The gross appearance of endometriosis at operation is usually quite characteristic and, to an experienced surgeon, is sufficient for diagnosis. The smallest (and presumably earliest) implants are red, petechial lesions on the peritoneal surface. With further growth, menstrual-like detritus accumulates within the lesion, giving it a cystic, dark brown, dark blue, or black appearance. The surrounding peritoneal surface becomes thickened and scarred. These “powder burn” implants typically attain a size of 5-10 mm in diameter. With progression of disease, the number and size of lesions increase, and extensive adhesions may develop. When present on the ovary, cysts may enlarge to several centimeters in size and are called “endometriomas” or “chocolate cysts.” Severe disease can erode into underlying tissues and distort the remaining organs with extensive adhesions. In addition to these traditional presentations, endometriosis lesions can have a variety of nonclassical appearances: clear vesicles, white or yellow spots or nodules, circular folds of peritoneum (“pockets”), and visually normal peritoneum (lesions so small they can only be detected microscopically).

The distribution of lesions also exhibits a characteristic pattern. Solitary lesions are possible, but multiple implantations are the rule. The most common site of disease is the ovary (approximately half of all cases), followed by the uterine cul-de-sac, uterosacral ligaments, the posterior surfaces of the uterus and broad ligament, and the remaining pelvic peritoneum.

Implants may occur over the bowel, bladder, and ureters; rarely, they may erode into underlying tissue and cause blood in the stool or urine, or their associated adhesions may result in stricture and obstruction of these organs. Implants can occur deep in tissue, especially on the cervix, posterior vaginal fornix, or within wounds contaminated by endometrial tissue. Very rarely, endometriosis is found distant from the pelvis, in such sites as the lung, brain, and kidney. Pleural implantations are associated with recurrent right pneumothoraces at the time of menses, termed “catamenial pneumothorax.” Similarly, lesions in the central nervous system can cause catamenial seizures.

The microscopic finding that these lesions are composed of tissue histologically resembling endometrial glands and stroma gives endometriosis its name (

Fig 40-2). The normal endometrial appearance is best seen in small, early lesions; with advanced disease, cyst formation, and fibrosis, the wall of the implant is lined by a monolayer of cells, if at all. Blood is present inside the cyst, and hemosiderin-laden macrophages are found in the cyst wall.

Although endometriosis resembles the uterine endometrium histologically, further assumptions about similarities between the tissues must be made with great caution. Simultaneous biopsies of implants and endometrium have found the implants often to be histologically out of phase with the uterine tissue. Also, the characteristic changes of estrogen and progesterone receptors present in endometrium across the menstrual cycle are absent in endometriosis implants. Endometriosis implants, unlike endometrium, do not respond to progesterone in vitro by the induction of 17β-hydroxysteroid dehydrogenase activity, the enzyme that in the luteal phase converts estradiol to the less potent estrone.

Figure 40-2. Histologic appearance of endometriosis. Left: Endometriosis of ovary. Right: Endometriosis of cervix. (Courtesy of Eugene H. Ruffolo, MD.)