Nausea and Vomiting

A comprehensive review of nausea and vomiting may be found in Chapter 20.

Palliative Care Considerations

• Up to 71% of palliative care patients will develop nausea and vomiting with approximately 40% experiencing these symptoms in the last 6 weeks of life. Chronic nausea can be defined as lasting longer than a week and without a well-identified


or self-limiting cause, such as chemotherapy, radiation, or infection.

• Four major mechanisms are correlated with the stimulation of the vomiting center (Fig. 4-3). Potentially reversible causes of nausea and vomiting should not be overlooked.

• Causes of chronic nausea in end-of-life patients may include: autonomic dysfunction, constipation, antibiotics, nonsteroidal anti-inflammatory drugs (NSAIDs), other drugs, infection, bowel obstruction, metabolic abnormalities (e.g., renal or hepatic failure, hypercalcemia), increased intracranial pressure, anxiety, radiation therapy, chemotherapy, or untreated pain.

Nonpharmacologic Treatment in Palliative Care

• Relaxation techniques may prove beneficial in some patients.

• Strong foods or odors should be avoided.

• If possible, eliminate offending medications.

Pharmacotherapy in Palliative Care

• The clinical features of nausea and vomiting should guide the choice of antiemetics used (for a more comprehensive review, refer to Chap. 20). The following are examples of managing nausea and vomiting as it correlates with the etiology:

• Chemoreceptor trigger zone (CTZ)-induced nausea and vomiting are caused by chemotherapeutic agents, bacterial toxins, metabolic products (e.g., uremia), and opioids. Dopamine (D2), serotonin (5-HT), and neurokinin-1 are the primary neurotransmitters involved in this process. Therapy is based on blocking D2 with D2-antagonists including butyrophenones (e.g., haloperidol), phenothiazines, and metoclopramide. Serotonin (5-HT3) antagonists (e.g., ondansetron) are mainly used for chemotherapy and radiotherapy-induced naus-


• Cerebral cortex-induced nausea and vomiting can be caused by anxiety, taste, and smell, as well as by increased intracranial pressure. Corticosteroids are administered to decrease intracranial pressure while anxiolytics such as benzo-diazepines are used to treat the "anticipatory," gustatory, and olfactory stimulation.

Ceiebrfl Cgrtix Vom it in 5 Center

Dopamine, 5HTS. NûurtOdrtir1- ! H Acetylcholine Histamine

Ceiebrfl Cgrtix Vom it in 5 Center

Dopamine, 5HTS. NûurtOdrtir1- ! H Acetylcholine Histamine

Nausea and Vomiting FIGURE 4-3. Mechanisms and associated neurotransmitters involved in nausea and vomiting.

• Vestibular nausea and vomiting is triggered by motion. Opioids can sensitize the vestibular center resulting in movement-induced nausea. Ambulatory patients are more susceptible to vestibular nausea and vomiting then bedbound patients. Because histamine and acetylcholine are the predominant neurotrans-

Vestibular Nerve

Cranial Nerve VIII

mitters here, antihistamines and anticholinergics are the drugs of choice in movement-induced nausea and vomiting.

• GI tract stimulation occurs through vagal and sympathetic pathways. These pathways can be triggered by stimulation of either mechanoreceptors or chemoreceptors located in the gut. Gastric stasis, GI obstruction, drugs, meta-static disease, bacterial toxins, chemotherapeutic agents, and irradiation can lead to nausea and vomiting. Glossopharyngeal or vagus nerve stimulation in the pharynx by sputum, mucosal lesions, or infection (e.g., Candida) can also evoke nausea. The major neurotransmitters in the upper GI tract are D2, acetylcholine, and 5-HT. Metoclopramide blocks 5-HT4 and increases gastric motility above the jejunum, whereas anticholinergics will decrease GI spasticity and motility in nausea induced by gut hyperactivity. In high doses, metoclopramide will also act as a 5-HT3 antagonist.

• Autonomic failure causes gastroparesis resulting in anorexia, nausea, early satiety, and constipation. Delayed gastric emptying is frequently observed in patients with diabetes mellitus, chronic renal failure, and neurologic disorders. Malnutrition, cachexia, lung and pancreatic cancers, HIV, radiotherapy, and drugs such as opioids, anticholinergics, antidepressants, and vasodilators have been associated with autonomic failure and resulting chronic nausea, poor performance, tachycardia, and malnutrition.

• In addition to their usefulness in reducing intracranial pressure, corticosteriods have been found to be effective in nonspecific nausea and vomiting. The mechanism of this action is unknown.

• If nausea is due to gastritis, hiatal hernia, gastroesophageal reflux disease (GERD), or peptic ulcer disease, histamine2 (H2) antagonists or proton pump inhibitors (PPIs) should be administered.

• Refractory cases of nausea and vomiting often require judiciously selected combinations of medications from different classes (e.g., various combinations of haloperidol, metoclopramide, diphenhydramine, lorazepam, dexamethasone).

• Serotonin 3 (5-HT3) antagonists, such as ondansetron, granisetron, dolasetron, and palonosetron, have limited usefulness in nausea and vomiting due to terminal illness caused by their high specificity for serotonin3. They are typically indicated with emetogenic chemotherapy and up to 10 to 14 days post-treatment.

• Aprepitant is a neurokinin-1 antagonist that is indicated for the treatment of nausea due to highly emetogenic chemotherapy and in combination with a 5-HT3 antagonist and corticosteroid. Aprepitrant should not be used as a sole agent.

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