Adhesions and fibrotic tissue in the uterus, particularly affecting the endometrium is characteristic of Asherman syndrome. This leads to loss of healthy endometrial mucosa.
Pelvic inflammatory disease (PID) can result in Asherman syndrome over time. The most common causative organisms are Chlamydia trachomatis and Neisseria gonorrhoeae. The longstanding inflammation can heal by fibrosis, thus decreasing functional endometrial tissue surface area.
The most common cause of Asherman syndrome is dilation and curettage (D&C) of the intrauterine cavity. This procedure might be necessary for spontaneous abortions or retained products of conception.
Patients may seek medical help after trying to conceive for several months or years without success. Infertility is an important clinical feature of this disease.
Recurrent pregnancy loss (RPL) is another feature of Asherman syndrome. The fibrotic tissue may allow fertilization, but after some weeks, the embryo/fetus becomes nonviable because of decreased placental/endometrial interfacing for survival.
Abnormal uterine bleeding (AUB), secondary amenorrhea, and periodic abdominal/pelvic pain are often seen in this disease.
The progesterone challenge can be performed to assess for Asherman syndrome. Progesterone is administered (oral or intramuscular injection). After about 2 weeks, withdrawal bleeding is a positive response indicating functional estrogen levels and uninterrupted outflow. A patient with Asherman syndrome may not experience significant bleeding after this 2-week time indicating a possible outflow tract obstruction due to intrauterine adhesions/synechiae or other fibrotic tissue.
Hysterosalpingoscopy will reveal a honeycomb or lacunar appearance of the uterus, which pertains to the adhesions. The adhesions presenting as filling defects often lack the ability to distend into the endometrial cavity.
A hysteroscopic resection of the endometrial adhesions is the only treatment of Asherman syndrome and should only be performed if the patient is symptomatic.
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