Adhesions (Figs. 10, 11, 13, 14, 19, 28, 29, 30, 31, 46) are scar tissue and are usually the end results of acute inflammation. This inflammation is either specific, due to the gonococcus, or septic and due either to the pyogenic organisms or in a small per cent of cases to the colon bacillus. Adhesions are sometimes apparently due to mechanical irritation of one serous surface when opposed to another under undue pressure. An example of this is when a retro-verted uterus becomes adherent to the posterior wall of the pelvis. As further examples may perhaps be placed those cases in which the pelvic colon is found adherent to the uterus and adnexa. In the female constipation is common and the pelvic colon is often distended with feces and from pressure the opposed serous surfaces may become irritated, abraded and then adherent. The colon bacillus as well as the streptococci and staphyloccocci often found in the colon, may also play a part in these processes.

It also seems possible that adhesions might result from long continued passive congestion with an outpouring of plastic lymph, followed by its ultimate organization. Here, too, the presence of a low grade of infection may be the determining factor.

It may be well in this connection to discuss the relationship of deranged spinal innervation (the osteopathic lesion) resulting from disturbed structural relations along the spine and intra-pelvic inflammation. Dr. Carl P. McConnell in Bulletin No. 1, The A. T. Still Research Institute, says, "The lesion effects upon viscus correspond definitely to the path of spinal innervation. It would seem that fundamentally, impairment of the vaso-motors plays the important role, though undoubtedly disturbance of viscero-motor, secretory and other nerves are necessary factors, and herein, probably vessel relaxation would take place as a reparative process. Congestion and inflammation are basic to the large majority of diseases, and in all our experiments we find vessel disturbance a constant feature whether in the immediate locality of the osteopathic lesion or as a remote effect, but still related physiologically by way of the nerve centers. Consequently, we conclude some involvement of the vaso-motor mechanism is fundamental to at least a large portion of visceral lesions. Remember we are considering only the osteopathic experimental field as it is presented to us, and not attempting to correlate it with other undoubted etiologic factors."

In the same bulletin the experiment of Dr. Louisa Burns showed that lesions through the lower dorsal and lumbar regions were regularly followed by dilatation of the blood vessels of the reproductive organs. Dr. Bums in Bulletin No. 5 says, "There seemed no doubt that vertebral lesions affecting the centers in the lower thoracic region are more apt to affect the ovaries or the testes; that lesions in the upper and mid-lumbar regions are more apt to affect the uterine and prostatic tissues; that lesions of the sacrum are more apt to affect the rectal, vesical and vaginal tissues. ... Bony lesions, with their disturbing influence upon circulation, innervation, secretion and nutrition must be considered important factors, but not the only factors, in controlling the localization of infections and the power of the tissues to overcome various infectious agents. Local circulatory disturbances may be due to the bony lesion exclusively."

Dr. Burns has also shown experimentally in rabbits that lesions affecting the spinal innervation of the pelvic tissues produce edema, decreased elasticity and lessened tensile strength of the broad ligaments and a localized acidosis. Clinical observation and experience give every evidence that similar lesions cause identical conditions in the pelves of women. These conditions undoubtedly lessen resistance and favor infection.

Adhesions occur in two tissues of the pelvis— peritoneum and connective tissue. It is unusual for either of these tissues to be involved alone. They are so closely related anatomically that pathology arising in one would inevitably spread to the other.

The gonorrhoeal inflammation causing adhesions travels by way of the mucous membrane of the uterus to the uterine tubes and from thence to the peritoneum through the fimbriated end of the tube. The progress of the infection is determined by the amount and virulence of the invading infection and the local and systemic resistance offered to it. It may result in a mild salpingitis with destruction of the ciliae of the tube and a mild thickening and infiltration of its walls. A slightly more severe type will extend through the tube walls involving their peritoneal coverings and the connective tissue between the layers of the mesosalpinx. Further invasion and involvement of the peritoneum may be prevented by the sealing of the fimbriated end of the tube by plastic lymph. There may now occur a serous exudate into the cube which is exceedingly likely to become purulent and unless the uterine end remains open and allows drainage, a pyo-salpinx, a collection of pus in the tube, results. If this does not occur the tube walls may become thickened and nodular and infiltrated with pus. Should the fimbriated end not become effectually sealed the pus leaks out, inflammation extends and involves the peritoneum on and about the ovary.

Plastic lymph is poured out and the fimbriae may become adherent to the ovary and an ovarian or a tubo-ovarian abscess form. The ovary may escape direct involvement only to be surrounded and covered by this fibrinous exudate which as it organizes and contracts not only interferes with the rupture of the Graffian follicles but may compress the ovary. Because of the inflammation of its peritoneal covering the ovary becomes closely adherent to all other peritoneal surfaces which come in contact with it. Should the stroma of the ovary become involved a true ovarian abscess, even to the size of an orange may develop. Escaping this an atrophic or "cirrhotic" ovary may result. The ovarian function is now damaged, if not destroyed, and severe symptoms may arise particularly with the onset of the menstrual congestion. The inflammation may extend further causing a more or less extensive peritonitis. If this is fibrinous in nature and sufficiently extensive, the coils of intestines in the pelvis will become adherent to the pelvic organs. If purulent, in addition, there will be one or a number of small collections of pus within the pelvis. These collections lie among the adherent organs or may have even burrowed into the connective tissue. The picture is now one of general pelvic inflammation-salpingitis, plus ovaritis or peri-ovaritis, plus peritonitis, plus cellulitis—with the involved tissues bathed in and infiltrated by pus and agglutinated with fibrinous exudate. (Fig. 10, 11).

Fig. 10. Pelvic Peritonitis. The uterus is displaced anteriorly and to the left. Adhesions bind it to the bladder and intestine and to the tubes and ovaries * * *. These plastic inflammations are due to gonorrhoeal salpingitis or to metritis or perimetritis from puerperal or operative lesions of the genital mucous membrane. (Schaeffer, Atlas and Epitome of Gynecology.) Left ovary contains multiple cysts.

Fig. 11. Pelvic Perintonitis, Perioophoritis, Perisalpingitis and Right-sided Pyosalpinx. View of the pouch of Douglas. Pseudoligaments fix the uterus and its adnexa to the sigmoid flexure. The left tube is bent at an angle, the right tube shows inflammatory redness and is transformed into a pyosalpinx by the agglutination of the abdominal ostium. The globular divisions of the tumor are characteristically shown. (Schaeffer, Atlas and Epitome of Gynecology.)