Endometrial cancer nursing: assessment, staging, and care priorities

Endometrial cancer is the most common gynecologic malignancy in the United States, accounting for approximately 66,000 new diagnoses annually. Unlike cervical cancer – which is declining due to vaccination and screening – endometrial cancer incidence has been rising steadily, driven largely by increasing rates of obesity and metabolic syndrome. Despite that trend, most endometrial cancers are diagnosed early: postmenopausal bleeding drives prompt evaluation, and the majority of patients present with Stage I disease, where survival rates exceed 90%.

For nurses and NCLEX candidates, endometrial cancer is high-yield across multiple domains: hormone biology, Lynch syndrome genetics, surgical nursing, radiation care, and an evolving targeted therapy landscape that now includes immunotherapy for mismatch repair-deficient tumors. This article completes the gyn-oncology cluster alongside cervical cancer nursing and ovarian cancer nursing. The oncology nursing reference covers the broader chemotherapy safety framework that applies to the systemic treatments described here.

Epidemiology and risk factors

Endometrial cancer arises from the endometrium – the glandular lining of the uterine body. It is the most common gynecologic malignancy and the fourth most common cancer overall in American women. Average age at diagnosis is 63; approximately 75% of cases occur after menopause, though premenopausal endometrial cancer is well recognized, particularly in women with PCOS and Lynch syndrome.

The central pathophysiologic driver of the dominant endometrial cancer subtype is unopposed estrogen – circulating estrogen that stimulates endometrial proliferation without the balancing effects of progesterone. This is the lens through which most risk factors should be understood.

Major risk factors:

• Obesity: The strongest modifiable risk factor. Adipose tissue converts androgens to estrone via peripheral aromatization, creating a chronic low-level estrogen state without progesterone opposition. Women with BMI >30 have 2–3× the risk; BMI >40 carries approximately 6× the risk.
• Nulliparity: Each pregnancy temporarily suppresses endometrial proliferation via progesterone; never being pregnant removes that protective window.
• Late menopause (after age 55): Extends the cumulative duration of estrogen exposure.
• Polycystic ovary syndrome (PCOS): Chronic anovulation means persistent estrogen stimulation without cyclic progesterone – a direct parallel to unopposed estrogen use.
• Exogenous unopposed estrogen: Estrogen-only hormone therapy (without progestogen) in a woman with an intact uterus substantially increases endometrial cancer risk. Combined estrogen-progestogen HRT does not carry this risk.
• Tamoxifen: A selective estrogen receptor modulator used in breast cancer treatment. Tamoxifen acts as an estrogen agonist in endometrial tissue, thickening the lining. Women on tamoxifen have approximately 2–3× the baseline risk. Nurses managing breast cancer patients on tamoxifen must instruct them to report any abnormal uterine bleeding immediately.
• Diabetes mellitus / insulin resistance: Independent of obesity, hyperinsulinemia promotes endometrial cell proliferation.
• Lynch syndrome: A hereditary mismatch repair (MMR) deficiency syndrome that dramatically elevates lifetime risk. Endometrial cancer is the most common Lynch-associated malignancy in women, with lifetime risk of 40–60%. Lynch syndrome is discussed in detail below.

Protective factors: Oral contraceptive use, multiparity, and physical activity are protective. Intrauterine devices (particularly levonorgestrel-IUDs) substantially reduce risk by delivering local progestogenic effect to the endometrium.

Histology: Type I vs Type II

Endometrial cancers are not biologically uniform. The most clinically useful classification divides them into two broad subtypes with different drivers, prognosis, and treatment implications.

The distinction matters clinically because Type II cancers can present in postmenopausal women without the expected obesity-estrogen background, reminding nurses not to dismiss bleeding as benign based on body habitus alone.

Clinical presentation

Postmenopausal bleeding is the cardinal symptom and the most important NCLEX principle for endometrial cancer. Any vaginal bleeding in a postmenopausal woman must be evaluated as endometrial cancer until proven otherwise – it is not acceptable to attribute it to vaginal atrophy or other benign causes without first ruling out malignancy. Approximately 90% of endometrial cancer cases present with this symptom, and the symptom predictably produces early-stage diagnoses.

In premenopausal women, abnormal uterine bleeding (AUB) – including intermenstrual spotting, heavy cycles, or irregular bleeding in a woman with known PCOS – warrants endometrial evaluation when other causes have been excluded or when clinical suspicion is high (age >45, obesity, Lynch syndrome history).

Additional symptoms that suggest more advanced disease:

• Pelvic pain or pressure: May indicate myometrial invasion or spread to adjacent structures
• Watery or blood-tinged vaginal discharge
• Urinary or bowel symptoms: Suggest parametrial, bladder, or rectal involvement

Early endometrial cancer is rarely associated with an abnormal physical examination; the uterus may feel normal on bimanual palpation even with active disease.

Diagnostics

Transvaginal ultrasound

Transvaginal ultrasound (TVUS) is typically the first imaging study performed. In a postmenopausal woman, an endometrial stripe thickness >4 mm on TVUS is the threshold that warrants tissue sampling. An endometrial stripe ≤4 mm carries a very low risk of malignancy and can – in low-clinical-suspicion cases – support a decision to defer biopsy. Note: this threshold does not apply to premenopausal women or women on tamoxifen, where normal endometrial thickness varies significantly.

Endometrial biopsy

Endometrial biopsy (EMB) is the first-line diagnostic test for suspected endometrial cancer. It is performed in the office without anesthesia, using a thin flexible cannula inserted through the cervix to obtain a tissue sample. Sensitivity for endometrial cancer is approximately 90–96%.

NCLEX point: endometrial biopsy is first-line – not dilation and curettage (D&C). D&C is reserved for cases where EMB is inadequate (insufficient tissue, cervical stenosis preventing biopsy, or high clinical suspicion despite negative EMB), or when full uterine curettage is needed for staging or therapeutic purposes.

Dilation and curettage (D&C) and hysteroscopy

D&C under anesthesia provides a larger, more complete tissue sample and is often combined with hysteroscopy – direct visual examination of the uterine cavity using a thin scope. Hysteroscopy identifies focal lesions (polyps, focal hyperplasia) that a blind biopsy might miss and allows directed biopsy under visualization. It is particularly useful when office biopsy is non-diagnostic.

CA-125

CA-125 is not useful as a primary diagnostic marker for endometrial cancer (far less specific than in ovarian cancer). However, it is used pre-operatively to assess for extrauterine disease – a significantly elevated CA-125 (>35 U/mL) may suggest lymph node involvement, peritoneal spread, or adnexal extension, influencing surgical planning. It is also used post-treatment to monitor for recurrence.

Imaging for staging

Once tissue diagnosis is confirmed, staging workup includes:

• MRI pelvis with contrast: Best modality for assessing depth of myometrial invasion and cervical involvement, which directly determines FIGO stage
• CT chest/abdomen/pelvis or PET-CT: Evaluates lymph nodes and distant metastases
• Molecular testing: MMR protein immunohistochemistry (IHC) or MSI testing – now recommended on all endometrial cancers per SGO guidelines, both for Lynch syndrome identification and to guide pembrolizumab eligibility

FIGO 2023 staging

The International Federation of Gynecology and Obstetrics released updated endometrial cancer staging in 2023. The revision added molecular subgroups and refined substage definitions to better reflect prognosis. This replaces the FIGO 2009 system – NCLEX questions may reflect either version, but the 2023 update is now the standard.

Treatment

Surgery: TH-BSO

Total hysterectomy and bilateral salpingo-oophorectomy (TH-BSO) is the standard surgical treatment for endometrial cancer. Removal of the uterus, fallopian tubes, and ovaries is the cornerstone for nearly all stages. The procedure can be performed via open laparotomy, laparoscopy, or robotic-assisted laparoscopy depending on tumor size, patient comorbidities, and surgeon experience. Minimally invasive approaches offer shorter hospital stays and lower complication rates without compromising oncologic outcomes for early-stage disease.

Pelvic and para-aortic lymph node dissection (PLND/PALND) is added for intermediate and high-risk cases to pathologically assess nodal spread. Sentinel lymph node (SLN) mapping – injecting dye (indocyanine green or blue dye) into the cervix to identify and remove the first draining lymph node – has become an alternative to full lymphadenectomy in low-to-intermediate risk cases, reducing lymphedema risk while maintaining accurate staging.

When lymph node dissection has been performed, nurses must be alert to post-operative lymphedema risk – particularly lower extremity lymphedema following pelvic node dissection. See lymphedema nursing for full management protocols.

Radiation therapy

Two radiation modalities are used in endometrial cancer:

Vaginal brachytherapy (VBT): A cylindrical applicator is inserted into the vagina to deliver focused radiation to the vaginal cuff – the surgical closure site after hysterectomy. This is the most common adjuvant treatment for Stage I–II endometrial cancer after TH-BSO in intermediate-risk cases. It reduces vaginal cuff recurrence rates significantly with low systemic toxicity. Administered as high-dose rate (HDR) in multiple outpatient fractions.

External beam radiation therapy (EBRT): Delivers radiation to the whole pelvis (and extended field to para-aortic nodes for Stage IIIC2). Used for higher-risk stages or where nodal coverage is needed. Can be combined with VBT or given alone.

Chemotherapy

Carboplatin and paclitaxel (carboplatin AUC 5–6 + paclitaxel 175 mg/m² IV q3 weeks) is the standard regimen for advanced or recurrent endometrial cancer (Stage III–IV) and for high-grade histologies (serous, clear cell, carcinosarcoma) even at early stages. This is the same doublet used in ovarian cancer, which means the same nursing monitoring priorities apply.

Key pharmacologic nursing points:

• Carboplatin hypersensitivity: Risk increases with cumulative exposure – patients who have received 6+ prior platinum cycles are at significantly elevated risk for infusion reactions, which can progress to anaphylaxis. Symptoms include facial flushing, urticaria, bronchospasm, back pain, and hypotension. Pre-treatment regimens include diphenhydramine and corticosteroids. Have epinephrine, antihistamines, and bronchodilators at bedside.
• Paclitaxel premedication protocol: Paclitaxel causes hypersensitivity reactions due to its Cremophor EL solvent. Standard premedication: dexamethasone 20 mg PO/IV the evening before and morning of infusion (or 12 and 6 hours before), plus diphenhydramine 50 mg IV and an H2 blocker (ranitidine or famotidine) IV 30–60 minutes before infusion.
• Peripheral neuropathy: Paclitaxel causes sensory neuropathy – numbness, tingling, burning in hands and feet – in proportion to cumulative dose. Assess neurologically before each cycle. Neuropathy that impairs function is grounds for dose reduction or discontinuation.
• Nephrotoxicity awareness: Carboplatin is renally cleared and dosed by AUC (Calvert formula using GFR). Renal function must be assessed before each cycle. See AKI nursing for monitoring principles.

Targeted and immunotherapy

Pembrolizumab (a PD-1 checkpoint inhibitor) has become a standard addition to carboplatin/paclitaxel for endometrial cancers with mismatch repair deficiency (dMMR) or microsatellite instability-high (MSI-H) status. The combination improves progression-free and overall survival compared to chemotherapy alone. MSI-H/dMMR endometrial cancer accounts for approximately 25–30% of all endometrial cancers – a substantial proportion.

Lenvatinib + pembrolizumab is approved for advanced endometrial cancer that is not MSI-H/dMMR (i.e., microsatellite stable, or MSS). Lenvatinib is a multi-targeted tyrosine kinase inhibitor; the combination exploits synergy between anti-angiogenic and immunotherapy effects.

Progestins (medroxyprogesterone acetate, megestrol acetate) are used for low-grade, hormone receptor-positive recurrent endometrial cancer – particularly in the fertility-sparing context where hysterectomy has been declined. Progestins counteract the estrogen-driven proliferation of Grade 1 endometrioid tumors. Response rates of 25–30% are achievable in well-selected patients.

Lynch syndrome and MMR testing

Lynch syndrome is a hereditary DNA mismatch repair (MMR) deficiency syndrome caused by germline mutations in one of four MMR genes: MLH1, MSH2, MSH6, or PMS2. It is the most common hereditary colorectal cancer syndrome, but endometrial cancer is the most common Lynch-associated malignancy in women – with lifetime risk estimates of 40–60% depending on the specific gene mutation.

Endometrial cancer as a sentinel Lynch malignancy: A substantial proportion of Lynch syndrome diagnoses are first recognized because a woman presents with endometrial cancer – before any colorectal cancer has occurred. This makes universal MMR testing of endometrial cancers a significant public health intervention: identifying a Lynch-associated endometrial cancer leads to cascade genetic testing in family members, enabling life-saving colorectal cancer surveillance and prophylactic procedures.

The Society of Gynecologic Oncology (SGO) now recommends universal MMR/MSI testing on all endometrial cancers – not just those in young patients or those with family history. Universal testing outperforms clinical criteria-based selection.

MMR testing methods:

• Immunohistochemistry (IHC): Tissue staining for the four MMR proteins (MLH1, MSH2, MSH6, PMS2). Loss of any protein staining (“dMMR”) triggers follow-up testing.
• MSI-PCR or next-generation sequencing: Detects microsatellite instability directly from DNA. MSI-H correlates with dMMR in most cases.
• MLH1 promoter methylation: When MLH1 protein is lost, methylation testing distinguishes sporadic epigenetic silencing (not Lynch) from germline MLH1 mutation (Lynch). If MLH1 methylation is present → sporadic; if absent → germline testing recommended.

Nurses play a key role in facilitating this pathway: ensuring tumor tissue is collected and sent for MMR testing at time of surgery, and supporting patients through the process of genetic counseling when germline testing is indicated.

Nursing priorities

Preoperative care (TH-BSO)

• Bowel preparation: Surgeon-specific; mechanical prep may be ordered, though evidence for routine pre-op bowel prep in gynecologic surgery is mixed.
• VTE prophylaxis education: Cancer patients undergoing major pelvic surgery carry a high VTE risk. Sequential compression devices (SCDs) are applied before induction of anesthesia and continued postoperatively. Low-molecular-weight heparin (LMWH) is typically initiated 12–24 hours post-operatively and continued 28 days in high-risk cases (extended prophylaxis). Refer to DVT nursing for full VTE risk stratification and prophylaxis protocols.
• Consent and counseling: Confirm patient understanding of surgical menopause (bilateral oophorectomy) in premenopausal women – acute onset of vasomotor symptoms, sexual health changes, and long-term bone and cardiovascular implications should be addressed.

Postoperative care (TH-BSO)

Drain management: A Jackson-Pratt (JP) drain is often placed in the pelvis at surgery. Nurses must:

• Record drain output (volume and character) at each assessment
• Assess for signs of lymphatic leak (high-volume, clear/straw-colored output) vs. normal sanguineous-to-serosanguineous drainage
• Watch for sudden decrease in output with new abdominal pain/distension (drain obstruction or hematoma)
• Teach patient drain care if discharged with drain in place

Urinary retention monitoring: Radical hysterectomy with extensive pelvic dissection can transiently impair bladder function (as detailed in the cervical cancer reference). Even standard TH-BSO affects pelvic anatomy and bladder positioning; assess for urinary retention when the urinary catheter is removed. Measure post-void residuals if the patient reports incomplete emptying.

VTE prophylaxis (ongoing): Continue SCDs while patient is in bed or ambulating minimally. Ensure LMWH prophylaxis is administered per protocol. Early ambulation is the most effective mechanical prophylaxis – get the patient out of bed on post-operative day 1 if hemodynamically stable.

Wound care: Assess laparoscopic port sites or laparotomy incision for signs of infection (redness, warmth, induration, purulent drainage), hematoma, or dehiscence. Document and report any abnormal findings promptly.

Lymphedema risk education: If pelvic lymph nodes were dissected, initiate early lymphedema education before discharge. Key instructions: avoid compression from tight clothing, avoid prolonged dependent positioning, skin protection, report any limb heaviness or swelling. See lymphedema nursing for full protocols.

Surgical menopause management (if premenopausal): Bilateral oophorectomy in premenopausal women triggers immediate surgical menopause. Counsel on hot flashes, sleep disruption, genitourinary symptoms, and mood changes. Hormone therapy discussion should involve the oncology team – it is generally avoided in endometrial cancer but may be considered case-by-case.

Radiation therapy nursing

Vaginal brachytherapy nursing care:

HDR brachytherapy for endometrial cancer is typically administered in 3–5 outpatient fractions. Patients are not radioactive between treatments, so no radiation precautions are needed outside the treatment room.

At each fraction:

• Confirm that no metallic pelvic implants or contraindications are present
• Provide analgesic per protocol before applicator insertion (a vaginal cylinder is inserted and held in place during treatment, which takes approximately 10–20 minutes)
• Monitor for vasovagal response during insertion
• Instruct the patient to remain still during treatment; the applicator must not be displaced

Vaginal stenosis prevention: Pelvic radiation causes progressive vaginal fibrosis. After completing brachytherapy, patients must be instructed on vaginal dilator use:

• Begin 2–4 weeks after radiation completes
• Use a vaginal dilator with water-based lubricant 3 times per week
• Start with the smallest size and progress gradually
• The purpose is to prevent stenosis that would cause dyspareunia and interfere with future gynecologic exams

This instruction is often omitted or delivered too briefly. Nurses should present it matter-of-factly as a necessary medical intervention and provide written instructions to reinforce verbal counseling.

External beam radiation nursing:

EBRT to the pelvis causes radiation enteritis (diarrhea, cramping, urgency) and radiation cystitis (dysuria, frequency, urgency, hematuria) during and after treatment. Nursing management:

• Bowel: Low-fiber diet during active treatment to reduce bulk transit; anti-diarrheal agents (loperamide) as needed; perineal skin care
• Bladder: Hydration to dilute urine; avoid bladder irritants (caffeine, alcohol); monitor urine output
• Skin: Radiation dermatitis in the pelvic field; gentle cleansing, moisture barriers, no topical products with alcohol, loose cotton clothing

Chemotherapy nursing (carboplatin/paclitaxel)

Before each cycle:

• Assess CBC, CMP, and renal function (GFR for carboplatin dosing)
• Assess for cumulative neuropathy (sensory symptoms in hands and feet)
• Administer paclitaxel premedication per protocol: dexamethasone, diphenhydramine, H2 blocker
• Review allergy history and cycle number for carboplatin hypersensitivity risk

During infusion:

• Infuse paclitaxel first (over 3 hours), then carboplatin (over 30–60 minutes)
• For paclitaxel: observe closely during the first 15 minutes; most hypersensitivity reactions occur in the first 2–3 cycles
• For carboplatin (especially after cycle 6): observe for flushing, urticaria, bronchospasm, back pain, hypotension. Have epinephrine 0.3 mg IM available
• Manage nausea with prescribed anti-emetics; carboplatin is moderately emetogenic; paclitaxel is moderately emetogenic

Post-infusion:

• Instruct patient to report peripheral neuropathy symptoms before next cycle
• Monitor ANC nadir (10–14 days); neutropenic fever precautions
• Carboplatin-induced thrombocytopenia: platelet nadir at days 14–21; assess for bruising, petechiae, prolonged bleeding

NCLEX differentiation: endometrial vs cervical vs ovarian

The three gynecologic cancers are frequently compared on NCLEX. This table organizes the distinguishing features that are most commonly tested.

The full cervical cancer reference is at cervical cancer nursing and ovarian at ovarian cancer nursing.

NCLEX high-yield tips

The following represent the most frequently tested endometrial cancer concepts. Each tip is written as a concise, exam-ready statement.

Tip 1 — Most common gynecologic malignancy Endometrial cancer is the most common gynecologic malignancy in the United States. Ovarian cancer is the deadliest. Cervical cancer is the most preventable. Know which superlative goes with which cancer.

Tip 2 — Postmenopausal bleeding = endometrial cancer until proven otherwise Any vaginal bleeding in a postmenopausal woman must be evaluated as endometrial cancer until tissue sampling confirms otherwise. Never accept atrophy or dryness as the explanation without first performing an endometrial biopsy. This is the single most important NCLEX principle for endometrial cancer.

Tip 3 — Endometrial biopsy is first-line (not D&C) Endometrial biopsy – performed in the office without anesthesia – is the first-line diagnostic test. D&C under anesthesia is reserved for inadequate biopsy samples, cervical stenosis, or high clinical suspicion with negative office biopsy.

Tip 4 — Type I vs Type II distinction Type I (endometrioid, estrogen-driven, ~80–85%, better prognosis) arises from unopposed estrogen and is associated with obesity and PCOS. Type II (serous, clear cell, carcinosarcoma – estrogen-independent, high-grade) arises de novo from atrophic endometrium in thin, older postmenopausal women who may lack the classic risk factor profile.

Tip 5 — Tamoxifen and endometrial cancer risk Tamoxifen is an estrogen agonist in endometrial tissue. Women taking tamoxifen for breast cancer treatment have approximately 2–3× the baseline endometrial cancer risk. Nurses must instruct all patients on tamoxifen to report any abnormal uterine bleeding immediately – it is not expected or benign.

Tip 6 — Lynch syndrome and universal MMR testing Endometrial cancer is the most common Lynch syndrome-associated malignancy in women. SGO recommends universal MMR/MSI testing on all endometrial cancers. A dMMR result that is not explained by MLH1 methylation should trigger germline genetic counseling. Identifying Lynch syndrome through an endometrial cancer diagnosis enables life-saving surveillance for the patient and family members.

Tip 7 — TH-BSO is standard surgical treatment Total hysterectomy and bilateral salpingo-oophorectomy (TH-BSO) is the standard treatment for endometrial cancer. Oophorectomy is included because ovaries are a site of potential spread and because removing them eliminates the source of endogenous estrogen.

Tip 8 — FIGO staging: confined to uterus = Stage I Stage I endometrial cancer is confined to the uterine corpus. Stage II extends to the cervix or parametrium. Stage III involves regional spread (adnexa, vagina, pelvic or para-aortic lymph nodes). Stage IV involves bladder/rectal mucosa (IVA) or distant metastasis (IVB).

Tip 9 — Vaginal dilators post-brachytherapy Pelvic radiation causes progressive vaginal fibrosis and stenosis. Start vaginal dilator therapy 2–4 weeks after brachytherapy is complete. Use with lubricant 3 times per week. This is a long-term survivorship intervention that nurses must initiate and normalize, not leave for patients to ask about.

Tip 10 — Carboplatin hypersensitivity after repeated cycles Carboplatin hypersensitivity risk accumulates with cumulative platinum exposure. Patients who have received 6 or more prior platinum-containing cycles are at elevated risk for infusion reactions, including anaphylaxis. Ensure epinephrine, antihistamines, and corticosteroids are available at bedside. Pre-medicate per protocol.

Tip 11 — Paclitaxel premedication Paclitaxel requires a standardized three-drug premedication protocol: dexamethasone (typically 20 mg PO/IV at 12 and 6 hours before, or IV 30 minutes before infusion), diphenhydramine 50 mg IV, and an H2 blocker (ranitidine or famotidine) IV, given 30–60 minutes before the infusion begins.

Tip 12 — Pembrolizumab for MSI-H/dMMR tumors Pembrolizumab is added to carboplatin/paclitaxel for endometrial cancers with mismatch repair deficiency (dMMR) or microsatellite instability-high (MSI-H) status. Monitor for immune-related adverse events (irAEs): pneumonitis, colitis, hepatitis, endocrinopathies (thyroid, adrenal, pituitary). irAEs may occur weeks to months after treatment begins.

Tip 13 — Lymphedema risk after lymphadenectomy Pelvic lymph node dissection disrupts lymphatic drainage from the lower extremities and pelvis. Educate all patients pre-operatively and post-operatively on lymphedema prevention: protect skin from injury, avoid compression, report limb swelling or heaviness early. Early intervention improves outcomes. See lymphedema nursing.

Tip 14 — Progestins for low-grade recurrent disease High-dose progestins (medroxyprogesterone acetate, megestrol acetate) are used for Grade 1 recurrent endometrial cancer in hormone receptor-positive tumors, particularly in the fertility-sparing context. Response rates are approximately 25–30%. This is the treatment choice when fertility preservation is the goal or when systemic chemotherapy is not appropriate.

Tip 15 — CA-125 monitoring post-treatment CA-125 is not an accurate diagnostic marker for endometrial cancer, but an elevated pre-operative CA-125 suggests extrauterine spread. Post-treatment, CA-125 is used to monitor for recurrence. A rising CA-125 in a patient with history of endometrial cancer warrants imaging evaluation.

Tip 16 — Endometrial stripe threshold On transvaginal ultrasound in a postmenopausal woman, an endometrial stripe >4 mm warrants tissue sampling (endometrial biopsy or D&C). A stripe ≤4 mm in a low-suspicion postmenopausal patient has a very low malignancy risk, but clinical judgment and follow-up still apply.

Tip 17 — Jackson-Pratt drain post-TH-BSO A Jackson-Pratt (JP) drain is commonly placed in the pelvis after TH-BSO with lymph node dissection. Document output character and volume. Sudden decrease with new abdominal pain or distension suggests obstruction or hematoma. Milky or high-volume clear drainage suggests lymph leak (chylous ascites or lymphocele formation).

Related references

Endometrial cancer nursing connects to several broader clinical areas covered in depth elsewhere on this site:

• Cervical cancer nursing — gyn-oncology cluster; FIGO staging comparison, HPV biology, brachytherapy nursing, and vaginal dilator protocols
• Ovarian cancer nursing — gyn-oncology cluster; BRCA genetics, CA-125, surgical debulking, carboplatin/paclitaxel nursing
• Oncology nursing reference — chemotherapy safety framework, hazardous drug handling, oncologic emergency recognition, and extravasation management
• DVT nursing — VTE prophylaxis in the perioperative period; cancer-associated thrombosis; LMWH protocols
• AKI nursing — renal monitoring for carboplatin dosing; nephrotoxicity surveillance
• Lymphedema nursing — post-lymphadenectomy risk, compression therapy, skin protection, and early intervention protocols