Endometriosis is a condition in which cells similar to those in the endometrium,

the layer of tissue that normally covers the inside of the uterus, grow outside of
it.[7][8] Most often this is on the ovaries, fallopian tubes, and tissue around the
uterus and ovaries; however, in rare cases it may also occur in other parts of the
body.[2] The main symptoms are pelvic pain and infertility.[1] Nearly half of those
affected have chronic pelvic pain, while in 70% pain occurs during menstruation.[1]
Pain during sexual intercourse is also common.[1] Infertility occurs in up to half
of women affected.[1] Less common symptoms include urinary or bowel symptoms.[1]
About 25% of women have no symptoms.[1] Endometriosis can have both social and
psychological effects.[9]

The cause is not entirely clear.[1] Risk factors include having a family history of
the condition.[2] The areas of endometriosis bleed each month, resulting in
inflammation and scarring.[1][2] The growths due to endometriosis are not cancer.
[2] Diagnosis is usually based on symptoms in combination with medical imaging,[2]
however, biopsy is the surest method of diagnosis.[2] Other causes of similar
symptoms include pelvic inflammatory disease, irritable bowel syndrome,
interstitial cystitis, and fibromyalgia.[1]

Tentative evidence suggests that the use of combined oral contraceptives reduces
the risk of endometriosis.[4] Exercise and avoiding large amounts of alcohol may
also be preventive.[2] There is no cure for endometriosis but a number of
treatments may improve symptoms.[1] This may include pain medication, hormonal
treatments or surgery.[2] The recommended pain medication is usually a non-
steroidal anti-inflammatory drug (NSAID), such as naproxen.[2] Taking the active
component of the birth control pill continuously or using an intrauterine device
with progestogen may also be useful.[2] Gonadotropin-releasing hormone agonist may
improve the ability of those who are infertile to get pregnant.[2] Surgical removal
of endometriosis may be used to treat those whose symptoms are not manageable with
other treatments.[2]

One estimate is that 10.8 million people are affected globally as of 2015.[5] Other
sources estimate about 6�10% of women are affected.[1] Endometriosis is most common
in those in their thirties and forties; however, it can begin in girls as early as
eight years old.[2][3] It results in few deaths.[10] Endometriosis was first
determined to be a separate condition in the 1920s.[11] Before that time,
endometriosis and adenomyosis were considered together.[11] It is unclear who first
described the disease.[11]

Contents
1 Signs and symptoms
1.1 Pelvic pain
1.2 Infertility
1.3 Other
2 Risk factors
2.1 Genetics
2.2 Environmental toxins
3 Pathophysiology
3.1 Formation
3.2 Localization
4 Diagnosis
4.1 Laparoscopy
4.2 Ultrasound
4.3 Magnetic resonance imaging
4.4 Staging
4.5 Markers
4.6 Histopathology
4.7 Pain quantification
5 Prevention
6 Management
6.1 Surgery
6.2 Hormonal medications
6.3 Other medication
6.4 Comparison of interventions
6.5 Treatment of infertility
7 Outcomes
7.1 Complications
8 Epidemiology
9 History
10 Society and culture
11 References
12 External links
Signs and symptoms

Drawing showing endometriosis

Pain and infertility are common symptoms, although 20-25% of women are
asymptomatic.[1]

Pelvic pain
A major symptom of endometriosis is recurring pelvic pain. The pain can range from
mild to severe cramping or stabbing pain that occurs on both sides of the pelvis,
in the lower back and rectal area, and even down the legs. The amount of pain a
woman feels correlates weakly with the extent or stage (1 through 4) of
endometriosis, with some women having little or no pain despite having extensive
endometriosis or endometriosis with scarring, while other women may have severe
pain even though they have only a few small areas of endometriosis.[12] The most
severe pain is typically associated with menstruation. Pain can also start a week
before a menstrual period, during and even a week after a menstrual period, or it
can be constant. The pain can be debilitating and result in emotional stress.[13]
Symptoms of endometriosis-related pain may include:

dysmenorrhea � painful, sometimes disabling cramps during the menstrual period;

pain may get worse over time (progressive pain), also lower back pains linked to
the pelvis
chronic pelvic pain � typically accompanied by lower back pain or abdominal pain
dyspareunia � painful sexual intercourse
dysuria � urinary urgency, frequency, and sometimes painful voiding [14]
mittelschmerz � pain associated with ovulation[15]
bodily movement pain � present during exercise, standing, or walking[14]
Compared with women with superficial endometriosis, those with deep disease appear
to be more likely to report shooting rectal pain and a sense of their insides being
pulled down.[16] Individual pain areas and pain intensity appear to be unrelated to
the surgical diagnosis, and the area of pain unrelated to area of endometriosis.
[16]

There are multiple causes of pain. Endometriosis lesions react to hormonal

stimulation and may "bleed" at the time of menstruation. The blood accumulates
locally if it is not cleared shortly by the immune, circulatory, and lymphatic
system. This may further lead to swelling, which triggers inflammation with the
activation of cytokines, which results in pain. Another source of pain is the organ
dislocation that arises from adhesion binding internal organs to each other. The
ovaries, the uterus, the oviducts, the peritoneum, and the bladder can be bound
together. Pain triggered in this way can last throughout the menstrual cycle, not
just during menstrual periods.[17]

Also, endometriotic lesions can develop their own nerve supply, thereby creating a
direct and two-way interaction between lesions and the central nervous system,
potentially producing a variety of individual differences in pain that can, in some
women, become independent of the disease itself.[12] Nerve fibres and blood vessels
are thought to grow into endometriosis lesions by a process known as
neuroangiogenesis.[18]

Infertility
Main article: Endometriosis and infertility
About a third of women with infertility have endometriosis.[1] Among women with
endometriosis about 40% are infertile.[1] The pathogenesis of infertility is
dependent on the stage of disease: in early stage disease, it is hypothesised that
this is secondary to an inflammatory response that impairs various aspects of
conception, whereas in later stage disease distorted pelvic anatomy and adhesions
contribute to impaired fertilisation.[19]

Other
Other symptoms include diarrhea or constipation,[14] chronic fatigue,[14] nausea
and vomiting, headaches, low-grade fevers, heavy and/or irregular periods, and
hypoglycemia.[20][21]

There is an association between endometriosis and certain types of cancers, notably

some types of ovarian cancer,[22][23] non-Hodgkin's lymphoma and brain cancer.[24]
Endometriosis is unrelated to endometrial cancer.[25]

Rarely, endometriosis can cause endometrial tissue to be found in other parts of

the body. Thoracic endometriosis occurs when endometrial tissue implants in the
lungs or pleura. Manifestations of this include coughing up blood, a collapsed
lung, or bleeding into the pleural space.[26]

Risk factors
Genetics
Endometriosis is a heritable condition that is influenced by both genetic and
environmental factors.[27] Daughters or sisters of women with endometriosis are at
higher risk of developing endometriosis themselves; low progesterone levels may be
genetic, and may contribute to a hormone imbalance.[28] There is an about six-fold
increased incidence in women with an affected first-degree relative.[29]

It has been proposed that endometriosis results from a series of multiple hits
within target genes, in a mechanism similar to the development of cancer.[27] In
this case, the initial mutation may be either somatic or heritable.[27]

Individual genomic changes (found by genotyping including genome-wide association

studies) that have been associated with endometriosis include:[30][31][32]

Chromosome Gene/Region of Mutation Gene Product Function

1 WNT4 Wingless-type MMTV integration site family member 4 Vital for
development of the female reproductive organs
2 GREB1/FN1 Growth regulation by estrogen in breast cancer 1/Fibronectin 1
Early response gene in the estrogen regulation pathway/Cell adhesion and
migration processes
6 ID4 Inhibitor of DNA binding 4 Ovarian oncogene, biological function
unknown
7 7p15.2 Transcription factors Influence transcriptional regulation of
uterine development
9 CDKN2BAS Cyclin-dependent kinase inhibitor 2B antisense RNA Regulation
of tumour suppressor genes
10 10q26
12 VEZT Vezatin, an adherens junction transmembrane protein Tumor suppressor
gene
19 MUC16 (CA-125) Mucin 16, cell surface associated Form protective mucous
barriers
There are many findings of altered gene expression and epigenetics, but both of
these can also be a secondary result of, for example, environmental factors and
altered metabolism. Examples of altered gene expression include that of miRNAs.[27]

Environmental toxins
Some factors associated with endometriosis include:

prolonged exposure to estrogen; for example, in late menopause[33] or early

menarche[34][35]
obstruction of menstrual outflow; for example, in M�llerian anomalies[33]
Several studies have investigated the potential link between exposure to dioxins
and endometriosis, but the evidence is equivocal and potential mechanisms are
poorly understood.[36] A 2004 review of studies of dioxin and endometriosis
concluded that "the human data supporting the dioxin-endometriosis association are
scanty and conflicting",[37] and a 2009 follow-up review also found that there was
"insufficient evidence" in support of a link between dioxin exposure and women
developing endometriosis.[38] A 2008 review concluded that more work was needed,
stating that "although preliminary work suggests a potential involvement of
exposure to dioxins in the pathogenesis of endometriosis, much work remains to
clearly define cause and effect and to understand the potential mechanism of
toxicity".[39]

Pathophysiology

Laparoscopic image of endometriotic lesions at the peritoneum of the pelvic wall

While the exact cause of endometriosis remains unknown, many theories have been
presented to better understand and explain its development. These concepts do not
necessarily exclude each other. The pathophysiology of endometriosis is likely to
be multifactorial and to involve an interplay between several factors.[27]

Formation
The main theories for the formation of the ectopic endometrium are retrograde
menstruation, M�llerianosis, coelomic metaplasia and transplantation, each further
described below.

Retrograde menstruation theory

The theory of retrograde menstruation (also called the implantation theory or
transplantation theory)[40] is the oldest theory for the formation of ectopic
endometrium in endometriosis.[27] It suggests that during a woman's menstrual flow,
some of the endometrial debris flow backwards through the Fallopian tubes and into
the peritoneal cavity, attaching itself to the peritoneal surface (the lining of
the abdominal cavity) where it can proceed to invade the tissue as endometriosis.
[27]

Retrograde menstruation alone is not able to explain all instances of

endometriosis, and additional factors such as genetic or immune differences need to
be invoked to account for the fact that many women with retrograde menstruation do
not have endometriosis. In addition, endometriosis has shown up in people who have
never experienced menstruation including men,[41] fetuses,[42] and prepubescent
girls.[43][44] Further detracting from the retrograde menstruation theory are cases
of endometriosis showing up in the brain[45] and lungs.[46] This theory has
numerous other associated issues.[47]

Researchers are investigating the possibility that the immune system may not be
able to cope with the cyclic onslaught of retrograde menstrual fluid. In this
context there is interest in studying the relationship of endometriosis to
autoimmune disease, allergic reactions, and the impact of toxic materials.[48][49]
It is still unclear what, if any, causal relationship exists between toxic
materials, autoimmune disease, and endometriosis. There are immune system changes
in women with endometriosis, such as an increase of macrophage-derived secretion
products, but it is unknown if these are contributing to the disorder or are
reactions from it.[50]

In addition, at least one study found that endometriotic lesions differ in their
biochemistry from artificially transplanted ectopic tissue.[51] This is likely
because the cells that give rise to endometriosis are a side population of cells.
[27] Similarly, there are changes in for example the mesothelium of the peritoneum
in women with endometriosis, such as loss of tight junctions, but it is unknown if
these are causes or effects of the disorder.[50]

In rare cases where imperforate hymen does not resolve itself prior to the first
menstrual cycle and goes undetected, blood and endometrium are trapped within the
uterus of the woman until such time as the problem is resolved by surgical
incision. Many health care practitioners never encounter this defect, and due to
the flu-like symptoms it is often misdiagnosed or overlooked until multiple
menstrual cycles have passed. By the time a correct diagnosis has been made,
endometrium and other fluids have filled the uterus and Fallopian tubes with
results similar to retrograde menstruation resulting in endometriosis. The initial
stage of endometriosis may vary based on the time elapsed between onset and
surgical procedure.[citation needed]

The theory of retrograde menstruation as a cause of endometriosis was first

proposed by John A. Sampson.

Other theories
Stem cells: Endometriosis may arise from stem cells from bone marrow and
potentially other sources. In particular, this theory explains endometriosis found
in areas remote from the pelvis such as the brain or lungs.[52]
Environment: Environmental toxins (e.g., dioxin, nickel) may cause endometriosis.
[53][54]
M�llerianosis: A theory supported by foetal autopsy is that cells with the
potential to become endometrial, which are laid down in tracts during embryonic
development called the female reproductive (M�llerian) tract as it migrates
downward at 8�10 weeks of embryonic life, could become dislocated from the
migrating uterus and act like seeds or stem cells.[55]
Coelomic metaplasia: Coelomic cells which are the common ancestor of endometrial
and peritoneal cells may undergo metaplasia (transformation) from one type of cell
to the other, perhaps triggered by inflammation.[56]
Vasculogenesis: Up to 37% of the microvascular endothelium of ectopic endometrial
tissue originates from endothelial progenitor cells, which result in de novo
formation of microvessels by the process of vasculogenesis rather than the
conventional process of angiogenesis.[57][clarification needed]
Neural growth: An increased expression of new nerve fibres is found in
endometriosis but does not fully explain the formation of ectopic endometrial
tissue and is not definitely correlated with the amount of perceived pain.[58]
[clarification needed]
Autoimmune: Graves disease is an autoimmune disease characterized by
hyperthyroidism, goiter, ophthalmopathy, and dermopathy. Women with endometriosis
had higher rates of Graves disease. One of these potential links between Graves
disease and endometriosis is autoimmunity.[59][60]
Oxidative stress: Influx of Iron is associated with the local destruction of the
peritoneal mesothelium, leading to the adhesion of ectopic endometrial cells.[61]
Peritoneal iron overload has been suggested to be caused by the destruction of
erythrocytes, which contain the iron-binding protein hemoglobin, or a deficiency in
the peritoneal iron metabolism system.[61] Oxidative stress activity and reactive
oxygen species (such as superoxide anions and peroxide levels) are reported to be
higher than normal in people with endometriosis.[61] Oxidative stress and the
presence of excess ROS can damage tissue and induce rapid cellular division.[61]
Mechanistically, there are several cellular pathways by which oxidative stress may
lead to or may induce proliferation of endometriotic lesions, including the mitogen
activated protein (MAP) kinase pathway and the extracellular signal-related kinase
(ERK) pathway.[61] Activation of both of the MAP and ERK pathways lead to increased
levels of c-Fos and c-Jun, which are proto-oncogenes that are associated with high-
grade lesions.[61]
Localization

Possible locations of endometriosis

Most often, endometriosis is found on the:

ovaries
fallopian tubes
tissues that hold the uterus in place (ligaments)
outer surface of the uterus[2]
Less common sites are:

vagina
cervix
vulva
bowel
bladder
rectum[2]
Rarely, endometriosis appears in other parts of the body, such as the lungs, brain,
and skin.[2]

Rectovaginal or bowel endometriosis affects approximately 5-12% of women with

endometriosis, and can cause severe pain with bowel movements.[62]

Endometriosis may spread to the cervix and vagina or to sites of a surgical

abdominal incision, known as "scar endometriosis."[63] Risk factors for scar
endometriosis include previous abdominal surgeries, such as a hysterotomy or
cesarean section, or ectopic pregnancies, salpingostomy puerperal sterilization,
laparoscopy, amniocentesis, appendectomy, episiotomy, vaginal hysterectomies, and
hernia repair.[64][65][66]

Endometriosis may also present with skin lesions in cutaneous endometriosis.

Less commonly lesions can be found on the diaphragm. Diaphragmatic endometriosis is

rare, almost always on the right hemidiaphragm, and may inflict the cyclic pain of
the right shoulder just before and during a menstrual period. Rarely, endometriosis
can be extraperitoneal and is found in the lungs and CNS.[67]

Diagnosis

Laparoscopic image of endometriotic lesions in the Pouch of Douglas and on the

right sacrouterine ligament
A health history and a physical examination can lead the health care practitioner
to suspect endometriosis. Although doctors can often feel the endometrial growths
during a pelvic exam, and these symptoms may be signs of endometriosis, diagnosis
cannot be confirmed by exam only.

In the UK, there is an average of 7.5 years between a woman first seeing a doctor
about their symptoms and receiving a firm diagnosis.[68]

Laparoscopy

Transvaginal ultrasonography showing a 67 x 40 mm endometrioma as distinguished

from other types of ovarian cysts by a somewhat grainy and not completely anechoic
content
Laparoscopy, a surgical procedure where a camera is used to look inside the
abdominal cavity, is the only way to officially diagnose the extent and severity of
endometriosis.[69] Laparoscopy permits lesion visualization unless the lesion is
visible externally (e.g., an endometriotic nodule in the vagina).[69] If the
growths (lesions) are not visible, a biopsy may be taken to determine the
diagnosis.[70] Surgery for diagnoses also allows for surgical treatment of
endometriosis at the same time.

During a laparoscopic procedure lesions can appear dark blue, powder-burn black,
red, white, yellow, brown or non-pigmented. Lesions vary in size.[71] Some within
the pelvis walls may not be visible, as normal-appearing peritoneum of infertile
women reveals endometriosis on biopsy in 6�13% of cases.[72] Early endometriosis
typically occurs on the surfaces of organs in the pelvic and intra-abdominal areas.
[71] Health care providers may call areas of endometriosis by different names, such
as implants, lesions, or nodules. Larger lesions may be seen within the ovaries as
endometriomas or "chocolate cysts", "chocolate" because they contain a thick
brownish fluid, mostly old blood.[71]

Frequently during diagnostic laparoscopy, no lesions are found in women with

chronic pelvic pain, a symptom common to other disorders including adenomyosis,
pelvic adhesions, pelvic inflammatory disease, congenital anomalies of the
reproductive tract, and ovarian or tubal masses.[73]

Ultrasound
Use of pelvic ultrasound may identify large endometriotic cysts (called
endometriomas). However, smaller endometriosis implants cannot be visualized with
ultrasound technique.[74]

Vaginal ultrasound has a clinical value in the diagnosis of endometrioma and before
operating for deep endometriosis.[75] This applies to the identification of the
spread of disease in women with well-established clinical suspicion of
endometriosis.[75] Vaginal ultrasound is inexpensive, easily accessible, has no
contraindications and requires no preparation.[75] Healthcare professionals
conducting ultrasound examinations need to be experienced.[75] By extending the
ultrasound assessment into the posterior and anterior pelvic compartments the
sonographer is able to evaluate structural mobility and look for deep infiltrating
endometriotic nodules noting the size, location and distance from the anus if
applicable.[76] An improvement in sonographic detection of deep infiltrating
endometriosis will not only reduce the number of diagnostic laparoscopies, it will
guide management and enhance quality of life.[76]

Magnetic resonance imaging

Use of MRIs is another method to detect lesions in a non-invasive manner.[69] MRI
is not widely used due to its cost and limited availability, however, it has the
ability to detect deep and small endometriotic lesions.[69]

Staging
Surgically, endometriosis can be staged I�IV by the revised classification of the
American Society of Reproductive Medicine from 1997.[77] The process is a complex
point system that assesses lesions and adhesions in the pelvic organs, but it is
important to note staging assesses physical disease only, not the level of pain or
infertility. A person with Stage I endometriosis may have a little disease and
severe pain, while a person with Stage IV endometriosis may have severe disease and
no pain or vice versa. In principle the various stages show these findings:[78]

Stage I (Minimal)
Findings restricted to only superficial lesions and possibly a few filmy adhesions
Stage II (Mild)

In addition, some deep lesions are present in the cul-de-sac

Stage III (Moderate)

As above, plus the presence of endometriomas on the ovary and more adhesions.
Stage IV (Severe)

As above, plus large endometriomas, extensive adhesions.

Markers
An area of research is the search for endometriosis markers.[79]

In 2010, essentially all proposed biomarkers for endometriosis were of unclear

medical use, although some appear to be promising.[79] The one biomarker that has
been in use over the last 20 years is CA-125.[79] A 2016 review found that in those
with symptoms of endometriosis; and, once ovarian cancer has been ruled out, a
positive CA-125 may confirm the diagnosis.[80] Its performance in ruling out
endometriosis is low.[80] CA-125 levels appear to fall during endometriosis
treatment, but has not shown a correlation with disease response.[79]

Another review in 2011 identified several putative biomarkers upon biopsy,

including findings of small sensory nerve fibers or defectively expressed �3
integrin subunit.[81] It has been postulated a future diagnostic tool for
endometriosis will consist of a panel of several specific and sensitive biomarkers,
including both substance concentrations and genetic predisposition.[79]

Histopathology

Endometriosis, abdominal wall

Micrograph showing endometriosis (right) and ovarian stroma (left). H&E stain.

Micrograph of the wall of an endometrioma. All features of endometriosis are

present (endometrial glands, endometrial stroma and hemosiderin-laden macrophages).
H&E stain.
Typical endometriotic lesions show histopathologic features similar to endometrium,
namely endometrial stroma, endometrial epithelium, and glands that respond to
hormonal stimuli. Older lesions may display no glands but hemosiderin deposits (see
photomicrograph on right) as residual.[citation needed]

Immunohistochemistry has been found to be useful in diagnosing endometriosis as

stromal cells have a peculiar surface antigen, CD10, thus allowing the pathologist
go straight to a staining area and hence confirm the presence of stromal cells and
sometimes glandular tissue is thus identified that was missed on routine H&E
staining.[82][better source needed]

Pain quantification
The most common pain scale for quantification of endometriosis-related pain is the
visual analogue scale (VAS); VAS and numerical rating scale (NRS) were the best
adapted pain scales for pain measurement in endometriosis. For research purposes,
and for more detailed pain measurement in clinical practice, VAS or NRS for each
type of typical pain related to endometriosis (dysmenorrhea, deep dyspareunia and
non-menstrual chronic pelvic pain), combined with the clinical global impression
(CGI) and a quality of life scale, are used.[83]

Prevention
Limited evidence indicates that the use of combined oral contraceptives is
associated with a reduced risk of endometriosis.[4]
Management
While there is no cure for endometriosis, there are two types of interventions;
treatment of pain and treatment of endometriosis-associated infertility.[84] In
many women, menopause (natural or surgical) will abate the process.[85] In women in
the reproductive years, endometriosis is merely managed: the goal is to provide
pain relief, to restrict progression of the process, and to restore or preserve
fertility where needed. In younger women, surgical treatment attempts to remove
endometrial tissue and preserve the ovaries without damaging normal tissue.[86]

In general, the diagnosis of endometriosis is confirmed during surgery, at which

time ablative steps can be taken. Further steps depend on circumstances: a woman
without infertility can be managed with hormonal medication that suppresses the
natural cycle and pain medication, while an infertile woman may be treated
expectantly after surgery, with fertility medication, or with IVF. As to the
surgical procedure, ablation (or fulguration) of endometriosis (burning and
vaporizing the lesions with an electric device) has shown a high rate of short-term
recurrence after the procedure. The best surgical procedure with much lower rate of
short-term recurrence is to excise (cut and remove) the lesions completely.
[citation needed]

Surgery
Surgery, if done should generally be laparoscopically (through keyhole surgery)
rather than open.[87] Treatment consists of the excision of the endometrium,
adhesions, resection of endometriomas, and restoration of normal pelvic anatomy as
much as is possible.[88] Endometrioma on the ovary of any significant size (Approx.
2 cm +) �sometimes misdiagnosed as ovarian cysts� must be removed surgically
because hormonal treatment alone will not remove the full endometrioma cyst, which
can progress to acute pain from the rupturing of the cyst and internal bleeding.
[citation needed] Laparoscopy, besides being used for diagnosis, can also be used
to perform surgery. It's considered a "minimally invasive" surgery because the
surgeon makes very small openings (incisions) at (or around) the belly button and
lower portion of the belly. A thin telescope-like instrument (the laparoscope) is
placed through one incision, which allows the doctor to look for endometriosis
using a small camera attached to the laparoscope. Small instruments are inserted
through the incisions to remove the endometriosis tissue and adhesions. Because the
incisions are very small, there will only be small scars on the skin after the
procedure, and all endometriosis can be removed, and women recover from surgery
quicker and have a lower risk of adhesions.[89]

55% to 100% of women develop adhesions following pelvic surgery,[90] which can
result in infertility, chronic abdominal and pelvic pain, and difficult reoperative
surgery. Trehan's temporary ovarian suspension, a technique in which the ovaries
are suspended for a week after surgery may be used to reduce the incidence of
adhesions after endometriosis surgery.[91][92]

Conservative treatment involves excision of endometriosis while preserving the

ovaries and uterus, very important for women wishing to conceive, but may increase
the risk of recurrence.[93]

Endometriosis recurrence following conservative surgery is estimated as 21.5% at 2

years and 40-50% at 5 years.[94]

Historically, a hysterectomy (removal of the uterus) was thought to be a cure for

endometriosis in women who do not wish to conceive. Removal of the uterus may, in
some people, be beneficial as part of the treatment when the uterus itself is
affected by adenomyosis. However, this should only be done when combined with
removal of the endometriosis by excision, as if endometriosis is not also removed
at the time of hysterectomy, pain may persist.[87]
For women with extreme pain, a presacral neurectomy may be very rarely performed
where the nerves to the uterus are cut. However, this technique is almost never
used due to the high incidence of associated complications including presacral
hematoma and irreversible problems with urination and constipation.[87]