FERTU.ITY AND STERILITY Copyright " 1981 The American Fertility Society Vol. 36, No. 6, December 1981 Printed in U.S A. PELVIC PERITONEAL DEFECTS AND ENDOMETRIOSIS: ALLEN-MASTERS SYNDROME REVISITED DONALD L. CHATMAN, M.D., F.A.C.O.G. Department of Obstetrics and Gynecology, Michael Reese Hospital and Medical Center and the Pritzker School of Medicine, The University of Chicago, Chicago, Illinois 60616 The peritoneum covering the pelvic viscera is usually smooth and glistening. Defects in the pelvic peritoneum are usually presumed to be acquired. Allen and Masters described such a clinical syndrome, the anatomic cornerstone of which was laceration.(s) of uterine supports with resultant defect(s) in the broad and/or uterosacral ligaments. This diagnosis has been made more often recently on the basis of laparoscopic findings alone. Twenty-five cases of pelvic peritoneal defects were documented in a series of 635 consecutive diagnostic laparoscopies done primarily for pelvic pain. None fit the criteria of the Allen-Masters syndrome. Sixty-eight percent had associated endometriosis. It is suggested that pelvic peritoneal defects may be causally related to endometriosis, the disease either attacking presumably previously altered peritoneal surfaces or causing peritoneal scarring, duplication, and reduplication secondary to the cyclic insults of the ectopic endometrium and thereby producing the appearance of traumatic lacerations. Further, it is suggested that when such defects are noted at laparoscopy, the presence of other associated pathologic abnormalities, including endometriosis, should be investigated. Fertil Steril36:751, 1981 Defects in the mesentery, congenital or acquired, are rare. Congenital defects have been reported in 0.5% of routine autopsies.1 Defects in the supporting structures and peritoneum of the pelvis are considered to be even more unusual. The peritoneum covering the abdominal surfaces of the female internal genitalia is usually smooth and glistening and conforms to the contour of the underlying organs. The origins of defects in the pelvic peritoneum are,. for the most part, unexplained. Pregnancy associated with unusual trauma has been cited as a cause of some such acquired defects. 2 No other causal relationship has been documented. Pelvic peritoneal defects acquire clinical significance when associated with pelvic pain, dyspareunia, acquired dysmenorrhea, and abnormal vaginal bleedings, as in the Allen-Masters syndrome. On rare occasions, herniation of the bowel Received April20, 1981; revised and accepted July 21, 1981. Reprint requests: Donald L. Chatman, M.D., 8811 South Stony Island Avenue, Chicago, Illinois 60617. 751 through the defect may cause intestinal obstruction.1 3 Alternatively, these defects may be completely asymptomatic and are found by chance at laparoscopy or laparotomy. This report describes a group of cases of pelvic peritoneal defects diagnosed at laparoscopy. These defects could not be classified as congenital or acquired. None was associated with the clinical characteristics of the Allen-Masters syndrome. However, the prevalence of endometriosis as associated disease suggests a possible causal relationship between endometriosis and some cases of pelvic peritoneal defects. MATERIALS AND METHODS Diagnostic laparoscopies were performed in 635 consecutive patients. The laparoscopies were done primarily for diagnosis of pelvic pain (75%). Pain was manifested as dysmenorrhea (usually acquired), deep dyspareunia, pain with defecation, and pain associated with other events. Twenty-five percent of patients were operated on for infertility. All patients were black.
752 CHATMAN December 1981 FIG. 1. Large defect in the left broad ligament with endometriosis. Twenty-five patients were noted to have pelvic peritoneal defects in this series, and these 25 cases form the basis of this report. The 25 patients found to have pelvic peritoneal defects reflected the age, parity, and symptomatic patterns of the entire group of 635 patients as a whole. Photography and peritoneal biopsies were done for documentation and confirmation of all visual impressions at laparoscopy. RESULTS Twenty-five patients with pelvic peritoneal defects were noted in the series of 635 consecutive diagnostic laparoscopies. In this group of 635 FIG. 2. Defect in the right broad ligament with endometriosis. symptomatic patients, consecutively laparoscoped, endometriosis was found in 192, an incidence of 30.3%. This represents continuing confirmation of an earlier analysis of the frequency of endometriosis in black women. 4 5 Illustrative examples of the pelvic peritoneal defects found in these patients are shown in Figures 1 to 8. Figure 1 shows a large defect in the left broad ligament with endometriotic implants on the borders of the defect and inside the defect itself. Figure 2 shows similar changes in the right broad ligament. The defect is smaller. Figure 3 shows a large cul-de-sac defect, the borders of which are studded with endometriosis. Figure 4 shows obliteration of the right uterosacral liga- FIG. 3. Large cul-de-sac defect with endometriosis on the borders. FIG. 4. Defect in the right uterosacral ligament with endometriosis.
Vol. 36, No.6 PELVIC PERITONEAL DEFECTS AND ENDOMETRIOSIS 753 FIG. 5. Defect in the left broad ligament with the ovary prolapsed into and adherent to the defect. FIG. 6. Two defects in the left broad ligament with endometriosis. ment by a defect, the inferior margin of which is marked by an endometriotic "knot." An additional defect is seen in the cul-de-sac to the left. In this figure it can be noted that the hue and color of the pelvic peritoneum and endometriotic disease has changed little from normal peritoneum, except for a slight dulling of its characteristic sheen. Figure 5 shows a defect in the left broad ligament into which the ovary has prolapsed and become adherent, a not uncommon occurrence associated with this phenqmenon. Endometriosis can be seen in the left uterosacral and broad ligaments. Figure 6 shows two defects in the left broad ligament, hemosiderin deposition above, and bloody cul-de-sac fluid below. After aspira- tion of the cul-de-sac fluid, multiple endometriotic implants were noted. Biopsy of the inferior edge of the larger defect histologically documented the disease. Figures 7 and 8 represent findings in one patient. Figure 7 shows vessels prolapsed through a large defect in the left broad ligament, as is characteristic in Allen-Masters syndrome. There is a defect in the right broad ligament just above the right uterosacral ligament. Biopsy of the inferior border of this defect and the right uterosacral ligament histologically documented endometriosis. In this study, the incidence of pelvic peritoneal defects was found to be 4% of all 635 cases, the incidence noted in a similar study. 6 If only those FIG. 7. Large defect in the left broad ligament with congested vessels prolapsed through the posterior left of the broad ligament. FIG. 8. The same patient as shown in Figure 7. Defect in the right broad ligament. The biopsy proved endometriosis.
754 CHATMAN laparoscopies done for pain are considered (75%), the incidence is 7%. Thus it would appear that the overall incidence of this pathologic finding at diagnostic laparoscopy is low. Table 1 shows the symptoms presented by the patients with pelvic peritoneal defects. Pain, in the form of chronic pelvic pain, dysmenorrhea, and dyspareunia, was a prominent complaint. Only two patients were free of pain, and laparoscopies were performed on them because of secondary infertility. Both of these patients had endometriosis. Abnormal vaginal bleeding in the form of menorrhagia and/or metrorrhagia occurred in fewer than half of the patients. The locations of pathologic defects were unevenly distributed between the broad and uterosacral ligaments, the defects having been noted in the broad ligament in 20 cases and in the uterosacral ligament in only 1 (Table 2). The cul-de-sac was involved in 10 cases. In 1 of these cases, it was felt that the origin of the defect was in the uterosacral ligament and extended into the culde-sac and left broad ligament. This extensive defect produced no pain. Of the 25 patients, only 7 (20%) had the pelvic peritoneal defect as the only positive finding at laparoscopy. Several of these patients had symptoms very suggestive of endometriosis, but no physical evidence of the disease. The majority of patients had associated pelvic pathology. Pelvic inflammatory disease was noted in one case, and salpingitis, along with endometriosis, was noted in another. Seventeen patients (68%) had pelvic endometriosis documented by biopsy of suspected lesions. When the incidence of endometriosis in patients with a pelvic peritoneal defect was compared with that of the entire group, it was found to be significantly elevated (Table 3). This fact suggests a strong association between the presence of these defects and endometriosis. In all 17 patients in which endometriosis and pelvic peritoneal defects were associated, the endometriosis was found inside the defects and/or on the borders of the defects themselves. In many cases, endometriosis was found in other areas of the pelvis as well. DISCUSSION In 1955, Allen and Masters described the gynecologic syndrome which now bears their names. 2 The syndrome was offered as a possible explanation for clinical observations made by previous investigators with reference to the so-called pel- December 1981 TABLE 1. Symptoms Presented by 25 Patients with Pelvic Peritoneal Defects Pain Dysmenorrhea Dyspareunia Abnormal bleeding 23 (92%) 17 (68%) 13 (52%) 11 (44%) vic congestion syndrome. 7-12 The essential pathology in the newly described syndrome was characterized by laceration(s) in the broad and sacro-uterine ligaments. The authors postulated that the "universal-joint cervix" developed as a result of traumatic laceration(s) of the supporting ligament(s) and that it developed along with characteristic symptomatology, which consisted of pelvic pain, deep dyspareunia, acquired dysmenorrhea, menorrhagia, and metrorrhagia. These symptoms are not unlike those associated with endometriosis. In fact, Lawry stated in the introduction of his article on the subject that "the presenting symptoms and findings are not always easy to evaluate, since they resemble other and commoner causes of pelvic pain, notably endometriosis, pelvic inflammatory disease, and pelvic congestion." 13 In current practice it is common to refer to such defects in the pelvic peritoneum alone as representative of this syndrome. 6 The diagnosis is thus made retrospectively and primarily on the basis of a pathologic finding rather than a composite of symptoms, physical findings, and pathologic changes. At laparoscopy, such pelvic peritoneal defects are easily seen, and the diagnosis may be made more often. The incidence of the Allen-Masters syndrome was stated to be 4.6% in a recent series of 475 laparoscopies done for pelvic pain. 6 This is a very high incidence, since Allen, in 1971, observed that at his institution over the previous 20 years, only 150 patients out of 7000 major cases were operated for the "universal-joint syndrome."14 Following the original report in 1955, over a decade passed before another report appeared in the English literature. In 1968 Lawry reported his 23 cases of traumatic lacerations of uterine supports. 13 Three of his patients had endometriosis as well, but he did not associate the two entities. TABLE 2. Location of Pelvic Peritoneal Defects in 25 Patients Undergoing Laparoscopy Location Right broad ligament Left broad ligament Right uterosacral ligament Left uterosacral ligament Cul-de-sac Number 12 (48%) 9 (36%) 0 1 (0.4%) 10 (40%)
Vol. 36, No.6 PELVIC PERITONEAL DEFECTS AND ENDOMETRIOSIS 755 TABLE 3. Frequency of Pelvic Peritoneal Defect:' Number of patients with pelvic peritoneal defects Number of patient without pelvic peritoneal defects Number 25 610 Patients with endometriosis 17 (68%)b 175 (28.7%) alncidence of endometriosis at laparoscopy in patients complaining of pelvic pain and/or infertility with or without pelvic peritoneal defects. bsignificantly different by x 2 ; P < 0.001. The so-called universal-joint syndrome is not a universally accepted entity. It has been said that the basic pathologic defect that is the cornerstone ofthis syndrome can be seen in patients who have no symptoms whatever. Moreover, the cause of pelvic peritoneal defects may not only be obstetric trauma, as has been postulated. Many cases may be related to endometriosis with peritoneal scarring, duplication, and reduplication of peritoneal scarring secondary to the cyclic insults of ectopic endometrium, producing defects similar to posttraumatic lacerations of uterine supports. Twenty of the 25 cases reported by Lawry had no history of obstetric trauma. Only 2 patients in our group may have sustained such trauma, but clinical preoperative assessment of these 2 patients excluded the features of Allen-Masters syndrome. Of the 25 patients found to have pelvic peritoneal defects, 4 were less than 20 years old, 12 were between 20 and 30 years of age, and 9 were older than 30. The age distribution is thus similar to a previously reported group of sympto"matic patients with endometriosis on whom laparoscopies were done. 4 5 The youngest patient was 16 and had symptoms of endometriosis, although only the defect was found at laparoscopy. Two teenagers had associated endometriosis, representing a 12% incidence of the total endometriosis cases in the group with defects. The oldest patient was 41, and her complaint was secondary infertility. She had associated severe endometriosis. The parity of the patients also reflects that of the group as a whole. Of the 25 patients, 9 were nulliparous, 15 had had one to three prior successful pregnancies, and only 1 had more than three children. Laparoscopic pelvic findings, as well as the symptoms that were originally described with the Allen-Masters syndrome, can be seen in many cases in association with endometriosis. In view of the frequent association, the observation at laparoscopy of such defects may lead one to suspect the possibility of associated disease such as endometriosis, and vice versa. The diagnosis of endometriosis may be very important in symptomatic patients, since even anatomically mild endometriosis may produce severe dysfunction. Endometriosis, because of its invasive properties and cyclic activity, may cause deep tissue damage, local scarring, and reduplication, with the resultant surface defects. In the absence of the characteristic blue-black raised typical lesions of endometriosis, the scarring associated with endometriosis may often go unnoticed. The appearance of endometriosis in the pelvis in these cases may be subtle, and the diagnosis may thus be very difficult to establish. The scar tissue may assume the same hue and color of the surrounding peritoneum, except for a slight dulling of its normal sheen. Adhesions may produce an appearance strongly suggestive of chronic inflammatory disease. The only clue may then be the presence of pelvic peritoneal defects. For accurate pathologic confirmation, biopsy of suspicious lesions and/or the edges of these defects may prove useful in documenting the associated pathology in many cases. With the widened use oflaparoscopy, the gynecologist has increased greatly the opportunity of diagnosing such defects. When defects are noted in the pelvic peritoneum, one must not assume that obstetrical trauma is the cause. The diagnosis of Allen-Masters syndrome should be made only in those typical cases where all the features of the syndrome are present. In all patients demonstrating pelvic peritoneal defects, possible associated pathology should be sought, since it is evident that such defects can be associated with other pathology. Our data indicate that endometriosis will be discovered frequently in such patients when properly investigated. It is unlikely that this increased frequency is due to chance, and a causal relationship seems clear. One can only postulate which comes first. It is purely speculative whether the pelvic peritoneal defects are caused by pelvic endometriosis or whether ectopic endometrium implants form more readily on peritoneum altered by previously existing anatomic defects. REFERENCES 1. Luvaudais W, Hartog JM, Otterson WN: Small bowel herniation through a defect in the broad ligament. Am J Obstet Gynecol 133:927, 1979 2. Allen WM, Masters WH: Traumatic laceration of uterine support. Am J Obstet Gynecol 70:500, 1955
756 CHATMAN 3. Kagahalju E, Harriluoto A: Strangulation of small intestine in an opening of the broad ligament. J Inti Surg 60:8, 1975 4. Chatman DL: Endometriosis and the black woman. Am J Obstet Gynecol126:987, 1976 5. Chatman DL: Endometriosis and the black woman. J Heprod Med 16:303, 1976 6. Frangenheim H, Kleindienst W: Chronic pelvic disease of unknown origin. In Laparoscopy, Edited by JM Phillips. Baltimore, Williams & Wilkins Co, 1977, p 43 7. Arkinson SM: The universal-joint syndrome. Obstet Gynecol 36:4, 1970 8. Harnett LJ, Edwards D, Knight WA, Woods R: Broad ligament laceration and pelvic congestive disease syndrome. Obstet Gynecol36:1, 1970 December 1981 9. Serreyn R, Vendererckhove D: Lacerations of the broad ligament: a critical approach to the Allen-Masters syndrome. Eur J Obstet Gynecol 2:133, 1972 10. Taylor HC Jr: Vascular congestion and hyperemia. Part I. Am J Obstet Gynecol 57:211, 1949 11. Taylor HC Jr: Vascular congestion and hyperemia. Part II. Am J Obstet Gynecol 57:654, 1949 12. Taylor HC Jr: Vascular congestion and hyperemia. Part TIL Am J Obstet Gynecol 57:654, 1949 13. Lawry EV: Traumatic laceration of uterine supports. Am J Obstet Gynecol 101:315, 1968 14. Allen WM: Chronic pelvic congestion and pelvic pain. Am J Obstet Gynecol 109:198, 1971