering the eroded and hemorrhagic subepithelial tissue. In a few of the cases the membranous inflammation did not involve the trachea itself, but only the larger and medium sized bronchi.

Not all the cases showed this intense diphtheritic necrosis; at times a membrane was entirely lacking, but the mucosa appeared rough and sandy and covered with shreds of fibrinopurulent exudate. It was always hyperemic and often dotted with punctate or larger hemorrhages. In later cases the membrane might be replaced by masses of soft crumbling purulent or bloody exudate. Careful dissection of the bronchial tree was very apt to show that the membranous casts which completely occluded the middle-sized bronchi as far as the third or fourth branches were replaced in the smallest branches by a softer purulent exudate. Examination of the lining of the bronchus showed a corresponding alteration from a rough hemorrhagic, ulcerated surface to a smoother, merely hyperemic one.

In later stages, when epithelial regeneration had occurred, the membrane or exudate was cleared away, and the surface was smooth, opaque, and thickened. How this regeneration occurred will become apparent in a study of the histological changes, but it may be noted here that even weeks or months after gassing, erosions, more or less localized or diffuse, might persist. This was the case where injury had been so deep-seated as to involve not only the superficial epithelium but also that of the ducts of the mucous glands, so that no possibility of regeneration obtained.

FIG. 8.- Mustard-gas poisoning. False membrane extending from epiglottis through entire trachea into bronchi


In a few of the cases the lesions of the upper respiratory tract were gangrenous rather than diphtheritic in character. (Pl. X.) The walls of the trachea and bronchi showed greenish discoloration, and the exudate had a characteristic foul odor. There were usually associated gangrenous areas in the lung itself. In two such cases the pathologist recorded the presence of extensive dental caries, indicating that, in his opinion, infection of the air passages had occurred, with the putrefactive bacteria from the mouth. This seemed a plausible idea, and in one of the cases it was supported by the finding of numerous fusiform bacilli in the necrotic exudate. Spirilla were not demonstrated, but were doubtless present.

The histological lesions found in the trachea and bronchi were studied in a severe case, dying two days after exposure. The trachea and large bronchi presented about the same picture. There was at thick, fibrinous membrane with coarse laminated threads running parallel to the surface. In the meshes lay scattered nuclear fragments and a few better preserved wandering cells masses of mucus, also, sometimes showing a curious concentric arrangement, were incorporated in the fibrinous membrane. Adherent to the under surface were the detached epithelial cells, many of which were surprisingly little altered, still conserving their cilia and showing good nuclear stain. The membrane lay loosely upon the exposed basement membrane, being

FIG. 9.- Diphtheritic necrosis of mucosa of upper respiratory tract after mustard-gas inhalation


attached only here and there by bridges of fibrin. The basement membrane itself was swollen and less sharply outlined than the normal structure. The subepithelial tissue was edematous; in places there was a definite fibrinous exudate between the connective tissuebundles. There was a moderate inflammatory infiltration with both mononuclear and polymorphonuclear leucocytes. As these approached the surface they appeared to undergo caryorrhexis, and in the superficial portion there was much nuclear debris. The nuclei of the connective tissue cells also showed the effects of the injury, their nuclei being, shrunken and pycnotic. The blood vessels were enormously distended, and there were small capillary extravasations. The endothelium showed no definite alteration. The mucous ducts were widely distended with plugs of mucus. Near the surface their epithelial cells were apt to be cast off and more or less degenerated. In the deeper portion the cells lost their orderly alignment and tended oto take on a squamous type. The mucous glands themselves at this stage were in a state of hypersecretion; only exception-

FIG.10.- Diphtheritic necrosis of mucosa of upper respiratory tract after mustard-gas inhalation


ally were there clearly defined degenerative changes in the gland cells to indicate a penetration of the poison. The loose cellular tissue about the perichondridum, and even between and external to the cartilages, might be edematous.

In the case described the injury had been limited to the superficial epithelium and had noted to the death of the tissue below the membrana propria. Many of the cases of the series, however, showed a more deep-seated injury, involving the subepithelial tissue to a variable depth. (Figs.12 and 13.) The basement membrane appeared to offer an obstacle to the penetration of the poison, but when this was overcome the necrosis of the connective tissue frequently extended to the bands of smooth muscle fibers lying superficial to the mucous glands. The muscle fibers again seemed to offer a resistance to the further penetration of the poisonous substance. Only exceptionally was there a direct necrosis of the mucous glands, and even in those cases the destruction involved only groups of acini and not the mucous glands in their entirety.

FIG. 11.- Diphtheritic necrosis of mucosa of upper respiratory tract after mustard-gas inhalation


A well-formed membrane was seen as early as 48 hours after gassing and might persist for many weeks. In cases where no membrane was present the surface of the trachea was formed by the exposed necrotic subepithelial tissue or by the smooth and wavy contour of the basement membrane. (Fig.14.) In the early stages shreds of epithelium were still to be found here and there, but these were rapidly cast off and replaced by regenerated cells in a manner to be described.

The reparative processes which followed the injury above described were most interesting. As early as four or five days after gassing, a beginning reinvestment of the trachea or bronchus might have taken place. The new cells were derived from little islands of epithelium still adherent to the membrana propria which had escaped the initial destruction and from the epithelial cells which had lined the ducts of the mucous glands. (Fig.15.) These

FIG. 12.- Mustard-gas burn. Deep-seated necrosis of bronchial mucosa

cells divided and crept out over the mouth of the duct covering the adljacent exposed basement membrane, first with a single layer of flattened cells, latter with a multilayered squamous epithelium. These duct cells seemed to play a very important role in elpithelial regeneration, and it was at common finding to see the entire duct filled with at solid nest of actively dividing cells. In this way, provided the destruction had not been too intense, the entire surface might he reinvested with a metaplastic epithelium of the squamous cell type. (Fig. 16.) Whether the superficial cells of this layer later became replaced by cylindrical ciliated cells can not be definitely stated until opportunity has presented to examine further material from late cases. In one of the cases after 167 days, in which typical mustard gas lesions were still present in the bronchi, the trachea showed a multilayered but ciliated epithelium. The majority of the late cases, however, showed epithelium of the squamous cell type, andl it is prolbable that. in most cases the metaplasia was at permanent change.

Certain of the cases showed interesting details in regard to the process of epithelial regeneration. Worth noting is the fact that regeneration might begin while the memlbrane was still present, so that it was not unusual to find a


layer of flattened cells showing many mitotic figures, often highly atypical in character, interposed between the fibrinous exudate and the basement membrane. Often it seemed as if the epithelial growth had outstripped the other processes of repair, so that the growing cells themselves, because of being improperly nourished, degenerated. (Fig.17.) Some of the preparations showed the new epithelium lifted up from the membrana propria by a granular coagulum, as if a new vesicle had been formed. This appearance leads one to

FIG. 13.- Case 22. Mustard-gas burn, 5 days' duration. Deep necrosis of tracheal mucosa

ask whether there may not have been a persistence of the poison and whether this late and secondary vesicle formation may not be comparable to the late appearance of skin vesicles four or five days after gassing.

One of the preparations showed the duet epithelium growing beneath the still preserved basement membrane. (Fig.18.) This anomalous growth was due to the proliferation of the duct epithelium beneath the partially loosened membrana propria. In one of the late cases, scattered through the, sub-epithelial tissue, were solid nests of cells which resembled very closely squamous-celled carcinoma. The cells were arranged as in epitheliomatous pearls; they


were definitely squamous, highly atypical, often multinucleated, and showed numerous mitotic figures. Intracellular fibrils even were to be seen between them. This appearance was brought about by the proliferation of the duct epithelium within the lumen. (Fig.19.)

FIG.14.- Case 21. Mustard-gas burn, 5days' duration. Necrosis and exfoliation of trachea lepitheliuim exposing basement membrane. Fibrinous edema of submucosa

As regards the lesions in the submucosa, it has been stated above that in the majority of cases he cellular response was not very marked, and in some cases, in the trachea at least, practically wanting. Bacterial stains showed that the organisms rarely penetrated below the surface. In one of the cases, however, in which there was an extreme edema not only of the submucosa tissue but also) of the areolar tissue external to the bronchus, a Gram stain showed unrestrained growth of Gram-positive cocci throughout the edematous area.


With the beginning of repair the connective tissue cells in the submucosa took on the character of fibroblasts. New blood vessels were formed which were sinusoidal in character and which formed wide channels extending to the basement membrane, where this was still intact. The inflammatory cells then became predominatingly lymphoid in character, and numerous plasma cells and other large mononuclear elements were present. This formation of a very vascular granulation tissue was found not only in the trachea and large bronchi, but in the medium-sized and smaller bronchioles, where it sometimes led to a

FIG. 15.- Case 61. Mustard-gas burn, 9 days' duration. Epithelial regeneration of trachea, proceeding from the mucous ducts

pronounced thickening of the wall, with narrowing of the lumen. As we have stated above, the granulation tissue might or might not be reinvested by epithelium according to whether the initial injury involved the epithelium of the mucous ducts or not.

In a few of the cases in which the mucous glands were injured it was possible to study a regeneration of these structures. The acinus was filled with a pink-staining, more or less hyaline, necrotic mass, embedded in which were nuclear particles. This represented the remains of the necrotic gland cells, and at the periphery the new secretory epithelium was seen pushing its way between the necrotic cells and the basement membrane of the gland.



The appearance of the lungs at autopsy presented a bewildering variety, and it is quite impossible to describe a composite picture which would distinguish the lungs of mustard-gas poisoning from those of the various types of pneumonia. Perhaps the most distinctive cases were the very early ones, in which the pulmonary lesions were largely confined to the bronchi and their immediate neighborhood. The lung was voluminous and did not collapse readily after removal. Occasionally the pleura was smooth, but in most cases there were patches of early fibrinous pleurisy. Darker sunken area of atelectasis

FIG. 16.- Case 41. Mustard-gas burn, 7 days' duration. Metaplasia of tracheal epithelium into squamous cell type. Numerous mitoses

associated with the occlusion of bronchi were visible on the surface. On section the most conspicuous features were the thickened bronchi filled with plulgs of creamy fibrinopurulent exudate, or in the case of the smaller bronchi a droplet of creamy pus might exude. Each bronchus was surrounded by a dlark reti sunken areola 2 or 3 mm. in width. This last feature is regardedl as particularly characteristic; the red peribronchial zone histologically was found to be composed of the adjacent alveoli, which were filled with red blood cells and more or less collapsed. Further outward from the bronchus the hemorrhage


gave place to a fibrinous exudate in which only a few desquamated alveolar cells and occasional leucocytes were included. (Pl. IX.) This peribronchial reaction did not appear to he due to a direct extension of the infection within the bronchus through the bronchial wall. It would seem that the hemorrhage was caused by the direct action of the toxic agent diffused through the wall of the bronchus. The collapse may perhaps be explained by the distension of the small bronchus with compression of the adjacent air spaces. Frequently, at least, the alveoli directly adjoining the bronchus appeared flattened.

FIG. 17.- Case 24. Mustard-gas burn, 5 days' duration. Between the false membrane and the congested sub-epithelial tissue are interposed hydropic epithelial cells of the squamous type

Aside from these bronchial and peribronchial lesions the lung, on section, showed emphysema and darker areas of partial collapse. Edema was present to a greater or less degree in about two-thirds of the cases. It was never so extensive as in the lung of phosgene or other asphyxiating gas and was often patchy in its distribution, being much more marked in some portions of the lobe than in others. From the autopsy records, which naturally vary greatly in detail and accuracy, it appears that excessive edema was noted in only three cases occurring two and three days after gassing, and in one case in which


the period of survival was not established; moderate general edema was present in 28 cases and slight patchy edema in 43 cases. In 18 cases the absence of edema is specifically reported, and in 6 cases no record was made.

As with so many of the pulmonary lesions, it was difficult to decide whether this edema wits the direct result of the action of the mustard gas upon the alveolar capillaries or whether it was due to secondary infection, to the failing circulation, or to other obscure factors. It is true that even in the early cases bacteria abounded in the bronchial and infundibular lesions. They were not usually present, however, in the edematous areas at a distance from the bronchi. This, and the fact that the most intense edema was recorded

FIG. 18.- Case 89. Mustard-gas burn 20 days' duration. Trachea. The regenerating epithelium is growing beneath the old swollen basement membrane, which covers the exposed surface

in relatively early cases, is perhaps an argument in favor of the direct edema- producing action of the mustard gas. Experimental observation also supports this view. It was possible in rabbits by intravenous injection to produce moderate pulmonary edema (Pappenheimer and Vance).6 Lynch, Smith, and Marshall made similar observations in dogs. 7 In cases which died late the edema, when present, was in all probability secondary and not due to the initial chemical injury.

The great majority of the cases showed, in addition to the bronchial and peribronchial lesions, areas of focal pneumonia, sometimes small and nodular, often large and confluent. There was no constancy in the appear-


ance of these pneumonic patches, nor could one find sharply cut differences in the appearances in cases dying early after gassing and in those which survived for weeks or even months. A fresh bacterial infection might develop at any stage after the initial chemical injury, and it was not uncommon to find in the same lung recent and older organizing lesions.

During the height of the influenzal epidemic in October and November, 1918, many of the gas pneumonias exhibited the characteristic gross features which had come to be associated with the pulmonary lesions of influenza. The lungs were heavy and voluminous and often a dusky red, especially in the posterior portions. There were fresh pleural hemorrhages and more or less fine fibrinous pleurisy which became organized in the later cases. Only twice was the pleurisy suppurative in character; in one of these cases (Case

FIG. 19.- Case 86. Mustard-gas burn, 18 days' duration. Bronchus. Proliferation of epithelium of ducts of mucous glands

99), the empyema was due to the extension of a traumatic liver abscess; in the other (Case 25), which occurred in August, the pleurisy was not extensive, and the resemblance of the pulmonary lesions to those found in influenza were less striking than in many other cases.

On section these lungs showed, in addition to the characteristic membranous bronchitis and bronchiolitis and peribronchial areola, diffuse, often incomplete areas of consolidation associated with much hemorrhagic edema. (Fig. 20.) The greater portion of one or several lobes was frequently affected. In some of the later cases there are described also opaque grayish areas of necrosis and groups of small abscesses. Organization was not infrequentlv recognized in the gross by some of the more experienced pathologists and confirmed histologically. (Fig. 21.)


In describing the histological changes associated with this type of pneu- monia attention is called again to the extraordinary resemblance of the finer changes to those observed in the primary influenzal cases. These lesions can not be ascribed wholly to the influenzal or postinfluenzal infection, in as much as they may be reproduced in animals by exposure to the gas alone, and have been present also in human cases dying at times when the epidemic was not active.

FIG. 20.- Case 28. Mustard-gas burn, 4-5 days' duration. Lung: Intense congestion, hemorrhagic edema, aplastic exudate. The lecuocytes are filled with minute Gram-negative bacillli

Leaving aside the larger bronchi, which have been described and in which the membranous character of the necrosis is usually more extreme than in the primary influenzal cases, the terminal bronchioles were found usually with their ciliated epithelium more or less conserved. There was an acute suppurative inflammation, which was in nowise distinctive. The atria, however, were often widely dilated; they might or might not themselves contain exudate. (Fig. 22.) The wall was lined by a wavy hyaline band, which sometimes, but not regularly, gave a faint fibrin stain with the Gram-Weigert-safranine method. (Pl.-VI.) It was a little difficult to be sure of the composition of this hyaline band. It


did not appear to be composed solely of the necrotic lining epithelial cells, although these probably took part in its formation. The continuity of the membrane with definite bands of fibrin in the walls of the atria or alveoli indicated that the fibrin was at least the chief constituent. Later, as it became more and more swollen and hyalinized, the specific staining was less readily obtained. In part it might have been due to the condensation of a highly albuminous material about the wall of the infundibulum.

FIG. 21.- Case 103. Mustard-gas burn, 5 days'duration. Lung: Organizing and interstitial pneumonia

The lesions found in the alveoli were manifold. The alveolar exudate in the vicinity of the bronchioles and atria was apt to be fairly cellular, containing, in addition to a variable number of red cells, leueocytes of various types, but predominantly polymorphonuclear. But there were large areas in which the exudate was characteristically poor in nucleated cells and was rather of the nature of a hemorrhagic edema. The fluid either contained a loose fibrin net or appeared merely as a homogeneous or fibrinous coagulum. There would be merely diapedesis of red cells or more profuse hemorrhages, leading to disruption and necrosis of the lung tissue and distinguishable from infarcts only by the absence of thrombi within the la roer arteries. The alveolar capillaries


in these portions of the lung were tremendously distended, bulging into the alveolar spaces. (Pl. VI.) Sometimes it appeared as if the membrane upon which the endothelium rests was swollen and thickened. Fibrin thrombi were fairly often found within the capillary lumen, and in some cases were quite abundant. It was very common also to see coarse fibrin threads deposited in the septa between the capillary wall and the epithelium. Edema of the alveolar

FIG. 22.- Case 81. Mustard-gas burn, 15 days' duration. Lung. Dilatation of atria, with hyaline necrosis

wall was often striking, and the still intact alveolar epithelium could be elevated at times as a continuous sheet of cells.

The alveolar epithelium itself in the early acute cases often appeared swollen and vacuolated, although it was only occasionally that degenerative changes could be recognized in the still adherent cells. There was always more or less exfoliation, the cast-off cells becoming rounded, taking up red cells, pigment granules, leucocytic nuclear fragments, losing their nuclear staining eventually, and becoming degenerated.


Necrosis of the capillary wall was observed repeatedly, with fragmentation of the endothelial nuclei and of the leucocytes, as recently described by Le Count in cases of primary influenzal pneumonia, and regarded by him as highly characteristic.8 (Fig. 23.)

Just as the bacteriological studies in influenzal pneumonia showed in the lung a varying flora, so the bacteriological data in the series of gas pneumonias studied failed to throw any light on the difference in anatomical types. Both

FIG. 23.- Case 22. Mustard-gas burn, 5 days' duration. Lung: Pneumonia, with necrosis of alveolar walls and nuclear fragmentation

culturally and in bacterial-stained sections a variety of forms was found. In a few cases, and these unfortunately were uncontrolled by cultures, the sections showed enormous numbers of minute Gram-negative rods as the predominating organism in the alveolar exudate. Many other cases, grossly and histologically similar, showed only Gram-positive cocci. So confusing were the findings that it seemed not worth while to attempt an analysis, particularly as no systematic study could be carried on.



The regenerative changes in the trachea and larger bronchi have already been described. Although bacteria were always present, the destruction produced by the chemical irritant was of so gross a character that the róle of the bacteria may well be regarded as altogether secondary, particularly as they rarely invaded the deeper tissues. The healing process also may be looked upon as a repair of the chemically injured tissue. But in the parenchyma of the lung,

FIG. 24.- Case 53. Mustard-gas burn (history of exposure also to green and blue cross shells), 8 days' duration. Lung, small bronchus, lined with dense granulation tissue; thickening of septa of adjacent alveoli, which contain plugs of dense fibrin undergoing early organization

where the original chemical injury was lost or overshadowed by the bacterial infection, it became quite impossible to say whether the reparative and organizing processes which were present in the later cases were in response to the chemical or the bacterial poison. But it was these late and permanent changes, however brought about, which were of the greatest practical interest, and it is necessary to describe them in some detail in order to form an approximate idea of the damage which may be expected to ensue upon the gassing


The thickening of the walls of the small bronchi was an alteration which was quite evident in gross sections of the lung. The section showed the bronchial wall replaced by a vascular granulation tissue, with lymphoid and plasma cells predominating. Where the epithelial lining had failed to regenerate this granulation surface lay exposed, and it can not be doubted that the further contraction of this tissue would lead to narrowing or complete occlusion, with the formation of bronchiectases distal to the stenotic area. (Fig. 24.)

Bronchial stenosis, also might result, though apparently not so frequently as one might expect, from the organization of the exudate within the bron-

FIG. 25.- Case 100. Death, 51 days after exposure to mixed vesicant and suffocant gases. Section through dilated bronchiole, containing a vascular organized plug

chiole. This seemed to occur more often in the ductus alveolaris, where the organizing fibrinous plugs extended into the contiguous alveoli. (Fig. 25.)

The zone of atelectasis, hemorrhage, and fibrinous edema which so often encircled the medium-sized and smaller bronchi has been described. In this zone, where the fibrin offered support to the growing cells, active organization was regularly found in progress, even when the pneumonic process at a distance from the bronchi was in full blast. It was in this peribronchial zone also that there was found, as in the later stages of the primary influenzal pneumonias, a remarkable proliferation of the alveolar epitheliums. The new cells, distinguished by their deeper Staining, their cuboidal form, and often


by numerous kinetic figures, not only reinvested the cavities of the alveoli but grew over and even into the plugs of fibrinous exudate (Fig. 26), and in some instances formed solid, carcinoma-like nests of cells. The alveolar septa also were thickened by the growth of fibroblasts, the new-formed connective tissue being continuous with the granulation tissue about the small bronchi, and also with the new-formed fibrous tissue which invaded the edematous tissue about the arteries and interlobular septa.

FIG. 26.- Case 74. Mustard-gas burn, 12 days' duiration. Lung. Proliferation of alveolar epithelium over a mass of fibrin and agglomerated red blood corpuscles


The study of human cases afforded little evidence that mustard gas, through cutaneous application or by inhalation, could be absorbed and could produce systemic effects in other organs. In dogs exposed to high concentrations in the chamber, the hydrolysis product, dihydroxyethylsulphide, has been dletected in the urine by reconverting it into dichlorethylsulphide and obtaining a vesicant action upon the human skin (Lynch and Marshall) .9 So far as is known no similar demonstration has been made in man.

Clinically there has been observed a group of cases with diffuse pigmentation, marked apathy andl asthenia, low blood pressure, and often pronounced mental disturbances, symptoms which it is difficult to correlate with the obvious lesions of the skin and respiratory tract. Indeed, in some of these


cases, respiratory damage may be quite insignificant. Such cases certainly suggest a systemic intoxication of some sort, and Satre and Gaos,10 and other French clinicians have attributed the symptoms to an acute adrenal insufficiency. No anatomical evidence has been brought forward to incriminate the adrenals, and the observations are not sufficiently definite to justifyany far-reaching conclusions. The lassitude and asthenia, and even the mental disturbances, in men freshly returned from combat, are perhaps more easily explained in other ways.

More direct proof of the absorption of dichlorethysulphide are the changes in the bone marrow and in the circulating blood. Zunz, 11 Stewart, 12 and later Krumbhaar 13 have shown that severely gassed cases, after an initial leucocytosis, may develop a marked leucopenia. and similar observations have been made by Muratet and Fauré &-Fremiet in animals. Pappenheimer and Vance 6 have also shown that intravenous injections of small doses in rabbits brought about a profound leuceopenia. with destruction of the granulocytes in the bone marrow, an effect comparable in its specificity with that of benzol. This has been confirmed by Warthin and Weller.14 Krumbhaar and Krumbhaar have brought confirmation of their clinical evidence by a study of the bone marrow in human cases.15 It may be taken as proved, therefore, that when introduced into the body dichlorethylsulphide is a specific poison for the hematopoietic tissue, and there are both clinical and experimental reasons for believing that a similar effect follows the inhalation of massive doses.


Abdominal tenderness, anorexia, nausea, vomiting, and less frequently diarrhea were observed clinically in a large proportion of mustard-gas cases. The experiments of Warthin and Weller, 12 Lynch, Smith, and Marshall, 8 Pappenheimer and Vance,6 and others, have shown that the intravenous or subcutaneous injection of dichlorethylsulpbide in animals may be followed by a hemorrhagic enteritis. Norris 16 refers the subimucous hemorrhages of the stomach and duodenum to the swallowing of contaminated saliva, but the possibility of the elimination of the absorbed substance or its hydrolysis products through the alimentary tract has not been disproved. This possibility is suggested by the experimnental facts citedl above and on clinical grounds by Ramon, Petit, and Carrié. 17

In the human protocols studied the alimentary tract was not examined in about half of the cases; in about 25 per cent of the cases the stomach and intestines are specifically stated to be normal; in the remainder there are noted injection or hyperemia, sometimes of the stomach, more commonly of the small intestine; hemorrhages in stomach, small or large intestines, erosions or small ulcers, in three cases in the stomach, once in the small intestine, once in the colon.

Too much weight should not be placed on these fragmentary references. The injection may be attributable to the general visceral stasis, which is the rule in the fatal cases. Hemorrhagic erosions of the stomach are so frequent a finding in any large series of autopsies that their oceasional presence in these cases does not seem very significant. On the other hand, a more careful scrutiny mligtht have shown a higher incidence of gastrointestinal lesions.



No changes were found apart from those common to all acute infections. Patients dying early have not shown degenerative changes which might be ascribed to a specific effect of the mustard gas.


No anatomical alterations of the myocardium were found which might throw light on the late circulatory disturbances (effort syndrome) noted in a certain proportion of gassed individuals. Dilatation of the right side of the heart is not infrequently mentioned and may be regarded as secondary to the pulmonary lesions. It was not always evident at autopsy. Suppurative pericarditis as a secondary infection with hemolytic streptococci is recorded in one case. Nor was there found a typical or characteristic vascular lesion in the lung or elsewhere, which could not be of infective origin. That the frequent occurrence of rather marked pulmonary edema in the severe early cases implies an alteration in the permeability of the blood vessels may be assumed, but the cellular changes in the endothelium are not sufficiently definite to warrant description.


Apart from incidental lesions, obviously antecedent to the gas poisoning, these organs showed only an intense venous and capillary congestion. In one case only were there hemorrhages into the capsular spaces and tubules. No alterations which would suggest a toxic effect upon the renal epithelium were noted. The intense congestion is probably sufficient to explain the diminished urinary output, albuminuria, presence of casts and red blood cells described by Hermann 18 as typical urinary findings during life.


Unfortunately there were available no data upon possible finer alterations in the central nervous system. In very few cases was the brain examined, and in none of these were significant gross changes detected, nor was material for histological study preserved. Stewart12 has described ring hemorrhages in the brain associated with swelling and degeneration of the endothelium, thrombosis, and slight leucocytic emigration.


No facts of value have been deduced from the incomplete study of the adrenal gland and other organs of internal secretion which have been occasionally included in the material studied.


The cases are arranged according to the period of survival after gassing. In the majority of the cases the date of gassing is accurately stated; in some it is inferred from the date of the first admission to field or evacuation hospital. Frequently additional data have been disclosed by the study of the reports of the gas officers of the Chemical Warfare Service, and the clinical records on file in the Oflice of the Surgeon General. Such information has been included


in the autopsy record. In a few instances, where the date of gassing is not given, it may be reasonably surmised from the fact that other members of the same company, battalion, or regiment were gassed about the same time and showed lesions similar in character. In only two cases was it not possible to obtain data roughly estimated from the character of the lesions.

While the effort has been made to present the records of the gross lesions as nearly as possible in the form and expressions used by the pathologist who performed the autopsy, it has been thought desirable to omit detailed descriptions of lesions irrelevant to the gassing and where necessary to alter the arrangement for the sake of uniformity. The reports will naturally be found to vary greatly in accuracy and completeness. Many of the autopsies were done under conditions where there was neither time nor facility for detailed observation and record. It seems hardly necessary to apologize for these defects.

CASE 1.- M. L., 64329, Pvt. Co. L, 192d Inf. Died, October 28, 1918, 2 p. m., Evacuation Hospital No. 7. Autopsy -hours after death, by Capt. James F. Coupal, M. C.
Clinical data.- Date of gassing not recorded. October 28, men of company were exposed to shell which had little odor, produced marked sneezing, with casualties five hours later. Severe dyspnea.
Anatomical diagnosis.– Not recorded.
Gross findings.- (The following note upon the lesions of the respiratory tract was made in the pathological laboratory, experimental gas field). The pharynx, larynx, and esophagus are normal. The trachea also shows no gross lesions. The primary and secondary bronchi show a reddened mucosa, covered with loose shreds of tenacious mucus. Their mucosa is intact. Right lung: Voluminous, weighs 735 grams. The pleura is smooth, mottled with darker patches which are slightly sunken. On section the lung is air containing in all lobes. There is a very moderate general edema, somewhat more marked in the anterior portion of the lung. Left lung: Weight, 705 grams; somewhat more voluminous than the right. The pleura is free from exudate. On section there is pretty marked general edema, with scattered patches of collapse. No pneumonic patches. The small bronchi are normal.

Microscopic examination
.- Trachea: In some places the epithelium is definitely necrotic and replaced by a mucopurulent exudate, the membrana propria being interrupted in some of the eroded places. In other places the nuclei of the epithelial cells, which are reduced to a single row, are definitely pycrotic in comparison with the vesicular nuclei of the uninjured cells. The vessels of the submucosa are congested. Lung: The epithelium of the smaller bronchi is uninjured; the lumina contain a small amount of coagulum, desquamated cells and a few leucocytes. Many of the alveoli contain homogeneous, pink-staining material which is practically cell free. The septa are thickened and edematous. There is a stasis of leucocytes in the capillaries. No bacteria are found in sections stained with Gram-saffranine. .myocardium: There is distinct edema about the intermuscular vessels and of the connective tissue between the muscle bundles. Liver, kidney, spleen, adrenal, and pancreas show no significant lesions.

NOTE.-The lesions suggest exposure to a mixture of the suffocant and irritant types of gas, possibly phosgene and arsene compounds. There was definite necrosis of the bronchial epithelium such as one would not expect to find after phosgene alone. The absence of bacterial growth and secondary pneumonic lesions may be taken as evidence of early death in this case, probably within 24 hours.

CASE 2.- A. D., 1429216, Pvt. Hdqrs. Co., 39th Inf. Died, October 11, 1918, 4.45 a. M., Evacuation Hospital No. 6. Autopsy, five hours after death, by Capt. James F. Coupal, M. C.

Clinical data
.- Gassed October 10, near Verdun, blue cross and green cross shells. Clinical diagnosis of phosgene poisoning.


Anatomical diagnosis.- Edema and congestion of lungs; emphysema; bronchopneumonia. External appearance.--Marked post-mortem lividity. No burns of skin. Quantities of frothy fluid exude from mouth.
Gross findings.- Pleural cavities: Very slight retraction of lungs after removal of sternum. Each cavity contains about 60 c. c. of straw-colored fluid. Lungs: Voluminous and extremely mottled, dark red areas of congestion alternating with pink areas of emphysema. On section the left lung especially shows numerous miliary areas, apparently connected with the finest bronchi. On examination with a hand lens these are found to be composed of aerated alveoli surrounded by dark red edematous and congested lung tissue. This appearance is less pronounced in the right lung. The parenchyma in general shows intense congestion but relatively little edema. Neck organs: Tonsils and lymphoid tissue at the base of the tongue enlarged. The mucosa is smooth, velvety, much congested, but there is no ulceration or exudate. The smaller bronchi appear normal. Heart: Cavities of right side extremely dilated. Remaining organs show no distinctive changes. Gastrointestinal tract: Not recorded.

Microscopic examination.- Trachea and bronchi of larger caliber: Ciliated epithelium is lost. The superficial cells show pycnosis of their nuclei and a homogenization of the cytoplasm. In occasional cells are found hydropic vacuoles with crescentic compression of the nucleus. The membrana propria is thick and swollen. The blood vessels of the sub-mucosa are congested, but there is no hemorrhage and little or no inflammatory reaction. (See fig. 3.) Lungs: The small bronchi show a normal epithelium which is often desquamated or elevated in strips from the underlying basement membrane by a collection of edematous fluid. The infundibula are dilated; they have no epithelial lining. The surrounding alveoli show marked changes consisting of edema, hemorrhage, desquamation of epithelium, and the presence of numerous pigment cells. There are excessive numbers of polynuclears in the capillaries, the nuclei of which, especially in the neighborhood of the infundibula, show striking distortion and fragmentation. Elsewhere there is patchy edema, the coagulum being homogeneous and containing little fibrin. Gram-positive cocci are found both in the bronchi and in the alveolar coagulum. Liver, spleen, and adrenals: No significant changes.

NOTE.- In spite of the clinical history of phosgene, and the gross appearance of the lung, the lesions suggested the admixture of an irritant gas, possibly an arsine compound, acting especially upon the infundibula and the adjoining lung tissue. There was no extensive bacterial infection of the lung, masses of bacteria being found only in the small bronchi.

CASE 3.- C. G., French soldier. Died, October 8, 1918, at 8 a. m., Gas Hospital, Julve-court. Autopsy, six hours after death, by Capt. James F. Coupal, M. C.

Clinical data
.- Gassed with phosgene on October 7. Died suddenly after sitting up, without great preceding dyspnea.
Anatomical diagnosis.- Massive pulmonary edema; dilatation of right heart; acute tracheitis.
External appearance.- The body shows marked lividity.
Gross findings.- Pleural cavities: Each contains about 300 c. c. of blood-stained fluid. Respiratory organs: (Note dictated upon receipt of specimens at the pathological laboratory, experimental gas field.) Larynx: Shows no edema. Trachea: Is discolored dark purplish- red. Bronchi: Contain frothy fluid and their mucosa is stained with blood. Right lung: Extremely large and dark purplish in color; the surface is smooth, the lobular markings being entirely obliterated. On section the lung is dark, firm, and rubbery, but showing no evident pneumonic consolidation; there is most intense edema, bloody fluid dripping from the cut section. The smaller bronchi do not contain purulent exudate. Left lung: Differs from the right in the appearance of the lower lobe, which, in its lower portion, is somewhat grayish, dryer, and more granular than elsewhere, suggesting early pneumonic consolidation. Gastrointestinal tract and remaining abdominal viscera normal save for congestion. Heart: Right side markedly dilated, left ventricle in extreme contraction.
Microscopic examination.- Trachea: There are definite lesions in certain areas. Where the epithelium is entirely defective the nuclei of the underlying connective tissue cells and lymphoid cells show marked caryorrhexis, and there is superficial necrosis, with groups of Gram-positive cocci in the necrotic tissue and in the blood vessels. There is also super-


ficial hemorrhage. Lesser injury to the epithelium is indicated by vacuolization of individual cells, or hyaline, pink staining of their cytoplasm. Where the epithelium is intact and composed of several layers, there is loss of cilia; but efforts at repair are suggested by the presence of numerous mitoses. Lungs: Sections of various blocks show similar picture. The alveoli are widely distended. The alveolar capillaries are wide and crowded with decolorized red blood cells. In the larger vessels the red cells are better preserved. In some of the septa it is possible to make out extravasation of cells between the capillary and the somewhat swollen basement membrane upon which the alveolar cells should rest. There is slight diapedesis into the alveolar spaces. The capillaries contain moderate numbers of mononuclear and polymorphonuclear leucocytes, some in process of emigration. A few alveoli contain dense collections of pycnotic leucocytes and much granular coagulum. The alveolar epithelium is not distinguishable. There is no fibrin. In some sections the edema is more evident, as shown by the abundant pink-staining coagulum. Sections stained for bacteria show enormous numbers of Gram-positive cocci in chains, pairs, and groups. They are found in the connective tissue about the blood vessels, in the septa outside the capillaries, and within the polymorphonuclear leucocytes of the alveolar exudate. No other types of bacteria are present. Liver, spleen, kidney, and adrenals show no significant changes.

NOTE.- A case of poisoning by suffocative gas, probably phosgene. There appears to have been complete death of alveolar epithelium, with massive invasion of bacteria (streptococci?) and hemolysis. The bacterial growth was probably not postmortal, since the autopsy was performed within six hours after death. There was very little inflammatory reaction.

CASE 4.- H. R., 76213, Pvt. Co. B, 18th Inf. Died, August 8, 1918, Gas Hospital No. 4. Autopsy, 11 hours after death, by Lieut. Russell W. Wilder, M. C.
Clinical data.- October 7, exposed to bombardment of phosgene and mustard-gas shells (77.105.150 mm.). Clinical diagnosis: Phosgene poisoning.
Anatomical diagnosis.- Diffuse generalized edema of lungs; anthracosis; hydro thorax, bilateral; dilatation of the heart; hyperenia of laryngeal and tracheal mucosa; cloudy swelling of liver and kidneys.
External appearance.- Marked cyanosis of ears, lips, and fingers, and extensive lividity of all dependent parts. Frothy serosanguineous discharge exudes from the mouth and nostrils. The skin shows no burns, scars, wounds, or abrasions. The eyes are clear, the lids edematous.
Gross findings.- Lymph glands are small. Lungs: Do not collapse and completely fill the pleural cavities. They show the imprint of the ribs. Right pleural sac contains 200 c. c. of serosanguineous watery exudate; the pleura is everywhere smooth and glistening. The left is like the right. The lungs are heavy and boggy, and when cut show an extremely wet surface. There is much anthracotic pigmentation. Several accumulations of air appear subpleurally over the surface, and the lung markings are emphysematous. Neck organs: There is moderate hyperemia of the mucosa of the pharynx and trachea, but no edema, tumefaction, exudation, or ulceration. The trachea shows slight hyperemia but no further change. It is filled with frothy serosanguineous fluid, which exudes in quantity when the lungs are pressed. Heart: Enormously dilated, especially the right auricle and ventricle, which are three times their normal size and filled with dark clotted blood. Liver: Intense congestion and cloudy swelling. Spleen: Four times normal size and very firm. Kidneys: Congestion and cloudy swelling. Gastrointestinal tract: Not recorded.
Microscopic examination.- Trachea: Lined with a single row of nonciliated cells, which are in some places completely exfoliated. The superficial cells have been desquamated. There is no edema or leucocytic infiltration of the submucosa, but the membrana propria unquestionably is thicker than normal. Lungs: Sections show advanced post-mortem changes, and finer details can not be made out. There are scattered patchy areas of edema. In some of the alveoli are many polymorphonuclear leucocytes, in the majority, the cellular elements are scanty and composed chiefly of desquamated epithelial cells containing pigment, red blood cells, and occasional leucocytes. Gram-positive bacteria are fairly numerous. There is little fibrin. Interspersed amongst the edematous and pneumonic areas are patches of collapse and emphysema.


NOTE.-The gross findings are very typical of acute poisoning by phosgene or similar suffocant gas, and confirm the clinical diagnosis. The histological material is of little value for finer study.

CASE 5.- H. E. McH., 3173285, Pvt. Co. H, 16th Inf. Died, October 4, 1918, Evacuation Hospital No. 6. Autopsy, October 5, 1918,--hours after death, by Capt. James F. Coupal, M. C.
Clinical data.- Mustard-gas burns and inhalation. Died while being evacuated.
Anatomical diagnosis.- Extensive superficial burns. Diphtheritic tracheobronchitis. Bronchopneumonia (bilateral).
External appearance.-Cloudiness of cornea and conjunctive. Burns of face, hands, elbows, and back.
Gross findings.- Pleural cavities: Left contains 40 c. c. of cloudy fluid. Right, negative. Heart: Right ventricle and auricle dilated. Otherwise normal. Lungs: Do not retract on opening chest cavity. Left: Early pleurisy over posterior portion. Lung on section is purple and yields quantity of blood and frothy mucus. Both lungs show areas of congestion and beginning consolidation scattered throughout. Trachea: Contains a false membrane which hangs to the wall and is surrounded by a quantity of thick mucus. Gastrointestinal tract: Negative except for injection of small intestine. The remaining organs are normal.
Microscopic examination.- Trachea and larger bronchi are covered by thick pseudo-membrane which is made up of a fibrinous network in the interstices, in which are numerous polymorphonuclear leucocytes. The mucous glands show epithelial degeneration, possibly in part post mortem. The cartilages are normal. Lungs: Marked injection of all blood vessels, including the alveolar capillaries. In some areas the alveoli contain an eosinophilic granular debris, and the exudate is frankly inflammatory, the alveoli being filled with plugs of fibrin and leucocytes or merely leucocytes. Some alveoli contain large epithelioid cells which are filled with brown pigment. The smaller bronchi are acutely inflamed. Some contain a fine, purulent pseudo membrane, or a covering of leucocytes. Around one bronchus is an especially marked zone of congestion, and even an infiltration of red blood cells into the adjacent alveoli. Liver: Shows extensive fat infiltration. The remaining organs are free from significant changes.

NOTE.-The case is a typical one of early mustard-gas poisoning, with very extensive tracheobronchitis and early bronchopneumonia, dying on the second day after exposure.

CASE 6.- W. D. F., 3173197, Pvt., Co. H, 16th Inf. Died, October 4, 1918, at 2.20 p. m., Gas Hospital, Julv ecourt. Autopsy, October 4, three and one half hours after death, by Capt. James F. Coupal, M. C.
Clinical data.- Mustard gas on the morning of October 2, 1918.
Anatomical diagnosis.- Multiple burns of skin; necrosis of tracheal and bronchial mucosa; bronchopneumonia; pulmonary edema.
External appearance.- Burns of face, neck, left hand, elbows, buttocks, and scrotum.
Gross findings.- Pleural cavities: The right pleural cavity contains 50 c. c. of clear fluid. Left, negative. Lungs: Contract only slightly. Pericardium: Contains 40 c. c. of clear fluid. The right heart is markedly dilated; left, in contraction. Otherwise negative. Lungs: The parenchyma of both lungs is congested. In the right middle lobe near the anterior border are patchy areas of atelectasis and bronchopneumonia in a stage of gray hepatization. Also a few areas of consolidation in right lower lobe. In the posterior portion of the left lung in both lobes are several deeply congested dark-red areas, somewhat resembling infarcts. The unconsolidated portion of the lung yields a quantity of frothy fluid. Mucosa of trachea appears necrotic and when stripped leaves an injected wall. The smaller bronchi contain a rather thin purulent exudate.
Microscopic examination.-Trachea: The epithelium is lost save for a single row of cuboidal cells here and there, and the epithelium of the ducts of the mucous glands which tends to creep over the adjacent tissue. The submucosa is slightly edematous. The nuclei of the connective tissue cells and of the wandering cells (chiefly polymorphonuclear leucocytes) which infiltrate the tissue in moderate numbers, are distorted and caryorrhectic. The blood vessels are rather wide and contain unaltered cells. Mucous glands normal. Lungs: Areas


of lobular pneumonia with foci of necrosis, patchy alveolar edema, and an excess of leucocytes in capillaries. (Fig. 27.) There is marked congestion and hemorrhage. The alveolar epithelium appears to be largely desquamated. It can rarely be made out distinctly. Bacteria are quite numerous, predominantly Gram-positive diplococci in the alveolar exudate and walls. Long chained streptococci and Gram-negative cocci and bacilli are also found, especially in bronchi. Bacteria are particularly numerous in the areas of necrosis. Fibrin is not abundant in the exudate, but is often present in the walls of the alveoli, apparently outside the capillary walls. A very interesting feature of the section is that many of the atria and alveoli are lined with a hyaline, wavy, refractile band, which in Gram-Weigert-safranine preparation stains bluish but has not the definiteness of fibrin. (See Pl. VI) No alveolar cells overlie this membrane. It is difficult to make out whether it is swollen fibrinous

FIG. 27.- Case 6. Mustard-gas burn, 2 days' duration. Lung showing patchy alveolar edema, stasis of leucocytes in capillaries, beginning lobular pneumonia, with areas of necrosis, dilatation of atria

exudate, the membrana propria of the alveolar epithelium, or the hyaline necrotic alveolar epithelium itself. In favorable places it is seen to be raised up from the alveolar capillary, polymorphonuclear leucocytes and red blood cells being found beneath it, as well as in the alveolar space. Liver: Normal.

NOTE.- Definite history of mustard-gas poisoning, patient dying on second day. Typical mustard-gas burns. Lesions of the upper respiratory passages were rather superficial. Pneumonia was of the influenzal type, with hemorrhagic edema and hyaline necrosis of the alveolar and bronchial walls. Bacterial infection was already established.


CASE 7.- V. O., 134765, Pvt., Battery B, 2d Mass. F. A. Died, October 13,1918, Julvécourt Gas Hospital. Autopsy, October 13, at 2 p. m., by Capt. James F. Coupal, M. C.
Clinical data.- Gassed with mustard gas 48 hours before death. Marked dyspnea.
Anatomical diagnosis.- Multiple superficial burns of skin; acute ulcerative tracheitis; purulent bronchitis; bronchopneumonia; acute fibrinous pleurisy; acute parenchymatous nephritis; mustard gas poisoning.
External appearance.- Marked post-mortem lividity. Burns of conjunctive, corneae, axillae, elbows, and scrotum.
Gross findings.- Heart: Markedly enlarged, right heart dilated. Muscle pale. Lungs: Retract only slightly upon opening the pleural cavity. Few fresh fibrinous adhesions over major portion of both lungs. Both lungs markedly edematous, especially in the posterior part, with the alternating areas of consolidation, congestion, and emphysema, the last especially along the anterior margins. Quantities of dark-red blood and frothy mucus can be scraped from the surface. Neck organs: Base of tongue and larynx are markedly congested. Mucosa of trachea is necrotic. Lumen filled with purulent exudate. Same condition extends throughout bronchial tree. Gastrointestinal tract: Not recorded. Liver, spleen, and kidneys show marked congestion.
Microscopic examination.- Trachea: Epithelium is desquamated over surface of mucosa except for a few flat epithelial cells in one area. Epithelium of gland ducts, however, though damaged, is more or less intact. A little fibrinous pseudo membrane is present. This is infiltrated with polymorphonuclear leucocytes and attached to the submucous layer. The latter is congested, edematous, and infiltrated with polymorphonuclear leucocytes, especially the superficial zone. The nuclei are caryorrhectic. The mucous glands and the deeper layers are not involved to the same extent. A few capillary thrombi are present. Lungs: The sections show no large bronchi, but some branches show desquamated epithelium and contain detritus and leucocytes. The alveolar walls are everywhere congested. Capillaries are distended with blood and contain leucocvtes in excess. In one section the alveoli contain granular debris in which are large epithelioid cells with relatively small spherical nucleus, often containing brown pigment in the cytoplasm, and are accompanied by mononuclear and polymorphonuclear leucocytes and little fibrin. There is also more definite bronchopneumonia. Gram-stained sections show great numbers of streptococci. Skin: Entire layer of stratified squamous epithelium has been raised from the subcutaneous surface except for small areas near the mouths of the hair follicles. This portion of the epithelium is thin and the cells distorted and deeply pigmented. The subepithelial layer contains inflammatory cells of various types, some of which show abundant chestnut-brown pigment. Capillaries are congested, and elsewhere vessels are surrounded by small round cells. Sebaceous glands and hair follicles are not much affected. Sweat glands are normal. Liver: Congested and atrophied with central fat infiltration. Spleen and kidneys are negative.

NOTE.- Mustard-gas poisoning, death after 48 hours, with skin burns. There was necrosis of the epithelium of the trachea and bronchi, with very little membrane formation. There was early lobular pneumonia, probably streptococcal.

CASE 8.- O. K. McD., 45325. Pvt., Co. L, 18th Inf. Died, October 5, 1918. Autopsy at Evacuation Hospital No. 7, on following day, by Capt. James F. Coupal, M. C.
Clinical data.- Gassed October 3, mustard-gas shell. No autopsy protocol.
Gross findings.-(The following note of lesions of the respiratory tract was made at the pathological laboratory of the experimental gas field.) The epiglottis and larynx show no edema. Mucous membrane of trachea and large bronchi is reddened. There is no evident necrosis, exudate, or false membrane. The lymph nodes at the bifurcation are calcareous, showing obsolete tuberculosis. Left lung: Over the upper lobe are organized apical adhesions. There is a small area of collapse near the anterior border. On section there is moderate general edema and congestion. At the base of the lower lobe there is a circumscribed dark red area of consolidation about 3 cm. in diameter. The lower lobe is somewhat more edematous, congested posteriorly, with small patches of collapse scattered throughout the lung. Near the base is an area of consolidation somewhat graver than that in the upper lobe. Right lung: The upper lobe shows edema and congestion, with a few small areas of consolidation near the hilus. The middle lobe is congested posteriorly, and anteriorly there are areas of atelectasis. There are a few small pneumonic areas in the base of the lower lobe. Sonic of the bronchi are found filled with thick mucopurulent exudate and surrounded by a narrow zone of collapse.


Microscopic examination.- Lung and trachea: There is a pseudo membrane present and the epithelium is destroyed. The submucous layers are edematous and infiltrated with polymorphonuclear leucocytes. The smaller bronchi are similarly inflamed but there is no pseudo membrane. The epithelium is intact in some bronchioles but the lumina contain masses of pus cells. The lung parenchyma is edematous and congested. The alveolar capillaries are infiltrated with leucocytes, some of which have wandered out into the alveolar spaces. In the alveoli are present also red blood cells, pigmented epithelial cells, and occasionally a small amount of fibrin. There is hyaline fibrinous material deposited in places in the alveolar septa. Skin: The normal epithelial covering is destroyed except around the mouths of two hair follicles. Even here the basal cells are in the process of vacuolization, elongation, and destruction, while the overlying layers are flattening out and disappearing. On the surface there is noncellular cornified membrane underneath which is a collection of red blood cells, leucocytes, and detritus, while the base of this blister is formed by the subcutaneous tissue, infiltrated by polymorphonuclear leucocytes, and is edematous. Liver, spleen, and kidneys show no significant lesions.

NOTE.- Mustard-gas poisoning, with typical skin lesions, death occurring on the second day after exposure. The respiratory lesions are rather indefinite and the histological description does not correspond with the gross findings, particularly as regards the presence of a membranous necrosis in the bronchi.

CASE 9.- C. H. W., 101135, Pvt., R. A. F., 3 Kite Balloon Section. Died, October 23, 1918, at 7.05 a. m., at Base Hospital No. 2. Autopsy, two hours after death, by Capt. B. F. Weems, M. C.
Clinical data.- October 21, 1918. Admitted to No. 47 Casualty Clearing Station, with gas-shell wound of right leg and groin. Gassed. October 22, admitted to Base Hospital No. 2. Face badly burned; eyelids edematous; slight cyanosis and dyspnea; rattle of moisture in trachea and bronchi; pulse 120. Chest: Good resonance, bronchial and tracheal rales. Heart: Cardiac dullness within normal limits. Abdomen: Superficial wound in epigastric region. Abdomen soft. Penetrating wound of left groin. Through-and-through wound of right thigh. October 23. No change in condition. Died suddenly at 7.05 a. m.
Anatomical diagnosis.- Extensive first and second degree burns of skin; acute conjunctivitis; membrano-ulcerative pharyngitis and tracheitis; laryngitis; membranous bronchitis; lobular pneumonia; congestion and edema of lungs; interstitial emphysema of lungs; acute fibrinous pleurisy, left; chronic fibrous pleurisy over right upper lobe; congestion of abdominal viscera; gas-shell wounds of both thighs.
External appearance.- Extensive burns over the trunk and extremities and large, pale-yellow blebs upon the anterior surface of both thighs, about the left knee, upon both forearms, and upon the neck and face. Besides these clear bullae, there are large areas of a peculiar dusky, pinkish-purple color, in most cases adjacent to the bulla and having approximately the same distribution. The face is swollen and covered over the beardy portions by scabby exudate; the skin about both eyes is swollen and discolored; there is purulent conjunctivitis. A mucopurulent exudate issues from the nostrils. There is extensive gingivitis. Skin over scrotum and penis edematous and in part blistered. Wounds: There is a through-and-through wound of right thigh, external to femur; wound of entrance just beneath anterior superior spine.
Gross findings.- Lungs: Marked inflation, anterior edges overlapping to level of third rib. Fibrous adhesions over right apex, no fluid in pleural cavities. Right, voluminous, color gray, becoming pink near posterior portion. The organ crepitates throughout. There are a few small slightly nodular areas in lower lobe. On section through upper lobe some small slightly sunken areas of a deep-red color are revealed, and a few small, rather cheesy plugs in the small bronchi. The lower lobe presents the same picture, except that there are a few patches of incomplete consolidation in lower portion and somewhat more congestion. Left, likewise voluminous, rather heavier than right, pleural surface shows a very slight fibrinous exudate, especially over anterior part of upper and lower lobes. There is some interstitial emphysema, most marked upon the anterior flap of upper lobe. The organ is closely nodular. There are lobular elevations over the anterior and inferior portions of upper lobe as well as lower. Upon section, surface is very moist, exuding bloody serum. There is patchy and extensive but incomplete consolidation. There are sunken brownish-red areas about the smaller bronchi. The bronchi themselves stand out sharply from the surrounding


tissue and appear almost occluded by fatty-looking plugs of exudate. Upon dissecting the larger bronchi these are found to contain large fatty looking casts coextensive with the tracheal membrane and extending downwards into the smallest bronchial tubes. Organs of neck: Tongue and regions about tonsils appear normal. The uvula is edematous and mucous membrane slightly macerated. The posterior pharyngeal wall is inflamed, with a slight fibrinous exudate. The laryngeal surface of the epiglottis and the epiglottic folds are edematous, deeply injected, and covered by a somewhat patchy grayish-yellow membrane. There is considerable erosion of the mucous membrane over both true and false vocal cords. The trachea is covered by a yellowish-gray necrotic membrane. Upon lifting the edge of this and stripping it back one has the impression of separating the mucous coat. The underlying surface is finely granular, with minute points of capillary hemorrhage. This membranous lesion extends down into the primary bronchi. The peribronchial glands are not enlarged. Heart normal. Gastrointestinal tract normal. Remaining organs show no significant lesions.
Microscopic examination.- Skin: The section shows definite necrosis, as evidenced by pink-staining cytoplasm, pyenosis of nuclei, vacuolization, separation of individual cells. There is loosening of the keratin lamellae. The section passes through the edge of a vesicle filled with shreddy fibrinous coagulum. The separation appears to have taken place within the epidermis, and not between epidermis and corium. The superficial layer of the corium is moderately edematous and contains a few pycnotic wandering cells. There is no marked hyperemia; no thrombosis and no striking alteration of the vascular endothelium. Primary bronchus: Lined with a thick fibrinous membrane, in places distinctly laminated and containing polynuclear leucocytes, especially on the surface. The ciliated mucosa is still present beneath the membrane, though largely detached from the basal layer of cells. The nuclei of these detached cells are perhaps somewhat pycnotic, but there is no very evident necrosis. The membrane is attached at intervals by vertical fibrinous strands to the submucosa. The ciliated cells are separated from the basal row in places by fresh hemorrhage. The submucosa is very edematous, fibrinous, hemorrhagic, with moderate cellular infiltration. The mucous glands are flattened and do not appear to be actively secreting. Medium-sized bronchus: Shows similar changes, except that the lumen is completely filled by a loose fibrinopurulent exudate. An attached bronchial lymph node shows the sinuses filled with pus and fibrin. Lungs: There is marked subpleural and interlobular edema. The capillaries are universally congested. There is a patchy, very loose exudate into the alveoli, composed of well-preserved mononuclear and polymorphonuclear leucocytes, few erythrocytes, and occasional swollen and exfoliated epithelial cells. Two small bronchi in the section show an intact mucosa. There are scattered emphysematous vesicles. Liver, spleen, kidney, pancreas, and adrenal show no significant lesion.
Bacteriological report.- Blood culture (post-mortem) anaerobic media streptococcus hemolyticus, aerobic in second generation. Lung culture: Pneumococcus, type(?); micrococcus catarrhalis.

NOTE.- A very characteristic case of poisoning with mustard gas, probably dying on the second day after exposure. There were extensive skin burns, and a severe membranous necrosis of the upper respiratory tract. The lung showed an early patchy lobular pneumonia, with areas of edema. There are no features deserving special comment except, perhaps, the preservation of the tracheal epithelium, which is included in the fibrinous membrane.

CASE 10.- B. B., 2252004, Pvt., Co. A, 39th Inf. Died, October 14, 1918, 10.45 a. m., Base Hospital No. 58. Autopsy, October 15, 23 hours after death, by Capt. M. Flexner, M. C.
Clinical data.- Gassed October 11, 1918, admitted to Base Hospital No. 58 on same day. Semicomatose, no history obtainable. Tincture digitalis and oxygen inhalation.
Anatomical diagnosis.- Mustard-gas poisoning. Bronchopneumonia.
External appearance.- Cyanosis of face and ears. Two superficial blisters on forehead about 3 cm. in diameter. Superficial burn on bend of left elbow. No other cutaneous lesions.
Gross findings.- Pleural cavities: The right is free. The left is obliterated by old fibrous adhesions. Pericardium: Contains about 20 c. c. of clear fluid. Heart: Left ventricle is contracted; the right is flabby; no other lesions. Right lung: Has old fibrous adhesions between the upper and middle lobes. Left lung: The pleura presents a shaggy appearance


over both lobes. Lung feels cottony with the exception of a few calcified areas. In the upper lobe is a small patch of bronchopneumonia about 2 by 3 cm. In general the cut surface is dry, mottled pinkish red in color. Purulent bronchitis, somewhat less marked than in right lung. Larynx, trachea, and large bronchi are injected and contain thick yellow pus. Gastrointestinal tract: Normal. The remaining organs show no significant lesions.
Microscopic examination.- Trachea: The epithelium for the most part is desquamated. (This may be largely post-mortem, autopsy 23 hours after death.) In places there is a layer of squamous epithelium which seems to originate from the glandular ducts. There is a moderate leucocytic infiltration of the submucous tissue, with congestion and edema. The leucocytes in the superficial zone are caryorrhectic. Section through medium-sized bronchus shows complete necrosis of epithelium and formation of definite membrane. Lung: Terminal bronchioles and alveoli are filled with exudate composed of polynuclear cells. In some areas red cells predominate and moderate numbers of pigmented epithelial cells also are seen There are small areas of emphysema and atelectasis. Alveolar capillaries are also congested. In sections stained by Gram method very few bacteria are seen. Skin: There is desquamation of the epidermis and remains of an old bleb. Slight leucocytic infiltration in subepithelial layer and some fibroblastic activity. There are a few polymorphic pigment cells.

NOTE.- A case of mustard-gas poisoning of three days' duration. Slight burns of skin; inflammatory changes of trachea and larger bronchi were rather superficial. No membrane except in smaller bronchi. Parenchyma of lung was very little affected.

CASE 11.- J. L. J., 2388735, Pvt., Co. M, 4th Inf. Died, October 17, 1918, 7 a. in., at Evacuation Hospital No. 6. Autopsy, three hours after death, by Capt. James F. Coupal, M. C.
Clinical data.- Mustard-gas burns and inhalation. Gassed on October 14. Area shelled daily with Yellow, Blue, and Green Cross shells; prolonged stay in contaminated vegetation and shell holes.
Anatomical diagnosis.- Multiple superficial burns of body with mustard gas. Acute ulcerative tracheitis and bronchitis. Bronchopneumonia. Acute fibrinous pleurisy.
External appearance.- Burns of face, scalp, conjunctivae, left shoulder, arm, and axilla, scrotum, and buttocks.
Gross findings.- Pleural cavities: Contain each about 200 c. c. of clear fluid. Few fresh fibrinous adhesions. Lungs: Both present a similar appearance, showing alternating areas of emphysema, edema, and congestion. On section they yield quantities of dark blood and frothy fluid. Posterior portions are especially edematous; anterior margins emphysematous. Organs of neck: Base of tongue, fauces, pharynx and larynx are markedly congested. Moderate edema of glottis. Trachea: Throughout is denuded of mucosa. Bronchi: There is a loose membrane which extends from the trachea into the larger bronchi. Secondary bronchi contain purulent exudate.
Microscopic examination.- Trachea: There is an adherent fibrinopurulent slough in which is incorporated a necrotic submucosa. Coarse network of fibrin, with many distorted and fragmented nuclei and superficial masses of bacteria, composes the exudate. Here and there the surface is covered by a layer of flattened cells, the connection of which with the proliferating cells of the mucous ducts does not appear in the section. The fibrinous edema and leucocytic infiltration of the fibrous tissue extends quite deeply. There is extensive congestion but little or no hemorrhage. Some of the glands show excessive mucous secretion; others are exhausted. Lung: Bronchi are filled with purulent exudate. Epithelium is largely preserved. Wall moderately congested and hemorrhagic. There is a fine fibrinous exudate in the surrounding alveoli. In these plugs of exudate are large well-preserved epithelioid nuclei, probably derived from alveolar cells. The alveolar epithelium under the immersion shows interesting changes. It is swollen and vacuolated. In many places there is an active growth of epithelial cells which creep along the alveolar walls or follow fibrin strands to invade or cover the plugs of exudate. In these places one finds the remains of the original epithelial lining. This epithelial reaction is the most striking feature of the section. Liver and spleen show no lesions of interest.


NOTE.- Case of typical mustard-gas poisoning, with extensive diphtheritic necrosis of trachea and bronchi and characteristic peribronchial reaction. There were interesting regenerative changes in the alveolar epithelium.
CASE 12.- J. R., 134681, Pvt., Co. B, 102d F. A. Died, October 13, 1918, 3 p. m., Evacuation Hospital No. 6. Autopsy No. 54. Autopsy, October 14, 19 hours after death, by Capt. James F. Coupal, M. C.
Clinical data.- Exposed on 9th and 10th of October to gas shelling (mustard gas and chloropicrin) over a period of five and one-half hours, 2,000 105-mm. and 150-mm. shells used over small area. Masks were removed too soon and soldiers slept in a gassed area. Diagnosis of mustard-gas poisoning.
Anatomical diagnosis.- Multiple mustard-gas burns of skin; acute ulcerative tracheitis; purulent bronchitis; bronchopneumonia; fibrinous pleurisy; acute parenchymatous nephritis.
External appearance.- Burns of face, neck, conjunctive, cornea-, elbows, axille, and scrotum.

Gross findings.- Pleural cavities: Lungs retract very slightly on opening the thorax, The right contains 400 e. c. of fluid with many fresh fibrinous adhesions.
(The following note was dictated at the pathological laboratory, Experimental Gas Field.)
Respiratory organs.- Trachea and bronchi are intensely congested. There is no membrane. Right lung: The upper lobe is voluminous and congested and markedly edematous. Middle lobe shows confluent lobular consolidation, affecting the entire lobe, with much fibrinous exudate about the pleural surface. The lower lobe shows extensive pneumonic consolidation, confluent in the lower portion. Left lung: Both upper and lower lobes are moderately congested and edematous and are free from pneumonic consolidation. Alimentary tract: Not examined. Kidneys: Cortex is mottled, alternately pale and hemorrhagic. The capsule is somewhat adherent. Vessels engorged. The remaining organs show no significant changes.
Microscopic examination.- Trachea: Shows complete loss of epithelium, with necrosis of the superficial portion of the submucosa. Associated with the leucocytic invasion, there is a fibrinous exudate and capillary hemorrhage. Nuclei of leucocytes show marked caryorrhexis. There is no false membrane. Epithelium of the ducts is conserved and in part widened. Mucous glands are degenerating. Bronchus: There are a few shreds of apparently proliferating epithelial cells beneath the fibrinopurulent membrane. Edema is intense. The bronchial wall is congested and there is early proliferation of the fibroblasts. Lung: Alveoli are very large. Many are partially filled with dense leucocytic exudate. Some edema of the interlobular septa and about the bronchi. There is also patchy alveolar edema. In the nonconsolidated areas there is marked congestion, with extensive exfoliation of the alveolar epithelium. Gram-stained section shows many Gram-positive cocci, morphologically staphylococci, occurring in groups in the alveolar exudate. Kidney: Shows acute hemorrhagic nephritis. There are no inflammatory lesions in the glomeruli. There is considerable epithelial necrosis, some of which may be autolytic. Liver and spleen show no significant lesions.

NOTE.- The lesions ate sufficiently typical of early mustard-gas poisoning (duration 3 days) except for the presence of an acute hemorrhagic nephritis. It is interesting to note that McNee recorded one case of hemorrhagic nephritis in his series of 18 mustard-gas cases.

CASE 13.- A. J. L., 1426227, Cpl., Co. G, 30th Inf. Died, August 13,1918, at 3.30 p. m. at Base Hospital No. 27. Autopsy, one and one-half hours after death, by Capt. H. H. Permar, M. C.
Clinical data.- August 10, admitted to Field Hospital No. 7. Diagnosis: Exposure to mustard gas. Eyes irrigated; soda bath. Transferred at 6.30 p. m. to Evacuation Hospital No. 6. August 12, admitted to Base Hospital No. 27. Surface burns of back and genitals, edema of lungs, rapid, weak heart. August 13, died at 3.30 p. m. Clinical diagnosis: Inhalation of deleterious gas, mustard gas and phosgene (?).


Summary of gross lesions.- Excoriations and second-degree burns of skin back and genitals. Both pleural cavities empty. Left lung: Weighed 960 grams; upper lobe congested and edematous, lower lobe shows peribronchial consolidation. Right lung: Weighed 70 grains; areas of consolidation in all lobes, which are markedly congested. Completed destruction of mucosa of primary bronchi. Right side of heart dilated.
Microscopic examination.- Trachea and large bronchi: No material preserved. Lung: The medium-sized bronchi show complete epithelial necrosis, with the formation of fibrino-purulent plugs, in some cases occluding the entire lumen. The epithelium in a few of the bronchi shows early regeneration. The bronchioli have an intact epithelium, normally ciliated, but contain purulent exudate. So also the atria. The lung tissue itself is the seat of confluent lobular pneumonia, the exudate in places being cellular, in others more fibrinous There are no distinctive features.

NOTE.- An incompletely studied, but apparently typical case, of mustard- gas poisoning of three days' duration. There is nothing in the findings at autopsy to confirm the clinical suspicion of exposure to phosgene in addition to mustard gas.

CASE 14.- J. M. P., 1630061, Pvt., Co. H, 30th Inf. Died, August 13, 1918, at 2 p.m. at Base Hospital No. 27. Autopsy No. 30, performed one and one-half hours after death by Capt. H. H. Permar, M. C.
Clinical data.- Gassed with mustard-gas shells at Chateau Thierry on August 10; admitted to Field Hospital No. 7 on same day. Eyes irrigated with novocaine; soda bath. August 12, admitted to Base Hospital No. 27. Extremely cyanotic and dyspneic; weak, rapid pulse; burns over entire body surface. Lungs: Moist rales throughout.
Summary of gross lesions.- Large blebs over back, chest, arms, face, and genitals. Few old adhesions in right pleura, left negative. Left lung: Weight, 466 grams; scattered areas of emphysema, atelectasis and consolidation in lower lobe; upper lobe congested. Bronchi filled with crust-like yellow slough. Right lung weighs 530 grams; voluminous, emphysematous, areas of consolidation in lower lobe. Trachea ulcerated and covered with pseudo- membrane. Right heart dilated. Old tuberculous lesions in peribronchial lymph-node.
Microscopic examination.- Medium-sized bronchus: There is complete denudation of the epithelium; the wall is formed by a dense granulation tissue, with distorted nuclei of inflammatory cells. No membrane is included in the section. The mucous glands are atrophic. Lungs: The smallest bronchi are filled with purulent exudate; their epithelium is intact. The alveoli contain a tense cellular exudate, the pneumonic process being diffuse and confluent. There are no special features.

NOTE.- An incompletely described case of early mustard-gas poisoning of three days' duration showing the usual findings at autopsy.

CASE 15.- A. L., 547297, Pvt., Co. H, 30th Inf. Died, August 13, 1918, at 5.30 a. m., at Base Hospital No. 27. Autopsy No. 29, performed three and one-half hours after death, by Capt. H. H. Permar, M. C.
Clinical data.- August 10, exposed to mustard-gas shelling. Admitted to Field Hospital No. 7. August 12, admitted to Base Hospital No. 27, with diagnosis of mustard-gas inhalation and contact burns of extremities, head, and back. Cardiac failure.
Anatomical diagnosis.- Burns of face, shoulders, back, chest, arms, thighs, and knees; pigmentation of skin of scrotum; laryngitis, tracheitis, and bronchitis, mucopurulent, with sloughing of mucosal lining; bronchopneumonia, early bilateral; edema and congestion of lungs. Heart: Dilatation of right side.
Microscopic examination.- Trachea: There is complete destruction of the surface epitheliuzn, but that of the ducts of the mucous glands is intact, and already actively proliferating. There are small shreds of false membrane adherent in places, but in general the trachea is lined by the necrotic submucous tissue. The zone of necrosis extends to the mucous glands, and the membrana propria is destroyed. In the necrotic tissue are many wandering cells, with pycnotic and distorted nuclei. The blood vessels are intensely congested. The glands appear somewhat compressed and flattened. Medium-sized bronchus: About the same picture as in the trachea. In one area, the necrotic epithelium in, the cells of


which have completely lost their staining, is lifted up from the membrana propria by a collection of leucocytes, forming a sort of pustule. A smaller bronchus shows in addition very extensive hemorrhage into the deeper portion of the submucosa. Lung: Bronchioli show a suppurative inflammation, but their epithelium is still intact. There is an extensive lobular pneumonia, without special features. The exudate is very cellular, and the leucocytes well preserved.

NOTE.- A very severe but typical case of mustard-gas poisoning of only three days' duration. An interesting point in the histological study of the trachea is the early proliferation of the epithelium of the mucous ducts.

CASE 16.- H. B., 2193795, Pvt., 314th F. S. B. Died, August 11, 1918, at Base Hospital No. 116. Autopsy by Lieut. B. S. Kline, M. C.

Clinical data.- Gassed with mustard-gas August 7; admitted to Base Hospital No. 116 on August 10, with cyanosis and extensive edema; severe burns all over body. Right heart dilated. Pulse rapid and weak. Treated with stimulants and venesection.
Anatomical diagnosis.- Extensive gas burns, upper respiratory tract. Superficial burns of skin, penis, and scotum. Acute seropurtulent conjunctivitis. Pigmentation of skin of face and scalp. Ulceration of mucosa of larynx, trachea, and bronchi. Acute membranous laryngitis, tracheitis, and bronchitis. Bronchopneumonia. Acute lymphadenitis. Cloudy swelling of parenchymatous organs. Cardiac dilatation, right side, moderate. Pulmonary edema, slight.

External appearance.- Body is that of an adult male, 192 cm. in length, well developed. Rigor is present to a considerable degree in the voluntary muscles. There is a moderate amount of hypostasis. In the skin of the back, particularly over the left shoulder and left axilla and to a less extent over the right scapular region; above this and between the scapulae are large superficial ulcerated areas. The base is clean and has a reddish-brown appearance. There is a similar smaller ulcerated area in the left lumbar region. There are others about the sacrum, the axilla on each side, the right upper arm, and over the chest anteriorly, particularly in the region of the ensiform. There is also superficial ulceration about the prepuce, the anterior surface of the scrotum showing a matted scab. These ulcerations are very superficial and extend into the dermis only. At the bend of the left elbow there is an area of vesiculation several centimeters in length and about 6 mm. in width. There is also another area on the left greater trochanter, a few centimeters in diameter. At the hand of the right elbow there is a superficial ulcerated area similar to those described above, and in addition over the head of the ulna there is an area of contusion. The skin of the face and scalp have a brownish color. There are beginning vesicles about the left side of the mouth. The inguinal glands are somewhat enlarged. The mucous membranes are pale. Eyes: The eyelids are somewhat swollen, the lids glued together by tenacious mucopurulent material. The conjunctiva e are edematous and there are patches of injection of the bulbar conjunctiva. There is a slight cloudiness of the cornea. The pupils, about 3 mm. in diameter, equal. Nose: In the nose there is a moderate amount of mucopurrulent material. Mouth: No abnormalities. Chest: Well formed, costal angle about 900. Abdomen and extremities: Natural looking.
Gross findings.- Pleural cavities: On opening the thorax the right pleural sac is free of fluid and adhesions. The left pleural sac is likewise free of fluid and adhesions. The heart lies in normal position. On incising the pericardial sac no abnormalities of or in the sac are visible. On the ventral surface of the right ventricle there is typical milky patch. Heart: Right auricle and ventricle moderately dilated. Otherwise normal. Right lung: All lobes voluminous, cushiony, somewhat soggy, palpable solid areas here and there, most marked in the tipper and median portion of the upper and middle lobes. The glands at the hilus are somewhat enlarged, pulpy, pigmented, and somewhat injected. Bronchus: The mucosa in the greater part ulcerated. Covering the denuded submucosa there is an elastic fibrinous membrane forming a cast of the bronchial tree. The vessels at the hilus show no abnormalities except perhaps some dilatation of the arteries. On section of the upper lobe a moist pinkish-red surface presents. The tissue is quite well aerated. In the air sacs there is a moderate amount of the frothy fluid. Medially there are vaguely outlined grayish-red solid patches varying ill size from a few millimeters to a few centimeters in diameter. Posteriorly the solid patches are fewer in number and the tissue is well aerated. The middle lobe oil section crepitates.


Medially there is a large walnut-sized, solid, dull reddish-gray patch. Nearby there are other solid patches of similar appearance. In the smaller bronchioles in this lobe viscid purulent exudate is visible. There is one peribronchial lymph node, grape seed in size, surrounded by a firm pigmented zone. On section of the lower lobe the tissue crepitates. The tissue is well aerated. In the air sacs there is a small amount of thin frothy fluid. The tissue is somewhat congested. In the large bronchial branches there is an adherent mass of exudate. On repeated section no definite solid areas can be made out. Left lung: The glands, vessels, and bronchi similar in appearance to those on the right. The pleura here, as on the right side, is thin and delicate. The lobes, as of the right, are very voluminous, cushiony. On section they crepitate. In the median portion there are good-sized reddish, dull gray areas of consolidation. In the left lower lobe the purulent exudate in the bronchioles is striking in amount. Neck organs: The larynx is filled with tenacious viscid mucopurulent exudate, most marked in the epiglottis and about the true vocal cords. The pouch behind them likewise is filled with a viscid exudate. The trachea is similar in appearance except that the exudate lessens in amount toward the bifurcation. Here the patchy ulceration of the mucosa is very striking. Below it the submucosa is intensely injected. Attached to the tip of the epiglottis there is an adherent elastic, friable plug of exudate. Throughout the upper respiratory tract the submucosa and the muscular coats are considerably edematous. The thyroid of average size and consistency. On section the tissue is spongy. The acini contain but a small amount of colloid. The tonsils of fair size and project somewhat above the general level. On section the tissue in great part is scarred. There is but a small amount lymphoid tissue present. The crypts are clean. Alimentary tract: The upper end of the esophagus and the base of the tongue show considerable injection of the mucosa. There is no ulceration present, however, and no exudate. The stomach contains some intensely bile-stained contents and a small amount of mucus. In the mucosa there are scatted areas of patchy injection. The duodenum shows no abnormalities. In the lower ileum there are patches of patchy injection of the mucosa. The solitary follicles are somewhat more prominent than normal in the lower ileum. Patchy injection of the cecum and of the transverse and descending colon. The appendix shows considerable patchy injection of the mucosa with tiny hemorrhages, especially marked in the tip. Kidneys show cloudy swelling.
Microscopic examination.- Lungs: No large bronchi are included in the sections. There is dilatation and hyaline necrosis of the walls of the infundibula. Small bronchioles still retain their epithelium but their walls are infiltrated with inflammatory cells. Alveolar walls are congested and contain many leucocytes. There is typical bronchopneumonia, the exudate being composed chiefly of well-preserved polymorphonuclear leucocytes. There is very little fibrin. Trachea: Well-formed laminated membrane invaded with leucocytes and containing in one area a large mass of mucus. Beneath the membrane in places a single row of epithelial cells with pycnotic distorted nuclei. Marked swelling of membrana propria. Edema, congestion, hemorrhage, and leucocytic infiltration of submucosa. The ducts of the mucous glands are distended with thick plugs of mucus. The epithelium in the superficial portion is destroyed. (Fig. 28.)
Bacteriological report.- Smears made from the exudate in larynx show innumerable organisms. The predominating one, a Gram-positive lancet-shaped diplococcus. In addition there are some rounded Gram-positive cocci, also a moderate number of small and large Gram-negative bacilli and a few Grain-negative cocci.

NOTE.- A typical case of mustard-gas poisoning of four days' duration. There was a diphtheritic tracheobronchitis, with patches of secondary broncho-pneumonia. Histologically the lung lesions differ from the influenzal pneumonias in the absence of extensive hemorrhagic edema and in the presence of large numbers of leucocytes in the exudate. There was, however, hyaline necrosis of the walls of the dilated atria, such as was commonly observed in the influenzal pneumonias.

CASE 17.- A. H., 1940705, Pvt., Co. E, 20th Inf. Died, October 7, 1918, Gas Hospital A. Autopsy, October 8, four hours after death, by Lieut. Russell WV. Wilder, M. C.

Clinical data.- Gassed on October 3, 1918. Burns of skin, eyes, and respiratory tract


Anatomical diagnosis.- Hyperemia of mucous membranes of larynx, pharynx, and trachea. Ulcerations of mucous membrane of bronchi. Emphysema and beginning atelectasis of lungs. Healed apical tuberculosis. Parenchymatous degeneration of liver and kidneys. Second-degree mustard-gas burns of face, arms, and trunk.
External appearance.-Moderate cyanosis and lividity. Large vesiculated burns of arms and trunk. Desquamation of skin of scrotum, leaving raw bloody surface. Purulent discharge from eyes.
Gross findings.- Lungs: Distended. No free fluid in pleural cavities. Pleura is smooth and glistening. Right, crepitates throughout. On section reveals small bronchi occluded with fibrinous exudate. Larger bronchi covered by membrane, which, when stripped away, reveals longitudinal muscle fibers. Extensive areas of emphysema and other areas of beginning atelectasis. Left, shows similar picture. There is a calcified scar 1 cm. in diameter in the apex of the upper lobe. Heart: Right ventricle moderately dilated. Mitral orifice somewhat stenotic, showing old endocardial scars. Abdomen: Adhesions about the site of old appendectomy. Gastrointestinal tract not examined. Pharynx intensely congested. Larynx and tracheal mucosa hyperemic, but not ulcerated or covered by exudate. Thin purulent material in tracheal lumen.

FIG. 28.- Case 16. Mustard-gas burn, 4 days' duration. Trachea. Low-power view, showing laminated false membrane attached to openings to mucous ducts

Microscopic examination.- Trachea. Tissue poorly preserved. Epithelium desquamated. Submucous layer is edematotis, congested, and infiltrated with leucocytes. There is no pseudo membrane. Section of medium-sized bronchus shows complete destruction of mucosa, with formation of false membrane composed of laminated fibrin. Lung: Sections unsatisfactory. Show only congestion of capillaries and desquamation of mononuclear epithelial cells.

NOTE.- A typical early ease of mustard-gas poisoning, dying four days after exposure. There was a membranous inflammation involving the bronchi, more deep seated than that in the trachea and extending into the smallest branches. Parenchyma, of the lung, aside from the emphysema and atelectasis, due to occlusion of the bronchi was very little affected.

CASE 18- C. P., 3171057 (rank and organization not given). Died, October 13, 1918, 11 a. m., Evacuation Hospital No. 6. Autopsy No. 53. Autopsy, October 14. 27 hours after death, by Capt. James F. Coupal, M. C.
Clinical data.- Gassed October 7 or 8. Died while being evacuated. Diagnosis: Mustard-gas poisoning.
Anatomical diagnosis.- Multiple superficial burns. Acute ulcerative tracheitis; purulent bronchitis; bronchopneumonia; acute fibrinous pleurisy; acute parenchymatous nephritis.


External appearance.- Burns of face, neck, conjunetiva , cornea, scrotum, buttock, and thighs. Multiple blisters. Marked subcutaneous emphysema at base of neck and extending down to first rib. Paraphiniosis.
Gross findings.-Pleural cavities: Lungs retract very slightly. Left pleural cavity contains 100 c. c. of sterile yellow fluid. Right, a similar amount, with few fibrinous adhesions over the diaphragm. Heart: The right ventricle is dilated.
(Note dictated at the pathological laboratory, experimental gas field.) Respiratory organs.-Trachea: Covered with tough continuous membrane extending into the smaller bronchi. The anterior portions of both lungs, including the right middle lobe, are emphysematous, while the posterior portions are congested and edematous. There are no gross pneumonic lesions. Alimentary tract: Intestines injected throughout. The remaining organs show no significant lesions.

Microscopic examination.- Trachea: Has a well-formed pseudo membrane composed of fibrin infiltrated with polymorphonuclear leucocytes. Submucous layer is congested, edematous and infiltrated with wandering cells, showing beginning caryorrhexis. An interesting point is the presence over large areas of a single row of epithelial cells beneath the pseudo membrane and still attached to the swollen membrana propria. The leucocytic infiltration is not dense. There is beginning caryorrhexis and capillary extravasation. The mucous glands do not appear to be in active secretion. Bronchus: Section through a medium-sized bronchus shows complete necrosis of the epithelium. The lumina are filled with purelent exudate. Lungs: There are a few small bronchi in the section showing generally exfoliation of the epithelium, probably post-mortem. The alveolar capillaries are congested, tortuous, and contain an increased number of polymorphonuclear and large mononuclear cells. A few air spaces are collapsed, others contain pink coagulum. There is slight exfoliation of the alveolar cells. No pneumonia. Skin: The epithelium is raised up from the corium in a continuous sheet, forming a blister, the contents of which consist of homogeneous, slightly fibrinous coagulum with a fair number of leucocvtes, chiefly polymorphonuclears. The epithelial cells show' varying degrees of necrosis. The underlying corium is moderately edematous and loosely invaded by wandering cells. The vessels are not extremely congested and are free from thrombi even in the superficial zone. Near the surface there are small irregular cells containing pigment, some of which seem to have been derived from the basal cells of the rete mucosum. Some of the brown pigment has been taken up by the polynuclears. At the margin of the blister the epidermal cells are in places detached from their neighbors, and there is considerable leucocytic infiltration, especially in the zone just above the pigment layer. Papillary processes are edematous. (See fig. 6.)

NOTE.- Mustard-gas case, five or six days' duration. There was a typical membranous tracheobronchitis, in addition to the typical cutaneous lesions. The pulmonary parenchyma, according to the gross description and the single histological block available, showed only emphysema, edema, and congestion. There was no pneumonia.

CASE 19.- D. B., 187, Pvt., 1/4 Highlanders R. Died, October 23, 1918, at 5.10 a. m., at Base Hospital No. 2. Autopsy, four and one-half hours after death, by Maj. A. M. Pappenheimer, M. C.
Clinical data.- October 20, admitted to No. 5 Casualty Clearing Station, with diagnosis of shell-gas poisoning (irritant). October 22 admitted to Base Hospital No. 2. Patient is pale; breathing with much difficulty; edematous; pulse 140, very weak; blood pressure 120-100). No sounds during respiration. Sputum mucopurulent. Chest: Good resonance, tracheal and bronchial r?les. Heart: Cardiac dullness within normal limits. Patient received an intravenous dose of strophanthin at 7 p. in. Oxygen administered, October 23. 4 a. m. Pulse very weak; pale; thirsty. Died at 5.10 a. m.
Anatomical diagnosis.- Membranous tracheobronchitis; lobular pneumonia; congestion and edema of lungs; pleural adhesions; acute conjunctivitis; congestion of viscera.
External appearance.- Conjunctiva are injected, slightly more so on left side. Abundant thin watery fluid flowing from mouth. The mucous membrane over the lower lip is a little macerated There are no burns or other cutaneous lesions.


Gross findings.- Pleural cavities: On both sides obliterated by organized adhesions. Lungs meet in median line to third interspace. Lungs: Voluminous and heavy, covered everywhere with edematous sheet-like adhesions. In all lobes there can be felt firm areas which are quite extensive. Right lung: On section, upper lobe shows very widespread areas of consolidation, which are grayish red and granular, forming patches 2 or 3 cm. in size, between which the lung tissue is very edematous and congested. The bronchi are thick, the larger ones lined with a continuation of the gray membrane present in the upper respiratory passages, the smaller ones completely filled with purulent fluid. In the lower and middle lobes the consolidation is less extensive but of the same character. The bronchi are surrounded by a sunken red zone. Left lung: Presents a similar picture. The most extensive consolidation is in the lower lobe, about two-thirds of which are completely consolidated. Organs of neck: Tongue normal. Tonsils small, normal on section. The pharynx congested, slight thickening of the arytenoepiglottidean folds. On the laryngeal surface of the epiglottis the mucous membrane in places is denuded and covered by a thin grayish membrane. The vocal cords and the entire lining of the trachea and primary bronchi are covered with a coherent, rather moist yellowish-gray membrane. This is readily detached, leaving a swollen red velvety surface, apparently covered by epithelium. Esophagus normal. Heart normal. Remaining viscera, including gastrointestinal tract, show no significant changes.
Microscopic examination.- Trachea: There is no membrane preserved in the section. The epithelium is reduced to occasional small groups of flattened cells, with pycnotic nuclei. The membrana propria is swollen. The submucous tissue is the seat of fibrinous edema. There is congestion, scattered hemorrhage, and loose inflammatory infiltration. The leucocytes as they approach the surface show pycnosis and caryorrhexis. The edema extends through the wall of the trachea to the neighboring fat and areolar tissue. Primary bronchus: The section shows a loose fibrinous membrane, to the base of which are attached strips of exfoliated epithelium. There is a curious arrangement of the fibrin. To the swollen membrana propria, are still adherent in places, flattened, deeply staining epithelial cells. The openings of the mucous ducts are dilated with mucus and exfoliated cells. The edema, congestion, hemorrhage, and leucocytic infiltration of the bronchial wall are like that in the trachea. Tonsils: No epithelial necrosis. Lungs: Bronchi filled with purulent exudate which in the terminal infundibula are in the form of fibrinopurulent plugs completely filling them. The epithelium is preserved in part. There is diffuse pneumonia, showing no special features. The exudate is rich in polymorphonuclear leucocytes, showing early pycnosis. The capillaries are extremely congested, and there is moderate diapedesis. There is rather marked periarterial edema. Another block shows a medium-sized bronchus, cut longitudinally and completely occluded by a fibrinopurulent plug. A few flattened epithelial cells persist here and there where the plug is less firmly attached. The wall is edematous and loosely invaded by wandering cells. The rest of the section shows edema, patchy in distribution, emphysema, and congestion. Liver, spleen, pancreas, and adrenals: Show no special features.

Bacteriological report.- Blood culture (post-mortem) anaerobic streptococcus, dying on transplant. Staphylococcus aureus. Lung culture: B. influenza and pneumococcus, Type IV.

NOTE.- This case, probably one of mustard-gas poisoning of three or four days' duration, is interesting and unusual because of the absence of cutaneous lesions. The diphtheritic necrosis of the trachea and bronchi were very severe and extensive and could hardly be ascribed to an influenzal infection alone. There was, moreover, a definite history of shell-gas inhalation. The eye lesions appear to have been very mild.

CASE 20.- J. A. A., 1681974, Pvt. (Co. not given), 306th Inf. Died, September 29, 1918, at Base Hospital No. 18. Autopsy No. 99, performed 16½ hours after death, by Lieut. B. S. Kline, M. C.
Clinical data.- Gassed on the night of September 25. Died shortly after admission to Base Hospital No. 18. No further data are available. The records at hand show four other casualties from gas on the night of September 25 in the 306th Infantry. One thousand five hundred 77 and 105 mm. Yellow Cross shells were used in the bombardment, which lasted one hour.


Anatomical diagnosis.- Gas burns of scrotum, conjunctiva , and respiratory tract; infected scrotal burn; acute conjunctivitis; acute esophagitis; laryngitis, tracheitis, and bronchitis; peribronchial and bronchopneumonia; acute lymphadenitis, regional lymph nodes; healed pleural adhesions; pulmonary edema, slight to moderate; chronic diffuse nephritis; myocardial scars, left; hypertrophy of left ventricle, considerable; anemia and emaciation, slight to moderate.
External appearance.- The skin is thin and sallow. The scrotum shows an area of superficial necrosis of the epidermis over each testis, also in the midline, several centimeters in diameter. Over this there is matted serum and a small amount of purulent exudate. The superficial lymph glands are palpable. The conjunctiva are diffusely injected. There is a small amount of fibrinopurulent secretion present; both corne are cloudy. There is superficial ulceration of the mucosa of the lips, covered with sores; many teeth poorly formed.
Gross findings.- Pleural cavities: Right pleural sac obliterated by sheetlike adhesions. On the left side, no abnormalities. Right lung: All lobes are voluminous, except the middle lobe, which is smaller than the average. The pleura in general is thickened. The lobes are bound to each other and to the pericardium by fibrous bands. Vessels at the hilum are normal. The lymph glands are enlarged, pulpy, injected, and edematous. The bronchus shows a striking picture; there is injection of the mucosa with patches of ulceration; in many places fibrinous and fibrinopurulent exudate adheres to the walls. On section of the upper lobe the tissue in the posterior part shows slight congestion and moderate edema. Throughout the lobe there are scattered areas of peribronchial consolidation, varying in size up to a few centimeters in diameter. In general they average only several millimeters. The middle lobe in its greater portion shows a patchy grayish-pink consolidation; about two-thirds of the lobes are involved. The right lower lobe on section resembles the upper. There is more uniform congestion, and the consolidation is more distinctly peribronchial. The bronchial branches throughout this side contain tightly adherent fibrinopurulent exudate. Left lung: Also voluminous in both lobes. The entire lung, except the apex of the upper lobe feels soggy and solid. Over the lower lobe posteriorly there is a small amount of fibrinous exudate. Glands at the hilum, vessels and bronchi are similar to those on the right side. On section of the upper lobe the upper part is well aerated and pink, but contains a few bronchopneumonic areas. In the lower portion there is considerable edema, slight congestion, and scattered areas of grayish consolidation, peribronchial and pneumonic. In the median portion of the lobe there is an area of consolidation several centimeters in diameter; the consolidation here is almost uniform grayish and red, finely granular. The lower lobe on section presents a picture similar to the lower portion of the upper, but is more extensive. The smaller bronchial branches are like those on the right side. Organs of neck: The larynx is lined with a necrotic white mucosa, covered in great part with tenacious, yellowish, slightly green tinged, coherent exudate. The true vocal cords and lower portion of the larynx are especially affected. A similar condition is present throughout the trachea, although the exudate is somewhat less abundant. Patchy injection and superficial ulceration of the mucosa is visible here and there. The posterior wall of the pharynx and the upper esophagus present a picture like that in the upper part of the larynx. The tonsils are slightly enlarged, edematous, pale, and scarred. Heart: Weighs 320 grams, the left ventricle about twice the average thickness. There are myocardial scars, and the muscle is coarse in texture. Sclerotic patches are seen in the coronaries and at the base of the aorta. Kidneys: Reduced in size and show irregular atrophy of the cortex and indistinct markings. Gastrointestinal tract: Not described. Remaining viscera show no changes of interest.
Microscopic examination.- Trachea: Longitudinal section cut. There is complete epithelial necrosis. Masses of tightly adherent fibriniopurulent exudate, in which are many bacterial colonies, cover the surface. The submucous tissue is only superficially infiltrated with inflammatory cells. The tissue is poorly preserved, and the red cells in the vessels are not stained. Pharynx: On the surface is an adherent fibrinopurulent slough; there is edema, intense congestion and inflammatory infiltration of the submucous tissue. Lungs: Tile smaller bronchi are lined with adherent fibrinopurulent exudate which is incorporated in the wall and does not form a distinct membrane. The terminal bronchioles and infundibula are filled with pus; their epitheliumn is still partially preserved. The parenchyma shows a diffuse pneumonia; the exudate is of varying composition, in places almost fibrinous, in others containing dense aggregations of leucocytes. There are no features of special interest.


The finer details are somewhat obscured by formalin pigment. Another section shows circum- scribed areas of pneumonia, in which there is great fragmentation of leucocytes and abundant bacterial growth. The appearance suggests beginning gangrene. Some of these consolidated foci are surrounded by zones of hemorrhagic edema. There is marked perivascular edema in some sections.

NOTE.-Typical early case of mustard-gas poisoning, of four days' duration, with severe diphtheritic necrosis of the upper respiratory passages.

CASE 21.- A. B., 240806, Pvt., Co. L, 309th Inf. Died, October 22, 1918, at 2.20 p. m., at Base Hospital No. 15. Autopsy (time not given) by Maj. Daniel Glomset, M. C.
Clinical data.- Gassed (inhalation and contact) October 17, 1918. October 20, diagnosis of lobar pneumonia right lower lobe was made.
Anatomical diagnosis.- Bronchopneumonia, all lobes, pseudo membranous tracheitis and bronchitis. Parenchymatous degeneration of liver and kidneys. Second-degree burns of skin. No detailed description of gross lesions available.
Microscopic examination.- Trachea: The membrane, only shreds of which are present, consists of coarse fibrin network in which are scattered pycnotic leucocytes. Surface is formed by the slightly swollen basement membrane. The outer half of the submucosa is necrotic. There is a coarse fibrinous exudate in the edematous tissue with deeply staining nuclei. Vessels are congested but there is no hemorrhage. The mucous ducts are apparently obstructed at their orifices. They are dilated, as are many of the mucous glands, and the epithelium is metaplastic, in places showing regenerative changes. Lungs: There are small patches of pneumonia definitely grouped about the bronchioles and atria, in which are found the usual lesions. Uninvolved lung is emphysematous. Kidney, myocardium, and adrenals show no lesions of interest.

NOTE.-Typical case of mustard-gas poisoning of five days' duration, with membranous tracheobronchitis. Lesions of the lung parenchyma are sharply limited to the peribronchial regions. It is of interest to note that regenerative changes in the epithelium of the mucous ducts are already in progress.

CASE 22.- S. D., 2250618, Pvt., Co. I, 39th Inf. Died, October 16, 1918, 8.30 a. in., at Base Hospital No. 59. Autopsy No. 7. Autopsy, four and one-half hours after death, by Capt. M. Flexner, M. C.
Clinical data.- Gassed October 11, 1918. Exposed to blue, green, and yellow cross shells. Admitted to Field Hospital the same day. Base Hospital No. 59 on October 13. On admission, conjunctivitis, sore throat, pain in chest, riles of all types throughout chest. Diagnosis of gas inhalation and bronchopneumnonia.
Anatomical diagnosis.- Mustard-gas burns. Fibrinopurulent tracheo-bronchopneumonia. Acute fibrinous pleurisy. Emphysema.
External appearance.- Skin about eves, nose, and mouth shows crusts from gas burns. Scrotum shows dense scab formation from old burns, and other severe superficial burns on the elbows. Eyes show conjunctivitis, bilateral keratitis. Cornea have steamed appearance.
Gross findings.- Pleural cavities: Right lung: Pleural surface is shaggy anteriorly, due to fibrous adhesions. There are more recent adhesions between the visceral pleura and the pericardial sac. Upper lobe is grayish white in color with a few darker patches, especially at the apex, and the lobe has a cottony feeling. On section, it is a pinkish-gray color with scattered flesh-colored areas from one-half to 3 cm. in diameter. On pressure bloody, frothy fluid escapes. The base of lower lobe is firm and darker in color. Excised piece of darker tissue sinks when placed in water. Left lung: Pleura over lower lobe is covered with fibrous tags. Upper lobe, on section, is pinkish gray in color. Contains scattered flesh-colored areas. Around smaller bronchioles are narrow dark colored zones. The upper two-thirds of the lower lobe are reddish brown with a few scattered purplish areas, which are dry and granular and apparently contain no air. Lower lobe is pinkish gray in color with few scattered elevations. Trachea and larger bronchi show erosions of mucous membrane, with fibrin. The remaining viscera show nothing of interest.