How is adenomyosis treated?

  Adenomyosis is a benign lesion caused by the invasion of the basal lining of the endometrium into the myometrium, with clinical manifestations of progressive dysmenorrhea, excessive menstruation, infertility and uterine enlargement. The age of onset is usually between 30 and 50 years. The conventional treatment includes total hysterectomy, focal resection and drug therapy, but there are many problems in the practical application of these methods.
  Treatment mechanism
Interventional treatment of adenomyosis is based on the basic role of vascular interventions, which is to embolize the blood vessels and block the blood flow to the lesion. Through relevant studies, it was found that.
(1) all ectopic endometrium is located in the myometrium: the lesions of adenomyosis show abundant blood flow under color ultrasound, with hyperechoic lesion areas surrounded by speckled, short rod-shaped low-velocity dynamic blood flow, and MRI shows ectopic endometrium with high signal, with or without bleeding microcystic cavities, and surrounded by hyperplastic muscle fibers forming miniature uterine structures, showing that their blood supply is small branches of the uterine artery, i.e. ectopic adenomyosis The endometrial lesions all receive blood supply through the uterine artery, which provides a vascular anatomical basis for interventional treatment.
(2) Ectopic endometrium originates from the basal layer of the endometrium: it is mostly in the proliferative stage and is sensitive to ischemia and hypoxia, which provides a pathological basis for interventional treatment.
(3) In uterine artery DSA angiography, contrast was found to be relatively concentrated in the adenomyosis lesion, indicating that blood flow is richer in this lesion than in the normal myometrium, which provides an imaging basis for the assessment of the efficacy and safety of interventional treatment.
Embolization of the uterine artery after interventional therapy results in.
(1) The blockage of blood flow causes necrosis of the ectopic endometrium and hyperplastic connective tissue due to ischemia and hypoxia, with non-inflammatory edema, followed by gradual dissolution and absorption, resulting in the reduction or even disappearance of the lesion, as well as the reduction of prostaglandin-like substances released from the lesion that cause dysmenorrhea due to uterine contraction, resulting in the relief or disappearance of dysmenorrheal symptoms.
(2) The shrinkage of the lesion causes the uterus to become softer and its volume and cavity area to be reduced, effectively reducing menstrual flow.
(3) Partial necrosis of the ectopic endometrium and the encapsulated myometrium causes contraction of the uterus and compression of the tiny channels by volume reduction, or necrotic closure of the channels themselves so that the normal endometrial basal layer can no longer enter the myometrium thereby, greatly reducing the recurrence rate.
(4) Necrosis of the ectopic endometrium decreases the local estrogen level and the number of estrogen receptors, etc., interrupting the vicious cycle of the spread of adenomyosis, eliminating the possible causes of endometrial adenomyosis and thus preventing recurrence, as well as improving the hyperplasia of the endometrium and reducing menstrual flow.
(5) Although mild necrosis also occurs in the functional layer of normal endometrium, it can be restored to normal function by gradual migration growth of the basal layer after revascularization or establishment of collateral circulation, whereas after necrosis of ectopic endometrium, such necrosis is irreversible due to lack of support from the basal layer, so when the embolized vessels are revascularized or collateral circulation is established and ischemia and hypoxia improve, the necrotic lesions cannot regrow, which ensures stability of the efficacy after quality.
  Operation method
  The femoral artery was punctured by Seldinger technique, and the 5F uterine catheter or Cobra catheter was super-selectively inserted into the bilateral uterine arteries, and after the imaging was clear, polyvinyl alcohol granules (PVA) + pinyamycin + appropriate amount of contrast agent were slowly pushed under fluoroscopy, and then embolized with gelatin sponge until the uterine artery blood flow was interrupted. The patients were closely monitored for pain, vaginal bleeding and other symptoms. All patients were asked to come to the hospital for review at the 3rd and 6th months after surgery, and ultrasound or MR examination was performed at the 6th month to observe the recovery of the lesion.
  Clinical efficacy
1, dysmenorrhea, dysmenorrhea relief rate: 70%-90% of patients with significant and effective dysmenorrhea relief after intervention;
2.Menstruation, 89% of patients have reduced menstrual flow after interventional treatment;
3, infertility, the chance of conception in infertile patients with adenomyosis is greatly increased after interventional treatment.
4.Vaginal discharge, leucorrhoea was significantly reduced after interventional treatment, and some patients were completely cured of various vaginitis due to long-term leucorrhoea and recurrent infections.
5.Uterus size, the uterus starts to soften and shrink in size 1-6 months after the intervention.
6.Anemia, after the intervention, the menstrual volume of the patient is significantly reduced. Patients usually return to normal or near normal hemoglobin level 3 months after the intervention.