When sufficient time elapses before death the brain may be softened in spots. This is probably due to the occlusion of vessels by coagula formed during the primary congestion.

Congestions also occur in other localities, and especially in the solid abdominal viscera. The liver and spleen have been found engorged in nearly every case. Jaminet has found clots of blood in the kidneys.2 The mucous membrane of the stomach, intestines, and bladder is often injected and marked with patches of ecchymosis. The lungs in cases of true caisson disease, though occasionally found in a state resembling red hepatization, seldom present any other change than simple hypostatic congestion.

2 Physical Effects of Compressed Air, p. 20.

PATHOLOGY.—It is probable that the pathology of this disease is not entirely uniform in all cases. Doubtless the chief element in it is the congestions already described, and especially of the brain and spinal cord. The mechanism, therefore, of these congestions becomes a subject of paramount importance.

It was suggested by François3 that the morbid phenomena might be due to the liberation in the vessels of air which had been absorbed by the blood while under pressure, but which was set free again when the pressure was removed. This theory has been reasserted by Paul Bert,4 with this difference: that he claims that bubbles of nitrogen instead of air are the cause of the interruption of the circulation. These bubbles he has discovered after death in the vessels of the brain and cord. But he states that when the pressure does not exceed five atmospheres three minutes allowed for the restoration of the normal pressure will be found to prevent the formation of these globules of nitrogen. Now, we find the caisson disease occurring when the pressure does not exceed two atmospheres and when six to eight minutes are allowed for locking out.5 It would seem that under these conditions the gas should escape through the lungs as rapidly as it is disengaged from the blood. Moreover, we find that the attack often comes on several minutes or even hours after leaving the caisson. During this time any free nitrogen in the blood should be constantly becoming less by diffusion through the pulmonary membrane, and if enough were not present at first to cause obstruction, such an effect could scarcely take place at a later period.6

3 Annales d'Hygien publique et de Méd. legale, t. xiv., 1860.

4 Comptes Rendus, August, 1872, and February and March, 1873.

5 I.e. passing from the caisson into the open air through the lock, or antechamber, where the pressure is gradually reduced.

6 In a private letter to the writer, T. Lauder Brunton suggests that a bubble of air might pass from a larger vessel, which it had only partially obstructed, into a smaller branch, which would be entirely occluded by it, or that additional nitrogen might be disengaged when the pressure was lessened by relaxation of vascular tension.

It is also very difficult to reconcile with Bert's theory the fact of the comparative immunity from danger which results from repeated exposures to the effects of compressed air. If the action were that of purely physical causes, habit could make no difference. The obstruction of the vessels, as described by Bert, is a condition of which the system could never become tolerant by frequency of repetition.