One, etiology
1. Congenital factors
(1) Long mesentery of the fallopian tube and ovary or variation in the length of the fallopian tube, with a spiral course, having the characteristic of being easily bendable.
(2) Underdeveloped mesentery at the distal end of the fallopian tube or excessive mobility.
(3) Congenital malformations of the reproductive organs, such as unilocular uterus, with both sides asymmetric, becoming a predisposing factor for adnexal torsion.
2. Acquired factors
(1) Lesions in the fallopian tube, increased weight, such as hydrosalpinx or hematosalpinx without adhesions.
(2) Dropout due to physiological cysts (follicular or corpus luteum cysts) in the ovary, which is prone to torsion.
(3) History of sterilization surgery using the Pomeroy technique (bilateral fallopian tube ligation and excision), where the free distal end of the fallopian tube is prone to torsion.
(4) Autonomic nervous system dysfunction, with abnormal peristalsis of the fallopian tubes.
3. External factors
(1) Pregnancy or uterine tumor, with the fundus of the uterus elevated, the appendages ascending to the abdominal cavity, and increased space for movement.
(2) Sudden changes in body position, such as sudden rotation or violent flipping over.
(3) Pelvic congestion during the premenstrual period or ovulatory phase.
(4) Drug-induced fallopian tube spasm.
All the above factors are triggers for the self-torsion of appendages. Under the combined action of one or more factors, complete and acute, irreversible torsion or incomplete and intermittent torsion can be caused.
Secondly, pathogenesis
1. After appendage torsion:Blood supply to the appendages is blocked, causing initial venous and lymphatic circulation disorders, while arterial perfusion continues, leading to appendage edema and thickening. The progression of torsion leads to intravascular thrombosis, starting with veins and eventually developing into arteries. If torsion is quickly resolved before the formation of arterial and venous thrombosis, appendage blood perfusion can quickly recover, and the organ can fully recover. If the torsion is complete and not resolved, it can rapidly progress from simple venous and lymphatic circulation disorders to arterial circulation blockage, and the fallopian tubes and ovaries can quickly turn deep black, leading to necrosis and gangrene. If treatment is not obtained, secondary infection can develop into peripancreatitis. In children, necrotic appendage torsion can be absorbed, and later, abdominal examination for other reasons may only find one side of the appendages, but the urinary system may show no abnormalities, which is an important differential diagnosis from congenital unilateral appendage agenesis. If it cannot be completely absorbed, calcification may occur.
2. If rotation is incomplete:Arterial perfusion is not completely occluded, leading to increased venous pressure, which can cause superficial vein rupture in the appendages, resulting in intra-abdominal hemorrhage. The surface of the ovary appears purple-red with hemorrhage, and when the ovary is incised, blood clots can be seen. Section examination can reveal the formation of hemorrhagic infarction. Sometimes, adhesions to other pelvic organs may also occur due to the degeneration of the surface tissue of the ovary. In severe cases, the ovary may become a parasitic organ.
3. If the torsion is incomplete:If venous return and lymphatic system circulation are blocked, but the arterial blood supply is not severely compromised, torsion can often be resolved spontaneously, and the appendages can fully recover within a few hours or a few days. However, the affected ovary may later show stromal luteinization, leading to clinical manifestations of masculinization; or excessive estrogen secretion can occur before the onset of menarche, promoting precocious puberty. Due to ovarian edema caused by incomplete torsion, severe cases may also be accompanied by Meig syndrome (ascites and pleural effusion).