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diff --git a/76801-0.txt b/76801-0.txt new file mode 100644 index 0000000..c4f6cd2 --- /dev/null +++ b/76801-0.txt @@ -0,0 +1,762 @@ + +*** START OF THE PROJECT GUTENBERG EBOOK 76801 *** + + + + + + _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. + + + +*** END OF THE PROJECT GUTENBERG EBOOK 76801 *** |