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Pathophysiology

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  • Results from stimulation of complex reflex coordinated by vomiting center; mediated by CNS, receives input from autonomic nervous system; numerous neurotransmitters can contribute to emetic process: dopamine, serotonin (5-HT3), substance P, histamine, acetylcholine (N Engl J Med 2008;358:2482)

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Types of Emesis

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(N Engl J Med 2008;358:2482; J Clin Oncol 2011;29:4189)

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  • Acute emesis: begins 1–2h of chemotherapy, peaks in 4–6h; may occur up to 18–24h after; typically responsive to drug therapy
  • Delayed emesis: >24h after chemotherapy, peaks in 2–3d; may occur up to 5d after (2/2 neurotransmitters other than serotonin); variable response to therapy
  • Anticipatory emesis: occurs prior to treatment; conditioned response in patients who previously developed significant CINV; not associated with neuroreceptors; often triggered by sights, smells, sounds; variable response to therapy → prevention is key

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CINV Risk Factors

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(J Clin Oncol 2011;29:4189; NCCN Nausea/Vomiting guideline v. 1.2012)

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  • Chemotherapy-related risk factors: daily PO chemotherapy may have specific recommendations for emesis management (NCCN Nausea/Vomiting guideline v. 1.2012); doxorubicin & cyclophosphamide (AC) regimen reclassified → manage per highly emetogenic regimen
  • Patient-related risk factors: ♀ > ♂, young > elderly, concomitant narcotics, history of motion sickness, prior chemotherapy, poor control with prior regimens, psychosocial issues
  • Negative risk factor: heavy alcohol use

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Table Graphic Jump Location
Table 20-1 Chemotherapy Associated with Emesis
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Minimize Risk of CINV

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(N Engl J Med 2008;358:2482; J Clin Oncol 2011;29:4189; NCCN guidelines)

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  • Prevention is key; chemotherapy with >10% incidence CINV → use prophylactic antiemetics; <10% incidence when given as a single agent → does not require prophylaxis; schedule antiemetics for delayed CINV
  • If >1 chemotherapy used → choose antiemetic regimen for highest risk category

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Table Graphic Jump Location
Table 20-2 CINV Prophylaxis

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