Gynecologic Oncology




PERIOPERATIVE CONSIDERATIONS AND COMPLICATIONS



Listen




Bowel Obstruction



Small Bowel Obstructions (SBO)




  • Workup may include imaging (abdominal x-ray, CT scan), CBC, CMP, lactate level



  • Trial of conservative (nonsurgical) management appropriate if no evidence of perforation, ischemia, or strangulation




    • Bowel rest and decompression with nasogastric (NG) tube are appropriate first steps



    • Start GI prophylaxis with Ranitidine (Zantac) 50 mg IV every 8 hours or proton pump inhibitor [eg, pantoprazole (Protonix)]



    • Replace NG tube output [1 cc NS (or LR) per cc NG tube output every 4 hours] and replete electrolyte losses




Note: If obstruction occurs acutely within 1 week of surgery, high likelihood of requiring surgical intervention





  • If conservative management fails




    • Consider risks/benefits of surgical intervention: Consent for exploratory laparotomy, possible bowel resection, possible bypass, possible ostomy



    • Consider preoperative Gastrografin enema to rule out concurrent large bowel obstruction (LBO)



    • Surgery not appropriate in patients with poor prognostic criteria (ie, diffuse intra-abdominal carcinomatosis, multifocal obstruction, poor performance status, or massive ascites)




Note: For women with ovarian cancer and bowel obstruction, data show 90% relieved with surgery, but major morbidity (fistulas and anastomotic leaks) occurred in 32% and perioperative death in 15%. Re-obstruction rate of 10–50%





  • If the patient is not a surgical candidate, consider percutaneous endoscopic gastrostomy (PEG) tube




    • Octreotide (100-300 μg subcutaneously 2-3 times daily) can decrease gastric secretions and slow intestinal mobility → decreases nausea/vomiting associated with SBO



    • Obstruction at cancer diagnosis and mucin histology are associated with recurrent obstructions




Large Bowel Obstruction (LBO)




  • Rare in ovarian cancer patients



  • In general, considered a surgical emergency



  • Surgical management generally involves creation of an ostomy



  • Endoscopic management with rectal stent is possible in select patients (stable, no peritoneal signs, partially obstructed, poor surgical candidate)




Closed Loop Obstruction




  • In general, considered a surgical emergency



  • Commonly due to adhesions. Occurs when two points along the small bowel are obstructed at the same junction, causing necrosis and edema of the internal segment



  • May look like a gasless abdomen on plain films. CT usually diagnostic and may show ground glass haziness in mid-abdomen, displacement of adjacent bowel, dilated clumps of edematous bowel, or classic U or C signs (pathognomonic)




Constipation



First-Line Medications




  • Bisacodyl (Dulcolax) 10 mg orally daily or 10 mg per rectum daily



  • Docusate sodium (Colace) 100 mg orally twice daily



  • Mineral oil 15–45 mL/day



  • Cascara 325 mg orally nightly




Second-Line/More Aggressive Medications




  • Polyethylene glycol (MiraLax) 240–720 mL/day



  • Lactulose 15–30 mL twice daily



  • Sorbitol 120 mL of 25% solution daily



  • Glycerin 3 g per rectum daily or 5–15 mL enemas




Remember: All patients on around-the-clock opiates should be on a bowel regimen



Antimotility Agents




  • Consider in patients with high-output ileostomies or short bowel syndrome in order to avoid dehydration and other electrolyte abnormalities, including hypocalcemia, hypomagnesemia, or hypokalemia



  • Be mindful of stoma outputs greater than 1000 cc/day



  • Loperamide (Imodium) 2 mg orally three times daily



  • Diphenoxylate/atropine (Lomotil)—requires narcotic prescription—2.5 mg orally three times daily



  • Tincture of opium 6 mg orally four times daily—sometimes in drop form (2 drops three times daily may be sufficient)—requires narcotic prescription




Note: Patient education on self-management is crucial



Electrolyte Abnormalities



Potassium


Hypokalemia (serum potassium <3.5 mEq/L)

Causes




  • Transcellular shift: Metabolic alkalosis, insulin, β agonists



  • Extrarenal: Decreased K intake, GI losses including vomiting and diarrhea



  • Renal: Diuresis, hyperaldosterone (primary, secondary), increased glucocorticoids (Cushing’s syndrome), renal tubule disease (renal tubular acidosis)



Signs and Symptoms




  • Diffuse muscle weakness; change in mental status



  • ECG changes: Earliest change is flattened T waves, followed by inversion, U waves may be visible, ST-segment depression, arrhythmias



  • Check magnesium as hypomagnesemia can cause refractory hypokalemia. Magnesium level must be corrected for potassium repletion to be effective



Treatment




  • <3 mEq/L: 40 mEq KCl IV minibag over 4 hours (administer twice)



  • 3.0–3.5 mEq/L: 40 mEq KCl IV minibag over 4 hours once, or 40 mEq potassium chloride (KDur) orally every 4 hours



  • <2.5 mEq/L: Obtain ECG and replace as above



  • Do not replace faster than10 mEq/h.



  • Serum K rises approximately 0.1 for every 10 mEq given




Hyperkalemia

Causes




  • Transcellular shift: Metabolic acidosis, insulin deficiency, β blockers, tissue damage



  • Extrarenal: Excessive potassium intake



  • Renal: Hypoaldosteronism, acute or chronic renal failure



  • Other: Decreased volume, K-sparing diuretics



  • Pseudo-hyperkalemia may be caused by blood draw secondary to hemolysis



Signs and Symptoms




  • ECG changes: Increased T wave amplitude, prolonged PR interval, increased QRS duration, loss of P waves, sine wave pattern, ventricular fibrillation, asystole (Figure 3-1)





Figure 3-1


EKG in hyperkalemia. (Used with permission from Ritchie JV, Juliano ML, Thurman R. Chapter 23. ECG Abnormalities. In: Knoop KJ, Stack LB, Storrow AB, Thurman R., eds. The Atlas of Emergency Medicine. 3rd ed. New York, NY: McGraw-Hill; 2010.)




Treatment




  • Calcium gluconate 1 g over 2-3 minutes (decreases membrane excitability)



  • Insulin/Glucose (shifts into cells)




    • Ex: Insulin 10 units followed by 1 amp D50, then D5-NS at 50 cc/h for 6 hours



    • OR 4 units insulin after 1 L bolus D5



  • Kayexalate (binds potassium)



  • Dialysis




Calcium


Hypocalcemia




  • Ca <8.4 mg/dL. Calcium gluconate 1 gram over 2 hours, or CaC03 650 mg orally three times daily



  • Need to correct Ca for serum albumin: for every 1.0 decrease in albumin less than 4.0, add 0.8 to Ca to replace for corrected calcium <8.4 mg/dL




Hypercalcemia

Differential Diagnosis




  • Primary hyperparathyroidism, malignancy, thyrotoxicosis, chronic kidney disease, milk alkali syndrome, hypervitaminosis D, sarcoidosis, lithium, thiazide diuretics, pheochromocytoma, adrenal insufficiency, rhabdomyolysis/acute renal failure, theophylline toxicity, familial hypocalciuric hypercalcemia, metaphyseal chondrodysplasia, congenital lactase deficiency



  • In cancer, hypercalcemia is often associated with advanced disease and poor outcomes



  • Labs




    • Serum parathyroid hormone (PTH) (if elevated, primary hyperparathyroidism is diagnosis). There is an increased frequency of primary hyperparathyroidism in the oncology population, so this is reasonable to evaluate



    • If serum PTH is low/normal, send PTH-related protein and vitamin D metabolites (calcidiol and calcitriol) to evaluate for hypercalcemia of malignancy and vitamin D intoxication.



    • Consider bone scan if you suspect malignancy



    • Additional labs that may be useful if picture still unclear: Serum and urinary protein electrophoresis (for possible multiple myeloma), TSH, vitamin A, serum phosphate, urinary 24 hour calcium



Treatment




  • Patients who are symptomatic, have an acute rise, or who have a calcium concentration over 14 mg/dL (3.5 mmol/L) require treatment




    • Isotonic saline at 200–300 cc/h (corrects hypovolemia and urinary salt wasting), tapered down to urine output of 100–150 mL/h. Monitor carefully especially in patients with edema/heart/kidney problems. If edema develops, stop IV fluids and consider loop diuretic



    • Calcitonin 5 IU/kg IM every 12 hours, but can increase to 6–8 IU/kg every 6 hours. Tachyphylaxis develops in 48 hours. Nasal calcitonin is not efficacious



    • Bisphosphonates (maximal effect occurs in 2–4 days)




Magnesium




  • Replacement (keep Mg above 1.7 mEq/L)




    • <1 mEq/L: MgSO4 6 g IV minibag over 6 hours



    • 1.1–1.3 mEq/L: MgSO4 4 g IV minibag over 4 hours



    • 1.4–1.6 mEq/L: MgSO4 2 g IV minibag over 2 hours



    • Oral: Magnesium oxide 400 mg orally three times daily




Phosphorus




  • Replacement




    • Phos <2.7 mg/dL: K-phos or Na-phos 15–20 mmol IV minibag over 6 hours. If taking orally, Neutra-Phos 250 mg orally three times daily



  • Neutra-Phos contains approximately 8 mmol Phos/250 mg and 7 mEq K/250 mg



  • Hyperphosphatemia may be seen in patients with chronic kidney disease. These patients should typically be on calcium acetate (PhosLo)




Sodium


Hyponatremia (Figure 3-2)



Figure 3-2


Hyponatremia. (Reprinted with permission from Douglas I. Hyponatremia: why it matters, how it presents, how we can manage it. Cleve Clin J Med 2006; 73(suppl 3):S4-S12. Copyright © 2006 Cleveland Clinic Foundation. All rights reserved.)







  • Calculate serum osmolality: 2 × Na + glucose/18 + BUN/2.8




    • Osm >295 (Hypertonic): Hyperglycemia or mannitol treatment



    • Osm 280–295 (Normal): Increased lipids



    • Osm <280 (Hypotonic): Evaluate volume status, check urine Na



  • Prevent central pontine myelinolysis—don’t correct too quickly



  • Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH): A condition when excess ADH is excreted, typically resulting in decreased urine output, hyponatremia




    • Treatment: Find the underlying cause that can be due to CNS disturbances of malignancy (especially lung). Treat the underlying cause and correct the sodium slowly with normal saline




Quick Reference Materials




  • IV fluid formulations and electrolyte content (Table 3-1)



  • Quick Management Guide (Table 3-2)





TABLE 3-1

IV FLUID FORMULATIONS






TABLE 3-2

ELECTROLYTE ABNORMALITIES: QUICK MANAGEMENT GUIDE





Imaging for Oncology Patients





  • CT Scan: Sensitive to tumors approximately 1–2 cm



  • PET Scan: Sensitive to approximately 8 mm



  • Contrast Dye Allergy




    • Pre-treat with Prednisone 40 mg orally 24 hours before scan, 12 hours before, and immediately before scan



  • Elevated Creatinine: Be particularly careful in patients with glomerular filtration rate (GFR) < 60mL/min or creatinine 1.5 or above (especially if diabetic). If there are no contraindications to volume expansion, pre-treat with IV isotonic bicarbonate (6 mL/kg) 1 hour prior to the procedure and 1 mL/kg/h for 6–12 hours following the procedure (longer for patients with severe renal impairment). If isotonic saline (1 mL/kg/h) is used, this can also be administered 6 hours prior to and 6 hours after the procedure




Pulmonary Embolism (PE)





  • Clinical suspicion: Dyspnea, tachycardia, hypoxia, sense of impending doom



  • Workup




    • Arterial Blood Gas (ABG)—look for A-a gradient [A-a grad = 148 – 1.2 (Paco2) – Pao2]




      • Equation presumes patient is breathing room air at sea level (Fio2 = 0.21)



      • A-a gradient is influenced by age and inspired oxygen. A normal gradient rises with age. Can be as high as 25–35 mm Hg for patients over age 40



      • For patients on supplemental O2, the normal A-a gradient increases 5–7 mm Hg for every 10% increase in Fio2



    • ECG if tachycardic



    • Chest x-ray to look for another cause of desaturation



    • Spiral CT of chest



  • Lower extremity Dopplers to evaluate for DVT




    • Wells Criteria: Determine likelihood of PE (>4 points—very likely)





| Download (.pdf) | Print



























  • Clinical signs/symptoms of DVT


3 points




  • Other causes of desaturation unlikely


3 points




  • Heart rate over 100 bpm


1.5 points




  • Immobilization >3 days OR surgery in past 4 weeks


1.5 points




  • Previous DVT/PE


1.5 points




  • Hemoptysis


1 point




  • Malignancy


1 point







  • Treatment




    • LMWH or UFH drip are equivalent treatment; then transition to warfarin (Coumadin) if appropriate (start 5 mg orally daily for 2 days, then adjust according to INR)



    • LMWH: Enoxaparin (Lovenox) 1 mg/kg SQ every 12 hours




      • LMWH doesn’t require monitoring or dose adjustment but has longer half-life (which makes it more difficult to have lines placed, epidurals pulled, etc)



    • UFH




      • BE CAREFUL BEFORE STARTING HEPARIN BOLUS ON POST-OP PATIENT DUE TO BLEEDING RISK!! CONSIDER STARTING MAINTENANCE DOSE ONLY



      • To Start UFH Treatment




        • Baseline labs: aPTT/PT/INR, CBC, basic metabolic panel



        • Monitor CBC daily until UFH is discontinued



        • If CBC is normal for 7 consecutive days, can decrease frequency of obtaining lab to not less than every 3 days up to day 14. If stable at that point, can obtain weekly



        • See Table 3-3 for UFH Nomogram



      • Anti-Xa UFH activity




        • Measures anticoagulant activity of UFH directed against factor Xa



        • Not affected by lupus anticoagulant, factor VIII or XII activity, warfarin levels



        • No lot-to-lot variations



        • Studies have shown that patients monitored with Anti-Xa UFH activity can achieve therapeutic levels more quickly and require fewer monitoring tests compared to patients monitored with aPTT



        • Therapeutic range remains constant (0.3–0.7 IU/mL)



        • Drawn every 6 hours after initiation of therapy (or dose change) until two therapeutic levels are obtained, then daily



        • CAREFUL: There are Anti-Xa LMWH tests (for monitoring LMWH) and Anti-Xa UFH tests (for monitoring UFH)



    • Transitioning




      • Transition from UFH to LMWH




        • Discontinue UFH concurrently with first dose of LMWH



      • UFH or LMWH to Warfarin Transition




        • During treatment of acute thrombosis, UFH (or LMWH) is continued for at least 5 days and the INR needs to be in goal range for at least 24 hours before UFH (or LMWH) is discontinued



        • Remember: Warfarin dose is not reflected in INR for 2–3 days post dose change; daily increases in dose are not recommended



    • Choice of long-term anticoagulant




      • Warfarin relies on a steady intake of vitamin K, and cancer patients have wide fluctuations in their dietary habits for a variety of reasons (chemotherapy, bowel obstructions, etc). Some data suggest that cancer patients have improved outcomes with LMWH compared to warfarin. However, LMWH is very expensive



      • See Table 3-4 for trials on anticoagulation





TABLE 3-3

UFH NOMOGRAM






TABLE 3-4

ANTICOAGULATION TRIALS





Blood Transfusions



Blood Products




  • Packed Red Blood Cells (PRBCs): Most plasma has been removed; total volume of 1 unit of PRBCs is about 250–300 cc; hematocrit should increase by 3% or hemoglobin by 1 g/dL



  • Platelets: 1 “pack” (6 units) should raise the count by 5000–8000.



  • When to transfuse platelets




    • Part of resuscitation with PRBCs



    • Platelets less than 10 000 (to prevent spontaneous hemorrhage)



    • Platelets less than 50 000 if about to undergo procedure, are actively bleeding, or have a qualitative platelet disorder



    • Platelets less than 100 000 (in patients with CNS injury, multisystem trauma, undergoing neurosurgery, or who require an intrathecal catheter)



    • Normal platelet count but ongoing bleeding and a reason for platelet dysfunction (congenital disorder, chronic aspirin therapy, uremia)



  • Cryoprecipitate: Contains Factor VIII, Factor XIII, von Willebrand’s Factor, and fibrinogen. One unit is about 10 cc



  • Fresh Frozen Plasma (FFP): Contains clotting factors. FFP must be thawed in a 37 degree C waterbath. This usually takes about 30 minutes. FFP has only a 24-hour shelf life; therefore, it is best ordered the same day it will be used. One unit is about 150–250 cc




Transfusion




  • When transfusing PRBCs




    • Premedicate with (prior to each unit)




      • Tylenol 650 mg orally/rectally once



      • Diphenhydramine (Benadryl) 25 mg orally/IV once



    • Each unit should be run in over 3–4 hours



    • Premedication does not necessarily decrease febrile non-hemolytic transfusion reactions



    • Patients with cardiac risk factors may need furosemide (Lasix) (10–20 mg) in between units to prevent volume overload (avoid Lasix in the sulfa-allergic patients)



  • When replacing large volumes of PRBCs, replace platelets and FFP accordingly



  • For acute blood loss anemia, contemporary protocols suggest a 1:1 or 1:2 replacement of PRBCs: FFP



  • In an emergency, anyone can receive type O PRBCs (preferably O negative), and type AB individuals can receive PRBCs of any ABO type. People with type O blood are “universal donors,” and those with type AB blood are “universal recipients.” In addition, AB plasma donors can give to all blood types




Risks of Transmission (Table 3-5)



TABLE 3-5

RISKS OF TRANSMISSION






CRITICAL CARE



Listen




Mechanical Ventilation—The Basics



Conventional Mechanical Ventilation




  • Improves gas exchange and decreases the work of breathing



  • Classified by manner in which inspiration is terminated. Most common are




    • Volume—cycled



    • Pressure—cycled



    • Flow—cycled



    • Time—cycled



  • Majority of postsurgical patients will be on volume-cycled ventilation with pressure support




Volume-Cycled Ventilation








      • Inspiratory phase terminated after delivery of a preset tidal volume



      • Physician sets inspiratory flow, tidal volume, and respiratory rate



      • Airway pressure and inspiratory time are patient related



      • Three common modes of volume-cycled ventilation




        • CMV: Controlled Mechanical Ventilation




          • The minute ventilation is completely a function of the preset respiratory rate and tidal volume. Patient’s efforts do not contribute to ventilation. Suitable for a patient making no respiratory effort



        • A/C: Assist-Control




          • The ventilator responds to patient’s inspiratory effort by supplying a preset tidal volume. A control mode backup ensures against hypoventilation



        • IMV: Intermittent Mandatory Ventilation




          • A preset tidal volume and respiratory rate triggers automatically at timed intervals. Most of these mechanical breaths are synchronized with an inspiratory effort by the patient [synchronized intermittent mandatory ventilation (SIMV)]




Flow-Cycled Ventilation










        • Triggered by patient’s inspiration; tidal volume and respiratory rate are not set



        • Inspiration is terminated when a set flow rate is reached



        • Pressure support [eg, positive end expiratory pressure (PEEP)] is a flow-cycled ventilation



        • Preset pressure is sustained until the patient’s inspiratory flow tapers to a set percentage of its maximum value



        • Pressure support decreases the work of breathing; requires the patient to initiate their own breath



        • Useful in combination with SIMV when weaning a patient




Settings




  • Tidal volume: Approximately 8 mL/kg ideal body weight. Inversely proportional to Paco2. This does not apply to patients on an acute respiratory distress syndrome (ARDS) protocol. Paco2 is affected by minute ventilation and tidal volume



  • Respiratory Rate: Product of respiratory rate and tidal volume is minute ventilation. Usually between 12 and 16 per minute



  • Trigger mode: Ventilator senses negative airway pressure and responds with a “triggered” breath. Usual sensitivity is –1 to –3 cm H2O



  • PEEP: Improves V/Q matching and therefore gas exchange



  • Fio2: Always attempt to minimize while maintaining SaO2



  • Flow rate: Adjusted to provide appropriate I/E ratio, typically 1:3




ARDS Criteria




  • Hypoxemic respiratory failure



  • Chest x-ray typically reveals bilateral alveolar infiltrates



  • Often accompanied with acute respiratory alkalosis and high A-a gradient



  • Pulmonary Capillary Wedge Pressure (PCWP) less than 18 is classic; however, not on updated criteria



  • Pao2/Fio2 less than 300



  • Attempt to keep plateau pressures less than 30 cm H2O




    • Keep tidal volumes low



    • Increase PEEP before Fio2



  • Refer to ARDSnet.org for protocol




Weaning Parameters




  • Certain goals must be met prior to weaning patients off the ventilator



  • First and foremost, a patient’s level of alertness should be assessed prior to extubation—a patient should be alert enough to handle their own secretions and be able to mentate



  • Assessing how a patient will do on minimal ventilator settings for a period of time prior to extubation is important—Minimal ventilator settings at our institution are pressure support 5, PEEP 5, Fio2 40%



  • Assessing a patient’s volume status prior to extubation is equally important. Patients who have required liters of fluid for resuscitation may benefit from Lasix to diurese some of this fluid (and hence increase lung compliance) prior to extubation



  • Tobin/RSBI




    • RSBI: Rapid Shallow Breathing Index (ratio of respiratory frequency/tidal volume) of less than 105 breaths/L/min has been associated with weaning success. Patients breathing in large tidal volumes and not hyperventilating will likely have lower RSBIs and an increased chance of weaning off sedation



    • Ideally their respiratory rate is under 25 breaths/min



  • NIF: Negative Inspiratory Force more negative than −20 mm Hg is ideal. The NIF measures the strength of respiratory muscles. Tested by asking patients to suck up air through the ET tube



  • A positive cuff leak (air moving through the trachea when the cuff is deflated) indicates that laryngeal edema is most likely NOT present; thus, the airway will not be compromised if extubated



  • Vital Capacity: For weaning this should be 10–15 mL/kg of ideal body weight, tidal volume 2–3 mL/kg of ideal body weight




Acid–Base Issues



Acid–Base Pearls




  • Sepsis: Anion gap metabolic acidosis



  • Renal Tubular Acidosis: Non-anion gap metabolic acidosis



  • Urinary diversion: Non-anion gap metabolic acidosis



  • Vomiting is least likely to produce acidosis



  • Prolonged NG tube use can lead to persistent metabolic alkalosis



  • Normal values




    • pH: 7.35–7.45



    • HCO3: 22–26



    • Paco2: 38–42



  • Patient Evaluation




    • Acidemic or Alkalemic?




      • Check pH: <7.38 is acidemic; >7.42 is alkalemic



    • Overriding problem respiratory or metabolic?




    • If metabolic acidosis present, is there an anion gap? (Check albumin)




      • Anion Gap = Na − (HCO3 + Cl)



      • Gap: >12; non-gap: <12



      • See Table 3-7



    • In metabolic disturbances, is the respiratory system compensating?




      • In metabolic acidosis




        • Check expected Paco2: [1.5 × HCO3] + 8 ± 2



        • If Paco2 < predicted, there is a coexisting respiratory alkalosis



        • If Paco2 > predicted, there is a coexisting respiratory acidosis



    • In metabolic alkalosis




      • If Paco2 < 40, there is a coexisting primary respiratory alkalosis



      • If Paco2 > 50, there is a coexisting primary respiratory acidosis



    • If a gap metabolic acidosis, are there other metabolic disturbances present?




      • Check corrected HCO3: Measure HCO3 + (anion gap−12)




        • If >24 there is a coexisting primary metabolic alkalosis



        • If <24, there is a coexisting non-gap metabolic acidosis





TABLE 3-6

METABOLIC PARAMETERS






TABLE 3-7

METABOLIC ACIDOSIS: ANION GAP VERSUS NON-GAP





Acute Renal Failure





  • Calculate Fractional Excretion of Sodium (FENa)




    • Determines if renal failure is due to prerenal, postrenal, or intrinsic renal pathology (Table 3-8)



    • FENa (%) = [(Urine Na × Plasma Cr/Plasma Na × Urine Cr) × 100]




      • Prerenal: FENa <1%: low volume, pump failure



      • Postrenal: Obstruction (cervical cancer, ureteral injury, etc)



      • Intrinsic: Tubular (granular casts, Urine Na >40, BUN/Cr <15; from ischemia, drugs, rhabdomyolysis); interstitial (white blood cells, eosinophils; from drugs, pyelonephritis); glomerular (RBCs, RBC casts, proteinuria; from post-strep, connective tissue diseases); vascular (vasculitis, DIC, malignant hypertension)




Remember: Renally dose Vancomycin. Obtain Vancomycin levels after the third dose and 1 hour prior to the fourth dose




TABLE 3-8

CAUSES OF RENAL FAILURE





Hemodynamics







TABLE 3-9

HEMODYNAMIC PARAMETERS






TABLE 3-10

TYPES OF SHOCK






CERVICAL CANCER



Listen




General





  • Most common gynecologic malignancy in the world



  • Second most frequently diagnosed cancer worldwide after breast cancer



  • Third most common gynecologic malignancy in the United States and third most common cause of gynecologic cancer death



  • 0.68% lifetime risk of cervical cancer (1 in 147 women) in the United States



  • Half of women diagnosed are 35 to 55 years old



  • Mean age at diagnosis is 48 years; bimodal distribution with peaks at 35–39 and 60–64 years



  • Overall 5-year survival rate (SEER data 1999–2006): 70.2%. If localized, 91%



  • Incidence by Race: Hispanic > Black > White > American Indian > Asian/Pacific Islander




Etiology





  • Infection: HPV 16, 18, 31, 33, 45, 51–53; HSV, chlamydia likely cofactors




    • HPV 16 accounts for 40–70% of invasive cervical cancers



    • HPV 18 is less prevalent but may be associated with cervical cancers that rapidly progress




Risk Factors





  • First intercourse less than age 16 (first intercourse over age 20 reduces risk)



  • Multiple partners



  • Increased parity



  • Cigarette smoking



  • Immunosuppression (HIV, Fanconi anemia, chronic steroids, transplant)



  • Low socioeconomic status




Types





  • Squamous cell carcinoma: Keratinizing, nonkeratinizing, verrucous, condylomatous, papillary, lymphoepithelioma-like



  • Adenocarcinoma: Mucinous (endocervical/intestinal/signet ring type), endometrioid (endometrioid AC with squamous metaplasia), clear cell, serous, minimal deviation (endocervical/endometrioid type), mesonephric, well-differentiated villoglandular



  • Other epithelial: Adenosquamous, glassy cell, mucoepidermoid, adenoid cystic, adenoid basal, carcinoid-like tumor, small cell, undifferentiated




Signs/Symptoms





  • Early: Asymptomatic



  • Late: Constitutional (anorexia, weight loss, weakness); vaginal bleeding (irregular, postcoital) serosanguineous or yellow discharge; pain (abdominopelvic, low back, dyspareunia); urinary frequency; lower extremity edema; hydronephrosis/acute renal failure; hemoptysis



  • Laboratory findings: Anemia, thrombocytosis, elevated creatinine




Diagnosis





  • Screening: Pap and HPV testing [see current American Society for Colposcopy and Cervical Pathology (ASCCP) guidelines]



  • Diagnosis: Colposcopy with biopsy, endocervical curettage (ECC), excisional procedures (cold knife cone (CKC), loop electrosurgical excision procedure (LEEP))



  • Assessing disease status: Ultrasound, abdomen/pelvis CT, MRI, PET/CT




Malignant Spread





  • Cervical cancer spreads via




    • Direct invasion into cervical stroma, corpus, vagina, and parametrium



    • Lymphatic spread into cardinal ligament (causing ureteral obstruction), parametrial lymph vessels, lymph nodes of obturator, external iliac, and hypogastric vessels; parametrial, inferior gluteal, and presacral nodes; common iliac, para-aortic, inguinal, supraclavicular nodes (usually left)



    • Hematogenous



    • Intraperitoneal




Staging—CLINICAL (not surgical)





  • FIGO standards




    • Permitted: Inspection, palpation, colposcopy, ECC, biopsies of cervix including conization, bladder, rectum, hysteroscopy, cystoscopy, proctoscopy, intravenous urography, and radiographic examination of the chest and skeleton



    • NOT included: Lymphangiograms, arteriograms, CT, MRI, PET, laparoscopy, laparotomy. (But, these may help plan treatment)



  • REVISED FIGO STAGING (2010) (Table 3-11)




    • Remains a clinically staged disease



    • Use of diagnostic imaging techniques to assess size of primary tumor is encouraged but is not mandatory. Imaging studies improve assessment/treatment of disease, but >80% of cervical cancer occurs where PET/CT/MRI are not readily available



    • Examination under anesthesia, cystoscopy, sigmoidoscopy, and IV pyelography is optional and no longer mandatory



    • Diagnostic excision technique recommended is CKC not LEEP





TABLE 3-11

FIGO STAGING—CERVICAL CANCER





Survival Statistics by Stage (Table 3-12)




TABLE 3-12

CERVICAL CANCER SURVIVAL BY STAGE





Surgical Management





  • Primary surgical management is limited to stages I–IIA (Table 3-13)



  • Advantages to surgical treatment, particularly for younger women: Allows for thorough pelvic/abdominal exploration, individualized therapy plan, and ovarian conservation with transposition out of radiation field



  • Ovarian function conserved in fewer than 50% of patients with radiation



  • Fertility sparing techniques (Table 3-14)



  • Types of hysterectomies (Table 3-15) and differences among the types (Table 3-16) are shown in the tables





TABLE 3-13

SURGICAL MANAGEMENT OF CERVICAL CANCER


Jan 12, 2019 | Posted by in GYNECOLOGY | Comments Off on Gynecologic Oncology

Full access? Get Clinical Tree

Get Clinical Tree app for offline access