5 things to know about pelvic inflammatory disease
Evidence links STIs to pelvic inflammatory disease (PID)
1. PID is underdiagnosed
PID is a non-notifiable syndrome comprising a spectrum of inflammatory disorders of the upper female genital tract, including any combination of endometritis, salpingitis, tubo-ovarian abscess and pelvic peritonitis. Clinical presentation varies widely in both severity and symptomatology, ranging from asymptomatic to fatal rupture of tubo-ovarian abscess.
There are no clear diagnostic criteria and laparoscopy remains the gold standard despite the cost, invasive nature and lack of both specificity and sensitivity.
Lower pelvic pain, dyspareunia, vaginal discharge and abnormal vaginal bleeding are all symptoms associated with PID, however diagnosis remains largely clinician dependant, so for women at risk of STI, particularly young women, a low threshold of diagnosis and treatment is needed to prevent long term sequelae.
2. Prompt treatment is essential to prevent long term sequelae
PID is associated with tubal factor infertility (TFI), ectopic pregnancy, chronic pelvic pain, reactive arthritis and Fitz-Hugh-Curtis syndrome or perihepatitis.4 There is compelling evidence linking STIs to PID and its associated long-term sequelae.
Women accessing treatment for tubal factor infertility (TFI) have significantly higher rates of chlamydia seropositivity 65–85% compared to 3–37% of controls. It is estimated that 20% of women with lower genital tract chlamydia will develop PID, 4% chronic pelvic pain and 3%TFI.2
It is tempting to assume, given the improved screening of chlamydia in Australia, rates of PID will fall. Certainly some studies have borne this out, with a drop in PID cases in younger women, i.e. those being screened. The relationship between rates of chlamydia and PID are far from straightforward. While some studies have noted a fall in PID in chlamydia-screened women, overall rates of PID have remained unchanged, and similarly unchanged are rates of ectopic pregnancy, a complication of PID.1,3
3. Sexually transmitted infections are usually involved despite failure to isolate causative organisms
Both chlamydia and/or gonorrhoea have been isolated from a third to a half of PID cases, however PID is a syndrome of polymicrobial aetiology – up to 70% of cases have an unidentified cause.5,6 The causative STI causes epithelial damage at cervix and facilitates change in cervicovaginal environment thereby allowing both the pathogen and vaginal bacteria to ascend to the upper genital tract.
Resulting infection and inflammation is therefore a result of both STI and the vaginal facultative bacteria (and hence the necessity of a multidrug treatment regimen). The role Mycoplasma genitalium plays in PID and long-term reproductive morbidity is emerging: tubal factor infertility patients have been found to have elevated M. genitalium antibodies. Cervical and vaginal swabs are often negative, as the infection has ascended above and no longer present at the cervix.
4. PID is managed in general practice
PID is managed largely in general practice and may present similarly to appendicitis, urinary tract infection and gastrointestinal disorders. Australian data estimates over 59,000 PID encounters annually in general practice of which only 0.3% resulted in hospital referral.1 Diagnosis is clinician dependant and an awareness of PID as a possible differential diagnosis and low index of suspicion is necessary. Even in areas specialising in sexual health medicine, diagnostic rates for PID differ significantly between clinicians resulting in cases being missed.7
5. A multidrug regimen is necessary for treatment
Due to the polymicrobial nature of infection, a multidrug regimen is required to treat PID. In young, sexually active women, common STIs should be covered, dependent upon local epidemiology. For iatrogenic PID, such as infection post dilatation and curettage of IUD insertion, differing microbes may be responsible. In both cases, vaginal facultative bacteria should be covered. To achieve adequate penetration of tissue, a minimum of two weeks treatment, close follow-up and monitoring is required. For women who have developed a tubo-ovarian abscess, are febrile, or where the diagnosis in unclear, hospitalisation is necessary. In all cases of suspected STI contact tracing is needed.
Treatment of PID
Suspected STI (2 weeks)
Azithromycin 1gm stat plusdoxycycline 100mg bd plus metronidazole 400gm bd or tinidazole 500mg daily +/- ceftriaxone 1gm stat IMI.
Suspected iatrogenic (2–4 weeks)
Amoxycillin + clavulanate bd plus doxycycline 100mg bd or amoxycillin + clavulanate bd plus metronidazole 400 mg tds.
Source: Antibiotic guidelines 2011.
1. Chen MY, Pan Y, Britt H, Donovan B. Trends in clinical encounters for pelvic inflammatory disease and epididymitis in a national sample of general practices. Intern J STD & AIDS. 2006;17(6):384-6
2. Currie MJ, Bowden FJ. The importance of chlamydial infections in obstetric and gynaecology: an update. Aust & New Zealand Journal of Obstets & Gynae. 2007;47(1):2-8
3. Bender N, Hermann B, Andersen B, Hocking JS, van Bergen J, Morgan J, van den Broek IVF, Zwahlen M, Low N. Chlamydia infection, pelvic inflammatory disease, ectopic pregnancy and infertility: cross national study. Sex Transm Infect. 2011;87(7):601-8
4. Westrom L, Joesoef R, Reynolds G, Hagdu A, Thompson SE. Pelvic inflammatory disease and fertility: a cohort study of 1,844 women with laparoscopically verified disease and 657 control women with normal laparoscopic results. Sexually Transmitted Diseases. 1992;19(4):185–192
5. Simms I, Eastick K, Mallinson H, et al. Associations between Mycoplasma genitalium, Chlamydia trachomatis and pelvic inflammatory disease. Journal of Clinical Pathology. 2003;56(8):616–618.
6. Hillier SL, Kiviat NB, Hawes SE, et al. Role of bacterial vaginosis-associated microorganisms in endometritis. American Journal of Obstetrics and Gynecology. 1996;175(2):435–441.
7. Doxanakis A, Hayes RD, Chen MY, Gurrin LC, Hocking J, Bradshaw CS, Williams H, Fairly CK. Missing pelvic inflammatory disease? Substantial differences in the rate at which doctors diagnose PID. Sex Transm Infect. 2008;84(7):518-23
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