Part 3

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.

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.

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.

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.

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.