Pelvic Inflammatory Disease several sexually transmitted infections,pptx (1).pptx

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1. Pelvic Inflammatory Disease

2. INTRODACTION. Pelvic inflammatory disease (PID) comprises a spectrum of inflammatory diseases of the upper genital tract of women. PID can involve infection of the endometrium (endometritis), the oviducts (salpingitis), the ovary (oophoritis), the uterine wall ( myometritis ), or portions of the peritoneum (peritonitis).

3. Acute PID mostly involves the tubes and the sequelae of tubal infection, such as destruction of tubal architecture and function and pelvic adhesions. Chronic PID is a misnomer because the chronic problems associates with PID - hydrosalpinx, infertility, adhesions, and pain – no longer have direct bacteriologic association.

4. Incidence PID is disease of the young woman. The peak incidence occurs in women in their late teens and early twenties. Acute PID occurs in 1% to 2% of young, sexually active women annually and is the most common serious infection in women 16 to 25 years of age. Initiation of intercourse at age 15 years results in a one in eight chance of PID. Fifty percent of these adolescents have four or more sexual partners that first year.

5. Medical sequelae develop in one of four women with acute PID. Ectopic pregnancy rate increases sixfold to tenfold in women with PID. Approximately 50% of all ectopic pregnancies are thought to result from the tubal damage caused by PID. Chronic pelvic pain develops in 20% of women with acute PID. Both chronic pelvic pain and dyspareunia (90,000 new cases each year) are related to PID. Infertility Morality, although rare, does occur, particularly in neglected cases in which a ruptured tuboovarian abscess can lead to septic shock and death.

6. Contraceptive use. Women who are not sexually active and use no contraception do not contract PID. Conversely, women who are sexually active but use no contraception contract 3.42 cases of PID per 100 woman-years. Condoms, when used consistenly and correctly, are very effective in preventing PID, as well as other STDs. Oral contraceptives appear to protect the user agains PID: only 0.91 case of PID per 100 woman-years has been reported among women using the pill. This relationship between the pill and PID may be the result of: Decreased menstrual flow Decreased ability of pathogenic bacteria to attach to endometrial cells

7. Other barrier methods of contraception (e.g., the diaphragm, sponge, the contraceptive foam) also protect against PID. Spermicides my also be bactericidal. Any barrier to spermatozoa also acts as a barrier to pathogenic bacteria. Intrauterine devices (IUDs) have been linked to an increased risk of PID (5.21 cases per 100 woman-years). The risk is confounded by epidemiologic factors such as history of STD and sexual promiscuity, and is lower in monogamous, healthy women. Possible mechanisms for the increased risk include:

8. BACTERIOLOGY. Acute PID is usually a polymicrobial infection caused by organisms that are considered normal flora of the cervix and vagina. Organisms cultured from the fallopian tube Neisseria gonorrhoeae , a gram-negative diplococcus Chlamydia trachomatis , an obligate intracellular organism due to its inability to produce adenosine triphosphate Endogenous aerobic bacteria, such as Escherichia coli and Proteus, Klebsiella , and Streptococcus sp Endogenous aerobic bacteria, such as Bacteroides , Peptostreptococcus , and Peptococcus sp Mycoplasma hominis Actinomyces israelii , which is found in 15% of IUD-associated cases of PID, particularly in unilateral abscesses. It is rarely found in women who do not use an IUD.

9. Organism prevalence N. gonorrhoeae is the only organism recovered by direct tubal or cul-de-sac culture in one third of women with acute PID. One third have a positive culture for Neisseria plus a mixture of endogenous aerobic and anaerobic flora. One third have only aerobic and anaerobic organisms. C. trachomatis alone is found in tubal cultures of approximately 20% of all women with salpingitis . N. gonorrhoeae and C. trachomatis coexist in the same individual 25% to 40% of the time.

10. PATHOPHYSIOLOGY: Menstrual periods. Degenerating endometrium is a good culture medium. Two thirds of acute PID cases begin just after menses . Sexual intercourse. Bacteria-laden fluids may be pushed into the uterus, and uterine contractions may assist their ascent. Iatrogenic events Elective abortion Dilation and curettage or endometrial biopsy IUD insertion or use Hysterosalpingography

11. Infection spreads to the tubal mascularis and serosa . It than spreads by direct extension to the abdominal cavity through the fimbriated end of the tube. Oophoritis develops over the surface other ovaries, and microabscesses may develop within the ovary. Peritonitis can develop, and upper abdominal infection may result either by direct extension of infection up the abdominal gutters or by lymphatic spread. Development of perihepatitis with adhesions and right-upper-quadrant abdominal pains is known as the Fitz-Hugh-Curtis syndrome. Low-grade, smoldering, or inadequately treated infections allow les virulent bacteria to contribute to the process, resulting in mixed infections. Anaerobes then play a major role in the development of pelvic abscesses.

12. Complications of PID are: Pyosalpinges (tubal abscesses) Hydrosalpinges (fluid-filled, dilated, thin-walled, destroyed tubes, usually totally obstructed) Partial tubal obstruction and crypt formation, resulting in ectopic pregnancies Total tubal obstruction and infertility Tuboovarian abscesses Peritubular and ovarian adhesions Dense pelvic and abdominal adhesions Ruptured abscesses, resulting in sepsis and shock Chronic pelvic pain and dyspareunia

13. DIAGNOSIS Signs and symptoms of PID are relatively nonspecific. Thus, they produce both a high false-positive rate and a high false-negative rate of diagnosis. Laparoscopic studies have revealed the inadequacy of diagnosing acute PID by means of the usual history and physical examination and laboratory studies

14. Based on symptoms, a high degree of suspicion is essential in making the diagnosis. Sometimes, only very mild symptoms appear in spite of serious infection. Women with C. trachomatis infection may present with a few symptoms but then exhibit a severe inflammatory process when examined with the laparoscope. Clinical criteria for diagnosis Minimum criteria for diagnosis. Empiric treatment of PID should given if all of the following criteria are met in the absence of another established cause for pelvic inflammation: Lower abdominal tenderness Adnexal tenderness Cervical motion tenderness

15. Additional criteria. For women with severe signs, these additional criteria are used to increase the specificity of the diagnosis: Oral temperature above 38.3 C Abnormal cervical or vaginal discharge Elevated erythrocyte sedimentation rate Elevated C-reactive protein Positive test for gonorrhea or chlamydia Tuboovarian abscess seen on ultrasound Evidence of endometritis on endometrial biopsy Laparoscopic evidence of PID Differential diagnosis for PID should include: Ectopic pregnancy Ruptured ovarian cyst Appendicitis Endometriosis Inflammatory bowel disease Degenerating fibroids Spontaneous abortion Diverticulitis

16. Ultrasound may help to define adnexal masses and intrauterine or ectopic pregnancies, especially when a patient has a tender abdomen and will not permit an adequate pelvic examination. Response to therapy can be measured objectively as pelvic masses and induration regress. Laparoscopy. If the disease process is unclear, this technique is the ultimate way to establish the diagnosis. Culdocentesis-( a procedure that checks for abnormal fluid in the space just behind the vagina) If purulent fluid is obtained, a culture may assist in antibiotic selection. However, infections may be secondary to another primary process.

17. Blood studies Leukocytosis is not a reliable indicator of acute PID. Less than 50% of women with acute PID have a white blood count greater than 10,000cells/ml. An increased sedimentation rate is a nonspecific finding, but the sedimentation rate is elevated in approximately 75% of women with laparoscopically confirmed PID.

18. THERAPY Individualized treatment and a high index of suspicion for infection are mandatory. Treatment should always include the sex partners. The physician must decide between outpatient management of the woman with close follow-up in 48 to 72 hours, or hospitalization. Many experts recommend that all patients be hospitalized. Hospitalization of PID patients should be especially considered if: The diagnosis is uncertain Surgical emergencies, such as appendicitis or ectopic pregnancy, must be excluded A pelvic abscess is suspected Severe illness (e.g., vomiting, dehydration, high fever, or signs of peritonitis) precludes outpatient management The patient is pregnant The patient is an adolescent, an my not comply with therapy The patient is nulliparous The patient has human immunodeficiency virus infection The patient is unable to follow or tolerate an outpatient regimen The patient has failed an outpatient course of management Clinical follow-up within 72 hours of beginning antibiotics cannot be arranged.

19. Mild PID. Outpatient regimens for patients with mild PID include: Ceftriaxone 250 mg ( third-generation cephalosporin  ) intramuscularly plus doxycycline 100 mg orally twice a day for 14 days Ofloxacin 400 mg ( broad-spectrum fluoroquinolone antibiotic ) orally twice daily for 14 days and either clindamycin 450 mg four times a day or metronidazole 500 mg orally two times a day for 14 days

20. Acute severe PID. One of the following combination antibiotic regimens that cover the three major pathogens – N. gonorrhoeae , C. trachomatis , and anaerobes – should be used. Cefoxitin 2 g ( is a beta-lactam antibiotic ) intravenously every 6 hours of cefotetan ( Cephalosporins, 2nd Generation ) 2 g intravenously every 12 hours plus doxycycline 100 mg intravenously or orally ever 12 hours Clindamycin 900 mg intravenously every 8 hours plus a gentamicin loading dose of 2.0 mg/kg intravenously, followed by gentamicin , 1.5 mg/kg intravenously every 8 hours Conservative therapy with intense intravenous antibiotics should be tried first. Sings of clinical improvement, which include defervescence , reduction in direct or rebound abdominal tenderness, and reduction in uterine and adnexal tenderness, should occur within 72 hours of initiating therapy.

21. If clinical improvement results, treatment should be continued for at least 48 hours after the patient demonstrates substantial clinical improvement, then followed by doxycycline 100 mg twice a day for 14 days total. Sonographic resolution of tuboovarian masses may take weeks. Surgical intervention must be considered if the patient shows no response to antibiotic therapy in 72 hours.

22. Laparoscopy may be considered for diagnosis, and may be followed by laparotomy. Unless a well-defined unilateral abscess allows a unilateral salpingo -oophorectomy, the treatment of choice is a total abdominal hysterectomy, bilateral salpingo -oophorectomy, and drainage of the pelvic cavity. The patient, regardless of her age, should be prepared for this possibility before surgery. If an abscess is accessible through the cul-de-sac or radiologically , catheter drainage may be possible.

23. Physical findings. Half the lesions are bilateral and are charctirzed by adnexal enlargement and tenderness. Presenting symptoms may be confused with those for appendicitis. Pathology. Grossly, there is tuboovarian inflammation, and there is copious necrotic material on sections of the tube. The tubal lumen may have an adenomatous appearance. Microscopically, actinomycotic “sulfur” granules are present . Club-like filaments radiate out form the center. A monocytic infiltrate is apparent, and giant cells may be present. Treatment. Therapy is a prolonged course of penicillin.

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