|Advances in equipment and techniques now allow many surgical procedures to be performed through tiny abdominal incisions. When performed by skilled operators “minimally invasive surgery” (MIS) results in dramatically shortened hospital stays and postoperative discomfort. Resumption of normal activity and return to work can occur much more rapidly than in surgeries requiring a traditional large abdominal incision. All GOA gynecologic oncologists are skilled endoscopic surgeons and perform hundreds of these surgeries yearly.MIS techniques can be divided into two categories:|
Advanced Laparoscopic Surgery
Laparoscopic instrumentation is directly manipulated by the operating surgeon. Articulating instrumentation, sophisticated power sources, 3-dimensional visualization systems etc., permit procedures to be be performed through fewer and smaller incisions. Some surgeries can even be performed through a single small incision (Single Incision Laparoscopic Surgery – SILS)!
“da Vinci” Robot Surgery
Robotic surgery consists of a surgeon’s console and and patient-side cart with four interactive robotic arms. This technology provides the surgeon with excellent 3-dimensional visualization of the operative field. The robotic instruments provide unparalleled dexterity, which mimics the range of motion of the human wrist. Robotic surgery was FDA approved for gynecologic surgery in 2005. GOA surgeons were early adopters of this technology and have performed more robotic surgeries than any group of Gynecologic Oncologists in Southern California.
Peruse the videos below to see the type of surgical procedures now performed endoscopically. All patients in these short films were discharged from the hospital either on the same day as the procedure or after an overnight stay.
Uterine cancer is the most common malignancy of the female genital tract, accounting for approximately 30,000 new cases annually and 6,000 deaths. Endometrial cancer is the fourth most common malignancy in women behind breast, lung and colon cancer.
The median age at onset is 63 years with up to 25% of cases occurring in pre-menopausal women and 5% in patients younger than 40 years.
The recognized risk factors often account for a chronic estrogenized state (endogenous and/or exogenous). These factors include nulliparity, early menarche, late menopause, obesity (35% of patients with endometrial cancer are not obese), chronic disease (e.g., diabetes, hypertension), unopposed estrogen therapy, and presence of atypical hyperplasia.
The most common endometrial tumor histologies are:
1. Adenocarcinoma (75%)
2. Adenosquamous (18%)
3. Papillary Serous (6%)
4. Clear Cell (1%)
Routes of Spread
Endometrial cancer can spread by the following routes:
1. Direct extension to adjacent structures.
2. Trans-tubal passage of exfoliated cells.
3. Lymphatic dissemination.
4. Hematogenous dissemination.
Abnormal uterine bleeding or post-menopausal bleeding are present in 90% of cases. Of interest, 15% of patients with post-menopausal bleeding have endometrial cancer. Other etiologies include atrophic vaginitis, exogenous estrogens, polyps, and other genital tract malignancy. Other associated nonspecific findings in patients with endometrial cancer include pyometria, hematometra, abnormal PAP smear, heavy menses and intermenstrual bleeding.
Patients suspected of having endometrial cancer should have pathologic confirmation of disease by either endometrial biopsy or dilation and currettage. Following confirmation of disease and careful physical exam the routine pre-operative evaluation consists of the following:
2. Blood tests which may include a CA-125.
3. Additional diagnostic tests may be performed if indicated.
StageIa – Tumor confined to the uterus, no or <50% myometrial invasion
Ib – Tumor confined to the uterus, >50% myometrial invasion
II – Cervical stromal invasion, but not beyond the uterus
IIIa – Tumor invades uterine serosa or adnexae
IIIb – Vaginal and/or parametrial involvement
IIIc1 – Pelvic node involvement
IIIc2 – Periaortic node involvement
IVa – Tumor invasion of bladder and/or bowel mucosa
IVb – Distant metastases including abdominal metastases and/or inguinal node involvement
G1 = 5% or less of a non-squamous or non-morular solid growth pattern.
G2 = 6-50% of a non-squamous or non-morular solid growth pattern.
G3 = More than 50% of a non-squamous or non-morular solid growth pattern.
A simplified approach to the treatment of patients with endometrial cancer can be achieved by subdividing the patients into high and low risk groups following hysterectomy and oophorectomy.
1. Disease confined to the uterus:
Sub-group 1: No further treatment (risk of recurrence<5%) G1, G2 with less than 10% myometrial invasion G3 with no myometrial invasion No cervix invasion Negative cytology No lymph vascular invasion Sub-group 2: Post-operative brachytherapy (risk of recurrence 5-10%) G1, G2 with 10-50% myometrial invasion G1, G2 with cervix invasion Negative cytology No lympho-vascular space invasion Note: The occasional patient with extensive cervical involvement may be considered for radical hysterectomy. Sub-group 3- Whole pelvis radiotherapy (risk of recurrence>10%)
All other cases of Stage I or Stage II disease.
2. Presence of extra-uterine disease:
Sub-group 1- Pelvic spread of disease:
Pelvic radiotherapy + vaginal brachytherapy and possible extended field if positive common or para-aortic lymph node involvement.
Sub-group 2- Optimally debulked < 2cm residual disease confined to the abdominal cavity. Whole abdominal radiation, chemotherapy and/or progestins. Sub-group 3- Suboptimally debulked >2cm residual disease or disease outside the abdominal cavity.
Chemotherapy and/or progestins. Radiotherapy also may have a role in local control of tumor related symptoms.
Recurrent Disease: Treatment is dependent on the extent of recurrence. Isolated local recurrences in patients who have received prior radiotherapy may be considered for pelvic exenteration. Unfortunately these are unusual and recurrent disease most often is not amenable to surgery. The remaining options include radiotherapy (in patients who have not had previous treatment) or chemotherapy.
The most important prognostic variable in endometrial cancer is the surgical stage. Other prognostic variables include myometrial invasion, vascular space invasion, nuclear grade, histologic type, tumor size, patient age, and peritoneal cytology.
Stage I- 75-100%
Stage II- 60%
Stage III- 50%
Stage IV- 20%
Follow-Up every 3 months for the first 2 years, every 6 months for years 3-5 and yearly thereafter. Routine pelvic exam performed at each visit and PAP smear on yearly basis. Chest X-ray may also be considered on annual basis, but the yield is low in the absence of symptoms.
Primary vaginal cancer represents 1-2% of malignancies of the female genital tract with average age of diagnosis at 60 years. The majority of vaginal neoplasms are metastatic lesions from other primary sources.
Postulated risk factors include low socioeconomic status, history of HPV infection, chronic vaginal irritation, prior abnormal PAP with CIN, prior hysterectomy (59% of patients with primary vaginal cancer), prior treatment for cervical cancer.
A subset of patients of special note are those who have had in-utero exposure to DES (DES was used from 1940 to 1971) during the first half of pregnancy. The risk of an exposed fetus to develop clear cell carcinoma of the vagina later in life is 1:1000 with peak age at diagnosis being 19 years.
The majority of primary vaginal cancers are of the squamous cell variety (85%) with adenocarcinoma representing the second most common variety (9%) and sarcoma, melanoma and less common types comprising the remainder.
Routes of Spread
1. Direct extension to adjacent structures
2. Lymphatic dissemination: Lesions of the upper 2/3 of the vagina metastasize directly to the pelvic lymph nodes. Lesions of the lower 1/3 of the vagina metastasize first to the inguino-femoral nodes and secondarily to the pelvic nodes.
3. Hematogenous dissemination: This represents a late occurence as the disease is confined primarily to the pelvis in the majority of cases.
Symptoms: Painless vaginal bleeding is the most common symptom followed by vaginal discharge. Other less common presenting features include bladder symptoms, tenesmus and pelvic pain (usually indicative of locally advanced disease).
Physical Findings: Lesions are primarily found in the upper 1/3 of the vagina, usually on the posterior wall. The appearance of lesions is variable with a range from exophytic to endophytic. Surface ulceration is usually not present except in advance cases. Visualization of the lesion identified on cytology may require colposcopy.
1. Colposcopy (unless lesion visible)
3. CT or CT/PET imaging
Stage 0: Carcinoma in situ, intraepithelial carcinoma
Stage I: Carcinoma limited to the vaginal wall.
Stage II: The carcinoma has involved the subvaginal tissue but has not extended to the pelvic wall.
Stage III: The carcinoma has extended to the pelvic wall.
Stage IV: The carcinoma has extended beyond the true pelvis or has involved the mucosa of the bladder or rectum.
IV A- Spread of growth to adjacent organs
IV B- Spread to distant organs
Stage 0: Surgical excision, laser ablation and in some cases 5-FU application
Stage I: These may be broken down into two treatment groups:
1. Lesions of the upper vaginal fornices may be treated surgically with radical hysterectomy (upper vaginectomy) and pelvic lymphadenectomy. Another alternative is radiotherapy alone.
2. All lesions of stage one, including those above, may be treated with radiotherapy usually in the form of an intracavitary cylinder.
Stage II, III, and IV: Treatment consists of external beam radiotherapy and intracavitary and/or interstitial therapy and if the lower 1/3 of the vagina is involved the groin should also be treated.
Recurrent Disease: Treatment is variable and depends on the extent of recurrence and includes wide local excision, partial vaginectomy, and exenteration. For distant metastatic disease, chemotherapy is an option, but because of the rarity of this tumor its role is unclear.
The most important prognostic factor is stage of disease.
Stage I- 80%
Stage II- 45%
Stage III- 35%
Stage IV- 10%
Physical examination every 3 months for years 1-2, every 6 months for years 3, 4 and 5, and annually thereafter.
3-5% of all female genital cancers and 1% of all malignancies in women. 2000-3000 new cases annually. The average age at diagnosis is approximately 65 years, but there is a trend to younger age at diagnosis.
The cause of vulvar cancer appears to be multifactorial but some associated risk factors appear to be advanced age, low socioeconomic class, hypertension, diabetes, prior lower genital tract malignancy (cervical cancer), and immunosuppression. HPV association is not as strong as that of cervix cancer.
Approximately 85% of vulvar malignancies are of the squamous cell variety. The second most common common histologic type is malignant melanoma representing 10% of cases of vulvar malignancies.
Routes of Spread
1. Direct extension
2. Lymphatic dissemination
3. Hematogenous dissemination
Symptoms: Chronic pruritis, ulceration, or nodule are the most common complaints.
Physical Findings: Generally these lesions arise from the labia majora (40%), labia minora (20%), periclitoral area (10%), and perineum/posterior fourchette (15%). They may appear as a dominant mass, warty area, ulcerated area, or thickened white epithelium. It is estimated that only 5% of cases are multi-focal. A general rule of thumb is to biopsy the center of any suspicious area.
1. Physical exam with special attention to the groin nodes and measurement of primary lesion
2. Routine labs
4. Cystoscopy/Proctoscopy (depending on site and extent of lesion)
Since 1988 Vulvar cancer has been staged using a surgical system which utilizes the TNM classification with modifications added in 1995.
Stage I and Stage IA:
T1N0M0- Tumor confined to the vulva and/or perineum 2cm or less in diameter with stromal invasion no greater than 1.0 mm, nodes are negative.
T1N0M0- Tumor confined to the vulva and/or perineum 2cm or less in diameter with stromal invasion greater than 1.0 mm, nodes are negative.
T2N0M0- Tumor confined to the vulva and/or perineum >2cm in diameter, nodes are negative.
T3N0M0- Tumor of any size with Adjacent spread to the lower urethra or the anus
T1N1M0 2. Unilateral regional lymph node metastases
Tumor invades any of the following:
Upper urethra, bladder mucosa, rectal mucosa, pelvic bone or bilateral regional node mets
T4 any N M0
Stage IV B:
Any distant mets including pelvic nodes.
Any T, any N, M1
Stage I- (<1 mm invasion=microinvasive) wide local excision. All other Stage I lesions require a radical wide local excision with a traditional 2cm gross margin and superficial dissection of the corresponding groin. If the lesion is close to the midline, bilateral superficial groins are dissected.
Stage II- Radical vulvectomy with bilateral node dissection including superficial and deep inguinal nodes. Radiotherapy may be indicated if high risk pathologic features are found ..
Stage III- Several treatment options exist and must be individualized in each patient:
1. Modified radical vulvectomy (Radical wide local excision is used in some institutions) with inguinal and femoral node dissection. Pelvic and groin radiation with positive groin nodes.
2. Preoperative radiotherapy (+/-radiosensitizer) may be used to increase operability and decrease the extent of resection followed by radical excision with bilateral superficial and deep groin node dissection.
3. Radiotherapy alone if the patient or extent of lesion deemed unsuitable for radical surgery.
Stage IV- Treatment options include the following and must be individualized:
1. Radical vulvectomy and pelvic exenteration
2. Radical vulvectomy followed by radiotherapy
3. Preoperative radiotherapy (+/- radiosensitizer) followed by radical surgical excision.
4. In cases of patient or lesion inoperability primary radiotherapy may be used (+/- radiosensitizer)
Recurrent Disease- Treatment depends on the site and extent of recurrence. For local recurrences a radical wide excision may be used with radiotherapy (dependent upon prior treatment). In selected cases, pelvic exenteration may be considered. Patients with regional or distant metastasis are more difficult to manage and often palliative therapy is the only option.
1. Stage (including lesion size)
2. Inguinal node metastases (this is the single most important prognostic variable)
3. Lymph-Vascular Space Invasion
4. Other important factors include site of lesion, histologic grade, and depth of invasion.
Stage I: 95%
Stage II: 75-85%
Stage III: 55%
Stage IV: A-20%, B-5%
Recommended Follow-Up Physical examination every 3 months for 2 years, every 6 months for years 3, 4 and 5, and annually thereafter.
One in 70 women will develop ovarian cancer during their lifetime. There are approximately 25,000 new cases of ovarian cancer and 14,000 deaths annually. Epithelial ovarian cancer comprises 90% of all ovarian cancers. This translates into 22,500 cases of epithelial ovarian cancer annually. The median age of onset is 61 years.
The risk of ovarian cancer increases with age and peaks at about 70 years. Patients of low parity, decreased fertility, and delayed child-bearing appear to be at greater risk for ovarian cancer. There also appears to be autosomal dominant inherited forms which account for only 3-5% of all cases of ovarian cancer. They tend to occur at younger ages (approximately 10 years before non-heritable ovarian cancer). A dysfunctional BRCA 1/2 gene plays a major role in these syndromes. There are three recognized hereditary forms which include the following:
1. Site Specific Familial Ovarian Cancer
2. Breast-Ovarian Familial Cancer Syndrome
3. Lynch II Syndrome (Non-polyposis colon cancer, endometrial cancer, breast cancer and ovarian cancer clusters in first and second degree relatives).
Note: Use of oral contraceptives appears to have a protective effect which may last up to 10 years.
PathologyThere are 8 different major histologic groups of epithelial ovarian cancer:
|Histologic Types||% of Ovarian Tumors||% Bilateral|
Routes of Spread
1. Transcoelemic (most common)- Exfoliated cells tend to assume the circulatory path of the peritoneal fluid and implant along this path.
2. Lymphatic dissemination
3. Hematogenous dissemination (uncommon)
The interval from onset of disease to diagnosis is often prolonged secondary to lack of specific diagnostic symptoms in early stage disease therefore diagnosis is often not made until patients have disseminated disease. It is estimated that more than half (60%) of patients with ovarian cancer are stage III or stage IV at time of diagnosis. Clinical signs and symptoms often seen in these patients are abdominal fullness, early satiety, dyspepsia, urinary frequency, and constipation. In some cases, an adnexal mass is noted on routine pelvic exam or a palpable ovary in a postmenopausal asymptomatic patient.
Note: Five percent of patients explored for presumed ovarian cancer have another primary which has metastasized to the ovary. The most common sources of metastatic lesions are the breast, GI tract, and pelvic organs.
1. Careful physical exam
2. Routine blood tests
3. Serum tumor markers: CA-125 is elevated in approximately 80-85% of cases of epithelial ovarian cancer. Unfortunately, the predictive power of pre-operative CA-125 is quite low.
4. Chest X-Ray
5. Imaging studies are often helpful but most often will not change the planned staging procedure. Computerized Axial Tomography (CT) may help determine the extent of disease and a Barium Enema (BE) will offer information on the status of the colon. Other imaging studies which are helpful in certain clinical situations include Intravenous Pyelography (IVP).
Stage I: Growth limited to the ovaries.
Ia- Growth limited to one ovary; no ascites; no tumor on the external surface; capsule intact.
IIB- Growth limited to both ovaries; no ascites; no tumor on external surface; capsules intact.
IC- Tumor either stage Ia or IIB, but with tumor on the surface of one or both ovaries; or with capsule ruptured; or with ascites present containing malignant cells or with positive peritoneal cytology.
Stage II: Growth involving one or both ovaries with pelvic extension.
IIA- Extension and/or metastases to the uterus and/or tubes.
IIB- Extension to other pelvic tissue.
IIC- Tumor either stage IIA or IIB, but with tumor on the surface of one or both ovaries; or with capsule(s) ruptured or with ascites present containing malignant cells or with positive peritoneal washings.
Stage III: Tumor involving one or both ovaries with peritoneal implants outside the pelvis and/or positive retroperitoneal or inguinal nodes. Superficial liver metastases equals stage III. Tumor is limited to the true pelvis but with histologically proven malignant extension to small bowel or omentum.
IIIA- Tumor grossly limited to the true pelvis with negative nodes but histologically confirmed microscopic seeding of abdominal peritoneal surfaces.
IIIB- Tumor involving one or both ovaries with histologically confirmed implants of abdominal peritoneal surfaces, none exceeding 2cm in diameter. Nodes are negative.
IIIc- Abdominal implants greater than 2cm in diameter and/or positive retroperitoneal or inguinal nodes.
Stage IV: Growth involving one or both ovaries with distant metastases. If pleural effusion is present, there must be positive cytology to allot a case to stage IV. Parenchymal liver metastases equals stage IV.
The initial step in treatment of epithelial ovarian cancer involves surgical exploration and appropriate staging procedures which include the following:
1. Abdominal Cytology
2. Careful exploration of all abdominal structures and surfaces.
3. Abdominal Hysterectomy and Bilateral Salpingoophorectomy (TAH/BSO). There are some exceptions to this when fertility is a concern and there is early stage disease.
4. Infracolic omentectomy, +/- appendectomy.
5. Selective pelvic and aortic lymph node sampling.
Primary cytoreduction is a key component of more advanced cases and survival is directly correlated to the amount of residual tumor remaining. Optimal tumor reduction surgery is loosely defined as the largest residual tumor diameter being less than or equal to 2cm. If residual is greater, the cytoreduction is deemed sub-optimal.
Note: There are certain exceptions to the initial treatment step, whereby primary chemotherapy may be employed followed by interval debulking procedures in certain subsets of patients with advanced disease, bulky disease or those patients not appropriately primarily cytoreduced. The impact on survival in this approach, however, is unproven in those patients with advanced and bulky disease.
Stage Ia , Grade 1 Tumors: Adjuvant chemotherapy is not necessary in this subset of patients. If fertility is an issue in those patients who have had a thorough staging procedure, the uterus and contra-lateral ovary may be conserved.
Stages Ia (Grades 2 and 3), IC, II, III, IV: Current treatment consists of Taxol and Carboplatin based regimens.
1. Histopathologic factors:
2. Clinical Factors:
Extent of residual disease remaining following primary cytoreduction
Volume of ascites
1. Overall – 40-60%
2. Residual Disease (All Stages) Five Year Survival:
Macroscopic (Optimal) 30-50%
Macroscopic (Suboptimal) 5-30%
3. Performance Status: As expected patients with poorer performance status (Karnofsky’s <70) prior to treatment have significantly shorter survival.
Follow-up for the first 2 years is every 3 months, every 6 months for years 3, 4 and 5 and yearly thereafter. Pelvic exam and CA-125 at each visit and PAP smear on an annual basis. Routine performance of imaging studies (CT scans, Chest X-ray, etc) should be individualized.
There are approximately 15,000 new cases of cervical cancer reported annually and 4,000-5,000 associated deaths.
Significant risk factors for cervical cancer include early age at first intercourse, multiple sexual partners, multiparity, infection with Human Papilloma Virus (HPV) (Specifically Types 16 and 18), non-barrier methods of birth control, sexual contact with high risk males and smoking.
Squamous carcinomas comprise the majority of cases (85%) followed by adenocarcinomas (10-15%), which include the less common adenosquamous carcinoma, and the remainder of cases comprised of the rarer tumors which includes small cell, sarcomas, lymphomas, and melanomas.
Routes of Spread
Cervical carcinoma spreads by one of three major routes:
1. Direct invasion into surrounding structures which include the parametria, corpus, and vagina.
2. Lymphatic dissemination
3. Hematogenous dissemination
4. Intraperitoneal implantation
The two predominant symptoms of cervical cancer are discharge and abnormal vaginal bleeding. Other complaints include urinary frequency and pain. The physical exam may vary depending on the site of the lesion (endocervix or exocervix). A careful visual inspection as well as both bimanual and rectovaginal palpation are necessary to identify the size and extent of the lesion.
All cases of cervical cancer should have as part of the pre-treatment work-up the following components:
1. Careful physical exam including biopsy of the lesion
2. Chest X-ray
3. Routine lab tests
Other procedures may be employed in more advanced disease or in the presence of symptoms (cystoscopy, proctoscopy, BE, CT or CT/PET scan, etc).
Stage I: Those lesions confined to the cervix (uterine involvement is disregarded).
Ia- Preclinical cervical cancers diagnosed by microscopy alone.
Ia1-Measured invasion of stroma no greater than 3 mm in depth and no wider than 7 mm.
Ia2- Measured invasion of stroma greater than 3 mm and no greater than 5 mm in depth and no wider than 7 mm.
IB- Lesions of greater dimension than Stage Ia whether seen clinically or not.
Ib1- Clinical lesions no greater than 4 cm in size.
Ib2- Clinical lesions greater than 4 cm in size.
Stage II: The carcinoma extends beyond the cervix, but has not extended to the pelvic sidewall or the lower 1/3 of the vagina.
IIA- No obvious parametrial involvement.
IIB- Parametrial involvement.
Stage III: The carcinoma has extended to the pelvic wall with no cancer free space between the tumor and the pelvic wall. The tumor involves the lower 1/3 of the vagina.All cases of hydronephrosis or non-functioning kidney unless secondary to unrelated cause.
IIIB- No extension to the pelvic sidewall, but involvement of the lower 1/3 of the vagina.
IIIB- Extension on the pelvic wall or hydronephrosis or nonfunctioning kidney.
Stage IV: The carcinoma has extended beyond the true pelvis or has clinically involved the mucosa of the bladder or rectum.
IVA- Spread of growth to adjacent organs.
IVB- Spread of growth to distant organs.
Note: The term microinvasive cervical cancer is sometimes applied to Stage Ia lesions. Unfortunately there are two separate definitions that are used which are important when considering therapy options. This diagnosis must be made from either a cone or hysterectomy specimen.
1. International Federation of gynecology and Obstetrics (FIGO) Definition: See definition above under FIGO stage Ia.
2. Society of Gynecologic Oncologists (SGO) Definition: Microinvasion as defined by the SGO must satisfy a depth of invasion in one or more foci of 3 mm or less and have no lymphovascular involvement.
Stage Ia- Lesions which satisfy the SGO definition of microinvasion may be treated conservatively with any of the following modalities:
1. Simple hysterectomy
2. Conization in cases where maintenance of fertility is at issue.
Lesions that do not satisfy the SGO definition (LVSI or invasion >3 mm) are at significantly increased risk for recurrence when treated conservatively therefore radical hysterectomy and lymph node dissection or radiotherapy should be employed.
Stages IB and IIA- Surgery or radiotherapy result in similar cure rates when patients are carefully selected. Squamous lesions less than 4-5 cm and adenocarcinomas less than 3 cm are potential surgical candidates. The standard treatment options are as follows:
1. Type III radical hysterectomy and pelvic lymph node dissection. In patients with risk factors on pathologic evaluation (e.g., lymph node metastases) are also given adjuvant radiotherapy.
2. Radiotherapy with 40-45 Gy external and two intracavitary applications.
3. Simple hysterectomy after pelvic radiotherapy; this primarily indicated in patients whose tumor responds slowly to radiotherapy or in whom vaginal anatomy precludes optimal intracavitary placement.
4. Radical trachelectomy (radical excision of the cervix alone) may be an option in selected Stage 1 cancers when preservation of potential fertility is desired.
Stages IIB through IVA- Radiotherapy is the treatment of choice for locally advanced disease. There are certain situations where surgery may be used as adjunctive therapy. For example, in cases of Stage IVA disease without parametrial involvement and cases of persistent central disease following radiotherapy.
Stage IVB- Chemotherapy for disseminated disease is the primary treatment for Stage IVB. Radiotherapy can be used for local control and palliation of symptoms in this setting.
Recurrent Disease- Patients with central recurrence may be managed with an exenteration in the absence of contraindicating factors. Those patients with prior radiation and extensive pelvic recurrence or distant metastatic disease are treated in a similar fashion as those patients with Stage IVB.
Stage I- Lymph vascular involvement, tumor size, depth of invasion, and presence of lymph node metastasis are important factors.
Stage II-IV- The major prognostic variables include stage, presence of lymph node metastasis, tumor volume, age, and performance status.
Stage I- Squamous 65-90%; Adenocarcinoma 70-75%
Stage II- Squamous 45-80%; Adenocarcinoma 30-40%
Stage III- Squamous up to 60%; Adenocarcinoma 20-30%
Stage IV- For both Squamous and Adenocarcinoma <15%
Of those patients who do have recurrence of their disease; 50% are diagnosed in the first year, 75% are diagnosed by 2 years and 95% are diagnosed within 5 years. Follow-up surveillance is recommended as follows:
1. Physical exam every 3 months for the 2 years every 6 months during the fourth through fifth year and yearly thereafter.
2. PAP smear with each exam.
3. CT or CT/PET scans at regular intervals for 2 years.