Urogenital Imaging

Salpingitis

inflammation in the Fallopian tube, a frequent component of pelvic inflammatory disease, and usually classified as either acute, chronic or granulomatous. Acute salpingitis is a purulent inflammatory process, usually caused by passage of bacteria from the uterine cavity into the tubal lumen. Neisseria gonorrhoea is thought to be the primary causative agent, but Chlamydia trachomatis, anaerobic bacteria (especially Bacteroides and peptostreptococci), Escherichia coli, Mycoplasma hominis, and Ureasplasma urealyticum have also been found. In response to gonococcal invasion, there is vascular engorgement and oedema of all layers of the Fallopian tube. In severe cases, there is transudation of plasma proteins resulting in a fibronous exudate on the serosal surfaces. As the lumen fills with granulocytes and cellular debris, the tube distends, and on laparoscopy pus may be seen dripping from the fimbrial end. These tubal changes, as well as focal peritonitis, produce fever and abdominal and pelvic pain. In typical gonococcal infections, the onset of pain corresponds to the onset of menses. Other bacteria in the uterus tend to spread into the tube via vascular or lymphatic channels, resulting in acute inflammation of the wall of the Fallopian tube, with relative sparing of the mucosa. In addition, the onset of acute salpingitis caused by other organisms is not related to menstruation. Chlamydial salpingitis may not be associated with any pelvic pain. The frequency of acute salpingitis is higher in women using intrauterine contraceptive devices and in those with multiple sexual partners. After resolution of acute salpingitis, residual chronic disease may be found in the Fallopian tube.

Chronic salpingitis is characterized by fibrous adhesions between the serosa and surrounding peritoneal surfaces as well as fibrotic changes in the tubal lumen. In addition, there may be widespread peritoneal inflammation. The bases of the fimbriae may coalesce in the centre, blocking the lumen, and tubo-ovarian adhesions may obliterate the tubal ostium. The ovary itself may become involved, and a tubo ovarian abscess may occur. Pyosalpinx may result in a severely scarred tube or a hydrosalpinx (see also hydrosalpinx).'

Because there are a variety of causes of granulomatous salpingitis, identification of granulomas requires further study to determine the precise aetiology. Of the infectious causes, tuberculosis is probably the most common (see tuberculous salpingitis), but other disorders such as actinomycosis and parasitic infections may be implicated. Salpingitis is also seen as part of systemic diseases such as sarcoidosis and Crohns disease, or may be the result of a foreign body introduced into the tube. Imaging evaluation of the salpingitis is rarely required.

The most sensitive imaging modality for the detection of salpingitis and its complications is hysterosalpingography (HSG). However, imaging findings are nonspecific and in the setting of acute inflammatory disease, imaging is not required. A hydrosalpinx is well demonstrated by either HSG, ultrasound or MRI. The latter is rarely clinically indicated. Hydrosalpinx demonstrates the tubular enlargement at the end of the Fallopian tube, and on HSG study no free spillage can be detected.

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