Scar tissue is the body’s natural response to injury, forming a fibrous patch to repair damaged areas. When this process occurs inside the uterus, it is known as intrauterine adhesions (IUAs) or, in severe cases, Asherman’s Syndrome. The uterus is a muscular organ with a central cavity lined by the endometrium, which has a functional layer that sheds monthly and a basal layer responsible for regeneration. Scar tissue forms when an injury damages this basal layer, causing the opposing walls of the uterine cavity to stick together. This abnormal scarring can partially or completely obliterate the uterine space, reducing its volume and interfering with normal function.
The Nature of Uterine Scar Tissue and Adhesion Formation
Intrauterine adhesions are composed of fibrous tissue, primarily collagen, deposited during an abnormal wound-healing process. Adhesion formation is triggered by trauma to the basal layer of the endometrium, the tissue necessary for rebuilding the functional lining. When this regenerative layer is damaged in opposing sections of the uterine cavity, the body repairs the wound by laying down fibrin and then scar tissue. This creates fibrous bands that bridge the space between the uterine walls.
The severity of adhesions varies widely, ranging from mild, thin, and filmy bands to thick, dense scars. Mild adhesions are often easily stretched and may contain residual endometrial tissue. Severe adhesions are thick and tough, lacking functional endometrial lining and causing the uterine walls to adhere tightly. The extent of the scarring determines the clinical impact, as these non-functional fibrous bands prevent the normal cyclical growth of the endometrium.
Clinical Events That Lead to Uterine Scarring
The most common cause of uterine scarring is instrumentation of the uterine cavity, especially when the uterus is pregnant or recently pregnant. Dilatation and Curettage (D&C) is the procedure most frequently linked to intrauterine adhesions. The risk for scarring is elevated when a D&C is performed to remove tissue following a miscarriage, retained placenta after childbirth, or an elective termination.
The uterine lining is vulnerable during the postpartum period due to decidual tissue and a low estrogen environment, which affects endometrial regeneration. Postpartum curettage performed between two and four weeks after delivery carries a high risk of adhesion formation. Other surgical procedures that cause deep endometrial damage include myomectomy (removal of uterine fibroids) and endometrial ablation (intended to scar the lining to control heavy bleeding).
Severe uterine infections, such as endometritis, can also lead to scar tissue formation without prior surgical trauma. Infections like genital tuberculosis can cause extensive inflammation and subsequent fibrosis, potentially leading to complete destruction of the endometrium and severe adhesions. The risk of developing scarring increases with the number of times the uterine cavity has been instrumented.
Recognizing the Physical and Reproductive Effects
Scar tissue in the uterus creates physical symptoms and significant reproductive challenges. A primary indicator is a change in the menstrual pattern, most commonly hypomenorrhea (extremely light periods). In severe cases, scarring can completely block the uterine cavity or cervical canal, leading to amenorrhea (the complete absence of menstrual bleeding).
Some individuals experience cyclic pelvic pain or severe cramping coinciding with menstruation. This pain occurs when scar tissue blocks the outward flow of menstrual blood, causing it to accumulate inside the uterine cavity, a condition known as hematometra. The physical obliteration of the cavity and impaired blood supply to the remaining lining also directly impact reproductive health.
Intrauterine adhesions frequently cause infertility because they interfere with an embryo’s ability to implant into the uterine wall. The condition is also a major risk factor for recurrent pregnancy loss, as the scarred lining cannot properly support a developing pregnancy. Scarring can contribute to serious complications later in pregnancy, such as placenta accreta, where the placenta abnormally attaches too deeply into the uterine wall. Diagnosis is achieved through imaging techniques like saline infusion sonography (SHG) or hysterosalpingography (HSG), which use fluid or dye to outline the uterine cavity and reveal defects caused by the scar tissue.
Surgical Removal and Post-Procedure Management
The definitive treatment for intrauterine adhesions is hysteroscopic lysis of adhesions, which is the surgical removal of the scar tissue. This minimally invasive surgery uses a hysteroscope, a thin, lighted camera inserted through the cervix, to guide specialized micro-scissors or electrosurgical tools to cut the adhesions. The goal is to restore the normal anatomy of the uterine cavity and maximize the functional surface area of the remaining endometrium.
The challenge following surgical removal is the high risk of the uterine walls re-adhering, with recurrence rates reaching over 60% in severe cases. To prevent this, post-procedure management keeps the separated walls apart and encourages healthy lining regeneration. Mechanical barriers, such as an intrauterine balloon or a pediatric Foley catheter, are often placed temporarily in the uterus for one to two weeks to act as a physical stent.
Pharmacological management is routinely employed, typically involving a course of high-dose estrogen therapy, sometimes followed by progesterone, for one to two months. This hormone regimen stimulates the remaining basal layer of the endometrium to proliferate and heal over exposed areas before the uterine walls can fuse again. Other methods, such as anti-adhesion barrier gels, may also be used in the uterine cavity to create physical separation during the initial healing phase.