Inflammation of the peritoneum is very seldom spontaneous in its origin. It seems remarkable that, compared with the pleura or pericardium, this membrane is so seldom the seat of independent inflammation as a result, for instance, of the irritation of the blood in acute rheumatism, or of the more vague causes of irritation designated as cold.
The peritoneum is, however, peculiarly liable to inflammations of a secondary character, the irritant proceeding either from without as in wounds of the abdomen, or from one of the organs lying beneath the membrane.
Mere exposure to the air or the entrance of air into the abdominal cavity does not induce peritonitis, and even a somewhat prolonged cooling of the membrane, as during an operation, does not seem to lead to inflammation.
These comprise the great proportion of acute inflammations of the peritoneum. Experiments (Grawitz, Waterhouse) seem to show that whilst the peritoneal cavity is a favourable place for the propagation of pyogenic microbes in respect to temperature and other conditions, yet that the absorbent power of the peritoneum is such that the introduction of these agents is not followed by inflammation when the peritoneum is strictly normal. On the other hand, if there be in the sac stagnant serous fluid, or irritating substances calculated to produce transudation, or if there is a septic wound communicating with the peritoneum so that the microbes are vigorously produced and nourished, then they multiply in the peritoneal cavity and evolve their specific toxines.
It is obvious that in actual cases in man the pyogenic microbes will rarely be introduced as in experiments, as pure cultures into a normal peritoneum. The septic inoculation may take place from a wound in the abdomen by accident or operation, and if the wound becomes septic one of the conditions mentioned above is satisfied. More frequently the source is an- underlying organ, as by rupture of the stomach, intestine, or vermiform appendage, or propagation of septic processes from the uterus in delivery. In the former case irritating matters from the alimentary canal are introduced along with the pyogenic agents, and in the latter the conditions are those of a septic wound communicating with the peritoneal cavity.
If the pyogenic agents once settle in the peritoneal sac they propagate with enormous rapidity in the warm and moist cavity, and it may happen that in comparatively few hours we may have such an absorption of toxines as to cause death by septic poisoning even before much evidence of inflammation has manifested itself.
The septic inflammations are pre-eminently acute, and tend rapidly towards suppuration. At first there is hyperemia and a serous and Fibrinous exudation. The exuded fibrine is visible on free surfaces as a soft yellow layer, and is often present in the fluid as yellow flakes. It glues together surfaces which are in contact, such as the loops of the intestine, but the adhesions are soft and readily separated. As the inflammation goes on, the fibrinous exudation, which from the first contains very numerous leucocytes and is correspondingly soft, becomes still more infiltrated with these, and assumes the characters of pus. Pus may be found in some parts, while in others there is still the soft fibrinous exudation. Thus pus may be found in the neighbourhood of the original source of the inflammation, as around the vermiform appendage, the inflammation being here more intense or of longer standing. The pus, and even any free fibrine that may exist, commonly gravitate to dependent parts, and we may find a collection of yellow pus in the pelvis, especially in Douglas's pouch.
The endothelial cells of the peritoneum take part in the inflammation. They multiply and enlarge (Orth), or they are shed. The underlying connective tissue is infiltrated with serous fluid and exudation, and all the underlying tissues are altered, more especially the wall of the intestine, whose coats are often oedematous and swollen. There is not infrequently considerable tympanitic distension of the intestine from paralysis of its muscular coat. This Meteorism is sometimes a peculiarly distressing feature in puerperal fever.
Septic peritonitis, if general, is almost necessarily fatal. Sometimes it is localized by adhesions, and, even after the occurrence of suppuration, may subside and give place to chronic inflammation.
A more localized acute peritonitis not infrequently occurs. It may be in connection with appendicitis (see ante), or with diseases of the uterus, or may be even a result of infarction of the spleen. If recovery occurs from such inflammations adhesion of the surfaces affected is the result.
Chronic peritonitis, whether developing out of the acute form or occurring in connection with disease in an underlying organ, is characterized by new-formation of connective tissue, frequently with adhesion of opposing surfaces (Peritonitis adhoesiva). The details of this process are similar to those in chronic pleurisy; it remains here to specify some of the more common occasions of the affection.
Local thickenings of the capsule of the liver and spleen are of frequent occurrence in connection with diseases in these organs or their neighbourhood. Sometimes the connective tissue is hard, almost like cartilage. Very commonly there is adhesion to the parts around, especially to the diaphragm. On the other hand, the diaphragm may be adherent by reason of the extension of an inflammation from the pleura, the irritant having passed downwards in a direction contrary to that of the usual circulation.
The peritoneum around the female generative organs is liable to very frequent local chronic inflammations (Perimetritis), resulting in complex adhesions and mattings of the pelvic organs. The contraction of the new-formed connective tissue may cause considerable distortion of these organs.
There is also a peritonitis from rupture of the gall-bladder or a bile duct (see p. 915).