I. Clinicopathological types of endometriosis
1. Peritoneal endometriosis: It refers to various endometriotic lesions in the peritoneum of the pelvic abdomen, mainly including red lesions (early lesions), blue lesions (typical lesions) and white lesions (old lesions).
2. Ovarian endometriosis: cysts can be formed, which are called endometriotic cysts (customarily called “chocolate cysts”). According to the size of cysts and the degree of infiltration of ectopic lesions, they are divided into:
Type I: the diameter of the cyst is less than 2 cm, the wall of the cyst has adhesions and the level of p is unclear, so it is not easy to peel off surgically.
Type II: subdivided into three types of ABC.
ⅡA: superficial foci of endoimplantation, involving the ovarian cortex, not reaching the cyst wall, often combined with functional cysts, easy to be peeled off surgically.
ⅡB: ectopic implantation foci have involved the wall of the chocolate cyst, but the boundaries with the ovarian cortex are clear and easier to be peeled off surgically.
ⅡC: ectopic implantation foci penetrate into the cyst wall and extend to the surrounding area. The cyst wall is closely adherent to the ovarian cortex with fibrosis or multiple compartments. The ovary is adherent to the pelvic side wall and is large in size, which is not easily stripped by surgery.
3.Deep infiltrative endometriosis: the depth of infiltration of the lesion is ≥5 mm, commonly in the uterosacral ligament p recto-uterine sulcus p vaginal vault p recto-vaginal septum. One is pseudo-vaginal endometriosis, i.e. the adhesions of the rectal fossa are closed and the lesion is located below the adhesions; the other is true endometriosis, i.e. the lesion is located outside the peritoneum, in the rectovaginal septum, and there is no obvious anatomical abnormality in the rectal uterine sulcus.
4. Endometriosis in other areas: it can involve digestive, urinary (U), respiratory (R) systems, scar endometriosis (S) can be formed, and other rare distant endometriosis.
II. Pathogenesis of endoheterotaxy
1.The pathogenesis is not fully understood, and the Sampson’s theory of epithelial metaplasia and induction is the leading theory.
2, the endometrium outside the uterine cavity needs to go through the process of adhesion p invasion and angiogenesis, and then develops after implantation and growth, the characteristics of the in situ endometrium may play a decisive role.
3. the systemic and local immune status and function of the body, hormones, cytokines and enzymes play an important role in the completion of the above process of ectopic endometrium.
4.Familial aggregation of endometriosis.
5, external environmental pollution may have some influence.
III. Clinical manifestations and auxiliary examination methods
1. Pain: 70%~80% have different degrees of pelvic pain, which are not exactly parallel to the degree of lesion, including
(1) dysmenorrhea: typically secondary, and progressively aggravated.
(2) non-menstrual abdominal pain: chronic pelvic pain.
(3) painful intercourse and painful defecation.
(4) Rupture of ovarian endometriosis cysts may cause acute abdominal pain.
(2) Infertility: about 50% of patients are combined with infertility.
(3) abnormal menstruation
(4) pelvic masses.
5.Special site of endoheterosis: various symptoms often have cyclic changes and can be combined with clinical manifestations of pelvic endoheterosis. For example
(1) Gastrointestinal endoheterosis: symptoms such as increased number of stools or constipation p blood in stool p painful defecation
(2) Urinary tract endoheterosis: urinary frequency, painful urination, hematuria and lumbar pain, even causing urinary obstruction and renal dysfunction.
(3) Respiratory tract endoanomalies: menstrual hemoptysis and pneumothorax.
(4) Scar endoheterosis including abdominal wall: nodules at the incision scar after surgery such as cesarean section, which increase in size and pain during menstruation;
(5) Perineum: perineal incision or wound scar nodules, increasing in size and pain during menstruation.
(6) Gynecologic examination: typically, the uterus is often posteriorly positioned and poorly mobile; the uterosacral ligament and rectal uterine sink or posterior fornix are painful nodules; cystic inactive adnexal masses may be present at the same time.
(7) Blood carcinoembryonic antigen 125 (CA125) test: CA125 level is mostly mild to moderately elevated.
(8) Imaging: Ultrasound scan is mainly meaningful for the diagnosis of ovarian endometriosis cysts. The typical ultrasound image is an anechoic mass in the adnexal region with strong light spots inside. Magnetic resonance imaging (MRI) is meaningful for the diagnosis and evaluation of ovarian endometriosis cysts p pelvic extranodal heterotrophy and deep invasive lesions.
(9) Other: other ancillary tests, such as intravenous pyelogram (IVP), cystoscopy, colonoscopy, etc., are feasible if necessary.
IV. Diagnosis
1. Pain: Infertility pelvic examination imaging and serum CA125 test are important clinical diagnostic indicators.
2.Laparoscopy is currently the common method for diagnosing endometriosis. The diagnosis is mainly based on the morphology of the lesion under laparoscopy, but it is difficult to confirm all of them by pathology.
3.Special sites: according to the symptoms and the corresponding examination.
V. Clinical staging
The commonly used staging method for endometriosis is the 1985 revised rAFS staging method, which is based on the size and depth of peritoneal p-ovarian lesions, the extent of ovarian-fallopian tube adhesions and the thickness of the adhesions, and the degree of closure of the recto-uterine sulcus.
The staging method is divided into 4 stages:
Stage I (microscopic lesions): 1~5 points;
Stage II (mild): 6~15 points;
Stage III (moderate): 16~40 points;
Stage IV (severe):>40 points.