We must distinguish two primary forms of softening, which present essential differences in numerous points; both, however, are to be carefully distinguished from cadaveric softening, the self-digestion of the stomach.

The one, a disease of infant life, is called gelatinous softening. It appears to be a metamorphosis - a softening - of the mucous membrane of the fundus, which extends to the muscular coat and the peritoneum, converting them and the intervening interstitial cellular tissue, into a grayish or grayish-red transparent jelly) with a yellowish tinge, through which single dark-brown streaks, the broken-down bloodvessels, are observed to pass. Inasmuch as the softened inner strata occasionally become detached, the fundus of the stomach may be found to consist of nothing else but thin, gauze-like, friable portions of the peritoneum.

The softened portion of the stomach tears at the slightest touch; it dissolves between the fingers, and perhaps in rare cases these rents occur during life, but probably oftener after death, giving rise to effusion of the gastric contents into the abdominal cavity.

The process is not, however, limited to the stomach, but frequently extends to the neighboring tissues, and chiefly to muscular organs, and especially to the diaphragm. Here, too, perforation is the final result, and with it there is effusion of the gastric contents into the left pleura.

Gelatinous softening of the stomach commonly runs a subacute course: general anaemia, which is particularly apparent throughout the intestinal canal, and general collapse and wasting, which are chiefly evident in the muscular tissue, are constant accompaniments of this disease. It is frequently founded upon a demonstrable affection of the brain, principally hypertrophy, or hydrocephalus: and this fact renders it probable that there is a similar causative nexus in those cases also, in which no visible anomalies have been hitherto detected in the infantine brain. Perhaps the proximate cause may be looked for in diseased innervation of the stomach, owing to a morbid condition of the vagus, and to extreme acidification of the gastric juice.

Nevertheless, the quaestio vexato as to the origin of the affection in irritation or inflammation remains. If we consider, in addition to the above remarks, the uniform localization of the disease, that in none of its stages it presents, either at the point of the softening or in its vicinity, hyperaeinia, injection, or reddening, and that we are still less able to demonstrate upon the inner surface of the stomach, or in the tissue of its coats, the products of inflammation, we are constrained to infer the non-inflammatory nature of the affection. This conclusion gives a key to the various kinds of softening that occur at advanced periods of life under similar circumstances, viz., in cerebral affections.

A second form, in which softening of the stomach takes place, is distinguished by an absence of pallor in the softened tissues, or rather by their color. The parietes of the stomach are converted into a more or less saturated dark-brown, or blackish pulp.

It occurs under two different circumstances, though in both the process has an acute character, and in both the color of the softening tissues is produced by an alteration of the blood contained in them, by an acid. They differ essentially in their genetic relations.

In the first instance, it occurs, both in children and adults as a sequela of acute affections of the brain and its membranes, and more especially of tubercular meningitis at the base of the brain. It is the same process as gelatinous softening of the stomach, and the theory to which we have alluded is the more applicable the more fully the affection at the base of the cerebrum is developed. But the development takes place with the greater rapidity, the less the acute disease of the brain has induced that degree of anaemia which commonly prevails in gelatinous softening; and, the tissue being still more or less injected, the superabundant acid acting upon the contained blood, produces the characteristic discoloration. The solitary fuliginous streaks above alluded to, as occurring in the pale, jellylike membranes of the stomach, are analogous to this condition. Besides, it not unfrequently presents itself in those cases of pulmonary paralysis which are probably caused by a reflex action of the oesophageal and gastric branches of the vagus.

In the second instance, the softening occurs, unconnected with the etiological relations we have hitherto discussed, under totally different circumstances. We now speak of it as a sequela of certain cachexiae, which were either originally acute, or became so under the influence of certain circumstances, viz., the exanthematic, the croupy, the typhoid in the widest senses, pyaemia, acute tuberculosis, acute cancer - it is then to be viewed as a fatal degeneration of these diseases. This form is developed from a congestion in the capillary network of the gastric membranes, and particularly of the mucous membrane of the fundus, which is generally accompanied by a more or less congested state of the spleen. It probably arises from the state of the blood itself which accumulates with an excess of acid in the vascular system of the fundus, and of the spleen. This too is the cause of the generally rapid course of the affection, the dark color of the softened tissues and their frequent perforation. It commences with a dark brown or black discoloration of the mucous membrane at the fundus, which is soon converted into a black pulp that may easily be detached. If it be removed or if it separate spontaneously, a pale, bluish-white, submucous cellular tissue is exhibited, in which vessels ramify whose coats are disorganized, and which contain a black (car-bonified) granular coagulum. The subjacent muscular coat is pale and thin, the peritoneum dull, and of a dirty gray color. The process extends from the mucous membrane to the subjacent tissues; they are converted into a black, grumous pulp, and thus more or less extensive perforations result, which are bounded by a furred margin. Here, too, the diaphragm is frequently involved, and softening and perforation of this organ follow. The stomach is found to contain large quantities of fluid resembling coffee-grounds or ink, which is often vomited during life - there is an admixture of more or less of the softened tissues, and of their fat, which floats in the mass in the shape of oil-globules. This fluid originates in the sanguineous effusion which takes place at the commencement of the disease; the latter proceeding from the vascular system, and first affecting the coats of the vessels. On the occurrence of perforation, the fluid is extravasated into the peritoneum, and into the left pleura; and it here gives rise to a similar process in the serous membrane, accompanied by the evolution of gas.

In rare cases this process only takes place at solitary, circumscribed spots, and does not then appear to run its course so rapidly. The mucous membrane disappears at these points, with the exception of a very thin, gauze-like, discolored layer, to the edges of which are attached a few jagged remains of the former.

The fundus is the seat of all the softening processes of the stomach - from here they extend to the large curvature of the stomach, in which respect they differ from the gastric diseases that we have already considered, or that we are about to examine, such as catarrhs, follicular erosions, the perforating ulcer, hypertrophy, cancer. It is there too that we find the perforations; and it is only in very rare cases that we see softening at the large curvature precede the development of softening at the fundus.

Softening, and especially the last-named form, occurs in company with softening of the fundus at the oesophagus. The lower third of this tube is liable to be attacked, and the side which is directed towards the left side of the thorax is chiefly so, as the perforations almost invariably occur here, producing effusions into the left half of the thorax, after the cellular sheath of the oesophagus and the mediastinum have been absorbed.

The softening is never distinctly circumscribed, but is shaded off gradually into the surrounding tissues. It is a fact of considerable importance, that softening may take place after death from the operation of cadaveric, chemical changes, which closely resemble the processes we have just described. It is not always easy to decide between this self-digestion and morbid softening; nay, it is a matter of impossibility for the conscientious pathologist, unless he take the previous disease and the mode of death into consideration.

The following circumstances may, however, serve to characterize cadaveric softening: a. The absence of all symptoms during life which indicated softening, or the morbid processes that gave rise to it.

b. Sudden death, from natural or other causes, during the digestive act, whilst the stomach is filled with chyme, without previous illness.

c. Limitation of the softening to the mucous membranes, and especially to the projecting folds, so as to form streaks.

d. And at the same time its extension beyond the ordinary boundaries of morbid softening - its development being most remarkable at those points at which there is a stagnation of the greatest quantity of the gastric contents.