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Volume XIV
THE MEDICAL DEPARTMENT OF THE
UNITED STATES ARMY IN THE WORLD WAR
VOLUME XIV
MEDICAL ASPECTS OF GAS WARFARE
PREPARED UNDER THE DIRECTION OF
MAJ. GEN. M. W. IRELAND
The Surgeon General
By
COL. WILDER D. BANCROFT, C. W. S. |
CAPT. E. K. MARSHALL, JR., C.W.S. |
MAJ. H. C. BRADLEY, C. W. S. |
MAJ. WALTER J. MEEK, C. W. S. |
MAJ. J. A. E. EYSTER, M. C. |
MAJ. A. A. PAPPENHEIMER, M. C. |
COL. H. L. GILCHRIST, M. C. |
MAJ. JAMES E. POORE, M. C. |
CAPT. SAMUEL GOLDSCHMIDT, C. W. S. |
TORALD SOLLMAN, M. D. |
CAPT. PAUL J. HANZLIK, M. C. |
SERGT. JESSE TARR, C. W. S. |
CAPT. ROBERT A. LAMBERT, M.C. |
LIEUT. COL. F. P. UNDERHILL, C.W.S. |
A. S. LOEVENHART, M. D. |
ALFRED S. WARTHIN, M. D. |
CAPT. D. W. WILSON, C.W.S. |
|
WASHINGTON: GOVERNMENT PRINTING OFFICE, 1926
ADDITIONAL. COPI ES
OF THIS PUBLICATION MAY BE PROCURED FROM
THE SUPERINTENDENT OF DOCUMENTS
GOVERNMENT PRINTING OFFICE
WASHINGTON, D.C.
AT
$3.00 PER COPY
LETTER OF TRANSMISSION
I have the honor to submit herewith Volume XIV of the history of the MEDICAL DEPARTMENT OF THE UNITED STATES ARMY IN THE WORLD WAR. The volume submitted is entitled "MEDICAL ASPECTS OF GAS WARFARE."
M. W. IRELAND,
Major General, The Surgeon General.
The SECRETARY OF WAR.
3
Lieut. Col. FRANK W. WEED, M. C., Editor
in Chief.
LOY MCAFEE, A. M., M. D., Assistant
Editor in Chief.
EDITORIAL BOARD a
Col. BAILEY K. ASHFORD, M. C.
Col. FRANK BILLINGS, M. C.
Col. THOMAS R. BOGGS, M. C.
Col. GEORGE E. BREWER, M. C.
Col. W. P. CHAMBERLAIN, M. C.
Col. C. F. CRAIG, M. C.
Col. HAVEN EMERSON, M. C.
Brig. Gen. JOHN M. T. FINNEY, M. D.
Col. J. H. FORI, M. C.
Lieut. Col. FIELDING 1H. GARRISON, M. C.
Col. H. L. GILCIHRIST, M. C.
Brig. Gen. JEFFERSON R. KEAN, M. D.
Lieut. Col. A. G. LOVE, M. C.
Col. CHARLES LYNCH, M. C.
Col. JAMES F. MCKERNON, M. C.
Col. S. J. MORRIS, M. C.
Col. R. T. OLIVER, D. C.
Col. CHARLES R. REYNOLDS, M. C.
Col. THOMAS W. SALMON, M. C.
Lieut. Col. G. E. DE SCHWEINITZ, M. C.
Col. J. F. SILER, M. C.
Brig. Gen. W. S. THAYER, M. D.
Col. A. D. TUTTLE, M. C.
Col. WILLIAM H.. WELCH, M. C.
Col. E. P. WOLFE, M. C.
Lieut. Col. CASEY A. WOOD, M. C.
Col. HANS ZINSSER, M. C.
______________________________________________________________________________
a The
highest rank held during the World War has been used in the case of
each officer.
4
PREFACE. a
In
this volume attempt is made to deal with only such problems of gas
warfare as
concerned the Medical Department directly, or through affiliation with
the Chemical Warfare
Service. The material seemed naturally to fall into three sections,
involving: (1) Organization
and administration of the gas service; (2) clinical features of gas
poisoning, including certain
statistical considerations; (3) experimental researches with respect to
the physiology, pathology,
and therapeutics of noxious gases.
The
connection of the Medical Department with the early development of the
defensive
aspects of gas warfare has been briefly detailed in Volume 1, which
gives the administrative
history of the Surgeon General 's Office. That account is elaborated,
with certain necessary
repetitions, in the present volume.
Reports
by the laboratory investigators concerning the progress of their
experimental
studies were submitted from time to time during and after the war, many
of which formed the
basis of contributions which appeared in professional journals or in
book form. A considerable
part, therefore, of the third, or experimental, section of the present
volume has been published. The purpose of this section is to assemble,
in one place and in convenient form the accounts of
the work of our most prominent students of the various aspects of gas
poisoning, as
experimentally investigated. The immediate editorial supervision of
this volume, in the earlier
stages of its preparation, and until official orders separated him from
the Historical Division, was
exercised by Lieut. Col. S. J. Morris. M. C.
______________________________________________________________________________
a For
the purposes of the History of the Medical Department of the United
States Army in the World War, the
period of war activities extends from Apr. 6. 1917, to Dec. 31, 1919.
In the professional volumes, however. in which
are recorded the medical and surgical aspects of the conflict as
applied to the actual care of the sick and wounded,
this period is extended, in some instances, to the time of the
completion of the history of the given service. In this
way only can the results of the methods employed be followed to their
logical conclusion.
TABLE OF CONTENTS
PREFACE
INTRODUCTION
SECTION I.-
ORGANIZATION
AND ADMINISTRATION OF GAS DEFENSE
CHAPTER I. Organization
in the United States. By Maj. H. C. Bradley, C. W. S.
II. Organization in the American
Expeditionary Forces. By Col. H. L. Gilchrist,
M. C
III. Classification and methods of use of war
gases. By Col. H. L. Gilchrist, M. C
IV. Field arrangements for gas defense and
the care of gas casualties. By
Col. H. L. Gilchrist, M. C
SECTION II.- CLINICAL
FEATURES
V.
Physiological action of war gases. By Maj.
H. C. Bradley, C. W. S
VI. Pathological action of war gases. By Maj.
A. M. Pappenheinmer, M. C .
[part 1, pages 87-137]
[part 2, pages 138-188]
[part 3, pages 189-249]
VII. Symptoms and treatment. By Col. H. L.
Gilchrist, M. C
VIII. Statistical consideration of gas
casualties:
(1) Gas casualties. By Col. H. L. Gilchrist,
M. C.
(2) After-effects of gas poisoning. By Maj.
James E. Poore, M. C
SECTION III.-EXPERIMENTAL
RESEARCHES
IX. The chemistry of war gases. By Col.
Wilder D. Bancroft, C. W. S
X. Physiological action
of phosgene,
chlorine, and chloropicrin. By Lieut. Col.
Frank P. Underhill, C. W. S
XI. Physiopathological action of acute
phosgene poisoning. By Maj. J. A. E.
Eyster, M. C., and Maj. Walter J. Meek, C. W. S
XII. Physiological action of
dichlorethylsulphide (mustard gas). By Capt. E.
K. Marshall, jr., C. W. S.
XIII.
Physiological action of miscellaneous
gases. By Lieut. Col. Frank P. Underhill,
C. W. S
XIV. Experimental pathology of war gases,
exclusive of mustard gas. By Capt.
Robert A. Lambert, M. C.
XV. Pathologic action of mustard gas
(dichlorethylsulphide). By Alfred S.
Warthin, M. D
XVI. The
comparative skin irritant properties
of mustard gas and other agents. By
Capt. Paul J. Hanzlik, M. C., and Sergt. Jesse Tarr, C.
W. S.
XVII. The influence of solvents, adsorbents,
and chemical antidotes on the severity
of human skin lesions caused by mustard gas. By Torald Sollman,
M. D
XVIII. Ointment protection against mustard
gas. By A. S. Loevenhart, M. D.
XIX. Experimental treatment of poisoning by
lung irritant or suffocallt gases. By
Lieut. Col. Frank P. Underhill, C. W.
S.
XX. The influence of oxygen administration on
the concentration of the blood which
accompanies the development of lung edema. By Capt. D. W. Wilson,
C. W. S., and Capt. Samuel Goldschmidt, C. W. S.
XXI. Researches of pathological and
physiological sections of Hanlon Field (experimental
gas field), American
Expeditionary Forces
APPENDIX.
Summary of
production, field supply section,
Gas Defense Service
Instructors in gas
defense methods, field
training section, Gas Defense Service
Quiz compend on the
use of gas in
warfare
A suggested
organization of the gas service
of the American Army (Church)
Gas defensive
organization of the British
armies in France
Abstract of plan for
organization of gas
service in United States Army (Flandin)
Gas and Flame
Service, offensive and
defensive (statement of action taken)
Inter-Allied gas
conferences (first, second,
and third)
The physiological
effect of warfare gases on
the human being, including symptomatology and general
treatment
Circular No. 34,
American Expeditionary
Forces résumé of symptoms and treatment of poisoning by irritant gases)
Report of
lectures for division medical gas
officers held in Paris in October, 1918
Report on gas
hospital, Justice Hospital
Group
LIST OF TABLES
1. Admission for gas
poisoning, by
organization, American Expeditionary Forces Absolute numbers and percentages of
total
number
2. Admissions for gas
poisoning, by months of
occurrence, American Expeditionary Forces. Absolute numbers and
percentages of
total number
3. Admissions for gas
poisoning, by gas,
American Expeditionary Forces. Absolute numbers, deaths, and case mortality rates
4. Admissions for gas
poisoning, by gas,
officers and enlisted men, American Expeditionary Forces
5. Deaths from
exposure to gas; by groups and
by months of occurrence
6. Medical and gas
officers' record of the
type of gas to which the fatal cases coming to autopsy had been
exposed
7. Series of fatal
cases coming to autopsy, by
groups, and by the gas believed to have been cause of lesions
found
8. Character of gas
attacks
sustained
9. Duration of life
after gassing, by groups
10. Causes of death
11. Associated
diseases other than those
mentioned in Table 10, as cause of death
12. Principal lesions described
in the autopsy protocols of Groups A and B
13.
Distribution of burns and pigmentation as
described at autopsy, by region and by group
14. Bacteriology of
cases
studied
15. Organisms
isolated in the series of
cases
16 A study of 3,014
gassed cases, American
Expeditionary Forces (1917-18), with a view to determining after-effects.
Numbers
and percentage of the total number of cases of the series and of certain
specific classes for each result. Average percentage of disability in specific
classes
16. A study of 3,015 gassed
cases, American Expeditionary Forces (1917-18), with a view of
determining after-effects. Numbers of percentage of the total numer of
cases of the series and of certain specific classes for each result
Average percentage of disability in specific classes continued
17. Toxicity of
chlorine gas
18. Toxicity of
phosgene
gas
19. Toxicity of
chloropicrin
gas
20. The influence of
chlorine poisoning Upon
the composition of the urine-
21. Chlorine
experiments
22. The influence of
chloropicrin poisoning
upon the composition of the urine
22. The influece of
chloropicrtin poisoning upon the composition of the urine continued
23. Hemoglobin
changes in the blood in
phosgene poisoning
24. The influence of chlorine gassing
upon
the leucocyte count
24. The influence of chlorine
gassing upon the leucocyte count continued
25. Chloride content
of blood plasma and
pulmonary exudate after phosgene gassing
26. Blood volumes in phosgene poisoning
27. Pulmonary
aeration during phosgene
poisoning
28. Irritating
effects of
dichlorethylsulphide applied locally
29. Irritating
effects of
dichlorethylsulplhide applied locally
30. Time of exposure
to vapor tests required
to produce a visible reaction
31. Skin irritation
from local application of
dichlorethylsulphide
32. Effect in
individuals of local
application of dichlorethylsulphide
33. Sensitivity of
negroes to
dichlorethylsulphide
34. Susceptibility of
skin of animals to
dichlorethylsulphide
35. Removal of
dichlorethylsulphide from skin
by washing with kerosene
36. Effects of
evaporation after application
of dichlorethylsulphide
37. Effects of
evaporation after application
of dichlorethylsulphide
38. Effect of
covering dichlorethysulphide
burns
39. Effect of
covering dichlorethylsulphide
burns
40. Effect of
covering exposures of varying
lengths
41. Effect of
covering exposures of varying
lengths
42. Transfer from
skin to skin of
dichlorethylsulphide burns
43. Sensitivity tests
of dichlorethylsulphide
burns
44. Persistence of
gas after
dichlorethylsulphide burns
45. Animals gassed
with cyanogen
chloride
45. Animals
gassed with cyanogen chloride continued
46. Animals gassed
with cyanogen
bromide
47. Toxicity of
diphosgene on dogs
48. Effect on the
respiratory tract of
different concentrations of diphosgene
49. Dogs gassed with
chlorine
50. Dogs gassed with
chlorine
51. Dogs gassed with
phosgene
52. Dogs gassed with
phosgene
53. Degree of
increase in lung weight after
gassing
54. Pulmonary
complications in dogs gassed
with phosgene
55. Dogs gassed with
chloropicrin
56. Dogs gassed with
chloropicrin-percent
showing pneumonia
57. Dogs gassed with
chloropicrin-degree of
edema of lungs
58. Blood changes
following gassing with
arsine
59. Relation of the
edema of lung and the
concentration of blood in gassed animals
60. Animals gassed
with
phosgene
61. Dogs dying of
malnutrition
62. Dogs dying of
chloropicrin
poisoning
63. Mean course of
experimental lesions
64. Effect of
venesection on chlorine
poisoning after standard gassing
65. Effect of
venesection and infusion of
salt solution
66. Influence of
various salt solutions in
the treatment of chlorine poisoning-
67. Treatment of
chlorine
poisoning
68. The influence of
various strengths of
sodium chloride solutions in the treatment of
chlorine poisoning
69. The influence of
the volume of fluid
injected in the treatment of chlorine poisoning
70. The influence of
repeated infusion in the
treatment of chlorine poisoning
71. The influence of
dextrose and acacia
solutions in the treatment of chlorine poisoning
72. The influence of
calcium and other salts
in the treatment of chlorine poisoning
73. Effect of
morphine in treatment of
chlorine poisoning
74. The influence of
subcutaneous injections
of calcium in the treatment of chlorine poisoning
75. Effect of
environmental conditions
(temperature) on the efficacy of the prescribed
treatment
76. The influence of
the element of time of
bleeding in the treatment of phosgene poisoning
77. The influence of
multiple small bleedings
78. Influence of
early infusion (recorded by
percentage)
79. Influence of
early bleeding and delayed
infusion
80. Influence of
various types of treatment
(recorded by percentage)
81. Modified treatment
82. Influence of
water intake upon treatment
83. Effect of
bleeding upon goats gassed with
chloropicrin
84. Effect of
bleeding upon goats gassed with
chloropicrin
85. Chloropicrin
treatment
86. The influence of
oxygen administration
upon the mortality of dogs gassed with phosgene
87. Comparison of
toxicity figures for
phosgene and those obtained by oxygen administration
88. The influence of
oxygen upon gassed dogs
treated by venesection
89.
Influence of
oxygen upon dogs gassed with
sublethal concentrations of phosgene and
treated by venesection
90. The influence of
oxygen upon dogs gassed
with chlorine treated by the standard method
91. The arterial and
venous oxygen content
and percentage saturation breathing air as compared with breathing oxygen
(approximately 50 percent). The capacity of the blood (oxygen-combining
power)
is also given
92. The influence of
oxygen administration
upon the percentage saturation and oxygen content of the blood of dogs gassed
with
phosgene (71 to 80 parts per million) (0.31 to 0.35 mgm. per
liter)
93. The
influence of oxygen administration
upon percentage saturation and oxygen content of the blood of dogs gassed with
phosgene (50 to 60 parts per million) (0.21 to
0.26 mgm. per liter)
94. Comparison of
calculated amounts of fluid
lost from blood and extra fluid in the lungs of
gassed animals
95. Alteration in the
blood count, following
the intravenous injection of dichlorethylsulphide
95. Alteration in the
blood count, following
the intravenous injection of dichlorethylsulphide
continued
95. Alteration in the
blood count, following
the intravenous injection of dichlorethylsulphide continued
95. Alteration
in the
blood count, following
the intravenous injection of dichlorethylsulphide continued
96. Effect of
dimethyltrithiocarbonate upon
animals
97. Pathological
report
97. Pathological
report continued
LIST OF
CHARTS
I. Factory protection
section, Gas Defense
Service, Surgeon General's Office
II. Medical Division,
Chemical Warfare
Service, July, 1918
III. Gas Service
organization, American
Expeditionary Forces
IV. The Medical
Department in the
organization for gas defense, training research and treatment, American
Expeditionary Forces
V. Organization chart
of Hanlon Field
(experimental gas field), American Expeditionary Forces, November 23, 1918
VI. Changes in total
solids of blood after
phosgene gassing, showing characteristic differences in the three gas
concentrations selected
VII. Changes
in total solids of blood, after
phosgene gassing, showing characteristic differences in the dogs that
died
acutely and those that survived the acute period
VIII. Comparison of
the changes in total
blood solids of dogs gassed with phosgene and those gassed
with chlorine
IX. Comparison
of total solids and
hemoglobin after chloropicrin gassing
X. Comparison of the
characteristic changes
of blood solids induced by chlorine,
phosgene, and chloropicrin
gases
XI. Comparison of
erythrocytes and hemoglobin
content of blood after chlorine gassing
XII. Comparison of
erythrocytes and
hemoglobin content of blood after chloropicrin gassing
XIII.
Changes in the chlorides
and total
solids of the lungs
after phosgene gassing
XIV. Changes in the
total solids of the blood
and lungs after phosgene gassing
XV. Water content of
lung tissue after
chloropicrin and phosgene gassing
XVI. Relation between
the changes of plasma
chlorides and lung solids after phosgene
gassing
XVII. Changes in the
chlorides of lung
tissues and blood plasma after phosgene gassing
XVIII. General
changes in the oxygen capacity
and content of the blood after phosgene gassing
XIX. Composite curve,
from 10 experiments, of
the changes in arterial blood pressure
after acute phosgene gassing
XX. Arterial blood
pressure record from a
case of acute phosgene poisoning
XXI. Composite curve,
from 14 experiments, of
the changes in the
heart rate after acute phosgene gassing
XXII. Composite curve
from 16 experiments, of
the changes in hemoglobin concentration after acute phosgene
gassing
XXIII.
Composite curve, from 9 experiments,
of the changes in the red blood
cell counts after acute phosgene gassing
XXIV. Duration of
life after chlorine
gassing
XXV. Duration of life
after phosgene
poisoning
XXVI. Degree of
pulmonary edema after
phosgene gassing, as determined by lung-heart and lung-body ratios
XXVII. Duration of
life after chloropicrin
gassing
XXVIII. Comparison of
the degree of pulmonary
edema and concentration
of the blood in gassed animals. Cross-hatched
columns represent percentage of increase in lung weight and are
arranged
in order. Solid black columns represent percentage of increase
in
red blood corpuscles. This chart clearly shows that there is no
relationship between the two
XXIX. Changes in
hemoglobin of the blood
after gassing with chloropicrin, 1 to 8,500, for 25 minutes. Solid
line, animals receiving extra oxygen; broken line, control animals
XXX. Changes in
hemoglobin of the blood after
gassing with chloropicrin,
1 to 8,500, for 30 minutes. Solid
line, animal
receiving extra oxygen; broken line, control animal
XXXI. Changes in
hemoglobin of the blood
after gassing with chloropicrin, 1 to 8,500, for 25 minutes. Solid line,
animals
receiving extra oxygen; broken line, control animals
XXXII. Rabbit No. 12,
serial No. 97, and
rabbit No. 13, serial No. 55 leucocyte counts, showing fluctuations due to
experimental changes of outside temperature. Counts plotted by
hour of day, space after each date representing 24 hours
XXXIII. Rabbit No.
20, serial No. 96
XXXIV. Rabbit No. 23,
serial No. 141, and
rabbit No. 24,
serial No. 104
XXXV. Rabbit No. 25,
serial No. 168
XXXVI. Rabbit No. 26,
serial No. 174
XXXVII. Rabbit No.
27, serial No. 177
LIST OF PLATES
I. Mustard-gas
inhalation. Diphtheritic
inflammation, with
formation of false membrane, upper respiratory tract
II. Mustard-gas burns
of external genitals,
with vesiculation and pigmentation
III. Experimental
mustard-gas burns (negro),
612 hours. Early
vesicle formation.
Absence of inflammatory reaction
IV. Experimental
mustard-gas burns (negro),
24 hours. Vesicle
formation, with necrosis of overlying epidermis, and
inflammatory reaction at margin of vesicle
V. Case 86.
Mustard-gas burn of scrotum, 18
days duration. Hyperkeratosis, hyperpigmentation, with irregular
distribution of pigment, chromatophores in corium
VI. Case 6. Mustard
gas, 2 days. Lung
VII. Mustard-gas burn
(contact) of neck
VIII. Mustard-gas
burns of body
IX. Case 24. Mustard
gas, 5 days. Section
through wall of small bronchus, showing false membrane replacing the
necrotic
epithelium, hemorrhage into adjacent alveoli, and
fibrinous exudate into
the alveoli external to the zone of hemorrhage
X. Gross changes in
larynx of a soldier who
died four days after inhalation mustard gas
XI. Heart and lungs
of dog dying 24 hours
after phosgene gassing. Light
colored patches of emphysema alternate with deep
red
congested and partially collapsed areas in the voluminous lung. Heart is
dilated, particularly the right side
XII. Lungs of dog
killed 14 days after
phosgene gassing. There
is marked emphysema with irregular patches of atelectasis. Microscopically a
widespread obliterative
bronchiolitis is present
XIII. Multiple
hemorrhages in wall of
bronchus of dog killed 6 days after exposure to chloropicrin
XIV. Higher
magnification of bronchus shown
in Plate XIII. Note
particularly the flattened character of the regenerating bronchial epithelium. A mitotic figure is seen on the left
XV. Pneumonia
complicated by multiple abscess
formation and pleurisy 5 days after exposure to
dichlorethylarsine. Only one lobe
is consolidated; others are relatively emphysematous
LIST OF FIGURES
1. Plan of mobile
degassing station
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
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
4. Case 8.
Mustard-gas burn of skin, of 2
days' duration. Necrosis of epidermis with beginning of intra-epidermal
vesicle
formation
5. Case 89.
Mustard-gas burn of 20 days'
duration. Regeneration of new epithelium beneath crust of necrotic
original
epithelium. Hyperemia. Absence of inflammatory reaction
6. Case 18.
Mustard-gas burn of 5 to 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
7. Case 18. Another
section, showing
condition similar to that seen in Figure 6
8. Mustard-gas
poisoning. False membrane
extending from epiglottis through entire trachea into bronchi
9. Diphtheritic
necrosis of mucosa of upper
respiratory tract after mustard-gas inhalation
10. Diphtheritic
necrosis of mucosa of upper
respiratory tract after mustard-gas inhalation
11.
Diphtheritic necrosis of upper
respiratory tract after mustard-gas
inhalation
12. Mustard-gas burn.
Deep-seated necrosis of
bronchial mucosa
13. Case22.
Mustard-gas burn,5 days'
duration. Deep necrosis of trachea mucosa
14.Case 21. Mustard-gas burn, 5 days'
duration.
Necrosis and exfoliation of tracheal epithelium, exposing basement
membrane. Fibrinous edema of submucosa
15. Case 61.
Mustard-gas burn, 9 days'
duration. Epithelial regeneration of trachea, proceeding from the mucous ducts
16. Case 41.
Mustard-gas burn, 7 days'
duration. Metaplasia of tracheal epithelium into squamous cell type. Numerous
mitoses
17. Case 24.
Mustard-gas burn, 5 days'
duration. Between the false membrane and the congested subepithelial tissue,
are
interposed hydropic epithelial cells of the
squamous type
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
19. Case 86.
Mustard-gas burn, 18 days'
duration. Bronchus. Proliferation of epithelium of ducts of mucous glands
20. Case 28.
Mustard-gas burn, 4 to 5 days'
duration. Lung. Intense congestion, hemorrhagic edema, aplastic exudate. The
leucocytes are filled with minute Gram-negative
bacilli
21. Case 103.
Mustard-gas burn, 58 days'
duration. Lung. Organizing and interstitial pneumonia
22. Case 81.
Mustard-gas burn, 15 days'
duration. Lung. Dilatation of atria, with hyaline necrosis
23. Case 22.
Mustard-gas burn, 5 days'
duration. Lung. Pneumonia with necrosis of alveolar walls and nuclear
fragmentation
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 contains plugs of dense fibrin undergoing early organization
25. Case 100. Death,
51 days after exposure
to mixed vesicant and suffocant gases. Section through dilated bronchiole,
containing a vascular organized plug
26. Case 74.
Mustard-gas burn, 12 days'
duration. Lung. Proliferation of alveolar epithelium over a mass of fibrin
and
agglomerated red-blood corpuscles
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
28. Case 16.
Mustard-gas burn, 4 days'
duration. Trachea. Low-power view, showing laminated false membrane
attached to
openings to mucous ducts
29. Case 25. Yellow,
blue,
and green cross
shell, exposure 5 or 6 days before death. Dilated bronchiole lined with laminated
fibrinopurulent membrane. Complete
loss of epithelium
30. Case 47.
Mustard-gas burn, 8 days'
duration. Longitudinal section of bronchiole, completely occluded by
fibrinopurulent exudate. A few shreds of epithelium
are still present
31. Case 61.
Mustard-gas burn, 9 days'
duration. Pharynx. Localized superficial
necrosis of epithelium with
inflammatory reaction
32. Case 67.
Mustard-gas burn, 9 days'
duration. Section through bronchus, showing regeneration of metaplastic
epithelium, fibroblastic thickening of bronchial wall, epithelial
proliferation,
edema, of adjacent alveoli
33. Case 75. Death,
probably 10 to 12 days
after exposure to mixed gases. Bronchiectases filled with purulent exudate.
Peribronchial and periarterial edema and beginning fibrosis
34. Case 88.
Exposure to yellow, blue, and
green cross shell gas. Death after 20 days. Lung. Section passes through
interlobular septum, which is edematous and in which there is active growth of
fibroblasts, and plasma cell infiltration. There are organizing plugs in the septal
lymphatics
35. Case 89.
Mustard-gas burn, 20 days'
duration. Lung. Area of bacterial necrosis with fibrinopurulent material
in the
adjacent alveoli
36. Same as Figure
35. Larger area of
gangrene in lung
37. Case 94. Death, 26 days
after exposure to mixture of
suffocant and vesicant gases. Obliterative bronchiolitis
38. Case 103.
Mustard-gas burn, 58 days'
duration. Lung. Low-power drawing through
bronchiectatic cavity.
Peribronchial
and periarterial fibrosis
39. Case 106.
Mustard-gas burn, 512 months'
duration. Lung, showing marked peribronchial and perivascular fibrosis,
interstitial fibrosis, organizing pneumonia, chronic edema, bronchiectasis
40. Case 106. Lung.
Section a. Edema of
alveoli and interlobular septum
41. Case 106. Lung.
Section b, through cavity
in the upper lobe
42. Case 106. Lung.
Section c. Taken from
opaque whitish tissue in anterior portion of upper lobe. Lung structures
over
large areas obliterated by poorly vascularized granulation tissue, densely
infiltrated with plasma cells
43. Case 106. Lung.
Section d,
through thickened bronchi at hilum of lower lobe
44. Case 107. Late
stricture of trachea
following mustard-gas inhalation
45. Superimposed
outlines of three X-ray
photographs taken at intervals during phosgene poisoning to show changes in
shape
of the heart. The solid line indicates the normal. The dotted line
shows
the right-sided dilatation 39
minutes after gassing. The broken line
is
from a photograph taken 11 hours and 53 minutes after exposure to the
gas. The
heart had then become pendular in shape and
much reduced in
size
46. Diagram of dog's
respiratory tract viewed
from behind. The interlobular fissures and the accessory caudate lobe are
well
shown
47. Diagram of
bronchial tree of dog showing
bronchi of first, second, and third order (A, B, C) and infundibula (D)
48. Normal bronchus.
Bronchiolar termination
in a dog's lung, showing transition from high ciliated epithelium of bronchi
to
the flattened epithielium of the infundibular
49. Bronchus plugged
with sloughs of "cooked"
epithelial lining. The cytoplasm of the cells is quite homogeneous and
hyalinized
50. Higher
magnification of necrotic lining
shown in Figure 49
51. Multiple areas of
focal necrosis in lung
of dog dying 20 hours after chlorine gassing
52. Higher
magnification of an area of focal
necrosis such as is shown in Figure 51. Death occurred 6 hours after gassing.
The
alveolar walls about an atrium are completely hyalinized and stain
deeply
with eosin
53. Marked
perivascular edema in acute death
from chlorine. The lymphatic channels of the adventitia are widely
distended with
fluid
54.
The cells of the
exudate are chiefly
polynuclears which accumulated in and about
an atrium
55. Organizing
bronchiolitis 5 days after
chlorine gassing. Lumen of bronchus is filled with a network of fibroblasts and
there is a similar organizing process going on in the adjacent pulmonary
alveoli. In the bronchial and
alveolar walls there is much old hyalinized
fibrin
56. Purulent
bronchitis in a dog dying 23
days after exposure to chlorine. The cells in the bronchi are chiefly
Polynuclears, but in the adjacent alveoli are many large mononuclear cells
57.
Obliterating bronchiolitis in a dog
killed 32 days after chlorine gassing. The main bronchus has a normal, probably
regenerated epithelial lining. The small tributary bronchus is occluded by
an
organized mass of tissue adherent
to the wall in places
58. Chronic
bronchitis and patchy emphysema
in a dog dying 58 days after chlorine gassing
59. Bronchiectatic
cavities in lung of dog
dying 39 days after chlorine gassing. The lung tissue supplied by these
bronchi is
completely atelectatic
60. Sloughing of
bronchial epithelium in dog
killed 3 hours after exposure to chlorine
61. Acute necrotizing bronchitis 10
hours
after chlorine gassing. There is complete sloughing of mucosa and a diffuse
inflammatory reaction throughout the bronchial wall. Note the marked edema of
tissue surrounding a large peribronchial
vessel
62. Regeneration of bronchial epithelium
4
days after chlorine gassing. One mitotic figure is
seen
63. Low magnification
of lung of dog dying 2
months after exposure to chlorine. Chronic bronchitis and bronchiectasis
with
atelectasis and occasional patches of
emphysema
64. Higher magnification
of one of the
bronchi shown in Figure 63. Bronchus is moderately dilated. Adjacent lung tissue
is
atelectatic
65. Higher
magnification of two bronchi shown
in Figure 63. Lumina are filled with a cellular inflammatory exudate. There
is
also a chronic peribronchial reaction
66. Lung of dog dying
2 days after exposure
to phosgene. Fibrin stain shows a heavy deposit along the alveolar walls,
outlining
them everywhere quite distinctly
67. Higher
magnification of an area shown in
Figure 66. In places the fibrin strands extend across the septa
68. Early
inflammatory reaction about
bronchiole 18 hours after phosgene gassing. Cells are chiefly polynuclears. There is
a
generalized edema of the lung tissue
69. Broncho pneumonia
causing death 7 days
after exposure to phosgene. The bronchial wall is necrotic and there is
considerable hemorrhage in the pneumonic
exudate. Lung is moderately
edematous
70. Early stage of
organization of pulmonary
exudate 4 days after phosgene gassing
71. Higher
magnification of bronchial wall
shown in Figure 70. Fibroblasts are seen extending in a loose growth from the
submucosa. One mitotic figure is present
72. Organizing
bronchiolitis in a dog killed
14 days after phosgene gassing. The lung grossly showed irregular patches of
emphysema and atelectasis, and tuberclelike nodules were felt
throughout the
lung
73. Higher
magnification of two bronchi shown
in Figure 72. The peribronchial thickening and the polypoid growths in
the
lumina are well shown
74. Necrosis of
bronchial epithelium and
subepithelial edema in acute death from chloropicrin
gassing
75. Widespread edema
of lung associated with
acute death from chloropicrin. Note occasional clear spaces (air bubbles) in
some
of the alveoli
76. Acute bronchitis
and bronchopneumonia
causing death 3 days after exposure to chloropicrin. The lung tissue
separating
the pneumonic patches is markedly edematous
77. Lung of
"recovered" dog killed 4 days
after chloropicrin gassing. In alveoli surrounding the bronchioles there are
structures resembling giant cells. As shown in Figure 78, the structures are
composed of fused mononuclear cells
inclosing hits of old fibrin and
degenerated
red cells
78. Higher
magnification of an alveolus from
Figure 77, showing the structure of phagocytic giant cells. Note their
resemblance to capillaries
79. Organizing
bronchiolitis in a dog killed
2 months after exposure to cyanogen bromide. The character of the cells
taking
part in the organization is well shown. The bronchiole has been partially
relined by an epithelium of irregular form but
mostly of the flattened type
80. Widespread edema
of lung in acute death
from dichlorethylarsine. The clear round spaces indicate the presence of
air
bubbles
81. Necrotization of
the bronchial lining
associated with acute death from dichlorethylarsine. A few air bubbles are seen
in
the exudate filling the lumen
82. Marked
perivascular edema and dilatation
of lymphatics in acute dichlorethylarsine
gassing
83. Ulceration of
cornea following exposure
to dichmlorethylarsine. Perforation of the cornea has taken place, with
infection of
the anterior chamber
84.
Blister formation in
epiglottis in a clog
dying acutely from exposure to dichlorethylarsine. The epidermis is severely
damaged and there is a widespread inflammatory
reaction in the tissues
beneath
85. A higher
magnification of one of the
blisters shown in Figure 84. The fluid of the bleb is rich in fibrin, which stains
deeply
86. Complete necrosis
of the mucosa of a
large bronchus, resulting from dichlorethylarsine gassing. There is a marked
inflammatory reaction throughout the wall of
the bronchus
87. Thick layer of
fibrin along the alveolar
wall 7 days after phosgene poisoning
88. Hemorrhage into a
perivascular sheath of
a pulmonary vessel in a dog dying 10 days after phosgene gassing
89. Necrosis of
bronchial epithelium with
acute inflammatory reaction 24 hours after chlorine gassing
90. Wall of small
bronchus showing
mucosa entirely destroyed by phosgene and a large bronchus of same animal with
uninjured
mucosa
91. A comparison of
the injury to the
tracheal mucosa by chloropicrin, phosgene, and chlorine. A, Chloropicrin, with damaged
but
intact epithelium; B, chloropicrin with sloughing of superficial epithelial
layer; C, phosgene, with undamaged mucosa; D,
chlorine, with killed and
exfoliated
mucosa
92. Mustard-gas
lesion at 1 hour
93. Mustard-gas
lesion at 3 hours
94. Mustard-gas
lesion at 18 hours
95. Mustard-gas
lesion at 22 hours
96. Mustard-gas
lesion at 46 hours
97. Mustard-gas
lesion at 72 hours
98. Mustard-gas
lesion at 4 days
99. Mustard-gas
lesion at 9
days
100. Mustard-gas
lesion at 18 days
101. Mustard-gas
lesion at 20 days
102. Mustard-gas
lesion at 49 days
103. Typical
mustard-gas vesicle about 20
hours after application
104. Lesion of human
skin one-half hour after
application of mustard gas
105. Human skin, 18
hours after application
of mustard gas, Transition between slightly damaged epitheliurn and
epithelium
showing hydropic degeneration. Early
blister formation
106. Human skin 18
hours after application of
mustard gas. Early vesicle formation
107. Human skin 18
hours after application of
mustard gas. High-power view of hydropic change, with early vesicle
formation
108. Human skin 18
hours after application of
mustard gas. High-power view of small
vesicle. Separation of epidermis
from
papillary layer
109. Human skin 36
hours after application of
mustard gas. Vesicle formation in epidermis and leucocyte infiltration of
papillae
110. Human skin 36
hours after application of
mustard gas. High-power view at border of lesion showing changes in
epidermis
and leucocyte infiltration and edema of papillary layer
111. Droplet lesion
of mustard gas on human
skin 7 days after application. Low- power view showing area of necrosis of
epidermis and upper portion of corium, with intense hyperemia of the
surrounding
vessels. Moderate edema and very little small-celled infiltration
112. Rabbit.
Application of mustard gas at
11.30 a. m. Droplet used was slightly larger than the standard. Marked
subcutaneous
edema as seen at 4 p. m. on the same day
113. Rabbit. Skin of
belly shows results of
four applications of standard drops of mustard gas. Above two areas of typical
edema; the one on the rabbit's right untreated, the one to the left washed
off in
5 minutes by water. The latter is more diffuse, larger in area, but less
intense. Below, on the rabbit's right, an area washed after 5 minutes with soap
containing an excess of free alkali. This area shows the least reaction. On the
lower
left is an area treated, after 5 minutes, with potassinm permanganate. The
reaction here is most marked
114. Rabbit. Two areas of
mustard-gas
application. Advanced eschar formation.
115. Rabbit.
Low-power view of mustard-gas
lesion in rabbit 2 hours after application. Extreme
subcutaneous edema.
Epidermis
but slightly changed.
116. Guinea pig.
Low-power view of
mustard-gas lesion 5 ½ hours after application. Extreme subcutaneous edema. Epidermis
necrosed in center of lesion
117. Rabbit. Border
of lesion 2 hours after
application of mustard gas. To the right of the middle, the epidermis is still
living;
to the left nearly completely necrosed, necrosis extending into the
upper
portion of the corium. Early edema
118. Rabbit. Two
hours after application of
mustard gas. Changes in epidermis and corium. Marked vascular change, with
beginning migration of leucocytes.Small hemorrhages by diapedesis. Early
edema
119. Guinea pig 5
½hours after application
of mustard gas to skin of abdomen. Deep
subcutaneous edema
120. Rabbit. Six days
after application of
mustard gas. Treatment with zinc oxide paste 5 minutes after use of
mustard
gas. Center of lesion, complete necrosis of epidermis, hair follicles,
and
upper portion of corium, extending even to the sweat glands. No reaction
121. Rabbit. Six days
after application of
mustard gas. Treatment with zinc ointment 5 minutes after application.
There
was no edema stage. Epidermis is dead, and there is a moderate
inflammatory
reaction in the corium. Reaction much less intense than in control
122. Rabbit. Six days
after application of
mustard gas. Treatment after 5 minutes with 2 percent solution of silver
nitrate
and 5 percent lead acetate. Primary edema was nearly completely controlled,
but
necrosis, 6 days later, is marked, extending
deep into the corium, with
more
rapid separation of the slough
123. Rabbit.
Periphery of same lesion as
Figure 122. Area of less damage
124. Rabbit. Six days
after application of
mustard gas, untreated. Border of lesion. Necrosis less marked. Beginning
repair
125. Rabbit. Six days
after application of
mustard gas, untreated. Intermediate zone. Separation of necrotic epidermis
and
papillary layer, with infiltration of leucocytes into the necrotic tissue.
Fibroblastic proliferation in lower part of
dermis, with regeneration of hair
follicles.
Intense congestion of subcutaneous vessels
126. Rabbit. Six days
after application,
untreated. Adherent slough, representing the necrotic epidermis and upper portion
of
the corium, involving the hair follicles
127. Section of skin
of penis, 8 days after
exposure to strong concentration of mustard-gas
vapor. Intense hyperemia
128. Section of skin
of scrotum, from same
individual as in Figure 127. Necrosis of epidermis; intense hyperemia
129. Human skin 1
week after exposure to
strong concentration of mustard-gas vapor. Microscopically, the changes
consist
of increased cornification, pycnosis of the cells of the epidermis,
and
necrosis of the papillary layer of the
corium. The only living cells in the
upper
portion of the corium are pigmented chromatophores
130. Human skin 1
week after exposure to
strong concentration of mustard-gas vapor. Edge of large vesicle showing the
necrosis of the upper portion of the corium, congestion of vessels, and
separation
of the epidermis
131. Section
of skin from same case as Figure
130. Area of collapsed vesicles; necrosis of epidermis and corium;
congestion
of vessels
132. Skin from axilla
of same patient as
Figure 130. Necrosis of skin to the depth of the large sweat glands. These show
also
partial necrosis, with some early regeneration
133 Infected
gangrenous area from skin of
back
134. Section of
corium from skin of same
patient as Figure 130, showing dlilated lymphatics filled with fibrin thrombi,
in the
lower portion of the corium.Some of these lymphatics contain
partially
hemolyzed red blood cells in small numbers
135. Microscopic
section of eschar 4 weeks
after exposure. Areas of regenerating epithelium from the sweat glands
136. Microscopic
appearance mustard-gas
decubitus 4 weeks after exposure. Destruction of tissue too great for
regeneration.
Necrosis extends below the level of the sweat glands
137. Photomicrograph
of regenerating
epidermis under the wet Dakin and saline method of treatment, 4 weeks after
injury.
Note the regeneration of the epithelium from the remains of the hair
follicles and sweat glands
138. Completely
healed mustard-gas lesion 4
weeks after injury treated 12 days with grease method, with increasing infection
and
gangrene. Under the wet Dakin and saline method infection was checked
promptly and healing begun. Regeneration of epidermis from hair
follicles
and sweat glands
139. Photograph taken
1 week after 40
minutes' exposure to strong concentration of mustard-gas vapor. Treated with grease
method
during this time, with increasing infection and gangrene of
epidermis.
Change of treatment to the wet Dakin saline method effected prompt
healing
140. Diffuse erythema
of the skin due to
exposure for 10 to 12 minutes to strong concentration of mustard gas. Treated 1
week
by the grease method, with increasing infection of the dead skin,
particularly around the genitals and
anus. Change of treatment to the wet
Dakin
and saline methods resulted in prompt healing
141. Rear view of
same patient shown in
Figure 140
142. Acute urethritis
and phimosis due to
mustard gas. One week after exposure
143. Buttocks of same
patient as Figure 142
144. Photograph 1
week after one-half hour
exposure to strong concentration of mustard gas. During this time treated by
the
grease method. Photograph shows very well the protection afforded
by
the tight belt. The more marked
lesions in the axillae, bends of the
elbows,
and genitals, and the large flaky character of the primary desquamation
and the
pigmentation are well shown
145. Back of patient
shown in Figure 144
146. Diagram
illustrating the distribution of
mustard-gas eschars, 4 weeks after exposure to strong concentration of
mustard
gas. The hatched areas represent the lesions
147. Mustard-gas
lesions of back at 1 week
148. Skin lesions of
mustard gassing 1 week
after exposure
149. Twenty-four
hours after direct
application of standard droplet of dichlorethylsulphide to cornea of right eye. Marked
edema
of lids and surrounding subcutaneous
tissue
150. Twenty-four
hours after direct
application of standard droplet of dichlorethysulphide to cornea. Marked edema of
lids,
flecks of purulent exudate. The marked congestion of the conjunctival
vessels
is best seen in the bulging edematous mass of the superior palpebral
conjunctiva
151. Twenty-four
hours after direct
application of standard droplet of crude mustard-gas liquid to the cornea. Extreme edema
of
conjunctiva, especially marked in upper lid and nictitating membrane.
Seropurulent exudate
152. One week after
direct application of
standard droplet of dichlorethylsulphide to the cornea. Lids still somewhat
edematous.
They were sealed by a marked purulent exudate which adheres along the
lid
margins and to the adjacent hair. A marked purulent rhinitis,
referable
to involvement of the mucosa through the nasolacrymal duct, is evident
153. Two weeks after
direct application of
standard droplet of dichlorethylsulphide to the cornea. Marked reduction of
edema.
Much less purulent exudate. Indurated lids exhibit the
characteristic
"ruffling" and partial entropion of the upper lid in the later stage and the
smooth ectropion of the lower lid. The lower half of the cornea shows a marked
clouding
154. Two weeks after
direct application of
standard droplet of dichlorethylsulphide to the cornea. Marked depilation about
the
eye. Characteristic "ruffling' and entropion of upper lid and marked
ectropion of lower lid. The corneal cloudiness and lack of luster are very
apparent, likewise the staphyloma in the lower half of the anterior quadrant
155. Two weeks after
direct application of
standard droplet of dichlorethylsulphide to cornea. Specimen obtained by excision
of
lids and orbital evisceration. Marked depilation especially at the
inner
canthus. Characteristic "ruffling" and entropion of upper lid. Corneal
cloudiness
156. Three weeks
after direct application of
standard droplet of dichlorethylsulplhide to center of cornea. Same rabbit as
Figure
154. Marked ectropion of lower lid. Porcelainlike cloudiness of the
cornea
most marked in the lower half
157. Three weeks
after direct application of
standard droplet of dichlorethylsulphide to cornea. Specimen obtained by excision
of
lids and evisceration of orbit. Anterior segment of globe in profile to
show
apparent staphyloma of cornea toward the inner canthus. The corneal
cloudiness is well shown
158. Rabbit's eye at
4 weeks after direct
application of standard droplet of dichlorethylsulphide to cornea
159. Six weeks after
direct application of
standard droplet of dichlorethylsulphlide to cornea. Combined ectropion and entropion
of upper lid with resulting "ruffling" of lid margin. Ectropion of
lower
lid. Organization of the necrotic cornea with extensive arborizations of
newly
formed blood vessels, best seen in the upper half of the cornea. Even in
the
photographs these can be traced from the sclera across the superior arc
of
the limbus to the central portion of the cornea. The same eye is shown in
Figures
160 and 161
160. Enlargement of
Figure 159, to show
details of changes
161. Seven weeks
after direct application of
standard droplet of dichlorethylsulphide to cornea. Same eye as in Figure 159.
Here
given in profile to show marked irregularity of covered surface. Note
especially the prominent apparent staphyloma in the selera toward the
inner
canthus
162. Five weeks after
direct application of
dichlorethylsulphide to cornea. Dosage about twice the size of the standard
droplet.
Lids not separated. Eye untreated. Resulting panophthalmitis,
with
collapse of eyeball
163. Cornea 2 hours
after application of
standard droplet of dichlorethylsulphide. First stage of necrosis of corneal
epithelium
and of the cells of the interstitial substance. Marked pycnosis of the
corneal
epithelium, the cells of the lowest layer alone being barely
distinguishable. The
nuclei of the interstitial substance and of the endothelial lining of
the
anterior chamber are also pycnotic. Section taken at corneal vertex
164. Section of
cornea at vertex 5 hours
after direct application of standard droplet of dichlorethylsulphide. Desquamation of
necrotic epithelium in center of vertex. Pycnosis of remaining epithelium
and
of cells of the interstitial substance.
Complete necrosis of endothelial
cells of anterior chamber
165. Section of
palpebral conjuntiva 8 hours
after application of standard droplet of dichlorethylsulphide. Complete necrosis
of
epithelium. Marked congestion. Minute hemorrhages. Polynuclear
infiltration
166. Palpebral
conjunctiva 26 hours after
application of standard droplet of dichlorethylsulphide, showing advancing
necrosis,
more marked infiltration, congestion, minute hemorrhages, and edema
167. Cornea 30 hours
after exposure to vapor
of dichlorethylsulphide. Complete necrosis of cornea
168. Palpebral
conjunctiva 34 hours after
application of standard droplet of dichlorethylsulphide. Section at fornix of upper
lid, showing the complete loss of the necrotic surface, extreme edema, and
polynuclear infiltration
169. Section from the
same region as in
Figure 168, but taken deeper down, showing the extreme edema and liquefaction
necrosis,
below the narrow band of the sphincter orbicularis
170. Cornea 42 hours
after application of
standard droplet of dichlorethylsulphide. Membrane of Descemet appears as a bright
hyaline line staining red with eosin
171. Cornea 3 ½ days
after application of
standard droplet of dichlorethylsulphide. Complete necrosis of corneal tissue;
ulceration of surface; beginning infiltration with polynuclear leucocytes and
collection of
polynuclear leucocytes along the line of the necrotic endothelium
172. Section of
sclerocorneal junction 3½
days after application of standard droplet of dichlorethylsulphide. Infiltration of
leucocytes, beginning fibroblastic and angioblastic proliferation
173. Section of upper
lid at palpebral margin
4 days after direct application of standard droplet of
dichlorethylsulphide.
Advanced ulceration, beginning repair
174. Section of same
lid, near fornix.
Regeneration of the conjunctival epithelium. Disappearance of the edema and advancing
cicatrization of the subconjunctival
tissues
175. Section of
corneal vertex 7 days after
application of standard droplet of dichlorethylsulphide. Ulcerated surface.
Infiltration of necrotic cornea with polynuclears and scattered fibroblasts.
Beginning regeneration of endothelium
176. Section of
corneal vertex 4 weeks after
application of standard droplet of dichlorethylsulphide, showing the marked
irregularities in the corneal surface; regeneration of corneal epithelium and
endothelium of anterior chamber;
edema of the interstitial substance with
some
fibroblastic repair
177. Sclerocorneal
junction of same eye as in
Figure 176, 4 weeks after application of standard droplet of
dichlorethylsulphide,
showing vascularization and repair proceeding from the sclera
178. Section of
corneal limbus 4 weeks after
application of standard droplet of dichlorethylsulphide. Advancing repair into the
cornea from the sclerocorneal junction
179. Section from the
inferior portion of the
cornea 7 weeks after application of the standard droplet of
dichlorethylsulphide.
Persistent ulcer; marked polynuclear infiltration of the cornea, and
repair.
Blood vessels have reached the
center of the cornea
180. Section from the
inferior portion of
corneal limbus, 7 weeks after application of standard droplet of
dichlorethylsulphide.
Partial regeneration of corneal epithelium. Marked polynuclear
infiltration
and advanced vascularization and repair of the substantia propria.
Regeneration of the endothelium of the anterior
chamber
181. Section from the
superior half of the
corneal vertex 7 weeks after application of standard droplet of
dichlorethylsulphide,
showing the greater degree of cicatrization usually found in this portion
182. Section of
corneal limbus from same eye
as Figure 181, showing advanced cicatrization
183. Ciliary body
from eye of rabbit exposed
12 hours in gassing chamber to a concentration of 1 to 50,000
dichlorethylsulphide
vapor. Animal died 92 hours later. Marked collection of polynuclear
leucocytes in anterior chamber, in the ciliary body, and in the iris of the
left
eye, which had received no treatment with the dichloramine-T solution
184. Iris of same eye
in Figure 183 showing congestion, edema, and polynuclear infiltration.
Marked polynuclear exudate in
the anterior chamber
185. Congestion of
the conjunctival vessels
persisting to a marked degree, 4 weeks after exposure to dichlorethlysulphide
vapor
186. Persistent
congestion 4 weeks after
exposure to dichlorethylsulphide vapor. Acute symptoms were very severe and the
patient still complained of dimness of vision when he left the hospital
after 5
weeks
187. Marked
conjunctival congestion and
hordeolum of left upper lid in a case of severe mustard-gas conjunctivitis, 4
weeks
after exposure. The hordeolum is a part of the general staphylococcus
furunculosis which may characterize the later stages of the severe skin burns
188.
Dichlorethylsulphide conjunctivitis 4
weeks after exposure to vapor. In the acute stage there was extreme
photophobia,
lacrymation, pain, edema, and purulent exudation. The residual
congestion
and seropurulent exudation are still evident
189.
Dichlorethylsulphide conjunctivitis 4
weeks after exposure to vapor. The severity of the original process is indicated by
the
severe skin changes. The persistent congestion is the sole evidence of the
severe
conjunctivitis that was present
190. Experimental
gassing apparatus.
Pathological laboratory, University of Michigan. A, washer containing sulphuric
acid; B, gas container; C, gassing box; D and E, degassing bottles; F,
standard
gas meter; G, suction pump
191. Rabbit. Exposed
40 minutes to a I to
110,000 concentration of dichlorethylsulphide vapor. Killed 12 hours after
removal
from gassing chamber. Section of lung. Marked congestion, edema,
and
areas of partial atelectasis alternating with those of emphysema
192. Exposed 20
minutes to a concentration of
1 to 15,000 dichlorethylsulphide vapor. Killed 36 hours after gassing. Section
of
trachea showing acute catarrhal desquamative tracheitis; marked mucoid
degeneration of the epithelium; congestion and edema of the submucosa.
Lumen
filled with mucous containing many desquamated cells
193. Rabbit. Exposed
30 minutes to a
concentration of 1 to 15,000 dichlorethylsulphide vapor. Killed 4 ¼ days after
gassing.
Section of larger bronchus, showing lumen filled with edema fluid.
Bronchial epithelium shows marked
mucoid and hydropic degeneration
194. Lung of same
rabbit as Figure 193. Acute
congestion and edema
195. Section of
laryngeal mucosa of rabbit.
Exposed 35 minutes to a concentration of 1 to 30,000 dichlorethylsulphide
vapor.
Killed 30 hours after gassing. Pycnosis and mucoid degeneration of the
epithelium. Marked congestion and- edema of the submucosa
196. Section of
tracheal wall of same rabbit
as Figure 195. Similar changes in epithelium and submucosa
197. Exposed 6 hours
to a concentration of 1
to 50,000 dichlorethylsulphide vapor. Died 60 hours after gassing. Section of
large
bronchus showing purulent necrotic
bronchitis
198. Section of lung
from same case as Figure
197. Area of purulent bronchopneumonia, with colony of cocci in the
center of
the field
199. Rabbit. Exposed
for 6 hours to a
concentration of 1 to 50,000 dichlorethylsulphide vapor. Died 7 days after
gassing.
Eschar from upper portion of larynx
200. Same rabbit as
in Figure 199. Section of
larynx showing diphtheritic ulcer
201. Mustard-gas
lesions of tongue, pharynx,
larynx, and trachea, in fatal human case. Dorsum of tongue shows
diphtheritic
eschars. Diphtheritic necrosis of pharynx, mucosa of larynx, and
trachea.
Marked edema, with diphtheritic
necrosis of the arytenoepiglottidean fold
202. Case I. Private
Ha. Mustard-gas lesion
of dorsum of tongue. Base of ulcer from which the diphtheritic membrane has
become detached
203. Case I. Private
Ha. Section of
diphtheritic lesion on vocal cord. Epithelium of mucosa completely destroyed and a
mucofibrinous membrane partly detached from the surface. Extreme
hyperemia of
the vessels. Some small-celled
infiltration
204. Case I. Private
Ha. Section of main
division of bronchus. Picture of catarrhal bronchitis. Marked mucoid
degeneration and vacuolation of the bronchial epithelium. Congestion,
small-celled infiltration, and edema of
the bronchial
wall
205. Case I. Private
Ha. Section of upper
lobe of lung. Congestion and edema. Acute emphysema
206. Case I. Private
Ha. Section of lower
lobe of lung. More intense congestion. Minute hemorrhages by diapedesis. Areas
of
partial atelectasis, alternating with emphysematous areas. Edema
207. Dog. Received 4
minims of
dichlorethylsulphide on meat. Died 5 days afterwards. Small mustard-gas eschar in
stomach
mucosa. Early fibroblastic proliferation
208. Dog. Received
0.06 c. c. of
dichlorethylsulphide in capsule. Died 12 days later. Portion of base of very large
eschar
of stomach wall, extending nearly to the serosa. Marked leucocyte
infiltration
209. Rabbit. Exposed
12 hours to a
concentration of 1 to 50,000. Died 92 hours after gassing. Mustard-gas eschar on
tongue
210. Rabbit. Eschar
resulting from
subcutaneous injection of 0.03 c. c. of dichlorethylsulphide, 18 days after
injection
211. Rabbit. Eschar
resulting from
subcutaneous injection of 0.06 c. c. of dichlorethylsulphide, 11 days after
injection
212. Rabbit. Received
subcutaneous injection
of 0.045 c. c. of dichlorethylsulphlide. Died on third day during mild diarrhea.
General mucoid degeneration
213. Rabbit. Received
subcutaneous injection
of 0.18 c. c. of dichlorethylsulphide. Began to have diarrhea 7 days after
injection
and died 4 days later. Section of upper portion of small intestine
showing
acute catarrhal enteritis
214. Same rabbit as
in Figure 213. Extreme
mucoid degeneration. Catarrhalenteritis. Mucous diarrhea
215. Section of cecal
wall from same rabbit
as in Figure 213. Marked catarrhal inflammation.
Mucous
diarrhea-
216. Rabbit. Received
subcutaneous injection
of 12 c. c. of dichlorethylsulphide. Diarrhea began on second day, the animal
dying 3 days later. Extreme mucoid degeneration of the entire
intestinal
epithelium. Mucous diarrhea
217. Dog. Received
subcutaneous injection of
0.24 c. c. of dichlorethylsulphide. Died in 4 days, with a very severe
diarrhea.
Extreme catarrhal desquamative enteritis.
Mucoid degeneration and
necrosis
of the glandular epithelium
218. Same dog as in
Figure 217. Middle
portion of small intestine showing desquamation of the superficial epithelium and
necrosis of the epithelium of the gland of Lieberkuehn.
Severe enteritis
219. Rabbit. Received
subcutaneous injection
of 0.06 c. c. of dichlorethylsulphide. Severe diarrhea from fourth to ninth
day.
Killed 15 days after injection. Mucosa of intestines intensely congested
and
edematous. Marked mucoid degeneration with cystic glands.
Regeneration of superficial epithelium
220. Rabbit. Received
subcutaneous injection
of 0.06 c. c. of dichlorethylsulphide. Very severe diarrhea on fifth to seventh
day
afterwards. Apparent recovery. Killed on the thirty-second day after
injection. Mucosa shows excessive
mucous formation
221. Rabbit. Received
subcutaneous injection
of 0.03 c. c. of dichlorethylsulphide. Very severe diarrhea on fourth to eighth
day.
Died on twelfth day after injection. Intestines showed severe
catarrhal
enteritis. Section of spleen showing
the great number of pigmented
phagocytes in the blood sinuses
222. Rabbit.
Sloughing lesion produced by
subcutaneous injection of 0.60 c. c. of hydrochloric acid, 24 hours after
injection
223. Detrimental
effects of water (Vapor
tests). Dichlorethylsulphide vapor was applied to the skin; 62, bare skin; 63,.
skin
coated with water; 64, skin coated with sodium bicarbonate water paste; 65,
skin
coated with soap; 66, skin coated with kaolin water paste. The photograph
was
taken 7 days after the application.
(The figures in parenthesis refer
to
experiments)
224. Protective
action of petrolatum when
dichlorethylsulphide is applied as "splash," and when applied through fabric. In
experiments No. 10 and No. 11 the alcoholic dichlorethylsulphide was
applied
directly to the skin; No. 11 was
previously vaselined. The protective
value of
the petrolatum in No. 11 is apparent. In No. 12 and No. 13 the
alcoholic
dichlorethylsulphide was dropped on a small square of cloth and
this
was applied to the skin; No. 13 was first oiled with
petrolatum. Note that
the two lesions are practically alike. The photograph was taken 19 days
after
the application
225. Value of
protective oiling. In No. 8 the
dichlorethylsulphide was applied to the bare skin, in No. 9 to oiled skin. Both
were
washed with oil, after 15 minutes. Observe the much greater effect on
the
unprotected skin in No. 8. The
photograph was taken 24 days after
the
application
226. Comparison of
oils. Observe the degree
of effect. Each area received 0.01 c. c. of 3 percent solution of
dichlorethylsulphide in the oil, spread over a surface of about one-half inch diameter.
The
photograph was taken 2 days
after application. The solvent oils were
as
follows: 110, liquid petrolatum; 111, raw linseed oil; 112, boiled
linseed
oil; 113, olive oil; 114, castor oil; 115, cod-liver
oil. (The figures refer to
experiments)
227. Protective value
of dichloramine-T.
Pieces of filter paper about 5 min. square, and containing about 0.001 c. c. of 95
per
cent dichlorethylsulphide were applied to the center of a square of
skin,
covered with the protectives. The
coatings were as follows: 117, raw
linseed
oil; 118, linseed oil and kaolin, 1 to 3; 119, same, with 3 per cent of soft
soap;
120, petrolatum kaolin, 1 to 1; 121, dichloramine-T, 10 percent in
chlorcosane; 122, solid paraffin. The photographs were made 1 day after the
application. Note that the reaction is less in 121 than in the others; 26 and
30 are
recrudescences of lesions 25 days old. (The figures refer to
experiments)
228. Efficiency of
dry powders.
Dichlorethylsulphide vapor was applied. Note the normal lesion in the bare skin (26); the
slight protection afforded 1b zinc stearate (30); and the complete
protection
from kaolin, fuller's earth, and
charcoal, indicated by the absence of
lesions
in a straight line drawn from (26) to (30). The photograph was taken 3 days
after the application. (The numbers in parenthesis refer to
experiments)
229. Rabbit No. 9,
serial No. 41. Death 2 1/2
hours after second injection of dichlorethylsulphide. Lung: Edema (oe) in part
fibrinous. Stasis of leucocytes (Lc) in capillaries. Coagulum in
bronchus (B)
and distension of peribronchial lymphatic vessel (L)
230. Rabbit No.
13, serial No. 55.
Died in less than 18 hours after intravenous injection of dichlorethylsulphide, 0.01 g.
per
kilo. Spleen, showing caryorrhexis of cells of follicles, with phagocytosis
of
chromatin fragments
231. Rabbit No. 20,
serial No. 96. Died 4
days after injection of 0.1 gin. per kilo intravenously. Small intestine: Complete
hemorrhagic necrosis of mucosa (AM); extreme fibrinous edema of submucosa (Oe)
232. Normal rabbit.
Bone marrow of femur.
Megacaryocyte (M)
233. Rabbit No. 24,
serial No. 104. Died 3
days after second injection of dichlorethylsulphide, 0.005 gm. per kilo
intravenously. Bone marrow of femur, showing extreme aplasia. The sinuses (B)
are
wide and congested. In the edematous pulp (oe) are many fat cells
(F).
Myelocytes, polymorphonuclears, and megacaryocytes are absent.
There
are few islands of normoblasts (N). The pale nuclei (R) are those of
the
reticular cells. (Somewhat lower magnification than Figure 232
234.
Dichlorethylsulphide, 11 hours after
exposure. Collagen fibers (C) separated by granular coagulum (oe). Distended
lymphatic vessel (L). Emigrated leucocytes (1c)
235.
Dichlorethylsulphide, 98 hours after
exposure. Superficial pustules (p) at margin of lesion. Increased pigmentation
(pq)
in adjacent epithelium. Leucocvtic infiltration of corium
236. Dichlorethylsulphide, 98 hours
after
exposure. Thinning of epithelium (E), infiltration of corium (C) with
leucocytes
showing caryorrhexis. Degenerated hair follicles (H)
237.
Dichlorethylsulphide, 7 days after
exposure. Beginning sequestration of necrotic epithelium (El) and superficial
corium (C) by ingrowth of regenerating epithelium
(E2). Proliferation of cells
of
sheaths of hair follicles (H1H2)
238.
Dichlorethylsulphide, 14 days after
exposure. The sequestration of the dead epidermis (El) and the underlying
necrotic
tissue (C,) by ingrowth of regenerating
epithelium (E2). Desquamated keratin
(K)
239.
Dichlorethylsulphide, 14 days after
exposure. Same designations as Figure 238
240.
Dichlorethylsulphide, 11 days after exposure. Hypertrophic cells at
margin of hair follicles
241. Lewisite No. 1,
24 hours after exposure.
Edema, leucocytes in corium (L). congestion of superficial capillaries
(B),
early degenerative changes and thinning of epidermis (E)
242. Lewisite No. 1,
48 hours after exposure.
Transition between living epidermis (El) and dead epidermis (E2). Leucocytic
infiltration at margin of lesion (Ic), edema of deeper layers (oe)