Images in Gynecologic Surgery
Allen Masters Peritoneal Defect: A Potential Pathway to Deep Infiltrating Rectovaginal Endometriosis? Farr R. Nezhat, MD, FACOG, FACS*, and Mohamad S. Mahmoud, MD, FACOG Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, St. Luke’s-Roosevelt Hospital, Columbia University, New York, New York (all authors).
DISCUSS
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Deep infiltrative endometriosis of the rectovaginal septum can be one of the most severe forms of endometriosis. It is characterized by spherically shaped lesions situated deep in the rectovaginal septum and often only visible as a small typical lesion at laparoscopy or not visible at all. This lesion is often more palpable than visible and can be tender during pelvic examination, especially if the patient is examined at the time of menstruation, and can cause severe dyspareunia, back pain, and sometimes bowel symptoms. Many theories have been suggested for this type of endometriosis including true deep infiltrating endometriosis caused by the invasion of a very active peritoneal lesion deep in the retroperitoneal space and pseudo-deep infiltrating endometriosis or ‘‘adenomyosis’’ of the rectovaginal septum and congenital endometriosis of the rectovaginal septum [1–4]. Cullen originally suggested that the adenomyotic lesion originates from the remnants of mullerian rectovaginal septum tissue and consists essentially of smooth muscle with active glandular epithelium and scanty stroma. We suggest a new potential mechanism of the development of deep infiltrating endometriosis of the rectovaginal septum [4]. Our patient is a 45-year-old woman with a chronic history of severe dysmenorrheal since menarche
The author declares no conflict of interest. Corresponding author: Farr R. Nezhat, MD, FACOG, FACS, Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, St. Luke’s-Roosevelt Hospital, Columbia University, 425 West 59th Street, Suite 9B, New York, NY 10019. E-mail: [email protected] Submitted October 2, 2013. Accepted for publication October 4, 2013. Available at www.sciencedirect.com and www.jmig.org 1553-4650/$ - see front matter Ó 2014 AAGL. All rights reserved. http://dx.doi.org/10.1016/j.jmig.2013.10.001
and menometrorrhagia. Upon exploratory laparoscopy, she was found to have endometriosis implants on her uterosacral ligaments bilaterally and a peritoneal defect window consistent with Allen-Masters syndrome [5] on the posterior cul-de-sac below the right uterosacral ligament, which was covered by a thin layer with a small opening. Behind the peritoneal area near this defect, there was a hematoma-like lesion (Figs. 1 and 2). The peritoneal defect was opened laparoscopically and after old blood was evacuated, endometriosis lesions that were completely resected were noticed and were confirmed on final pathology. We suggest that endometriosis implants could have started either by retrograde menstruation and implanting in this defect or congenitally through the m€ullerian remnant of the rectovaginal septum. Gradually, because blood cannot escape and via retroperitoneal buildup, an endometrioma is developed, which as time goes on becomes more and
Fig. 1 The peritoneal window and hematoma-like lesion behind the peritoneum.
322
Fig. 2 Endometriotic lesions can be seen on the bottom of the defect.
Journal of Minimally Invasive Gynecology, Vol 21, No 3, May/June 2014
We recommend that whenever a peritoneal defect is present in a patient with suspected endometriosis, it has to be thoroughly examined, and its content needs to be resected completely in order to remove any hidden endometriosis that could otherwise go undiagnosed and develop further into a deeper nodular lesion. References
more advanced. Chatman [6] recognized up to 60% of patients with an Allen-Masters defect had biopsy-proven endometriosis.
1. Donnez J, Nisolle M, Casanas-Roux F, Bassil S, Anaf V. Rectovaginal septum, endometriosis or adenomyosis: laparoscopic management in a series of 231 patients. Hum Reprod. 1995;10:630–635. 2. Nezhat C, Nezhat F, Nezhat C. Endometriosis: ancient disease, ancient treatments. Fertil Steril. 2012;98(suppl):1–62. 3. Sampson JA. Peritoneal endometriosis due to the menstrual dissemination of endometrial tissue into the peritoneal cavity. Am J Obstet Gynecol. 1927;14:442. 4. Hudelist G, Keckstein J, Wright JT. The migrating adenomyoma:past views on the etiology of adenomyosis and endometriosis. Fertil Steril. 2009;92:1536–1543. 5. Allen MM, Masters WH. Traumatic laceration of uterine support. Am J Obstet Gynecol. 1955;70:500. 6. Chatman DL. Pelvic peritoneal defects and endometriosis: AllenMasters syndrome revisited. Fertil Steril. 1981;36:751–756.
Allen Masters Peritoneal Defect: A Potential Pathway to Deep Infiltrating Rectovaginal Endometriosis? Farr R. Nezhat, MD, FACOG, FACS*, and Mohamad S. Mahmoud, MD, FACOG Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, St. Luke’s-Roosevelt Hospital, Columbia University, New York, New York (all authors).
DISCUSS
You can discuss this article with its authors and with other AAGL members at http://www.AAGL.org/jmig-21-3-JMIG-D-13-00541
Use your Smartphone to scan this QR code and connect to the discussion forum for this article now* * Download a free QR Code scanner by searching for ‘‘QR scanner’’ in your smartphone’s app store or app marketplace.
Deep infiltrative endometriosis of the rectovaginal septum can be one of the most severe forms of endometriosis. It is characterized by spherically shaped lesions situated deep in the rectovaginal septum and often only visible as a small typical lesion at laparoscopy or not visible at all. This lesion is often more palpable than visible and can be tender during pelvic examination, especially if the patient is examined at the time of menstruation, and can cause severe dyspareunia, back pain, and sometimes bowel symptoms. Many theories have been suggested for this type of endometriosis including true deep infiltrating endometriosis caused by the invasion of a very active peritoneal lesion deep in the retroperitoneal space and pseudo-deep infiltrating endometriosis or ‘‘adenomyosis’’ of the rectovaginal septum and congenital endometriosis of the rectovaginal septum [1–4]. Cullen originally suggested that the adenomyotic lesion originates from the remnants of mullerian rectovaginal septum tissue and consists essentially of smooth muscle with active glandular epithelium and scanty stroma. We suggest a new potential mechanism of the development of deep infiltrating endometriosis of the rectovaginal septum [4]. Our patient is a 45-year-old woman with a chronic history of severe dysmenorrheal since menarche
The author declares no conflict of interest. Corresponding author: Farr R. Nezhat, MD, FACOG, FACS, Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, St. Luke’s-Roosevelt Hospital, Columbia University, 425 West 59th Street, Suite 9B, New York, NY 10019. E-mail: [email protected] Submitted October 2, 2013. Accepted for publication October 4, 2013. Available at www.sciencedirect.com and www.jmig.org 1553-4650/$ - see front matter Ó 2014 AAGL. All rights reserved. http://dx.doi.org/10.1016/j.jmig.2013.10.001
and menometrorrhagia. Upon exploratory laparoscopy, she was found to have endometriosis implants on her uterosacral ligaments bilaterally and a peritoneal defect window consistent with Allen-Masters syndrome [5] on the posterior cul-de-sac below the right uterosacral ligament, which was covered by a thin layer with a small opening. Behind the peritoneal area near this defect, there was a hematoma-like lesion (Figs. 1 and 2). The peritoneal defect was opened laparoscopically and after old blood was evacuated, endometriosis lesions that were completely resected were noticed and were confirmed on final pathology. We suggest that endometriosis implants could have started either by retrograde menstruation and implanting in this defect or congenitally through the m€ullerian remnant of the rectovaginal septum. Gradually, because blood cannot escape and via retroperitoneal buildup, an endometrioma is developed, which as time goes on becomes more and
Fig. 1 The peritoneal window and hematoma-like lesion behind the peritoneum.
322
Fig. 2 Endometriotic lesions can be seen on the bottom of the defect.
Journal of Minimally Invasive Gynecology, Vol 21, No 3, May/June 2014
We recommend that whenever a peritoneal defect is present in a patient with suspected endometriosis, it has to be thoroughly examined, and its content needs to be resected completely in order to remove any hidden endometriosis that could otherwise go undiagnosed and develop further into a deeper nodular lesion. References
more advanced. Chatman [6] recognized up to 60% of patients with an Allen-Masters defect had biopsy-proven endometriosis.
1. Donnez J, Nisolle M, Casanas-Roux F, Bassil S, Anaf V. Rectovaginal septum, endometriosis or adenomyosis: laparoscopic management in a series of 231 patients. Hum Reprod. 1995;10:630–635. 2. Nezhat C, Nezhat F, Nezhat C. Endometriosis: ancient disease, ancient treatments. Fertil Steril. 2012;98(suppl):1–62. 3. Sampson JA. Peritoneal endometriosis due to the menstrual dissemination of endometrial tissue into the peritoneal cavity. Am J Obstet Gynecol. 1927;14:442. 4. Hudelist G, Keckstein J, Wright JT. The migrating adenomyoma:past views on the etiology of adenomyosis and endometriosis. Fertil Steril. 2009;92:1536–1543. 5. Allen MM, Masters WH. Traumatic laceration of uterine support. Am J Obstet Gynecol. 1955;70:500. 6. Chatman DL. Pelvic peritoneal defects and endometriosis: AllenMasters syndrome revisited. Fertil Steril. 1981;36:751–756.
