Diagnosis and treatment of global endometrial ablation failure

Causes of EA failure

Untreated uterine cornua, and untreated submucous leiomyomas and endometrial polyps, are common causes of EA failure. Among the 50 women included in our retrospective review of ultrasound-guided reoperative hysteroscopy after GEA failure, 44% had intraoperative evidence of untreated cornua and nearly one-fourth had persistent or enlarging submucous leiomyomas.

Contrary to what some believe, most endometrial ablations will not adequately destroy submucous or intramural leiomyomas. Therefore, we recommend that these fibroids be entirely removed immediately before EA.

Moreover, GEA will not always provide adequate thermal destruction to the entire endometrial cavity. The cornua regions are particularly at risk; they are difficult to reach under ideal circumstances, and especially difficult to treat in patients who have a uterine septum or a T-shaped uterus (with the ostia and cornua deeply recessed). We have also seen late-onset EA failures in patients with an extended uterine transverse diameter. The limits of GEA are greatest when a device with a fixed configuration or geometry is used.

A history of abnormal hysteroscopy or other evidence of such anatomic distortions are therefore among the reported risk factors for GEA failure (J Minim Invasive Gynecol. 2015 Mar-Apr;22[3]:323-31). A history of tubal ligation also confers risk; the procedure further increases susceptibility for failure when functioning endometrial tissue remains or regrows at the cornua, because any retrograde menstrual bleeding that occurs will be constrained by the obstructed proximal portion of the fallopian tubes.

Obesity is another risk factor for GEA failure in that the condition increases the risk of endometrial cancer, making the need for reliable biopsies in the case of spotting or other signs or symptoms even more important. On the other hand, obesity may also worsen a patient’s status as a candidate for hysterectomy.

There is much to consider with these patients. For some obese patients, GEA may be less risky than hysterectomy while for others, such as those who also have polycystic ovarian syndrome (in whom the risk for developing endometrial cancer is further increased) the scale may tip in favor of hysterectomy.

Age at the time of the primary GEA may be the single most important risk factor for GEA failure and is an important predictor of success in patient selection. Numerous investigators have shown that women younger than 35 years of age at the time of their EA had a significantly increased risk for hysterectomy, compared with women who were at least 45 years old. The younger the patient, the longer the “bridge” to menopause and the greater the likelihood that bridge will fail.

While age is not necessarily a contraindication, it is worthy of serious consideration. We generally discourage GEA for patients younger than 35. We also advise ensuring that each patient undergoing initial EA is highly self-motivated to have a uterine-sparing procedure; if not, symptoms she may experience later will likely drive her toward hysterectomy anyway.

Additionally, we caution against performing GEA in patients who have chronic pelvic pain; these patients tend to have poorer outcomes with any type of hysteroscopic surgery.
 

Diagnosing failed EA

Delayed complications manifest in several ways: Renewed and increasing vaginal bleeding after a period of improvement, cyclic pelvic pain (unilateral, bilateral, or suprapubic), or both bleeding and pain. Some women – likely an underreported number of them – present with postmenopausal bleeding and proceed to have unsuccessful attempts at an endometrial biopsy due to EA-associated endometrial scarring.

The cyclic pelvic pain associated with endometrial persistence or regrowth tends to worsen over time and is often described as sharp or laborlike. In our experience, a description of “laborlike” pain and a history of EA is almost fully predictive of a finding of endometrial growth. Often a hematometra can be demonstrated on transvaginal ultrasound, but this isn’t always the case.

Pain typically precedes bleeding in patients who demonstrate both. In such cases, blood from functioning endometrial tissue or other sources becomes blocked from exiting the uterine cavity by EA-induced intrauterine scarring and contracture. Painful uterine contractions then aim to expel the pooled blood. In other cases of pain – mainly those without significant vaginal bleeding – the pain is often attributed to cornual and central hematometra.

For the majority of EA failures, the diagnosis lies in the history and current symptoms. Unfortunately, the traditional methods of assessing the endometrial cavity have little merit for women presenting with delayed-onset EA complications. A sonographically assisted pelvic examination can be useful in evaluating complications, but the interpretation of ultrasounds in women with a prior EA can be challenging and is often beyond the training of most radiologists and gynecologists.

It is not uncommon for images to be incorrectly interpreted in the emergency department or physicians’ offices as “normal” and for such readings to set off a chain of CT scans, MRIs, laparoscopies, ovarian cystectomies, and other procedures that miss the root causes of pain.

Unfortunately, there is little in the literature that describes and defines ultrasound findings after EA. We do know that sonography should be timed with episodes of pain, and that the absence of a demonstrable hematometra does not exclude a diagnosis of EA failure.