Chronic Peritonitis

I have doubted whether any disease deserving this name really exists independent of such low inflammatory action as may arise from the irritations of tumors or heterologous deposits. This statement refers to general not local peritonitis. I have never seen anything that would lead me to believe that acute diffuse peritonitis can be deprived of its acute character and still continue an inflammation. With me it has always been death or cure. I have already referred to a case in which after recovery the bowels were greatly disturbed by tympanitis for years. But this came from adhesions: her general health was good. I have at long intervals met with cases of ascites in which the peritoneal membrane was redder than natural, and in which no obstruction to the portal circulation was discovered. This, however, I have regarded as hyperæmia rather than inflammation.

Bauer, however, gives to these cases the title latent general peritonitis, especially when after death an abnormal adhesion is found here and there. In the cases that I have seen there was a peculiar state of the surface of the abdomen. The skin there was more or less scaly and dry, but I do not remember whether there were internal adhesions. Bauer regards the diagnosis of this form of disease as difficult, but refers to the constantly present meteorism as well as serous fluid. I have met with three or four instances in which at the time of puberty an abdominal dropsy has rather suddenly occurred, lasting one to three months, and disappearing on the use of diuretics. I have had no reason to attribute this effusion to inflammatory action, except in one case. A lady of extraordinary symmetry and beauty of form, in excellent health, whom I had treated for this disorder twelve years before, applied to know whether there was anything in that disease that would prevent her having children. She had been married seven or eight years, and had not been pregnant. The question then occurred to me, At the time of the dropsy could there have been lymphy exudation that has since confined the ovaries in an unnatural position? The question I could not answer. The treatment which Bauer prefers for his latent peritonitis consists in "painting with iodine, the use of diuretics, and the regulation of diaphoresis by means of Turkish baths."

Cyclopædia of the Practice, etc., vol. viii. pp. 297-302.

Another form of general chronic peritonitis is, according to Bauer, that which follows acute peritonitis. He quotes several authorities in support of his views. I must draw on him for a description of it, for, as I have said, practically I know nothing about it.

The symptoms of acute peritonitis are all toned down, but do not all disappear. Vomiting occurs occasionally; tenderness is diminished, but is quite perceptible; meteorism diminishes, but fluctuates greatly; appetite is poor or variable; constipation alternates with diarrhoea or is followed by dysentery; now there is a febrile heat, and then the temperature is normal—this fever is most likely to come in the evening; the pulse is frequent and varying; ultimately extreme emaciation and anæmia. The most striking feature of this condition appears to be sacculation of the fluid in the abdomen, wholly or partially; this fluid then is not freely movable, but will give dulness on percussion, which may contrast well with intestinal resonance in its immediate neighborhood. When the tension of the abdominal wall is diminished these sacs can be felt by the hand as uneven tumors. Colicky pains occur, and in a case cited it was at one time very severe, at another only slight. The majority of the cases terminate, after a protracted course, fatally. Recovery may occur by absorption or external evacuation of the fluid. He gives no special treatment.

Bauer makes still another class of cases of chronic peritonitis—those arising in the course of old ascites; he, however, does not make much out of it. He thinks the cases of this kind occur with cardiac and hepatic disease, and particularly with the nutmeg liver. The symptoms, he admits, are neither well defined nor severe, and the anatomical changes consist "in thickening of the serous membrane by a slight deposit of fibrin, slight turbidity of the ascitic fluid, and a few flakes of fibrin suspended in it." He then, strangely, gives, as if they were illustrations of such a disease, two cases in which death by acute peritonitis followed the last of many tappings, in one of which a pool of pus was found encysted in front of the intestines. Both are borrowed.

Probably most practitioners who are in the habit of making post-mortem examinations have seen the flakes of lymph in the ascitic fluid, etc., but the German physicians have been the first, I believe, to regard such cases as belonging to separate forms of disease.

William Pepper has published a case observed by himself and G. A. Rex which shows non-malignant chronic peritonitis better than any I can recall to mind. The report forms the sequel to the case of the young woman on whom he successfully performed paracentesis of the pericardium.

Am. Journ. of Med. Sci., April, 1874.

This young woman began to have double pleuritic effusion, and this was soon followed by ascites three and a half months after the operation. From that time the ascites was better or worse, but did not wholly leave her, and became considerable before her death. This was sudden, she having some convulsive movements in extremis. Lesions were found in the thoracic cavity like those discovered in the abdominal, showing, it was believed, a special tendency in this person to plastic exudation on the serous membranes. "The lower part of the abdomen was found occupied by an extensive effusion. The intestines were floated upward. There were few if any signs of inflammation of the intestinal peritoneum, but marked changes were observed in the parietal peritoneum and in the capsules of the liver and spleen. The peritonitis was most marked in the upper segment of the abdomen, while the parietal membrane presented large patches of irregular thickening. No tubercles were found on any part of the peritoneum. The capsules of the liver and spleen were greatly thickened, whitish, opaque, and densely fibrous. The liver was enlarged and heavy, and so tightly bound by its thickened capsule that its shape was somewhat altered.

"The diaphragm, especially that part of it underlying the pericardial sacs, had undergone marked fibroid degeneration. The muscular tissue was much atrophied; many fasciculi had evidently disappeared, while many others were markedly narrowed, some of them shading off to a width of less than /3000 of an inch, and finally disappearing altogether. They retained, however, even in their narrowest dimensions, their transverse striæ."

(It may be remarked, in passing, that this substitution of fibrous for muscular tissue follows the same law that it does in the heart when that organ is the seat of fibrosis or fibrous degeneration. Here it was supposed to be the consequence of a low grade of inflammatory action. Is it when it occurs in the heart?)

In the abdomen these observers found nothing which suggested the possibility of tubercles or any obscure form of cancer. In the pericardium, on the heart side, were found numerous small nodular roughnesses. Irregularities of the pericardial false membrane are so common that nothing but the close and universal adhesions would raise any question of these relations. But tubercles would hardly be here and nowhere else.

Delafield says that one form of the chronic disease is the continuance of his cellular peritonitis. In this, he says, the surface of the omentum is covered with cells which look as if they were derived from the endothelium and connective-tissue cells, although they differ from the normal shape of these. The new cells are for the most part polygonal, of different size, with one or several nuclei, and giant-cells—large granular masses filled with nuclei. Although these new cells are produced over the entire surface of the peritoneum, yet, as a rule, they are more numerous in little patches here and there. These little patches may be heaped together in such numbers as to form nodules visible to the naked eye. There is never any stroma between these cells.

This form of peritonitis occurs most frequently with organic heart disease, with cirrhosis of the liver, with chronic pulmonary phthisis, and with acute general tuberculosis. In the two latter diseases he thinks they have been improperly called tubercles.

He describes a form of chronic adhesion of peritoneal surfaces that occurs without the intervention of fibrin, but, as he supposes, by coalescence of the branching cells and a production from them of a fibrillated basement substance, the fibrils crossing in all directions. In the midst of these fibrils he finds the nuclei of these cells. He finds also in the immediate neighborhood of these adhesions thousands of branching cells that are attached one to another and float free in the water, the fixed end being attached to the peritoneum. He regards such a peritonitis with adhesions as a more advanced stage of the forms of cellular peritonitis already described, and the new cells are changed into membrane.

Sayre has published an extraordinary case in the Transactions of the Pathological Society. He calls it chronic proliferative peritonitis; it might be called more aptly the consequence of peritonitis.

A large, strong man fell from a hammock, the rope breaking, upon his shoulders, and felt a severe pain in his stomach, and soon developed symptoms of peritonitis. This pain never entirely subsided. The peritonitis was recognized. About one month after he was tapped, and 240 ounces of serum were drawn. He was tapped one hundred and eighty-seven times, and 1203/16 pounds of fluid were taken from him during the remainder of his life. At post-mortem examination 3000 cc. of yellow serum were found. The liver and spleen were covered by a thick layer of false membrane, intestines were glued together in the upper part of the abdomen, and the stomach was adherent to the lower surface of the liver. The portal vein was contracted by this membranous coating. There were numerous other lesions in the heart and pleura, but these will account for the dropsy.

This man was unusually strong and hearty until 1876, when he had an attack of double pleuro-pneumonia, and in 1878 he slipped on the front steps and fell, but seemed to recover from the effects of this. The fall from the swing occurred in July, 1879. He died in February, 1884.

Med. Record, April 19, 1884.