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Pelvic Inflammatory Disease (PID) Last updated 6/20/2011
PID is a community-acquired ascending infection that may affect the uterus, fallopian tubes, ovaries, and peritoneal cavity as it ascends. Strictly speaking, it is caused by a sexually transmitted agent, most commonly Neisseria gonorrhea and/or Chlamydia trachomatis. Rapid diagnosis and treatment are important to prevent the development of recurrent infections, chronic pain, infertility, ectopic pregnancy, and peritonitis. Epidemiology 1. Every year in the United States PID accounts for 2.5 million outpatient visits, 200,000 hospitalizations, and 100,000 surgical procedures. It is the most frequent gynecologic cause for emergency department visits (350,000/year) and costs an estimated total of $2 billion/year.[1,2] 2. Risk factors include age range 15 - 25 (a > 35 year old have 1/7 chance of having PID), poor contraceptive habits, and many sexual partners ( > 4 in 6 months; RR 3.4), and frequent sex (> 6 times/week; RR 3.2) [3,4] Clinical Presentation 1. Most common presentation is lower abdominal pain of less than 2 weeks duration, bilateral, and not predominantly referable to the GI or urinary tract. May also have dysuria, dysmenorrhea, irregular uterine bleeding. and dyspareunia. 2. On physical examination, there is usually diffuse tenderness in the lower quadrants with rebound tenderness and decreased bowel sounds being common. On pelvic examination PID is very likely if there is purulent endocervical discharge, cervical motion tenderness (chandelier sign), and adnexal tenderness with bimanual examination. Rectovaginal examination can further support these findings. Fever occurs in about half of patients with PID. 3. Gonorrhea infections account for about one third of PID cases, presenting often with acute symptoms of fever, nausea, vomiting, vaginal discharge and peritoneal signs. [5] 4. Chlamydial infections may have an insidious onset and present with tubular disease and infertility without a history of PID (subclinical PID). [6] 5. CDC criteria for the Diagnosis of PID a. Minimum criteria- treatment should be initiated in the absence of other established causes of the following symptoms. i. lower abdominal tenderness ii. Adnexal tenderness iii. Cervical motion tenderness b. The following additional criteria can support the diagnosis i. Oral temperature > 38.3 C (101 F or 311.3 Kelvin) ii. Abnormal cervical or vaginal mucopurulent discharge iii. elevated ESR or CRP iv. Presence of many WBCs on saline microscopy of vaginal secretions c. Definitive Criteria i. Biopsy confirming endometritis ii. Imaging showing thickened fluid in the tubes or tubo-ovarian abscess. iii. Laporoscopic evidence of PID 6. Suspicion of PID should be high and antibiotic therapy should be initiated even without definitive diagnosis because the risk of developing sequelae left untreated is very high. Testing The following tests are recommended [7]: 1. Pregnancy test to rule out an ectopic pregancy 2. Microscopic exam of vaginal discharge in saline - assessing for WBCs 3. CBC 4. nucleic acid amplification tests for chlamydia and gonococcus 5. Urinalysis 6. FOBT - positive test can suggest other diagnoses. 7. CRP (optional) 8. Ultrasound to rule out ectopic pregnancy if there is a positive pregnancy test and to rule out ovarian torsion, cysts, and TOA if there is suspicion Treatment 1. Most authorities recommend inpatient treatment for those who are pregnant, cannot take oral medication, have poor compliance, have severe clinical illness (high fevers, nausea, vomiting, severe pain), have an abscess, or for whom surgerical intervention is possible. 2. Adolescent females and women > 35 years of age are often routinely treated as inpatients, but there is no data to support this practice. 3. The most important pathogens that must be targeted are chlamydia and gonococcus. Inpatient regimens cover a broader spectrum including strep, gram-negative enterics, and anaerobic organisms. 4. Parental therapy [8]: a. Cefoxitin (2g IV q6) or cefotetan (2g iV q12) plus doxycycline (100 mg PO q12) b. Clindamycin (900 mg IV q8) plus gentamicin (2mg/kg loading dose followed by 1.5mg/kg q8 maintenance dose). c. After 24 hours of sustained clinical improvment, oral therapy can be started.
5. Oral therapy [ibid]: a.
Ceftriaxone (250 mg IM single dose) plus doxycycline (100 b. Cefoxitin (2 g
IM single dose) concurrently with probenecid (1 g
6. Imperative to treat partners regardless of whether they have positive cultures. 7. Counsel patients about contraception and they should notify a physician if they become pregnant to rule out an ectopic pregnancy. 8. Abstinence from sexual intercourse until symptoms resolve and treatment is completed 9. Reculture 10 days after treatment is completed. Prognosis and complications 1. High recurrence rates. One study of low income AA age <19 and > 19 showed recurrence rates of 25 and 20 percent, respectively, at 84 months post-treatment. 2. Tuboovarian abscess is the most serious complication since rupture can lead to sepsis, shock and death. 3. Chronic pelvic pain develops in up to one third of cases, with the more important risk factor being recurrence. 4. Infertility is increased several-fold in prevalence among those with PID. The most important risk factors are Chlamydial infection, delay in seeking care, multiple episodes of PID, and severity of infection. [9] 5. PID is an important risk factor for ectopic pregnancies. The ratio of ectopic pregnancy to intrauterine pregnancy was 1:15, 1:6, and 1:3 after one, two, and three episodes of PID. And in women with a single, milk, or severe episode of PID the ratio of ectopic to intrauterine pregnancy was 1:35, 1:25, and 1:5. [ibid]
References: 1. Washington AE, Katz P. Cost of and payment source for pelvic inflammatory disease. Trends and projections, 1983 through 2000. JAMA 1991; 266:2565. 2. Curtis KM, Hillis SD, Kieke BA Jr, et al. Visits to emergency departments for gynecologic disorders in the United States, 1992-1994. Obstet Gynecol 1998; 91:1007. 3. Lee NC, Rubin GL, Grimes DA. Measures of sexual behavior and the risk of pelvic inflammatory disease. Obstet Gynecol 1991; 77:425. 4. Weström L. Incidence, prevalence, and trends of acute pelvic inflammatory disease and its consequences in industrialized countries. Am J Obstet Gynecol 1980; 138:880. 5. Rendtroff RC, Curran JW, Chandler RW, et al. Economic consequences of gonorrhea in women: experience from an Urban hospital. J Am Vener Dis Assoc 1974; 1:40. 6. Keilani A, Boulieu D, Raudrant D, et al. [Role of Chlamydia trachomatis in tubal pathology (acute salpingitis and tubal sterility). Microbiological study of 175 samples of peritoneal fluid]. J Gynecol Obstet Biol Reprod (Paris) 1989; 18:167. 7. Kahn JG, Walker CK, Washington AE, et al. Diagnosing pelvic inflammatory disease. A comprehensive analysis and considerations for developing a new model. JAMA 1991; 266:2594. 8. UpToDate: Treatment of pelvic inflammatory disease 9. Weström L, Joesoef R, Reynolds G, et al. Pelvic inflammatory disease and fertility. A cohort study of 1,844 women with laparoscopically verified disease and 657 control women with normal laparoscopic results. Sex Transm Dis 1992; 19:185.
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