Asherman's syndrome can occur after any type of gynecologic surgery, and we must shift our thinking and heighten our index of suspicion to accommodate the growing body of data that supports this claim.
A literature review published in Fertility and Sterility 15 years ago reported that approximately 90% of all cases of Asherman's syndrome occurred after curettage, mainly after D&C for a spontaneous abortion or one performed to control a postpartum hemorrhage. Although these two antecedent factors remain the most common causes, there has been a significant increase in the number of patients who develop endometrial scarring after gynecologic surgery, particularly following abdominal and hysteroscopic myomectomy.
Women who have had myomectomy or other types of uterine surgery make up an increasing proportion of all patients with adhesion formation and a variant of Asherman's syndrome known as endometrial sclerosis.
Endometrial sclerosis, commonly called an “unstuck Asherman's,” is an end-stage disease in which the basalis layer of the endometrium has been severely damaged or even removed. In these women, the hysterosalpingography (HSG) may demonstrate a normal cavity or one of slightly reduced size, but with little or no scarring.
This change presents new challenges because the damage that follows gynecologic surgery other than curettage is a much less curable condition.
Our Index of Suspicion
Key to our role as gynecologists is suspecting the problem. Any change in menstrual flow and pattern—from amenorrhea to any decrease in the duration or amount of bleeding—that follows any type of uterine surgery, irrespective of how minimal that surgery might have been, must prompt us to suspect that this patient may have scarring in her uterus. All patients with a history of intrauterine trauma must be considered at risk.
In addition to endometrial trauma, pregnancy (or recent pregnancy) and hypoestrogenism are important keys. The pregnant or recently pregnant uterus appears to be more vulnerable to scar formation.
Concomitantly, breast-feeding increases the risk of adhesion formation because women who breast-feed remain estrogen deficient. Estrogen has a tremendous effect in promoting the healing of the uterus and regeneration of the endometrium. Women who breast-feed don't have that stimulus.
To a lesser extent, infection also can play a role. Decades ago, infection was viewed as critical, in that it was the “infected abortion” that was thought to cause Asherman's syndrome. Today, infections are an uncommon cause of the problem. I have treated more than 1,000 patients with Asherman's, and fewer than 5 had any clinical evidence of infection around the time of their original surgery. Still, the possibility of Asherman's resulting from infections still exists.
Pelvic tuberculosis by itself, without any surgical trauma, causes scarring in the uterus. Considering the diversity of our society and the rise in antibiotic-resistant TB, we ought to keep it in mind.
It is also important to appreciate the fact that the presence of normal menstrual flow does not rule out the presence of intrauterine adhesions. Approximately three-quarters of women with Asherman's syndrome have amenorrhea or hypomenorrhea, but the remainder have menses of normal flow and duration. Other symptoms of intrauterine adhesions include infertility, recurrent miscarriage, and placenta accreta or its more severe variants.
Methods of Diagnosis
The diagnosis will most frequently be made by either HSG or a saline-infusion sonogram. However, these methods provide us with only a presumptive diagnosis. Both will demonstrate irregular, lacunalike defects spaced throughout the cavity. Access to the oviducts may or may not be blocked. A definitive diagnosis comes only with hysteroscopy.
We should individualize our diagnostic methods depending on the patient's history and symptoms and our own index of suspicion. For instance, a patient who presents with amenorrhea and monthly cramping following a D&C would benefit from a pelvic ultrasound. This study is likely to demonstrate fluid in the uterus. Her hematometra is secondary to outflow tract obstruction. There is no reason in this case to do a saline-infusion sonogram or an HSG. The next appropriate step is hysteroscopy, which will allow the diagnosis to be made with certainty so that treatment can commence.
Consider another patient with postcurettage amenorrhea. She has little or no fluid in the uterus and her endometrium is thin and/or irregular. A pregnancy test is negative and a uterine sound cannot be passed into the cavity. In this case, it is wise to proceed to hysteroscopy because it would not be possible to pass the contrast material for HSG—or the saline for a saline-infusion sonogram—beyond the site that blocked passage of the sound.
Hysteroscopy provides us with absolute proof of intrauterine adhesions. It allows us to directly inspect the uterine cavity and assess the extent, nature, and location of the adhesions. This also allows us to classify the disease, which is critical because classification enables us to make meaningful comparisons among different types of treatment regimens or adjunctive therapies. Finally, adhesiolysis under hysteroscopic guidance is more efficacious and less traumatic to the adjacent normal tissue.