Endometriosis Dr. Shaimaa al-hasani

Endometriosis Is a common benign gynecologic disorder defined as the presence of endometrial glands and stroma outside of the normal location. It is most commonly found on the pelvic peritoneum, on the ovaries, rectovaginal septum, ureter, rarely in the bladder, pericardium, and pleura. Endometrial tissue located within the myometrium is termed adenomyosis (endometriosis in situ).

It is a hormonally dependent (estrogen) disease and as a result,is chiefly found in reproductive- aged women. Women with endometriosis may be asymptomatic, subfertile, or suffer varying degrees of pelvic pain. Endometriosis should be suspected in women with sub fertility, sever dyspareunia and/or chronic pelvic pain

Incidence The incidence of endometriosis is difficult to quantify, as women with the disease are often asymptomatic, and imaging modalities have low sensitivities for diagnosis. The primary method of diagnosis is laparoscopy, with or without biopsy for histological diagnosis, the annual incidence of surgically diagnosed endometriosis is 1.6 cases per 1000 women aged between 15 and 49 years (Houston, 1987). In asymptomatic women, the prevalence of endometriosis ranges from 2 to 22 percent, depending on the population studied (Eskenazi, 1997; Moen, 1997).

PATHOPHYSIOLOGY Although the definitive cause of endometriosis remains unknown, several theories with supporting evidence have been described. I.Retrograde Menstruation: The earliest and most widely accepted theory describes retrograde menstruation through the fallopian tubes and subsequenent dissemination of endometrial tissue within the peritoneal cavity adhere to and invade the peritoneal mesothelium and develop a blood supply, which leads to continued implant survival and growth. II.Lymphatic or Vascular Spread: Evidence also supports the concept of endometriosis originating from aberrant lymphatic or vascular spread of endometrial tissue. Findings of endometriosis in unusual locations, such as groin or perineum.

III. Coelomic Metaplasia This theory suggests that the parietal peritoneum is a pluripotential tissue that can undergo metaplastic transformation to tissue histologically indistinguishable from normal endometrium. Because the ovary and the progenitor of the endometrium, (the müllerian ducts) are both derived from coelomic epithelium, metaplasia may explain the development of ovarian endometriosis, this theory is attractive in instances of endometriosis in the absence of menstruation, such as in premenarchal and postmenopausal women, and in males estrogen and orchiectomy for prostatic treated with carcinom

This theory proposes that some hormonal or biologic factor(s) may induce the differentiation of und ifferentiated cells into endometrial tissue. These substances may be exogenous or released directly from the endometrium. In vitro studies have demonstrated the potential for ovarian surface epithelium, in response to estrogens, to undergo transformation to form endometriotic lesions. V. Genetics and immunological factors: This may alter the susceptibility of a women and allow her to develop endometriosis. It is more in women with 1st degree relative with the disorder and racial differences (more in oriental and less in Afro-Caribbean origin). IV. Induction Theory:

Symptoms of endometriosis in relationship to :site of endometriotic implants Site Symptoms Female reproductive tract Dysmenorrhoea Lower abdominal and pelvic pain Dyspareunia Infertility Menstrual irregularity Acute pelvic pain due to rupture/torsion endometrioma Low back pain Urinary tract Cyclical haematuria/pain Ureteral obstruction Gastrointestinal tract Cyclical tenesmus/rectal bleeding Diarrhoea Colonic obstruction Surgical scars, umbilicus Cyclical pain and bleeding Lung Cyclical haemoptysis

Disease risk factors: Endometriosis is a multi factorial genetic trait similar to DM, asthma but there are several risk factors including: 1.Age. 2. Increased peripheral body fat. 3. Greater exposure to menstruation (short cycle, long duration of flow). 4. Low parity. 5.Racial : It is less in African and more in oriental.

Classification systems: American Society for Reproductive Medicine (ASRM) classification system (1997) allows description of disease extent, differentiation between superficial and invasive disease, better correlation of surgical findings with this system has limitations and is not a good predictor of pregnancy following treatment and does not correlate well with symptoms of pain (American College of Obstetricians and Gynecologists, 1999). In this system, endometriosis is classified as stage I (minimal), stage II (mild), stage III (moderate), and stage IV (severe) This newest classification does not include certain endometriosis locations, such as bowel, in staging of the disease clinical outcomes.

Differential Diagnosis of Endometriosis Gynecologic Pelvic inflammatory disease Tubo-ovarian abscess Salpingitis Endometritis Hemorrhagic ovarian cyst Ovarian torsion Primary dysmenorrhea Degenerating leiomyoma Ectopic pregnancy Other pregnancy complications Nongynecologic Interstitial cystitis Chronic urinary tract infection Renal calculi Inflammatory bowel disease Irritable bowel syndrome Diverticulitis Mesenteric lymphadenitis Musculoskeletal disorders

Infertility and endometriosis – possible mechanisms Ovarian function Luteolysis caused by PG Oocyte maturation defects Luteinized unruptured follicle syndrome Altered prolactin release Anovulation Tubal function Impaired fimbrial oocyte pick-up Altered tubal mobility Coital function Deep dyspareunia reduced coital frequency sperm function Antibodies causing inactivation Macrophage phagocytosis Early pregnancy PG induced Immune reaction failure Luteal phase deficiency

Diagnosis: I. History & Examination: Endometriosis cannot be diagnosed by symptoms alone. It may be suspected if patient having fertility problems, severe menstrual cramps, pain during intercourse, or chronic pelvic pain or when there is a persistent ovarian cyst. Endometriosis is often found in close family members like a mother or sister. Remember, however, that many women with endometriosis have no symptoms at all. II. Visual Inspection: abnormalities during visual inspection are often lacking. Some exceptions include endometriosis within an episiotomy scar or surgical scar, most often within a Pfannenstiel incision, Rarely, endometriosis may develop spontaneously within the perineum or perianal region.

IIII. Speculum Examination: Examination of the vagina and cervix often reveals no signs of endometriosis. Occasionally, blue or red powder-burn lesions may be seen on the cervix or the posterior fornix of the vagina. These lesions may be tender or bleed with contact. IV. Bimanual Examination: Pelvic organ palpation may reveal anatomic abnormalities suggestive of endometriosis: Uterosacral ligament nodularity and tenderness. An enlarged, cystic adnexal mass may represent an ovarian endometrioma, which may be mobile or adhered to other pelvic structures. Retroverted, fixed, tender uteru. firm, fixed posterior cul-de-sac. However, examination is generally inaccurate in assessing the extent of endometriosis, especially if the lesions are extragenital.

Laboratory Testing They are often undertaken to exclude other causes of pelvic pain.Initially, CBC, serum or urine HCG assay, urinalysis and urine cultures, vaginal cultures, and cervical swabs may be obtained to exclude infections or pregnancy complications. Serum CA125 : CA125 in the diagnosis of endometriosis revealed a sensitivity of only 28 percent and a specificity of 90 percent. This marker appeared to be a better test in diagnosing stage III and IV endometriosis. Other Serum Markers Cancer antigen 19-9 (CA 19-9), Serum placental protein 14, Interleukin-6 (IL-6) serum levels above 2 pg/mL,

Comparison of ovulation induction protocols after endometrioma resection. Long GnRH-a and GnRH-ant protocols both present similar IVF outcomes in patients with endometriosis who have undergone laparoscopic endometrioma resection surgery. A long GnRH-a protocol may lead to a higher number of embryos that can be cryopreserved, providing the possibility of additional embryo transfers without having to go through the process of ovarian stimulation again. (3) There is still not enough evidence to support the use of anti- TNF-α drugs in the management of women with endometriosis for the relief of pelvic pain (4) Anti-angiogenic compounds may inhibit the establishment of new endometriotic lesions in early stages of the disease or after surgical treatment. Further experimental studies needed (5)

References 1.William gyn.(2 nd edition 2012 ) 2.Ten teachers (19 th edition 1011) 3. JSLS Jul;18(3) IstanbulJSLS. 4. Cochrane Database Syst Rev., Lu D1, Song H, Shi G Mar 28.Cochrane Database Syst Rev.Lu DSong H Shi G 5. Hum Reprod Update Nov-Dec;18(6). Epub 2012 Jun 19Hum Reprod Update.