Aetiology
I. Planting theory The earliest (1921) that the occurrence of pelvic endometriosis, endometrial fragments of the endometrium with the menstrual blood reflux, through the fallopian tubes into the pelvic cavity and planted in the ovary or other parts of the pelvic cavity caused. Clinically, menstrual blood can be found in the pelvic cavity during the menstrual period when performing a cesarean section, and the endometrium can be found in the menstrual blood. The abdominal wall scar endometriosis formed after cesarean section is a good example of the implantation doctrine.
The plasma membrane theory, also known as the chemotaxis theory, believes that ovarian and pelvic endometriosis is chemotaxis from the peritoneal mesothelial cell layer. The paramedian mesonephric duct is developed from the primitive peritoneal invagination, and the ovarian germinal epithelium, the pelvic peritoneum, the atresia peritoneal invagination, such as the peritoneal sheath of the inguinal area (Nukes), the rectovaginal septum, the umbilicus and so on, are all from the body cavity epithelium differentiation. All tissues arising from the corpora cavernosa epithelium have the potential ability to chemotaxis into tissues that are virtually indistinguishable from the endometrium, and thus the peritoneal mesothelial cells may be susceptible to chemotaxis into an ectopic endometrium when stimulated by mechanical (including tubal ventilation, retroverted uterus, and cervical obstruction), inflammatory, and ectopic pregnancy factors. The germinal epithelium on the surface of the ovary has more potential for differentiation because it is a primitive somatic epithelium. Under the influence of hormones and inflammation, it can differentiate into all kinds of tissues that can be formed at the time of embryo, including endometrium. The ovary is the most involved site in extrinsic endometriosis and is easily explained by the chemotaxis theory. The implantation doctrine does not explain the occurrence of endometriosis beyond the pelvis.
Third, immunological theory In 1980, Weed et al. reported that the ectopic endometrium is surrounded by lymphocytes, plasma cells infiltration, macrophages containing ferritin deposits and varying degrees of fibrosis. They believed that it was due to the ectopic endothelial lesion as a foreign body, which activated the body's immune system. Since then, many scholars have explored the etiology and pathogenesis of ectopic endothelial disease from the aspects of cellular immunity and humoral immunity.
(I) cellular immune defects 1.T lymphocyte function defects; 2.natural killer cell (NK) function defects: NK cells are a heterogeneous group of multifunctional immune cells, whose function is characterized by the fact that they do not need the presence of antibodies, do not need to be sensitized to the antigen to kill certain tumor cells or viral cells, and they play an important role in the body's immune guardianship. It plays an important role in the body's immune guardianship.
(2) Humoral immune deficiency There are other theories about endometriosis: (1) the theory of lymphatic dissemination. It is believed that the endometrium can be disseminated through the lymphatic channel, and it has been found that the paracolic lymph nodes and the internal iliac lymph nodes contain endometrial tissue. However, the weakness of this theory is that endometrial tissue is seldom seen in the center of regional lymph nodes, and the frequent sites are not in line with normal lymphatic drainage; ② hemorrhagic dissemination theory. According to the literature, ectopic endometrium has been found in the veins, pleura, liver parenchyma, kidneys, upper arms and lower limbs. Some scholars believe that it is most likely that the endometrium spreads to the above mentioned tissues and organs through the bloodstream, and experimental endometriosis has been caused in the lungs of rabbits. However, it has been suggested that although these cases may be caused by hematogenous dissemination, localized chemotaxis cannot be excluded because the pleura is also differentiated from the epithelium of the corpora cavernosa. In the embryonic stage, when the germ and the mesonephric ducts are produced, it is possible that the corpora cavernosa epithelium is ectopically located in them, and the tissue may later metaplasia and form endometriosis in each of these parts.
No matter what the source of the ectopic endometrium is, its growth is related to the endocrine secretion of the ovary, and the clinical data can show that this disease occurs mostly in women in their childbearing years (more than 80% of them are 30-50 years old), and it is often accompanied by ovarian dysfunction. After removal of the ovaries, the ectopic endometrium atrophies. The growth of ectopic endometrium mainly relies on estrogen, and with the higher secretion of progesterone during pregnancy, the ectopic endometrium is inhibited. Prolonged oral synthetic progesterone such as acetylenolone, resulting in false pregnancy, can also make the ectopic endometrium atrophy.
Pathological changes
I. Intrinsic endometriosis The endometrium grows from the base to the myometrium and is confined to the uterus, so it is also called adenomyosis. Ectopic endometrium is often diffuse throughout the myometrial wall, due to endometrial invasion caused by fibrous tissue and myofibers reactive hyperplasia, so that the uterus consistency distension, but rarely more than the full-term fetal head size. Uneven or focal distribution is usually more common in the posterior wall, and because it is confined to one part of the uterus, it tends to make the uterus irregularly enlarged, resembling a fibroid tumor. On the cut surface, the proliferated muscle tissue is also similar to fibroids in a swirling structure, but there is no peritoneal tissue that separates the fibroids from the surrounding normal muscle fibers. In the middle of the lesion, there is an area of softening, and occasionally, small cavities containing a small amount of old blood can be seen scattered. Microscopically, the endometrial glands are identical to endometrial glands and are surrounded by endometrial mesenchyme. The ectopic endometrium changes with the menstrual cycle, but the changes are less pronounced during the secretory phase, indicating that the ectopic endometrial glands are less affected by progesterone. When conception occurs, the mesenchymal cells of the ectopic endometrium may show marked metaplasia, as has been described above.
Second, interstitial endometriosis is a special type of intrinsic endometriosis, less common, that is, the ectopic endometrium only endometrial interstitial tissue, or endometrial invasion of the myometrium after the development of the interstitial tissue far more than the degree of glandular components. Generally, the uterine consistency increases, the ectopic cells are scattered in the myometrium or concentrated in a certain area, yellow in color, often with elastic rubber-like hardness, softer than fibroids, and in the section can often be seen in the cord-like worm-like protrusions, which can be used to establish the diagnosis. Ectopic tissue can also be developed to the uterine cavity to form polypoid masses, multiple, smooth surface, wide and uterine myometrial wall has a large area of direct connection, and can be from the uterine wall to the uterine cavity or along the uterine blood vessels to the broad ligament protruding. Those protruding into the uterine cavity may result in excessive menstruation or even postmenopausal bleeding; those protruding into the broad ligament may be detected by gynecologic double diagnosis. Interstitial endometriosis can have pulmonary dissemination, even years after hysterectomy. Because of this feature, it has been suggested that interstitial endometriosis is a sarcoma with low-floor malignancy.
Third, extrinsic endometriosis Endometrial invasion of tissues (including ectopic endometrium invading the plasma layer of the uterus from the pelvis) or organs outside the uterus, often involving multiple organs or tissues.
The ovary is the most frequent site of extrinsic endometriosis, accounting for 80% of cases, followed by the peritoneum of the uterorectal fossa, including the uterosacral ligament, the anterior wall of the uterorectal fossa corresponding to the area of the posterior fornix of the vagina, and the posterior wall of the uterine cervix corresponding to the endocervical opening. Sometimes the ectopic endometrium invades the anterior wall of the rectum, forming dense adhesions between the intestinal wall and the posterior wall of the uterus and ovaries, which are difficult to separate intraoperatively. Extrinsic endometriosis can also invade the rectovaginal septum and form scattered black-purple dots on the mucosa of the posterior vaginal fornix, or even form cauliflower-like protrusions, which resembles cancerous tumors, and can only be confirmed as endometriosis by biopsy. In addition, as mentioned earlier, the fallopian tube, cervix, vulva, appendix, umbilicus, abdominal wall incision, hernia sac, bladder, lymph nodes, and even pleura and pericardium, upper limbs, thighs, the skin may have ectopic endometriosis growth.
Ectopic endometrium in the uterorectal fossa may also form purple-black hemorrhagic spots on the peritoneum or blood-accumulating vesicles, which are embedded in fibrous tissues with severe adhesions, and can be seen microscopically as typical endometrium. The ectopic endometrial tissue may also extend into the rectovaginal septum and uterosacral ligament to form a firm nodule that is painful to the touch. Or it may penetrate the mucosa of the posterior vaginal fornix to form a bluish-purple papillary mass, which may appear as many small bleeding spots during menstruation. If the anterior wall of the rectum is involved, menstrual pain may occur. Sometimes the endometriosis extends around the rectum to form a narrow ring, which is very similar to carcinoma, and intestinal invasion accounts for about 10% of endometriosis. The lesions are often located in the plasma membrane and muscular layer, and rarely the mucosa is invaded and ulceration occurs. Occasionally, intestinal obstruction occurs due to the formation of a mass in the intestinal wall or fibrous stenosis or adhesions causing excessive flexion of the intestinal tubes, and irritation symptoms, such as intermittent diarrhea, are more severe during menstruation.
Clinical manifestations
Signs and symptoms of endometriosis vary with the location of the ectopic endometrium and are closely related to the menstrual cycle.
I. Symptoms
(1) Dysmenorrhea: a common and prominent symptom, mostly secondary, that is, since the occurrence of endometriosis, the patient complained of no pain during the previous menstrual period, and dysmenorrhea began to appear from a certain period. They may occur before, during and after menstruation. In some cases, the dysmenorrhea is so severe and intolerable that bed rest or medication is needed to relieve the pain. The pain often worsens with the menstrual cycle. Due to high estrogen levels, the ectopic endometrium proliferates and swells, and bleeds if affected by progesterone, irritating the local tissues and causing pain. In cases of intrinsic endometriosis, uterine muscle contracture can be induced, and dysmenorrhea will be more pronounced. In cases where there is no bleeding from the ectopic tissue, the dysmenorrhea may be caused by vascular congestion. After menstruation, the ectopic endometrium gradually shrinks and the dysmenorrhea disappears. In addition, in pelvic endometriosis, many inflammatory processes can be detected, and it is likely that localized inflammatory processes are accompanied by active peritoneal lesions, which produce prostaglandins, kallikreins, and other peptides causing pain or tenderness.
But the degree of pain often does not reflect the degree of disease detected by laparoscopy. Clinically significant endometriosis without dysmenorrhea occurs in about 25% of cases. A woman's psychological condition can also influence pain perception.
(ii) Hypermenorrhea: In intrinsic endometriosis, menstrual flow tends to increase and menstrual period is prolonged. It may be due to increased endometrium but is mostly associated with ovarian dysfunction.
(3) Infertility: patients with endometriosis are often associated with infertility. According to reports from Tianjin and Shanghai, primary infertility accounts for 41.5-43.3% and secondary infertility accounts for 46.6-47.3%. The causal relationship between infertility and endometriosis is still debated. Pelvic endometriosis can often cause adhesions around the fallopian tubes affecting oocyte pickup or causing lumen blockage. Or it may cause infertility due to ovarian pathology that affects the normal progression of ovulation. However, it is also believed that long-term infertility, menstruation without closing period, can cause endometriosis opportunity; and once pregnant, the ectopic endometrium is inhibited and atrophy.
(4) pain in sexual intercourse: endometriosis occurring in the uterine rectal fossa, vaginal rectal septum, so that the surrounding tissues are swollen and affect sexual life, pre-menstrual sexual discomfort aggravated.
(E) stool swelling: usually occurs in the premenstrual period or after menstruation, the patient feels pain when the feces passes through the rectum, but not at other times, for the uterorectal fossa and rectum near the endometriosis of the typical symptoms. Occasionally, if the ectopic endometrium reaches the rectal mucosa, there is rectal bleeding during menstruation. The endometriotic lesions around the rectum to form a narrowing of the person has a rapid and obstructive symptoms, so it is similar to the cancer tumor.
(6) Bladder symptoms: in endometriosis to the bladder, there are symptoms of cyclic dysuria and dyspareunia; when the mucosa of the bladder is invaded, cyclic hematuria may occur.
Endometriosis in the abdominal wall scar and umbilicus is characterized by periodic localized lumps and pain.
Zhang Linghao reported that of 490 cases of infertility laparoscopy, 229 cases were endometriosis of different dates. The fallopian tubes were bilaterally patent in 50 cases (21.8%), patent on one side and incompetent or obstructed on the other in 73 cases (31.7%), incompetent bilaterally or incompetent on one side and obstructed on the other in 72 cases (31.3%), and incompetent bilaterally in 49 cases (21.3%). Bilateral tubal impassability certainly can't cause pregnancy naturally, accounting for 1/5 of the infertility of endometriosis; bilateral or one side of the pass but not pass accounted for 1/3 of the weak; 1/5 both sides of the pass or one side of the pass accounted for 1/3 of the weak. Obstructed or incomplete fallopian tubes, as well as adhesions around the umbrella end, all affect the entry of egg cells into the fallopian tube. However, infertility also occurs when one side of the tube is open, or even both sides are open. In addition, destruction of the ovaries by ectopic endometrium also affects oocyte development or ovulation and luteal insufficiency. The above changes easily explain the mechanism of infertility. Autoimmune reactions in patients with endometriosis are also detrimental to sperm and fertilized eggs.
Patients with endometriosis also have a higher rate of miscarriage. According to Jones and Jones and Naples et al, the miscarriage rate in those conceived with endometriosis can be as high as 44 to 47%.Naples also reported that the miscarriage rate in patients with endometriosis decreased to 8% after surgical treatment.
Signs Patients with intrinsic endometriosis tend to have a distended uterus, but seldom more than 3 months gestation. Most of the consistency of distension, may also feel a part of the more prominent as if fibroids. If the uterus is posterior, it is often fixed by adhesions. In the uterine rectal fossa, the uterosacral ligament or the posterior wall of the cervix can often be palpated one or two or more hard nodules, such as mung bean or soybean size, mostly with obvious tenderness, anal examination is more obvious, this is very important. Occasionally, large black-purple bleeding spots or nodules may be seen in the posterior vaginal vault. If there are more lesions in the rectum, a hard lump can be touched and even misdiagnosed as rectal cancer.
Ovarian hematoma often adheres and fixes with the surrounding area, and a mass with large tension and pressure pain can be palpated during gynecological double diagnosis, which is easy to be misdiagnosed as an adnexal inflammation mass when combined with the history of infertility. After rupture, internal bleeding occurs, manifesting as acute abdominal pain.
Diagnosis
The disease occurs most often in women aged 30 to 40 years. The chief complaint is secondary progressive severe dysmenorrhea, and endometriosis should be highly suspected. The patient is often accompanied by infertility, menorrhagia and dyspareunia. Endometriosis is diagnosed when the uterus is slightly distended on gynecologic examination and nodules are palpable in the sacral ligament of the uterus or the posterior wall of the cervix. In the presence of endometrioid cysts of the ovary, a cystic or cystic-solid mass can be palpated on one or both sides of the double commissurotomy, usually within 10cm in diameter, with a sense of adhesion to the surrounding area.
Periodic bleeding from the rectum and bladder and painful defecation during menstruation should be considered as endometriosis of the rectum and bladder firstly, and cystoscopy or proctoscopy can be done if necessary, and tissues should also be taken for pathological examination when there are ulcers.
The diagnosis can also be established if there is periodic hardness and pain in the abdominal wall scars, and if there is a history of transabdominal uterine abdominal wall suspension, cesarean section, or cesarean surgery.
The diagnosis can also be made in suspected cases where drug therapy is effective.
Where a localized mass is formed close to the surface, the diagnosis can be confirmed by taking tissues (cut out or taken by hepatic puncture needle) and sending them for pathologic examination.
B ultrasound sonogram of endometrioid cysts showed granular fine echoes. If the cystic fluid is viscous, there are endothelial fragments floating inside, it is easy to be similar to the echo characteristics of teratoma fat containing hairs, that is, small thin light bands are seen in the fluid, distributed in parallel dashed lines. Sometimes the internal separation, divided into several cystic cavities of varying sizes, the echogenicity between the various cystic cavities is inconsistent, often with the uterine adhesion, and the border between the two is unclear. Teratomas, on the other hand, generally have clear cystic borders. Ovarian endometrioid cysts, also easy to confuse with adnexitis block and tubal pregnancy sonogram, so should be combined with the clinical characteristics of each to be identified. In addition, the application of vaginal probe, so that the mass is in the near field of high-frequency sound, located in the pelvic mass nature of identification, has its superiority, can determine the nature of the mass and the source of the mass, but also in the ultrasound under the guidance of the puncture extraction of cystic fluid or biopsy, in order to clarify the diagnosis.
X-ray examination: can be done alone pelvic insufflation contrast, pelvic insufflation contrast and uterine tubal iodine oil contrast and alone uterine tubal contrast. Most patients with endometriosis have adhesions to the internal reproductive organs and to the bowel curvature. Ectopic endometrium is most likely to be implanted in the uterorectal folds, so adhesions to the internal genital organs tend to occur in the uterorectal folds, making them shallower, especially on pelvic insufflation angiography lateral films. Tubal ovary may form adhesion mass, which is more clearly shown in filling film or in pneumogram. Iodized oil hysterosalpingography may remain patent or be patent but not patent. Often, poor application of iodized oil due to adhesions is seen on 24-hour review films, with small clumps or dots of varying thickness appearing as snow-like manifestations. The combination of ruling out other causes of infertility and having a history of dysmenorrhea may help in the diagnosis of endometriosis.
Laparoscopy: an effective method of diagnosing endometriosis. The freshest foci of implantation seen on microscopic examination are small yellow blisters; the most biologically active are large flame-like hemorrhagic foci; most of the scattered foci merge to form coffee-colored plaques and implant deeper; the sacral ligament is thickened, sclerotic, and shortened; the pelvic floor peritoneal scars are formed, which makes the uterorectal fossa shallower; the ovarian implantation foci are mostly originated in the free margins of the ovary and its dorsal side, and they are initially 1~3mm granulomatous foci which gradually develop to the ovarian cortex, forming a Chocolate capsule with grayish-orchid surface, mostly bilateral, interconnected and adhering to each other, inverted to the uterorectal fossa, widely adhering to the uterus, rectum and surrounding tissues. There is no abnormality of the fallopian tubes in stage I-II, and the oviducts in stage III-IV span over the coelomic sacs, which are passively prolonged, edematous, with limited peristalsis, and the umbilical portion is mostly normal, patent, or passive but not patent. Uterine tubal ligation should be done when doing laparoscopy.
1. Anti-endometrial antibody (EMAb): In 1982, Mathur used hemagglutination and indirect immunofluorescence to find EMAb in the blood, cervical mucus, vaginal secretion and endometrium of patients with endometriosis. many scholars reported different cases and used different methods to side out the blood of patients with endometriosis containing EMAb, with sensitivity of 56-75% and specificity of 90-100%. 90 to 100%. After the patients were treated with danazol and gonadotropin-releasing hormone agonist (GNRHa), the serum EMAb concentration decreased significantly. Therefore, serum EMAb testing is an effective aid in the diagnosis and observation of the therapeutic effects in patients with endogamy.
2. CA-125: In the late 70's, Knapp and Bast firstly prepared human ovarian epithelial cell carcinoma cell membrane antigen and antibody plates, named CA-125 (antigen) and OC-125 (antibody), which was a prominent good start for clinical molecular biology research. Barbeiri attributed the elevated CA-125 in patients with endometriosis to the fact that endometriotic endothelial cells regurgitate into the pelvic cavity and undergo biochemical coelomic metaplasia, which results in the production of higher amounts of CA-125 antigen. In addition, endometriosis is associated with inflammation, which increases the CA-125 antigen. This antigen is often found in the patient's blood and antibodies are produced.
Differential Diagnosis
I. Uterine Fibroids Uterine fibroids often show similar symptoms. Generally endometriosis dysmenorrhea is heavier, secondary and progressive. The uterus is consistently distended, but not very large. If accompanied by ectopic endometrium elsewhere, it helps to differentiate. Drug therapy may be tried in those with real difficulties, and if symptoms improve rapidly (1 to 2 months of medication), the diagnosis favors endometriosis. It should be noted that adenomyosis can coexist with fibroids (about 10%). It is usually difficult to differentiate preoperatively, pending pathologic examination of the surgically removed uterus.
Two, adnexitis Endometriosis of the ovary is often misdiagnosed as adnexitis. Both can form a solid mass in the pelvis with pressure and pain. However, patients with endometriosis do not have a history of acute infection, and patients are often treated with various anti-inflammatory treatments to no avail. And should be asked in detail about the period of the beginning of dysmenorrhea and the degree of pain. Such cases often have ectopic endometriotic nodules in the uterorectal fossa, which can be detected if carefully examined and can help in the diagnosis. If necessary, drugs can be used to test the treatment and observe whether there is any therapeutic effect to identify. In general, in endometriosis of the ovaries, the fallopian tubes are often patent. Therefore, the tubal fluid test can be tried, such as fluent, can be ruled out tubal inflammation.
Three, ovarian malignant tumors Ovarian cancer misdiagnosed as endometriosis in the ovary, then delayed treatment, so must be careful. Ovarian cancer does not necessarily have symptoms of abdominal pain, and if it does, it is often persistent, unlike the periodic abdominal pain of endometriosis. On examination, ovarian cancer is parenchymal, with uneven surface and large size. Endometriosis of the ovary may also be associated with endometriosis in other parts of the uterus, with signs and symptoms of lesions in those parts of the uterus. For patients who can not be identified, the older should be carried out caesarean section, the younger can be a short period of time according to the endometriosis treatment, in order to observe the efficacy of the treatment.
Four, rectal cancer When endometriosis invades the rectum and sigmoid colon and the range is wide, it often forms hard lumps in the place, causing partial obstruction, and in some cases, the ectopic endometrium invades the intestinal mucosa and causes hemorrhage, which is more like rectal cancer. However, the incidence of rectal cancer is much higher than that of intestinal endometriosis. Generally, patients with rectal cancer have obvious weight loss, more frequent intestinal bleeding, which is not related to menstruation, without dysmenorrhea. The tumor is fixed in the intestinal wall during anal diagnosis, and the intestinal wall is narrowed all around. Barium enema saw uneven intestinal mucosa and small range of poor barium filling. Sigmoidoscopy sees ulcers, bleeding, and biopsy confirms the diagnosis. Intestinal endometriosis weight loss, intestinal rarely bleeding, individual bleeding also occurs during menstruation, dysmenorrhea is heavier. The mucosa is not adherent to the mass at its base during anal examination, and only the anterior wall is hard. Barium enema showed smooth intestinal mucosa and wide range of poor barium filling.
Therapeutic measures
The diagnosis is made as clearly as possible before treatment, and the patient's age, fertility requirements, severity of the disease, symptoms and the extent of the lesion are taken into account.
I. Hormone therapy
(I) DANAZOLE: It is a derivative of the synthetic steroid 17α-ethinyltestosterone. Its main role is to inhibit the production of hypothalamic GnRH, thus reducing the synthesis and release of FSH and LH, resulting in the suppression of ovarian function. It also directly inhibits ovarian steroid hormone synthesis or competitively binds to estrogen and progesterone receptors, resulting in ectopic endothelial atrophy, anovulation and amenorrhea. DANAZOL also has mild androgenic effects, producing masculinization such as increased hairiness, lowered voice, smaller breasts and acne. Another common side effect of danazol is water retention and weight gain. It should not be used by people with high blood pressure, heart disease or renal insufficiency. Dannazol is mainly metabolized by the liver and may cause some damage to liver cells, so it is contraindicated in women with liver disease.
The usual dose is 400mg/d, 2～4 times orally, starting from menstruation, usually in about 1 month the symptoms will be reduced. If it is ineffective, it can be increased to 600-800mg/d, and then gradually reduced to 400mg/d after the effect is achieved. The course of treatment is usually 6 months, and 90-100% of them have achieved the effect of amenorrhea.
Danazol is more effective in pelvic peritoneal endometriosis, and less effective in ovarian ectopic masses larger than 1cm in diameter.
(2) Nemestran: 3-enkephalin (R2323), a 19-nortestosterone derivative, has high anti-progestin activity and moderate anti-estrogen effect, inhibits the secretion of FSH and LH, so that the body's estrogen level decreases, and the ectopic endothelium atrophies and is absorbed.
(3) Gonadotropin-releasing hormone agonist (GnRHa): In 1982, Meldtum and Lemay reported that the application of LHRHa for the treatment of endometriosis had good results. LHRH has a biphasic effect on the pituitary gland, and its large number of sustained application makes the pituitary cells show a down-regulation response, i.e., the pituitary cells' receptors are full of hormones and are unable to synthesize and release FSH and LH, The pituitary cells are unable to synthesize and release FSH, LH, and LH due to hormone overload. Side effects are hot flashes, vaginal dryness, headache, and small amounts of vaginal bleeding.
(4) Tamoxifen (TMX): a bis-styrene derivative. The dose is 10mg x 2/d, starting on the fifth day of menstruation, with 20 days as a course of treatment.
(5) Synthetic progestins: Cyclic treatment with ethynylisodone, kynurenine, or megestrol (aminoglutethimide) can be used to degrade the ectopic endothelium. Starting from the sixth day of the menstrual cycle to the twenty-fifth day, one of the above drugs can be taken orally daily for 5 to 10 mg. The duration of treatment depends on the therapeutic effect, and this method can inhibit ovulation. Therefore, for those who wish to procreate, kynurenine or kynurenone 10mg can be applied daily from the sixteenth day of the menstrual cycle to the twenty-fifth day, which can control endometriosis without interfering with ovulation. In some cases, there are heavy side effects during the treatment period such as nausea, vomiting, headache and swelling, uterine cramps, breast pain and excessive weight gain due to water retention and improved appetite, which can be alleviated by giving tranquilizers, antiemetics, diuretics and a low-salt diet.
Testosterone: It is also effective in this disease. The dose should be determined by the patient's tolerance. The best starting dose is 10mg twice a day, taken orally 2 weeks after the menstrual cycle. This dose rarely affects the menstrual cycle and has few masculinizing side effects. However, it is often necessary to continue taking it for several cycles to achieve pain relief. Thereafter, the dose may be reduced and maintained for a further period of time before being discontinued for observation. If pregnancy is possible, the disease can be cured.
Two, surgical treatment
Surgery is the main method of endometriosis, because the scope and nature of the lesions can be basically clear under direct vision, to relieve the pain, to promote the effect of reproductive function is better, the course of treatment is short, especially for the severe cases, fibrosis, adhesion tight, the drug is not easy to work. Large ovarian endometrioid cysts, drug treatment is ineffective, surgery is still possible to retain effective ovarian tissue. Surgery can be divided into conservative surgery, semi-radical surgery and radical surgery 3 kinds.
(I) Conservative surgery: mainly used for young, fertile people. Preserve the uterus and adnexa (try to keep both sides), just remove the lesions, separate adhesions, rebuild the ovaries and repair the tissues. In recent years, microsurgery has been applied to excise the ectopic lesion, carefully suture the wound, rebuild the pelvic peritoneum, carefully stop the bleeding, and thoroughly flush, so that the surgical effect can be perfected, and the success rate of post-surgical pregnancy can be improved and the recurrence rate can be reduced.
1. Laparoscopic surgery: Through laparoscopy, a clear diagnosis can be made, and special designed knives, scissors, pliers, etc. can be used to excise the lesions and separate the adhesions. Under laparoscopy, the lesion can be cauterized with a CO2 laser or a helium-neon laser, i.e., a second incision is made 2cm above the pubic symphysis, and the laser knife is inserted into the pelvis through the cannula of the incision, and the lesion is cauterized under the direct vision of the laparoscope. The cystic fluid can also be aspirated via laparoscopic puncture, then rinsed with saline, then injected with 5-10 ml of anhydrous ethanol, fixed for 5-10 minutes and then aspirated.
Tubal fluids are also feasible under laparoscopy.
2. Ultrasound puncture of endometrioid cysts of the ovary: in cases of recurrence after surgical stripping or after laparoscopic puncture, ultrasound puncture and drug treatment can be considered.
3. Conservative laparotomy: for patients with more serious lesions adherent, especially without laparoscopic equipment or laparoscopic mastery of unskilled, can be practiced laparotomy to separate the adhesion, dig out the ovary endometrioid cysts, as far as possible to retain the normal ovarian tissue, such as lesions are limited to one side and heavy, the other side of the normal, it is advocated that the side of the attachment of the disease will be excised. This has a higher pregnancy rate than that following preservation of the diseased ovary. Simple uterine suspension can also be done. It is debatable whether to do presacral neurectomy or not.
One of the important goals of conservative surgery is to achieve a full-term delivery of the pregnancy, so the couple should be thoroughly screened for infertility before surgery. Conservative surgery can still be used again in cases of postoperative recurrence and can still be effective.
(2) Semi-radical surgery: no fertility requirements, serious lesions, and younger (<45 years old), the uterus and lesions can be completely cut, but as far as possible to retain the normal ovarian tissue on one side, in order to avoid the premature appearance of menopausal symptoms. The recurrence rate after semi-radical surgery is generally considered to be low with few sequelae. Removal of the uterus removes the source of viable endometrial cell implantation, thus reducing the chance of recurrence. However, recurrence is still possible because the ovaries are preserved.
(3) radical surgery: near menopause, especially those with severe disease and recurrence, total hysterectomy and bilateral adnexa should be performed. Surgery should be performed to avoid rupture of the endometrial ovarian cysts as much as possible. The cyst fluid should be aspirated and flushed out as soon as possible. If menopausal syndrome occurs after surgery, sedatives and nil estradiol can be used.
If endometriosis occurs at the abdominal wall and perineal incision, it should be completely removed or it will recur.
Endometriosis patients are often combined with ovulatory dysfunction, so no matter the use of hormone therapy or conservative surgical treatment, can be used to promote follicular maturation and ovulation with HMG or / and clomiphene.
If conservative surgical treatment is practiced for infertility, hormonal treatment can be applied for 3 to 6 months to consolidate the therapeutic effect. However, some people believe that 1 year after surgery is the most likely time for pregnancy to occur, and the use of danazol or pseudo-pregnancy treatment, on the contrary, to reduce the chances of conception and do not advocate the use of.
Three, radiation therapy
Although radiotherapy for endometriosis has been used for many years, but the application of a variety of drugs and surgery to achieve a high degree of efficacy, generally does not destroy the ovarian function, and the role of radiation therapy for endometriosis, lies in the destruction of the ovarian tissue, thereby eliminating the influence of ovarian hormones, so that the ectopic endothelium atrophy, to achieve the purpose of treatment. The destructive effect of radiation on the ectopic endometrium is not obvious, but for individual patients who can neither tolerate hormone therapy nor have foci located in the intestinal tract, urinary tract and extensive pelvic adhesions, especially those who are combined with serious diseases such as cardiac, pulmonary or renal diseases, and who are very fearful of surgery, extracorporeal radiotherapy can also be used to destroy the function of the ovaries and achieve the therapeutic purpose. Even if an individual receives radiotherapy, must first be clearly diagnosed, especially can not be malignant ovarian tumor misdiagnosed as endometrial cysts, so that the wrong treatment and delay the correct treatment.
Prevention
Based on the currently recognized causes of the disease, attention to the following points may prevent the occurrence of endometriosis.
I. Avoid unnecessary, repetitive, or overly rough gynecological doublets near the time of menstruation, which may push the endometrium into the fallopian tubes and cause abdominal implantation.
Second, gynecological surgery should be avoided as much as possible near the menstrual period. If it is necessary, the operation should be gentle and avoid squeezing the uterus, otherwise the endometrium may be squeezed into the fallopian tube and the abdominal cavity.
Three, timely correction of excessive retroflexion of the uterus and cervical canal stenosis, so that the menstrual blood drainage, to avoid stagnation, causing backflow.
Four, strict control of the tubal patency test (ventilation, fluid) and the operating procedures of imaging, not in the menstrual period just clean or directly in the scraping of this cycle, so as to avoid the endothelial debris through the fallopian tubes pressed into the abdominal cavity.
Fifth, cesarean section and cesarean section to remove the fetus should be careful to prevent the contents of the uterine cavity overflow into the abdominal cavity, in the suture uterine incision, do not make the suture line through the endometrial layer, suture the abdominal wall before the incision should be rinsed with saline, to prevent the endometrial implantation.
Because the causes are multiple, the above preventive advice is only applicable to a few cases, and whether menstrual blood flow itself causes endometriosis is still controversial.