Treatment mechanism
Embolization of the blood supplying artery of leiomyosarcoma causes ischemic and anoxic necrosis and absorption of the leiomyosarcoma, resulting in a significant reduction of the total number of leiomyosarcoma cells and shrinkage of the tumor, which can relieve or eliminate a series of clinical symptoms associated with it. The efficacy is stable and not easy to recur.
Clinical applications.
1.Arterial embolization of uterine fibroids.
2. Arterial embolization of uterine adenomyosis.
Uterine fibroids and other benign lesions
Uterine fibroids, also known as uterine smooth muscle tumors, are the most common benign tumors of the female reproductive system, with an incidence of 20-25% in pregnant women, formed mainly by the proliferation of uterine smooth muscle cells, surrounded by a layer of connective tissue peritoneum, often multiple and varying in size. It is often multiple and varies in size. It can be classified into three types: submucosal leiomyoma, interstitial leiomyoma, and subplasma leiomyoma according to their locations. Clinical symptoms include excessive menstrual flow and non-menstrual bleeding, often complicated by anemia, increased leucorrhea, abdominal masses, lower abdominal cramping or other pelvic pressure symptoms such as frequent urination and irregular bowel movements, and even miscarriage and infertility. Interventional treatment: Embolization of uterine fibroids was first introduced in France in 1995. The principle is that embolization of the uterine artery causes necrosis, absorption, reduction or disappearance of fibroids rich in blood supply, while normal uterine tissues can tolerate ischemia better and are minimally affected. This is done by first performing a bilateral internal iliac arteriogram via femoral artery puncture to clarify the origin and course of the uterine arteries bilaterally and whether the fibroids are rich in blood supply. The uterine artery is superselected for embolization. The embolic agent is slowly released under fluoroscopic surveillance until the uterine artery is blocked or the tumor stains. The embolic agent is usually pindamycin-iodine oil emulsifier or PVA pellets. The procedure is best performed 3 to 7 days after menstruation. In case of heavy bleeding, it may not be necessary to perform the procedure electively.
Indications: Not all uterine fibroids require uterine artery embolization. The main indications are
1.Uterine fibroids cause corresponding symptoms, such as prolonged menstrual period, high volume, dysmenorrhea, symptoms of rectal and bladder compression, obvious abdominal mass, causing infertility and miscarriage, as well as obvious psychological symptoms caused by the discovery of tumor.
2.Age less than 58 years old.
3.Recurrence after surgery.
Contraindications.
1.Subplasmalemma with tissues.
2, pelvic infection, pregnancy.
Evaluation: Traditional treatments for uterine fibroids include hysterectomy, myomectomy, laparoscopic myomectomy and hormonal therapy. In recent years, uterine artery embolization has been used to treat this disease because it has the advantages of less trauma, less side effects, good efficacy (efficiency above 90%), preservation of the uterus and normal fertility. Fine embolization of the uterine arteries usually does not affect the ovarian blood supply and therefore has minimal impact on the function of the ovaries.
Other benign uterine pathologies: Other benign pathologies that are suitable for uterine artery embolization include uterine hemorrhage from various causes, such as postpartum hemorrhage and traumatic hemorrhage, as well as dysfunctional uterine bleeding and adenomyosis. For the former, good hemostatic effect can be obtained with gelatin sponge granule embolization. The latter two are treated in the same way as uterine fibroids, but with less efficacy than uterine adenomyosis.
Principle of interventional treatment for adenomyosis
Treatment principle: Necrosis and absorption of the lesions in the uterus by embolization of the uterine artery. Following embolization of the uterine artery the lesion undergoes the following changes.
Due to the loss of blood supply, the ectopic endometrium and the hyperplastic connective tissue become necrotic due to ischemia and hypoxia, and then gradually dissolve and absorb, making the lesion shrink or even disappear.
After the lesion shrinks, it releases fewer irritating substances that make the uterus contract, which leads to improvement of dysmenorrhea symptoms. The shrinking of the lesion causes the uterus to soften, the volume of the uterus and the area of the uterine cavity are correspondingly reduced, and the menstrual flow can be correspondingly reduced.
After necrosis of the ectopic endometrium, the necrotic part closes and the myometrium closes due to the corresponding decrease in volume and compression of the original tiny channels, while the normal endometrium also loses access to the myometrium. This greatly reduces the possibility of recurrence. The necrosis of the ectopic endometrium reduces the amount of local estrogen and its receptors. This allows the vicious cycle of adenomyosis spreading to be controlled. It also eliminates one of the possible factors of adenomyosis and reduces the possibility of recurrence.
After embolization, although mild necrosis may occur in normal endometrium, it can regrow and resume normal function after revascularization or establishment of collateral circulation. Ectopic endothelium, on the other hand, cannot regenerate after necrosis because it lacks the support of the basal lamina.