2. cord neurotransmitter and interneuron activity, the
transmission of these nociceptive signals from the
periphery. Deterioration of these regulatory processes
were thought to potentially account for development
of chronic pain states by allowing too many peripheral
signals to pass through the spinal cord “gates.” Vari-ation
in patients’ relative degree of gate opening could
thus explain why similar amounts of physical tissue
damage result in different degrees of pain perception.6
While these theory changes were stimulating the
field of pain research, gynecologists were busy devel-oping
laparoscopy and with it the hope that treating
visible pathology could fix chronic pelvic pain. A
focus on “laparoscopy-negative” patients in chronic
pelvic pain clinics emerged, implying that if some
pathology were found, it must be a “real” cause for
pain. Subsequent experience has shown that although
treatment of laparoscopically diagnosed pathology
can be helpful, the clinical reality is more complex:
1) in many instances, visible pathology found at lapa-roscopy
may be incidental and not related to the pain;
2) in those with pathology that does contribute to
nociception, the pain experienced by the patient
may differ from another patient with anatomically
similar pathology; and 3) pain from a laparoscopic
finding is often best understood in the larger context
of a centralized pain disorder.
Research of the 1980s added the observation of
distressingly high rates of physical and sexual abuse,
especially in the chronic pelvic pain population. These
observations led to the speculation that the experience
of abuse may make a person more vulnerable to the
development of chronic pelvic pain or perhaps be
a specific cause for pain. In relation to pain, abuse,
particularly that which occurs in formative years, may
serve to alter the response to nociception and central
pain processing. That said, not all abused patients go
on to have chronic pain nor do all patients with pain
have a history of abuse, so it might be the response to
trauma that plays a key role in development of chronic
pain. Health care providers need to take into account
the presence of abuse in a patient’s history when de-tected
but be careful to avoid necessarily concluding
a causal relationship in that patient’s pain.
Melzack’s neuromatrix theory7 added the pivotal
notion of neuroplasticity, which suggests that experi-ence
can change the neurophysiologic behavior of the
central nervous system in a manner that influences the
subsequent processing of nociceptive stimuli. It may
explain the apparent development of pain responses
to stimuli usually thought of as nonpainful (allodynia)
as well as exaggerated responses to painful stimuli
(hyperalgesia). Every practicing gynecologist has seen
patients whose pain responses seem out of proportion
to the pathology found. This may reflect the emo-tional
meaning of the problem for the patient as well
as past or present trauma, but it may also be the result
of sensitization of spinal cord interneurons that have
become pain amplifiers as a result of being on the
receiving end of peripheral nociceptive stimuli for pro-longed
periods. On the positive side, neuroplasticity
suggests that given enough time and the right treat-ment,
even seemingly intractable chronic pain prob-lems
can improve substantially.
The concept of central sensitization adds the
most recent layer to theoretical understanding of
chronic pain: the notion that multiple repetitions of
lower-level stimuli may over time result in a more
severe central perception of pain. This centralized
pain hypersensitivity helps us understand how mul-tiple
organ systems can be recruited into the syn-drome,
incorporating genetic and social factors in
pain amplification. Whatever the nociceptive stimulus
(bowel, bladder, muscle, uterus), it can register as pain
at a lower threshold in the patient with a centralized
pain disorder (Box 1).
Box 1. Definitions of Pain Terms
Allodynia—pain resulting from a nonnoxious stimulus
Hyperalgesia—painful sensation of abnormal severity
after noxious stimulation
Neuropathic pain—pain persisting after healing of
disease or trauma-induced tissue damage
Neuroplasticity—the malleability of central pain perception
mechanisms in response to chronic pain states
Nociceptor—a nerve receptor for pain
This understanding contributes to the framework
a clinician needs when taking a clinic history of pelvic
pain and performing the physical examination. The
inquiry should set out in pursuit of all the factors
relevant to a person’s pain, not simply trying to identify
one factor with an acceptably plausible relationship to
her complaints. Once the patient is aware that the cli-nician
is keeping an open mind about multiple contrib-uting
factors, she may become less defensive about any
inquiries in emotional areas.
EVALUATION OF PATIENTS WITH CHRONIC
PELVIC PAIN
History-Taking
The site, duration, pattern during activities, relation to
position changes, and association with bodily func-tions
are all important elements of pain. For example,
pain that is absent in the morning but worsens
VOL. 124, NO. 3, SEPTEMBER 2014 Steege and Siedhoff Chronic Pelvic Pain 617
3. progressively during the day may be associated with
pelvic floor muscle dysfunction, whereas a tender
“spot” of dyspareunia might be related to nodular cul
de sac endometriosis. A previous review supplies a very
detailed description of both history-taking and physical
examination techniques that are useful in the evalua-tion
of chronic pelvic pain.8 We focus here on the most
frequently useful elements of this process.
The chronology of a patient’s pain is critical. As a
pain syndrome develops, pain can be present over a
progressively larger area despite stable detectable
pathology. Interpreting this as the breakdown or wear-ing
out of physiologic systems that deal with pain sig-nals
has some biologic validity and may make sense to
the patient. The clinician may need to counter the idea
patients sometimes have that endometriosis “flares”
like rheumatoid disease or spreads like a malignancy.
From a cognitive perspective, it is invaluable to
discern the patient’s and her family’s ideas about the
causes of and future for her pain. Fears of cancer can
be discovered even if this diagnosis was never even
remotely considered by the clinician. Less dramatic
but equally powerful attributions of cause can emerge
such as pelvic infection that is the result of sexual acts
remote in time, arguments with a spouse, divine ret-ribution,
and so forth.
When a patient has been under that care of
previous health care providers, it is important to
review the effects of previous treatments and the
evolution of how the patient has thought about her
own disease. For example, when a prior treatment
for mild endometriosis was only briefly successful,
did she (and her health care provider?) see this as
evidence for increasing severity of disease or did it
make them question the diagnosis in the first place?
In a referral-based practice, it is a frequent event to
deal with a patient with mild disease who has not
responded to any of four or five medical or surgical
measures that would ordinarily improve symptoms.
She then sees herself as having increasing and
invasive disease, prompting even more aggressive
treatment, rather than wondering if something else is
contributing to her pain.
Physical Examination
The physical examination begins with observing the
patient’s gait, comfort with sitting, ease of going from
sitting to standing, and from sitting on the table to
lying down. Dysfunctions of the pelvic floor and hip
muscles may be manifested by discomfort with these
motions. For example, if the patient sits up on one
buttock during the interview, one might suspect pelvic
floor muscle pain.
With the patient sitting on the examination table,
it can be helpful to begin the examination with the
back, evaluating for tenderness of the spine, para-spinous
muscles, and sacroiliac joints. This may
identify pain generators and sites for therapeutic
intervention, but it also allows for touch to begin in
a very nonthreatening way. Gynecologic assessment is
uncomfortable to some degree for almost all women,
but the patient with chronic pelvic pain is particularly
vulnerable. Moving from back to abdomen to pelvis
can establish trust and reduce fear.
The patient is then asked to recline on the table,
observing how comfortably she can do this. The
abdominal wall is examined with and without flexed
rectus muscles. A positive Carnett sign (increased
tenderness when palpation is done in the presence of
abdominal wall flexion) implies at least a contribution
to the pain from abdominal wall myofascial sources.
Decreased pain during this maneuver implies a higher
contribution from visceral sources. On occasion, gentle
fingertip palpation of the abdominal wall can detect
such trigger points in the musculature. Rarely, a sub-cutaneous
abdominal wall endometrioma is discov-ered,
a diagnosis supported by a history of predictable,
cyclic, focal tenderness. An abdominal wall endome-trioma,
or a hernia, is often more readily appreciated
by examining the patient in the standing position.
Pelvic examination then begins with external
review of the vulva and vestibule. Gentle palpation
with a cotton swab can detect areas of sensitivity
consistent with vulvar vestibular syndrome in the
introitus or trigger points higher in the vagina.
Intrinsic cervical allodynia (from cervical conization
or after obstetric cervical laceration) may be detected
in the same manner with gentle cotton-tipped appli-cator
palpation.
Guiding a patient through contraction–relaxation
sequences of the abdominal, thigh, and vaginal introi-tal
muscles can reduce the discomfort of the examina-tion
and can indicate the patient’s degree of control
over muscle tension. Single-digit palpation of the leva-tor
plate, piriformis, and obturator muscles can elicit
the tenderness of pelvic floor tension myalgia. This
condition can present as a sequel to some other pelvic
pain or a problem in itself. Discomfort is usually felt as
pelvic pressure and radiation pain to the sacrum, near
the insertions of the levator plate muscles. The exact
sequence of the examination should be adjusted in
view of the information obtained during the history:
examine the areas less likely to be tender first, saving
the more tender areas for the end. Palpating the most
tender areas first can elevate anxiety and distort pain
responses from subsequent areas.
618 Steege and Siedhoff Chronic Pelvic Pain OBSTETRICS & GYNECOLOGY
4. Single-digit palpation should also be used to
discover areas of tenderness in the cervix, uterus,
adnexa, bladder, and urethra. Premature addition of
the abdominal hand to the examination adds in
nociceptive signals from abdominal wall myofascial
components that may lead the examiner to over-attribute
pain to the viscera. Finally, the abdominal
hand is added to assess size, shape, and mobility of
pelvic structures. Adnexal thickening and mobility,
pelvic relaxation, coccygeal tenderness, and foci of
pain that reproduce dyspareunia should be noted. A
rectovaginal examination is important when deep
infiltrating endometriosis is suspected.
During all components of the physical examina-tion,
it is important to not only ask the question “Does
this hurt?,” but also “Do you feel pain where I am
pressing or somewhere else?” and “Is this the pain
you were describing earlier—is this your pain?” If
a patient answers affirmatively to the final question,
it can be helpful to point out what structure you are
palpating (eg, pelvic floor muscle compared with
ovary). As you are going along through the examina-tion,
it can be useful to mention the items you are
adding to the list of possible contributing factors to
her pain, thus reinforcing what you discussed during
the history in terms of pain being multifactorial.
Having concluded the most important part of the
evaluation, the history and physical, you are now
prepared to discuss diagnostic possibilities and a treat-ment
plan. What follows is a review of the commonly
described contributors to pelvic pain, which might be
part of that discussion.
CONTRIBUTIONS OF PERIPHERAL
PAIN GENERATORS
This section deserves an important caveat. Although we
believe that types of tissue damage or other nociceptive
input can generate pain, they cannot be viewed in
isolation of the patient’s individual central pain process-ing.
Management strategies are discussed in more
detail, but, in general, the goal of the treating health
care provider involves trying to dampen overall pain
signaling sensitivity—“turning down the master vol-ume”—
and looking for areas in the periphery that can
be “tuned up” toward better functioning. This effort is
more likely to be successful in the patient who takes an
active role in her own improvement and avoids seeing
herself as helpless in the face of her discomforts.9
The following peripheral generators represent areas
where we can intervene but should not be described to
patients with chronic pelvic pain as the only cause of
their pain. Because these conditions can be completely
asymptomatic in many patients, their importance needs
interpretation in the context of her overall health, taking
into account her other pain disorders and general
capacity for dealing with life’s challenges.
Endometriosis
Evidence that endometriosis causes pain results from
observations that the disease is more commonly
encountered in women undergoing laparoscopy for
pain than for other reasons10 and that laparoscopic
treatment results in better pain reduction than diagnos-tic
surgery alone.11–13 However, amount of disease does
not correlate with symptom severity14,15; endometriosis
is a frequently encountered incidental finding, and peri-toneal
implants do not localize to symptom location.16
A variety of proposed mechanisms explaining pain
associated with endometriosis exist, including inflam-matory,
nociceptive, and neuropathic.17 There is no
pathognomonic symptom associated with endometri-osis,
however. Many of the symptoms often attributed
to endometriosis (eg, dyspareunia, dysmenorrhea,
abnormal bowel or bladder function) are commonly
found in functional disorders such as irritable bowel
syndrome or interstitial cystitis, making it difficult to
understand the relevant contribution of endometriosis
to chronic pelvic pain. Deeply infiltrating endometri-osis—
fibrotic, vascular, desmoplastic tissue destruction—
is a biologically different disease, in which detectable
physical examination or imaging findings relate to spe-cific
symptoms such as tender rectovaginal nodularity
or ovarian endometrioma with dyspareunia or dysche-zia
with intrinsic rectal involvement.18–20 The relation-ship
of a related condition, adenomyosis, to pelvic pain
is less established, but the disease should be considered,
especially when symptoms include dysmenorrhea or
heavy bleeding.21
Pelvic Adhesions
Early reviews supported the role of adhesions as
a significant contributor in chronic pelvic pain.10,22
More recent investigations23 demonstrate a relatively
weak correlation between adhesions and chronic
pelvic pain, much less than other factors such as psy-chosomatic
symptoms and substance abuse. Few, if any,
well-designed studies demonstrate effective treatment of
chronic pelvic pain with adhesiolysis. Unfortunately, in
an effort to provide some explanation for complex pain
disorders, health care providers often still posit adhe-sions
as an etiology, even when a patient’s surgical his-tory
includes only laparoscopy with findings of minimal
or no endometriosis, pelvic inflammatory disease, or
other conditions associated with meaningful adhesions.
This explanation can happen even when the patient’s
pain escalation is remote from her last surgery.
VOL. 124, NO. 3, SEPTEMBER 2014 Steege and Siedhoff Chronic Pelvic Pain 619
5. Adhesions may play some role in pain conditions in
some women, but the relative contribution is probably
small. Also, the putative treatment—repeat surgical
intervention—can add new contributions to pain syn-dromes
such as the effect of surgical trauma, disappoint-ment
from lack of pain relief, feeding the psychological
need of being “ill” with more surgery, and, in the worst
case, generating a complication such as enterotomy.
Pelvic Support
Most women in pain clinics are in their third or fourth
decade of life, whereas pelvic organ prolapse affects
significantly older women, suggesting a very minimal
role for support problems in chronic pelvic pain.
Pelvic relaxation usually leads to reports of heaviness,
pressure, dropping sensations, or aching. In attempt-ing
to hold in prolapsing organs, the patient may tense
the levator plate, leading to tenderness during daily
activities and intercourse. Fear of (or actual) loss of
urinary control during coitus can add to the discom-fort
by impairing physiologic sexual response.
The retroverted uterus is another potential contrib-utor
to chronic pelvic pain, particularly in the form of
deep dyspareunia. Clearly for many women, retrover-sion
is an innocent anatomic variant, but for those with
pain, uncontrolled clinical series of uterine suspension
procedures suggest changing the position of the uterus
to an axial or anteverted position can improve dyspar-eunia
by elevating the fundus out of the posterior cul de
sac24–26 and allowing for better vaginal expansion as
a natural part of the sexual response cycle.27
Pelvic Congestion
Overfilling (congestion) of the pelvic venous system
has been implicated as a cause of dull chronic aching
pain that usually is bilateral, worse at the end of the
day after prolonged standing, premenstrually, and
postcoitally. Some studies suggest the condition is
present in nearly one-third of women with chronic
pelvic pain,28 but there is no agreed-on reference stan-dard
for diagnosis despite individual technical regi-mens
involving venography, magnetic resonance,
and ultrasonography.29 Hormonal suppression,30,31
percutaneous embolotherapy, and surgery (vein liga-tion,
hysterectomy and salpingo-oophorectomy) rep-resent
available treatments,32 but study protocols
involving these interventions are diverse and few have
been investigated in controlled trials.33
Residual Ovary
When the uterus has been removed, with or without
removal of one ovary, the remaining ovary or ovaries
become symptomatic in a small percentage of women.34
Pain from the ovary can be increased by confinement
within postoperative adhesions, rupture or leakage of
a cyst prompting additional adhesion formation, or
attachment of the ovary to the sigmoid colon or vaginal
apex by postoperative adhesions. In the case of attach-ment
to the vaginal apex, deep dyspareunia can result
when the area is struck.
Ovarian Remnant
A more difficult situation can develop if a small
fragment of ovarian tissue is left behind during
attempted oophorectomy.35 In most instances, this
happens when challenging dissection is required, such
as cases of extensive pelvic adhesions or deeply infil-trating
endometriosis. Within 1–3 years of the attemp-ted
oophorectomy, continued follicle-stimulating
hormone stimulation will result in growth of the ovar-ian
fragment, often producing an intermittently symp-tomatic
pelvic mass located along the course of the
ovarian vascular supply. A postulated mechanism for
pain generation includes the cystic enlargement of the
mass confined within fibrotic adhesions. If the rem-nant
developed because endometriosis made for diffi-cult
oophorectomy, that disease is often found in the
remnant and probably also serves as a pain generator.
Classic remnant symptoms include absence of vaso-motor
symptoms after ostensible bilateral oophorec-tomy
and the presence of cyclic unilateral pain. Like
in the case of the residual ovary, the remnant can
produce dyspareunia if it is located close to the vaginal
apex. When performing oophorectomy, it is best to
open the pararectal space and completely skeletonize
the infundibulopelvic ligament not only to avoid com-plications
such as ureteral injury, but also to prevent
ovarian remnant syndrome. In difficult cases, dividing
the pedicle at or above the pelvic brim, like in risk-reduction
prophylactic oophorectomy, is prudent.
Vaginal Apex Pain
After hysterectomy, pain may persist or recur because
of intrinsic sensitivity of the vaginal apex. Although the
cuff may appear to have healed perfectly well, gentle
examination with a cotton-tipped applicator may reveal
focal sensitivity of a moderate to severe degree, many
times located in one lateral fornix or the other and often
replicating the reported pain of dyspareunia. When the
cotton applicator examination is not done, the unaware
examiner may then, noting pain on traditional biman-ual
examination, mistakenly conclude that the source of
nociception lies cephalad, for example, in a remaining
ovary, pelvic scarring, or bowel adhesions.
The diagnosis may be confirmed by noting
elimination of the pain after injection of a local
620 Steege and Siedhoff Chronic Pelvic Pain OBSTETRICS & GYNECOLOGY
6. anesthetic. The condition is generally considered
neuropathic by virtue of the character of the pain
(burning, stinging, sharp) and that neuropathic treat-ments
(overnight application of lidocaine, oral medi-cations
such as nortriptyline, amitriptyline, gabapentin,
etc) seem to benefit some patients. Laparoscopic
revision of the vaginal cuff may give good initial relief
in approximately two-thirds of patients, but pain tends
to recur to a degree over the subsequent 2–3 years,
although perhaps at a less intense level.36,37
Musculoskeletal Problems
Musculoskeletal changes can become involved with
chronic pelvic pain, either as the primary problem or
as a secondary reaction to the pelvic pain. The
muscular problem that most often produces pelvic
pain is pelvic floor tension myalgia (also called levator
spasm or levator ani syndrome).38 The clinical symp-tom
profile commonly includes pain with sitting flat
on a chair, worsening pelvic pressure over the course of
the day, and midvaginal dyspareunia. Intermittent or
constant painful contraction of the levator plate can be
present as a primary problem or a reaction to some
other source of pain. The patient with levator pain will
often sit up on one buttock during the interview and will
report that pelvic floor soreness persisted for 1–2 days
after palpation of the muscles during pelvic examination.
The piriformis and obturator muscles warrant
further emphasis because they are seldom appreciated
as possible sources of pain. These muscles are external
rotators of the leg, and rotation against resistance can
allow detection of tender spasm of the muscles during
the pelvic examination. The sciatic nerve can traverse
the belly of the piriformis as a normal anatomic variant,
producing symptoms similar to sciatica when the muscle
is in spasm. Pain caused by the iliopsoas complex can
manifest as anterior hip or groin pain and is diagnosed
with passive or active extension at the hip.
The mainstay of treatment of muscular compo-nents
of pelvic pain is physical therapy, most com-monly
performed by a therapist with specialized
training in the treatment of female pelvic pain. This
subspecialty of the field has grown enormously over
the past 15 years in obvious response to growing
recognition of muscular elements to pelvic pain and in
recognition that it works.39 Most physical therapists
specializing in women’s care will address pelvic floor
and hip muscles issues with transvaginal muscle treat-ments
as well as other treatment measures. Other
measures that are sometimes helpful are self-directed
pelvic floor contraction and relaxation exercises, mus-cle
relaxants, vaginal valium, and Botox injections.
When the problem is severe enough to require these
measures, it is generally advised that they be used
along with simultaneous physical therapy.
Medical Comorbidity
Peripheral pain generation in chronic pelvic pain
often involves nongynecologic systems.40,41 A careful
history and close physical examination of gastrointes-tinal,
urologic, musculoskeletal, and neurologic sys-tems
are needed to evaluate these additional
contributions to chronic pelvic pain. Most of the avail-able
literature examines these problems indepen-dently
of each other and without reference to their
relevance to chronic pelvic pain or to the overall prev-alence
of these disorders in chronic pelvic pain. The
gastrointestinal system is the most common nongyne-cologic
contributor to chronic pelvic pain, typically
manifesting as irritable bowel syndrome. Perhaps sec-ond
in terms of prevalence, functional urinary prob-lems
(ie, interstitial cystitis) are another common
comorbid contributor in chronic pelvic pain. These
as well as others such as migraine, temporomandibu-lar
joint disorder, and fibromyalgia should be viewed
in the context of a larger centralized pain problem and
treatment should be symptom-specific.
Psychological comorbidity also travels with
chronic pelvic pain. Depression, anxiety, anger–hos-tility,
somatization, and catastrophization9 (the belief
that things are as bad as they can be and are not likely
to improve) are all more common among women with
chronic pain than in women in a control group.42,43
Whether mood disorder is a predisposing factor to, or
a result of, chronic pain is not clear and may differ
from patient to patient, but the situation is symbiotic
at a minimum. Many women with chronic pelvic pain
fear physicians’ recognition of mood disorder leads to
the conclusion that their pain problem is not “real” or
“in her head.” Thus, from a treatment perspective, it
makes sense to attend to each disorder to the degree it
manifests, but not necessarily attempt to discern cau-sality
in a gynecologic visit.
Studies vary in describing the prevalence of sexual
abuse,44,45 but regardless, it is difficult to judge whether
these events are directly relevant to present pain and
hence demand attention or whether they contribute to
a psychologically vulnerable substrate influenced by
subsequent physical and emotional events. In these
circumstances, it may be worthwhile to suggest further
mental health evaluation as an exploratory measure,
being careful not to imply that the patient is being
referred because the physician is certain that the abuse
is related to the development of the pain.
Lastly, marital distress and sexual dysfunction,
particularly dyspareunia, are common further
VOL. 124, NO. 3, SEPTEMBER 2014 Steege and Siedhoff Chronic Pelvic Pain 621
7. burdens for patients with pain. Although some
women report satisfactory sexual functioning before
the onset of pain symptoms, others appear to have
long-standing impairments in sexual response. In our
experience, sexual difficulties are often the problem
that makes a person seek (or is encouraged by her
partner to seek) help for her pain.
DIAGNOSTIC STRATEGIES
Recognizing a Chronic Pain Syndrome
Many women can experience pain for longer than 6
months without becoming debilitated. Although their
pain is chronic, such women are not described as
having a chronic pain syndrome. The following are the
common clinical hallmarks of this syndrome46: 1) dura-tion
of 6 months or longer, 2) incomplete relief by most
previous treatments, 3) significantly impaired physical
function at home or at work, 4) signs of depression
(sleep disturbance, weight loss, loss of appetite), 5)
hypersensitive response to nociceptive stimuli, and 6)
altered family roles.
Of the signs of depression, sleep disturbance is
usually the first to appear. Careful questioning is
needed to distinguish awakening caused by pain from
awakening that just happens. In the true vegetative
sign, the person usually cannot get back to sleep even
if pain is relieved (by medication or other means).
The alteration of family roles is perhaps the most
important of those mentioned. This includes changed
responsibilities for household, children, finances, and
so forth. Initially intended as helpful, such changes
may eventually diminish the patient’s self-esteem and
progressively reduce her family’s interactions with her
to little more than checking on her pain. Over time,
this covertly reinforces the symptom of pain and im-parts
to it unintended value as a major means of main-taining
communication within the family.
Imaging Studies
If the physical examination is relatively benign and is
not severely limited by body habitus, extensive
imaging usually adds little to the database needed
before laparoscopy is performed. This is especially
true in the case of organ-specific studies (intravenous
pyelography, barium enema, colonoscopy) in the
absence of symptoms or signs pointing to an explicit
organ problem (eg, blood in the stools). Intervening
for chronic pelvic pain on the basis of an imaging study
finding alone is unlikely to be fruitful. On the other
hand, with a specific question in mind—for example,
pelvic ultrasonography to confirm ovarian endometrio-ma,
magnetic resonance imaging when adenomyosis is
suspected, or lower endoscopic ultrasonography to rule
out invasive rectal endometriosis—imaging can be quite
helpful.
Laboratory Studies
Relatively few hematologic or chemical measures are
useful in diagnosing chronic pelvic pain. An elevated
leukocyte count and erythrocyte sedimentation rate
may make the clinician suspect chronic pelvic inflam-matory
disease even when cervical probes are nega-tive
for the most common sexually transmitted
infections. Serum CA-125 can confirm suspicions of
deeply infiltrating endometriosis in those without
prior surgical evaluation but is not sufficiently sensi-tive
to detect early-stage disease. In those with
advanced endometriosis, the anti-Müllerian hormone
level, a measure of ovarian reserve, can help fertility
counseling in a woman considering extirpative surgical
treatment for her disease. In those status postbilateral
oophorectomy with remnant ovarian tissue, follicle-stimulating
hormone and estradiol levels remain in
premenopausal ranges. Women using replacement
estrogen therapy should stop 3 weeks before these
levels are measured.
Anesthetic Blocks
Injection of small volumes of a local anesthetic, 1–5
mL of 1% lidocaine or 0.25–0.5% bupivacaine, blocks
pain from either an entrapped segmental nerve (eg,
ilioinguinal) or an abdominal wall trigger point. Such
blocks can be therapeutic as well as diagnostic. Many
anesthesia pain clinics administer epidural or spinal
anesthetics to distinguish pain arising from peripheral
organs from pain that has become completely central
in origin.
In some instances, it is useful to attempt diagnos-tic
and therapeutic transvaginal blocks with the same
local anesthetics for vaginal apex pain, as discussed
previously. A series of three or four blocks adminis-tered
1–2 weeks apart may provide durable relief in
some instances.
Psychologic Tests and Interviews
In the attempt to distinguish physical from psycho-logical
contributions to pain, many studies of chronic
pelvic pain have used traditional psychological instru-ments
that were developed to measure general
psychopathology or personality factors. These psy-chometric
instruments generally have uncertain face
value for patients with chronic pain, and their use can
support the patient’s fears that the health care pro-vider
thinks her pain is imagined. Psychometric tests
are most useful when they are interpreted by a psy-chologist
who has interviewed the patient, and they
622 Steege and Siedhoff Chronic Pelvic Pain OBSTETRICS & GYNECOLOGY
8. serve best as a means to better understand the pa-tient’s
strengths and weaknesses rather than as a means
to decide who has “organic” compared with “psycho-logical”
pathology or who needs surgery. The newer
specialty of pain psychology holds promise in assist-ing
women dealing with chronic pelvic pain to better
focus on the positives in their lives and encourages
them to take an active role in dealing with their pain.
Laparoscopy
Great strides have been made in operative laparoscopy
in the past three decades. Laparoscopy can be useful
diagnostically and therapeutically (even in the face of
negative findings), but when a chronic pain syndrome
is clinically evident, results of laparoscopic treatment
alone, despite comparable pathology, are much less
impressive. For a patient with the clinical markers of
chronic pain syndrome listed earlier, a complete
workup should be performed before laparoscopy.
In some puzzling cases, laparoscopy under local
anesthesia can be used to “pain map” the pelvis.47 A 2-
mm laparoscope and a small suprapubic probe are
placed with the use of short-acting, reversible intrave-nous
analgesia (eg, remifentanil) and local anesthetic.
Having been oriented to the procedure beforehand, as
each organ is touched, the patient is asked if the site is
painful, to rate it on an ordinal scale from 1 to 10, and
if the discomfort represents her pain. It is possible in
some cases to block the superior hypogastric plexus
during pain mapping to better predict benefit from
presacral neurectomy.48 In this approach, mapping
is done before and after injecting 10 mL of 1% lido-caine
just underneath the peritoneum over the sacrum
using a 7-inch, 22-gauge spinal needle.
Limiting patient characteristics for using pain
mapping include high states of anxiety and obesity,
in which the torque required to move an instrument
against a thick abdominal wall can provide a distract-ing
nociceptive stimulus. Once thought to be the
“holy grail” of chronic pelvic pain diagnostics, better
understanding of the central mechanisms of chronic
pain and the relationship among various named pain
disorders has led to diminished use of laparoscopic
pain mapping in routine practice.
The enthusiasm for laparoscopy has its negative
aspects as well. When pain recurs after the first
laparoscopic treatment of endometriosis, for example,
many patients and their gynecologists will automati-cally
assume that this is the result of a return of their
disease. The surgeon must also consider the possibil-ity
that the improvement seen after the first laparos-copy
was a nonspecific effect of the surgery and that,
in fact, the “disease” seen and treated was not actually
relevant to the pain. The second laparoscopy, in
perhaps the majority of circumstances, reveals less
disease than was present at the first surgery.49 This
would suggest that the pain is multifactorial and that
over time, in many cases, the relative importance of
the endometriosis may diminish. Ironically, in most
practices, medical and surgical treatment is neverthe-less
escalated in such situations. We would recom-mend
instead starting all over again, making no
assumption ahead of time that the endometriosis is
playing a role at all.
MANAGEMENT
Relatively straightforward pain problems are not
challenging to manage such as treating isolated
dysmenorrhea with hormonal suppression or
a chronic tubo-ovarian abscess with adnexectomy.
More often, however, chronic pelvic pain represents
a complex and nuanced syndrome in which treatment
may vary considerably depending on the patient. When
pain itself is the disease, the goal of treatment is not
necessarily complete eradication of pain, but rather
finding strategies that afford more functional living.
Neuromodulatory medications (eg, tricyclic antidepres-sants,
neurotransmitter reuptake inhibitors, neuroleptics),
psychological adjuncts (eg, cognitive–behavioral ther-apy,
pain psychotherapy, sexual counseling), and com-plementary
strategies (eg, mindfulness-based medication,
yoga, acupuncture) can be useful to dampen central
hypersensitivity. For the peripheral elements, physical
therapy, diet modification, peripheral nerve blocks,
and surgery can be helpful depending on the target pain
generator. In all cases, good sleep hygiene, exercise,
smoking cessation, healthy eating, and social support
are important foundational elements that improve the
effectiveness of chronic pelvic pain treatment.
Medication Use
Analgesics
Analgesics such as nonsteroidal anti-inflammatory
drugs and opioid narcotics can be quite effective for
acute conditions, but their use in chronic pain is
marred by a host of adverse outcomes and limited
efficacy associated with long-term use. Dose-related
effects of medications such as acetaminophen (liver
toxicity) and cyclooxygenase inhibitors (gastric and
renal damage) are well known, but they are not major
offenders in the realm of tolerance and withdrawal.
Opioid narcotics, on the other hand, are notoriously
dangerous in regard to these consequences in addition
to problems such as narcotic bowel syndrome and
opioid-induced hyperalgesia. Some patients benefit
from structured narcotic therapy, but, if they are to be
VOL. 124, NO. 3, SEPTEMBER 2014 Steege and Siedhoff Chronic Pelvic Pain 623
9. used for chronic pelvic pain, clinicians should screen
carefully for factors associated with high risk for
misuse50,51 and set nonnegotiable ground rules such
as limiting prescriptions to one health care provider,
not entertaining requests for early refills, mandating
scheduled urine drug screens, and refraining from
uncontrolled dose escalation. Newer opioid medica-tions
such as oxymorphone and tapentadol are con-sidered
less euphoria-generating than the more
commonly used narcotics such as hydrocodone, oxy-codone,
and hydromorphone (Table 1).
Antidepressants and Neuroleptics
These classes of drugs are commonly used in the
treatment of chronic pain, including chronic pelvic
pain, although few controlled trials have been
carried out specifically in this population. Although
no longer first line for mood disorders, tricyclic
Table 1. Narcotics Used in Pain Management
Drug Dosing Side Effects
Hydrocodone bitartrate with
acetaminophen
5–10 mg hydrocodone either every
6 or every 8 h
Lightheadedness, dizziness, sedation, nausea
and vomiting, constipation (these are common
side effects of all narcotics)
Lortab 2.5/500, 5/500, or
7.5/500
Can use additional acetaminophen
between doses
Vicodin 5/750
Lorcet 10/650
Lorcet Plus 7.5/650
Oxycodone hydrochloride 1 tablet every 6 or every 8 h Common effects
Percocet 5/325 Additional acetaminophen
between doses
Oxycodone controlled release 10–40 mg every 12 h Common effects
Oxycontin
Methadone hydrochloride 2.5 mg every 8 h to 10 mg every 6 h Common effects, lower extremity edema or joint
swelling may occur and require discontinuation,
concurrent use of desipramine may increase
methadone blood level, cautious use in patients
on monoamine oxidase inhibitors
Dolphine 5 or 10 mg scored
tablets
Commonly 15–20 mg per day total
Acetaminophen with codeine 1–2 tablets every 6–8 h Common effects, constipation very likely, nausea
and vomiting more common than with other
narcotics, more common allergy—rash
Tylenol #3: 300 mg
acetaminophen with 30 mg
codeine
Morphine sulfate 15–60 mg every 12 h (controlled-release
tablets)
Common effects, higher doses increase risk
of respiratory depression
MS Contin
Oramorph
Avinza
Fentanyl transdermal system 25-microgram patch, 1 every 72 h Common effects, patch must be kept from heat
sources or dose may be increased, extreme
caution in patients on other central nervous
system medications, respiratory depression
can result
Duragesic Also available in 50 or 75
micrograms
Actiq Always start with lowest dose
Fentora
Tramadol 50 mg every 6–8 h Common adverse effects, less gastrointestinal,
less euphoric effects
Ultram
Tapentadol 50 mg every 6–8 h; 50–100 mg daily
for extended release
Nucynta, Nucynta ER
624 Steege and Siedhoff Chronic Pelvic Pain OBSTETRICS & GYNECOLOGY
10. antidepressants such as amitriptyline, nortriptyline,
and desipramine have a long record of being effective
in treating chronic pain.52 Newer-generation neuro-transmitter
reuptake inhibitors such as duloxetine and
desvenlafaxine can also be useful. Neuroleptics such as
gabapentin, pregabalin, and lamotrigine are generally
used when symptoms are more specifically neuropathic
in nature. It is important to discuss with patients that,
although they tend to diminish with continued use, all
of these medications have central side effects, some of
which are predictable and others quite idiosyncratic.
When higher doses or multiple agents are used, it
can be helpful to consult with a psychiatrist or psy-chopharmacologist
to avoid complications such as
severe mood dysregulation or serotonin syndrome
(Table 2).
Anxiolytics
Anxiolytic drugs are certainly widely prescribed by
gynecologists, although it is uncertain how often they
are given for pain. In one study, alprazolam had
a surprising degree of analgesic effect in moderate-to-high
doses in patients with chronic pain of malignant
origin and concomitant mood changes or anxiety.53
These patients were already receiving narcotics,
which may suggest that alprazolam potentiates the
analgesic effect of narcotics. Their role in conjunction
with nonnarcotic analgesics is uncertain, and the
addiction potential is obvious.
Hormonal Medications
Combined oral contraceptives are effective in reduc-ing
dysmenorrhea and cyclic symptoms associated
with endometriosis. It is not uncommon, however, to
meet resistance to using these medications in women
with chronic pelvic pain—either because they were pre-viously
used and did not cure the entirety of the pain
syndrome and were thus deemed ineffective or because
of sensitivity to side effects such as nausea, an under-standable
consequence in a viscerally hypersensitive
group. Avoiding ultralow-dose 20-microgram ethinyl
estradiol formulations can help reduce unscheduled
bleeding, important for women who may closely asso-ciate
bleeding with pain. Outside of deeply infiltrating
endometriosis, progestin-only formulations, by enteral
or parenteral route, run the risk of exacerbating depres-sive
symptoms in a vulnerable population. A notable
exception includes the levonorgestrel intrauterine sys-tem,
which has little systemic absorption and can con-trol
dysmenorrhea and pain from endometriosis in
a low-risk, reversible, long-acting manner.
The use of gonadotropin-releasing hormone
agonists deserves special mention. They have been
recommended to distinguish gynecologic from
Table 2. Antidepressants and Neuroleptics Used in Pain Management
Medication Class Dosing Consideration, Side Effects
Tricyclic antidepressants Tricyclics commonly cause sedation, dry mouth,
weight gain, constipation; this can be exploited
for urinary frequency problems; nortriptyline or
desipramine used more frequently when patients
have constipation, generally administer at night
Amitriptyline Start 10–25 mg nightly, titrate
to 75–150 mg
Nortriptyline Start 25 mg nightly, titrate to
50–150 mg
Desipramine Start 25 mg nightly, titrate to
50–150 mg
Serotonin–norepinephrine
reuptake inhibitors
Most common side effects are nausea and central
nervous effects such as lethargy and dizziness,
provide warning signs of serotonin syndrome for
patients on other serotonergic drugs and do not
stop abruptly
Duloxetine Start 30 mg daily, titrate to 60,
occasionally 90 mg
Desvenlafaxine 50–100 mg daily
Gamma-aminobutyric
acid analogues
No major drug interactions, reduce central nervous
effects by slow titration (for example, over 4 wk);
do not stop abruptly
Gabapentin 100–300 mg divided 3 times daily
Pregabalin 75 mg twice daily
VOL. 124, NO. 3, SEPTEMBER 2014 Steege and Siedhoff Chronic Pelvic Pain 625
11. nongynecologic sources of pain based on interpreta-tion
of some data,54 but pain relief after gonadotropin-releasing
hormone treatment does not make a gyneco-logic
(including endometriosis) diagnosis. In that
study, patients without endometriosis improved with
the same the frequency as those with the disease, and
these agents also relieve symptoms of other functional
conditions such as irritable bowel syndrome. Further-more,
pain thresholds have been shown to be lower
premenstrually, even in women without chronic pelvic
pain. The effect of the menstrual cycle itself in patients
with chronic pain has not been well-explored, but it
seems likely that it may impart some cyclicity even to
conditions unrelated to the reproductive tract. Cyclic-ity
of symptoms must therefore be interpreted with
caution, and the disappearance of symptoms or of
their cyclicity by pharmacologically obliterating the
menstrual cycle does not demonstrate a gynecologic
cause. Gonadotropin-releasing hormone agonists can
be useful when differential diagnosis includes ovarian
remnant syndrome or residual ovary syndrome or in
the treatment of deeply infiltrating endometriosis, but
its use in treating general chronic pelvic pain is limited
by cost and morbidity. Contrary to popular belief,
gonadotropin-releasing hormone agonists are not
more effective than other more benign hormonal ma-nipulations
directed at pelvic pain.55–57 For deeply
infiltrating endometriosis, aromatase inhibitors with
norethindrone may work similarly without as signifi-cant
hypoestrogenic effects.58,59
Surgery
Two basic surgical approaches have been used to treat
chronic pelvic pain: removing pelvic organs and
treating visible disease while leaving the pelvic organs
in place. The use of both approaches is guided by
clinical experience, because high-quality scientific
data regarding the role of surgery in pelvic pain are
sparse. Expansion of literature on the topic, including
stratification for characteristics that lead to strong or
poor response, would be most welcome.
In the United States, approximately 12% of
hysterectomies are performed with pelvic pain as the
primary indication.60,61 Although hysterectomy should
not be viewed as a final curative step in an algorithm
for treating chronic pelvic pain in general, it can be
quite helpful for central uterine pain, dyspareunia asso-ciated
with fundal tenderness, dysmenorrhea, abnor-mal
bleeding, and cyclic symptoms. Quality of life,
with particular attention to the effect of pain and
depression on outcomes, was studied using data from
the Maryland Women’s Health Study, in which 1,249
women were evaluated at several-month intervals up to
2 years after hysterectomy. Not surprisingly, women
without pain or depression had the highest functional
levels, but even among women with pain and depres-sion,
pelvic pain decreased from 97% to 19%, and there
was a reduction by half in limited physical and social
function. Women with depression only had improve-ment
in impaired mental health (85% down to 33%)
and dyspareunia decreased in all groups.62 Another
study suggests hysterectomy done for various condi-tions,
including pelvic pain, outperforms medical or
uterus-preserving surgical treatment on quality-of-life
measures.63 Furthermore, the majority of hysterecto-mies
in these studies were performed using laparot-omy.
Newer randomized controlled trial data suggest
improved quality of life laparoscopic over abdominal
hysterectomy durable to 4 years out from surgery.64
When considering hysterectomy in the treatment of
chronic pelvic pain, it is essential to discuss with pa-tients
which pain symptoms are likely to improve after
surgery and that some may remain. Just because hys-terectomy
does not fix every problem does not exclude
it from being a helpful aspect of treatment provided
attention is still provided to centralized pain disorders
and symptoms linked to other organ systems.
Although many patients and health care providers
still consider endometriosis nearly synonymous with
pelvic pain, as discussed previously, the relationship
is probably more tenuous than previously thought.
Laparoscopic treatment, even of mild disease, however,
does provide pain relief.10–13 Some studies suggest
superiority of excision to ablation of endometriosis im-plants,
and this approach probably makes good clinical
sense, but there is insufficient evidence to conclude one
is definitively superior to the other in pain reduc-tion.
65,66 Specific symptom improvement after deeply
infiltrating endometriosis (gastrointestinal, urologic, cul
de sac) resection is best documented in the litera-ture.
67,68 Given the complexity of these operations
and the potential for harm to adjacent vital structures,
advanced endometriosis resection should be performed
by experienced surgeons. The benefits of surgical exci-sion
may be prolonged by subsequent medical therapy.
Numerous studies have been done of postsurgical treat-ment
with hormonal medications. Oral contraceptive
pills, danazol, progestins, aromatase inhibitors, and
gonadotropin-releasing hormone agonists (with and
without add-back estrogen and progestin) have all been
shown to be effective.69–74 Although gonadotropin-releasing
hormone agonists have become perhaps the
most widely used of these, definitive evidence for their
superiority is lacking. The more economical and less
physiologically intrusive approach would seem to favor
sex steroids over gonadotropin-releasing hormone
626 Steege and Siedhoff Chronic Pelvic Pain OBSTETRICS & GYNECOLOGY
12. agonists. Most troublesome in reviewing all of these
studies is the observation that dyspareunia is the symp-tom
that is most refractory to treatment, testifying to its
multifactorial nature.
Presacral neurectomy through surgical interrup-tion
of the superior hypogastric plexus has been
described in clinical series as effective at treating central
uterine pain, dysmenorrhea, and endometriosis.75,76 In
the most rigorous study, Zullo et al4 investigated the
question with a double-masked randomized trial and
demonstrated a 20% difference in pain improvement
when presacral neurectomy was added to endometri-osis
excision in women with a midline component to
their pain. When considering presacral neurectomy,
patients must be counseled about risks of postoperative
bowel and bladder dysfunction and should also be
offered more conservative (eg, levonorgestrel intrauter-ine
systemic) as well as more definitive (ie, hysterec-tomy)
treatments.
An ovarian remnant should be removed if it is
persistently symptomatic despite attempts at medical
suppression and if menopause cannot be expected in
the patient’s near future. The dissection should be
detailed and should include all the peritoneum sur-rounding
the mass. The pararectal space, and paraves-ical
space if needed, should be opened systematically
and the ureter and pelvic sidewall vessels exposed and
carefully freed fromthe specimen.Usually there is a vas-cular
supply along the tract of the infundibulopelvic
ligament, and it is prudent to divide the pedicle well
above the pelvic brim. When a gonadotropin-releasing
hormone agonist has been used preoperatively for
symptom control or to distinguish the relative contribu-tions
made by the remnant and other pelvic pathology,
the remnant tissue may become so small as to make it
difficult to identify. Hence, if a palpable (or visible by
imaging) mass disappears after gonadotropin-releasing
hormone agonist treatment, it may be wise to allow
time for it to regrow before pursuing surgical excision.
When the remnant is small, some surgeons have stim-ulated
the remnant with clomiphene citrate to make it
easier to find.77
Alternative Treatments
Psychological disorders should be treated in chronic
pelvic pain, whether independently present or the result
of a long-standing pain disorder. Some practitioners
may find cognitive–behavioral or biofeedback therapy
useful in reducing automatic responses to painful stim-uli.
Sexual counseling, couples counseling, and psycho-therapy
can be helpful adjuncts. Alternative strategies
such as mindfulness-based meditation, yoga, and acu-puncture
may have roles in individual cases, but none is
so clearly applicable or effective that its automatic use is
supported in cases of chronic pelvic pain.
Management Overview
The most effective clinical approach requires simul-taneous
treatment of as many factors as possible:
anatomic, musculoskeletal, functional bowel and
bladder, psychological, and so forth. The patient and
physician must contract for the long term and work
from a rehabilitation perspective rather than hope that
the latest single addition to the treatment will prove to
be the answer. The physician, to prevent frustration
and feelings of defeat, must often play the role of
helping to manage and relieve the pain while helping
to maximize function, even when pain persists. To the
surgically trained gynecologist who prefers a clear-cut
single answer to a clinical problem, this can be the
most difficult part of dealing with the problem of
chronic pelvic pain. It is important to free oneself
from the responsibility of needing to “fix” a patient’s
chronic pelvic pain. Although the compassionate
health care provider can be an invaluable aide, much
of the work in improving from pelvic pain is the bur-den
of the patient herself.
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