miércoles, 30 de noviembre de 2011

Pelvic inflammatory disease - Williams review


Pelvic Inflammatory Disease


Pelvic inflammatory disease (PID) is an infection of the upper reproductive tract organs. Another diagnosis given to this disease is acute salpingitis. Although all may be involved, the organ of importance, with or without abscess formation, is the fallopian tube. Because of difficulty in accurately diagnosing this infection, its true magnitude is unknown. Many women report that they have been treated for PID when they did not have it, and vice versa.
Microbiology and Pathogenesis
The exact microbiologic pathogens in the fallopian tube cannot be known for any given patient. Studies have shown that transvaginal culture of the endocervix, endometrium, and cul-de-sac contents revealed different organisms from each site in the same patient. In laparoscopic studies, cervical pathogens and those recovered from the fallopian tube or cul-de-sac were not identical. For that reason, treatment protocols are designed so that most potential pathogens are covered by antibiotic regimens.
Classic salpingitis is that associated with and secondary to N gonorrhoeae (Table 3-25). Another sexually transmitted disease species frequently recovered from acutely symptomatic women is T vaginalis. The lower reproductive tract flora in those patients and in women with bacterial vaginosis are those in which anaerobic species predominate. However, Ness and colleagues (2004) and others have shown that bacterial vaginosis is not a risk factor for development of PID. The sexually transmitted disease species commonly recovered from women diagnosed with PID and reported in Scandinavian studies is C trachomatis. It does not, however, cause an acute inflammatory response.




Upper tract infection is believed to be caused by bacteria from the lower reproductive tract that ascend into the upper tract. It is assumed that ascension of bacteria into the upper tract is enhanced during menstruation due to loss of endocervical barriers. The gonococcus can cause a direct inflammatory response in the human endocervix, endometrium, and fallopian tube and is one of the true pathogens of human fallopian tube epithelial cells. If normal human fallopian tube cells in cell culture are exposed to potential pathogens such as E coli, Bacteroides fragilis, or Enterococcus faecalis, no inflammatory response results. If the above bacteria are introduced into a fallopian tube cell culture in which gonococci are present and have caused inflammatory damage, an exaggerated inflammatory response results.
In contrast, with intracellular C trachomatis, cell-mediated immune mechanisms may be responsible for resulting tissue injury. Little direct permanent damage results from chlamydial tubal involvement (Patton, 1983). Tubal destruction in women with repeated asymptomatic chlamydia may be the result of a delayed hyperimmune response.
Women with pulmonary tuberculosis can develop salpingitis and endometritis. It is assumed that this pathogen is blood-borne, but ascension may still be a possible route. The fallopian tubes also can be infected by direct extension from inflammatory gastrointestinal disease, especially ruptured abscess, i.e., appendiceal or diverticular
Diagnosis
Pelvic inflammatory disease can be segregated into "silent" PID and PID. Of these, PID can be further subdivided into acute and chronic.
Silent Pelvic Inflammatory Disease
It is presumed that this condition results from multiple or continuous low-grade infection in asymptomatic women. Silent PID is not a clinical diagnosis. Rather, it is an ultimate diagnosis given to women with tubal-factor infertility who lack a history compatible with upper tract infection. Many of these patients have antibodies to C trachomatis and/or N gonorrhoeae. At laparoscopy or laparotomy, these patients may have evidence of prior tubal infection such as adhesions, but for the most part the fallopian tubes are grossly normal. Internally, however, there are flattened mucosal folds, extensive deciliation, and secretory epithelial cell degeneration (Patton, 1989).
Acute Pelvic Inflammatory Disease
Criteria for Diagnosis of Acute Disease
In women who are symptomatic, symptoms develop during or following menstruation. The most recent recommended diagnostic criteria presented by the CDC (2006) are for sexually active women at risk for STDs who have pelvic or lower abdominal pain and other etiologies are not feasible. Their diagnosis should be PID if they have uterine tenderness, adnexal tenderness, or cervical motion tenderness. One or more of the following enhances diagnostic specificity: (1) oral temperature >38.3°C (101.6°F), (2) mucopurulent cervical or vaginal discharge, (3) abundant WBCs on saline microscopy of cervical secretions, (4) elevated erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP), and (5) presence of cervical N gonorrhoeae or C trachomatis
Symptoms and Physical Findings
Presenting symptoms may include lower abdominal and/or pelvic pain, yellow vaginal discharge, menorrhagia, fever, chills, anorexia, nausea, vomiting, diarrhea, dysmenorrhea, and dyspareunia. Patients also may have infective urinary symptoms. Unfortunately, there is no single symptom or symptom associated with a physical finding that is specific for this diagnosis. Accordingly, other possible sources of acute pelvic pain should be considered (see Table 11-1).
In women with acute PID, leukorrhea or mucopurulent endocervicitis is common and is diagnosed microscopically. In women suspected of having acute PID, endocervical testing for both N gonorrhoeae and C trachomatis should be performed.
During bimanual pelvic examination, women with acute pelvic inflammatory disease will usually have pelvic organ tenderness. Cervical motion tenderness (CMT) is typically elicited by quickly displacing the cervix laterally with examining vaginal fingers. If a woman has pelvic peritonitis secondary to bacteria and purulent debris that has exuded from the fallopian tubes, this rapid peritoneal movement usually causes a marked pain response. Tapping the cul-de-sac with examining finger(s) will give the examiner similar information. This maneuver usually causes a patient significantly less pain because less inflamed peritoneum is involved.
Abdominal peritonitis may be identified by deep probing and quick release of a hand placed on the abdomen. Alternatively, an examining hand may be positioned with a palm against a woman's mid-abdomen and gently and quickly moved back and forth (shake). This will identify abdominal peritonitis, often with less patient discomfort. In women with PID and peritonitis, usually only the lower abdomen is involved. If all quadrants are involved, suspicion of a ruptured tubo-ovarian abscess should be heightened
Laparoscopy
In Scandinavian countries, women suspected of having acute PID undergo laparoscopy for diagnosis. Tubal serosal hyperemia, tubal wall edema, and purulent exudate issuing from the fimbriated ends of the fallopian tubes and pooling in the cul-de-sac confirm this diagnosis.
Because of this routine practice, Hadgu and co-workers (1986) assembled criteria that preoperatively clinically predicted acute pelvic inflammatory disease and assessed their validity by the absence or presence of disease at laparoscopy. Criteria included: (1) single status, (2) adnexal mass, (3) age younger than 25 years, (4) temperature >38°C, (5) cervical N gonorrhoeae, (6) purulent vaginal discharge, and (7) ESR >15 mm/hr. The preoperative clinical diagnosis of PID was 97-percent accurate if a woman met all seven criteria. Accordingly, due to the cost of laparoscopy, antimicrobial therapy based on a clinical diagnosis in patients with historical and physical findings suggestive of acute PID is prudent.
Sonography
In women with marked abdominal pain and tenderness, appreciation of upper reproductive tract organs during bimanual examination may be limited. In these patients, vaginal sonography may be used to identify tubo-ovarian abscess or exclude other pathology as the pain source (Figs. 2-15 and 2-16) (Molander, 2001). If sonography does not lead to a clear diagnosis, computed-tomography (CT) scanning may be indicated
Endometrial Biopsy
In women suspected of acute PID, some recommend endometrial biopsy to diagnose endometritis. Polymorphonuclear leukocytes on the endometrial surface correlate with acute endometritis, whereas plasma cells in the endometrium are found with chronic endometritis. However, women with uterine leiomyomas or endometrial polyps and no PID frequently also have plasma cells present in the endometrium at endometrial biopsy, as do essentially all women in the lower uterine segment. This, in the opinion of many, indicates that in women with mucopurulent secretions, an endometrial biopsy would not provide useful information to alter the diagnosis or therapy (Achilles, 2005).
Chronic Pelvic Inflammatory Disease
This diagnosis is given to women who describe a history of acute PID and who have pelvic pain. Accuracy of this diagnosis clinically is orders of magnitude less than for acute PID. A hydrosalpinx might qualify as a criterion for this diagnosis (Figs. 9–17 and 9–18). Realistically, however, it is a histologic diagnosis (chronic inflammation) made by a pathologist. Thus, the clinical utility of this diagnosis is limited
Treatment
The most beneficial patient outcomes follow early diagnosis and prompt, appropriate therapy. The primary goal of therapy is to eradicate bacteria, relieve symptoms, and prevent sequelae. Tubal damage or occlusion resulting from infection may lead to infertility. Rates following one episode approximate 15 percent; two episodes, 35 percent; and three or more episodes, 75 percent (Westrom, 1975). Also, ectopic pregnancy risk is increased six- to 10-fold and may reach a 10-percent risk for those who conceive. Other sequelae include chronic pelvic pain (15 to 20 percent), recurrent infection (20 to 25 percent), and abscess formation (5 to 15 percent). Unfortunately, women with mild symptoms may remain at home for days or weeks prior to presentation for diagnosis and therapy.
Exactly where a patient should be treated remains controversial. There are proposed criteria that predict better outcome for certain patients with in-hospital parenteral antimicrobial therapy (Table 3-26). However, the high cost of in-hospital treatment prevents routine hospitalization for all women given this diagnosis



Oral Treatment
In women with a mild to moderate clinical presentation, outpatient treatment and inpatient therapy yield similar results. Clinical treatment with oral therapy is also appropriate for women with HIV infection and PID. These women have the same species recovered compared with non-HIV infected patients and response to therapy is similar.
However, if women have more than moderate disease, they require hospitalization. Dunbar-Jacob and associates (2004) showed that women treated as outpatients took 70 percent of prescribed doses, and for less than 50 percent of their outpatient treatment days. If patients are to be treated as outpatients, an initial parenteral dose may be beneficial. If women do not respond to oral therapy within 72 hours, re-evaluation is indicated and parenteral therapy should be initiated either as an inpatient or as an outpatient if home nursing care is available. This assumes that the diagnosis was confirmed at re-evaluation.
Specific treatment recommendations from the CDC are found in Table 3-27. As mentioned earlier (Treatment), if patients have been recently to California, Hawaii, the east coast, or other areas with increased quinolone-resistant strains of N gonorrhoeae, quinolones should not be used. Anaerobes are believed by some to play an important role in upper tract infection and should be treated. Although prospective clinical trials have established that quinolones alone have excellent cure rates, anaerobes are not predictably covered. Hence, metronidazole may be added to improve anaerobic coverage. If patients have BV or trichomoniasis, then metronidazole addition is required, although perhaps not for 14 days






Parenteral Treatment
Any woman who has criteria as outlined in Table 3-26 should be hospitalized for parenteral treatment for at least 24 hours. Following this, if home parenteral treatment is available, this is a reasonable option. Alternatively, if a woman will be appropriately treated by one of the oral regimens in Table 3-27, then she can be discharged on those medications.
Recommendations for parenteral antibiotic treatment of pelvic inflammatory disease are found in Table 3-28. Of these antibiotics, oral and parenteral routes of doxycycline have almost identical bioavailability, but parenteral doxycycline is caustic to veins. Many prospective clinical trials have shown that either of the listed cephalosporins alone, without doxycycline, will bring a clinical cure. For that reason, doxycycline administration could be reserved until the patient can take oral medication. The recommendation is to continue parenteral therapy until 24 hours after the patient clinically improves and the oral doxycycline should continue to complete 14 days of therapy. Alternatively, if the primary reason for providing doxycycline is to eradicate chlamydia, a 1-g oral dose of azithromycin while the patient is in the hospital will also achieve that goal








For women with an abscess, some also administer oral clindamycin (450 mg every 6 hours) or metronidazole (as shown) to complete therapy. Treatment of a patient with an abscess should include parenteral antimicrobial therapy until the patient has been afebrile for at least 24 hours, preferably 48 to 72 hours. Surgery is rarely required. Although older recommendations for abscess include hysterectomy and adenexectomy, current antibiotics obviate most surgery. If antibiotic treatment fails, then abscess drainage alone typically will suffice. Often this is possible percutaneously by a radiologist with CT guidance and should be considered initially for abscesses larger than 8 cm.


References: Williams Ginecology 9th edition