Endometriosis

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Endometriosis
Classification and external resources

ICD-10 ICD-9 OMIM DiseasesDB MedlinePlus eMedicine MeSH

N80 617.0 131200 4269 000915 med/3419 ped/677emerg/165 D004715

Endometriosis (from Greek - endon, "within", and - mtra, "womb") is a gynecological medical condition in which cells from the lining of the uterus (endometrium) appear and flourish outside the uterine cavity, most commonly on the ovaries. The uterine cavity is lined by endometrial cells, which are under the influence of female hormones. These endometrial-like cells in areas outside the uterus (endometriosis) are influenced by hormonal changes and respond in a way that is similar to the cells found inside the uterus. Symptoms often worsen with the menstrual cycle.

Endometriosis is typically seen during the reproductive years; it has been estimated that endometriosis occurs in roughly 510% of women.[1] Symptoms may depend on the site of active endometriosis. Its main but not universal symptom is pelvic pain in various manifestations. Endometriosis is a common finding in women with infertility.[2]

Contents
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o o o o o o o o o o o o o o o o o o

1 Signs and symptoms 1.1 Pelvic pain 1.2 Fertility 1.3 Other 1.4 Complications 2 Risk factors 2.1 Genetics 2.2 Environmental 2.3 Aging 3 Pathophysiology 3.1 Metabolic changes 3.2 Formation of ectopic endometrium 3.3 Generation of pain 3.4 Localization 4 Diagnosis 4.1 Staging 4.2 Markers 4.3 Histopathology 5 Prevention 6 Management 6.1 Hormonal medication 6.2 Other medication 6.3 Surgery 6.4 Comparison of medicinal and surgical 6.5 Treatment of infertility

interventions
o

o o

6.6 Other treatments 7 Prognosis 7.1 Recurrence 8 Epidemiology 9 Notable cases 10 References 11 External links

[edit]Signs [edit]Pelvic

and symptoms
pain

A major symptom of endometriosis is recurring pelvic pain. The pain can be mild to severe cramping 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 poorly 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, on the other hand, other women may have severe pain even though they have only a few small areas of endometriosis.[3]Symptoms of endometriosis-related pain may include:[4]

dysmenorrhea painful, sometimes disabling cramps during menses; 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 sex dysuria urinary urgency, frequency, and sometimes painful voiding

Throbbing, gnawing, and dragging pain to the legs are reported more commonly by women with endometriosis.
[5]

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.[5] Individual pain areas and pain intensity appears to be unrelated to the surgical diagnosis, and the area of pain unrelated to area of endometriosis.[5]

[edit]Fertility
Many women with infertility may have endometriosis. As endometriosis can lead to anatomical distortions and adhesions (the fibrous bands that form between tissues and organs following recovery from an injury), the causality may be easy to understand; however, the link between infertility and endometriosis remains enigmatic when the extent of endometriosis is limited.[6] It has been suggested that endometriotic lesions release factors

which are detrimental to gametes or embryos, or, alternatively, endometriosis may more likely develop in women who fail to conceive for other reasons and thus be a secondary phenomenon; for this reason it is preferable to speak of endometriosis-associated infertility[7] in such cases. In some cases it can take a woman with endometriosis 710 years to conceive her first child, to most couples this can be stressful and daunting.

[edit]Other
Other symptoms may be present, including:

Constipation[5] chronic fatigue[8]

In addition to pain during menstruation, the pain of endometriosis can occur at other times of the month. There can be pain with ovulation, pain associated with adhesions, pain caused by inflammation in the pelvic cavity, pain during bowel movements and urination, during general bodily movement like exercise, pain from standing or walking, and pain with intercourse. But the most desperate pain is usually with menstruation and many women dread having their periods. Pain can also start a week before menses, during and even a week after menses, or it can be constant. There is no known cure for endometriosis. [9] There are some additional conditions that are seen in increased frequency among people with endometriosis, but where there is uncertainty whether these are factors that predispose to endometriosis or vice versa. Endometriosis bears no relationship to endometrial cancer. Current research has demonstrated an association between endometriosis and certain types of cancers, notably ovarian cancer, non-Hodgkin's lymphoma and brain cancer.[10][11][12] Endometriosis often also coexists with leiomyoma or adenomyosis, as well as autoimmune disorders. A 1988 survey conducted in the US found significantly moreHypothyroidism, fibromyalgia, chronic fatigue syndrome, autoimmune diseases, allergies and asthma in women with endometriosis compared to the general population.[13]

[edit]Complications

Endoscopic image of a rupturedchocolate cyst in left ovary.

Complications of endometriosis include:

Internal scarring Adhesions[14] Pelvic cysts Chocolate cyst of ovaries Ruptured cyst Bowel obstruction

Infertility can be related to scar formation and anatomical distortions due to the endometriosis; however, endometriosis may also interfere in more subtle ways: cytokines and other chemical agents may be released that interfere with reproduction. Other complications of endometriosis include bowel and ureteral obstruction resulting from pelvic adhesions. Also, peritonitis from bowel perforation can occur. Ovarian endometriosis may complicate pregnancy by decidualization, abscess and/or rupture.[15] It is the most common adnexal mass detected during pregnancy, being present in 0.52% of deliveries as studied in the period 2002 to 2007.[15] Still, ovarian endometriosis during pregnancy can be safely observed conservatively.[15] Pleural implantations are associated with recurrent right pneumothoraces at times of menses, termed catamenial pneumothorax.

[edit]Risk

factors

[edit]Genetics
Genetic predisposition plays a role in endometriosis.[16] It is well recognized that daughters or sisters of patients with endometriosis are at higher risk of developing endometriosis themselves; for example, low progesterone levels may be genetic, and may contribute to a hormone imbalance. There is an about 10-fold increased incidence in women with an affected first-degree relative.[17] One study found that in female siblings of patients with endometriosis the relative risk of endometriosis is 5.7:1 versus a control population.[18] 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.[16] In this case, the initial mutation may be either somatic or heritable.[16] Individual genomic changes (found by genotyping) that have been associated with endometriosis include:

Changes in chromosome 10 at region 10q26.[19] Changes in the 7p15.2 region.[20]

In addition, 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.[16]

[edit]Environmental
There is a growing suspicion that environmental factors may cause endometriosis, specifically some plastics and cooking with certain types of plastic containers with microwave ovens.[21] Dioxin exposure has been found a very likely cause of endometriosis in one well known study by The Endometriosis association that found that 79% of monkeys developed Endometriosis after receiving doses of dioxin.[22] Other sources suggest that pesticides and hormones in our food cause a hormone imbalance.

Tobacco smoking: The risk of endometriosis has been reported to be reduced in smokers.[23] Smoking

causes decreased estrogens with increased breakthrough bleeding and shortened luteal phases. Smokers have an earlier than normal (by about 1.53 years) menopause which suggests that there is some toxic effect of smoking on the follicles directly. Chemically, nicotine has been shown to concentrate in cervical mucous and metabolites have been found in follicular fluid and been associated with delayed follicular growth and maturation. Finally, there is some effect on tubal motility because smoking is associated with an increased incidence of ectopic pregnancy as well as an increased spontaneous abortion rate.

[edit]Aging
Aging brings with it many effects that may reduce fertility. Depletion over time of ovarian follicles affects menstrual regularity. Endometriosis has more time to produce scarring of the ovary and tubes so they cannot move freely or it can even replace ovarian follicular tissue if ovarian endometriosis persists and grows. Leiomyomata (fibroids) can slowly grow and start causing endometrial bleeding that disrupts implantation sites or distorts the endometrial cavity which affects carrying a pregnancy in the very early stages. Abdominal adhesions from other intraabdominal surgery, or ruptured ovarian cysts can also affect tubal motility needed to sweep the ovary and gather an ovulated follicle (egg). Endometriosis in postmenopausal women does occur and has been described as an aggressive form of this disease characterized by complete progesterone resistance and extraordinarily high levels of aromatase expression.[24] In less common cases, girls may have endometriosis symptoms before they even reach menarche.[25][26]

[edit]Pathophysiology

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.[16] Broadly, the aspects of the pathophysiology can basically be classified as underlying predisposing factors, metabolic changes, formation of ectopic endometrium, and generation of pain and other effects. It is not certain, however, to what degree predisposing factors lead to metabolic changes and so on, or if metabolic changes or formation of ectopic endometrium is the primary cause. Also, there are several theories within each category, but the uncertainty over what is a cause versus what is an effect when considered in relation to other aspects is as true for any individual entry in the pathophysiology of endometriosis.[16] Also, pathogenic mechanisms appear to differ in the formation of distinct types of endometriotic lesion, such as peritoneal, ovarian and rectovaginal lesions.[16]

[edit]Metabolic

changes

Endoscopic image of endometriotic lesions at the peritoneum of the pelvic wall.

Endometriosis correlates with abnormal amounts of multiple substances, possibly indicating a causative link in its pathogenesis, althoughcorrelation does not imply causation:

Endometrial cells in women with endometriosis demonstrate increased adherence to peritoneal cells

and increased expression of splice variants of CD44, a cell-surface protein involved in cell adhesions.[27]

The matrix metalloproteinases MMP-1 and MMP-2 are also increased, and appear to be major factors

involved in the invasion of endometrium into the peritoneum and in vascularization of endometriosis.[28]

Endometriosis patients also have elevated levels of vascular endothelial growth factor A (VEGF-

A), soluble vascular endothelial growth factor receptors-1 and -2 (sVEGFR-1 and -2) and angiopoietin2 (Ang-2).[29] IL-4 may induce angiogenesis in endometriosis by inducing expression of eotaxin.[30]

Increased oxidative stress is also implicated in the pathophysiology of endometriosis, as well as 8-iso-

PGF2 and oxysterols, being potential causative links in this oxidative stress.[31]

Endometriosis is a condition that is estrogen-dependent and thus seen primarily during the reproductive years. In experimental models, estrogen is necessary to induce or maintain endometriosis. Medical therapy is often aimed at lowering estrogen levels to control the disease. Additionally, the current research intoaromatase, an estrogen-synthesizing enzyme, has provided evidence as to why and how the disease persists after menopause and hysterectomy.

[edit]Formation

of ectopic endometrium

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

[edit]Retrograde menstruation
The theory of retrograde menstruation is the most widely accepted theory for the formation of ectopic endometrium in endometriosis.[16] It suggests that during a woman's menstrual flow, some of the endometrial debris exits the uterus through the fallopian tubes and attaches itself to the peritoneal surface (the lining of the abdominal cavity) where it can proceed to invade the tissue as endometriosis.[16] While most women may have some retrograde menstrual flow, typically their immune system is able to clear the debris and prevent implantation and growth of cells from this occurrence. However, in some patients, endometrial tissue transplanted by retrograde menstruation may be able to implant and establish itself as endometriosis. Factors that might cause the tissue to grow in some women but not in others need to be studied, and some of the possible causes below may provide some explanation, e.g., hereditary factors, toxins, or a compromised immune system. It can be argued that the uninterrupted occurrence of regular menstruation month after month for decades is a modern phenomenon, as in the past women had more frequent menstrual rest due to pregnancy and lactation. Retrograde menstruation alone is not able to explain all instances of endometriosis, and it needs additional factors such as genetic or immune differences to account for the fact that many women with retrograde menstruation do not have endometriosis. Research is focusing on 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 toxins.
[32][33]

It is still unclear what, if any, causal relationship exists between toxins, autoimmune disease, and

endometriosis In addition, at least one study found that endometriotic lesions are biochemically very different from artificially transplanted ectopic tissue.[34] The latter finding, however, can in turn be explained by that the cells that establish endometrial lesions are not of the main cell type in ordinary endometrium, but rather of a side population cell type, as supported by exhibitition of a side population phenotype upon staining with Hoechst dye and by flow cytometric analysis.[16]

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 patient until such time as the problem is resolved by surgical incision. Many health care practitioners never encounter this defect, and due to the flulike 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. The theory of retrograde menstruation as a cause of endometriosis was first proposed by John A. Sampson.

[edit]Other theories of endometrial formation

Mllerianosis: A competing theory states that cells with the potential to become endometrial are laid

down in tracts during embryonic development and organogenesis. These tracts follow the female reproductive (Mullerian) tract as it migrates caudally (downward) at 810 weeks of embryonic life. Primitive endometrial cells become dislocated from the migrating uterus and act like seeds or stem cells. This theory is supported by foetal autopsy.[35]

Coelomic metaplasia: This theory is based on the fact that coelomic epithelium is the common

ancestor of endometrial and peritoneal cells and hypothesizes that later metaplasia(transformation) from one type of cell to the other is possible, perhaps triggered by inflammation.[1] This theory is further supported by laboratory observation of this transformation.[36]

Transplantation: It is accepted that in specific patients endometriosis can spread directly. Thus

endometriosis has been found in abdominal incisional scars after surgery for endometriosis. It can also grow invasively into different tissue layers, i.e., from the cul-de-sac into the vagina. On rare occasions endometriosis may be transplanted by blood or by thelymphatic system into peripheral organs such as the lungs and brain.[citation needed] It appears that that 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 vasculogenesis rather than the conventional process of angiogenesis.[37]

[edit]Generation

of pain

The way endometriosis causes pain is the subject of much research. Because many women with endometriosis feel pain during or around their periods and may spill further menstrual flow into the pelvis with each menstruation, some researchers are trying to reduce menstrual events in patients with endometriosis.

Endometriosis lesions react to hormonal stimulation and may "bleed" at the time of menstruation. The blood accumulates locally, causes swelling, and triggers inflammatory responses with the activation of cytokines. It is thought that this process may cause pain. Pain can also occur from adhesions (internal scar tissue) binding internal organs to each other, causing organ dislocation. Fallopian tubes, ovaries, the uterus, the bowels, and the bladder can be bound together in ways that are painful on a daily basis, not just during menstrual periods. 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.[3]

[edit]Localization
Most endometriosis is found on these structures in the pelvic cavity:[citation needed]

Ovaries (the most common site) Fallopian tubes The back of the uterus and the posterior cul-de-sac The front of the uterus and the anterior cul-de-sac Uterine ligaments such as the broad or round ligament of the uterus Pelvic and back wall Intestines, most commonly the rectosigmoid Urinary bladder and ureters

Bowel endometriosis affects approximately 10% of women with endometriosis, and can cause severe pain with bowel movements.[citation needed] Endometriosis may spread to the cervix and vagina or to sites of a surgical abdominal incision.[citation needed] 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 cyclic pain of the right shoulder just before and during menses. Rarely, endometriosis can be extraperitoneal and is found in the lungs and CNS.[38]

[edit]Diagnosis

Endometriosis, abdominal wall

Micrograph showing endometriosis (right) and ovarian stroma (left). H&E stain.
A health history and a physical examination can in many patients lead the physician to suspect endometriosis. Surgery is the gold standard in diagnosis. However, in the United States most insurance plans will not cover surgical diagnosis unless the patient has already attempted to become pregnant and failed. Use of imaging tests may identify endometriotic cysts or larger endometriotic areas. It also may identify free fluid often within the cul-de-sac. The two most common imaging tests are ultrasound and magnetic resonance imaging (MRI). Normal results on these tests do not eliminate the possibility of endometriosis. Areas of endometriosis are often too small to be seen by these tests.

Endoscopic image of endometriotic lesions in the Pouch of Douglas and on the right sacrouterine ligament.

The only way to diagnose endometriosis is by laparoscopy or other types of surgery with lesion biopsy.[citation
needed]

The diagnosis is based on the characteristic appearance of the disease, and should be corroborated by

a biopsy. Surgery for diagnoses also allows for surgical treatment of endometriosis at the same time. Although doctors can often feel the endometrial growths during a pelvic exam, and these symptoms may be signs of endometriosis, diagnosis cannot be confirmed without performing a laparoscopic procedure. To the eye, lesions can appear dark blue. powder-burn black, red, white, yellow, brown or non-pigmented. Lesions vary in size. Some within the pelvis walls may not be visible to the eye, as normal-appearing peritoneum of infertile women reveals endometriosis on biopsy in 613% of cases.[39] Early endometriosis typically occurs on the surfaces of organs in the pelvic and intra-abdominal areas. 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 ovarian endometriomas or "chocolate cysts", "chocolate" because they contain a thick brownish fluid, mostly old blood. Often the symptoms of ovarian cancer are identical to those of endometriosis. If a misdiagnosis of endometriosis occurs due to failure to confirm diagnosis through laparoscopy, early diagnosis of ovarian cancer, which is crucial for successful treatment, may have been missed.[40] If surgery is not performed, then a diagnosis of exclusion process is used. This means that all of the other plausible causes of pelvic pain are ruled out. For example, internal hernias are difficult to identify in women, and misdiagnosis with endometriosis is very common. One cause of misdiagnosis is that when the woman lies down flat on an examination table, all of the medical signs of the hernia disappear, but the woman typically has tenderness and other symptoms associated with endometriosis in a pelvic exam. The hernia can typically only be detected when symptoms are present, so diagnosis requires positioning the woman's body in a way that provokes symptoms.[41]

[edit]Staging

possible locations of endometriosis

Surgically, endometriosis can be staged IIV (Revised Classification of the American Society of Reproductive Medicine).[42] 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 patient with Stage I endometriosis may have little disease and severe pain, while a patient with Stage IV endometriosis may have severe disease and no pain or vice versa. In principle the various stages show these findings: 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 presence of endometriomas on the ovary and more adhesions. Stage IV (Severe) As above, plus large endometriomas, extensive adhesions. Endometrioma on the ovary of any significant size (Approx. 2 cm +) 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. Endometrioma is sometimes misdiagnosed as ovarian cysts.

[edit]Markers
An area of research is the search for endometriosis markers. These markers are substances made by or in response to endometriosis that health care providers can measure in biopsies, in the blood or urine. Detection of such a marker may result in an earlier diagnosis of endometriosis than can be made by the rather non-specific symptoms, and may replace the invasive surgical procedures to verify the disease.[43] A biomarker could also be used to identify early signs of therapeutic efficacy or disease recurrence, as symptomatic relief or aggravation usually is hard to quantify.[43] However, as the benefits of treating women with asymptomatic endometriosis are unclear, it is likely that any biomarker would be used only to investigate women with symptoms suggestive of endometriosis.[43] Therefore, a prospective biomarker needs to distinguish women with endometriosis from women with similar presentations (for example, dysmenorrhoea, pelvic pain or subfertility).[43] A systematic review in 2010 of essentially all proposed biomarkers for endometriosis in serum, plasma and urine came to the conclusion that none of them have been clearly shown to be of clinical use, although some appear to be promising.[43] Another review in 2011

identified several putative biomarkers upon biopsy, including findings of small sensory nerve fibers or defectively expressed 3 integrin subunit.[44] The one biomarker that has been used in clinical practice over the last 20 years is CA-125.
[43]

However, its performance in diagnosing endometriosis is low, even though it shows some

promise in detecting more severe disease.[43] CA-125 levels appear to fall during endometriosis treatment, but has not shown a correlation with disease response.[43] Research is also being conducted on potential genetic markers associated with endometriosis so that a saliva-based diagnostic may replace surgical procedures for basic diagnosis.[45]However, this research remains very preliminary. It has been postulated a future diagnostic tool for endometriosis will consist of a panel of several biomarkers, including both substance concentrations and genetic predisposition.[43]

[edit]Histopathology

Micrograph of the wall of an endometrioma. All features of endometriosis are present (endometrial glands, endometrialstroma and hemosiderinladenmacrophages. 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 hemosiderindeposits as residual.

[edit]Prevention
Use of combined oral contraceptives is associated with a reduced risk of endometriosis, apparently giving a relative risk of endometriosis of 0.63 during active use, yet with limited quality of evidence according to a systematic review.[46]

[edit]Management

While there is no cure for endometriosis, in many people menopause (natural or surgical) will abate the process. In patients 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 with unfulfilled reproductive potential, surgical treatment attempts to remove endometrial tissue and preserving the ovaries without damaging normal tissue. In general, the diagnosis of endometriosis is confirmed during surgery, at which time ablative steps can be taken. Further steps depend on circumstances: patients without infertility can be managed with hormonal medication that suppress the natural cycle and pain medication, while infertile patients may be treated expectantly after surgery, with fertility medication, or with IVF. Sonography is a method to monitor recurrence of endometriomas during treatments. Treatments for endometriosis in women who do not wish to become pregnant include:

[edit]Hormonal

medication

Progesterone or Progestins: Progesterone counteracts estrogen and inhibits the

growth of the endometrium. Such therapy can reduce or eliminate menstruation in a controlled and reversible fashion. Progestins are chemical variants of natural progesterone.

Avoiding products with xenoestrogens, which have a similar effect to naturally

produced estrogen and can increase growth of the endometrium.

Hormone contraception therapy: Oral contraceptives reduce the menstrual pain

associated with endometriosis.[47] They may function by reducing or eliminating menstrual flow and providing estrogen support. Typically, it is a long-term approach. Recently Seasonale was FDA approved to reduce periods to 4 per year. Other OCPs have however been used like this off label for years. Continuous hormonal contraception consists of the use of combined oral contraceptive pills without the use of placebo pills, or the use of NuvaRing or thecontraceptive patch without the break week. This eliminates monthly bleeding episodes.

Danazol (Danocrine) and gestrinone are suppressive steroids with some androgenic
activity. Both agents inhibit the growth of endometriosis but their use remains limited as they may cause hirsutism and voice changes.

Gonadotropin Releasing Hormone (GnRH) agonist: These agents work by increasing

the levels of GnRH. Consistent stimulation of the GnRH receptors results

in downregulation, inducing a profound hypoestrogenism by decreasing FSH and LH levels. While effective in some patients, they induce unpleasant menopausal symptoms, and over time may lead toosteoporosis. To counteract such side effects some estrogen may have to be given back (add-back therapy). These drugs can only be used for six months at a time.

Lupron depo shot is a GnRH agonist and is used to lower the hormone levels

in the woman's body to prevent or reduce growth of endometriosis. The injection is given in 2 different doses: a 3 month course of monthly injections, each with the dosage of (11.25 mg); or a 6 month course of monthly injections, each with the dosage of (3.75 mg).[48]

Aromatase inhibitors are medications that block the formation of estrogen and have
become of interest for researchers who are treating endometriosis.[49]

[edit]Other

medication

NSAIDs: Anti-inflammatory. They are commonly used in conjunction with other

therapy. For more severe cases narcotic prescription drugs may be used. NSAID injections can be helpful for severe pain or if stomach pain prevents oral NSAID use.

MST: Morphine sulphate tablets and other opioid painkillers work by mimicking the
action of naturally occurring pain-reducing chemicals called "endorphins". There are different long acting and short acting medications that can be used alone or in combination to provide appropriate pain control.

Following laparoscopic surgery women who were given Chinese herbs were reported
to have comparable benefits to women with conventional drug treatments, though the journal article that reviewed this study also noted that "the two trials included in this review are of poor methodological quality so these findings must be interpreted cautiously. Better quality randomised controlled trials are needed to investigate a possible role for CHM [Chinese Herbal Medicine] in the treatment of endometriosis.",[50]

Pentoxifylline, an immuno-modulatory agent

[edit]Surgery
Procedures are classified as

conservative when reproductive organs are retained, semi-conservative when ovarian function is allowed to continue,

Conservative therapy consists of the excision (called cystectomy) of the endometrium, adhesions, resection of endometriomas, and restoration of normal pelvic anatomy as much as is possible.[6] There are combinations as well, notably one consisting of cystectomy followed by ablative surgery (removal of endometrium) using a CO2 laser to vaporize the remaining 1020% of the endometrioma wall close to the hilus.[51] Laparoscopy, besides being used for diagnosis, can also be an option for 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 into 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 tissue and adhesions. Because the incisions are very small, there will only be small scars on the skin after the procedure. The patient usually can go home the day of the surgery and should be able to return to their usual activities.[52] Semi-conservative therapy preserves a healthy appearing ovary, but also increases the risk of recurrence.[53] For patients with extreme pain, a presacral neurectomy may be indicated where the nerves to the uterus are cut. However, strong clinical evidence showed that presacral neurectomy is more effective in pain relief if the pelvic pain is midline concentrated, and not as effective if the pain extends to the left and right lower quadrants of the abdomen.[6] This is because the nerves to be transected in the procedure are innervating the central or the midline region in the female pelvis. Furthermore, women who had presacral neurectomy have higher prevalence of chronic constipation not responding well to medication treatment because of the potential injury to the parasympathetic nerve in the vicinity during the procedure. After surgical treatment of deeply infiltrating endometriosis with colorectal involvement, a review study estimated the overall endometriosis recurrence rate to be approximately 10% (ranging between 525%).[54]

[edit]Comparison

of medicinal and surgical

interventions
Efficacy studies show that both medicinal and surgical interventions produce roughly equivalent pain-relief benefits. Recurrence of pain was found to be 44 and 53 percent with medicinal and surgical interventions, respectively.[17] However, each approach has its own advantages and disadvantages.[1]

[edit]Advantages of medicinal interventions

1. 2. 3.

Decrease initial cost Empirical therapy (i.e. can be easily modified as needed) Effective for pain control

[edit]Disadvantages of medicinal interventions

1. 2. 3. Adverse effects are common Not likely to improve fertility Some can only be used for limited periods of time

[edit]Advantages of surgery
1.
2. 3. Has significant efficacy for pain control.[55] Has increased efficacy over medicinal intervention for infertility treatment Combined with biopsy, it is the only way to achieve a definitive diagnosis Can often be carried out as a minimally invasive (laparoscopic) procedure to

4.

reduce morbidity and minimize the risk of post-operative adhesions[56]

[edit]Treatment

of infertility

While roughly similar to medicinal interventions in treating pain, the efficacy of surgery is especially significant in treating infertility. One study has shown that surgical treatment of endometriosis approximately doubles the fecundity (pregnancy rate).[57] The use of medical suppression after surgery for minimal/mild endometriosis has not shown benefits for patients with infertility.[7] Use of fertility medication that stimulates ovulation (clomiphene citrate, gonadotropins) combined with intrauterine insemination (IUI) enhances fertility in these patients.[7] In-vitro fertilization (IVF) procedures are effective in improving fertility in many women with endometriosis. IVF makes it possible to combine sperm and eggs in a laboratory and then place the resulting embryos into the woman's uterus. The decision when to apply IVF in endometriosis-associated infertility takes into account the age of the patient, the severity of the endometriosis, the presence of other infertility factors, and the results and duration of past treatments.

[edit]Other

treatments

 One theory above suggests that endometriosis is an auto-immune condition and if the
immune system is compromised with a food intolerance, then removing that food from the diet can, in some people, have an effect. Various dietary recommendations are made in popular media. For example, common intolerances in people with endometriosis are claimed to be wheat, sugar, meat and dairy.[58] Avoiding foods high in hormones and inflammatory fats also appears to be important in endometriosis pain management.[citation needed] Eating foods high in indole-3-carbinol, such as cruciferous vegetables appears to be helpful in balancing hormones and managing pain.
[59]

However, these popular claims are typically not supported by scientific studies.

According to one scientific study, diets high in fat and low in fruit and -carotene were associated with a lower risk of endometriosis,[60] contradicting the typical idea of a healthy diet. Consumption of omega 3 fatty acids, particularly EPA, as a food supplement has been suggested as a therapy for endometriosis.[61] The use of soy has been reported to both alleviate pain and to aggravate symptoms, making its use questionable.[62]

Physical therapy for pain management in endometriosis has been investigated in a

pilot study suggesting possible benefit.[63] Physical exertion such as lifting, prolonged standing or running does exacerbate pelvic pain. Use of heating pads on the lower back area, may provide some temporary relief.

Laboratory studies indicate that heparin may alleviate endometriosis-associated

fibrosis.[64]

[edit]Prognosis
Proper counseling of patients with endometriosis requires attention to several aspects of the disorder. Of primary importance is the initial operative staging of the disease to obtain adequate information on which to base future decisions about therapy. The patient's symptoms and desire for childbearing dictate appropriate therapy. Not all therapy works for all patients. Some patients have recurrences after surgery or pseudo-menopause. In most cases, treatment will give patients significant relief from pelvic pain and assist them in achieving pregnancy.[65] It is important for patients to be continually in contact with their physician and keep an open dialog throughout treatment. This is a disease without a cure but with the proper communication, a woman with endometriosis can attempt to live a normal, functioning life. Using cystectomy and ablative surgery, pregnancy rates are approximately 40%.[51]

[edit]Recurrence
The underlying process that causes endometriosis may not cease after surgical or medical intervention. The most recent studies have shown that endometriosis recurs at a rate of 20 to 40 percent within five years following conservative surgery,[66] unless hysterectomy is performed or menopause reached. Monitoring of patients consists of periodic clinical examinations and sonography. Also, the CA 125 serum antigen levels have been used to follow patients with endometriosis. With combined cystectomy and ablative surgery, one study showed recurrence of a small endometrioma in only one case among fifty-two women (2%) at a mean follow-up of 8.3 months.[51] Vaginal childbirth decreases recurrence of endometriosis. In contrast, endometriosis recurrence rates have been shown to be higher in women who have not given birth vaginally, such as in Cesarean section.[67]

[edit]Epidemiology
Endometriosis can affect any female, from premenarche to postmenopause, regardless of race or ethnicity or whether or not they have had children. It is primarily a disease of the reproductive years. Estimates about its prevalence vary, but 510% is a reasonable number, more common in women with infertility (2050%) and women with chronic pelvic pain (about 80%).[17] As an estrogen-dependent process, it can persist beyond menopause and persists in up to 40% of patients following hysterectomy.[68] In some cases, it may also begin beyond menopause and it has also been described in men taking high-dose estrogen therapy.[69][70]

[edit]Notable

cases

Emma Bunton singer [71] Annabel Croft tennis player, radio presenter and television presenter [72] Karen Duffy model, television personality and actress [73] Anna Friel actress [74] Julianne Hough professional ballroom dancer, country music singer and actress [75] Padma Lakshmi cookbook author, actress, model and television host [76] Jillian Michaels (personal trainer) celebrity personal trainer, reality show personality,
direct-response television pitchwoman and entrepreneur [77]

Marilyn Monroe actress [78] Tia Mowry actress [79]

 Dolly Parton singer-songwriter, author, multi-instrumentalist, actress and

philanthropist [80]

Queen Victoria monarch [81] Louise Redknapp singer [82] Susan Sarandon actress and social activist [83] Lacey Schwimmer ballroom dancer and singer [84] Stephanie St. James actress [85] Kirsten Storms actress [86] Anthea Turner television presenter and media personality [87]

[edit]References

Ectopic pregnancy
From Wikipedia, the free encyclopedia

This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (November 2010)

Ectopic pregnancy
Classification and external resources

Ectopic by Reinier de Graaf ICD-10 ICD-9 O00 633

DiseasesDB MedlinePlus eMedicine MeSH

4089 000895 med/3212 emerg/478radio/231 D011271

An ectopic pregnancy, or eccysis , is a complication of pregnancy in which the embryo implants outside the uterine cavity.[1] With rare exceptions, ectopic pregnancies are not viable. Furthermore, they are dangerous for the parent, since internal haemorrhage is a life threatening complication. Most ectopic pregnancies occur in the Fallopian tube (so-called tubal pregnancies), but implantation can also occur in the cervix, ovaries, and abdomen. An ectopic pregnancy is a potential medical emergency, and, if not treated properly, can lead to death. In a normal pregnancy, the fertilized egg enters the uterus and settles into the uterine lining where it has plenty of room to divide and grow. About 1% of pregnancies are in an ectopic location with implantation not occurring inside of the womb, and of these 98% occur in the Fallopian tubes. Detection of ectopic pregnancy in early gestation has been achieved mainly due to enhanced diagnostic capability. Despite all these notable successes in diagnostics and detection techniques ectopic pregnancy remains a source of serious maternal morbidity and mortality worldwide, especially in countries with poor prenatal care.[2] In a typical ectopic pregnancy, the embryo adheres to the lining of the fallopian tube and burrows into the tubal lining. Most commonly this invades vessels and will cause bleeding. This intratubal bleeding hematosalpinx expels the implantation out of the tubal end as a tubal abortion. Tubal abortion is a common type of miscarriage. There is no inflammation of the tube in ectopic pregnancy. The pain is caused by prostaglandins released at the implantation site, and by free blood in the peritoneal cavity, which is a local irritant. Sometimes the bleeding might be heavy enough to threaten the health or life of the woman. Usually this degree of bleeding is due to delay in diagnosis, but sometimes, especially if the implantation is in the proximal tube (just before it enters the uterus), it may invade into the nearby Sampson artery, causing heavy bleeding earlier than usual. If left untreated, about half of ectopic pregnancies will resolve without treatment. These are the tubal abortions. The advent of methotrexatetreatment for ectopic pregnancy has reduced the need for surgery; however, surgical intervention is still required in cases where the Fallopian tube has ruptured or is in danger of doing so. This intervention may be laparoscopic or through a larger incision, known as a laparotomy.

Contents
[hide]
o o

1 Classification 1.1 Tubal pregnancy 1.2 Nontubal ectopic 1.3 Heterotopic pregnancy 1.4 Persistent ectopic 2 Signs and symptoms 3 Causes
o

pregnancy
o o

pregnancy

3.1 Cilial damage and tube 3.2 Other 4 Diagnosis 5 Treatment

occlusion
o o o o

5.1 Medical 5.2 Surgical 6 Complications 7 Prognosis 7.1 Future fertility 8 Cases with live birth 9 In other animals 10 References 11 External links

[edit]Classification [edit]Tubal

pregnancy

The vast majority of ectopic pregnancies implant in the Fallopian tube. Pregnancies can grow in the fimbrial end (5% of all ectopics), the ampullary section (80%), the isthmus (12%), and the cornual and interstitial part of the tube (2%).[3] Mortality of a tubal pregnancy at the isthmus or within the uterus (interstitial pregnancy) is higher as there is increased vascularity that may result more likely in sudden major internal hemorrhage. A

review published in 2010 supports the hypothesis that tubal ectopic pregnancy is caused by a combination of retention of the embryo within the fallopian tube due to impaired embryo-tubal transport and alterations in the tubal environment allowing early implantation to occur.[4]

[edit]Nontubal

ectopic pregnancy

Two percent of ectopic pregnancies occur in the ovary, cervix, or are intraabdominal. Transvaginal ultrasound examination is usually able to detect a cervical pregnancy. An ovarian pregnancy is differentiated from a tubal pregnancy by the Spiegelberg criteria.[5] While a fetus of ectopic pregnancy is typically not viable, very rarely, a live baby has been delivered from an abdominal pregnancy. In such a situation the placenta sits on the intraabdominal organs or the peritoneum and has found sufficient blood supply. This is generally bowel or mesentery, but other sites, such as the renal (kidney), liver or hepatic (liver) artery or even aorta have been described. Support to near viability has occasionally been described, but even in third world countries, the diagnosis is most commonly made at 16 to 20 weeks gestation. Such a fetus would have to be delivered by laparotomy. Maternal morbidity and mortality from extrauterine pregnancy is high as attempts to remove the placenta from the organs to which it is attached usually lead to uncontrollable bleeding from the attachment site. If the organ to which the placenta is attached is removable, such as a section of bowel, then the placenta should be removed together with that organ. This is such a rare occurrence that true data are unavailable and reliance must be made on anecdotal reports.[6][7][8]However, the vast majority of abdominal pregnancies require intervention well before fetal viability because of the risk of hemorrhage.

[edit]Heterotopic

pregnancy

In rare cases of ectopic pregnancy, there may be two fertilized eggs, one outside the uterus and the other inside. This is called a heterotopic pregnancy. Often the intrauterine pregnancy is discovered later than the ectopic, mainly because of the painful emergency nature of ectopic pregnancies. Since ectopic pregnancies are normally discovered and removed very early in the pregnancy, an ultrasound may not find the additional pregnancy inside the uterus. When hCG levels continue to rise after the removal of the ectopic pregnancy, there is the chance that a pregnancy inside the uterus is still viable. This is normally discovered through an ultrasound. Although rare, heterotopic pregnancies are becoming more common, likely due to increased use of IVF. The survival rate of the uterine fetus of an ectopic pregnancy is around 70%.[9] Successful pregnancies have been reported from ruptured tubal pregnancy continuing by the placenta implanting on abdominal organs or on the outside of the uterus.

[edit]Persistent

ectopic pregnancy

A persistent ectopic pregnancy refers to the continuation of trophoplastic growth after a surgical intervention to remove an ectopic pregnancy. After a conservative procedure that attempts to preserve the affected fallopian tube such as a salpingotomy, in about 15-20% the major portion of the ectopic growth may have been removed, but some trophoblastic tissue, perhaps deeply embedded, has escaped removal and continues to grow, generating a new rise in hCG levels.[10] After weeks this may lead to new clinical symptoms including bleeding. For this reason hCG levels may have to be monitored after removal of an ectopic to assure their decline, also methotrexate can be given at the time of surgery prophylactically.

[edit]Signs

and symptoms

Early symptoms are either absent or subtle. Clinical presentation of ectopic pregnancy occurs at a mean of 7.2 weeks after the last normal menstrual period, with a range of 5 to 8 weeks. Later presentations are more common in communities deprived of modern diagnostic ability. Early signs include:

Pain in the lower abdomen, and inflammation (Pain may be confused with a strong stomach pain, it

may also feel like a strong cramp)

Pain while urinating Pain and discomfort, usually mild. A corpus luteum on the ovary in a normal pregnancy may give very

similar symptoms.

Vaginal bleeding, usually mild. An ectopic pregnancy is usually a failing pregnancy and falling levels of

progesterone from the corpus luteum on the ovary cause withdrawal bleeding. This can be indistinguishable from an early miscarriage or the 'implantation bleed' of a normal early pregnancy.

Pain while having a bowel movement

Patients with a late ectopic pregnancy typically experience pain and bleeding. This bleeding will be both vaginal and internal and has two discrete pathophysiologic mechanisms:

External bleeding is due to the falling progesterone levels. Internal bleeding (hematoperitoneum) is due to hemorrhage from the affected tube.

The differential diagnosis at this point is between miscarriage, ectopic pregnancy, and early normal pregnancy. The presence of a positive pregnancy test virtually rules out pelvic infection as it is rare indeed to find pregnancy with an active Pelvic Inflammatory Disease (PID). The most common misdiagnosis assigned to early ectopic pregnancy is PID. More severe internal bleeding may cause:

Lower back, abdominal, or pelvic pain. Shoulder pain. This is caused by free blood tracking up the abdominal cavity and irritating the

diaphragm, and is an ominous sign.

There may be cramping or even tenderness on one side of the pelvis. The pain is of recent onset, meaning it must be differentiated from cyclical pelvic pain, and is often

getting worse. Ectopic pregnancy can mimic symptoms of other diseases such as appendicitis, other gastrointestinal disorder, problems of the urinary system, as well as pelvic inflammatory diseaseand other gynaecologic problems.

[edit]Causes
There are a number of risk factors for ectopic pregnancies. However, in as many as one third[11] to one half[12] of ectopic pregnancies, no risk factors can be identified. Risk factors include: pelvic inflammatory disease, infertility, use of an intrauterine device (IUD), previous exposure to DES, tubal surgery, intrauterine surgery (e.g. D&C), smoking, previous ectopic pregnancy, and tubal ligation.[13] Although older texts suggests an association between endometriosis and ectopic pregnancy this is not evidence based and current research suggests no association between endometriosis and ectopic pregnancy.
[14]

[edit]Cilial

damage and tube occlusion

Hair-like cilia located on the internal surface of the Fallopian tubes carry the fertilized egg to the uterus. Fallopian cilia are sometimes seen in reduced numbers subsequent to an ectopic pregnancy, leading to a hypothesis that cilia damage in the Fallopian tubes is likely to lead to an ectopic pregnancy.[15] Women with pelvic inflammatory disease (PID) have a high occurrence of ectopic pregnancy.[16] This results from the build-up of scar tissue in the Fallopian tubes, causing damage to cilia.[3] If however both tubes were completely blocked, so that sperm and egg were physically unable to meet, then fertilization of the egg would naturally be impossible, and neither normal pregnancy nor ectopic pregnancy could occur. Tubal surgery for damaged tubes might remove this protection and increase the risk of ectopic pregnancy[citation needed]. Intrauterine adhesions (IUA) present in Asherman's syndrome can cause ectopic cervical pregnancy or, if adhesions partially block access to the tubes via the ostia, ectopic tubal pregnancy.[17][18][19] Asherman's syndrome usually occurs from intrauterine surgery, most commonly after D&C.[17] Endometrial/pelvic/genital tuberculosis, another cause of Asherman's syndrome, can also lead to ectopic pregnancy as infection may lead to tubal adhesions in addition to intrauterine adhesions.[20] Tubal ligation can predispose to ectopic pregnancy. Seventy percent of pregnancies after tubal cautery are ectopic, while 70% of pregnancies after tubal clips are intrauterine[citation needed]. Reversal of tubal sterilization

(Tubal reversal) carries a risk for ectopic pregnancy. This is higher if more destructive methods of tubal ligation (tubal cautery, partial removal of the tubes) have been used than less destructive methods (tubal clipping). A history of a tubal pregnancy increases the risk of future occurrences to about 10%.[3] This risk is not reduced by removing the affected tube, even if the other tube appears normal. The best method for diagnosing this is to do an early ultrasound.

[edit]Other
Although some investigations have shown that patients may be at higher risk for ectopic pregnancy with advancing age, it is believed that age is a variable which could act as a surrogate for other risk factors. Also, it has been noted that smoking is associated with ectopic risk. Vaginal douching is thought by some to increase ectopic pregnancies.[3] Women exposed todiethylstilbestrol (DES) in utero (also known as "DES Daughters") also have an elevated risk of ectopic pregnancy, up to 3 times the risk of unexposed women[citation needed]. It has also been suggested that pathologic generation of nitric oxide through increased iNOS production may decrease tubal ciliary beats and smooth muscle contractions and thus affect embryo transport, which may consequently result in ectopic pregnancy.[21]

[edit]Diagnosis

An opened oviduct with an ectopic pregnancy at about 7 weeks gestational age.

An ectopic pregnancy should be considered in any woman with abdominal pain or vaginal bleeding who has a positive pregnancy test. Anultrasound showing a gestational sac with fetal heart in the fallopian tube is clear evidence of ectopic pregnancy. An abnormal rise in blood -human chorionic gonadotropin (-hCG) levels may indicate an ectopic pregnancy. The threshold of discrimination ofintrauterine pregnancy is around 1500 IU/ml of -hCG. A high resolution, transvaginal ultrasound showing no intrauterine pregnancy is presumptive evidence that an ectopic

pregnancy is present if the threshold of discrimination for -hCG has been reached. An empty uterus with levels higher than 1500 IU/ml may be evidence of an ectopic pregnancy, but may also be consistent with an intrauterine pregnancy which is simply too small to be seen on ultrasound. If the diagnosis is uncertain, it may be necessary to wait a few days and repeat the blood work. This can be done by measuring the -hCG level approximately 48 hours later and repeating the ultrasound. If the -hCG falls on repeat examination, this strongly suggests a spontaneous abortion or rupture. A laparoscopy or laparotomy can also be performed to visually confirm an ectopic pregnancy. Often if a tubal abortion or tubal rupture has occurred, it is difficult to find the pregnancy tissue. A laparoscopy in very early ectopic pregnancy rarely shows a normal looking fallopian tube. Culdocentesis, in which fluid is retrieved from the space separating the vagina and rectum, is a less commonly performed test that may be used to look for internal bleeding. In this test, a needle is inserted into the space at the very top of the vagina, behind the uterus and in front of the rectum. Any blood or fluid found may have been derived from a ruptured ectopic pregnancy. Cullen's sign can indicate a ruptured ectopic pregnancy.

[edit]Treatment [edit]Medical
Early treatment of an ectopic pregnancy with methotrexate is a viable alternative to surgical treatment[22] since at least 1993.[23] If administered early in the pregnancy, methotrexate terminates the growth of the developing embryo; this may cause an abortion, or the tissue may then be either resorbed by the woman's body or pass with a menstrual period. Contraindications include liver, kidney, or blood disease, as well as an ectopic mass > 3.5 cm.

[edit]Surgical
If hemorrhage has already occurred, surgical intervention may be necessary. However, whether to pursue surgical intervention is an often difficult decision in a stable patient with minimal evidence of blood clot on ultrasound.[citation needed] Surgeons use laparoscopy or laparotomy to gain access to the pelvis and can either incise the affected Fallopian and remove only the pregnancy (salpingostomy) or remove the affected tube with the pregnancy (salpingectomy). The first successful surgery for an ectopic pregnancy was performed by Robert Lawson Tait in 1883.[24]

[edit]Complications

The most common complication is rupture with internal haemorrhage which may lead to hypovolaemic shock. Death from rupture is rare in women who have access to modern medical facilities.

[edit]Prognosis [edit]Future

fertility

Fertility following ectopic pregnancy depends upon several factors, the most important of which is a prior history of infertility.[25] The treatment choice, whether surgical or nonsurgical, also plays a role. For example, the rate of intrauterine pregnancy may be higher following methotrexate compared to surgical treatment.[26] Rate of fertility may be better following salpingostomy than salpingectomy.[26]

[edit]Cases

with live birth

There have been cases where ectopic pregnancy lasted many months and ended in a live baby delivered by laparotomy. In July 1999, Lori Dalton gave birth by Caesarean section in Ogden, Utah, USA to a healthy baby girl who had developed outside of the uterus. Previous ultrasounds had not discovered the problem. "Sage Dalton's delivery was slated as a routine Cesarean birth at Ogden Regional Medical Center in Utah. When Dr. Naisbitt performed Loris Cesarean, he was astonished to find Sage within the amniotic membrane outside the womb."[27] " But what makes this case so rare is that not only did mother and baby survive-- they're both in perfect health. John Dalton (the father) took home video inside the delivery room. Saige came out doing extremely well because even though she had been implanted outside the womb, a rich blood supply from a benign fibrous tumor along the outer uterus wall had nourished her with a rich source of blood."[28] On 19 April 2008 an English woman, Jayne Jones (age 37) who had an ectopic pregnancy attached to the omentum, the fatty covering of her large bowel, gave birth. The baby, Billy Jones was delivered by a laparotomy at 28 weeks gestation. The surgery, the first of its kind to be performed in the UK, was successful, and both mother and baby survived.[29] On May 29, 2008 an Australian woman, Meera Thangarajah (age 34), who had an ectopic pregnancy in the ovary, gave birth to a healthy full term 6 pound 3 ounce (2.8 kg) baby girl, Durga, via Caesarean section. She had no problems or complications during the 38-week pregnancy.[30][31] The case of Olivia, Mary and Ronan had an extrauterine fetus (Ronan) and intrauterine twins. All three survived. The intrauterine twins were taken out first.[32]

[edit]In

other animals

Ectopic gestation exists in other mammals.

In sheep, it can go to term, with mammary preparation to parturition, and expulsion efforts. The fetus can be removed by caesarian section. Pictures of caesarian section of a euthanized ewe, 5 days after parturition signs.

Leg of fetal lamb appearing out of the uterus during cesarian section.

External view of fetal sac, necrotic distal part.

Internal view of fetal sac, before resection of distal necrotic part.

Internal view of fetal sac, the necrotic distal part is to the left.

External side of fetal sac, proximal end, with ovary and uterine horn.

Resected distal part of fetal sac, with attached placenta.