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to the viscera. He also admits that the whole subject of visceroptosis is a complicated one.

In a recent article, Dr. Hazen states that about ninety-six per cent of the cases that he operated upon were congenital. He describes an embryologic basis, which consists in defective agglutination and fusion of the peritoneum of the back with that of the large intestine, and so causing a malfusion, which may be either hyper or hypofusion. These errors in fusion of the peritoneum result in ptosis of abdominal organs which may cause angulations, constrictions, and traction strains, and which, in turn, give rise to a trend of symptoms. Hypofusion is a laxity of attachment permitting abnormalities in the position and the relation of organs. Hyperfusions are localized adhesion bands. Fibrous hypertrophy and constrictions may result from these bands.

It would be well to disregard all the extreme views on the causation of organ prolapse, since they afford unlimited ground for disagreement. Not all cases of visceroptosis can be attributed to neurasthenia or congenital predisposition.

Undoubtedly, there is sufficient evidence that any wasting condition, resulting in loss of weight and general muscular atony, will predispose to organ prolapse. Toxemia, focal infections, prolonged fevers, and wasting diseases, such as cancer, diabetes, and nephritis, may all result in the loss of muscular tone, and so cause visceroptosis.

I prefer to think, that, in the majority of cases, neurasthenia is not the cause but the sequel of ptosis. When an advanced case of neurasthenia plus visceroptosis appears to us for relief, who could unhesitatingly state which was the first to start the trouble? I also believe that it is not the malposition of organs that causes the neurosis but the autointoxication that may be incidental to it. An hepatic flexure sequence has been described by several authors, in which, primarily, the hepatic flexure comes down from its housing underneath the liver, and frequently prolapses considerably below the crest of the ileum. This leaves a fossa which permits the liver to rotate inward and forward and so constitutes ptosis of the liver. The inward rotation of the liver

[graphic]

FIG. 1. Hepatic flexure below the crest of the ileum, ptosis of splenic flexure, transverse colon V-shaped and dipping into the pelvis, angulation at hepatic flexure.

FIG. 2. Hepatic flexure at crest of ileum, splenic flexure high in the hypochondriac region, pronounced V-shape of the transverse colon, the filling defect in colon not constant.

[graphic]

FIG. 3.

Prolapse of hepatic flexure, also splenic flexure in lesser degree, stomach resting on transverse colon, visualized kinked appendix, filling defect at antrum.

FIG. 4. Marked elongation of atonic stomach, lower end almost reaching pelvic floor, cardiac end still held in normal position.

[graphic]

The transverse

carries with it the pylorus and the stomach. colon and right kidney also take part in the downward movement. It would be plausible likewise to consider the probability of a gastric sequence. An elongated, atonic stomach, exerting a constant pressure on the transverse colon, carries it into the pelvic fossa and drags with it the hepatic flexure from its housing, and thus causes the other organs to prolapse.

The stomach assumes an enteroptotic habitus which is of the fishhook variety. The lower end sometimes reaches the pelvic floor.

The hepatic flexure is more frequently prolapsed than the splenic flexure. In severe, long-standing cases the transverse colon, dipping down into the pelvis, assumes a V-shaped position. It may be much elongated and it may lose its saculations. Schlesinger maintains that the cardia must take part in the ptotic process.

In the limited number of gastroptotic cases that I have roentgenographed, I have usually found an elongated stomach with the cardiac end in the normal position under the diaphragm, held by the gastrophrenic ligament. I consider it rather a stretching of the longitudinal fibers of the stomach, due to atony and an elongation of the organ, than a true prolapse. In aggravated cases gastroctasia may also be present. Considerable trouble may arise from Lane's kinks and hyperfusion bands. Extreme ptosis may cause interference with the blood supply and innervation of the organs involved and may result in serious disturbances. I shall not speak of subjective symptoms of uncomplicated visceroptosis. A misplaced organ will perform its function and not give rise to any symptoms unless there is an interference with its innervation, blood supply and secretions, or unless it is distorted by adhesion bands. I believe that there are many people who go through life enjoying good health, ignorant of misplaced organs. One of my patients, S. K., age 60, has complete transposition of the thoracic and abdominal organs. The heart apex is to the right, the stomach on the right, with the pylorus towards the left, the liver on the left, the cecum on the left, and the spleen on the right. This patient was enjoying good health until a few

years ago, when he developed diabetes which resulted in debility and general muscular weakness, and he now shows visceroptosis.

Roentgenologically, gastroptosis is the rule and not the exception. Of far greater importance than the prolapse itself are the habitus and other conditions accompanying the prolapse.

Stiller characterizes the visceroptotic as one with a slight skeleton, a long, narrow, sunken thorax, movable tenth rib (costal stigma), steeply falling ribs, wide intercostal spaces, an acute epigastric angle, a thin, weak musculature, a poor panniculus, and pallor of the skin. In the absence of symptoms of uncomplicated visceroptosis, I find that the authorities dwell on the symptoms of its complications.

Thus, disturbances in the motor functions of the stomach may give rise to digestive disturbances, such as fermentation, anorexia, hyper or hyposecretion, and epigastric distress. Gastroctasia from the atonic condition results in delayed evacuation of its contents and adds to the above symptoms. Sharp angulation in the intestines and Lane's kinks and bands may produce intestinal stasis which in turn may give rise to autointoxication resulting in a group of symptoms incidental to the autointoxication. These patients absorb toxic substances which have a degenerating effect upon the nerve tissue, especially the sympathetic ganglions, terminating in neurasthenia.

Spasm in any portion of the alimentary canal will cause severe pain in the abdomen. Kinks may also cause reversed peristalsis with nausea and vomiting. Constipation is the rule except in thyroid cases.

There has been much controversy as to whether the surgeon or the internist should treat the visceroptotic patients. Several authors, including Rehfuss, think that the sphere of visceroptosis is a purely medical one. I do not think that either one or the other should claim all the cases. It would be just as unwise for the internist to undertake to treat medically a case of visceroptosis complicated with intestinal stasis due to kinks and adhesions, as it would be for the surgeon to operate on a case of general visceroptosis accompanied by muscular atony and neurasthenia due to some chronic disease. Among the visceroptotics there are undoubtedly either purely medical cases or

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