The endometrium is the “soil” of the embryo. If the “soil” is not good, even the best seeds will not grow into a big tree. Introduction: Uterine adhesions originate from trauma within the uterus. The degree of adhesion formation and the impact of adhesions on the contours of the uterine cavity vary widely. Mild lesions are characterized only by the formation of an involved band of filiform strip-like tissue on the surface of the uterine cavity, whereas severe disease is characterized by complete occlusion of the uterine cavity, in which the anterior wall of the uterus is densely adherent to the posterior wall of the uterus. Etiology: Approximately 90% of cases of severe uterine adhesions are associated with curettage for pregnancy complications (e.g., induced abortion, incomplete miscarriage, postpartum hemorrhage, or retained placenta). Repeated curettage for pregnancy loss increases the risk of adhesion formation from 8% after the 1st curettage to more than 30% after the 3rd curettage. The basal endometrium appears to be most vulnerable in the first 4 weeks after delivery or miscarriage; however, adhesions can also occur in the nonpregnant uterus, for example, as a result of endometrial damage from myomectomy or nonpostpartum curettage. The role of postpartum or post-abortion infection in the formation of uterine adhesions is controversial and data are limited. A study using hysteroscopy to evaluate 28 patients with severe endometritis after cesarean delivery reported that the incidence of uterine adhesions in these women was similar to that of control women without post-cesarean infection. Another study reported increased but not statistically significant formation of uterine adhesions when dilation and curettage were performed in the setting of co-infection. Trauma is the main cause of uterine adhesions, while infection may play only a minor contributing role. In developing countries, germline tuberculosis is one of the causes of uterine adhesions, which are usually more severe with complete occlusion of the uterine cavity. These patients are usually seen for amenorrhea and cyclic pelvic pain. It is generally accepted that adhesion formation is secondary to chronic inflammation of the endometrium. Clinical presentation: Uterine adhesions may be asymptomatic and not clinically significant. Symptoms associated with clinically significant uterine adhesions include infertility, irregular menstruation (hypomenorrhea, amenorrhea), cyclic pelvic pain, and recurrent pregnancy loss. Infertility is the most common reason for patient visits: 43% of women with uterine adhesions have varying degrees of infertility. Irregular menstruation is also a common clinical presentation; however, the degree of adhesions shown by hysteroscopy does not correlate well with the degree of irregular menstruation, and nearly 40% of patients with hysteroscopically confirmed adhesions do not complain of irregular menstruation. amenorrhea (absence of menstruation) due to hysterocutaneous adhesions was first reported in 1894. The condition was further defined by Asherman in 1948 and 1950 and is therefore often referred to as Asherman syndrome. Women who experience infertility, menstrual disorders, cyclic pelvic pain, or recurrent pregnancy loss, especially in patients who have undergone curettage for pregnancy, require diagnostic evaluation. Diagnosis: Diagnosis is based on direct hysteroscopic demonstration or indirect demonstration of uterine adhesions on imaging. The gold standard for the diagnosis of uterine adhesions is diagnostic hysteroscopy. The advantage of this approach is that once the adhesions are identified, they can be removed by hysteroscopic surgery. Compared to blind adhesion release, this method allows simultaneous diagnosis and treatment in a single operation and reduces the potential for damage to the surrounding endometrium. Other diagnostic imaging modalities include hysterosalpingogram, hysterosalpingogram (HSG), or transvaginal ultrasonography (TVUS). A study comparing HSG, hysterosalpingogram, and TVUS with hysteroscopy in 65 infertile women found that HSG and hysterosalpingogram were equally sensitive for the diagnosis of uterine adhesions (both detected 3 of 4 cases with a sensitivity of 75%). In this case series study, TVUS alone appeared to be less effective (undetectable in all 4 cases of uterine adhesions). Another study using hysteroscopy as a reference standard found that HSG had a sensitivity of 81.2% and a specificity of 80.4%. The advantage of hysterosonography is that it is not radioactive and some clinicians can perform this test under outpatient conditions. In contrast, HSG must be performed in the radiology department. Although newer techniques using combined water/air perfusion may improve the assessment of tubal patency with hysterosonography, the ability of HSG to assess tubal patency (if needed) remains a potential advantage. Experienced sonographers have reported a sensitivity of 80-90% for the diagnosis of uterine adhesions using TVUS (detected in 8 of 10 cases, and 10 of 11 cases, respectively). Considering that the sensitivity of TVUS depends to a large extent on the operator of this examination, we recommend the use of hysterosonography for the initial diagnostic evaluation of such patients rather than ultrasonography alone. Treatment must be performed separately. Once the diagnosis is clear, TVUS may help to predict the outcome of surgical treatment of hysterocutaneous adhesions. One study evaluated seven patients with severe uterine adhesions before hysteroscopic resection and found that patients with well-formed endometrial bands resumed normal menstruation after surgery, whereas patients with very thin endometrium found by preoperative ultrasound evaluation had an occluded uterine cavity and ineffective surgical intervention. Pathology: adhesions can originate from the endometrium, myometrium or connective tissue. They can vary in size from thin and fragile to thick and dense, wider at the ends than in the middle. They may occur peripherally or diffusely in the endometrial cavity; in severe cases they may completely occlude the uterine cavity. Peripheral adhesions may be crescentic or drapery-shaped. Mucosal adhesions usually appear the same color as the endometrium and are fragile, whereas fibrous adhesions are pale and firm. The endometrial cavity of tuberculosis-induced adhesions is often honeycomb-shaped. Classification: Several classification systems have been proposed for uterine adhesions. The classification system of the American Fertility Society (now the American Society for Reproductive Medicine) classifies adhesions into 3 stages based on the degree of uterine cavity involvement (<1/3, 1/3-2/3, >2/3), the type of adhesions seen on hysteroscopy (membranous adhesions, both membranous and dense adhesions, dense adhesions), and the patient’s menstrual pattern (normal, hypomenorrhea, amenorrhea). Although alternative classification systems have been proposed by other groups, no clear consensus has been reached. Treatment: There are no randomized clinical trials guiding the treatment of this group of patients. Our management is based on the experience of individual physicians, small case series studies, and case reports. Adhesion release: The standard treatment for uterine adhesions is surgical release under direct visualization guidance. This is usually performed as an outpatient procedure using a surgical hysteroscope. The procedure aims to restore the size and shape of the uterine cavity, as well as endometrial function and fertility. In patients with a severely occluded uterine cavity, care must be taken when dilating the cervix, as it can easily result in faulty access and uterine perforation. Intraoperative simultaneous ultrasonography helps to clarify the connection between the endocervix and the uterine cavity, as well as to guide the separation procedure in which the hysteroscope is first placed at the endocervix and sharp separation is used to loosen the adhesions. We prefer to use small rigid surgical scissors. The adhesion zone is identified through the hysteroscope and then the connection between the adhesion zone and the endometrium is cut to remove the adhesions (in contrast, a longitudinal septum should be dissected). Careful separation continues until the entire uterine cavity is free of adhesions. The goal is to restore the normal anatomy of the uterine cavity. The procedure can also be done using the bipolar electrosurgery technique. This technique will vaporize the adhesions. If there are adhesions in the wall of the uterine cavity, a more extensive separation is required. In this case, we recommend intraoperative concomitant guidance with laparoscopy or ultrasound to reduce the risk of uterine perforation. Fluoroscopic techniques may also be used to guide the separation in severe cases. If the adhesions are so severe that the hysteroscope cannot enter the uterine cavity, a cesarean hysterotomy is required. Each procedure may be unique and requires the operator to have a detailed knowledge of the anatomy of the uterus and to perform the separation with patience and skill. For a completely occluded uterine cavity, ultrasound-guided separation starting from the midline and widening out to the sides may be feasible. If there are areas of less dense adhesions where normal anatomy can still be observed (e.g., the uterine horns), the separation should be started in this area. Invasive separations that may enter the myometrium should be avoided. Prevention of adhesion re-formation: Postoperative management should focus on reducing the risk of adhesion re-formation. One approach is to give high doses of estrogen postoperatively to promote endometrial regrowth in the area of adhesion-induced endometrial exfoliation. Estrogen therapy can be started on postoperative day 1. The standard dose is 5 mg of conjugated estrogen or 8 mg of estradiol given in daily divided doses for 30 days. Progesterone is then administered to induce withdrawal bleeding. Progesterone is administered by giving 10 mg/d medroxyprogesterone acetate or 2.5 mg/d vinblastine concurrently with the last 10 days of estrogen therapy. Alternatively, a bladder catheter (e.g., an 8-gauge pediatric catheter with a 5-mL balloon) or an intrauterine device (IUD) should be placed in the uterus immediately after the adhesions are released; the IUD should be removed after 3 months, and the bladder catheter should be removed from the uterus after 10 days. Antibiotics should be given at the same time as the bladder catheter is placed, as this means that a foreign body is placed in the uterus that is connected to the germ-bearing vagina. We recommend placing a Foley catheter in the uterine cavity immediately after surgery to reduce the re-formation of adhesions. Comparing outcomes after Foley catheter placement with IUD placement, we found that patients with Foley catheters had a higher rate of return to normal menses postoperatively (81% vs. 63%), a higher pregnancy rate (34% vs. 23%), and a decreased need for reoperation. There are no good data comparing the use of these methods with the use of estrogen after hysteroscopic release of adhesions. Outcome: Menstruation resumes in 73%-92% of patients. One study reported that 40 patients seen for recurrent pregnancy loss were able to become pregnant after surgical treatment of adhesions. Other case series studies have reported live birth rates of 32%-76%, with the lowest rates in women with more severe adhesion lesions and/or other risk factors for low fertility. In addition, some of these pregnancies are complicated by adherent placenta, which may be associated with persistent abnormalities on the endometrial surface or complications related to the amniotic band. Follow-up: Postoperative evaluation of the uterine cavity to assess whether it has regained its normal shape is recommended by the American Association of Gynecologic Laparoscopy. We recommend an HSG or hysterosonography 2-3 months after hysteroscopic removal of hysterosal adhesions. If it is determined that significant adhesive lesions are present, a repeat procedure may be required. However, the size of the uterine cavity does not correlate well with the ability to conceive and carry a pregnancy to term. There are no studies on the risk or prevention of recurrence of adhesions after pregnancy. Summary and recommendations: Severe adhesive uterine disease is mainly caused by curettage to treat pregnancy complications (e.g., induced abortion, incomplete miscarriage, or postpartum hemorrhage). Clinical manifestations of severe uterine adhesive lesions include infertility, irregular menstruation (hypomenorrhea, amenorrhea), cyclic pelvic pain, and recurrent pregnancy loss. The diagnosis is based on direct hysteroscopic demonstration of adhesions or indirect demonstration of adhesions by hysterosalpingography (HSG) or hysterosalpingography. Treatment is hysteroscopic adhesion release. We recommend placement of a Foley catheter in the uterine cavity immediately after surgery to reduce the re-formation of adhesions (Grade 2C). Postoperative evaluation of the uterine cavity was performed to clarify whether the cavity had returned to its normal shape.