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  • Introduction
  • 1. Advance Care Planning
  • 2. Communicating Bad News
  • 3. Whole Patient Assessment
  • 4. Pain Management
  • 5. Assisted Suicide Debate
  • 6. Anxiety, Delirium
  • 7. Goals of Care
  • 8. Sudden Illness
  • 9. Medical Futility
  • 10. Common Symptoms
  • 11. Withholding Treatment
  • 12. Last Hours of Living
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  • 15. Legal Issues
  • 16. Social and Psychological
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    Site Index
    Back to Module 10: Common Physical Symptoms
    Specific Symptoms

    Breathlessness (Dyspnea)
    Nausea and Vomiting Constipation
    Fluid Balance/Edema

    Nausea and Vomiting

    Case Example

    PT is a 92-year-old farmer with colon cancer metastatic to the liver. Right upper quadrant pain is well controlled with extended-release morphine 60 mg po bid and dexamethasone 4 mg po q am. However, he complains of constant nausea that limits his ability to eat.



    • Commonly associated with many advanced diseases
    • Awareness of nausea, the inability to keep food or fluids down, the associated acid and bitter tastes, and the unpleasant smells associated with vomitus can be very distressing for patients, families, and caregivers
    • Nausea
      • Subjective sensation
      • Stimulation
        • Gastrointestinal lining, chemoreceptor trigger zone, vestibular apparatus, cerebral cortex
    • Vomiting
      • Neuromuscular reflex
      • Constitutes a final common pathway after stimulation of one or more of these areas



    • Multiple potential causes for both nausea and vomiting (see the table that follows)
    • Fortunately, symptomatic relief is relatively easy to achieve if the right medications are chosen
    • Unfortunately, lack of understanding and unsophisticated prescribing contributes to inadequate relief and unnecessary suffering for the patient, family, and caregivers
    • Pathophysiology
      • There are 2 organ systems that are particularly important in nausea and vomiting:
        • Brain
        • GI tract

      • Usual process
        • The gastric lining, the chemoreceptor trigger zone in the base of the fourth ventricle, the vestibular apparatus, and the cortex are all involved in the intricate physiology of nausea

        • The vomiting center is where the neuromuscular reflex that constitutes the final common pathway after stimulation from one or more of these areas emanates

        • Stimulation is mediated through the neurotransmitters serotonin, dopamine, acetylcholine, and histamine

        • All 4 neurotransmitters can be demonstrated in the chemoreceptor trigger zone

        • Although all are present in the lining of the GI tract, serotonin is particularly important

        • Acetylcholine and histamine are important in the vestibular apparatus

      • However, when mediated by the cortex, nausea and vomiting is more complex
        • Not associated with specific neurotransmitters

        • Seem to be learned responses (e.g., the anticipatory nausea associated with chemotherapy, nausea related to anxiety, etc)



    • Assessment
      • Which of the potential etiologies is operating?
      • What is the likely pathophysiology?
      • What would be the most appropriate intervention to prescribe?
    • Different causes will require very different interventions if the symptoms are to be controlled effectively
    • Focus here on general symptomatic management of nausea and vomiting
    • Not frequently possible to identify or specifically correct underlying etiology
    • Therapeutic trials may provide both relief and clues to underlying causes
    • When causes are known, burden of disease-modifying intervention may outweigh it potential benefit
    • Empirical therapy with antiemetics
      • Usually begins with a single medication
      • Target the presumed mechanism of nausea/vomiting
    • Dose optimized before a second medication with a different mechanism of action is added
    • Sequential combination therapy may be required

    Management of Nausea/Vomiting





    Cerebral (increased ICP)



    increased ICP, direct CTZ effect

    toxin buildup


    steroids, mannitol, anti-DA/Hist


    Meningeal irritation

    increased ICP



    vestibular stimulation (may be worse with morphine)


    Mentation, e.g., anxiety


    anxiolytics e.g., benzodiazepines, THC




    (NSAIDs, see Mucosal Irritation)


    CTZ, vestibular effect, GUT

    CTZ, GUT



    anti-DA/Hist, anti-Ach, prokinetic agents, stimulant cathartics

    anti-5HT/DA, steroids


    Mucosal irritation


    Hyperacidity, gastroesophageal reflux


    GUT, gastritis

    GUT, gastritis, duodenitis


    cytoprotective agents


    Mechanical obstruction




    Constipation, obstipation

    Tumor, fibrotic stricture


    manage constipation


    irreversible—manage fluids, steroids, , inhibit secretions w. octreotide, scopolamine


    Opioids, ileus, other medications


    GUT, CNS


    prokinetic agents, stimulant laxatives


    Hypercalcemia, hyponatremia, hepatic/renal failure




    anti-DA/Hist, rehydration, steroids


    Local irritation,
    e.g., esophagitis, gastritis from Candida, H pylori, herpes, CMV

    Systemic sepsis





    antibacterials, antivirals, antifungals, antacids

    anti-DA/Hist, antibacterials, antivirals, antifungals


    Ischemia, congestive heart failure


    Vagal stimulation, cortical, CTZ,


    Oxygen, opioids, anti-DA/Hist

    anti-Ach = Acetylcholine antagonists
    anti-DA = Dopamine antagonists

    anti-Hist = Histamine antagonists
    anti-5HT = Serotonin antagonists
    CTZ = Chemoreceptor trigger zone

    GUT = Gastrointestinal tract
    ICP = Intracranial pressure
    THC = Tetrahydrocannabinol


    Antiemetic Types

    Dopamine Antagonists

    • Dopamine-mediated nausea is probably the most common form of nausea
    • Frequently targeted for initial symptom management, even when the precise mechanism of nausea is not known
    • These medications are phenothiazines or butyrophenone neuroleptics
    • Potential to cause drowsiness and extrapyramidal symptoms, particularly in young women
    • Haloperidol is less sedating
      • Haloperidol 0.5–2.0 mg PO, IV, SC q 6h, titrate

      • Prochlorperazine
        • 10–20 mg PO q 6h, or
        • 25 mg PR q 12h, or
        • 5–10 mg IV q 6h

      • Droperidol 2.5–5 mg IV q 6h

      • Thiethylperazine 10–20 mg PO q 6h

      • Promethazine
        • 12.5–25 mg IV q 4–6h, or
        • 25 mg PO, PR q 4–6h

      • Perphenazine 2–8 mg PO, IV q 6h

      • Trimethobenzamide
        • 250 mg PO q 6–8h, or
        • 200 mg PR q 6–8h


    Antihistamines (Histamine Antagonists)

    • Antihistamines typically used to control nausea may also cause sedation
    • In some patients, this adverse effect may be an added benefit
    • Because the antihistamines also have anticholinergic properties, they may do "double duty" as a single agent and cover both mechanisms
    • Types:
      • Diphenhydramine 25–50 mg PO q 6h
      • Meclizine 25–50 mg PO q 6h
      • Hydroxyzine 25–50 mg PO q 6h


    Anticholinergics (Acetylcholine Antagonists)

    • Opioids and anesthetics can trigger acetylcholine-mediated nausea in the vestibular apparatus
    • A medication from this class may be added to other antiemetics in empirical therapy
    • Scopolamine
      • 0.1–0.4 mg SC, IV q 4h, or
      • 1–3 transdermal patches q 72h, or
      • 10–80 mg/h by continuous IV or SC infusion


    Serotonin Antagonists

    • Serotonin has been particularly implicated in chemotherapy-associated nausea
    • This class of medications can be exceedingly effective, but they are very expensive
    • They can be useful for refractory nausea of diverse types
    • Typically tried only when other medications have failed
    • They should be promptly stopped if they are not effective after a short trial
    • Types:
      • Ondansetron 8 mg PO tid
      • Granisetron 1 mg PO q d or bid


    Prokinetic Agents

    • A "sluggish" or dyskinetic gut (due to carcinomatosis, opioid therapy, other medications, etc) may be a profound source of nausea and vomiting in patients with advanced disease
    • A large liver may be causing a "squashed stomach"
    • Ascites or peritoneal disease may be causing pseudo-obstruction
    • Constipation can be an exacerbating factor
    • Types:
      • Metoclopramide 10–20 mg PO q 6h
      • Cisapride 10–20 mg PO q 6h



    • Hyperacidity, with or without gastroesophageal reflux and/or gastric or duodenal erosions, may produce considerable
      • Nausea
      • Heartburn
      • Acidity
      • Bitter taste
    • Also associated with vomiting
    • Types:
      • Antacids 1–2 tablespoons q 2h prn
      • H2 receptor antagonists (cimetidine, famotidine, ranitidine)
      • Proton pump inhibitors (omeprazole, lansoprazole)


    Cytoprotective Agents

    • Mucosal erosion secondary to NSAIDs may be associated with significant nausea
    • Types:
      • Misoprostol 200 mg bid–qid
      • Proton pump inhibitors (omeprazole, lansoprazole)


    Other Medications

    • This heterogeneous class of medications has unclear mechanisms of action, but uncontested benefits in some patients
      • Dexamethasone 6–20 mg daily
      • Tetrahydrocannabinol 2.5–5 mg po tid
      • Lorazepam 0.5–2 mg po q 4–6h
    • The symptoms of bowel obstruction represent a special case
      • With complete obstruction, accumulation of intraluminal fluid from epithelial sources is principally response for the symptoms of bloating, crampy abdominal pain, nausea and vomiting

      • Octreotide, a synthetic analog of somatostatin, selectively inhibits secretion of fluids and electrolytes into the gut lumen

        • Octreotide may be started by continuous IV at 10 mg/hr or intermittent subcutaneous injection 100 mg q 8-12 h

        • Titrated every 24-48 hours to relief of symptoms
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