Ureteral displacement associated with pelvic peritoneal defects and endometriosis

Ureteral displacement associated with pelvic peritoneal defects and endometriosis

February 2000, Vol. 7, No. 1 TheJournal of the American Association of Gynecologic Laparoscopists Ureteral Displacement Associated with Pelvic Perito...

965KB Sizes 1 Downloads 104 Views

February 2000, Vol. 7, No. 1 TheJournal of the American Association of Gynecologic Laparoscopists

Ureteral Displacement Associated with Pelvic Peritoneal Defects and Endometriosis Anna Chan Nackley, M.D., and Timothy R. Yeko, M.D.

Abstract Ten women had endometriosis and pelvic peritoneal defects of the posterior leaf of the broad ligament, with the consistent finding of medial displacement of the ureter toward the uterosacral ligament. Ureterolysis at the time of surgery revealed the underlying course of the ureter and its proximity to the uterosacral ligament, making it susceptible to surgical injury. It is important for surgeons to be aware of this anatomic alteration associated with these specific peritoneal defects. (J Am Assoc Gynecol Laparosc7:(1):131-133, 2000)

Defects of the pelvic peritoneum can be asymptomatic or symptomatic and their origin can be congenital or acquired. They may be accompanied by pain and abnormal bleeding I and may be associated with endometriosis. 2,~For example, endometriosis was found in 68% of patients with peritoneal defects at the time of diagnostic laparoscopy, and up to 30% of women with endometriosis also had pelvic peritoneal defects. 4 These findings were consistent with a report that 18% of patients diagnosed with endometriosis at the time of laparoscopy had peritoneal pockets, and 60% of those who had peritoneal pockets had identifiable endometriotic lesions. 5 It is believed that the invasive nature of endometriosis leads to inflammation, scarring, and reduplication of peritoneal tissue, forming the thickened appearance at margins of the peritoneal defect. The most frequent anatomic locations of peritoneal defects in women with associated endometriosis are posterior cul-de-sac and posterior leaves of the fight and left broad ligaments. The literature to date has not reported a relationship between peritoneal defects, specifically located in the broad ligament as it covers the ovarian fossa,

and the course of the underlying ureter in this area. We identified a series of 10 cases in which ureterolysis was performed as a safeguard against ureteral injury before resection of endometriosis near or within the broad ligament peritoneal defect. In each case the relationship between the pelvic ureter and margins of the peritoneal defect was determined. Materials and Methods Over 8 years from January 1992 to May 1999, l0 women who underwent laparoscopy performed by a single surgeon for pelvic pain were noted to have coexisting endometriosis and peritoneal defects specifically located within the posterior broad ligament as it covers the ovarian fossa and lateral to the uterosacral ligament. In each case, ureterolysis was begun at the level of the pelvic brim in an area free of pathology. Peritoneum overlying the ureter was dissected free and cut with monopolar scissors. The course of the ureter was systematically exposed down to and beyond the peritoneal defect, usually to the level of the uterine artery at the base of the broad ligament, similar to a published technique. 6 The degree of endometriosis

From the Department of Obstetrics and Gynecology, Division of Reproductive Endocrinology and Infertility, University of South Florida, Tampa, Florida (both authors). Address reprint requests to Timothy R. Yeko, M.D., Department of Obstetrics and Gynecology, University of South Florida, Harbourside Medical Tower, Suite 529, 4 Columbia Drive, Tampa, FL 33606; fax 813 254 9040. Accepted for publication September 27, 1999.

131

Ureteral Displacement Nackley and Yeko

was staged according to the American Society for Reproductive Medicine classification. Results Endometriosis was staged as mild in nine women and severe in one. The location of the defects was distributed between the right (67%) and bilateral (33%) broad ligaments (left broad ligament 0%). In each case, dissection of the ureter revealed a remarkably consistent finding that the ureter always coursed around the thickened medial margin of the peritoneal defect. Of interest, it never deviated along the lateral margin of the defect even when the lateral margin was closer to its natural course. These defects therefore were uniformly associated with medial displacement of the ureter. The size of the defects ranged from 2 to 4 cm, with the largest ones producing the greatest degree of ureteral displacement. Figure 1 is a laparoscopic view of one large defect that appears to form a cradle around the entire ovary. Frequently the medially displaced ureter created a peritoneal fold that ran parallel to and confluent with the uterosacral ligament. Figure 2 shows the ovary elevated with the defect exposed. The ureter runs along the medial edge of the defect, which grossly mimics the appearance of the uterosacral ligament. Ureterolysis revealed that the ureter was medially displaced to the point that it completely overrode the uterosacral ligament. Fibrous encapsulation of the ureter was not encountered in any of these cases. This made dissec-

FIGURE 2. With the ovary elevated, the defect is exposed and the ureter runs along the medial edge mimicking the appearance of the uterosacral ligament. An implant of endometriosis is present in the middle of the defect.

tion and mobilization of the ureter away from the margin of the defect technically easy, since its attachment consisted only of simple retroperitoneal fibroareolar tissue. Discussion Laparoscopic diagnosis of endometriosis is often based on dark lesions scattered throughout the pelvic peritoneal surface. However, the disease may be more subtle and take the form of clear, red, or white lesions, adhesions, retroperitoneal nodules, and defects on the peritoneal surface. Defects in pelvic peritoneum are infrequent and may indicate previous pelvic trauma or existing pathology. These areas of scarring or reduplication of peritoneal tissue are often referred to as AllenMasters windows. Those authors described the defects as part of the universal joint syndrome, which was characterized by lacerations of the broad and uterosacral ligaments. It was accompanied by pain, deep dyspareunia, dysmenorrhea, menorrhagia, and metrorrhagia, 1symptoms that are similar to those of endometriosis. The age distribution of women with peritoneal windows is also similar to that of women with symptomatic endometriosis. In a series of 635 women undergoing laparoscopy for pelvic pain, 4% had peritoneal defects and 30% had visible endometriosis? Of those with peritoneal defects, 68% had coexisting endometriosis.

FIGURE 1. Laparoscopic view of peritoneal defect on the right side forms a cradle around the entire ovary.

132

February 2000, Vol. 7, No. 1 TheJournalof the American Association of Gynecologic Laparoscopists

Histologic findings of the defects were consistent with endometriosis. More recently, in a study of 309 patients who underwent laparoscopy for pelvic pain, approximately 80% with peritoneal defects had associated endometriosis and 28% with endometriosis had peritoneal defects. 4 The three most commons sites of defects were posterior cul-de-sac (31%) and right (29%) and left (29%) broad ligaments. In our study, ureterolysis was performed in 10 women with broad ligament defects and endometriosis to determine the effect of these defects on the course of the ureter. In all patients the ureter was consistently medially displaced by broad ligament defects, a previously undescribed finding, and the degree of ureteral displacement was proportionate to the size of the defect. This finding is relevant to the gynecologic surgeon who encounters such a broad ligament defect at laparoscopy for pelvic pain. The surgeon must be vigilant in identifying the ureter before undertaking any surgical treatment around the area of the defect. Specifically, patients undergoing fulguration of peritoneal endometriosis, resection of an endometriotic nodule on the uterosacral ligament, uterosacral nerve ablation for dysmenorrhea, and hysterectomy would be most susceptible to ureteral injury. Underscoring the safeguarding of the ureter is the fact that the most common site of ureteral injury at laparoscopy for endometriosis is near the uterosacral ligament. The author of a review of the world literature on this subject concluded, "the extent of endometriosis along the uterosacral ligaments upon which one can safely operate at laparoscopy is not k n o w n . ''7 In this context, the presence of a broad ligament defect should be considered an added risk factor due to predictable alteration of the ureter.

Conclusion

Ureteral displacement is a consistent finding associated with pelvic peritoneal defects due to endometriosis. This alteration of pelvic anatomy places the ureter at a potentially high risk of surgical injury. In the presence of a peritoneal window located lateral to the ureter in the broad ligament, the surgeon must make a special effort to visualize the structure in its entirety as it courses through the area of interest, or perform ureterolysis to ensure its distance from areas being ligated, fulgurated, or resected. References

1. Allen WM, Masters WH: Traumatic laceration of uterine support. Am J Obstet Gynecol 70:500-513, 1955 2. Sampson JA: Peritoneal endometriosis due to menstrual dissemination of endometrial tissue into the peritoneal cavity. Am J Obstet Gynecol 14:422-469, 1927 3. Chatman DL, Zbella EA: Pelvic peritoneal defects and endometriosis: Further observations. Fertil Steril 46:711-714, 1986 4. Chatman DL: Pelvic peritoneal defects and endometriosis: Allen-Masters syndrome revisited. Fertil Steril 36:751-756, 1981 5. Redwine DB: Peritoneal pockets and endometriosis. J Reprod Med 34:270-272, 1989 6. Kadar N: Dissecting the pelvic retroperitoneum and identifying the ureters. J Reprod Med 40:116-122, 1995 7. Grainger DA, Soderstrom RM, Schiff SEet al: Ureteral injuries at laparoscopy: Insights into diagnosis, management and prevention. Obstet Gynecol 75:839-843, 1990

133