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Endometriomas: Classification and surgical management
Related article:
Endometriosis: Expert answers to 7 crucial questions on diagnosis
Etiology
Endometriomas are extensively described in the literature, and their origin is the subject of several theories. In 1921, Sampson noted luteal membrane and ovarian epithelial tissues within endometriomas and was the first to indicate that endometriomas may result from the invasion of functional cysts by endometrial tissue.2,4,5 In 1979, Czernobilsky and Morris6 found endometrial and oviduct-like epithelium in ovarian endometriosis and concluded that ovarian tissue may be a common histologic precursor. Several other authors subsequently have reported finding different types of tissue within ovarian endometriomas, and not all of these chocolate cysts showed histologic evidence of endometriosis.4,7,8
Read about the classification of endometriomas
Disease classification
Our classification system identifies 2 types of endometriomas on the basis of their etiologies and characteristics. Type I, which arise from endometrial tissue implanted on the ovarian surface, are also called true endometriomas. Invagination of cortex and subsequent hemorrhage from endometrial tissue result in cyst formation. Endometrial tissue (endometrial stroma and glands) is histologically present in all type I endometriomas.1,4,9 These endometriomas usually are small (<5 cm in diameter) and have a densely adherent fibrous capsule.4 Often, there is no clear plane between cyst wall and ovarian stroma.3
Type II endometriomas arise from functional cysts involved in or invaded by cortical or pelvic side-wall endometrial implants or by type I endometriomas. Type II endometriomas are subclassified by the extent of endometrial implant involvement in the cyst wall. Type IIA endometriomas are hemorrhagic cysts with less than 10% of endometrial tissue within the cyst wall. Similar to the functional cysts from which they originate, type IIA endometriomas have a cyst wall that is separated easily from ovarian tissue during surgery.4,7,9 Although type II endometriomas tend to be larger than their type I counterparts, in some cases they are identified at an early stage of 2 to 5 cm. Endometriomas larger than 5 cm are almost always type II.4
Type IIB and IIC endometriomas have endometrial implants and fibrosis within their cyst walls, with progressively more endometrial invasion in type IIC endometriomas (>50%) than in type IIB (10% to 50%). Consequently, type IIB cysts are relatively easy to dissect from ovarian tissue, except adjacent to an endometriotic area where the cyst densely adheres to the ovarian stroma. In type IIC, endometrial tissue more extensively penetrates the capsule, making dissection of diseased tissue from the ovarian stroma more difficult; in fact, separating type IIC cyst wall from ovarian stroma can be as challenging as excising a type I endometrioma.7 In most cases, a type IIC cyst is attached by adhesions and fibrosis to the pelvic side wall or uterus and ruptures during mobilization (TABLE).
Related article:
Imaging the endometrioma and mature cystic teratoma
Presentation and diagnosis
Almost all patients with an endometrioma concurrently have peritoneal endometriosis, which is characterized by dysmenorrhea, dyspareunia, chronic pelvic pain, infertility, and, in some cases, gastrointestinal or genitourinary dysfunction.1 Pelvic examination may reveal an adnexal mass that is an endometrioma, or an endometrioma may appear on imaging obtained in a pelvic pain or infertility work-up. Given its 73% sensitivity, 94% specificity, safety, and low cost, transvaginal ultrasonography is the preferred imaging modality for endometrioma.3 The characteristic ultrasonographic appearance is that of a round, homogeneous, fluid-filled mass with low-level echoes.1 Magnetic resonance imaging is appropriate when a more sensitive imaging modality is indicated, as for a patient with risk factors for malignancy.3,10–12
Read about the surgical management of endometriomas
Surgical management
Indications for surgical excision of endometriomas include pelvic pain, infertility, and prevention and diagnosis of malignancy. Endometriomas may be excised prior to use of assisted reproductive technology.13–15 Medical therapy, such as oral contraceptives, can be used to reduce the size of endometriomas but does not improve fertility.3 Certain ovarian cancers are more common in women with endometriosis, and ovarian tumors are thought to develop in about 1% of ovarian endometriosis cases.1,12 Therefore, endometrioma excision may reduce the risk of malignancy. As with other ovarian cysts, large endometriomas may be excised to reduce the risks of rupture and torsion.
Approach
Laparoscopy is the preferred approach for endometrioma excision. Controversy exists regarding the ideal procedure: complete excision (with stripping of the cyst capsule) or drainage and ablation of the cyst wall. Compared with drainage and ablation, excision reduces recurrence of endometriomas; relieves dysmenorrhea, dyspareunia, pelvic pain, and other symptoms; and improves fertility.13,16 The recurrence rate may be as low as 5.8% with complete excision but is 90% with simple transvaginal aspiration.17,18 If not performed properly, however, cyst capsule stripping may damage nearby ovarian stroma and decrease the ovarian reserve.14 Some authors have advocated combining excision and ablation—performing cystectomy until there is no longer a clear plane between capsule and ovarian stroma and then ablating any remaining endometrial tissue.8
With type I and IIC endometriomas, we have seen the endometrial cyst wall infiltrating the ovarian stroma so deeply there is not always a definable plane. By contrast, type IIA and IIB endometriomas typically have a plane between the cyst wall and the ovarian cortex. In type II endometriomas, endometrial implants on the ovarian cortex infiltrate the plane of the cyst wall such that the juxtaposing lipomatous follicular cyst detaches with minimal intraoperative traction. Portions of type II endometriomas containing fibrosis and adhesions may become more difficult to peel off the cyst wall. For most endometriomas, at least 1 spot is difficult to peel off the ovary, and extra care must be taken at the hilum of ovary to avoid excising healthy ovarian cortex.4,5,7,8
Our surgical approach accounts for the described variations in type I and II endometriomas. Endometrial contents often spill as the endometrioma is dissected off neighboring structures. When possible, endometriomas should be aspirated and irrigated prior to cystectomy to avoid seeding the pelvis and abdomen with spilled endometriotic contents. We use hydrodissection, the injection of dilute vasopressin with a laparoscopic needle, to create a plane between cyst wall and ovarian stroma and strip the cyst capsule with laparoscopic graspers. Type I endometriomas adhere densely to the ovary. Given the presence of fibrosis and adhesions, the cyst is excised in a piecemeal fashion. Care is taken to remove any endometrial implants from the ovary while preserving as much of the ovarian tissue as possible.1
Type II endometriomas are larger cysts originating from the invasion of endometrial implants or type I endometrioma into functional cysts. The difficulty of capsule excision varies according to the extent of endometrial invasion. Type IIA endometriomas contain less than 10% endometrial tissue within the cyst capsule. Thus, the standard ovarian cystectomy stripping technique is successful in removing more than 90% of the cyst capsule. Special care is taken in stripping the residual small portion that involves the endometrial glands and stroma and adheres densely to the ovary.
The larger proportion of endometrial tissue present in type IIB and IIC endometriomas degrades the plane between the cyst capsule and the ovarian stroma, making excision more difficult. Similar to the type I excision, a piecemeal approach is often necessary. If complete stripping of the cyst capsule would result in extensive loss of healthy ovarian tissue, then electrocautery, plasma energy, or laser ablation can be selectively used to destroy focal areas of endometrial invasion. Complete ablation may be difficult, as the endometrioma wall can be up to 5 mm thick.19 For these thick-walled endometriomas, we recommend excision (vs ablation), which lowers the risk of endometrioma recurrence.
Related article:
Endometriosis and pain: Expert answers to 6 questions targeting your management options
- Endometriomas are common adnexal masses in women affected by endometriosis and may exacerbate pelvic pain and impair fertility. Classification of endometriomas into type I and type II,depending on their etiology and characteristics, can guide minimally invasive surgical management.
- Type I endometriomas arise from invagination of endometrial implants on the ovarian cortex, resulting in dense fibrosis and adhesions. These lesions typically require piecemeal excision in order to completely remove the cyst capsule.
- Type II endometriomas result from invasion of endometrial tissue into preexisting functional cysts and are further subclassified by the proportion of cyst capsule containing endometrial tissue (IIA <10%, IIB 10% to 50%, IIC >50%).
- The difficulty of excising type II endometriomas correlates with the degree of endometrial invasion, with type IIA being relatively straightforward and type IIC being as challenging and piecemeal as type I.
- We generally favor complete excision rather than ablation of the cyst capsule, except for when excision would result in an unacceptable loss of healthy ovarian tissue.
Conclusion
Endometriomas, common adnexal masses in women affected by endometriosis, may exacerbate pelvic pain and impair fertility. Gynecologists should be prepared to excise endometriomas completely and exercise care in preserving as much of the ovarian stroma as possible. We classify endometriomas into 2 types: type I, which develop from invagination of endometrial implants in the ovarian cortex, and type II, which stem from invasion of functional cysts by endometrial implants or type I endometrioma. This distinction guides surgical management. We hope this article and its accompanying video will be helpful in guiding laparoscopic excision of type I and II endometriomas.
Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.
- Nezhat C, Buescher E, Paka C, et al. Video-assisted laparoscopic treatment of endometriosis. In: Nezhat C, Nezhat F, Nezhat C, eds. Nezhat’s Video-Assisted and Robotic-Assisted Laparoscopy and Hysteroscopy. 4th ed. New York, NY: Cambridge University Press; 2013:265–302.
- Burney RO, Giudice LC. Pathogenesis and pathophysiology of endometriosis. Fertil Steril. 2012;98(3):511–519.
- Keyhan S, Hughes C, Price T, Muasher S. An update on surgical versus expectant management of ovarian endometriomas in infertile women. Biomed Res Int. 2015;2015:204792.
- Nezhat F, Nezhat C, Allan CJ, Metzger DA, Sears DL. Clinical and histologic classification of endometriomas. Implications for a mechanism of pathogenesis. J Reprod Med. 1992;37(9):771–776.
- Burney RO, Giudice LC. The pathogenesis of endometriosis. In: Nezhat C, Nezhat F, Nezhat C, eds. Nezhat’s Video-Assisted and Robotic-Assisted Laparoscopy and Hysteroscopy. 4th ed. New York, NY: Cambridge University Press; 2013:252–258.
- Czernobilsky B, Morris WJ. A histologic study of ovarian endometriosis with emphasis on hyperplastic and atypical changes. Obstet Gynecol. 1979;53(3):318–323.
- Nezhat F, Nezhat C, Nezhat C, Admon D. A fresh look at ovarian endometriomas. Contemp Ob Gyn. 1994;39(11):81–94.
- Donnez J, Lousse JC, Jadoul P, Donnez O, Squifflet J. Laparoscopic management of endometriomas using a combined technique of excisional (cystectomy) and ablative surgery. Fertil Steril. 2010;94(1):28–32.
- Nezhat C, Nezhat F, Nezhat C, Seidman DS. Classification of endometriosis. Improving the classification of endometriotic ovarian cysts. Hum Reprod. 1994;9(12):2212–2213.
- Nezhat FR, Pejovic T, Reis FM, Guo SW. The link between endometriosis and ovarian cancer: clinical implications. Int J Gynecol Cancer. 2014;24(4):623–628.
- Nezhat F, Apostol R, Mahmoud M, el Daouk M. Malignant transformation of endometriosis and its clinical significance. Fertil Steril. 2014;102(2):342–344.
- Nezhat FR, Apostal R, Nezhat C, Pejovic T. New insights in the pathophysiology of ovarian cancer and implications for screening and prevention. Am J Obstet Gynecol. 2015;213(3):262–267.
- Hart RJ, Hickey M, Maouris P, Buckett W. Excisional surgery versus ablative surgery for ovarian endometriomata. Cochrane Database Syst Rev. 2008;(2):CD004992.
- Yates J. Endometriosis and infertility: expert answers to 6 questions to help pinpoint the best route to pregnancy. OBG Manag. 2015;27(6):30–35.
- Littman E, Giudice L, Lathi R, Berker B, Milki A, Nezhat C. Role of laparoscopic treatment of endometriosis in patients with failed in vitro fertilization cycles. Fertil Steril. 2005;84(6):1574–1578.
- Exacoustos C, Zupi E, Amadio A, et al. Laparoscopic removal of endometriomas: sonographic evaluation of residual functioning ovarian tissue. Am J Obstet Gynecol. 2004;191(1):68–72.
- Gonçalves FC, Andres MP, Passman LJ, Gonçalves MO, Podgaec S. A systematic review of ultrasonography-guided transvaginal aspiration of recurrent ovarian endometrioma. Int J Gynaecol Obstet. 2016;134(1):3–7.
- Alborzi S, Momtahan M, Parsanezhad ME, Dehbashi S, Zolghadri J, Alborzi S. A prospective, randomized study comparing laparoscopic ovarian cystectomy versus fenestration and coagulation in patients with endometriomas. Fertil Steril. 2004;82(6):1633–1637.
- Nezhat C, Crowgey SR, Garrison CP. Surgical treatment of endometriosis via laser laparoscopy. Fertil Steril. 1986;45(6):778–783.
Dr. Falik is from the Center for Special Minimally Invasive and Robotic Surgery and Stanford University Medical Center, Palo Alto, California.
Dr. Li is from the Center for Special Minimally Invasive and Robotic Surgery and Stanford University Medical Center.
At the time of this writing, Dr. Farrimond was medical student, University of California–San Francisco, and is currently resident, Obstetrics and Gynecology, Kaiser Santa Clara Medical Center, Santa Clara, California.
Dr. Razavi is from the Center for Special Minimally Invasive and Robotic Surgery.
Dr. C. Nezhat is Fellowship Director, Atlanta Center for Minimally Invasive Surgery and Reproductive Medicine, Atlanta, Georgia.
Dr. F. Nezhat is Clinical Professor, Obstetrics and Gynecology, Weill Cornell Medical College, Cornell University, New York, New York, and Adjunct Professor, Obstetrics, Gynecology, and Reproductive Medicine, School of Medicine, Stony Brook University, Stony Brook, New York.
Dr. F. Nezhat reports being a speaker for Ambry Genetics. The other authors report no financial relationships relevant to this article.
Dr. Falik is from the Center for Special Minimally Invasive and Robotic Surgery and Stanford University Medical Center, Palo Alto, California.
Dr. Li is from the Center for Special Minimally Invasive and Robotic Surgery and Stanford University Medical Center.
At the time of this writing, Dr. Farrimond was medical student, University of California–San Francisco, and is currently resident, Obstetrics and Gynecology, Kaiser Santa Clara Medical Center, Santa Clara, California.
Dr. Razavi is from the Center for Special Minimally Invasive and Robotic Surgery.
Dr. C. Nezhat is Fellowship Director, Atlanta Center for Minimally Invasive Surgery and Reproductive Medicine, Atlanta, Georgia.
Dr. F. Nezhat is Clinical Professor, Obstetrics and Gynecology, Weill Cornell Medical College, Cornell University, New York, New York, and Adjunct Professor, Obstetrics, Gynecology, and Reproductive Medicine, School of Medicine, Stony Brook University, Stony Brook, New York.
Dr. F. Nezhat reports being a speaker for Ambry Genetics. The other authors report no financial relationships relevant to this article.
Dr. Falik is from the Center for Special Minimally Invasive and Robotic Surgery and Stanford University Medical Center, Palo Alto, California.
Dr. Li is from the Center for Special Minimally Invasive and Robotic Surgery and Stanford University Medical Center.
At the time of this writing, Dr. Farrimond was medical student, University of California–San Francisco, and is currently resident, Obstetrics and Gynecology, Kaiser Santa Clara Medical Center, Santa Clara, California.
Dr. Razavi is from the Center for Special Minimally Invasive and Robotic Surgery.
Dr. C. Nezhat is Fellowship Director, Atlanta Center for Minimally Invasive Surgery and Reproductive Medicine, Atlanta, Georgia.
Dr. F. Nezhat is Clinical Professor, Obstetrics and Gynecology, Weill Cornell Medical College, Cornell University, New York, New York, and Adjunct Professor, Obstetrics, Gynecology, and Reproductive Medicine, School of Medicine, Stony Brook University, Stony Brook, New York.
Dr. F. Nezhat reports being a speaker for Ambry Genetics. The other authors report no financial relationships relevant to this article.
Related article:
Endometriosis: Expert answers to 7 crucial questions on diagnosis
Etiology
Endometriomas are extensively described in the literature, and their origin is the subject of several theories. In 1921, Sampson noted luteal membrane and ovarian epithelial tissues within endometriomas and was the first to indicate that endometriomas may result from the invasion of functional cysts by endometrial tissue.2,4,5 In 1979, Czernobilsky and Morris6 found endometrial and oviduct-like epithelium in ovarian endometriosis and concluded that ovarian tissue may be a common histologic precursor. Several other authors subsequently have reported finding different types of tissue within ovarian endometriomas, and not all of these chocolate cysts showed histologic evidence of endometriosis.4,7,8
Read about the classification of endometriomas
Disease classification
Our classification system identifies 2 types of endometriomas on the basis of their etiologies and characteristics. Type I, which arise from endometrial tissue implanted on the ovarian surface, are also called true endometriomas. Invagination of cortex and subsequent hemorrhage from endometrial tissue result in cyst formation. Endometrial tissue (endometrial stroma and glands) is histologically present in all type I endometriomas.1,4,9 These endometriomas usually are small (<5 cm in diameter) and have a densely adherent fibrous capsule.4 Often, there is no clear plane between cyst wall and ovarian stroma.3
Type II endometriomas arise from functional cysts involved in or invaded by cortical or pelvic side-wall endometrial implants or by type I endometriomas. Type II endometriomas are subclassified by the extent of endometrial implant involvement in the cyst wall. Type IIA endometriomas are hemorrhagic cysts with less than 10% of endometrial tissue within the cyst wall. Similar to the functional cysts from which they originate, type IIA endometriomas have a cyst wall that is separated easily from ovarian tissue during surgery.4,7,9 Although type II endometriomas tend to be larger than their type I counterparts, in some cases they are identified at an early stage of 2 to 5 cm. Endometriomas larger than 5 cm are almost always type II.4
Type IIB and IIC endometriomas have endometrial implants and fibrosis within their cyst walls, with progressively more endometrial invasion in type IIC endometriomas (>50%) than in type IIB (10% to 50%). Consequently, type IIB cysts are relatively easy to dissect from ovarian tissue, except adjacent to an endometriotic area where the cyst densely adheres to the ovarian stroma. In type IIC, endometrial tissue more extensively penetrates the capsule, making dissection of diseased tissue from the ovarian stroma more difficult; in fact, separating type IIC cyst wall from ovarian stroma can be as challenging as excising a type I endometrioma.7 In most cases, a type IIC cyst is attached by adhesions and fibrosis to the pelvic side wall or uterus and ruptures during mobilization (TABLE).
Related article:
Imaging the endometrioma and mature cystic teratoma
Presentation and diagnosis
Almost all patients with an endometrioma concurrently have peritoneal endometriosis, which is characterized by dysmenorrhea, dyspareunia, chronic pelvic pain, infertility, and, in some cases, gastrointestinal or genitourinary dysfunction.1 Pelvic examination may reveal an adnexal mass that is an endometrioma, or an endometrioma may appear on imaging obtained in a pelvic pain or infertility work-up. Given its 73% sensitivity, 94% specificity, safety, and low cost, transvaginal ultrasonography is the preferred imaging modality for endometrioma.3 The characteristic ultrasonographic appearance is that of a round, homogeneous, fluid-filled mass with low-level echoes.1 Magnetic resonance imaging is appropriate when a more sensitive imaging modality is indicated, as for a patient with risk factors for malignancy.3,10–12
Read about the surgical management of endometriomas
Surgical management
Indications for surgical excision of endometriomas include pelvic pain, infertility, and prevention and diagnosis of malignancy. Endometriomas may be excised prior to use of assisted reproductive technology.13–15 Medical therapy, such as oral contraceptives, can be used to reduce the size of endometriomas but does not improve fertility.3 Certain ovarian cancers are more common in women with endometriosis, and ovarian tumors are thought to develop in about 1% of ovarian endometriosis cases.1,12 Therefore, endometrioma excision may reduce the risk of malignancy. As with other ovarian cysts, large endometriomas may be excised to reduce the risks of rupture and torsion.
Approach
Laparoscopy is the preferred approach for endometrioma excision. Controversy exists regarding the ideal procedure: complete excision (with stripping of the cyst capsule) or drainage and ablation of the cyst wall. Compared with drainage and ablation, excision reduces recurrence of endometriomas; relieves dysmenorrhea, dyspareunia, pelvic pain, and other symptoms; and improves fertility.13,16 The recurrence rate may be as low as 5.8% with complete excision but is 90% with simple transvaginal aspiration.17,18 If not performed properly, however, cyst capsule stripping may damage nearby ovarian stroma and decrease the ovarian reserve.14 Some authors have advocated combining excision and ablation—performing cystectomy until there is no longer a clear plane between capsule and ovarian stroma and then ablating any remaining endometrial tissue.8
With type I and IIC endometriomas, we have seen the endometrial cyst wall infiltrating the ovarian stroma so deeply there is not always a definable plane. By contrast, type IIA and IIB endometriomas typically have a plane between the cyst wall and the ovarian cortex. In type II endometriomas, endometrial implants on the ovarian cortex infiltrate the plane of the cyst wall such that the juxtaposing lipomatous follicular cyst detaches with minimal intraoperative traction. Portions of type II endometriomas containing fibrosis and adhesions may become more difficult to peel off the cyst wall. For most endometriomas, at least 1 spot is difficult to peel off the ovary, and extra care must be taken at the hilum of ovary to avoid excising healthy ovarian cortex.4,5,7,8
Our surgical approach accounts for the described variations in type I and II endometriomas. Endometrial contents often spill as the endometrioma is dissected off neighboring structures. When possible, endometriomas should be aspirated and irrigated prior to cystectomy to avoid seeding the pelvis and abdomen with spilled endometriotic contents. We use hydrodissection, the injection of dilute vasopressin with a laparoscopic needle, to create a plane between cyst wall and ovarian stroma and strip the cyst capsule with laparoscopic graspers. Type I endometriomas adhere densely to the ovary. Given the presence of fibrosis and adhesions, the cyst is excised in a piecemeal fashion. Care is taken to remove any endometrial implants from the ovary while preserving as much of the ovarian tissue as possible.1
Type II endometriomas are larger cysts originating from the invasion of endometrial implants or type I endometrioma into functional cysts. The difficulty of capsule excision varies according to the extent of endometrial invasion. Type IIA endometriomas contain less than 10% endometrial tissue within the cyst capsule. Thus, the standard ovarian cystectomy stripping technique is successful in removing more than 90% of the cyst capsule. Special care is taken in stripping the residual small portion that involves the endometrial glands and stroma and adheres densely to the ovary.
The larger proportion of endometrial tissue present in type IIB and IIC endometriomas degrades the plane between the cyst capsule and the ovarian stroma, making excision more difficult. Similar to the type I excision, a piecemeal approach is often necessary. If complete stripping of the cyst capsule would result in extensive loss of healthy ovarian tissue, then electrocautery, plasma energy, or laser ablation can be selectively used to destroy focal areas of endometrial invasion. Complete ablation may be difficult, as the endometrioma wall can be up to 5 mm thick.19 For these thick-walled endometriomas, we recommend excision (vs ablation), which lowers the risk of endometrioma recurrence.
Related article:
Endometriosis and pain: Expert answers to 6 questions targeting your management options
- Endometriomas are common adnexal masses in women affected by endometriosis and may exacerbate pelvic pain and impair fertility. Classification of endometriomas into type I and type II,depending on their etiology and characteristics, can guide minimally invasive surgical management.
- Type I endometriomas arise from invagination of endometrial implants on the ovarian cortex, resulting in dense fibrosis and adhesions. These lesions typically require piecemeal excision in order to completely remove the cyst capsule.
- Type II endometriomas result from invasion of endometrial tissue into preexisting functional cysts and are further subclassified by the proportion of cyst capsule containing endometrial tissue (IIA <10%, IIB 10% to 50%, IIC >50%).
- The difficulty of excising type II endometriomas correlates with the degree of endometrial invasion, with type IIA being relatively straightforward and type IIC being as challenging and piecemeal as type I.
- We generally favor complete excision rather than ablation of the cyst capsule, except for when excision would result in an unacceptable loss of healthy ovarian tissue.
Conclusion
Endometriomas, common adnexal masses in women affected by endometriosis, may exacerbate pelvic pain and impair fertility. Gynecologists should be prepared to excise endometriomas completely and exercise care in preserving as much of the ovarian stroma as possible. We classify endometriomas into 2 types: type I, which develop from invagination of endometrial implants in the ovarian cortex, and type II, which stem from invasion of functional cysts by endometrial implants or type I endometrioma. This distinction guides surgical management. We hope this article and its accompanying video will be helpful in guiding laparoscopic excision of type I and II endometriomas.
Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.
Related article:
Endometriosis: Expert answers to 7 crucial questions on diagnosis
Etiology
Endometriomas are extensively described in the literature, and their origin is the subject of several theories. In 1921, Sampson noted luteal membrane and ovarian epithelial tissues within endometriomas and was the first to indicate that endometriomas may result from the invasion of functional cysts by endometrial tissue.2,4,5 In 1979, Czernobilsky and Morris6 found endometrial and oviduct-like epithelium in ovarian endometriosis and concluded that ovarian tissue may be a common histologic precursor. Several other authors subsequently have reported finding different types of tissue within ovarian endometriomas, and not all of these chocolate cysts showed histologic evidence of endometriosis.4,7,8
Read about the classification of endometriomas
Disease classification
Our classification system identifies 2 types of endometriomas on the basis of their etiologies and characteristics. Type I, which arise from endometrial tissue implanted on the ovarian surface, are also called true endometriomas. Invagination of cortex and subsequent hemorrhage from endometrial tissue result in cyst formation. Endometrial tissue (endometrial stroma and glands) is histologically present in all type I endometriomas.1,4,9 These endometriomas usually are small (<5 cm in diameter) and have a densely adherent fibrous capsule.4 Often, there is no clear plane between cyst wall and ovarian stroma.3
Type II endometriomas arise from functional cysts involved in or invaded by cortical or pelvic side-wall endometrial implants or by type I endometriomas. Type II endometriomas are subclassified by the extent of endometrial implant involvement in the cyst wall. Type IIA endometriomas are hemorrhagic cysts with less than 10% of endometrial tissue within the cyst wall. Similar to the functional cysts from which they originate, type IIA endometriomas have a cyst wall that is separated easily from ovarian tissue during surgery.4,7,9 Although type II endometriomas tend to be larger than their type I counterparts, in some cases they are identified at an early stage of 2 to 5 cm. Endometriomas larger than 5 cm are almost always type II.4
Type IIB and IIC endometriomas have endometrial implants and fibrosis within their cyst walls, with progressively more endometrial invasion in type IIC endometriomas (>50%) than in type IIB (10% to 50%). Consequently, type IIB cysts are relatively easy to dissect from ovarian tissue, except adjacent to an endometriotic area where the cyst densely adheres to the ovarian stroma. In type IIC, endometrial tissue more extensively penetrates the capsule, making dissection of diseased tissue from the ovarian stroma more difficult; in fact, separating type IIC cyst wall from ovarian stroma can be as challenging as excising a type I endometrioma.7 In most cases, a type IIC cyst is attached by adhesions and fibrosis to the pelvic side wall or uterus and ruptures during mobilization (TABLE).
Related article:
Imaging the endometrioma and mature cystic teratoma
Presentation and diagnosis
Almost all patients with an endometrioma concurrently have peritoneal endometriosis, which is characterized by dysmenorrhea, dyspareunia, chronic pelvic pain, infertility, and, in some cases, gastrointestinal or genitourinary dysfunction.1 Pelvic examination may reveal an adnexal mass that is an endometrioma, or an endometrioma may appear on imaging obtained in a pelvic pain or infertility work-up. Given its 73% sensitivity, 94% specificity, safety, and low cost, transvaginal ultrasonography is the preferred imaging modality for endometrioma.3 The characteristic ultrasonographic appearance is that of a round, homogeneous, fluid-filled mass with low-level echoes.1 Magnetic resonance imaging is appropriate when a more sensitive imaging modality is indicated, as for a patient with risk factors for malignancy.3,10–12
Read about the surgical management of endometriomas
Surgical management
Indications for surgical excision of endometriomas include pelvic pain, infertility, and prevention and diagnosis of malignancy. Endometriomas may be excised prior to use of assisted reproductive technology.13–15 Medical therapy, such as oral contraceptives, can be used to reduce the size of endometriomas but does not improve fertility.3 Certain ovarian cancers are more common in women with endometriosis, and ovarian tumors are thought to develop in about 1% of ovarian endometriosis cases.1,12 Therefore, endometrioma excision may reduce the risk of malignancy. As with other ovarian cysts, large endometriomas may be excised to reduce the risks of rupture and torsion.
Approach
Laparoscopy is the preferred approach for endometrioma excision. Controversy exists regarding the ideal procedure: complete excision (with stripping of the cyst capsule) or drainage and ablation of the cyst wall. Compared with drainage and ablation, excision reduces recurrence of endometriomas; relieves dysmenorrhea, dyspareunia, pelvic pain, and other symptoms; and improves fertility.13,16 The recurrence rate may be as low as 5.8% with complete excision but is 90% with simple transvaginal aspiration.17,18 If not performed properly, however, cyst capsule stripping may damage nearby ovarian stroma and decrease the ovarian reserve.14 Some authors have advocated combining excision and ablation—performing cystectomy until there is no longer a clear plane between capsule and ovarian stroma and then ablating any remaining endometrial tissue.8
With type I and IIC endometriomas, we have seen the endometrial cyst wall infiltrating the ovarian stroma so deeply there is not always a definable plane. By contrast, type IIA and IIB endometriomas typically have a plane between the cyst wall and the ovarian cortex. In type II endometriomas, endometrial implants on the ovarian cortex infiltrate the plane of the cyst wall such that the juxtaposing lipomatous follicular cyst detaches with minimal intraoperative traction. Portions of type II endometriomas containing fibrosis and adhesions may become more difficult to peel off the cyst wall. For most endometriomas, at least 1 spot is difficult to peel off the ovary, and extra care must be taken at the hilum of ovary to avoid excising healthy ovarian cortex.4,5,7,8
Our surgical approach accounts for the described variations in type I and II endometriomas. Endometrial contents often spill as the endometrioma is dissected off neighboring structures. When possible, endometriomas should be aspirated and irrigated prior to cystectomy to avoid seeding the pelvis and abdomen with spilled endometriotic contents. We use hydrodissection, the injection of dilute vasopressin with a laparoscopic needle, to create a plane between cyst wall and ovarian stroma and strip the cyst capsule with laparoscopic graspers. Type I endometriomas adhere densely to the ovary. Given the presence of fibrosis and adhesions, the cyst is excised in a piecemeal fashion. Care is taken to remove any endometrial implants from the ovary while preserving as much of the ovarian tissue as possible.1
Type II endometriomas are larger cysts originating from the invasion of endometrial implants or type I endometrioma into functional cysts. The difficulty of capsule excision varies according to the extent of endometrial invasion. Type IIA endometriomas contain less than 10% endometrial tissue within the cyst capsule. Thus, the standard ovarian cystectomy stripping technique is successful in removing more than 90% of the cyst capsule. Special care is taken in stripping the residual small portion that involves the endometrial glands and stroma and adheres densely to the ovary.
The larger proportion of endometrial tissue present in type IIB and IIC endometriomas degrades the plane between the cyst capsule and the ovarian stroma, making excision more difficult. Similar to the type I excision, a piecemeal approach is often necessary. If complete stripping of the cyst capsule would result in extensive loss of healthy ovarian tissue, then electrocautery, plasma energy, or laser ablation can be selectively used to destroy focal areas of endometrial invasion. Complete ablation may be difficult, as the endometrioma wall can be up to 5 mm thick.19 For these thick-walled endometriomas, we recommend excision (vs ablation), which lowers the risk of endometrioma recurrence.
Related article:
Endometriosis and pain: Expert answers to 6 questions targeting your management options
- Endometriomas are common adnexal masses in women affected by endometriosis and may exacerbate pelvic pain and impair fertility. Classification of endometriomas into type I and type II,depending on their etiology and characteristics, can guide minimally invasive surgical management.
- Type I endometriomas arise from invagination of endometrial implants on the ovarian cortex, resulting in dense fibrosis and adhesions. These lesions typically require piecemeal excision in order to completely remove the cyst capsule.
- Type II endometriomas result from invasion of endometrial tissue into preexisting functional cysts and are further subclassified by the proportion of cyst capsule containing endometrial tissue (IIA <10%, IIB 10% to 50%, IIC >50%).
- The difficulty of excising type II endometriomas correlates with the degree of endometrial invasion, with type IIA being relatively straightforward and type IIC being as challenging and piecemeal as type I.
- We generally favor complete excision rather than ablation of the cyst capsule, except for when excision would result in an unacceptable loss of healthy ovarian tissue.
Conclusion
Endometriomas, common adnexal masses in women affected by endometriosis, may exacerbate pelvic pain and impair fertility. Gynecologists should be prepared to excise endometriomas completely and exercise care in preserving as much of the ovarian stroma as possible. We classify endometriomas into 2 types: type I, which develop from invagination of endometrial implants in the ovarian cortex, and type II, which stem from invasion of functional cysts by endometrial implants or type I endometrioma. This distinction guides surgical management. We hope this article and its accompanying video will be helpful in guiding laparoscopic excision of type I and II endometriomas.
Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.
- Nezhat C, Buescher E, Paka C, et al. Video-assisted laparoscopic treatment of endometriosis. In: Nezhat C, Nezhat F, Nezhat C, eds. Nezhat’s Video-Assisted and Robotic-Assisted Laparoscopy and Hysteroscopy. 4th ed. New York, NY: Cambridge University Press; 2013:265–302.
- Burney RO, Giudice LC. Pathogenesis and pathophysiology of endometriosis. Fertil Steril. 2012;98(3):511–519.
- Keyhan S, Hughes C, Price T, Muasher S. An update on surgical versus expectant management of ovarian endometriomas in infertile women. Biomed Res Int. 2015;2015:204792.
- Nezhat F, Nezhat C, Allan CJ, Metzger DA, Sears DL. Clinical and histologic classification of endometriomas. Implications for a mechanism of pathogenesis. J Reprod Med. 1992;37(9):771–776.
- Burney RO, Giudice LC. The pathogenesis of endometriosis. In: Nezhat C, Nezhat F, Nezhat C, eds. Nezhat’s Video-Assisted and Robotic-Assisted Laparoscopy and Hysteroscopy. 4th ed. New York, NY: Cambridge University Press; 2013:252–258.
- Czernobilsky B, Morris WJ. A histologic study of ovarian endometriosis with emphasis on hyperplastic and atypical changes. Obstet Gynecol. 1979;53(3):318–323.
- Nezhat F, Nezhat C, Nezhat C, Admon D. A fresh look at ovarian endometriomas. Contemp Ob Gyn. 1994;39(11):81–94.
- Donnez J, Lousse JC, Jadoul P, Donnez O, Squifflet J. Laparoscopic management of endometriomas using a combined technique of excisional (cystectomy) and ablative surgery. Fertil Steril. 2010;94(1):28–32.
- Nezhat C, Nezhat F, Nezhat C, Seidman DS. Classification of endometriosis. Improving the classification of endometriotic ovarian cysts. Hum Reprod. 1994;9(12):2212–2213.
- Nezhat FR, Pejovic T, Reis FM, Guo SW. The link between endometriosis and ovarian cancer: clinical implications. Int J Gynecol Cancer. 2014;24(4):623–628.
- Nezhat F, Apostol R, Mahmoud M, el Daouk M. Malignant transformation of endometriosis and its clinical significance. Fertil Steril. 2014;102(2):342–344.
- Nezhat FR, Apostal R, Nezhat C, Pejovic T. New insights in the pathophysiology of ovarian cancer and implications for screening and prevention. Am J Obstet Gynecol. 2015;213(3):262–267.
- Hart RJ, Hickey M, Maouris P, Buckett W. Excisional surgery versus ablative surgery for ovarian endometriomata. Cochrane Database Syst Rev. 2008;(2):CD004992.
- Yates J. Endometriosis and infertility: expert answers to 6 questions to help pinpoint the best route to pregnancy. OBG Manag. 2015;27(6):30–35.
- Littman E, Giudice L, Lathi R, Berker B, Milki A, Nezhat C. Role of laparoscopic treatment of endometriosis in patients with failed in vitro fertilization cycles. Fertil Steril. 2005;84(6):1574–1578.
- Exacoustos C, Zupi E, Amadio A, et al. Laparoscopic removal of endometriomas: sonographic evaluation of residual functioning ovarian tissue. Am J Obstet Gynecol. 2004;191(1):68–72.
- Gonçalves FC, Andres MP, Passman LJ, Gonçalves MO, Podgaec S. A systematic review of ultrasonography-guided transvaginal aspiration of recurrent ovarian endometrioma. Int J Gynaecol Obstet. 2016;134(1):3–7.
- Alborzi S, Momtahan M, Parsanezhad ME, Dehbashi S, Zolghadri J, Alborzi S. A prospective, randomized study comparing laparoscopic ovarian cystectomy versus fenestration and coagulation in patients with endometriomas. Fertil Steril. 2004;82(6):1633–1637.
- Nezhat C, Crowgey SR, Garrison CP. Surgical treatment of endometriosis via laser laparoscopy. Fertil Steril. 1986;45(6):778–783.
- Nezhat C, Buescher E, Paka C, et al. Video-assisted laparoscopic treatment of endometriosis. In: Nezhat C, Nezhat F, Nezhat C, eds. Nezhat’s Video-Assisted and Robotic-Assisted Laparoscopy and Hysteroscopy. 4th ed. New York, NY: Cambridge University Press; 2013:265–302.
- Burney RO, Giudice LC. Pathogenesis and pathophysiology of endometriosis. Fertil Steril. 2012;98(3):511–519.
- Keyhan S, Hughes C, Price T, Muasher S. An update on surgical versus expectant management of ovarian endometriomas in infertile women. Biomed Res Int. 2015;2015:204792.
- Nezhat F, Nezhat C, Allan CJ, Metzger DA, Sears DL. Clinical and histologic classification of endometriomas. Implications for a mechanism of pathogenesis. J Reprod Med. 1992;37(9):771–776.
- Burney RO, Giudice LC. The pathogenesis of endometriosis. In: Nezhat C, Nezhat F, Nezhat C, eds. Nezhat’s Video-Assisted and Robotic-Assisted Laparoscopy and Hysteroscopy. 4th ed. New York, NY: Cambridge University Press; 2013:252–258.
- Czernobilsky B, Morris WJ. A histologic study of ovarian endometriosis with emphasis on hyperplastic and atypical changes. Obstet Gynecol. 1979;53(3):318–323.
- Nezhat F, Nezhat C, Nezhat C, Admon D. A fresh look at ovarian endometriomas. Contemp Ob Gyn. 1994;39(11):81–94.
- Donnez J, Lousse JC, Jadoul P, Donnez O, Squifflet J. Laparoscopic management of endometriomas using a combined technique of excisional (cystectomy) and ablative surgery. Fertil Steril. 2010;94(1):28–32.
- Nezhat C, Nezhat F, Nezhat C, Seidman DS. Classification of endometriosis. Improving the classification of endometriotic ovarian cysts. Hum Reprod. 1994;9(12):2212–2213.
- Nezhat FR, Pejovic T, Reis FM, Guo SW. The link between endometriosis and ovarian cancer: clinical implications. Int J Gynecol Cancer. 2014;24(4):623–628.
- Nezhat F, Apostol R, Mahmoud M, el Daouk M. Malignant transformation of endometriosis and its clinical significance. Fertil Steril. 2014;102(2):342–344.
- Nezhat FR, Apostal R, Nezhat C, Pejovic T. New insights in the pathophysiology of ovarian cancer and implications for screening and prevention. Am J Obstet Gynecol. 2015;213(3):262–267.
- Hart RJ, Hickey M, Maouris P, Buckett W. Excisional surgery versus ablative surgery for ovarian endometriomata. Cochrane Database Syst Rev. 2008;(2):CD004992.
- Yates J. Endometriosis and infertility: expert answers to 6 questions to help pinpoint the best route to pregnancy. OBG Manag. 2015;27(6):30–35.
- Littman E, Giudice L, Lathi R, Berker B, Milki A, Nezhat C. Role of laparoscopic treatment of endometriosis in patients with failed in vitro fertilization cycles. Fertil Steril. 2005;84(6):1574–1578.
- Exacoustos C, Zupi E, Amadio A, et al. Laparoscopic removal of endometriomas: sonographic evaluation of residual functioning ovarian tissue. Am J Obstet Gynecol. 2004;191(1):68–72.
- Gonçalves FC, Andres MP, Passman LJ, Gonçalves MO, Podgaec S. A systematic review of ultrasonography-guided transvaginal aspiration of recurrent ovarian endometrioma. Int J Gynaecol Obstet. 2016;134(1):3–7.
- Alborzi S, Momtahan M, Parsanezhad ME, Dehbashi S, Zolghadri J, Alborzi S. A prospective, randomized study comparing laparoscopic ovarian cystectomy versus fenestration and coagulation in patients with endometriomas. Fertil Steril. 2004;82(6):1633–1637.
- Nezhat C, Crowgey SR, Garrison CP. Surgical treatment of endometriosis via laser laparoscopy. Fertil Steril. 1986;45(6):778–783.
IN THIS ARTICLE
Cesarean scar defect: What is it and how should it be treated?
Cesarean delivery is one of the most common surgical procedures in women, with rates of 30% or more in the United States.1 As a result, the rate is rising for cesarean scar defect—the presence of a “niche” at the site of cesarean delivery scar—with the reported prevalence between 24% and 70% in a random population of women with at least one cesarean delivery.2 Other terms for cesarean scar defect include a niche, isthmocele, uteroperitoneal fistula, and diverticulum.1–9
Formation of cesarean scar defect
Cesarean scar defect forms after cesarean delivery, at the site of hysterotomy, on the anterior wall of the uterine isthmus (FIGURE 1). While this is the typical location, the defect has also been found at the endocervical canal and mid-uterine body. Improper healing of the cesarean incision leads to thinning of the anterior uterine wall, which creates an indentation and fluid-filled pouch at the cesarean scar site. The exact reason why a niche develops has not yet been determined; however, there are several hypotheses, broken down by pregnancy-related and patient-related factors. Surgical techniques that may increase the chance of niche development include low (cervical) hysterotomy, single-layer uterine wall closure, use of locking sutures, closure of hysterotomy with endometrial-sparing technique, and multiple cesarean deliveries.3,4 Patients with medical conditions that may impact wound healing (such as diabetes and smoking) may be at increased risk for niche formation.
Viewed hysteroscopically, the defect appears as a concave shape in the anterior uterine wall; to the inexperienced eye, it may resemble a second cavity (FIGURE 2).
Pelvic pain and other serious consequences
The presence of fibrotic tissue in the niche acts like a valve, leading to the accumulation of blood in this reservoir-like area. A niche thus can cause delayed menstruation through the cervix, resulting in abnormal bleeding, pelvic pain, vaginal discharge, dysmenorrhea, dyspareunia, and infertility. Accumulated blood in this area can ultimately degrade cervical mucus and sperm quality, as well as inhibit sperm transport, a proposed mechanism of infertility.5,6 Women with a niche who conceive are at potential risk for cesarean scar ectopic pregnancy, with the embryo implanting in the pouch and subsequently growing and developing improperly.
Read about evaluation and treatment.
Evaluation and treatment
Patients presenting with the symptoms de-scribed above who have had a prior cesarean delivery should be evaluated for a cesarean scar defect.9 The best time to assess for the abnormality is after the patient’s menstrual cycle, when the endometrial lining is at its thinnest and recently menstruated blood has collected in the defect (this can highlight the niche on imaging). Transvaginal ultrasonography (FIGURE 3) or saline-infusion sonohysterogram serve as a first-line test for in-office diagnosis.7 Magnetic resonance imaging (MRI), 3-D ultrasonography, and hysteroscopy are additional useful imaging modalities that can aid in the diagnosis.
Treatments for cesarean scar defect vary dramatically and include hormonal therapy, hysteroscopic resection, vaginal or laparoscopic repair, and hysterectomy. Nonsurgical treatment should be reserved for women who desire a noninvasive approach, as the evidence for symptom resolution is limited.8
To promote fertility and decrease symptoms, the abnormal, fibrotic tissue must be removed. In our experience, since 2003, we have found that use of a laparoscopic approach is best for women desiring future fertility and that hysteroscopic resection is best for women whose childbearing is completed.9 Our management is dictated by the patient’s fertility plans, since there is concern that cesarean scar defect in a gravid uterus presents a risk for uterine rupture. The laparoscopic approach allows the defect to be repaired and the integrity of the myometrium restored.9
What are the coding options for cesarean scar defect repair?
Melanie Witt, RN, CPC, COBGC, MA
As the accompanying article discusses, the primary treatment for a cesarean scar defect depends on whether the patient wishes to preserve fertility, but assigning a procedure code for either surgical option will entail reporting an unlisted procedure code.
Under Current Procedural Terminology (CPT) guidelines (which are developed and copyrighted by the American Medical Association), procedure code selected must accurately describe the service/procedure performed rather than just approximate the service. This means that when a procedure-specific code does not exist, an unlisted procedure code that represents the type of surgery, the approach, and the anatomic site needs to be selected.
When an unlisted CPT code is reported, payment is based on the complexity of the surgery, and one way to communicate this to a payer is to provide additional documentation that not only includes the operative report but also suggests one or more existing CPT codes that have a published relative value unit (RVU) that approximates the work involved for the unlisted procedure.
The coding options for hysteroscopic and laparoscopic treatment options are listed below. The comparison codes offered will give the surgeon a range to look at, but the ultimate decision to use one of those suggested, or to choose an entirely different comparison code, is entirely within the control of the physician.
ICD-10-CM diagnostic coding
While the cesarean scar defect is a sequela of cesarean delivery, which is always reported as a secondary code, the choice of a primary diagnosis code can be either a gynecologic and/or an obstetric complication code. The choice may be determined by payer policy, as the use of an obstetric complication may not be accepted with a gynecologic procedure code. From a coding perspective, however, use of all 3 of these codes from the International Classification of Diseases, 10th Revision, Clinical Modification (ICD-10-CM) paints the most accurate description of the defect and its cause:
- N85.8 Other specified noninflammatory disorders of uterus versus
- O34.21 Maternal care for scar from previous cesarean delivery plus
- O94 Sequelae of complication of pregnancy, childbirth, and the puerperium.
Hysteroscopic resection codes:
- 58579 Unlisted hysteroscopy procedure, uterus
- The codes that may most closely approximate the physician work include 58561 (Hysteroscopy, surgical; with removal of leiomyomata) with 15.48 RVUs or 58560 (Hysteroscopy, surgical; with division or resection of intrauterine septum [any method]) with 10.92 RVUs.
Laparoscopic repair codes:
- 58578 Unlisted laparoscopy procedure, uterus
- The codes that may most closely approximate the physician work include 58520 (Hysterorrhaphy, repair of ruptured uterus [nonobstetrical] 24.25 RVUs or 58662 (Laparoscopy, surgical; with fulguration or excision of lesions of the ovary, pelvic viscera, or peritoneal surface by any method) with 20.14 RVUs.
You may also want to report a diagnostic hysteroscopy (code 58555), but keep in mind that payment will depend on documentation that clearly indicates that the use of the hysteroscope was for diagnostic purposes. Use of the hysteroscope to simply identify the surgical site to be repaired via the laparoscope will usually not be reimbursed separately.
Ms. Witt is an independent coding and documentation consultant and former program manager, department of coding and nomenclature, American Congress of Obstetricians and Gynecologists.
The author reports no financial relationships relevant to this article.
Read about techniques for repair.
Techniques for repairing cesarean scar defect
For hysteroscopic resection of a niche, the uterus is distended and the intrauterine defect is visualized hysteroscopically, as seen in FIGURE 2. Using a bipolar or unipolar resectoscope, resect the fibrotic tissue of the defect and endometrial-like glands present within the niche. The goal of this relatively quick procedure is to open up the reservoir and facilitate the complete drainage of menstrual blood, thus alleviating the patient’s symptoms.Postoperatively, follow the patient for symptom resolution, and evaluate for defect resolution with transvaginal ultrasonography.
For a laparoscopic repair, first identify the niche hysteroscopically. At the same time as hysteroscopic examination of the cavity, the defect can be evaluated laparoscopically (FIGURE 4). The light from the hysteroscope can be visualized easily laparoscopically because of the thinned myometrium in the area of the defect. Map out the niche by transvaginally passing a cervical dilator into the defect in the uterine cavity (FIGURE 5). Again, given the thinning of this segment of the uterus, the dilator can be easily visualized laparoscopically. Be cautious when placing this dilator, as there is often overlying bladder. Prevent incidental cystotomy by gently advancing the dilator into the defect only until the niche can be adequately detected.9At this point, develop a bladder flap by opening the vesicovaginal and vesicocervical space, mobilizing the bladder inferiorly (FIGURE 6). With the guide of the dilator mapping out the defect (FIGURE 7), excise the fibrotic edges of the niche with thermal energy (monopolar cautery or CO2 laser) or sharp dissection (FIGURE 8). This leaves healthy myometrial tissue margins. Reapproximate these margins with absorbable suture (2-0 polyglactin 910 [Vicryl]) in an interrupted or running fashion, in 2 layers9 (FIGURE 9). Following the laparoscopic repair, perform hysteroscopic evaluation of the uterine cavity to assure complete resolution of the defect (FIGURE 10). With the hysteroscope in place, perform concurrent laparoscopic assessment of the repair. Check for impermeability by assuring no hysteroscopic fluid escapes at the site of repaired hysterotomy.9
Postoperative care requires following the patient for symptom resolution and counseling regarding future fertility plans. We recommend that patients wait 6 months following the procedure before attempting conception.
When it comes to recommendations regarding preventing cesarean scar defects, additional randomized controlled trials need to be performed to evaluate various surgical techniques. At this time, there is no conclusive evidence that one method of hysterotomy closure is superior to another in preventing cesarean scar defect.
Symptoms often resolve with repair
When a patient with a prior cesarean delivery presents with symptoms of abnormal uterine bleeding, vaginal discharge, dysmenorrhea, dyspareunia, pelvic pain, or infertility that remain unexplained, consider cesarean scar defect as the culprit. Once a diagnosis of niche has been confirmed, the treatment approach should be dictated by the patient’s plans for future fertility. Hysteroscopic resection has been reported to have a 92% to 100% success rate for resolving symptoms of pain and bleeding, while 75% of patients undergoing laparoscopic niche repair for infertility achieved pregnancy.10,11 In our practice, a majority of patients experience symptom relief and go on to carry healthy pregnancies.
Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.
Dr. Camran Nezhat is Director of the Center for Special Minimally Invasive and Robotic Surgery, Palo Alto, California.
Dr. Grace is a Fellow of the Society of Laparoendoscopic Surgeons at the Center for Special Minimally Invasive and Robotic Surgery, Palo Alto.
Ms. Soliemannjad is an Intern at the Center for Special Minimally Invasive and Robotic Surgery, Palo Alto.
Dr. Meshkat Razavi is Fellow at the Center for Special Minimally Invasive and Robotic Surgery, Palo Alto.
Dr. Azadeh Nezhat is Co-Director of the Center for Special Minimally Invasive and Robotic Surgery, Palo Alto.
The authors report no financial relationships relevant to this article.
Dr. Camran Nezhat is Director of the Center for Special Minimally Invasive and Robotic Surgery, Palo Alto, California.
Dr. Grace is a Fellow of the Society of Laparoendoscopic Surgeons at the Center for Special Minimally Invasive and Robotic Surgery, Palo Alto.
Ms. Soliemannjad is an Intern at the Center for Special Minimally Invasive and Robotic Surgery, Palo Alto.
Dr. Meshkat Razavi is Fellow at the Center for Special Minimally Invasive and Robotic Surgery, Palo Alto.
Dr. Azadeh Nezhat is Co-Director of the Center for Special Minimally Invasive and Robotic Surgery, Palo Alto.
The authors report no financial relationships relevant to this article.
Dr. Camran Nezhat is Director of the Center for Special Minimally Invasive and Robotic Surgery, Palo Alto, California.
Dr. Grace is a Fellow of the Society of Laparoendoscopic Surgeons at the Center for Special Minimally Invasive and Robotic Surgery, Palo Alto.
Ms. Soliemannjad is an Intern at the Center for Special Minimally Invasive and Robotic Surgery, Palo Alto.
Dr. Meshkat Razavi is Fellow at the Center for Special Minimally Invasive and Robotic Surgery, Palo Alto.
Dr. Azadeh Nezhat is Co-Director of the Center for Special Minimally Invasive and Robotic Surgery, Palo Alto.
The authors report no financial relationships relevant to this article.
Cesarean delivery is one of the most common surgical procedures in women, with rates of 30% or more in the United States.1 As a result, the rate is rising for cesarean scar defect—the presence of a “niche” at the site of cesarean delivery scar—with the reported prevalence between 24% and 70% in a random population of women with at least one cesarean delivery.2 Other terms for cesarean scar defect include a niche, isthmocele, uteroperitoneal fistula, and diverticulum.1–9
Formation of cesarean scar defect
Cesarean scar defect forms after cesarean delivery, at the site of hysterotomy, on the anterior wall of the uterine isthmus (FIGURE 1). While this is the typical location, the defect has also been found at the endocervical canal and mid-uterine body. Improper healing of the cesarean incision leads to thinning of the anterior uterine wall, which creates an indentation and fluid-filled pouch at the cesarean scar site. The exact reason why a niche develops has not yet been determined; however, there are several hypotheses, broken down by pregnancy-related and patient-related factors. Surgical techniques that may increase the chance of niche development include low (cervical) hysterotomy, single-layer uterine wall closure, use of locking sutures, closure of hysterotomy with endometrial-sparing technique, and multiple cesarean deliveries.3,4 Patients with medical conditions that may impact wound healing (such as diabetes and smoking) may be at increased risk for niche formation.
Viewed hysteroscopically, the defect appears as a concave shape in the anterior uterine wall; to the inexperienced eye, it may resemble a second cavity (FIGURE 2).
Pelvic pain and other serious consequences
The presence of fibrotic tissue in the niche acts like a valve, leading to the accumulation of blood in this reservoir-like area. A niche thus can cause delayed menstruation through the cervix, resulting in abnormal bleeding, pelvic pain, vaginal discharge, dysmenorrhea, dyspareunia, and infertility. Accumulated blood in this area can ultimately degrade cervical mucus and sperm quality, as well as inhibit sperm transport, a proposed mechanism of infertility.5,6 Women with a niche who conceive are at potential risk for cesarean scar ectopic pregnancy, with the embryo implanting in the pouch and subsequently growing and developing improperly.
Read about evaluation and treatment.
Evaluation and treatment
Patients presenting with the symptoms de-scribed above who have had a prior cesarean delivery should be evaluated for a cesarean scar defect.9 The best time to assess for the abnormality is after the patient’s menstrual cycle, when the endometrial lining is at its thinnest and recently menstruated blood has collected in the defect (this can highlight the niche on imaging). Transvaginal ultrasonography (FIGURE 3) or saline-infusion sonohysterogram serve as a first-line test for in-office diagnosis.7 Magnetic resonance imaging (MRI), 3-D ultrasonography, and hysteroscopy are additional useful imaging modalities that can aid in the diagnosis.
Treatments for cesarean scar defect vary dramatically and include hormonal therapy, hysteroscopic resection, vaginal or laparoscopic repair, and hysterectomy. Nonsurgical treatment should be reserved for women who desire a noninvasive approach, as the evidence for symptom resolution is limited.8
To promote fertility and decrease symptoms, the abnormal, fibrotic tissue must be removed. In our experience, since 2003, we have found that use of a laparoscopic approach is best for women desiring future fertility and that hysteroscopic resection is best for women whose childbearing is completed.9 Our management is dictated by the patient’s fertility plans, since there is concern that cesarean scar defect in a gravid uterus presents a risk for uterine rupture. The laparoscopic approach allows the defect to be repaired and the integrity of the myometrium restored.9
What are the coding options for cesarean scar defect repair?
Melanie Witt, RN, CPC, COBGC, MA
As the accompanying article discusses, the primary treatment for a cesarean scar defect depends on whether the patient wishes to preserve fertility, but assigning a procedure code for either surgical option will entail reporting an unlisted procedure code.
Under Current Procedural Terminology (CPT) guidelines (which are developed and copyrighted by the American Medical Association), procedure code selected must accurately describe the service/procedure performed rather than just approximate the service. This means that when a procedure-specific code does not exist, an unlisted procedure code that represents the type of surgery, the approach, and the anatomic site needs to be selected.
When an unlisted CPT code is reported, payment is based on the complexity of the surgery, and one way to communicate this to a payer is to provide additional documentation that not only includes the operative report but also suggests one or more existing CPT codes that have a published relative value unit (RVU) that approximates the work involved for the unlisted procedure.
The coding options for hysteroscopic and laparoscopic treatment options are listed below. The comparison codes offered will give the surgeon a range to look at, but the ultimate decision to use one of those suggested, or to choose an entirely different comparison code, is entirely within the control of the physician.
ICD-10-CM diagnostic coding
While the cesarean scar defect is a sequela of cesarean delivery, which is always reported as a secondary code, the choice of a primary diagnosis code can be either a gynecologic and/or an obstetric complication code. The choice may be determined by payer policy, as the use of an obstetric complication may not be accepted with a gynecologic procedure code. From a coding perspective, however, use of all 3 of these codes from the International Classification of Diseases, 10th Revision, Clinical Modification (ICD-10-CM) paints the most accurate description of the defect and its cause:
- N85.8 Other specified noninflammatory disorders of uterus versus
- O34.21 Maternal care for scar from previous cesarean delivery plus
- O94 Sequelae of complication of pregnancy, childbirth, and the puerperium.
Hysteroscopic resection codes:
- 58579 Unlisted hysteroscopy procedure, uterus
- The codes that may most closely approximate the physician work include 58561 (Hysteroscopy, surgical; with removal of leiomyomata) with 15.48 RVUs or 58560 (Hysteroscopy, surgical; with division or resection of intrauterine septum [any method]) with 10.92 RVUs.
Laparoscopic repair codes:
- 58578 Unlisted laparoscopy procedure, uterus
- The codes that may most closely approximate the physician work include 58520 (Hysterorrhaphy, repair of ruptured uterus [nonobstetrical] 24.25 RVUs or 58662 (Laparoscopy, surgical; with fulguration or excision of lesions of the ovary, pelvic viscera, or peritoneal surface by any method) with 20.14 RVUs.
You may also want to report a diagnostic hysteroscopy (code 58555), but keep in mind that payment will depend on documentation that clearly indicates that the use of the hysteroscope was for diagnostic purposes. Use of the hysteroscope to simply identify the surgical site to be repaired via the laparoscope will usually not be reimbursed separately.
Ms. Witt is an independent coding and documentation consultant and former program manager, department of coding and nomenclature, American Congress of Obstetricians and Gynecologists.
The author reports no financial relationships relevant to this article.
Read about techniques for repair.
Techniques for repairing cesarean scar defect
For hysteroscopic resection of a niche, the uterus is distended and the intrauterine defect is visualized hysteroscopically, as seen in FIGURE 2. Using a bipolar or unipolar resectoscope, resect the fibrotic tissue of the defect and endometrial-like glands present within the niche. The goal of this relatively quick procedure is to open up the reservoir and facilitate the complete drainage of menstrual blood, thus alleviating the patient’s symptoms.Postoperatively, follow the patient for symptom resolution, and evaluate for defect resolution with transvaginal ultrasonography.
For a laparoscopic repair, first identify the niche hysteroscopically. At the same time as hysteroscopic examination of the cavity, the defect can be evaluated laparoscopically (FIGURE 4). The light from the hysteroscope can be visualized easily laparoscopically because of the thinned myometrium in the area of the defect. Map out the niche by transvaginally passing a cervical dilator into the defect in the uterine cavity (FIGURE 5). Again, given the thinning of this segment of the uterus, the dilator can be easily visualized laparoscopically. Be cautious when placing this dilator, as there is often overlying bladder. Prevent incidental cystotomy by gently advancing the dilator into the defect only until the niche can be adequately detected.9At this point, develop a bladder flap by opening the vesicovaginal and vesicocervical space, mobilizing the bladder inferiorly (FIGURE 6). With the guide of the dilator mapping out the defect (FIGURE 7), excise the fibrotic edges of the niche with thermal energy (monopolar cautery or CO2 laser) or sharp dissection (FIGURE 8). This leaves healthy myometrial tissue margins. Reapproximate these margins with absorbable suture (2-0 polyglactin 910 [Vicryl]) in an interrupted or running fashion, in 2 layers9 (FIGURE 9). Following the laparoscopic repair, perform hysteroscopic evaluation of the uterine cavity to assure complete resolution of the defect (FIGURE 10). With the hysteroscope in place, perform concurrent laparoscopic assessment of the repair. Check for impermeability by assuring no hysteroscopic fluid escapes at the site of repaired hysterotomy.9
Postoperative care requires following the patient for symptom resolution and counseling regarding future fertility plans. We recommend that patients wait 6 months following the procedure before attempting conception.
When it comes to recommendations regarding preventing cesarean scar defects, additional randomized controlled trials need to be performed to evaluate various surgical techniques. At this time, there is no conclusive evidence that one method of hysterotomy closure is superior to another in preventing cesarean scar defect.
Symptoms often resolve with repair
When a patient with a prior cesarean delivery presents with symptoms of abnormal uterine bleeding, vaginal discharge, dysmenorrhea, dyspareunia, pelvic pain, or infertility that remain unexplained, consider cesarean scar defect as the culprit. Once a diagnosis of niche has been confirmed, the treatment approach should be dictated by the patient’s plans for future fertility. Hysteroscopic resection has been reported to have a 92% to 100% success rate for resolving symptoms of pain and bleeding, while 75% of patients undergoing laparoscopic niche repair for infertility achieved pregnancy.10,11 In our practice, a majority of patients experience symptom relief and go on to carry healthy pregnancies.
Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.
Cesarean delivery is one of the most common surgical procedures in women, with rates of 30% or more in the United States.1 As a result, the rate is rising for cesarean scar defect—the presence of a “niche” at the site of cesarean delivery scar—with the reported prevalence between 24% and 70% in a random population of women with at least one cesarean delivery.2 Other terms for cesarean scar defect include a niche, isthmocele, uteroperitoneal fistula, and diverticulum.1–9
Formation of cesarean scar defect
Cesarean scar defect forms after cesarean delivery, at the site of hysterotomy, on the anterior wall of the uterine isthmus (FIGURE 1). While this is the typical location, the defect has also been found at the endocervical canal and mid-uterine body. Improper healing of the cesarean incision leads to thinning of the anterior uterine wall, which creates an indentation and fluid-filled pouch at the cesarean scar site. The exact reason why a niche develops has not yet been determined; however, there are several hypotheses, broken down by pregnancy-related and patient-related factors. Surgical techniques that may increase the chance of niche development include low (cervical) hysterotomy, single-layer uterine wall closure, use of locking sutures, closure of hysterotomy with endometrial-sparing technique, and multiple cesarean deliveries.3,4 Patients with medical conditions that may impact wound healing (such as diabetes and smoking) may be at increased risk for niche formation.
Viewed hysteroscopically, the defect appears as a concave shape in the anterior uterine wall; to the inexperienced eye, it may resemble a second cavity (FIGURE 2).
Pelvic pain and other serious consequences
The presence of fibrotic tissue in the niche acts like a valve, leading to the accumulation of blood in this reservoir-like area. A niche thus can cause delayed menstruation through the cervix, resulting in abnormal bleeding, pelvic pain, vaginal discharge, dysmenorrhea, dyspareunia, and infertility. Accumulated blood in this area can ultimately degrade cervical mucus and sperm quality, as well as inhibit sperm transport, a proposed mechanism of infertility.5,6 Women with a niche who conceive are at potential risk for cesarean scar ectopic pregnancy, with the embryo implanting in the pouch and subsequently growing and developing improperly.
Read about evaluation and treatment.
Evaluation and treatment
Patients presenting with the symptoms de-scribed above who have had a prior cesarean delivery should be evaluated for a cesarean scar defect.9 The best time to assess for the abnormality is after the patient’s menstrual cycle, when the endometrial lining is at its thinnest and recently menstruated blood has collected in the defect (this can highlight the niche on imaging). Transvaginal ultrasonography (FIGURE 3) or saline-infusion sonohysterogram serve as a first-line test for in-office diagnosis.7 Magnetic resonance imaging (MRI), 3-D ultrasonography, and hysteroscopy are additional useful imaging modalities that can aid in the diagnosis.
Treatments for cesarean scar defect vary dramatically and include hormonal therapy, hysteroscopic resection, vaginal or laparoscopic repair, and hysterectomy. Nonsurgical treatment should be reserved for women who desire a noninvasive approach, as the evidence for symptom resolution is limited.8
To promote fertility and decrease symptoms, the abnormal, fibrotic tissue must be removed. In our experience, since 2003, we have found that use of a laparoscopic approach is best for women desiring future fertility and that hysteroscopic resection is best for women whose childbearing is completed.9 Our management is dictated by the patient’s fertility plans, since there is concern that cesarean scar defect in a gravid uterus presents a risk for uterine rupture. The laparoscopic approach allows the defect to be repaired and the integrity of the myometrium restored.9
What are the coding options for cesarean scar defect repair?
Melanie Witt, RN, CPC, COBGC, MA
As the accompanying article discusses, the primary treatment for a cesarean scar defect depends on whether the patient wishes to preserve fertility, but assigning a procedure code for either surgical option will entail reporting an unlisted procedure code.
Under Current Procedural Terminology (CPT) guidelines (which are developed and copyrighted by the American Medical Association), procedure code selected must accurately describe the service/procedure performed rather than just approximate the service. This means that when a procedure-specific code does not exist, an unlisted procedure code that represents the type of surgery, the approach, and the anatomic site needs to be selected.
When an unlisted CPT code is reported, payment is based on the complexity of the surgery, and one way to communicate this to a payer is to provide additional documentation that not only includes the operative report but also suggests one or more existing CPT codes that have a published relative value unit (RVU) that approximates the work involved for the unlisted procedure.
The coding options for hysteroscopic and laparoscopic treatment options are listed below. The comparison codes offered will give the surgeon a range to look at, but the ultimate decision to use one of those suggested, or to choose an entirely different comparison code, is entirely within the control of the physician.
ICD-10-CM diagnostic coding
While the cesarean scar defect is a sequela of cesarean delivery, which is always reported as a secondary code, the choice of a primary diagnosis code can be either a gynecologic and/or an obstetric complication code. The choice may be determined by payer policy, as the use of an obstetric complication may not be accepted with a gynecologic procedure code. From a coding perspective, however, use of all 3 of these codes from the International Classification of Diseases, 10th Revision, Clinical Modification (ICD-10-CM) paints the most accurate description of the defect and its cause:
- N85.8 Other specified noninflammatory disorders of uterus versus
- O34.21 Maternal care for scar from previous cesarean delivery plus
- O94 Sequelae of complication of pregnancy, childbirth, and the puerperium.
Hysteroscopic resection codes:
- 58579 Unlisted hysteroscopy procedure, uterus
- The codes that may most closely approximate the physician work include 58561 (Hysteroscopy, surgical; with removal of leiomyomata) with 15.48 RVUs or 58560 (Hysteroscopy, surgical; with division or resection of intrauterine septum [any method]) with 10.92 RVUs.
Laparoscopic repair codes:
- 58578 Unlisted laparoscopy procedure, uterus
- The codes that may most closely approximate the physician work include 58520 (Hysterorrhaphy, repair of ruptured uterus [nonobstetrical] 24.25 RVUs or 58662 (Laparoscopy, surgical; with fulguration or excision of lesions of the ovary, pelvic viscera, or peritoneal surface by any method) with 20.14 RVUs.
You may also want to report a diagnostic hysteroscopy (code 58555), but keep in mind that payment will depend on documentation that clearly indicates that the use of the hysteroscope was for diagnostic purposes. Use of the hysteroscope to simply identify the surgical site to be repaired via the laparoscope will usually not be reimbursed separately.
Ms. Witt is an independent coding and documentation consultant and former program manager, department of coding and nomenclature, American Congress of Obstetricians and Gynecologists.
The author reports no financial relationships relevant to this article.
Read about techniques for repair.
Techniques for repairing cesarean scar defect
For hysteroscopic resection of a niche, the uterus is distended and the intrauterine defect is visualized hysteroscopically, as seen in FIGURE 2. Using a bipolar or unipolar resectoscope, resect the fibrotic tissue of the defect and endometrial-like glands present within the niche. The goal of this relatively quick procedure is to open up the reservoir and facilitate the complete drainage of menstrual blood, thus alleviating the patient’s symptoms.Postoperatively, follow the patient for symptom resolution, and evaluate for defect resolution with transvaginal ultrasonography.
For a laparoscopic repair, first identify the niche hysteroscopically. At the same time as hysteroscopic examination of the cavity, the defect can be evaluated laparoscopically (FIGURE 4). The light from the hysteroscope can be visualized easily laparoscopically because of the thinned myometrium in the area of the defect. Map out the niche by transvaginally passing a cervical dilator into the defect in the uterine cavity (FIGURE 5). Again, given the thinning of this segment of the uterus, the dilator can be easily visualized laparoscopically. Be cautious when placing this dilator, as there is often overlying bladder. Prevent incidental cystotomy by gently advancing the dilator into the defect only until the niche can be adequately detected.9At this point, develop a bladder flap by opening the vesicovaginal and vesicocervical space, mobilizing the bladder inferiorly (FIGURE 6). With the guide of the dilator mapping out the defect (FIGURE 7), excise the fibrotic edges of the niche with thermal energy (monopolar cautery or CO2 laser) or sharp dissection (FIGURE 8). This leaves healthy myometrial tissue margins. Reapproximate these margins with absorbable suture (2-0 polyglactin 910 [Vicryl]) in an interrupted or running fashion, in 2 layers9 (FIGURE 9). Following the laparoscopic repair, perform hysteroscopic evaluation of the uterine cavity to assure complete resolution of the defect (FIGURE 10). With the hysteroscope in place, perform concurrent laparoscopic assessment of the repair. Check for impermeability by assuring no hysteroscopic fluid escapes at the site of repaired hysterotomy.9
Postoperative care requires following the patient for symptom resolution and counseling regarding future fertility plans. We recommend that patients wait 6 months following the procedure before attempting conception.
When it comes to recommendations regarding preventing cesarean scar defects, additional randomized controlled trials need to be performed to evaluate various surgical techniques. At this time, there is no conclusive evidence that one method of hysterotomy closure is superior to another in preventing cesarean scar defect.
Symptoms often resolve with repair
When a patient with a prior cesarean delivery presents with symptoms of abnormal uterine bleeding, vaginal discharge, dysmenorrhea, dyspareunia, pelvic pain, or infertility that remain unexplained, consider cesarean scar defect as the culprit. Once a diagnosis of niche has been confirmed, the treatment approach should be dictated by the patient’s plans for future fertility. Hysteroscopic resection has been reported to have a 92% to 100% success rate for resolving symptoms of pain and bleeding, while 75% of patients undergoing laparoscopic niche repair for infertility achieved pregnancy.10,11 In our practice, a majority of patients experience symptom relief and go on to carry healthy pregnancies.
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