CHAPTER 197

Pelvic Inflammatory Disease

Tori Hudson, ND

DIAGNOSTIC SUMMARY
Dyspareunia
Mucopurulent cervical discharge
Pelvic pain; bilateral adnexal tenderness
Palpable adnexal mass
Elevated temperature (above 101oF)
Cervical motion tenderness
White blood cell count (WBC) 20,000/L, with marked leukocytosis, elevated
sedimentation rate, or both
Neisseria gonorrhoeae (GC) and Chlamydia trachomatis (CT) most common, followed by Ureaplasma urealyticum, Mycoplasma hominis, Streptococcus species,
Escherichia coli, Haemophilus influenzae, Peptostreptococcus, and Peptococcus*
Transvaginal ultrasound shows thickened fluid-filled tubes or tubo-ovarian mass
Acute and chronic endometritis on endometrial biopsy
Laparoscopythe gold standard
GENERAL CONSIDERATIONS
Pelvic inflammatory disease (PID) is a categorical name for a range of pelvic infections and inflammations. The CDC defines PID by the presence of abdominal and
adnexal tenderness and cervical motion tenderness in the absence of another definable cause of the patients symptoms. The diagnosis does not require the presence of
elevated WBC, erythrocyte sedimentation rate (ESR), or of fever.
PID causes women to make an estimated 2.5 million outpatient visits to health
care providers each year. One fourth of these women will suffer serious long-term
sequelae and all are at risk for recurrence.1
The social and physical costs of PID are also significant: the risk of ectopic pregnancy increases sixfold after a single episode of PID, and there is an estimated 13%
risk of infertility after one infection and a 70% risk after three infections.2 For these
reasons as well as costs, prevention and aggressive full-spectrum care of the acute
phase are vital.

CHAPTER CONTENTS
D iagnostic Summary, 1695
General Considerations, 1695
Etiology, 1695
Complications, 1696
Risk Factors, 1697
Pathogen Access to the Upper Female Tract, 1697
Diagnosis, 1697
T herapeutic Considerations, 1698
Antibiotics, 1698
Oral Treatment, 1698
Physical Medicine, 1699
Nutritional Supplements, 1699
Botanical Medicines, 1700
Prevention, 1700
T herapeutic Approach, 1701
Diet, 1701
Supplements, 1701
Botanical Medicines, 1701
Physical Medicine, 1701

Etiology
Several organisms (listed in Table 197-13) are known to be implicated in the etiology of PID, but GC and CT are the most common. Because of the complexities
and inconsistencies involved in sampling and laboratory verification, it is difficult
to make definitive statements about the causal agents in PID. Asymptomatic chlamydial infections are an important cause of PID. An estimated 1 million new
*Testing methods for GC and CT include cell culture (the gold standard), direct fluorescent
antibody (DFA) testing, enzyme immunoassay (EIA) antigen detection technique, nucleic
acid hybridization tests (DNA probes), nucleic acid amplification (polymerase chain reaction
[PCR] or ligase chain reaction [LCR]), and the newer ThinPrep Pap Collection system. The new
Centers for Disease Control and Prevention (CDC) recommendations are that all sexually
active adolescents undergo routine screening for CT during annual pelvic examinations. The
CDC also recommends that routine screening of asymptomatic women between 20 and 24
years of age should be considered, particularly if they have a new male sex partner, more than
one male sex partner, or do not use barrier contraception.
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TABLE 197-1Microorganisms Involved in Pelvic

Inflammatory Disease
ORGANISM
Neisseria gonorrheae
Chlamydia trachomatis
Mycoplasma hominis
Ureaplasma urealyticum

INCIDENCE (%)
40-60
30
8
4

Data from Karchmer AW. Sexually transmitted diseases. In Dale DC, Federman DD, eds.
Scientific American medicine. New York: Scientific American, 1996:7:XXII-10-13.

infections with GC occur in the United States annually. More

than 4 million infections occur annually due to CT. The true incidence of CT infection is probably higher because not all states
require reporting. A higher proportion of PID has been ascribed
to CT than to GC.4
Neisseria gonorrhea

The incidence of GC in the United States increased by a factor of

2.7 from 1960 to 1980.5 The infection has reached pandemic proportions in the United States, where it is estimated that for each
reported case, four cases go unreported.6 Gonococci have been
recovered from the urethra of 2.2% of sexually active servicemen
who had minimal or no symptoms and from 40% of asymptomatic males who had contact with symptomatic women.7 In addition, an estimated 80% of the men and women exposed to
Gonococcus will develop infections.8
For a seemingly delicate and fastidious species, Neisseria has
impressive infective abilities, preferring human columnar and
transitional epithelia. In less than 1 hour after intercourse, Gonococcus can establish itself on the urethral mucosa, where it successfully resists the flow of urine.9 Favored sites in the lower female
genital tract are Bartholins and Skenes glands, the urethra, and
the endocervical canal.6 Direct spreading can occur from the
endocervix across the endometrial surface to the tubal mucosa, or
migration can occur through subendothelial vascular and lymphatic channels.2 Perhaps the most common method of spreading, however, is by vector: GC attached to spermatozoa are
physically carried to the fallopian tubes.6 Primary pathogens can
also enter the upper tract from retrograde menstruation or uterine
contractions during intercourse.10
In the acute state, the gonococci and polymorphonuclear lymphocytes accumulate in the subepithelial connective tissue, resulting in patchy destruction of the overlying mucosa.9,11 The
consequent thinning of the mucosal lining is thought to facilitate
the penetration of GC into deeper tissue.9 It is probably for this
reason that gonococci are reported to survive only a short time in
the fallopian tubes.12 However, they may be not only surviving
but thriving. The descent of the microbe beyond the surfaces
being examined makes detection difficult.12
Concomitant infections are known to occur with GC.13 Some
researchers have even proposed that GCs primary role appears to
be paving the way for secondary invaders from normal vaginal
flora, allowing access to the upper tract.14 The associated infection will frequently be CT, but a superinfection can also be present, in which case one will find that anaerobic bacteria have
colonized as well.13
Chlamydia trachomatis

In the United States it is estimated that 20% to 30% of PID cases

are caused by CT.3,15 Further, one study found that acute

chlamydial PID may be subclinical or silent in 66% to 75% of

the cases.16 Laboratory diagnosis of chlamydial infection is difficult, which, combined with CTs propensity to be asymptomatic,
renders thorough assessment of the scope of these infections
nearly impossible.
A 5-year study conducted in urban Sweden showed that, despite
a decrease in the incidence of gonococcal PID, the total number
of cases of acute PID were unchanged or even increased in the last
year of the study.17 Another European study, conducted in 1977,
found that 62% of women with acute salpingitis had elevated
(titer 1:64) chlamydial IgG antibodies.18 However, most other
studies completed to date show much lower percentages. These
numbers will no doubt change as diagnostic technology improves
and the clinical presentation of CT is more widely understood.
Anaerobic Infections

Anaerobes are the organisms most commonly isolated from the

fallopian tubes or culs-de-sac of patients with PID.19 Anaerobic
bacteria are probably not the chief causative agents but rather
opportunists, establishing themselves in unsuccessfully
defended tissues.
Anaerobic infections are commonly found in immunocompromised hosts and are generally of endogenous origin.20 The
cervix and vagina of a normal healthy woman contain both
anaerobic and aerobic bacteria.21 Anaerobic infections establish
themselves more often in older patients and in women with a
history of prior PID.5
Other Organisms

Facultative aerobic organisms found in tuboperitoneal fluids from

women with salpingitis have included coliforms, H. influenzae, S.
species, and M. hominis.22
M. hominis has not been demonstrated as a sole etiologic agent
but rather seems to be a common contributor to the polymicrobial
milieu that is often discovered in PID. One study found M. hominis in cervical cultures from 81% of women patients with GC and
64% of those without GC.23
Complications
There are serious physical consequences for women who have had
PID. It has been estimated that, in the postinfection state, one of
four women suffers from one or more sequelae such as abdominal
pain, infertility, or ectopic pregnancy.5 Dyspareunia is a symptom
that is often not investigated but which, when relevant questions
are asked, is frequently found in the post-PID sufferer.
Death from salpingitis is rare and is generally due to rupture of
the tubo-ovarian abscess with subsequent peritonitis. A mortality
rate of 5.2% to 5.9% has been calculated for tubo-ovarian
abscesses; before 1950, mortality was 80% to 100%.24,25 Better
diagnostic understanding of this complication, treatment with
antibiotics, and prompt surgical intervention have phenomenally
improved both morbidity and mortality statistics.
The Fitz-HughCurtis syndrome is a perihepatitis complicating
the primary condition of PID. Characteristic violin-string adhesions attach the liver to the abdominal wall.20,26 These adhesions
are due to local peritonitis involving the anterior liver surface and
the adjacent abdominal wall.27 Historically, GC was thought to be
the main contributor to this syndrome, but CT is now found
more frequently.20,21
Infertility is a serious concern. Once a woman has had PID, she
is at risk for additional attacks. This is in part because, after the
fallopian tubes have been damaged by the infectious process,

CHAPTER 197 Pelvic Inflammatory Disease

normal defense mechanisms are impaired. Reinfection has been

found to be the most important cause of infertility after PID.28
One study comparing the rate of nonsurgical infertility in 1973
with that of 1976 noted a 45% increase. This translates to 122,000
infertile couples per year.29 This increased incidence is consistent
with the concurrent epidemic of sexually transmitted disease
(STD)associated PID.
An alarming statistical analysis has shown that for each 1000
girls born in 1950, a total of 138 had one or more bouts of PID
by age 30; 26 were infertile because of the PID; and 9 had surgery
for ectopic pregnancy.5 Further, it has been postulated that by the
year 2000 there will be one episode of salpingitis for each two
women reaching reproductive age in 1970.21
Ectopic pregnancy is a severe sequelae, and any woman with a
history of PID faces a sevenfold to tenfold increased risk.5 Ectopic
pregnancies tripled in the United States from 1967 to 1977. In
1977 ruptured ectopic pregnancies accounted for 12% of maternal deaths and were the leading cause of maternal death in nonwhite women.29 In another study that followed women with PID
for 9.5 years, 12.8% were infertile after one infection, 35.5% after
two, and 75% after three infections. The same study showed that
1 in 24 women with PID will have an ectopic pregnancy.30
Risk Factors
In addition to the obvious factor of sexual contact, the main risk
factors are age, use or history of use of an intrauterine device
(IUD), and previous history of PID. An earlier sexual debut
puts a young woman in a high-risk group for PID, especially
when there are multiple sex partners. The risk in sexually active
15-year-olds is 1 in 8, whereas in the average 24-year-old it is 1 in
80.5 One interesting hypothesis for these data is that the cervical
mucus in the younger woman may be estrogen-dominated, creating an environment that is more accessible to pathogens.22
Women with multiple partners have a 4.6-fold greater risk than
women in monogamous relationships.21
A woman faces an increased risk of PID if she uses an IUD.
Oral contraceptive (OC) users are somewhat less likely to have
GC; on the other hand, they are at increased risk for chlamydial
invasion. Birth control remains a potent issue, with barrier methods being the techniques of choice because of their decreased PID
risk. It should also be noted that one author included his own
clinical observation that women in his practice who had vasectomized men as partners only seldom developed PID.31
The last risk factor to be considered is iatrogenic. This occurs
when invasive procedures have introduced pathogens, or in some
other way disturbed the tract flora and induced PID. Among these
procedures are the following:
Cervical dilation
Abortion
Curettage
Tubal insufflation
Hysterosalpingography
Insertion of an IUD
A hospital in Lund, Sweden, reported that 15% of its PID cases
were iatrogenic. This indicates that PID may not be strictly an STD.20
Pathogen Access to the Upper Female Tract
The route by which the pathogens gain access to the upper female
tract has only recently been explored. Menstruation, sperm, and
trichomonads have all been shown to be important in the transportation of pathogens into the salpinx.

1697

Often the onset of menses corresponds with the onset of an

episode of PID. Infections occurring around the menses tend to
be GC rather than CT, a clinical curiosity that may ultimately
shed light on the etiology. One hypothesis is that menstrual regurgitation assists the inflammatory response by carrying sloughed
endometrial epithelium, which may have attached GC or intracellular CT. These organisms can then proliferate in the tubal epithelium or on peritoneal surfaces.10,32
Human sperm has proved to be an interesting and multifaceted
variable in the precipitation of PID. Some of the research targets
bacteriospermia as a cause of infertility in men, findings that are
clearly relevant to PID. Increasingly, STD research is noting the
incidence of asymptomatic male carriers.6,7,31,33-36 A large population study discovered that 66% to 75% of the men who tested
positive for GC were asymptomatic.7
Designed to travel during intercourse, sperm also serve as effective vectors. Researchers took a look at this most basic interaction
between a man and a woman by means of a laboratory experiment.
They introduced organisms into capillary tubes containing cervical mucus, either alone or with added spermatozoa, and observed
microbial motility. Cervical mucus had already been considered
an effective mechanical and immunologic barrier between the
abundant flora of the vagina and the upper tract, and the test
results confirmed this idea. However, they also demonstrated that
organisms attached to sperm could easily traverse the length of the
mucus column. This may be particularly important during menses, because sperm migration has been observed through menstrual plasma but not during the luteal phase or through the
cervical mucus of pregnancy.
Electron microscopy has produced amazing photographic evidence of organisms attached to sperm.6,37 The mechanism observed
with piliated GC is that pili twist together with the tails of the
spermatozoa in a rope-in-a-spider-web arrangement around the
bacteria. Sperm have also been found intimately associated with
cytomegalovirus, Toxoplasma, Ureaplasma urealyticum,32 and CT.38
Motile trichomonads serve as another transporter of PID. They
can ascend from the vagina to the fallopian tubes, carrying additional invaders. In fact, it has been observed that trichomonads are
never isolated from humans when heavy bacterial contamination
is absent.32
DIAGNOSIS
Pelvic or lower abdominal pain is the most dependable symptom
of PID; unfortunately, however, it is not specific. Rebound tenderness is not reliably reported; cervical motion tenderness and
adnexal tenderness are much more common. The clinical picture
of the various types of PID can easily mislead. In a large study, the
clinical diagnosis of PID was confirmed at laparoscopy in only
65% of the patients. Appendicitis, hemorrhagic corpus luteum,
pelvic endometriosis, ectopic pregnancy, mesenteric adenitis, and
ovarian tumors accounted for 12%, while 23% were found to be
normal.39 Many PID patients have atypical signs and symptoms
and some have no signs or symptoms at all.5 Table 197-2 lists
those most commonly found.
The woman with GC may appear more toxic and febrile and
manifest leukocytosis, while CT-caused PID may give her an elevated sedimentation rate (ESR). Most episodes of gonococcal PID
occur at or shortly after menses.40 Gonococcal PID has a generally
more severe clinical picture, but tissue damage and long-term
sequelae can be more severe in CT. This attempt to differentiate
clinical pictures becomes meaningless, of course, in the presence
of mixed infections.


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TABLE 197-2Common Signs and Symptoms in Acute

Pelvic Inflammatory Disease
SYMPTOM
Lower abdominal pain
Adnexal tenderness on palpation
Pain on movement of the cervix
Vaginal discharge
Adnexal mass or swelling
Fever or chills
Irregular vaginal bleeding
Anorexia, nausea, and vomiting

INCIDENCE (%)
90
90
90
55
50
40
35
25

Data from Karchmer AW. Sexually transmitted diseases. In Dale DC, Federman DD, eds.
Scientific American medicine. New York: Scientific American, 1996:7:XXII-10-13.

BOX 197-1Differential Diagnosis of Pelvic Inflammatory

Acute appendicitis
Acute cholecystitis
Acute pyelonephritis
Ectopic pregnancy
Endometriosis
Hemorrhagic ovarian cysts

Intrauterine pregnancy
Mesenteric lymphadenitis
Ovarian cyst with torsion
Ovarian tumor
Pelvic thrombophlebitis
Septic abortion

Any mucopurulent discharge should yield oxygen-sensitive

organisms because offensive odor is considered diagnostic of
anaerobic infection. Any woman who has such a discharge probably has well-developed PID, with opportunistic anaerobes following the primary invaders.28 Box 197-1 shows the differential
diagnoses of PID. Potentially lethal conditions to consider include
ectopic pregnancy, tubo-ovarian abscess, ovarian cyst rupture with
hemorrhage, and appendicitis.
In light of the Fitz-HughCurtis syndrome, symptoms from
the upper right quadrant in a sexually active woman may be an
indirect sign of genital infection. The pain usually has a sudden
onset and can overshadow the signs and symptoms of the
underlying PID.27
In the event of rupture of a tubo-ovarian abscess, a sudden
severe exacerbation of the pain can be observed. The pain is
referred to the side of the rupture and is typically followed by
generalized peritonitis and collapse. Shoulder pain may be present. The pulse will likely be elevated out of proportion to the fever
and is frequently as high as 170.25 Surgery must be performed
within 12 hours or mortality becomes probable.
A careful history is, as always, invaluable. The patients risk factors and history should be assessed for likelihood of infection with
a sexually transmitted organism. The patient should be questioned
about any new sex partner, method of contraception, and recent
medical procedures. The source, severity, and characteristics of the
pelvic/abdominal pain should be evaluated. Mucopurulent cervicitis should be considered as well, and the cervix should be cultured for GC and CT.
Empiric treatment of PID should be initiated in sexually
active young women and other women at risk for STDs if they
are experiencing pelvic or lower abdominal pain, if no cause
for the symptoms other than PID can be identified, and if
one or more of the following minimal criteria are present on
pelvic examination:
Cervical motion tenderness or uterine tenderness or adnexal
tenderness

The following additional criteria above and beyond the minimal

criteria may enhance the diagnosis of PID:
Oral temperature above 101F or 38.3C
Abnormal cervical or vaginal mucopurulent discharge
Presence of abundant numbers of WBCs on saline microscopy
of vaginal secretions
Elevated erythrocyte sedimentation rate
Elevated C-reactive protein
Laboratory documentation of cervical infection with GC or CT
The following criteria for hospitalization are suggested:
Surgical emergencies (e.g., appendicitis) cannot be excluded.
The patient is pregnant.
The patient does not respond clinically to oral antimicrobial
therapy.
The patient is unable to follow or tolerate an outpatient oral
regimen.
The patient has severe illness, nausea and vomiting, or high fever.
The patient has a tubo-ovarian abscess.
THERAPEUTIC CONSIDERATIONS
Criteria for hospitalization include surgical emergency or septicappearing patient, pregnancy, failure to respond to oral antibiotics,
and suspicion of tubo-ovarian abscess. Referral is necessary if the
diagnosis is uncertain or a surgical emergency threatens. Should the
physician decide not to hospitalize, a regimen of antibiotic therapy
combined with the supportive therapies discussed later, can be tried
if the patients clinical and laboratory status can be reassessed in 48
to 72 hours. Laboratory values and objective patient criteria should
direct all acute-phase treatment. The CDC leaves it to the individual practitioner to decide on the severity of the disease and the optimal treatment. Its guidelines do say that Most experts encourage
hospitalization and treatment with intravenous antibiotics.
Antibiotics
PID is a complex syndrome, with inconsistent and variable presentations in different women and including a range of symptoms
and etiologic microorganisms. Because of this, broad-spectrum
antibiotic regimens are employed that allow for some flexibility on
the part of the practitioner. Regimens are tailored on the basis of
clinical severity and laboratory findings, patient compliance, cost
of medications, and availability of medications. Because some
antibiotics cover only one organism, the CDC outpatient recommendations take into account the limited anaerobic activity of any
one regimen.
Oral Treatment
Oral therapy can be considered for women with mild to moderately severe acute PID, because the clinical outcomes among
women treated with oral therapy are similar to those in women
treated with parenteral therapy. Women who do not respond to
oral therapy within 72 hours should be reevaluated to confirm the
diagnosis and should be given parenteral therapy (see Box 197-2).
Fifteen percent of women with PID fail to respond to primary
antimicrobial treatment, 20% have at least one recurrence, and
15% are rendered infertile.19
Given the polymicrobial nature of PID, the complexities of isolation, antibiotic-resistant strains of microorganisms, and the
realities of recurrence rate with antibiotic use, an approach that
combines immune system enhancement and nontoxic therapies
concurrently with antibiotics seems sound. However, there are no
evidence-based therapies using natural therapies exclusively for

CHAPTER 197 Pelvic Inflammatory Disease

1699

BOX 197-2Recommended CDC Oral Regimen (last updated 2010)

Recommended Regimen
Ceftriaxone 250 mg IM in a single dose
PLUS
Doxycycline 100 mg orally twice a day for 14 days
WITH or WITHOUT
Metronidazole 500 mg orally twice a day for 14 days
OR
Cefoxitin 2 g IM in a single dose and Probenecid, 1 g orally administered
concurrently in a single dose
PLUS
Doxycycline 100 mg orally twice a day for 14 days
WITH or WITHOUT
Metronidazole 500 mg orally twice a day for 14 days
OR
Other parenteral third-generation cephalosporin (e.g., ceftizoxime or cefotaxime)
PLUS
Doxycycline 100 mg orally twice a day for 14 days
WITH or WITHOUT
Metronidazole 500 mg orally twice a day for 14 days
Parenteral and oral therapy appear to have similar clinical efficacy treating women with PID of mild or moderate severity. Clinical experience should
guide decisions regarding transition to oral therapy, which usually can be
initiated within 24 hours of clinical improvement.

Recommended Parenteral Regimen A

Cefotetan 2 g IV every 12 hours
OR
Cefoxitin 2 g IV every 6 hours
PLUS
Doxycycline 100 mg orally or IV every 12 hours
Intravenous infusion of doxycycline is painful and should be administered
orally when possible. Bioavailability of oral and IV is similar.
Parenteral therapy may be discontinued 24 hours after clinical improvement,
but oral therapy with doxycycline (100 mg twice a day) should continue to complete 14 days of therapy. When tubo-ovarian abscess is present, clindamycin or
metronidazole along with doxycycline can be used for continued therapy because
it provides more effective anaerobic coverage than doxycycline alone.
Recommended Parenteral Regimen B
Clindamycin 900 mg IV every 8 hours
PLUS
Gentamicin loading dose IV or IM (2 mg/kg of body weight), followed by a
maintenance dose (1.5 mg/kg) every 8 hours. Single daily dosing (3-5 mg/
kg) can be substituted.
Parenteral therapy may be discontinued 24 hours after clinical improvement; ongoing oral therapy should consist of doxycycline 100 mg orally twice
a day, or clindamycin 450 mg orally four times a day to complete a total of 14
days of therapy. When tubo-ovarian abscess is present, clindamycin or metronidazole along with doxycycline can be used for continued therapy because
it provides more effective anaerobic coverage than doxycycline alone.

Data from Centers for Disease Control and Prevention, Sexually Transmitted Diseases: Treatment Guidelines, 2010: Pelvic Inflammatory Disease, http://www.cdc.gov/std/
treatment/2010/pid.htm, accessed May 15, 2012.

the treatment of PID. Antibiotics can help with the first phase of
treatment but may not offer sufficient intervention for the devastation that regularly occurs in the wake of the primary infection.
Physical Medicine
Diathermy

In the 1920s and 1930s, pulsed, high-frequency diathermy was first

reported to be beneficial in the treatment of women with PID.41-43
Pulsing electric energy for a short duration (65 mcs every 1600
mcs) at high intensity achieves the desired therapeutic result without the hyperpyrexia typically associated with diathermy. Local
recovery is enhanced, the reticuloendothelial system is stimulated,
and gamma-globulin fractions are increased.21 There is no modern
research on using this therapy, and practitioners should be very
cautious in using it as a substitute for antibiotic therapy.
Sitz Baths

Traditionally, sitz baths have been an important component of the

naturopathic treatment of PID. The contrast sitz bath is primarily
used to increase pelvic circulation, bring an influx of macrophages
to the area, and provide decongestion of the pelvic inflammatory
reaction (for further discussion, see Chapter 40).
Nutritional Supplements
Vitamin C

Vitamin C may be useful in the treatment of women with PID for

the following reasons:
Its antiinflammatory effects help to decrease tissue destruction.
Its support of collagen tissue repair helps to prevent the spread
of infection (especially important in GC infections, which can

spread through the subepithelial connective tissue, resulting in

disorganization of the collagen matrix8).
Its fibrinolytic activity helps to prevent pelvic scarring.
Beta-carotene

The normal ovary has a high concentration of beta-carotene. As

these structures are bombarded by inflammation and the unwelcome company of aggressive microbes, it is essential to maintain
optimal levels of carotene to allow for an optimal defense. Betacarotene potentiates the beneficial effects of interferon and enhances
numerous other immune functions such as antibody levels and
WBC activity.44,45 Beta-carotene is also important as an antioxidant, helping to limit the cell damage induced by the inflammatory
process (see Chapter 69 for a full discussion of this nutrient).
Bromelain

Bromelain should be considered an important component of the

treatment regimen. Adnexal exudate in PID frequently suppurates
to form abscesses. If tissue irritation is relieved or ameliorated during the acute stage, much of the exudate can be absorbed and fewer
adhesions will be formed.41 Adhesions will form as the exudate
lingers, the structures being overwhelmed by the inflammation.
Also, after resolution, agglutination of the villous fold in the lumen
of the tube may occur, resulting in scarring and tubal occlusion.6
Bromelain activates fibrinolysis, which can greatly diminish the
enduring sequelae of the inevitable exudate. Bromelain also demonstrates antimicrobial properties, and an Italian study has shown that
it penetrates the salpinx46 (see Chapter 71 for further discussion).
Probiotics

When individuals take antibiotics, the gastrointestinal, vaginal,

and bladder microflora are disrupted. This can cause side effects


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with antibiotic use or after such use, including diarrhea, candidal

vulvovaginits, and acute cystitis. Probiotics are generally defined as
live microorganisms whose function is dependent on the ability of
a strain to benefit the host when it is administered orally.
There are many species and strains that have been proved to
have adhesive properties and can proliferate in these organs and
thus prevent opportunistic overgrowth, as well as the side effects
from antibiotics, and also restore the normal microflora. No one
species or strain can be recommended here, but combination
products to be considered should include at least one or more of
the following: Lactobacillus rhamnosus, L. plantarum, L. rheuteri, L. acidophilus, Bifidobacterium bifidum, B. lactis, B. breve,
and B. longum.
Botanical Medicines
Many botanicals have been shown to have antimicrobial and
immunostimulating effects. Allicin extracts from garlic, golden
seal and Oregon grape root, and echinacea should all be considered at least as part of a treatment plan and as adjuncts to antiobiotic therapy.
Vaginal Depletion Packs

Use of the vaginal depletion pack has historically been a part of

traditional PID treatment, because it promotes the drainage of
exudate from the involved tissues. (This is discussed in more detail
in Appendix 12.) It may also stimulate the immune cells within
the vagina to provide a first line of defense.
Hydrastis canadensis

The immune-potentiating specific antimicrobial properties and

the general antibacterial nature of goldenseal make it indispensable in the care of PID. Since Hydrastis canadensis is also a trophorestorative to mucous membranes, the herb should be used
throughout the rehabilitation period. (H. canadensis is discussed
in more detail in Chapter 97.)
Prevention
STD prevention is an extremely important issue for all heterosexually and bisexually active women. The woman with no history of
PID should still be concerned about the significant population of
asymptomatic male carriers of STDs. The choice of birth control
is pivotal. Women who use barrier methods of contraception have
a lower risk of PID.
Oral Contraceptives

A surprising number of articles laud the use of oral contraceptives

(OCs) for their apparent inhibition of GC.21 Burnham19 has suggested OC use after a first episode of PID to prevent recurrence.
Apparently, estrogens create a thicker cervical plug, which offers
protection against gonococci.8,10 OCs also decrease the length and
volume of menstrual flow, thus decreasing the exposure of the GC
to this handy culture medium.
On the other hand, OC users have a higher risk of chlamydial
infections.8,32,40,47 Progesterone can produce cervical eversion,
exposing the endocervical columnar epitheliumthe target tissue
of CT.40 Estradiol has been implicated in suppressing the endocervical antibodies necessary for resolution of CT.40 Animal experimentation finds that estrogen-treated individuals have a higher
number of infected cervical cells and a longer duration of infection.48 Because women are probably not selectively exposed to GC
versus CT, OCs are not recommended.

Intrauterine Devices

The IUD has a bad reputation in PID.* This reputation is a carryover from the former Dalkon Shield, which is no longer available. Current IUDs such as the Copper T and the Mirena are
generally considered safe. However, the use of an IUD is associated with a slightly increased risk of PID, especially in the first 4
months of use. An IUD allows the colonization of bacteria on its
surface while simultaneously reducing local immunologic capacity.49 If a woman with suspected PID has an IUD, it must be
removed 12 to 24 hours after initiation of antibiotic therapy in
order to prevent the spread of the infection during its removal.
Barrier Methods

Barrier methods of contraception are excellent choices for the prevention of PID. The condom is preferred to cervical protectors, as
with this method the sperm more rarely reach the vaginal vault.
Douching

Haphazard douching is to be avoided because it disturbs the vaginal flora. All forms of douching increase the risk of PID and can
cause organisms to ascend into the upper genital tract.
One study compared 100 consecutive patients hospitalized for
PID with 762 controls and 119 women suspected of having PID.50
Current douching (defined as any douching during the previous
2 months) was more common among those with PID than among
those in both control groups. Among current douchers, PID was
related to the frequency of douching. Those who douched three or
more times per month were 3.6 times more likely to develop PID
than those who douched less than once per month.
A much larger study surveyed 6984 women older than 18 years
of age and found that 32% said they had douched within the previous week; 13% reported regular douching more than once a week.51
Intercourse During Menses

Intercourse during menses is not recommended unless a condom

is used. GC risk is increased by the loss of the protective cervical
mucus plug and by the prevalence of blood, a medium of choice
for Gonococcus. The endometrium is also thought to offer local
protection against bacterial invasion, and it is this layer that is
being sloughed off during menses.
Smoking

When 197 women hospitalized for their first PID infection were
compared with 667 controls with nongynecologic conditions, it
was found that cigarette smokers, compared with women who had
never smoked, had an elevated risk of PID of 1.7, and former cigarette smokers had an elevated risk of 2.3. There was no doseresponse relationship.52
A more rigorous study found similar results. This was a casecontrolled population-based study of 131 women between 18 and
40 years of age who were treated for their first episode of PID
compared with 294 randomly selected patients from the same
health maintenance organization. Current smokers compared
with those who had never smoked had an increased risk of PID.
Women who smoked 10 or more cigarettes a day had a higher risk
than those who smoked less.53
Education

A physician should review the signs and symptoms of PID with all
sexually active women and encourage any woman to seek counsel
if she appears to fit the clinical picture for PID. The diagnosis is
*References 5, 16, 19, 22, 27, 54, 55.

CHAPTER 197 Pelvic Inflammatory Disease

easier to make and the recovery more rapid when treatment is

instituted early.
THERAPEUTIC APPROACH
Treatment consists of two phases, both of which are important.
The first therapeutic goal is to eliminate all pathogens and normalize the microflora of the adnexa. The second is to rehabilitate the
damaged tissues.
Women should avoid intercourse until all signs and symptoms are
resolved and their male partners have been examined and treated. In
addition, all partners from up to 2 months before the illness should
be examined19 and treated if a diagnosis of PID is made. Increased
bed rest must also accompany all forms of treatment.
These therapies are recommended as adjuncts to appropriate
antibiotic treatment and immune support, as discussed in
Chapter 56.
Diet
All dietary inhibitors of immune function (sugar, alcohol, saturated fats, simple carbohydrates) should be limited during both
phases of treatment.
Supplements
Beta-carotene: 100,000 IU/day for 2 or more months
Vitamin E: 400 IU/day for 3 months
Vitamin C: 500 mg four times a day for the first week of treatment and then decreased over 3 days to 250 mg three times a day
Chlorophyll: 10 mg of fat/oil-soluble four times a day for
1 month

1701

Bromelain: 250 mg (1800 milk clotting unites [MCU]) four

times a day for the first week and three times a day for 6 weeks
Probiotics supplement: minimum 1 billion CFU per day, consider up to 24 billion CFU per day during antibiotic treatment
and for 2 months thereafter
Botanical Medicines
H. canadensis: 500 mg of the solid extract (4:1 or 8% to 12%
alkaloid content) three times a day during the acute phase;
250 mg three times a day during recovery
Vaginal packs: daily during the acute phase until there is adequate clinical and laboratory response. After the acute phase,
vaginal packs need to be used three times a week, alternating
with chlorophyll douches, for 3 weeks.
Physical Medicine
Diathermy: pulsed, high-intensity diathermy for 10 minutes
over the suprapubic area, 10 minutes over the liver, and 10 minutes in the area of the left adrenal (the right being presumably
stimulated with the liver).
Sitz baths: one to two times/day throughout the acute phase.
Contrast sitz baths are given in groups of three alterations of hot
to cold. Two separate tubs are necessary during this process. The
hot is at 105oF to 115oF, the cold at 55oF to 85oF, with the
temperatures dependent on the patients tolerance. The standard treatment is 3 minutes hot and 30 seconds cold, with this
cycle being repeated three times in one sitting. The water level
in the hot tub is set 1 inch higher than in the cold. Adequate
draping is necessary to prevent chilling. As with all hydrotherapy treatments, one always finishes with the cold.

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