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KembaraXtra-Medicine – Asherman Syndrome (Intrauterine Adhesions)
Asherman syndrome refers to symptomatic intrauterine adhesions (IUA), which are bands of scar tissue, also known as synechiae, that form within the uterine cavity and sometimes the cervix. Synechiae develop when two opposing areas of endometrial tissue lose their epithelial lining and heal together, creating fibrous bridges. These adhesions may distort, narrow, or completely obliterate the uterine cavity. The term Asherman syndrome is reserved for cases in which intrauterine adhesions cause symptoms, whereas asymptomatic, incidentally discovered adhesions should be described simply as intrauterine adhesions.
The true incidence and prevalence of intrauterine adhesions in the general population are unknown because many cases are asymptomatic. Among individuals undergoing evaluation for infertility, approximately 1.5% are found to have intrauterine adhesions on hysterosalpingography, a figure that increases to over 20% in those with a prior history of dilation and curettage. Higher rates are also observed in women with recurrent miscarriage and in those who have undergone hysteroscopic uterine surgery, particularly repeat procedures. Asherman syndrome most commonly affects individuals of reproductive age, reflecting both exposure to intrauterine procedures and presentation with menstrual abnormalities or infertility.
Risk factors include dilation and curettage performed for miscarriage, abortion, abnormal uterine bleeding, or retained products of conception. Additional risks include placenta accreta, cesarean section, uterine compression sutures such as B-lynch sutures, abdominal or hysteroscopic myomectomy, pelvic inflammatory disease, genital tuberculosis, and surgical treatment of Müllerian anomalies. The risk of adhesion formation increases with repeated intrauterine procedures.
Many individuals with intrauterine adhesions are asymptomatic and never diagnosed. Symptomatic patients typically present with secondary amenorrhea, hypomenorrhea, infertility, or recurrent pregnancy loss. Some experience cyclic pelvic pain due to obstruction of menstrual flow. The severity of symptoms correlates with the extent and density of adhesions, which may range from thin, filmy bands to dense fibrotic tissue causing near-total obliteration of the uterine cavity. Adhesions are not palpable on bimanual examination and require imaging or direct visualization for diagnosis.
The pathophysiology of Asherman syndrome involves damage to the basal layer of the endometrium, which is responsible for regenerating the functional layer during the menstrual cycle. When the basal layer is destroyed, the endometrium cannot regenerate normally, leading to decreased or absent menstruation and impaired implantation. Inflammatory healing between opposing denuded uterine surfaces results in fibrous adhesion formation. The American Fertility Society classifies intrauterine adhesions as mild, moderate, or severe. Mild disease involves less than one-third of the uterine cavity and is associated with normal or mildly decreased menses. Moderate disease involves one- to two-thirds of the cavity with hypomenorrhea. Severe disease affects more than two-thirds of the cavity and typically presents with amenorrhea.
The differential diagnosis overlaps with that of secondary amenorrhea and infertility and includes cervical stenosis, thyroid disease, hypothalamic or pituitary dysfunction, premature ovarian insufficiency, polycystic ovarian syndrome, and androgen-secreting tumors. Intrauterine adhesions account for approximately 7% of cases of secondary amenorrhea.
Evaluation begins with laboratory assessment of ovarian and pituitary function, including follicle-stimulating hormone, luteinizing hormone, and estrogen levels. If these values are normal, a progesterone challenge test is performed. Failure to produce a withdrawal bleed suggests an outflow tract abnormality such as Asherman syndrome. Imaging is then pursued to evaluate the uterine cavity.
Saline-infusion sonography is the preferred screening modality and is more accurate than hysterosalpingography or transvaginal ultrasound alone. Adhesions appear as hypoechoic bands or filling defects within the uterine cavity. Hysterosalpingography may show compartmentalization or multiple filling defects. Definitive diagnosis is often made by hysteroscopy, which allows direct visualization of the adhesions.
Treatment is indicated for patients with symptomatic Asherman syndrome, including those with infertility, amenorrhea, hypomenorrhea, or cyclic pelvic pain. The primary goal is restoration of the normal uterine cavity through hysteroscopic adhesiolysis. Filmy adhesions may be divided with the hysteroscope alone, while denser adhesions require scissors or energy-based instruments. Adhesion division should proceed carefully from the center of the cavity outward to minimize further endometrial injury. There is no specific pharmacologic therapy for Asherman syndrome, although nonsteroidal anti-inflammatory drugs may be used for menstrual pain.
Prognosis depends on disease severity. Patients with mild adhesions generally have favorable outcomes, with improvement in menstrual function and fertility. Those with moderate to severe disease have lower fertility rates, even after surgical correction, as regeneration of the endometrial lining may be incomplete or delayed. Asymptomatic individuals who do not desire fertility do not require treatment.
Prevention focuses on minimizing unnecessary intrauterine procedures, particularly repeated dilation and curettage. When uterine evacuation is required, hysteroscopic techniques may reduce the risk of adhesion formation compared with blind curettage. Patients should be counseled about the risk of amenorrhea and infertility associated with intrauterine adhesions. Effective contraception can reduce the need for abortion-related procedures and thereby lower the risk of developing Asherman syndrome.
Asherman syndrome refers to symptomatic intrauterine adhesions (IUA), which are bands of scar tissue, also known as synechiae, that form within the uterine cavity and sometimes the cervix. Synechiae develop when two opposing areas of endometrial tissue lose their epithelial lining and heal together, creating fibrous bridges. These adhesions may distort, narrow, or completely obliterate the uterine cavity. The term Asherman syndrome is reserved for cases in which intrauterine adhesions cause symptoms, whereas asymptomatic, incidentally discovered adhesions should be described simply as intrauterine adhesions.
The true incidence and prevalence of intrauterine adhesions in the general population are unknown because many cases are asymptomatic. Among individuals undergoing evaluation for infertility, approximately 1.5% are found to have intrauterine adhesions on hysterosalpingography, a figure that increases to over 20% in those with a prior history of dilation and curettage. Higher rates are also observed in women with recurrent miscarriage and in those who have undergone hysteroscopic uterine surgery, particularly repeat procedures. Asherman syndrome most commonly affects individuals of reproductive age, reflecting both exposure to intrauterine procedures and presentation with menstrual abnormalities or infertility.
Risk factors include dilation and curettage performed for miscarriage, abortion, abnormal uterine bleeding, or retained products of conception. Additional risks include placenta accreta, cesarean section, uterine compression sutures such as B-lynch sutures, abdominal or hysteroscopic myomectomy, pelvic inflammatory disease, genital tuberculosis, and surgical treatment of Müllerian anomalies. The risk of adhesion formation increases with repeated intrauterine procedures.
Many individuals with intrauterine adhesions are asymptomatic and never diagnosed. Symptomatic patients typically present with secondary amenorrhea, hypomenorrhea, infertility, or recurrent pregnancy loss. Some experience cyclic pelvic pain due to obstruction of menstrual flow. The severity of symptoms correlates with the extent and density of adhesions, which may range from thin, filmy bands to dense fibrotic tissue causing near-total obliteration of the uterine cavity. Adhesions are not palpable on bimanual examination and require imaging or direct visualization for diagnosis.
The pathophysiology of Asherman syndrome involves damage to the basal layer of the endometrium, which is responsible for regenerating the functional layer during the menstrual cycle. When the basal layer is destroyed, the endometrium cannot regenerate normally, leading to decreased or absent menstruation and impaired implantation. Inflammatory healing between opposing denuded uterine surfaces results in fibrous adhesion formation. The American Fertility Society classifies intrauterine adhesions as mild, moderate, or severe. Mild disease involves less than one-third of the uterine cavity and is associated with normal or mildly decreased menses. Moderate disease involves one- to two-thirds of the cavity with hypomenorrhea. Severe disease affects more than two-thirds of the cavity and typically presents with amenorrhea.
The differential diagnosis overlaps with that of secondary amenorrhea and infertility and includes cervical stenosis, thyroid disease, hypothalamic or pituitary dysfunction, premature ovarian insufficiency, polycystic ovarian syndrome, and androgen-secreting tumors. Intrauterine adhesions account for approximately 7% of cases of secondary amenorrhea.
Evaluation begins with laboratory assessment of ovarian and pituitary function, including follicle-stimulating hormone, luteinizing hormone, and estrogen levels. If these values are normal, a progesterone challenge test is performed. Failure to produce a withdrawal bleed suggests an outflow tract abnormality such as Asherman syndrome. Imaging is then pursued to evaluate the uterine cavity.
Saline-infusion sonography is the preferred screening modality and is more accurate than hysterosalpingography or transvaginal ultrasound alone. Adhesions appear as hypoechoic bands or filling defects within the uterine cavity. Hysterosalpingography may show compartmentalization or multiple filling defects. Definitive diagnosis is often made by hysteroscopy, which allows direct visualization of the adhesions.
Treatment is indicated for patients with symptomatic Asherman syndrome, including those with infertility, amenorrhea, hypomenorrhea, or cyclic pelvic pain. The primary goal is restoration of the normal uterine cavity through hysteroscopic adhesiolysis. Filmy adhesions may be divided with the hysteroscope alone, while denser adhesions require scissors or energy-based instruments. Adhesion division should proceed carefully from the center of the cavity outward to minimize further endometrial injury. There is no specific pharmacologic therapy for Asherman syndrome, although nonsteroidal anti-inflammatory drugs may be used for menstrual pain.
Prognosis depends on disease severity. Patients with mild adhesions generally have favorable outcomes, with improvement in menstrual function and fertility. Those with moderate to severe disease have lower fertility rates, even after surgical correction, as regeneration of the endometrial lining may be incomplete or delayed. Asymptomatic individuals who do not desire fertility do not require treatment.
Prevention focuses on minimizing unnecessary intrauterine procedures, particularly repeated dilation and curettage. When uterine evacuation is required, hysteroscopic techniques may reduce the risk of adhesion formation compared with blind curettage. Patients should be counseled about the risk of amenorrhea and infertility associated with intrauterine adhesions. Effective contraception can reduce the need for abortion-related procedures and thereby lower the risk of developing Asherman syndrome.
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