Assessment and Plan

Differential diagnosis of the patient’s pelvic pain and right adnexal mass includes endometriosis, ovarian cyst, and ovarian tumor. She was offered diagnostic laparoscopy for further assessment. Multiple preoperative laboratory studies were ordered, including urinalysis and culture (UA&C), urine human chorionic gonadotropin (HCG), complete blood count with differential, complete metabolic panel, testosterone (free and total), folate, dehydroepiandrosterone sulfate (DHEAS), follicle-stimulating hormone, luteinizing hormone, progesterone, prolactin, estradiol, cancer antigen 125, and serum HCG. The UA&C and urine HCG were negative; all other results were within normal limits.

Operative Findings and Diagnosis

Operative findings were consistent with stage IV endometriosis. Laparoscopic visualization and histology revealed scattered superficial endometriosis on the anterior cul-desac and paravesical areas (Figure 1). The posterior cul-de-sac, uterosacral ligaments, and rectovaginal area had deeper lesions that penetrated through the fibroadipose tissue (Figure 2). The posterior aspect of the right ovary also contained vascular adhesions and endometriosis. All the lesions were treated with vaporization or excision techniques (Figure 3).

The large right ovarian cyst appeared benign but adhered to the pelvic sidewall and portions of the loops of bowel. The cyst caused partial torsion of the right fallopian tube (Figure 4) and compression over the loops of bowel, which led to partial distension of the bowels and sigmoid colon. The cyst was aspirated and found to contain a chocolate-like material. Ovarian cystectomy was performed and an endometrioma was confirmed by histologic evaluation of the specimen.

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Further exploration revealed multiple benign paratubal serous cysts in the left fallopian tube (Figure 5); the largest of these was excised and the rest were aspirated. The left distal ureter also was involved, with dense adhesions that were lysed to restore normal anatomy. The left ovary contained multiple functional cysts.

The uterus was normal in shape and contour. Hysteroscopy with endometrial biopsy was performed, and no evidence of malignancy or hyperplasia was found. Peritoneal washing and cytology were free of malignancy.

Proctosigmoidoscopy and rectovaginal examination performed at the conclusion of surgery revealed resolution of the thickening and irregularity at the sites of endometriosis treatment. The patient recovered well, with resolution of symptoms.


Endometriosis is a chronic inflammatory disorder caused by the growth of endometrial-like tissue outside the uterine cavity.1 The most common sites of endometriosis are the ovaries, uterosacral ligaments, posterior cul-de-sac, rectosigmoid colon, and bladder.2 It affects approximately 10% of women of reproductive age, with peak prevalence occurring in those aged 25 to 35 years.1,2 Risk factors include first-degree relatives with endometriosis, early menarche, short menstrual cycles, nulliparity, and low body mass index.3

The exact etiology of endometriosis is unclear, but several theories have been proposed. The most widely promoted is Sampson’s theory of retrograde menstruation. During this phenomenon, endometrial tissue enters the peritoneal cavity through the fallopian tubes and implants itself in the peritoneum and surrounding organs, leading to adhesions, inflammation, and chronic pain.1,4 However, retrograde menstruation is a normal occurrence in 90% of women and thus does not explain why only some develop endometriosis.2,3

More recent theories suggest immunologic dysfunction and genetic/epigenetic components are involved in the pathogenesis of endometriosis.3 Studies have shown that women with endometriosis appear to have lower cell-mediated immunity with decreased T-cell and natural killer cell responses, which may alter the ability of the immune system to target and destroy the endometriotic lesions.2,3 A third theory, the theory of Müllerianosis, suggests that during fetal organogenesis, Müllerian cells remain in the pelvis and differentiate into functioning endometrial glands and stroma under the influence of estrogen.2,3 Still, these theories fail to explain why the tissue of endometriosis has a similar histologic appearance to the endometrium yet functions differently.3