Treatment of pelvic inflammatory disease

Early detection of PID is important to reduce fertility risks, say Dr Suneeta Kochhar and Mr Lawrence Mascarenhas.

Pelvic inflammatory disease (PID) describes infection and inflammation of the upper genital tract. This may involve the endometrium, fallopian tubes and/or ovaries, as well as the surrounding peritoneum.

A diagnosis of PID is made in 1.6 per cent of women aged 16 to 45 years attending general practice in England and Wales.

On occasion, this may lead to Fitz-Hugh-Curtis syndrome, where infection spreads along the upper peritoneum to the liver capsule causing perihepatic 'violin string' adhesions.

Sexual transmission

Generally, PID is caused by a cervical sexually transmitted infection, usually as a result of ascending infection with Chlamydia trachomatis or Neisseria gonorrhoeae.

Initial epithelial damage by these bacteria appears to allow opportunistic entry of other organisms.

Sexually active women in their teens or early 20s are at increased risk of PID, as are women from lower socio-economic backgrounds.

Previous pelvic infections and unprotected sexual intercourse are risk factors for PID. Less commonly, instrumentation of the cervix and/or of the uterus can result in endogenous bacteria inoculating the endometrium and consequently PID.

Most studies have suggested that the newer contraceptive IUDs do not in themselves cause pelvic infection.

Clinical features

Usually there is a history of acute pelvic pain and fever which occurs during or after a menstrual period.

PID attributed to chlamydia infection may not present with any symptoms and tends to be diagnosed retrospectively when a patient presents with subfertility due to tubal adhesions.

In contrast, PID caused by Neisseria gonorrhoeae tends to be acute. Nausea and vomiting may be a feature in PID.

On examination, there may be a mild tachycardia and fever. There is likely to be bilateral lower abdominal pain; rebound tenderness and guarding may be elicited.

If there is right upper quadrant tenderness, Fitz-Hugh-Curtis syndrome should be suspected.

Bimanual examination is likely to reveal adnexal tenderness and cervical excitation; there may be a tubo-ovarian abscess that may be appreciated on bimanual palpation.

Mucopurulent discharge from the cervix or vagina may be seen on speculum examination, and high vaginal and endocervical swabs should be taken.

An elevated white cell count and C-reactive protein supports the diagnosis of PID. Liver function tests may be deranged in the presence of Fitz-Hugh-Curtis syndrome.

Ultrasound examination is not helpful in diagnosis but may demonstrate tubo-ovarian abscesses.

Visualising the fallopian tubes by laparoscopy is the best diagnostic tool, but is not used first line in clinical practice as it is invasive.

Differential diagnoses

Differential diagnoses may include appendicitis, diverticulitis, urinary tract infection, ectopic pregnancy, ovarian torsion or rupture.

Urine or serum beta -human chorionic gonadotrophin (beta hCG) may rule out septic abortion or ectopic pregnancy, but may not rule out PID entirely. If a diagnosis of PID is made, testing for other STIs is recommended.

Long-term effects

With a single episode of PID, the incidence of subfertility is 20 per cent due to tubal and ovarian adhesions. There is a risk of tubo-ovarian abscess, chronic pelvic pain (20 per cent) and an increased risk of ectopic pregnancy (10 per cent).

Repeated episodes of PID may increase the risk of permanent tubal damage fivefold.

Since there are no widely accepted clinical criteria for PID, early empirical treatment is common.

Antibiotic regimens for the treatment of PID must cover Chlamydia trachomatis, Neisseria gonorrhoeae, anaerobes, Gram- negative aerobes and streptococci.

This provides cover for the most likely STIs as well as endogenous vaginal and lower gastrointestinal flora.

Early treatment

Treatment should be started as early as possible to minimise the risk of a future ectopic pregnancy and tubal infertility.

However, seeking medical attention may be delayed as clinical features may not be apparent or appreciated by patients. Several regimens of parenteral antibiotics followed by oral antibiotics are effective, with the most common treatment period being 14 days (see box right).

However, there is not very good evidence on the optimal duration of treatment, and no significant difference has been shown between antibiotic therapy in hospital and in outpatients.

The patient needs to be re-assessed to ensure response to treatment, and sexual partners may potentially need to be treated for an STI.

PID is a serious condition that can cause substantial morbidity. Preventing gonococcal and chlamydial infections represents the most effective means of reducing the incidence of PID.

Educating women about the sequelae of untreated sexually transmitted infections, as well as emphasising how to prevent transmission of such infections, is important.

- Dr Suneeta Kochhar is an SHO in surgery, Queen Mary's Hospital, Sidcup, Kent and Mr Lawrence Mascarenhas is consultant obstetrician and gynaecologist, St Thomas' Hospital, London.

TREATMENT REGIMENS

- Oral ofloxacin 400mg twice a day, plus oral metronidazole 400mg twice a day for 14 days.

- Intramuscular ceftriaxone 250mg immediately, followed by oral doxycycline 100mg twice a day, plus metronidazole 400mg twice a day for 14 days.

Source: Royal College of Obstetricians and Gynaecologists. Management of acute pelvic inflammatory disease. Guideline No 32. May 2003. RCOG, London.

REFERENCES

- Ross J D C. Pelvic inflammatory disease. BMJ 2001; 322: 658-9.

- Ross J D C. Outpatient antibiotics for pelvic inflammatory disease. BMJ 2001; 322: 251-2.

- Buchan H, Vessey M, Goldacre M, Fairweather J. Morbidity following pelvic inflammatory disease. Br J Obstet Gynaecol 1993; 100: 558-62.

- Washington A E, Cates W, Wasserheit J N. Preventing pelvic inflammatory disease. JAMA 1991; 266: 257-480.

- Kamwedo F, Forslin L, Bodin L, Danielsson D. Programmes to reduce pelvic inflammatory disease - the Swedish experience. Lancet 1998; 351 (suppl 3): 2,528.

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