[Tissue injury observation caused by thermal effects of microwave endometrial ablation]

To investigate the thermal effects on tissue structures during microwave endometrial ablation (MEA) and seek a feasible method of endometrial thinning and a fitting mode of applicator radiating microwaves.

Operations were performed between the group of thorough uterine curettage and the group of early follicular phase in in vitro or in vivo uterus. The former was treated with MEA after thorough uterine curettage; while the latter was treated with MEA in the early follicular phase directly. The applicator radiating microwaves were moved in "Z" or "Z + W" shape inside uterine cavity. At the same time the serosal temperature was measured in the uterine fundus, tael cornua uteri, the posterior wall and the lower part of anterior wall. After operations the uterine specimens were stained by hematoxylin-eosin, and respiratory enzyme dehydronicotinamide adenine dinucleotide phosphate diaphorase (NADH-d) methods. The morphologic changes and the depth of tissue thermal damage were evaluated using an optical microscope and electron microscope.

(1) Under the optical microscope the endometrial glands became distorted, the cell boundaries disappeared, the nucleoli turned condensed and were stained darker. A large number of acute inflammatory cells appeared in fibrous tissue. In the shallow muscle layer cells were arrayed thickly, nucleoli were solidified and condensed, and cellular plasm were concentrated. The endometrial and the superficial muscle layers were damaged and colorless with NADH-d staining. The scope of the tissue thermal damage was clearly seen. Under an electron microscope, some smooth muscle cells, chromatin, karyotheca and cellular membranes were destroyed. The mitochondria were swollen, membranes were ruptured, and the crista disappeared. Many organelles were destroyed. The chromatin was lightly wrecked in the transitional area between putrescence and the normal smooth muscle tissue. Karyotheca and cellular plasm still existed, the mitochondria were highly edematous and the crista were disappeared, and the granular endoplasmic reticula were slightly expanded and degranulated. (2) The serosal temperature in in vitro uterus was significantly higher than that in in vivo uterus (P < 0.01). However, the highest temperature in in vitro or in vivo uterus were all taken in the posterior wall, being 50.9 degrees C and 37.6 degrees C, respectively. (3) The injury depth in in vitro uterus was 4.0 - 8.8 mm in the uterine body, 1.6 - 3.8 mm in the cervix uteri-uterine body junction; while those of in vivo uterus were 4.1 - 6.6 mm, 0 - 2.8 mm, respectively. The highest injury depth of tissue was in the posterior wall, significantly different from the other parts (P < 0.01). The injury depth of the corresponding part in in vitro or in vivo uterus all had a significant difference (P < 0.05). The depth of thermal damage had no significant difference between the group of thorough uterine curettage and the group of early follicular phase (P > 0.05). The injury depth of the "Z + W" radiation group increased significantly than that of the "Z" radiation group (P < 0.05).

(1) The depth of thermal damage is safe and controllable. (2) MEA with preoperative thorough uterine curettage or scheduling treatment at the follicular phase is efficient. (3) It is the ideal performing mode that the applicator radiating microwaves move in "Z + W" shape inside uterine cavity. (4) The thermal damage of MEA occurs more frequently in the portion with a shortage of blood supply.