A 32-year-old woman, G1P1001, presented with two years of increasing abdominal distension. She had also experienced poor appetite and weight loss. Her menstrual period was regular, and she had neither abnormal vaginal bleeding nor pelvic pain.
Six years prior to this visit, she experienced chronic pelvic pain and had been treated with injectable progestin for clinical suspicion of pelvic endometriosis.
One year prior to this visit, she had visited the provincial hospital due to abdominal distension. A computerized tomography (CT) scan of the abdominopelvic region revealed a large amount of ascites with peritoneal nodule and pleural effusion. Abdominal paracentesis and pleural tapping were performed, which indicated exudative fluid, but no malignant cells were noted. She was then referred to another hospital for further work-up. Another CT scan of the abdominopelvic region was performed, which revealed circumferential wall thickening at the mid to upper rectum suggesting rectal cancer with a large amount of ascites and right pleural effusion. Colonoscopy and tissue biopsy at the rectum showed only acute colitis with no dysplasia or malignancy detected. However, she did not return to follow up after this operation.
Upon presentation at our hospital, the patient appeared chronically ill and emaciated with a body mass index of 14.9 kg/m2. Her abdomen was markedly distended due to a large amount of ascites (Figure 1). There were no masses or pain upon palpation. Vaginal examination revealed bulging of the anterior vaginal wall due to ascites with no palpated pelvic mass. A CT scan of the abdominopelvic region performed at our hospital showed infiltrative enhancing lesions involving the cul-de-sac and perirectal region with massive loculated ascites and internal septation. The uterus and both ovaries appeared unremarkable (Figure 2). A chest X-ray revealed bilateral pleural effusion and passive atelectasis of both lower lobes. Her CA-125 level was 112 IU/mL, CA19-9, and CEA levels were within the normal range.
We performed abdominal paracentesis, which yielded a clear yellowish fluid. Cytologic examination suggested inflammation without malignant cells. The ascites sample was also sent for tuberculosis PCR and acid-fast bacilli staining, both of which were negative. Exploratory laparotomy was scheduled for tissue diagnosis. Upon laparotomy, we noted a large amount of serosanguinous ascites, thickened matted bowel loops, and necrotic debris covering the entire peritoneal surface (Figure 3). The right adnexa and uterus were partially identified. No gross focal mass lesions were found. The surgical procedures included drainage of 6.5 liters of ascites, lysis adhesion, biopsy of the peritoneum, and right salpingo-oophorectomy.
Histologic examination of peritoneum tissue showed benign endometrial glands with stroma deposited within a thick fibrous tissue and chronic inflammation background (Figure 4). Immunohistochemical studies of peritoneal tissue showed positive staining for estrogen receptor (ER) and progesterone receptor (PR) within the foci of endometriosis. Endometriotic foci at the broad ligament were found adjacent to an unremarkable right fallopian tube (Figure 5). Sections of the right ovary were unremarkable. There were no malignant cells in any of the tissues examined. Cytologic examination of ascites fluid revealed inflammation without malignant cells. A final diagnosis of endometriosis was made based on these pathological and cytological findings.
The patient's postoperative course was uneventful. GnRH analog was prescribed for six months postoperatively. The patient has subsequently been on a daily regimen of oral progestin. At fifteen months following the operation, the patient had no symptoms and the results of a physical examination were unremarkable.