Part 4

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.

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.

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.

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.

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.

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.

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.