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.
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
Pelvic
inflammatory disease can be segregated into "silent" PID and PID. Of these, PID can be further subdivided
into acute and chronic.
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).
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
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
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.
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
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).
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
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
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
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
