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Abdominal pain in an intrauterine contraceptive device user

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Q1: What does the abdominal computed tomogram show?

The abdominal computed tomogram (see p 602) shows large multiloculated collections in the pelvis with thickening (arrow) of surrounding tissues. Wall thickening of the upper sigmoid (arrow head) corresponds to the sigmoid stricture in the barium enema study.

Q2: What does the barium enema show?

The barium enema study (see p 602) shows a stricture (opposing arrows) in the lower sigmoid colon. The IUCD is also shown (single arrow).

Clinical course

The patient was initially treated with intravenous fluids and nasogastric tube aspiration. She continued to experience bouts of severe lower abdominal pain and vomiting necessitating laparotomy (10 days after admission). At surgery, a large pelvic abscess was seen with dense adhesions between the pelvic viscera, appendix, and bowel loops. Appendectomy and hysterectomy with right salpingo-oopherectomy were performed along with a covering loop colostomy.

Histology of the uterus showed severe chronic endometritis with numerous branching Gram positive rods in the endometrial cavity and endocervix. Sections from the Fallopian tube showed numerous actinomycotic granules (fig 1 above). No evidence of malignancy was detected. The appendix and right ovary showed non-specific inflammation only. Although bacterial culture was not performed, the clinical and histological findings were consistent with pelvic actinomycosis. She was treated with intravenous benzylpenicillin 9.6 million units daily for four weeks and then intravenous ceftriaxone 2 g daily for two weeks as an outpatient. She is currently taking oral amoxycillin 1.5 g daily, which is to be continued for a year. She remains well at six months of follow up and the colostomy was closed recently.

Figure 1

The edge of a typical “sulphur” granule showing filamentous actinomyces embedded along the periphery of the matrix, surrounded by inflammatory cells (haematoxylin and eosin stain × 500).

Discussion

Actinomycosis is a bacterial infection caused by members of the genus actinomyces, a group of Gram positive, filamentous, and microaerophilic bacilli. Actinomyces israelii is most commonly associated with human disease. They occur as commensals in the oropharynx and gastrointestinal tract and do not usually breach mucosal barriers, unless there is disruption of tissue planes after surgery, trauma, or perforation. Presence of necrotic tissue or foreign bodies may also favour the development of actinomycosis.1

Three major clinical patterns are recognised: cervicofacial, thoracic, and abdominal. Florid granulation tissue, abscesses, cutaneous sinuses, and fistulae are common.1 Diagnosis is established by biopsy, fine needle aspiration of abscess contents, or culture. Examination of the purulent exudate shows characteristic “sulphur” granules, which are clusters of actinomyces colonies embedded in an amorphous matrix (fig 1). The presence of “sulphur” granules is suggestive but not pathognomonic of actinomycosis. Other organisms may show similar appearances and only the Gram stain (showing Gram positive, branching, filamentous rods) can differentiate these from actinomyces.2 Definitive identification is obtained only by culture or species specific antibodies.

Abdominal actinomycosis usually occurs in the ileocaecal area and appendix (65% of cases).1 It typically follows emergency gallbladder or colonic surgery. Clinical features include fever, weight loss, abdominal pain, abdominal mass, and signs of partial intestinal obstruction. Fistulae develop in about one third of abdominal actinomycotic abscesses. Abdominal actinomycosis is well recognised as a “great imitator” and is readily mistaken for neoplastic disease, Crohn's disease, or tuberculosis. Preoperative diagnosis is infrequent (<10%). Crohn's disease and ovarian malignancy were the preoperative diagnoses being considered in this patient.

Actinomycosis of the female genital tract is much less common (less than 1/100 000 women discharged from hospital).3 The spectrum of pelvic actinomycosis includes endometritis, pelvic inflammatory disease, and pelvic abscess. Occasionally, the disease may be confined to the bowel, bladder, abdominal wall, or retroperitoneum. Rarely systemic (liver, brain, and lung) abscesses may develop.4 5 Pelvic actinomycosis results from ascending perineal infection or through orogenital/anogenital contact.5

The presence of the IUCD is an important factor in the pathogenesis of pelvic actinomycosis. Occasionally, other foreign bodies (for example, vaginal pessaries) may be involved. Actinomyces can be demonstrated by cervical smears or immunofluorescence in about 7% (range 0%–31%) of IUCD users. However, a higher rate of deep pelvic infection has not been clearly demonstrated in those with positive smears. The relationship between a positive cervical smear and subsequent pelvic actinomycosis is therefore uncertain and the utility of the cervical smear as a screening tool is controversial. However, a positive smear in an IUCD user with a pelvic abscess should at least prompt further evaluation.

Pelvic abscess associated with the modern IUCD was first reported in 1973. Most reported cases have occurred in long term IUCD or pessary users (average eight years).5 Symptoms include abdominal pain (85%), weight loss (44%), and vaginal discharge (24%). Anaemia (70%), leucocytosis (76%), and a raised erythrocyte sedimentation rate are other features. Physical examination is unhelpful except in those with obvious pelvic masses or skin sinuses. Radiological appearances are not distinctive. Ultrasound and computed tomography studies may demonstrate a solid mass with areas of attenuation, a cystic mass with wall thickening, or diffuse tissue thickening.1 6 Fine needle aspiration performed at the same time may help in establishing the diagnosis.

Clinically stable patients are treated with a prolonged course of antibiotics. Surgery is reserved for bowel obstruction, abscess drainage, or antibiotic failure. High dose intravenous penicillin G is the treatment of choice and is given for four to six weeks, followed by a prolonged course (6–12 months) of oral penicillin. Alternatives to penicillin are ceftriaxone, tetracycline, erythromycin, and clindamycin. Superinfection with other organisms particularlyActinobacillus actinomycetemitans should be considered if there is poor progress after four weeks of treatment.

Removal of the IUCD and antibiotic treatment is recommended in the presence of pelvic inflammatory disease. Antibiotics are usually withheld when actinomyces are detected on a routine cervical smear or culture from an asymptomatic IUCD user. Further management in this situation varies from centre to centre. Most but not all authors advocate IUCD removal, repeating the cervical smear in 6–12 weeks, and IUCD reinsertion if the repeat smears are negative.4

In conclusion, actinomycosis should be considered in the differential diagnosis of any unexplained abdominal or pelvic mass, abdominal pain or intestinal obstruction. This is particularly important in young women with an IUCD in situ.

References

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