Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Radical Hysterectomy

  • Author: Jori S Carter, MD, MS; Chief Editor: Warner K Huh, MD  more...
 
Updated: Apr 16, 2015
 

History of the Procedure

Clark performed the first radical hysterectomy for cervical cancer at Johns Hopkins Hospital in 1895. In 1898, Wertheim, a Viennese physician, developed the radical total hysterectomy with removal of the pelvic lymph nodes and the parametrium. In 1905, Wertheim reported the outcomes of his first 270 patients. The operative mortality rate was 18%, and the major morbidity rate was 31%.

In 1901, Schauta described the radical vaginal hysterectomy and reported a lower operative mortality rate than the abdominal approach. In the late 20th century, radiation therapy became the favored approach because of the high mortality and morbidity of the surgical approach.

In 1944, Meigs repopularized the surgical approach when he developed a modified Wertheim operation with removal of all pelvic nodes (the Wertheim-Clark plus Taussig operation). Meigs reported a survival rate of 75% for patients with stage I disease and demonstrated an operative mortality rate of 1% when these procedures were performed by a specially trained gynecologist. Throughout the remainder of the 20th century, various modifications have been made for this radical procedure, especially in light of improvements in the areas of anesthesia, intensive care, antibiotics, and blood product transfusion science. Finally, the concurrent decrease in the incidence of invasive cervical cancer, the most common rationale for this procedure, has declined over the past several decades and has led to more conservative procedures (ie, conization for early-stage disease) or nonsurgical modalities (ie, radiotherapy).[1]

Next

Problem

Radical hysterectomy was initially developed as a surgical treatment for cervical cancer due to the absence of other modalities for treatment. Squamous cell carcinoma and adenocarcinoma are the most common variants that arise in the cervix. The uterine cervix comprises the distal third of the uterus. The cervix projects into the vagina and continues up to the lower uterine segment. The portion of the cervix exposed to the vagina is most commonly covered with squamous epithelium. The squamous epithelium transitions to columnar epithelium at the squamocolumnar junction, which is also known as the transformation zone. It is this vulnerable area of the cervix, where columnar cells are actively undergoing metaplastic change to squamous epithelium, in which the majority of cervical malignancies occur.

Previous
Next

Epidemiology

Frequency

In 2009, there were 12,357 cervical cancer cases in the United States, and 3,909 women died from the disease.[2] The death rate from cervical cancer has decreased dramatically since the American Cancer Society recommended the use of the Papanicolaou test (Pap test) for cervical cancer screening in the mid 1940s. Over the next 40 years, the death rate from cervical cancer decreased by more than 70% because preinvasive lesions and cervical cancers were detected at an earlier stage.

Worldwide, cervical cancer is the third most common cancer in women. More than 85% of the global burden occurs in developing countries.[3] The lack of a screening cytology program (ie, Pap test) has resulted in this significant problem in the area of women's health. Thus, the most effective strategy of prevention of this malignancy due to the detection of a preinvasive phase is negated and most cases of cervical cancer are not diagnosed until they are advanced in stage and the patient becomes symptomatic.

Previous
Next

Etiology

Multiple factors have been associated with the development of cervical cancer. This malignancy most commonly arises at the squamocolumnar junction, where cells are most actively undergoing metaplastic change from columnar epithelium to squamous epithelium.

Infection with human papillomavirus (HPV) is detected in more than 99% of cervical cancers. Although more than 70 different subtypes of HPV have been identified, women infected with high-risk subtypes have an increased risk of developing dysplasia and a subsequent malignancy. The most common high-risk subtypes are HPV-16 and HPV-18, which account for 70% of cervical cancers in the United States.[4] The E6 protein product of these high-risk HPVs binds to the tumor suppressor protein p53, which is thought to disrupt the p53-dependent control of the cell cycle.[5] The E7 protein causes an inactivation of the tumor suppressor retinoblastoma gene (Rb) via its interaction with the Rb protein, whose normal function is seen with the negative control of cell growth.[6]

Risk factors associated with HPV infection include multiple sexual partners, history of other sexually transmitted infections, high parity, immunosuppression, and cigarette smoking.[7]

Cigarette smoking has been associated with an increased severity of dysplasia and squamous cell carcinoma in women with underlying HPV infection.[8] Nicotine, co-nicotine, hydrocarbons, and tars, carcinogenic breakdown products of cigarette smoke, have been seen concentrated in cervical secretions.[9]

The effect of oral contraceptive use on the risk of cervical cancer is controversial because it is difficult separate sexual behavior from contraceptive use in studies. However, several studies have demonstrated that long-term oral contraceptive use resulted in an increased incidence of cervical cancer.[7, 10, 11] To adequately demonstrate an association, such studies must control for sexual behavior and for the interval of last cervical screening in all study groups. Finally, there are no proven benefits from the cessation of oral contraceptives in the clinical management of cervical dysplasia.

Immunosuppression, either induced or acquired (eg, from HIV infection), is a risk factor for the development of significant preinvasive disease for cervical cancer.[12] In the era of organ transplantation and chronic diseases that require systemic immunosuppression, there exists a cohort of patients with increased risk for the development of cervical cancer.

Sexually transmitted diseases, such as those caused by Chlamydia trachomatis, Neisseria gonorrhoeae, herpes simplex virus, and Trichomonas vaginalis, may be associated with preinvasive disease of the cervix and ultimately a risk for malignancy.[13] With the evidence of HPV as an etiologic agent, such diseases may represent more than a co-infective process, and, in fact, they may be a cofactor in the ability for the establishment of the viral infection via disruption of epithelial integrity.

Previous
Next

Pathophysiology

Squamous cell carcinoma is the most common histologic variant of cervical cancer. HPV is now known to be definitively associated with cervical carcinogenesis and its precancerous precursors, low-grade squamous intraepithelial lesions (LSIL) and high-grade squamous intraepithelial lesions (HSIL). The molecular basis for the malignant potential of these viruses has been determined in the dysregulation of the cell cycle by the viral oncogenes E6 and E7.[14]

The progression rate of mild dysplasia to a severe dysplasia or worse is approximately 1% per year; high-grade lesions (moderate and severe dysplasia) have demonstrated a progression to a worsening lesion in approximately 16-36% of cases. Therefore, the treatment strategy for a high-grade lesion usually involves removal of the lesion, but a colposcopically confirmed low-grade lesion can be conservatively managed. The progression time to an invasive malignancy is variable and can span a period of 1 year to several decades.

Adenocarcinoma, the second most common histologic type of cervical cancer, arises from the subcolumnar reserve cells of the columnar endocervical epithelium. A strong association has been demonstrated between cervical adenocarcinoma and HPV-18. The overall incidence for this variant has increased and is associated with women younger than 35 years. Approximately 15% will exhibit no visible lesion due to its endocervical point of origin. Adenocarcinoma in situ of the cervix is strongly associated with an underlying squamous dysplastic lesion and/or cancer in more than 50% of cases, thus making this a high-risk cytologic finding.

Other histologic findings of malignancy involving the cervix include minimal-deviation adenocarcinoma, papillary villoglandular adenocarcinoma, endometrioid adenocarcinoma, serous adenocarcinoma, mesonephric adenocarcinoma, glassy cell carcinoma, adenoid basal carcinoma, basal cell carcinoma, verrucous carcinoma, clear cell adenocarcinoma, adenosquamous carcinoma, adenoid cystic carcinoma, adenoid basal epithelioma, and neuroendocrine tumors.[15] Rarely, cervical lesions result from direct invasion by advanced endometrial, vaginal, bladder, urethra, or colon cancers.

Previous
Next

Presentation

Patients with early-stage cervical cancer are relatively asymptomatic; these cases are usually detected via cytologic screening. With the advancement of the disease, signs and symptoms of abnormal bleeding and vaginal discharge may occur. Postcoital bleeding may be the first reported sign in sexually active women; in women who are not sexually active, cervical cancer may not produce clinical manifestations, such as postmenopausal or abnormal uterine bleeding, until the malignancy is in an advanced stage.

As tumors enlarge and outgrow their blood supply, they may become necrotic and produce a malodorous discharge. Larger tumors may cause size-related symptoms such as urinary frequency or retention, rectal pressure, constipation, neurologic symptoms (ie, sciatic pain due to local extension), lower extremity pain, and swelling. Urinary or fecal incontinence due to a local tumor eroding into the bowel or bladder may be the symptom that prompts patients to seek care. Symptomatic anemia may be encountered due to persistent bleeding of the cervical lesion.

The most common sign of cervical cancer is a grossly visible lesion upon a vaginal speculum examination. An exophytic or ulcerative lesion may be obvious during the clinical examination, but an endocervical lesion may remain occult and demonstrate a normal-appearing ectocervical mucosa in the presence of a firm, enlarged cervix. With microinvasive cervical cancer, colposcopic evaluation may provide the means of detection. Colposcopic detection of atypical vessels that demonstrate irregular distribution, unusual caliber, and acute angles are associated with an early invasive tumor of the ectocervix. Presence of any ulcerative or erosive lesion warrants a histologic evaluation by biopsy despite a normal cytologic (Pap test) antecedent result.

The size of the cervix is most accurately determined via a rectal examination, which can also determine the involvement of the adjacent parametrial tissue and/or pelvic side wall. Endocervical lesions expanding or prolapsing through the cervical os can be mistaken for cervical or prolapsing leiomyomata. Biopsy of any abnormally firm or grossly abnormal lesions of the cervix should be undertaken.

The remainder of the physical examination for a patient suspected of a diagnosis of cervical cancer should include a careful evaluation of the vagina, vulva, and rectum for the presence of locally advanced disease. In addition, surveillance of the inguinal, femoral, and supraclavicular lymph nodes by careful palpation should be performed in search of overt evidence of advanced distal disease.

Previous
Next

Indications

Radical hysterectomy is indicated for patients with International Federation of Gynecology and Obstetrics (FIGO) stage IA2-IIA cervical cancer who are medically fit enough to tolerate an aggressive surgical approach and wish to avoid the long-term adverse effects of radiation therapy. Prospective randomized trials have validated equal curative rates from radical surgery and radiotherapy (overall survival similar at 83%).[16]

Increased complication rates are noted with combined radical therapies (ie, requirement for adjuvant radiotherapy). However, adjuvant radiotherapy is recommended after radical hysterectomy if there is parametrial involvement, positive surgical margins, or pelvic lymph node metastases, and it should be considered if there is a combination of lymphovascular space invasion, tumor size greater than 2 cm, and deep invasion.[17, 18]

Currently, with stage IB disease, approximately 54% of patients with tumors 4 cm or less in size (stage IB1) and 84% with tumors greater than 4 cm (stage IB2) will require postoperative adjuvant radiotherapy. Recent encouraging data for improved outcomes with combined chemoradiation therapy and the increased morbidity noted with the combined surgical and adjuvant radiotherapy has brought into question the role of radical surgery with stage IB2 and stage IIA. However, a review of survival in 4,885 women with stage IB1-IIA cervical cancer in the Surveillance, Epidemiology, and End Results database showed that radical hysterectomy is superior to primary radiation for the treatment of cervical cancer lesions smaller than 6 cm, and especially for those smaller than 4 cm.[19]

Young patients who desire ovarian preservation and retention of a functional, nonirradiated vagina are ideal candidates for this procedure. Patients who have relative or absolute contraindications to radiation therapy, such as a pelvic kidney or a history of pelvic abscess or pelvic irradiation, should be afforded surgical treatment. In the setting of recurrence, radical hysterectomy has been performed for very small, centrally recurrent or persistent cancers after radiation therapy. Radical hysterectomy is also indicated for other disease processes that involve the cervix (eg, primary upper vaginal carcinoma, endometrial cancer with involvement of the lower uterine segment or cervix).

Previous
Next

Relevant Anatomy

Knowledge of the relevant anatomy of the pelvis is important. Radical hysterectomy includes removal of the uterus with parametrial and paracervical tissue, proximal vagina, and proximal uterosacral ligaments. The uterine artery is transected at its origin, lateral to the ureter. In order to complete this dissection, the ureter is unroofed from the paracervical tunnel until the point of entry into the bladder. In order to resect the parametrial and paracervical tissue and unroof the ureter, the paravesical and pararectal spaces must be developed. The pertinent boundaries are the paravesical space and the pararectal space.

The paravesical space is bordered as follows:

  • Medially by the obliterated umbilical artery
  • Laterally by the obturator internus muscle
  • Posteriorly by the cardinal ligament
  • Anteriorly by the pubic symphysis

The pararectal space is bordered as follows:

  • Medially by the rectum
  • Laterally by the hypogastric artery (the internal iliac artery)
  • Posteriorly by the sacrum
  • Anteriorly by the cardinal ligament

The pelvic lymphadenectomy is performed in a systematic fashion. The anatomy of this procedure involves removal of all nodal tissue and skeletonization of all vessels from the mid portion of the common iliac vessels and the internal and external iliac vessels to the level of the circumflex iliac vein distally, from the mid portion of the psoas muscle laterally to the ureter medially, with preservation of the genitofemoral nerve on the psoas muscle. The nodal tissue in the obturator fossa is removed from above the obturator nerve to the external iliac vein superiorly and laterally to the pelvic sidewall. Care must be taken in the obturator fossa to avoid injury to the obturator nerve or to an accessory obturator vein, which is present in approximately 20% of patients.

Previous
Next

Contraindications

Contraindications to radical hysterectomy include patients who are medically infirm and those who refuse surgical treatment. Because between one third and two thirds of surgical patients require transfusion, radiation therapy should be considered for patients whose religious or personal beliefs prohibit blood product transfusion. As with any other surgery, careful preoperative risk assessment must be performed. A relative contraindication concerns the possible requirements for adjuvant radiotherapy (ie, stage IB2/IIA or intraoperative findings of locally advanced disease with overt parametrial involvement or grossly positive pelvic or para-aortic lymph nodes).

Previous
 
 
Contributor Information and Disclosures
Author

Jori S Carter, MD, MS Assistant Professor, Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, Virginia Commonwealth University School of Medicine

Jori S Carter, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American College of Obstetricians and Gynecologists, Society of Gynecologic Oncology, Association of Women Surgeons, International Society for Magnetic Resonance in Medicine, American Society of Clinical Oncology

Disclosure: Nothing to disclose.

Chief Editor

Warner K Huh, MD Professor, Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, Senior Scientist, Comprehensive Cancer Center, University of Alabama School of Medicine

Warner K Huh, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American College of Surgeons, Massachusetts Medical Society, Society of Gynecologic Oncology, American Society of Clinical Oncology

Disclosure: I have received consulting fees for: Merck; THEVAX.

Acknowledgements

Margarett C Ellison, MD Consulting Staff, Kaiser Permanente, Los Angeles Medical Center

Disclosure: Nothing to disclose.

Jeffrey B Garris, MD Chief, Assistant Professor, Department of Obstetrics and Gynecology, Division of Urogynecology and Reconstructive Pelvic Surgery, Tulane University School of Medicine

Jeffrey B Garris, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Institute of Ultrasound in Medicine, American Medical Association, American Urological Association, Association of Professors of Gynecology and Obstetrics, Louisiana State Medical Society, Royal Society of Medicine, and Sigma Xi

Disclosure: Nothing to disclose.

Michael J Sundborg, MD, FACOG Assistant Professor, Department of Obstetrics and Gynecology, Uniformed Services University of the Health Sciences, F Hebert School of Medicine; Chief and Principle Investigator, Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, Brooke Army Medical Center

Michael J Sundborg, MD, FACOG is a member of the following medical societies: Alpha Omega Alpha, American Association of Gynecologic Laparoscopists, American College of Obstetricians and Gynecologists, American Medical Association, Association of Professors of Gynecology and Obstetrics, and Society of Gynecologist Oncologists

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. O'Dowd MJ, Philipp EE. The History of Obstetrics and Gynaecology. Vol 1. New York, NY: Parthenon Publishing Group; 1994:. 543-70.

  2. Department of Health and Human Services, Centers for Disease Control and Prevention, and National Cancer Institute. U.S. Cancer Statistics Working Group. United States Cancer Statistics: 1999–2009 Incidence and Mortality Web-based Report. Centers for Disease Control and Prevention. Available at http://www.cdc.gov/uscs. Accessed: January 7, 13.

  3. American Cancer Society. American Cancer Society. Global Cancer Facts & Figures. 2nd ed. Atlanta, Ga: American Cancer Society; 2011.

  4. Bosch FX, de Sanjose S. Chapter 1: Human papillomavirus and cervical cancer: burden and assessment of causality. J Natl Cancer Inst Monogr. 2003. 31:3-13. [Medline].

  5. Scheffner M, Werness BA, Huibregtse JM, et al. The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53. Cell. 1990 Dec 21. 63(6):1129-36. [Medline].

  6. Jones RE, Wegrzyn RJ, Patrick DR, et al. Identification of HPV-16 E7 peptides that are potent antagonists of E7 binding to the retinoblastoma suppressor protein. J Biol Chem. 1990 Aug 5. 265(22):12782-5. [Medline].

  7. Castellsague X, Munoz N. Chapter 3: Cofactors in human papillomavirus carcinogenesis--role of parity, oral contraceptives, and tobacco smoking. J Natl Cancer Inst Monogr. 2003. 20-8. [Medline].

  8. Louie KS, Castellsague X, de Sanjose S, et al. Smoking and passive smoking in cervical cancer risk: pooled analysis of couples from the IARC multicentric case-control studies. Cancer Epidemiol Biomarkers Prev. 2011. 20(7):1379-90. [Medline].

  9. McCann MF, Irwin DE, Walton LA, Hulka BS, Morton JL, Axelrad CM. Nicotine and cotinine in the cervical mucus of smokers, passive smokers, and nonsmokers. Cancer Epidemiol Biomarkers Prev. 1992 Jan-Feb. 1(2):125-9. [Medline].

  10. Smith JS, Green J, Berrington de Gonzalez A, Appleby P, Peto J, Plummer M, et al. Cervical cancer and use of hormonal contraceptives: a systematic review. Lancet. 2003 Apr 5. 361(9364):1159-67. [Medline].

  11. Castle PE. Beyond human papillomavirus: the cervix, exogenous secondary factors, and the development of cervical precancer and cancer. J Low Genit Tract Dis. 2004 Jul. 8(3):224-30. [Medline].

  12. Lehtovirta P, Finne P, Nieminen P, et al. Prevalence and risk factors of squamous intraepithelial lesions of the cervix among HIV-infected women: a long-term follow-up study in a low-prevalence population. Int J STD AIDS. 2006. 17(12):831-4. [Medline].

  13. Anttila T, Saikku P, Koskela P, Bloigu A, Dillner J, Ikäheimo I. Serotypes of Chlamydia trachomatis and risk for development of cervical squamous cell carcinoma. JAMA. 2001 Jan 3. 285(1):47-51. [Medline].

  14. Ibeanu OA. Molecular pathogenesis of cervical cancer. Cancer Biol Ther. 2011 Feb 1. 11(3):295-306. [Medline].

  15. Randall ME, Michael H, Long 3rd H, Tedjarati S. Uterine cervix. Barakat RR, Markman M, Randall ME. Principles and Practice of Gynecologic Oncology. 5th ed. 2009. 623-682.

  16. Landoni F, Maneo A, Colombo A, et al. Randomised study of radical surgery versus radiotherapy for stage Ib-IIa cervical cancer. Lancet. 1997 Aug 23. 350(9077):535-40. [Medline].

  17. Peters WA, Liu PY, Barrett RJ, et al. Concurrent chemotherapy and pelvic radiation therapy compared with pelvic radiation therapy alone as adjuvant therapy after radical surgery in high-risk early-stage cancer of the cervix. J Clin Oncol. 2000 Apr. 18(8):1606-13. [Medline].

  18. Sedlis A, Bundy BN, Rotman MZ, Lentz SS, Muderspach LI, Zaino RJ. A randomized trial of pelvic radiation therapy versus no further therapy in selected patients with stage IB carcinoma of the cervix after radical hysterectomy and pelvic lymphadenectomy: A Gynecologic Oncology Group Study. Gynecol Oncol. 1999 May. 73(2):177-83. [Medline].

  19. Bansal N, Herzog TJ, Shaw RE, Burke WM, Deutsch I, Wright JD. Primary therapy for early-stage cervical cancer: radical hysterectomy vs radiation. Am J Obstet Gynecol. 2009 Nov. 201(5):485.e1-9. [Medline].

  20. Scheidler J, Hricak H, Yu KK, et al. Radiological evaluation of lymph node metastases in patients with cervical cancer. A meta-analysis. JAMA. 1997 Oct 1. 278(13):1096-101. [Medline].

  21. Mitchell DG, Snyder B, Coakley F, Reinhold C, Thomas G, Amendola M. Early invasive cervical cancer: tumor delineation by magnetic resonance imaging, computed tomography, and clinical examination, verified by pathologic results, in the ACRIN 6651/GOG 183 Intergroup Study. J Clin Oncol. 2006 Dec 20. 24(36):5687-94. [Medline].

  22. Sahdev A, Sohaib SA, Wenaden AE, Shepherd JH, Reznek RH. The performance of magnetic resonance imaging in early cervical carcinoma: a long-term experience. Int J Gynecol Cancer. 2007 May-Jun. 17(3):629-36. [Medline].

  23. Rajendran JG, Greer BE. Expanding role of positron emission tomography in cancer of the uterine cervix. J Natl Compr Canc Netw. 2006 May. 4(5):463-9. [Medline].

  24. Rose PG, Adler LP, Rodriguez M, Faulhaber PF, Abdul-Karim FW, Miraldi F. Positron emission tomography for evaluating para-aortic nodal metastasis in locally advanced cervical cancer before surgical staging: a surgicopathologic study. J Clin Oncol. 1999 Jan. 17(1):41-5. [Medline].

  25. Lai CH, Yen TC, Ng KK. Surgical and radiologic staging of cervical cancer. Curr Opin Obstet Gynecol. 2010 Feb. 22(1):15-20. [Medline].

  26. Pecorelli S, Zigliani L, Odicino F. Revised FIGO staging for carcinoma of the cervix. Int J Gynaecol Obstet. 2009 May. 105(2):107-8. [Medline].

  27. Doll KM, Donnelly E, Helenowski I, Rosenbloom L, Small W Jr, Schink JC, et al. Radical Hysterectomy Compared With Primary Radiation for Treatment of Stage IB1 Cervix Cancer. Am J Clin Oncol. 2012 Sep 18. [Medline].

  28. Uzan C, Merlot B, Gouy S, Belghiti J, Haie-Meder C, Nickers P, et al. Laparoscopic Radical Hysterectomy after Preoperative Brachytherapy for Stage IB1 Cervical Cancer: Feasibility, Results, and Surgical Implications in a Large Bicentric Study of 162 Consecutive Cases. Ann Surg Oncol. 2012 Aug 30. [Medline].

  29. Fanfani F, Fagotti A, Ferrandina G, Raspagliesi F, Ditto A, Cerrotta AM, et al. Neoadjuvant chemoradiation followed by radical hysterectomy in FIGO Stage IIIB cervical cancer: feasibility, complications, and clinical outcome. Int J Gynecol Cancer. 2009 Aug. 19(6):1119-24. [Medline].

  30. Guo L, Liu X, Wang L, et al. Outcome of International Federation of Gynecology and Obstetrics stage IIB cervical cancer from 2003 to 2012: an evaluation of treatments and prognosis: a retrospective study. Int J Gynecol Cancer. 2015 Apr 10. [Medline].

  31. Takatori E, Shoji T, Omi H, et al. Analysis of prognostic factors for patients with bulky squamous cell carcinoma of the uterine cervix who underwent neoadjuvant chemotherapy followed by radical hysterectomy. Int J Clin Oncol. 2015 Apr. 20(2):345-50. [Medline].

  32. Plante M. Vaginal radical trachelectomy: an update. Gynecol Oncol. 2008 Nov. 111(2 Suppl):S105-10. [Medline].

  33. Plante M, Renaud MC, Hoskins IA, Roy M. Vaginal radical trachelectomy: a valuable fertility-preserving option in the management of early-stage cervical cancer. A series of 50 pregnancies and review of the literature. Gynecol Oncol. 2005 Jul. 98(1):3-10. [Medline].

  34. Patsner B. Radical abdominal hysterectomy using the ENDO-GIA stapler: report of 150 cases and literature review. Eur J Gynaecol Oncol. 1998. 19(3):215-9. [Medline].

  35. Cibula D, Velechovska P, Sláma J, Fischerova D, Pinkavova I, Pavlista D, et al. Late morbidity following nerve-sparing radical hysterectomy. Gynecol Oncol. 2009 Nov 9. [Medline].

  36. Skret-Magierlo J, Naróg M, Kruczek A, Kluza R, Kluz T, Magon T, et al. Radical hysterectomy during the transition period from traditional to nerve-sparing technique. Gynecol Oncol. 2009 Dec 9. [Medline].

  37. Mabuchi S, Okazawa M, Kinose Y, Matsuo K, Fujiwara M, Suzuki O, et al. Comparison of the Prognoses of FIGO Stage I to Stage II Adenosquamous Carcinoma and Adenocarcinoma of the Uterine Cervix Treated With Radical Hysterectomy. Int J Gynecol Cancer. 2012 Sep 12. [Medline].

  38. Qiu JT, Abdullah NA, Chou HH, Lin CT, Jung SM, Wang CC, et al. Outcomes and prognosis of patients with recurrent cervical cancer after radical hysterectomy. Gynecol Oncol. 2012 Aug 14. [Medline].

  39. Lowe MP, Chamberlain DH, Kamelle SA, Johnson PR, Tillmanns TD. A multi-institutional experience with robotic-assisted radical hysterectomy for early stage cervical cancer. Gynecol Oncol. 2009 May. 113(2):191-4. [Medline].

  40. Roy M, Plante M. Pregnancies after radical vaginal trachelectomy for early-stage cervical cancer. Am J Obstet Gynecol. 1998 Dec. 179(6 Pt 1):1491-6. [Medline].

  41. Keys HM, Bundy BN, Stehman FB, et al. Cisplatin, radiation, and adjuvant hysterectomy compared with radiation and adjuvant hysterectomy for bulky stage IB cervical carcinoma. N Engl J Med. 1999 Apr 15. 340(15):1154-61. [Medline].

  42. Rose PG, Bundy BN, Watkins EB, et al. Concurrent cisplatin-based radiotherapy and chemotherapy for locally advanced cervical cancer. N Engl J Med. 1999 Apr 15. 340(15):1144-53. [Medline].

  43. Campion MJ. Preinvasive disease. Berek JS, Hacker NF, eds. Practical Gynecologic Oncology. 4th ed. 2005. 265-336.

  44. Randall ME, Michael H, Vermorken J. Uterine Cervix. Hoskins WJ, Perez CA, Young RC, et al, eds. Principles and Practice of Gynecologic Oncology. 4th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2005. 743-822.

  45. Schorge JO, Boruta 2nd DM. Uterine procedures. Karlan BY, Bristow RE, Li AJ, eds. Gynecologic Oncology: Clinical Practice and Surgical Atlas. New York, NY: McGraw-Hill; 2012. 493-530.

  46. Ziebarth AJ, Kim KH, Huh WK. Cervical cancer. Karlan BY, Bristow RE, Li AJ, eds. Gynecologic Oncology: Clinical Practice and Surgical Atlas. New York, NY: McGraw-Hill; 2012. 85-104.

 
Previous
Next
 
Radical hysterectomy specimen demonstrating the vaginal margin.
Radical hysterectomy specimen demonstrating the parametrial margins.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.