Uterine adhesions: Abortion may be the culprit
 Encyclopedic 
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As a primary remedial measure following contraceptive failure, the safety of induced abortion and its potential risks to women's reproductive health have garnered increasing attention. In recent years, with the widespread adoption of abortion techniques, the number of abortions and repeat procedures has risen annually. Consequently, the incidence of postoperative intrauterine adhesions has also increased, becoming a significant concern warranting attention.
I. What Are Intrauterine Adhesions?
Intrauterine adhesions (IUA), also known as Asherman's syndrome, refer to the adhesion of uterine walls caused by detachment and damage to the basal layer of the endometrium following any trauma.Under normal circumstances, the anterior and posterior walls of the uterine cavity are closely apposed. However, due to the integrity of the endometrium, even when the endometrium is shed during menstruation, adhesions do not form. This is because only the functional layer of the endometrium is shed, while the basal layer remains intact and can rapidly regenerate and repair itself.
II. Causes of Intrauterine Adhesions
The primary etiologies of intrauterine adhesions (IUA) include:
(1) Pregnancy-related intrauterine procedures: Studies indicate that 66.7% of IUA cases occur after abortion, 21.5% after full-term delivery, 2% after cesarean section, and 0.6% after evacuation of hydatidiform mole.
(2) Non-pregnancy-related uterine trauma. Examples include diagnostic curettage, myomectomy, polypectomy, and intrauterine device insertion.
(3) Secondary genital tuberculosis in women.
(4) Infection: Whether chronic or subacute endometritis causes intrauterine adhesions remains controversial.
(5) Congenital uterine anomalies, particularly septate uterus, where recurrent miscarriages often lead to intrauterine adhesions, creating a vicious cycle.
(6) Genetic predisposition.
(7) Procedures involving uterine vessel ligation, embolization, or pelvic radiation therapy.
III. Clinical Manifestations Following Intrauterine Adhesions
The clinical presentation of intrauterine adhesions (IUA) is based on its pathological changes and closely correlates with the location, type, extent of intrauterine adhesions, and the degree of endometrial damage. It primarily manifests in three categories:
(1) Menstrual disorders: Hypomenorrhea, amenorrhea.
(2) Cyclic abdominal pain and anal heaviness.
(3) Pregnancy complications: early-to-mid-term miscarriage, recurrent or habitual miscarriage, post-term pregnancy, ectopic pregnancy, preterm labor, intrauterine fetal death, and abnormal placental implantation.
(4) Secondary infertility. However, some patients with intrauterine adhesions exhibit no obvious clinical symptoms, necessitating vigilance regarding the condition's insidious onset.
IV. Classification and Grading of Intrauterine Adhesions
Based on histological type, three pathological categories exist:
(1) Endometrial adhesions.
(2) Myofibrous adhesions.
(3) Connective tissue adhesions.
V. Diagnosis of Intrauterine Adhesions
(1) Hysterosalpingography (HSG): Prior to hysteroscopy, HSG served as the primary diagnostic method for IUA. Approximately 36% of IUA cases can be definitively diagnosed via HSG.
(2) Transvaginal Sonography (TVS): TVS is an effective method for diagnosing IUA. It serves as a viable non-invasive alternative when HSG is contraindicated due to uterine cavity obstruction. Common ultrasonic features of IUA include dense intrauterine echoes, discontinuity of the endometrial lining, and scattered fluid-filled dark areas.Literature reports indicate TVS has a sensitivity of 52% for diagnosing intrauterine adhesions, with a specificity of only 11%.
(3) Sonohysterography (SHG): SHG combines transvaginal ultrasound with intrauterine saline injection to detect adhesions. Its accuracy has been demonstrated to be comparable to HSG and superior to TVS alone.
(4) Hysteroscopy: Hysteroscopy is the most accurate method for diagnosing intrauterine adhesions (IUA). Direct visualization during hysteroscopy not only excludes 30% of abnormal HSG results but also determines the location, extent, nature, and severity of adhesions.
VI. Treatment of Intrauterine Adhesions
The goal of treating intrauterine adhesions is to restore normal uterine cavity volume and shape, prevent recurrence of adhesions, promote endometrial repair and proliferation, and restore fertility. Treatment methods include:
(1) Watchful Waiting: Primarily for patients without significant symptoms and no desire for pregnancy.
(2) Hysteroscopic adhesiolysis: Currently the most common approach, it is simple, safe, effectively restores normal uterine cavity, improves menstrual patterns, and increases pregnancy rates.
(3) Laparoscopic monitoring: Primarily used to monitor hysteroscopic procedures and prevent uterine perforation.
(4) Fluorescence-guided adhesiolysis: Primarily used for severe cervical canal adhesions to prevent uterine perforation during hysteroscopic procedures.
(5) Transabdominal ultrasound-guided hysteroscopic adhesiolysis.
(6) Blind dilation and curettage: Discontinued due to high uterine perforation rates and poor therapeutic outcomes.
(7) Radiopaque dye-guided hysteroscopic adhesiolysis: Reduces patient discomfort but remains an immature technique with uncertain efficacy.
(8) Hysterectomy: Indicated for severe intrauterine adhesions causing complete obstruction, but rarely performed today.
(9) Other techniques: Such as ultrasound-guided saline lavage of the uterine cavity. Due to limited reports, efficacy remains unknown.Postoperative outcomes for IUA vary considerably. Studies report: 58%–98% regain normal anatomical structure, 52%–88% resume normal menstruation postoperatively, pregnancy rates in infertile patients are 29% pre-surgery and 54% post-surgery, and live birth rates in recurrent miscarriage patients are 18% pre-surgery and 69% post-surgery.The prognosis for intrauterine adhesions caused by endometrial tuberculosis is poor, with a high recurrence rate.
VIII. Preventing Postoperative Recurrence of Intrauterine Adhesions
(1) Postoperative insertion of an intrauterine device (IUD) for 2–3 months, most commonly a copper IUD.
(2) Hormonal therapy: Currently, the most common regimen is 2–6 mg/day of estradiol valerate for 22 days to 3 months, with or without progestin added during the latter phase.
(3) Postoperative placement of a Foley catheter with a balloon for 3–10 days. Some studies suggest catheters offer slightly better adhesion prevention than IUDs. Complications include patient discomfort, ascending infection, and potential endometrial ischemia from balloon pressure on the uterine wall, which may impair endometrial growth.
(4) Intrauterine hyaluronic acid placement.
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