INTRAUTERINE ADHESIONS (ASHERMAN’S SYNDROME)
Intrauterine adhesions (IUA) or formerly known as Asherman’s syndrome is a condition characterized by the presence of adhesions or scar tissue (synechea) in the endometrium. When the endometrium is scarred and injured, amenorrhea (cessation of menstruation), recurrent pregnancy loss and infertility may follow. IUA can result from post-partum or post-abortion inflammation of the uterine lining, but it can also occur following uterine surgery such as removal of polyps and fibroids (myomectomy) resected abdominally or hysteroscopically.
The degree of IUA significantly impacts clinical and pregnancy outcome. Severe cases may result in a reduction in the days and the amount of menstrual blood flow and can be closely related with repeated pregnancy loss and infertility. Mild cases may even go unrecognized for a long time or until pregnancy is desired. Additionally, IUA may block the junction where the uterus connects with the fallopian tubes (internal tubal ostia). In such cases, embryo implantation may be compromised and the pregnancy may implant in the fallopian tube, resulting in an ectopic pregnancy.
Treatment involves a procedure called hysteroscopic lysis of adhesions (or adhesiolysis), where a camera type instrument (hysteroscope) is introduced vaginally into the uterine cavity to allow direct surgical treatment of scar tissue under anesthesia. The objective is to remove all of the scar tissue or at least as much as possible within the safety margin of the procedure. In order to perform hysteroscopy, special distention liquid needs to be utilized to visualize the endometrial cavity. If excessive amount of the distention fluid is used before the completion of the procedure, procedure is stopped for safety reasons and a repeat hysteroscopy may be necessary to correct remaining disease. Multiple hysteroscopic procedures may be necessary in severe cases of IUA although majority of the time, adhesions can by treated with a single procedure with high success rates.
Post-operatively, a small catheter with a balloon at the end called a “uterine stent” can be placed in the endometrial cavity to keep the opposing surfaces separated, in the hope of preventing recurrence of adhesion formation. The stent is usually kept inside the endometrial cavity for 5-7 days to allow adequate healing of the endometrium along with supplemental antibiotic treatment. The patient usually receives supplemental estrogen to stimulate endometrial development, followed by progesterone administration to induce a period. Neither uterine stent placement nor postoperative estrogen supplementation has been documented to significantly improve outcome and prevent adhesion formation.
In some cases, endometrial lining may be relatively thin following hysteroscopic treatment of IUA. Additional estrogen administered vaginally along with vaginal Viagra treatment may help improve the thickness of the inner lining of the uterus. Vaginal Viagra has been postulated to improve the blood flow and deliver more estrogen into the uterine lining, but medical literature on its efficacy is still very much limited. In most cases, increasing the estrogen dose or the route of administration has been sufficient enough to thicken the lining to satisfactory levels. If lining is not improved with such measures, additional causes should be ruled out, including total destruction of the basal layer of the endometrium or uterine malformations that may be associated with poor vascular support to the uterus. In such severe cases, using a gestational carrier appears to be the best option for a healthy pregnancy and overall outcome.