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Title: An atlas of gas poisoning
Creator: Great Britain. Medical Research Committee
Release date: September 2, 2025 [eBook #76801]
Language: English
Original publication: London: Medical Research Committee, 1918
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*** START OF THE PROJECT GUTENBERG EBOOK AN ATLAS OF GAS POISONING ***
_For official use only_
MEDICAL RESEARCH COMMITTEE
AN ATLAS
OF
GAS POISONING
[Illustration: [Logo]]
1918
The Medical Research Committee have made the necessary arrangements for
the preparation and reproduction of the drawings shown in this Atlas.
The Atlas is printed for distribution in size uniform with the series of
Reports issued by the Chemical Warfare Medical Committee with the
sanction of the Director-General A.M.S. and of the Controller of the
Chemical Warfare Department, Ministry of Munitions. The arrangements
have been facilitated by the co-operation of the American Red Cross
Society, who have undertaken to provide part of the present issue of
this Atlas for official distribution in the American Army Medical
Service.
The following Reports of the Chemical Warfare Medical Committee have
already been issued:
No. 1. Notes on the Pathology and Treatment of the Effects of Pulmonary
Irritant Gases. (_March_, 1918.)
No. 2. The Histological Effects produced by Gas Poisoning and their
Significance. (_April_, 1918.)
No. 3. The Symptoms and Treatment of the Late Effects of Gas Poisoning.
(_April_, 1918.)
No. 4. Polycythæmia after Gas Poisoning and the Effect of Oxygen
Administration in the Treatment of Chronic Cases. (_April_, 1918.)
No. 5. The Reflex Restriction of Respiration after Gas Poisoning.
(_April_, 1918.)
No. 6. Investigations into the Reaction of the Blood after Gas
Poisoning, and the Results of the Administration of Saline and other
Substances. The Effects of Bleeding and of the Injection of Calcium
Chloride. (_April_, 1918.)
No. 7. Changes observed in the Heart and Circulation and the general
After-Effects of Irritant Gas Poisoning. (_April_, 1918.)
No. 8. Reports on Fatal Cases of Poisoning. (i.) Ethyl iodoacetate.
(_June_, 1918).
AN ATLAS
OF
GAS POISONING
These drawings have been reproduced by the permission of the
Director-General of Medical Services, B. E. F., and they are presented
as a supplement to the official memoranda on the Nature and Treatment of
Gas Poisoning that have already been issued by General Headquarters to
Medical Officers.
The drawings illustrate only the chief features in the pathology of the
lesions produced by Enemy Gas, and the primary aim of their distribution
is that of general instruction for Officers who are not already familiar
with the subject by experience in the field.
The copyright of all these drawings is reserved and the contents of the
Atlas must be regarded as confidential and not to be communicated to the
press.
B. E. F. FRANCE.
AUGUST 1, 1918.
Out of all the various substances used by the Enemy in Gas Warfare only
two have been chosen for illustration of their effects in this Atlas.
They are Phosgene (COCl_{2}), and Di-chlorethyl-sulphide,
(C_{2}H_{4}Cl)_{2}S, or ‘Mustard Gas’.
=Phosgene= is the chief of all the many gasses and liquids that are used
for their effects as _pulmonary irritants_. Chlorine belongs to this
group and was the first Poison Gas used by the Germans in April 1915,
but it has long since been superseded by more effective chemical
substances. The pulmonary irritants are inhaled as gasses or vapours.
They may cause some watering of the eyes, but the chief effect noticed
at once is a catching of the breath or a choking sensation so that the
chest feels gripped and incapable of free respiration. Coughing and
vomiting may follow, and then after a delay of time varying from a few
minutes to several hours an inflammatory reaction appears in the lungs
themselves, with the development of an acute oedema that may commence
insidiously and yet progress so rapidly as soon to be an immediate
menace to life itself.
The alveoli fill with oedema fluid, which then rises into the bronchial
tubes and may appear in a most abundant expectoration of thin frothy
fluid. Aeration of the blood is seriously interfered with, because the
air sacs are either drowned with oedema fluid or burst by the efforts of
coughing. Moreover the actual circulation through the lungs is
embarrassed, both by the pressure of the oedema fluid on the capillary
vessels and by the local thrombosis that occurs in many places in the
smaller lung vessels. The blood itself is concentrated by the loss of
serum so that the count may rise to even eight or nine million red
corpuscles to the cu. mm. and this change probably adds to the
difficulties of the circulation.
The gassed man can no longer get the oxygen that he wants, and he either
dies in obvious asphyxia with progressive circulatory failure, or he
collapses as the result of some muscular effort that suddenly makes a
greater call for oxygen and so reveals the deficiency of the supply.
Death is the result simply of this inflammatory oedema of the lung, and
it occurs chiefly in the first and second day after exposure to
Phosgene. A few cases may chance to develop secondary bacterial
infections of the lungs and to succumb to a later broncho-pneumonia, but
they are relatively rare.
The main clinical features of acute Phosgene poisoning may therefore be
summarized as follows:
(i) Catching of the breath, choking, and coughing _immediately_ on
exposure to the gas.
(ii) Inability to expand the chest in a full breath after removal from
the poisoned air.
(iii) Vomiting, hurried shallow respiration, and sometimes coughing with
an abundant expectoration, follow. Pain is felt behind the sternum and
across the lower part of the chest. Fine râles are heard in the axillae
and over the back.
(iv) Cyanosis next appears, in association either with a full venous
congestion or with the pallid face of circulatory failure. The
development of these dangerous symptoms may occur after many hours’
delay, and sometimes with unexpected rapidity in an apparently slight
case as the result of muscular effort.
(v) Death, which may or may not be preceded by mild delirium or
unconsciousness, rarely occurs after the first or second day.
=Di-chlor-ethyl-sulphide= is spoken of as being a _vesicant_. It may
exert its irritant action either as a vapour in low concentration in the
air or by direct contact from splashes of the liquid. The liquid or
vapour clings to the clothing of men exposed to Yellow Cross shells, and
thus slowly exerts its continuously irritant action on their bodies.
No irritant effect at all is felt on first exposure, whatever the
concentration may be, but after a delay of about two to six hours the
skin and mucous membranes begin to react with a progressive inflammation
that may result in local necrosis and desquamation of these covering
membranes. There is intense conjunctivitis; the skin turns an angry red,
and this erythema is soon followed by skin blistering here and there
over the face and body. The passage of the vapour down the respiratory
tract may cause such severe injury to the lining mucous membranes of the
trachea and bronchioles that they are eventually destroyed and sloughed
away. Bacterial infection then seizes upon these raw surfaces, and the
patient may die from secondary septic broncho-pneumonia.
Death is never the direct result of the action of the poisonous vapour.
From the 2nd day onward through the first and second week severely
affected men may die, but only as the result of secondary bacterial
infection. This poison therefore differs entirely from the lung
irritants such as Phosgene, which kill directly and speedily by flooding
the lungs with oedema fluid.
The main features of poisoning from Mustard Gas may be resumed as
follows:
(i) _Delay_ of the irritant effect for at least two to three hours, and
then a comparatively slow development of the various inflammatory
reactions.
(ii) Vomiting, and a sense of burning in the eyes, with discomfort in
the throat, hoarse cough, and some retro-sternal pain.
(iii) Intense conjunctivitis that temporarily ‘blinds’ the man.
(iv) Burning of the exposed skin surfaces and of the moist areas in the
axillae and groin, followed by blistering, excoriation, and brown
staining.
(v) Inflammatory necrosis of the mucous membrane of the trachea and
bronchi, with the secondary development of infective bronchitis or
septic broncho-pneumonia.
(vi) Death is relatively uncommon: it occurs later than the first day
and only as the result of septic complications.
No.
I. Microscopic section of human lung from phosgene shell poisoning.
Death at the nineteenth hour after gassing.
II. Blue type of asphyxia from phosgene poisoning, with intense venous
congestion.
III. Pallid type of asphyxia from phosgene poisoning, with circulatory
failure.
IV. Gangrene of foot caused by vascular thrombosis from chlorine
poisoning.
V. Erythema of skin from general exposure to the vapour of Yellow
Cross substance.
VI. Blistering of buttocks by mustard gas.
VII. Burning of scrotum and penis by mustard gas.
VIII. Brown staining from mustard gas.
IX. Ulceration of trachea by mustard gas.
X. Microscopic section of human lung from mustard gas poisoning, with
death at end of second day (40 hours).
XIA. Severely burned eye in the acute stage.
XIB. Slightly later stage of acute burning.
XIIA. Stage of resolution after severe burning.
XIIB. Late stage of resolution.
XIIIA. Drawing of the cornea in the acute stage of severe burning.
XIIIB. Drawing of cornea in the stage of resolution after severe burning.
PLATE NO. I
Microscopic section of human lung from phosgene shell poisoning. Death
at the nineteenth hour after gassing.
The piece of lung shown is almost entirely useless for aeration of the
blood. Most of the pulmonary alveoli are filled with oedema fluid, and
the walls of the air sacs are burst asunder in many places. The rounded
edges of these torn walls can be recognized both in the areas of
emphysema and in the parts that are flooded with oedema fluid. The
bronchus also is filled with oedema fluid, but it should be noted that
its lining epithelium is intact and pus cells have not accumulated in
the secretion. The blood vessels of the alveolar network are congested;
and intravascular thrombosis is frequently found in these smaller
vessels, though it is not actually shown in the area of this section.
The main changes in the lung are:
Congestion, and occasional thrombosis, of the network of pulmonary
blood vessels.
Abundant outpouring of inflammatory oedema fluid both into the tissues
and into the air spaces of the alveoli and bronchi.
Disruptive emphysema of the weakened lung tissue.
The result of these changes is that the blood circulation through the
lungs is impeded, and the respiratory exchange of gasses between the
blood and the air in the lung is seriously diminished. The gassed man is
in danger of death by asphyxia so long as his lung is drowned in oedema
fluid.
From the third day onwards the oedema fluid is reabsorbed or
expectorated, and the lung soon resumes its functions. Bronchopneumonic
complications may develop from secondary infections, but they are not
very common.
The recovery of the lung, even after severe gassing appears to be
functionally good. In the earlier stages of convalescence there may
still be signs of persisting oxygen want, so that tachycardia with
excessively rapid respiration is the result of even slight physical
effort. Later these disabilities vanish. The microscopic examination of
lungs in these stages of recovery has not been made.
[Illustration: PLATE I.]
PLATE NO. II
Blue type of asphyxia from phosgene poisoning, with intense venous
congestion.
_History of case._ Drawing made early on second day after gassing; when
there was copious frothy sputum, frequent cough, and hurried shallow
respiration of 40 to 48 with temperature of 101° and pulse 100. The
patient was bled 15 ozs. and oxygen added to the air that he breathed.
He soon made a complete recovery.
Such venous congestion was more frequent with chlorine poisoning than it
now is with phosgene. It is associated with a full strong pulse at the
outset, though later the pulse may fail and the asphyxia change to the
pallid type shown in Plate III. The patient as a rule is fully conscious
and complains chiefly of headache and pains in the chest; he turns
restlessly to and fro in extreme general discomfort, and his hurried
breathing is interrupted from time to time by short bursts of coughing
and of expectoration. The lung is in the oedematous state shown in Plate
I.
Oxygen, when given by an efficient apparatus, will at once change the
blue tint of the face to a full pink colour, showing that it can still
be absorbed by the blood through the lungs. Venesection relieves the
discomfort felt by the patient, and probably lessens the embarrassment
of the circulation.
[Illustration: PLATE II.]
PLATE NO. III
Pallid type of asphyxia from phosgene poisoning, with circulatory
failure.
The cyanotic hue of the ears and lips, despite the general pallor caused
by the failure of the circulation, indicates the intense want of oxygen
from which the patient is suffering. Respiratory difficulty is shown in
the strained effort of the muscles around the nostrils.
_History of case._ Drawing made on second day after gassing, when there
was profuse frothy expectoration, hurried shallow breathing of 50 a
minute and a rapid running pulse of 132. The patient died two hours
later.
This pallid or leaden-hued type of asphyxia is characteristically
frequent after phosgene, and it may either develop at once with a
rapidly progressive failure of the circulation or follow a stage of
venous congestion.
The patient is restless, often semi-delirious, and his skin may be dry
and hot, or cold in the final collapse, though it is not often damp with
perspiration. The hurrying small pulse and the panting rapid shallow
breathing, often with sounds of fluid in the trachea, are both
characteristic. Examination of the chest finds physical signs very
similar to those of the blue congested type, a little dulness on
percussion and numerous fine râles and rhonchi, especially in the
axillae and over the back. In both cases the intensity of the pulmonary
oedema is hidden from physical examination by the presence everywhere in
the lungs of scattered islets of emphysema.
[Illustration: PLATE III.]
PLATE NO. IV
Gangrene of foot caused by vascular thrombosis from chlorine poisoning.
_History of case._ Gassed by chlorine in 1915 under conditions which
could not have induced frost-bite. Severe dyspnoea from pulmonary
oedema.
Drawing of foot made on fifth day. Both feet were then anaesthetic,
stone cold, and no pulsation could be felt in the dorsalis pedis artery.
The right hand also was mottled, cold, and painful. The circulation was
restored in a few days with complete recovery, except that two toes
became black and shrivelled.
Such arterial thrombosis, of slowly progressive onset, is quite uncommon
in the extremities, though it is occasionally seen with phosgene. The
obstruction is very rarely so complete as to cause gangrene and death of
the tissues. But this drawing of a visible condition is introduced in
order to emphasize the fact that an unseen vascular thrombosis of
smaller vessels in deeper organs of the body is frequently found with
phosgene poisoning. Such thrombosis is revealed by the microscope in
fatal cases in the smaller lung vessels, in the kidney, in the mucous
membrane of the stomach, and in the brain. Indeed in deaths with
prolonged asphyxia from gassing by phosgene the white matter of the
brain is often seen to be thickly sown with brownish-red petechial spots
around each tiny arterial thrombus. The obstruction to the lung
circulation has already been referred to; the kidney thrombosis does not
appear to have any serious results; and, except where larger
haemorrhages have burst in the brain, the scattered cerebral thrombi do
not appear to be of grave clinical import. The petechial areas within
the stomach may occasionally become the seat of a superficial
ulceration. Large thrombi are sometimes found within the heart, but they
also are associated with rather than the cause of the other changes that
lead to death.
[Illustration: PLATE IV.]
PLATE NO. V
Erythema of skin from general exposure to the vapour of yellow cross
substance. Dermatitis of this distribution and associated with
conjunctivitis forms a characteristic picture of poisoning by this
vesicant.
_History of case._ Exposed to ‘mustard gas’ at Ypres on July 12, 1917,
when this substance was first employed by the enemy. Wore box respirator
for only 30 minutes, so that he was exposed without any protection for
nearly four hours. No symptoms were felt until some hours later, when
severe vomiting commenced and conjunctivitis developed.
Drawing made on the fifth day. The laryngitis and bronchitis were
slight, so that the poisonous vapour must have acted only in low
concentration. But the reddening of the skin was fairly intense because
the man had been sweating freely when exposed to the gas, and he was not
washed afterwards nor was his clothing changed. The erythema was
succeeded by staining in the same areas of the skin.
This reddening, as though the skin had been scorched or deeply
sun-burned, is the first cutaneous reaction to mustard gas, though it
sometimes may not appear until several days after exposure. It is
accompanied by only a slight feeling of warmth and irritation. In
addition to the face and arms which are directly exposed to the vapour
in the air, the moist surfaces of the axillae, the flexures of the
elbows, and the perineum and inner surfaces of the thighs are
particularly affected, that is in the places where the skin is often
sodden with fatty perspiration. This special distribution of the diffuse
erythema characterizes the general dermatitis of mustard gas vapour; but
the reaction may be limited to a smaller area in any part of the body,
for example where the clothing may have chanced to be splashed by the
liquid.
The inflammatory reaction is chiefly superficial, and it is not
accompanied by much oedema of the subcutaneous tissues except in the
eyelids and over the penis and scrotum. Later the dusky red colour
deepens, and patches of cyanotic or whitish oedema may arise amid it.
Blisters then appear, and the cuticle becomes excoriated; or the skin
may be retained while the erythema fades and a brown staining slowly
darkens the original area of irritation.
[Illustration: PLATE V.]
PLATE NO. VI
Blistering of buttocks by mustard gas.
_History of case._ The man sat down on ground that was contaminated by
the poison and the vapour passed through his clothing, causing
inflammation of the buttocks and of the scrotum. A diffuse reddening
appeared twenty-four hours after exposure, and this was followed by an
outcrop of superficial blisters. On the eighth day the erythema began to
be replaced by a brown staining, and the drawing was made on the
eleventh day during this change of tints. Infection of the raw surface
was avoided, and the healing was complete in three weeks.
The blisters in this case were probably aggravated by pressure, for the
inflamed skin becomes very fragile, so that the surface layer is readily
loosened by pressure or careless rubbing. The blisters may be very tiny
bullae, as on the eyelids, or they may coalesce into areas many inches
across, covering a collection of serous fluid which perhaps itself
contains enough of the irritant substance to injure other skin if it is
allowed to flow over it.
The blisters are usually quite superficial and almost painless in their
development. But the raw surface that is left after the blister has
burst becomes most acutely sensitive to all forms of mechanical
irritation. Deeper destruction of the dermis may be caused by spreading
necrosis where the substance attacks the skin locally in high
concentration, or when secondary infections are implanted on the raw
surface. Chronic and painful sores then result, and in this event the
skin does not regenerate completely, so that thinly covered scars for a
long time will mark the site of the burn.
[Illustration: PLATE VI.]
PLATE NO. VII
Burning of scrotum and penis by mustard gas.
_History of case._ From the same incident as that described under Plate
No. VI. Inflammation commenced at the close of the first day after
exposure. Drawing made on the eleventh day when the red erythema had
almost faded from the inner aspects of the thighs. The scrotum is
oedematous and the raw surfaces have become the seat of a mild secondary
eczematisation. The injuries were soon and completely healed.
The perineum is peculiarly liable to be inflamed after exposure to the
vapour of mustard gas, and the penis and scrotum become oedematous as
well as reddened. Balanitis and pain with micturition may be
troublesome. When the skin is excoriated, secondary infections of the
raw surface are very likely to develop unless adequate precautions are
taken to prevent sepsis. But with careful cleansing of the skin and
clothes of a casualty after exposure to the vapour, inflammation of the
perineum can be reduced to a comparatively trifling incidence.
[Illustration: PLATE VII.]
PLATE NO. VIII
Brown staining from mustard gas.
This purplish-brown, or brown, or brownish-black tint usually appears in
areas that were first inflamed and red, but it may arise without such
preceding erythema. Its distribution is in the same areas as those in
which erythema occurs, that is over the exposed skin surfaces of the
neck and hands, or on the sheltered moist flexures of the body. It may
appear at any time from the fifth or sixth day onwards, and it persists
for several weeks, until the stained cuticle desquamates. There is no
deep pigmentation.
The drawing was made from a case on the eighteenth day after exposure to
gas, and the brown tint was present on the sixth day.
[Illustration: PLATE VIII.]
PLATE NO. IX
Ulceration of trachea by mustard gas.
The characteristic feature is the sloughing of the tracheal mucous
membrane. The reddening of the base of the tongue and of the pharynx,
with a sharp delimitation where the oesophagus has refused ingress to
the toxic vapour, is seen also with chlorine and other irritant gasses.
But the pharyngeal inflammation with mustard gas may proceed further to
a local ulceration that will cause dysphagia for many days.
The mucous membrane of the trachea and bronchi is affected by
di-chlor-ethyl-sulphide in much the same way as is the skin. It reacts
with an intense inflammation, and death of the surface layers soon
results. The mass of necrotic tissue, exuded fibrin, and pus cells may
form a yellowish-grey slough in which all manner of organisms flourish.
Subsequently this false membrane comes away in patches or in entire
casts from the raw surface of the bronchial wall.
Meantime the infected débris and secretions tend to accumulate in the
bronchial ramifications at the bases of the lungs, and infection may
spread from them into the lung tissues and alveoli. Septic
broncho-pneumonia, localised abscesses, superficial pleurisy, and even
empyema or pyopneumothorax then develop and cause death.
The drawing is of a trachea at the twelfth day after gassing. The base
of the tongue and the pharynx show characteristic inflammation. Yellow
necrotic sloughs lie on the larynx and at the bifurcation of the
trachea. Between these the trachea is red and glistening, because it is
now completely denuded of both mucous membrane and of slough. The dotted
line points to a little group of ulcers on the posterior wall from which
bleeding has occurred. The trachea and bronchi contained an abundance of
thin yellow pus.
[Illustration: PLATE IX.]
PLATE NO. X
Microscopic section of human lung from mustard gas poisoning, with death
at end of second day (40 hours).
The bronchiole is filled with fibrin and pus cells, and its lining
epithelium has been completely destroyed. The inflammation has caused a
characteristic ring of haemorrhage in the tissues around the bronchial
tube, and infection is beginning to appear in the alveoli nearest to
these inflamed tissues. But there is no generalised pulmonary oedema and
no disruptive emphysema.
Di-chlor-ethyl-sulphide may cause some catarrhal desquamation of the
pulmonary endothelial cells, but it rarely excites an outpouring of
oedema fluid from the pulmonary vessels. The pathological changes in the
bronchioles and in the alveoli are therefore in the sharpest contrast
with those caused by phosgene (see Plate No. I). As infection spreads
into the lung tissues, patches of septic broncho-pneumonia and small
abscesses develop, and these often excite an inflammatory oedema around
them.
If the patient lives, his bronchial mucous membrane is slowly
regenerated; and during this time he is naturally subject to reflex
spasms of coughing or even to a protracted bronchitis.
[Illustration: PLATE X.]
PLATE NO. XIA
Severely burned eye in the acute stage.
Early in the second day after exposure to mustard gas vapour the eyelids
and the external surface of the globe show an intense inflammatory
reaction. Tears stream from between the closed oedematous eyelids, which
may even be blistered, and there is often severe pain behind the eyes
and in the forehead. The conjunctiva is swollen, oedematous, and bright
red from injection of the blood vessels. The injury of the cornea, even
when severe, is not so obvious, and careful examination is of great
importance for its detection. Photophobia and blepharospasm render
examination of the eye very difficult.
The majority of gassed eyes exhibit inflammation of a general character
that is not illustrated in this Atlas. But examples are continually
occurring in which the eye is more severely burned, and these may be
recognized by certain characteristic features that are depicted in the
drawing, Plate No. XIA. Whenever a dead white band crosses the exposed
area of the conjunctiva, while the parts of this membrane covered by the
upper and lower lids are red and oedematous, serious injury from the
burning is likely to have occurred.
In the case illustrated, the caustic effect of the vapour is seen
chiefly in the interpalpebral aperture. On each side of the cornea there
is a dead white band due to coagulative oedema, which compresses the
vessels, impairs the circulation, and thus acts as a menace to the
nutrition of the cornea. The swelling in the region of this white band
is slight, while the protected conjunctiva above and below it is greatly
swollen and injected and may even bulge between the lids.
The exposed portion of the cornea is grey and hazy; it has lost its
lustre, and when viewed with a bright light and a magnifying glass it
shows a blurred ‘window reflex’ and a typical ‘orange-skinned’ surface.
The haze gradually fades off above in the region of the protected part
of the cornea where the surface is usually bright and smooth. The pupil
is at first contracted as the result of irritation and congestion. In
this drawing it is shown as artificially dilated by atropine ointment,
which should always be used early in severe cases or where there is much
pain and blepharospasm.
PLATE NO. XIB
Slightly later stage of acute burning.
The swelling in the conjunctiva above and below has subsided, but the
vascular injection remains, and the solid white oedema in the palpebral
aperture is still well marked. The cornea is grey in the exposed area.
[_For_ History of the case _see page facing Plate XII_.
[Illustration: PLATE XI.]
_History of the case._ The casualty was caused by the bursting of a
Yellow Cross shell close to the man when he was riding a restive mule,
and his box respirator was momentarily displaced. A fine spray of the
liquid must have splashed lightly over his right side, for cutaneous
blisters developed on the neck, the cheek, and the forehead on this side
only. The right eye showed serious burning with the central white band,
while the left eye was only in the state of general red conjunctivitis.
With the lowering of the nutrition of the corneal epithelium, secondary
infection is liable to take place. In this case an infiltrated corneal
ulcer is seen associated with a hypopyon. It is therefore important when
there is conjunctival discharge, which indicates secondary infection,
that in addition to the use of atropine the conjunctival sac should be
cleansed by frequent bland irrigations and by the instillation of
antiseptic drops so as to check infection of any corneal ulceration
which may develop. Otherwise the infective progress which has led to
hypopyon may progress till panophthalmitis supervenes.
PLATE NO. XIIA
Stage of resolution after severe burning.
The vascular injection is passing off, the solid oedema is becoming
absorbed, and the corneal epithelium has regained its normal lustre. In
this stage the use of atropine should be discontinued.
PLATE NO. XIIB
Late stage of resolution.
The earlier vascular injection above and below the cornea has
practically disappeared; the solid white oedema has been absorbed, and
the conjunctiva in the palpebral aperture now shows definite injection,
often of a bright violet tint. The entire picture has changed, so that
the parts which were red in the acute stage are now white and the part
which was formerly white is now red. This drawing would illustrate
equally well the condition that may follow immediately on a very slight
exposure to the irritant gas, when only a slight central band of red
injection develops instead of the bloodless state of white oedema that
is caused by the more severe burns.
At this stage atropine and shades should be abandoned. Astringent drops
should be instilled and photophobia combated with cold douching, &c.,
while fresh air and occupation will help to restore the general health
of the individual and mitigate any tendency to neurasthenia.
[Illustration: PLATE XII.]
PLATE NO. XIIIA
Drawing of the cornea in the acute stage of severe burning.
This corresponds with Plate No. XIA. The exposed central area shows grey
haze and loss of lustre on its stippled surface, which gradually fades
off to the bright lustrous normal surface in the part above that has
been protected by the eyelid. Injection of the conjunctival vessels is
seen only in relation to this upper and less burned area.
PLATE NO. XIIIB
Drawing of cornea in the stage of resolution after severe burning.
The cornea is now smooth and bright with a clear light reflex on its
surface. But some grey superficial nebulae are seen in the centre, and
these may persist for several weeks. The injection of the conjunctival
vessels is now limited to the central band.
[Illustration: PLATE XIII.]
------------------------------------------------------------------------
TRANSCRIBER’S NOTES
● Typos fixed; non-standard spelling and dialect retained.
● Enclosed italics font in _underscores_.
● Subscripts are shown using an underscore (_) with curly braces { },
as in H_{2}O.
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