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    Back to Module 10: Common Physical Symptoms
    Specific Symptoms

     
    Breathlessness (Dyspnea)
    Nausea and Vomiting Constipation
    Diarrhea
    Anorexia/Cachexia
    Fatigue/Weakness
    Fluid Balance/Edema
    Skin
    Odors
    Insomnia

    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.

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    Definition/Description

    • 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

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    Causes

    • 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)

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    Management

    • 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

    Etiology

    Pathophysiology

    Therapy

    Metastases

    Cerebral (increased ICP)

    Liver

     

    increased ICP, direct CTZ effect

    toxin buildup

     

    steroids, mannitol, anti-DA/Hist

    anti-DA/Hist

    Meningeal irritation

    increased ICP

    Steroids

    Movement

    vestibular stimulation (may be worse with morphine)

    anti-Ach

    Mentation, e.g., anxiety

    Cortical

    anxiolytics e.g., benzodiazepines, THC

    Medications

    Opioids

    Chemotherapy

    Others
    (NSAIDs, see Mucosal Irritation)

     

    CTZ, vestibular effect, GUT

    CTZ, GUT

    CTZ

     

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

    anti-5HT/DA, steroids

    anti-DA/Hist

    Mucosal irritation

    NSAIDs

    Hyperacidity, gastroesophageal reflux

     

    GUT, gastritis

    GUT, gastritis, duodenitis

     

    cytoprotective agents

    antacids

    Mechanical obstruction

    Intraluminal

    Extraluminal

     

    Constipation, obstipation

    Tumor, fibrotic stricture

     

    manage constipation

    reversible—surgery

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

    Motility

    Opioids, ileus, other medications

     

    GUT, CNS

     

    prokinetic agents, stimulant laxatives

    Metabolic

    Hypercalcemia, hyponatremia, hepatic/renal failure

     

    CTZ

     

    anti-DA/Hist, rehydration, steroids

    Microbes

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

    Systemic sepsis

     

    GUT

    CTZ

     

    antibacterials, antivirals, antifungals, antacids

    anti-DA/Hist, antibacterials, antivirals, antifungals

    Myocardial

    Ischemia, congestive heart failure

     

    Vagal stimulation, cortical, CTZ,

     

    Oxygen, opioids, anti-DA/Hist
    anxiolytics

    Legend:
    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

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    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

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    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

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    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

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    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

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    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

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    Antacids

    • 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)

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    Cytoprotective Agents

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

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    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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