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Invasive cervical cancer

Also known as: Cervical cancer

DiseaseUpdated: 2026-02-09

Summary

Cervical cancer is the third most common cancer of the female genital tract in the US, with a peak incidence in women between 35–44 years of age. Persistent infection with any high-risk HPV genotype is the most common cause of cervical cancer. Consequently, the main risk factors are those that increase the likelihood of contracting HPV infection (e.g., multiple sexual partners) and/or decrease the clearance of ongoing infection (e.g., immunosuppression). Early-stage cervical cancer is typically asymptomatic. Symptoms, such as abnormal vaginal bleeding, dyspareunia, and pelvic pain, usually manifest later in the disease course. Diagnostics for individuals with concerning symptoms include colposcopy with cervical biopsy. Once the diagnosis is confirmed, invasive cervical cancer should be staged (FIGO staging for cervical cancer is preferred) to determine the appropriate treatment and likely prognosis. Surgery (e.g., conization, trachelectomy, hysterectomy) may be appropriate for early-stage disease. Management options for advanced disease include concurrent chemoradiotherapy, systemic chemotherapy, and palliative radiotherapy. Management of pregnant individuals with invasive cervical cancer or precancerous lesions should be individualized. Patients with invasive cervical cancer should be closely followed up for recurrence after management. HPV immunization, counseling on safe sex practices, and screening for cervical cancer are the most effective prevention measures.

Cervical cancer screening and management of precursor lesions are detailed in a separate article.

Epidemiology

  • Incidence: 7.4:100,000 [1]
    • Cervical cancer is the 3rd most common gynecological malignancy in the US after endometrial and ovarian cancer.
    • Incidence is higher in countries without screening programs and HPV vaccination.
    • Incidence has declined over the past 40 years due to screening and HPV vaccination.
  • Peak incidence: 35–44 years of age [2][3]
  • Mortality: 2.2:100,000 women per year [1]
    • Cervical cancer is the third most common cause of death due to a gynecological malignancy after endometrial and ovarian cancer.
    • Mortality is highest in individuals aged 55–64 years.

One in 161 female individuals in the US (∼ 0.6%) will develop cervical cancer during their lifetime. [1]

Cervical intraepithelial neoplasia (CIN), a precursor of cervical cancer, typically occurs in young adults (25–35 years).

Epidemiological data refers to the US, unless otherwise specified.

Etiology

Human papillomavirus virus (HPV) infection [4][5][6]

  • Infection with high-risk HPV genotypes is the main cause of cervical cancer.
  • Nearly all squamous cell carcinoma of the cervix and approximately 90% of adenocarcinoma of the cervix are positive for HPV infection. [4][6]
  • The major high-risk HPV types are HPV 16 and HPV 18. [6]

Risk factors [4]

  • For contracting HPV infection
    • Multiple sexual partners (strongest risk factor)
    • Early-onset of sexual activity
    • Multiparity
    • Immunosuppression (e.g., HIV infection, post-transplantation)
    • History of sexually transmitted infections (e.g., herpes simplex, chlamydia)
  • Environmental risk factors
    • Cigarette smoking and/or exposure to second-hand smoke (for squamous cell cancer types only) [7]
    • In-utero exposure to diethylstilbestrol (DES)
    • Low socioeconomic status [8]

The most common risk factors for cervical cancer are those that increase the likelihood of HPV infection (e.g., multiple sexual partners) and/or decrease the clearance of ongoing infection (e.g., immunosuppression). [4]

Immunocompromised individuals, those who were exposed to DES in-utero, and those with a current or past history of a high-grade precancerous cervical lesion are considered to have a high risk of developing invasive cervical cancer. Screening modalities and intervals in these groups of individuals should account for the increased risk (see “Screening recommendations for individuals at high risk of cervical cancer”). [9][10][11]

Pathophysiology of the development of cervical cancer
Pathophysiology of the development of cervical cancer

Almost all cases of cervical cancer are caused by an infection of the transformation zone (rectangular box) with high-risk types of human papillomavirus (HPV).

HPVs infect the stem cells of the basal cell epithelium. Cell proliferation and migration of virus-infected daughter cells into the suprabasal cell layer allow the infection to spread. At the beginning of the process, the DNA of the virus is episomal. As the disease progresses, the DNA is integrated into the cervical epithelium's DNA. A noninvasive precursor lesion, cervical intraepithelial neoplasia (CIN), may develop from an HPV infection over months to years, which may ultimately progress to invasive carcinoma.

In most cases, complete recovery will occur during the early stages of an HPV infection.


© AMBOSS

Clinical features

Cervical cancer is usually asymptomatic in the early stages; symptoms typically develop later in the course of the disease.

  • Early symptoms
    • Abnormal vaginal bleeding: irregular vaginal bleeding; heavy, irregular menstrual bleeding; postcoital spotting
    • Abnormal vaginal discharge: blood-stained or purulent malodorous discharge
    • Dyspareunia
    • Pelvic pain
  • Late symptoms: hydronephrosis, lymphedema, fistula formation
  • Cervical examination: ulceration, induration, or an exophytic tumor (see “Overview of colposcopy findings”)

Always consider cervical cancer as a cause of postcoital bleeding.

Diagnosis

Invasive cervical cancer is confirmed on colposcopy with biopsy and histological evaluation. Diagnosis of cervical cancer precursor lesions is detailed in “Cervical cancer screening”.

Colposcopy [12][13] [14][15]

Indications [12][13][14]

  • Individuals with symptoms suggestive of cervical cancer
  • Abnormal findings on pelvic examination
  • Asymptomatic individuals with immediate risk of CIN3 ≥ 4% on cervical cancer screening who do not meet the threshold for or do not wish to undergo expedited treatment
  • Certain results on cervical cancer screening (see “Exceptions to the risk-based approach”)

Findings

Overview of colposcopy findings [12][14][15]
Features of epithelium
Normal
  • Ectopy/ectropion
  • Squamous or columnar epithelium
  • Nabothian cysts
  • Submucosal branching vessels
  • No acetowhitening
Features suggestive of precancerous lesions [12][14]
  • Acetowhitening (most common): an area that appears white after the application of acetic acid
    • Low-grade features of acetowhitening: translucent, flat, fine punctation/mosaic, indistinct border
    • High-grade features of acetowhitening: thick, coarse punctation/mosaic, sharp border, peeling edge
Features suggestive of invasive cervical cancer
  • Gross exophytic or endophytic neoplasm
  • Ulceration
  • Necrosis
  • Acetowhitening may or may not be present.
  • Atypical growth of the vessels (e.g., corkscrew or comma-like shape)
Nonspecific
  • Cervical leukoplakia: a white membrane on the cervix that cannot be scraped off [6]
  • Erosion
  • Friable tissue

The cervical transformation zone or squamocolumnar junction is the most common site for squamous cell carcinoma and its precursors and should always be evaluated during colposcopy. Failure to do so may cause cervical cancer or precancerous lesions to be missed. [15]

Cervical punch biopsy [11][12][13][14][16]

  • Indications and procedure [12][14]
    • Abnormal colposcopy findings: Obtain multiple (2–4) colposcopy-directed biopsies targeting all areas of cervical abnormalities (e.g., acetowhitening, metaplasia) and the squamocolumnar junction. [12][16]
    • Normal colposcopy findings in individuals at high risk of CIN3 who do meet the threshold for or do not wish to undergo expedited treatment: Consider random, nontargeted biopsies OR biopsy the squamocolumnar junction.
  • Findings: See “Pathology” section. [6][17]

Nontargeted (random) biopsies are not recommended in individuals with normal findings on colposcopy who are at low risk for CIN (i.e., HPV negative and cytology less than HSIL). [12][14]

Expedited treatment (without a preceding biopsy) is recommended for asymptomatic women at high risk of CIN3 with normal findings on colposcopy. Observation is recommended for women with normal colposcopy findings who are at very low risk of CIN. [11][13]

Ectocervix
Ectocervix

Colposcopy with application of acetic acid

The external os of the cervix is circular and the mucosa is smooth and pale pink.

These findings are characteristic of a normal ectocervix in a nulliparous woman.


Source: “Fig. 1, in: VIA and Challenges of a Single Visit Approach in Malawi” by Haeok Lee, Mary Sue Makin, Jasintha T Mtengezo, and Address Malata, Published in clinmed - international library, licensed under CC BY 4.0.
Cervical intraepithelial neoplasia (CIN 2)
Cervical intraepithelial neoplasia (CIN 2)

Colposcopy after application of acetic acid to cervix (acetowhitening reaction)

The epithelium on the entire anterior lip appears white. The white lesion ascends into the endocervical canal; therefore, its distal margin is not visible.

An acetowhitening reaction suggests a precancerous lesion.


Source: “Fig 4, In: The Accuracy of Cytology, Colposcopy and Pathology in Evaluating Precancerous Cervical Lesions” by Pleş L, Radosa JC, Sima RM et al., MDPI, licensed under CC BY 4.0.
Low-grade squamous intraepithelial lesion (LSIL) of the cervix
Low-grade squamous intraepithelial lesion (LSIL) of the cervix

Colposcopy after application of acetic acid to cervix demonstrating acetowhitening reaction.

At 12 and 6 o'clock of the ectopic epithelium, the thin white areas of the epithelium (acetowhite epithelium) show a fine mosaic pattern. A cervical gland can be seen at 7 o’clock.

The fine mosaic pattern of the epithelium is suggestive of a low-grade lesion. Biopsy confirmed LSIL.


Source: “Fig 2, In:The Accuracy of Cytology, Colposcopy and Pathology in Evaluating Precancerous Cervical Lesions” by Pleş L, Radosa JC, Sima RM et al., MDPI, licensed under CC BY 4.0. Modifications: image cropped.
High-grade squamous intraepithelial lesion of the cervix (HSIL)
High-grade squamous intraepithelial lesion of the cervix (HSIL)

Colposcopy after application of acetic acid to cervix demonstrating acetowhitening reaction

A significant amount of acetowhite epithelium is noted with sharp borders (though the margin of the distal end of it is indistinct). Around 11 o'clock, a coarse mosaic pattern and punctation can also be seen.

These features suggest high-grade cervical cancer. Biopsy confirmed HSIL.


Source: “Fig 8, In: The Accuracy of Cytology, Colposcopy and Pathology in Evaluating Precancerous Cervical Lesions” by Pleş L, Radosa JC, Sima RM et al., MDPI, licensed under CC BY 4.0. Modifications: image cropped.
High-grade squamous intraepithelial lesion (HSIL) of the cervix
High-grade squamous intraepithelial lesion (HSIL) of the cervix

Colposcopic image of an HSIL cytology result:

Acetowhite epithelium at 7 o’clock as well as atypical irregular and petechial vascularization are visible.

Atypical growth of vessels is highly suggestive of an invasive lesion.


Source: “Fig 12, In: The Accuracy of Cytology, Colposcopy and Pathology in Evaluating Precancerous Cervical Lesions” by Pleş L, Radosa JC, Sima RM et al., MDPI, licensed under CC BY 4.0.
High-grade squamous intraepithelial lesion (HSIL) of the cervix
High-grade squamous intraepithelial lesion (HSIL) of the cervix

Colposcopy prior to application of acetic acid.

The structure of the cervix appears disorganized. The tissue is friable, bleeding easily when touched.

Friable cervical tissue is suggestive of a high-grade lesion. Biopsy confirmed HSIL.


Source: “Fig 3A, In: The Influence of SARS-CoV-2 Pandemic in the Diagnosis and Treatment of Cervical Dysplasia” by Istrate-Ofițeru AM, Berbecaru EIA, Ruican D et al., MDPI, licensed under CC BY 4.0. Modifications: image cropped + removal of the letter A and in-image text.

Pathology

  • Invasive cervical carcinoma is characterized by invasion of the tumor beyond the basement membrane of the cervical epithelium.
  • HSIL and invasive cervical carcinoma most commonly arise from metaplastic squamous cell epithelium in the cervical transformation zone (see “Microscopic anatomy of the cervix” in “Female reproductive organs” for more information on the histology of the cervix).

Squamous cell carcinoma (∼ 80% of cases) [18]

  • Subtypes include large cell keratinizing, large cell nonkeratinizing, and papillary squamous cell carcinoma.
  • Irregular cell morphology
  • Hyperchromatic cells with nonspherical nuclei, mitotic activity, and prominent nucleoli
  • Loss of basal membrane
  • Precursor lesion: CIN or SIL [19]

Adenocarcinoma (∼ 20% of cases) [20]

  • Subtypes include mucinous, endometrioid, clear-cell, and serous adenocarcinoma
  • The most common is the endocervical mucinous subtype
  • Precursor lesion: endocervical adenocarcinoma in situ [19]

Clear-cell carcinoma of the cervix (CCC) [21]

  • Rare form of cervical cancer (∼ 4% of all cervical adenocarcinomas)
  • Frequently associated with exposure to diethylstilbestrol (DES).

Atypical columnar epithelium with elongated nuclei

  • Small-cell carcinoma: ∼ 2% of cases [22][23]
    • Neuroendocrine tumor
    • Infiltration of monotonous round atypical cells, arranged in a nesting pattern
    • Nuclei with salt-and-pepper chromatin

Almost all squamous cell carcinomas and approx. 90% of adenocarcinomas of the cervix are positive for HPV. [6]

Cervical carcinoma and HSIL most commonly arise from metaplastic squamous cell epithelium in the cervical transformation zone. [6]

Histopathological grades of cervical cancer
Histopathological grades of cervical cancer

LSIL: low-grade squamous intraepithelial neoplasia
HSIL: high-grade squamous intraepithelial neoplasia
CIN: cervical intraepithelial neoplasia


© AMBOSS
Squamous cell carcinoma of the cervix
Squamous cell carcinoma of the cervix

Photomicrograph of cervical tissue (H&E stain; low magnification)

Cancer cells with nuclear atypia are growing within the subepithelial stroma (purple area). Tumor necrosis is present throughout the cancerous mass, seen here as an amorphous eosinophilic accumulation of cell debris. The abundance of neutrophils accompanying the invasive component is a sign of active inflammation secondary to malignant neoplasia.

This is the typical appearance of squamous cell carcinoma of the cervix.

Click on the Smartzoom button to view the entire specimen through a virtual microscope.


Source: © Smart Zoom, Smart In Media. Image and annotations in digital microscopy: PD Dr. Alberto Perez Bouza
Adenocarcinoma in situ (AIS) of the cervix
Adenocarcinoma in situ (AIS) of the cervix

Photomicrograph of a PAP smear showing glandular cells of the cervix (Papanicolaou stain, very high magnification)

A cluster of atypical endocervical cells showing hyperchromatic elongated nuclei (examples indicated by yellow overlay), overlapping nuclei (indicated by (dashed) lines), and an increased nuclear-cytoplasmic ratio (indicated by distance lines) is seen in the center.
A normal intermediate squamous epithelial cell can be seen on the left.

These findings are typical of dysplastic cells and represent AIS of the cervix.


Source: “Adenocarcinoma in Situ of the Cervix” by Ed Uthman, flickr, licensed under CC BY 2.0. The supplementary image with overlays of relevant areas was adapted from the image mentioned above (© AMBOSS).
Endocervical Adenocarcinoma
Endocervical Adenocarcinoma

Photomicrograph of a pap smear showing endocervical glandular cells (Papanicolaou stain, high magnification)

On the right side a normal intermediate squamous cell with a regular nucleus and cyanophilic cytoplasm is shown (arrow).
In the center a thick, three-dimensional appearing cluster of atypical glandular cells with irregular, crowded hyperchromatic nuclei can be seen. Additionally, binucleate cells (examples indicated by yellow dashed overlay) and prominent nucleoli (examples indicated by arrowheads) are present. Some of the cells contain unstained intracytoplasmic vacuoles filled with mucin indicating endocervical glandular origin (examples indicated by yellow overlay).

These findings are indicative of endocervical adenocarcinoma.


Source: “Adenocarcinoma on pap test 1” by Nephron, Wikimedia Commons, licensed under CC BY-SA 3.0. The supplementary image with overlays of relevant areas was adapted from the image mentioned above and licensed under CC BY-SA 3.0.
Endocervical adenocarcinoma
Endocervical adenocarcinoma

Photomicrograph of an endocervical biopsy specimen (H&E stain; high magnification)

Atypical columnar epithelial cells with elongated nuclei are visible (green overlays). There is an abundance of neutrophils (as a sign of inflammation secondary to neoplasia; yellow overlays) within the subepithelial stroma indicating an invasive tumor. Parts of the invasive component can be seen in the center and at the bottom of the image (red overlays).

This appearance is characteristic of endocervical adenocarcinoma.


Source: “Endocervical adenocarcinoma (1)” by KGH, Wikimedia Commons, licensed under CC BY-SA 3.0. The supplementary image with overlays of relevant areas was adapted from the image mentioned above and licensed under CC BY-SA 3.0.

Staging

  • Staging of invasive cervical cancer is based on the extent of the primary tumor and spread; routes of spread include: [5]
    • Direct extension into the vagina, uterus, parametrium, pelvic wall, and adjacent organs (e.g., bladder, rectum)
    • Lymphatic spread, first to the regional pelvic lymph nodes, and then to the paraaortic lymph nodes.
    • Hematogenous spread causing distant metastases (e.g., to lungs, liver, bone) occurs late in the course.
  • The revised (2018) FIGO staging is preferred to determine the appropriate treatment of cervical cancer and the likely prognosis of the disease. [5][17][24]
  • FIGO staging aligns closely with the American Joint Committee on Cancer (AJCC) tumor, node, metastasis (TNM) staging. [5][25]
  • The TNM classification also includes a stage 0 (Tis) for carcinoma in situ (CIN III). [25]

Determination of stage [5][26][27]

Refer patients with confirmed invasive cervical cancer to a specialist (e.g., gynecologic oncologist, surgical oncologist) for staging. Staging is based on the following parameters. [5]

  • Clinical examination: comprehensive physical exam, bimanual pelvic examination, colposcopy
  • Cervical biopsy and lymph node biopsy findings
  • Imaging [5][24][28][29]
    • Evaluation of primary tumor size and local extent: MRI pelvis without and with IV contrast (preferred)
    • Lymph node involvement: FDG-PET scan
    • Local extent: evaluation for hydronephrosis, cystoscopy, and sigmoidoscopy
    • Distant metastasis: chest imaging, FDG-PET scan

Assessment of the primary tumor and lymph node involvement on imaging and/or intraoperatively is not mandatory for cervical cancer staging. In resource-poor settings, staging can be based on clinical examination and diagnostic histopathology results. [26]

Histopathological assessment and imaging are adjuncts to clinical findings in assessing the pretreatment stage of invasive cervical cancer. Histopathological findings take precedence over imaging findings. [5][26]

FIGO staging of cervical cancer [5][26][27]

FIGO staging of cervical cancer (2018) [5][26][27]
Tumor location and spread
I
  • Tumor strictly confined to the cervix
    • IA: microscopic stromal invasion ≤ 5 mm
    • IB: gross or microscopic stromal invasion > 5 mm in depth
II
  • Extension beyond the uterus but does not involve the pelvic wall or lower third of the vagina
    • IIA: upper two-thirds of the vagina, no parametrial invasion
    • IIB: with parametrial invasion
III
  • Tumor invades pelvic wall and/or lower third of the vagina and/or causes hydronephrosis or nonfunctioning kidney
    • IIIA: tumor involves lower third of the vagina, no extension to the pelvic wall
    • IIIB: tumor invades pelvic wall and/or hydronephrosis or nonfunctioning kidney
    • IIIC: tumor involves pelvic and paraaortic lymph nodes (including micrometastases)
IV
  • Tumor extends beyond the true pelvis or (biopsy-proven) involvement of the vesical or rectal mucosa
    • IVA: tumor spread to adjacent organs
    • IVB: tumor spread to distant organs

If there is any discrepancy in staging, the lower stage should be assigned. [26]

Treatment

Management of invasive cervical cancer in nonpregnant individuals is described here. Management of cervical cancer precursors and management of invasive cervical cancer during pregnancy are detailed separately. [5]

Early disease (FIGO stages IA, IB1, IB2 IIA1)

  • Surgery is preferred.
    • Conization (with or without pelvic lymphadenectomy) and radical trachelectomy are fertility-sparing options.
    • Hysterectomy (simple hysterectomy, modified radical hysterectomy, and radical hysterectomy) with bilateral pelvic lymphadenectomy is usually recommended for more advanced disease (stage ≥ IA2)
  • If surgery is not feasible: Radiotherapy may be considered.

Locally advanced disease (FIGO stages IB3, IIA2, III, IVA)

  • Concurrent chemoradiotherapy (CCRT) using platinum-based agents is preferred.
  • Pelvic exenteration may be considered in select patients with stage IVA cervical cancer that has not extended to the pelvic side wall.

Distant metastases (FIGO Stage IVB)

  • Palliative systemic chemotherapy for disease and symptom control
  • Palliative radiotherapy, CCRT, or immunotherapy may be considered depending on patient performance status and extent of metastatic disease.

Prior to surgery, patients who opt for fertility-preserving options should be counseled on potential postoperative obstetric complications and be referred to a fertility specialist to discuss future reproductive plans. [5][30]

Consider hormone replacement therapy for patients < 50 years of age who have lost ovarian function. [5]

Follow-up [5]

  • General principles
    • A thorough clinical examination and history should be taken at each follow-up visit.
    • Imaging is not routinely indicated.
  • After treatment for invasive cervical cancer: Follow-up is recommended at the following intervals.
    • Every 3–4 months for 2–3 years
    • Followed by every 6 months for 3–5 years
    • Then annually for life
  • After fertility-sparing surgery for microinvasive cancer: Resume routine age-appropriate screening for cervical cancer if follow-up testing is negative for 5 consecutive years.

Surgical interventions for cervical cancer

Conization (cervical excisional procedure) [31]

A fertility-preserving diagnostic and therapeutic procedure in which a cone-shaped portion of the cervix including the ectocervix, endocervix, and cervical transformation zone are excised

  • Indications [5][11]
    • Treatment of high-grade cervical abnormalities on screening
    • Treatment of early-stage cervical cancer
  • Important contraindications include pregnancy and severe cervicitis [11]
  • Methods
    • Cold-knife conization
      • A scalpel is used to remove a cone-shaped portion of cervical tissue.
      • Typically requires general or regional anesthesia
    • Loop electrosurgical excision procedure (LEEP)
      • A thin electric wire loop is used to remove abnormal cervical tissue.
      • Can be performed under local anesthesia as an office procedure
    • Laser conization
  • Common complications: bleeding, infection, obstetric complications (preterm delivery) [31]

LEEP is usually the preferred method of conization. [11]

Radical trachelectomy [30]

A surgical procedure that includes removal of the cervix, upper vagina, and parametrium with or without bilateral pelvic lymphadenectomy; followed by anastomosis of the uterus and vagina. [5][30]

  • Indication: fertility-sparing procedure for early-stage cervical cancer [5][11][30]
  • Complications include: [30]
    • Anastomosis-related (e.g., dyspareunia, internal cervical stenosis, secondary endometriosis)
    • Obstetric complications: cervical insufficiency, chorioamnionitis, PPROM, preterm delivery

Hysterectomy [5]

  • Types
    • Simple hysterectomy: removal of the uterus and cervix; vagina and parametrium are preserved
    • Modified radical hysterectomy: en bloc removal of the uterus, cervix, upper ¼ of the vagina, and the parametrium
    • Radical hysterectomy: en bloc removal of uterus, cervix, upper ⅓ to upper ½ of the vagina, the parametrium , and, if needed, resection of involved aspects of the adjacent organs
  • Indication (for cervical cancer): early-stage disease
  • Approach: laparotomy, laparoscopy, or robotic surgery through a transabdominal or transvaginal approach
  • Complications include: bleeding, infections, and injury to surrounding organs (e.g., ureter, bladder, pelvic nerves) [32]

Pelvic exenteration (gynecology)[33]

A radical procedure that involves an en bloc resection of the uterus, ovaries, fallopian tubes, vagina, the lower urinary tract, rectosigmoid, and pelvic lymph nodes. Associated with high morbidity.

  • Indication: a potentially curative option for locally advanced cervical cancer
  • Complications include: [33]
    • Hemorrhage
    • Infection
    • Intestinal obstruction
    • Intestinal and urinary fistulas
Cervical conization
Cervical conization

Excision of dysplastic cervical tissue including the entire transformation zone

Left: In premenopausal women, most of the transformation zone is located in the ectocervix (the visible portion of the cervix), with only a small portion extending into the endocervix. Therefore only a small, flat cone of tissue needs to be removed.

Right: In postmenopausal women, the transformation zone extends much deeper into the endocervix, with only a small portion located in the ectocervix. Therefore, a deeper cone must be excised to remove the entire transformation zone.


© AMBOSS
Radical trachelectomy
Radical trachelectomy

A surgical procedure that involves removing approximately two-thirds of the cervix, the surrounding parametrium, and a small vaginal cuff.

Left image: preoperative condition with resection margins (indicated by dashed lines).

Right image: postoperative condition after the vagina is reattached to the remaining cervix (dashed line).


© AMBOSS

Special patient groups

Management of invasive cervical cancer during pregnancy [5]

  • Treatment should be individualized and carried out by a multidisciplinary team (e.g., gynecologic oncologist, maternal-fetal specialist).
  • Treatment options are the same as those for nonpregnant individuals (see “Treatment of cervical cancer” for details).
  • The timing of treatment depends on the cancer stage, gestational age, and the patient's wish to maintain the current pregnancy.
Treatment of invasive cervical cancer during pregnancy [5]
< 20 weeks' gestation
  • Consider treatment without delay.
> 20 weeks' gestation Early stage (FIGO stages IA1, IA2, IB1, IB2)
  • Consider delaying treatment until the postpartum period.
  • Early delivery (within the 34th week of gestation) can be considered to facilitate earlier treatment.
Advanced stage
  • The effect of delaying treatment on prognosis is not known.
  • Locally advanced disease (FIGO stages IB3, IIA2, III, IVA)
    • Consider neoadjuvant chemotherapy in women who do not wish to terminate the pregnancy.
    • Administer definitive treatment in the postpartum period.

Complications

Direct complications of invasive cervical cancer

  • Local infiltration of organs
    • Infiltration and compression of ureter → urinary obstruction → hydronephrosis → kidney failure (bilateral obstruction is a potentially fatal complication)
    • Other organs often affected by the spread of cervical cancer include the rectum, bladder, and vagina.
  • Fistula formation in locally advanced disease (e.g., rectovaginal, vesicovaginal, urethrovaginal fistula)
  • Compression of veins or lymphatic vessels in the lesser pelvis → lymphedema of the lower extremities
  • Metastasis [34]
    • Bone metastasis: bone pain, pathologic fractures, spinal compression, hypercalcemia
    • Liver metastasis: abdominal pain, abdominal distention, nausea, jaundice
    • Lung metastasis: cough, hemoptysis, dyspnea, chest pain
    • Brain metastasis: headaches, seizures, cognitive deficits, focal neurological deficits
  • Cancer anorexia-cachexia syndrome (CACS) [35]

Complications of radiation therapy [36]

  • Vaginal stenosis
  • Postirradiation vaginitis (e.g., vaginal dryness, dyspareunia)
  • Radiogenic cystitis/proctitis
  • Radiation may increase the risk of complications like fistula formation. [37]

We list the most important complications. The selection is not exhaustive.

Prognosis

  • Cervical cancer has the best prognosis out of the three main gynecological cancers (ovarian, endometrial, and cervical cancer).
  • The survival rates decrease with increasing FIGO stage [38]
    • Stage 0: > 93%
    • Stage I: 93%
    • Stage II: 63%
    • Stage III: 35%
    • Stage IV: 16%
  • Patients without lymph node involvement have a very good prognosis, regardless of FIGO stage.
  • Main cause of death: uremia, often occurs secondary to bilateral ureteral obstruction.

Prevention

  • Primary prevention [7][39][40]
    • HPV immunization (see “ACIP immunization schedule” for details)
    • Use of barrier protection (condoms) during sexual intercourse
  • Secondary prevention: adherence to cervical cancer screening recommendations

External Resources

References

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