Management of Common Symptoms in Terminally Ill Patients: Part I. Fatigue, Anorexia, Cachexia, Nausea and Vomiting



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Physical symptoms other than pain often contribute to suffering near the end of life. In addition to pain, the most common symptoms in the terminal stages of an illness such as cancer or acquired immunodeficiency syndrome are fatigue, anorexia, cachexia, nausea, vomiting, constipation, delirium and dyspnea. Management involves a diagnostic evaluation for the cause of each symptom when possible, treatment of the identified cause when reasonable, and concomitant treatment of the symptom using nonpharmacologic and adjunctive pharmacologic measures. Part I of this two-part article discusses fatigue, anorexia, cachexia, nausea and vomiting. Fatigue is the most common symptom at the end of life, but little is known about its pathophysiology and specific treatment. Education of the patient and family is the foundation of treatment, with the possible use of adjunctive psychostimulants. Anorexia and cachexia caused by wasting syndromes are best managed with patient and family education, as well as a possible trial of appetite stimulants such as megestrol or dexamethasone. For appropriate pharmacologic treatment, it is helpful to identify the pathophysiologic origin of nausea in each patient.

Although pain is commonly associated with end-of-life distress, other physical symptoms often contribute to the suffering of terminally ill patients.15 In patients who have cancer, fatigue and anorexia rank as the top two reasons for emotional and physical distress, with pain ranked third. Nausea, constipation, altered mental state (e.g., delirium) and dyspnea are the next most common symptoms.3,4 This two-part article focuses on the more prevalent nonpain physical symptoms found in patients who have cancer, acquired immunodeficiency syndrome (AIDS) or other terminal illnesses.

In managing a nonpain symptom at the end of life, the physician should search for the cause of the symptom by obtaining the proper historical, physical and laboratory data (to the extent that is appropriate in terminally ill or hospice patients). Efforts are directed at alleviating the symptom, as well as preventing or treating the underlying cause when possible or reasonable. Effective management requires that the physician be thoroughly familiar with the drugs and treatments prescribed. Frequent re-evaluation of the patient is also important.

Treatments often change as the patient approaches the end of life. The continued presence of physicians and a steadfast commitment to ameliorating symptoms are particularly important when it is impossible to cure or even slow the progression of an underlying disease process.

Fatigue

The terms “asthenia” and “fatigue” are often used interchangeably. Used in relation to a terminal illness, however, the word “fatigue” has multiple components, including the symptoms of tiredness, a general lack of energy not relieved by rest, diminished mental capacity and the subjective weakness associated with difficulty in performing activities of daily living.6 When conducting a review of systems, the physician is advised to use terms that are more familiar to patients than “asthenia.” In addition to “fatigue,” appropriate terms include “tiredness” and “lack of energy.”

Fatigue can be extremely debilitating and may have a severe negative impact on quality of life. This symptom is a problem in 75 to 90 percent of patients with cancer or other chronic illnesses.47 Even survivors of cancer and other life-threatening illnesses report chronic fatigue lasting months to years after the completion of treatment. Despite the high prevalence of fatigue, little is known about its pathogenesis. Consequently, treatment for fatigue may be less successful than treatment for other symptoms at the end of life.

In medical practice, fatigue is frequently undiagnosed or ignored. Recent reports indicate that patients with cancer seldom discuss this symptom with their oncologist.6,8,9 A number of multidimensional fatigue assessment tools have been validated,1013 but family physicians may be most interested in recently proposed practical criteria for the bedside diagnosis of cancer-related fatigue.6,8 The Brief Fatigue Inventory is a straightforward diagnostic tool (Figure 1).13 (This inventory can also be obtained from the Internet at http://prg.mdanderson.org/bfi.pdf.)

Pathologic fatigue can arise from both physical and psychologic stresses.6 Physical causes include the direct consequences of a disease process, such as diminished oxygen-carrying capacity as a result of anemia or heart failure. Cancer, hepatic or renal failure, and many chronic illnesses (including chronic pain) can cause fatigue. In addition, treatments such as cancer therapy or anti-hypertensive and cardiac therapy can cause this symptom. Psychologic causes of fatigue include anxiety and depression.

Determining the severity of a patient's fatigue is important. The physician should note the factors that worsen or relieve fatigue, the presence of potentially treatable causes (i.e., anxiety or depression, concurrent medications, anemia, pain, infection, cancer, sleep disorder) and the impact of fatigue on the patient's daily activities and quality of life.6

The management of fatigue with an unidentified underlying treatable cause is summarized in Table 1.6,14 Patient and family education can be of great value. For example, family members may interpret fatigue to mean that the patient is “giving up,” when the symptom is actually beyond the patient's control. To decrease pressure on the patient to be more energetic, the physician may need to give the patient “permission” to rest.14

Brief Fatigue Inventory

FIGURE 1.

Brief Fatigue Inventory. Family physicians may find this tool useful for evaluating fatigue in patients who are approaching the end of life.

Adapted with permission from Mendoza TR, Wang XS, Cleeland CS, Morrissey M, Johnson BA, Wendt JK, et al. The rapid assessment of fatigue severity in cancer patients: use of the Brief Fatigue Inventory. Cancer 1999;85:1186–96.

View Large

Brief Fatigue Inventory


FIGURE 1.

Brief Fatigue Inventory. Family physicians may find this tool useful for evaluating fatigue in patients who are approaching the end of life.

Adapted with permission from Mendoza TR, Wang XS, Cleeland CS, Morrissey M, Johnson BA, Wendt JK, et al. The rapid assessment of fatigue severity in cancer patients: use of the Brief Fatigue Inventory. Cancer 1999;85:1186–96.

Brief Fatigue Inventory


FIGURE 1.

Brief Fatigue Inventory. Family physicians may find this tool useful for evaluating fatigue in patients who are approaching the end of life.

Adapted with permission from Mendoza TR, Wang XS, Cleeland CS, Morrissey M, Johnson BA, Wendt JK, et al. The rapid assessment of fatigue severity in cancer patients: use of the Brief Fatigue Inventory. Cancer 1999;85:1186–96.

Medications, notably corticosteroids and psychostimulants, are sometimes beneficial adjuncts to nonpharmacologic interventions directed at relieving fatigue in patients nearing the end of life. Dexamethasone (Decadron), 2 to 20 mg taken orally once daily in the morning, can bring about feelings of well-being and increased energy, although these effects may diminish after the drug has been used for four to six weeks.14 In the end-of-life setting, the long-term side effects of morning doses of corticosteroids are usually not an issue. Of the psychostimulants, methylphenidate (Ritalin) is most commonly prescribed, although dextroamphetamine (Dexedrine) and pemoline (Cylert) also are used.

Antidepressants have been used empirically in patients without clinical depression who have fatigue that does not respond to non-pharmacologic interventions, corticosteroids or psychostimulants. In addition to elevating mood, antidepressants (particularly selective serotonin reuptake inhibitors) can have an energizing effect.6

Erythropoietin therapy can be beneficial in relieving fatigue and improving quality of life in patients with chronic anemia who have human immunodeficiency virus (HIV) infection/AIDS or end-stage renal disease, and in those who are undergoing cancer chemotherapy.15,16 However, erythropoietin therapy is expensive, and beneficial effects may not become apparent for four to six weeks. The expense and “time to effect” for this treatment should be compared with the cost and inconvenience of transfusions in patients who have symptomatic anemia at the end of life.

TABLE 1
Management of Fatigue When an Underlying Treatable Cause Cannot Be Found

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Anorexia and Cachexia

Systemic illnesses such as cancer, chronic organ failure, infections or AIDS sometimes cause wasting syndromes. These syndromes are characterized by lack of appetite (anorexia) and weight loss (cachexia), frequently accompanied by fatigue.1719

Little is known about the pathogenesis of wasting syndromes. In cancer, humoral factors elaborated by the tumor appear to be involved, because cachexia can be transferred from cancer-bearing to noncancer-bearing animals in parabiotic experiments.20 It is likely that elevated levels of cytokines, notably interferons and tumor necrosis factors, play a role in the metabolic alterations observed in patients with wasting syndromes.20,21 There is no relationship between tumor size and the degree of cachexia.17

Despite the appearance of malnutrition, the wasting syndrome associated with cancer and hypermetabolic states is caused by the underlying disease process and is usually not reversible with improved nutrition. Orally or parenterally administered nutrition frequently results in increased body fat, not increased protein. The findings of a number of studies indicate that aggressive alimentation in patients with a wasting syndrome related to cancer may actually increase their discomfort.22,23 This differs for patients with AIDS.

The physician can be of particular assistance in helping the patient and family understand that cachexia is an expected consequence of the underlying disease process. Frequently, family caregivers believe that wasting is the result of their provision of inadequate care and nutrition. They can be taught to replace their “need to feed” with behaviors that alleviate symptoms, such as moistening the patient's lips and oral cavity with a sponge, offering small amounts of food as desired by the patient, providing light massage, reading to the patient or playing soft music for the patient.

Treatable causes of anorexia and cachexia in patients who are near the end of life include chronic pain, mouth conditions (dryness, mucositis resulting from chemotherapy, and infections such as oral candidiasis or oral herpes), gastrointestinal motility problems (e.g., constipation) and reflux esophagitis. In patients with cancer who are being treated with chemotherapy, radiation therapy and/or medications such as opioids or nonsteroidal anti-inflammatory drugs, an attempt should be made to determine whether anorexia and weight loss are due to mucositis, changes in gastrointestinal motility and nausea as the effects of treatment, rather than progressive disease.

In the absence of specific treatable causes, symptomatic management of cachexia at the end of life includes both nonpharmacologic and pharmacologic interventions (Table 2).14 It is important to emphasize that cachexia is part of the “normal” end-of-life process. Wasting in dying patients may result in the natural release of endorphins, causing euphoria.

Nausea and Vomiting

Nausea and vomiting can be extremely debilitating symptoms at the end of life. With available methods, effective control of these symptoms can be achieved in most patients.

The brain (chemoreceptor trigger zone, cerebral cortex, vestibular apparatus and vomiting center) and the gastrointestinal tract are the key organs involved in nausea and vomiting. Neurotransmitter receptors that mediate nausea and vomiting include those for serotonin, dopamine, acetylcholine and histamine.14 Identification of the pathophysiologic origin of nausea is helpful in prescribing effective pharmacologic interventions.

TABLE 2

Management of Weight Loss Once Treatable Causes Have Been Ruled Out

Nonpharmacologic therapy

Provide patient and family education about the pathophysiology of the anorexia and cachexia in terminal illness, and the ineffectiveness of forced feeding and hydration.

Eliminate dietary restrictions: allow the patient to choose favorite foods and fluids, and to have them when desired and in the amount desired.

Reduce portion size and eliminate foods whose odor the patient finds unpleasant.

Explore the emotional and spiritual issues related to the patient's weight loss.

Pharmacologic therapy*

Dexamethasone (Decadron), 2 to 20 mg taken orally each morning; effect may diminish after 4 to 6 weeks of use.

Megestrol (Megace), 200 mg taken orally every 6 to 8 hours; titrate dosage to achieve and maintain desired effect.

Dronabinol (Marinol), 2.5 mg taken orally two or three times daily; titrate dosage to patient tolerance and to achieve and maintain desired effect.

Androgens (e.g., oxandrolone [Oxandrin], nandrolone [Durabolin]) are currently under investigation for their effects on appetite and weight.


*— Pharmacologic therapy should be considered an adjunct to general nonpharmacologic measures; a drug should be discontinued if no benefit occurs after two to six weeks of treatment.

Information from Module 10: Common physical symptoms. In: Education for physicians on end-of-life care. Chicago: EPEC Project, The Robert Wood Johnson Foundation, 1999.

TABLE 2   Management of Weight Loss Once Treatable Causes Have Been Ruled Out

View Table

TABLE 2

Management of Weight Loss Once Treatable Causes Have Been Ruled Out

Nonpharmacologic therapy

Provide patient and family education about the pathophysiology of the anorexia and cachexia in terminal illness, and the ineffectiveness of forced feeding and hydration.

Eliminate dietary restrictions: allow the patient to choose favorite foods and fluids, and to have them when desired and in the amount desired.

Reduce portion size and eliminate foods whose odor the patient finds unpleasant.

Explore the emotional and spiritual issues related to the patient's weight loss.

Pharmacologic therapy*

Dexamethasone (Decadron), 2 to 20 mg taken orally each morning; effect may diminish after 4 to 6 weeks of use.

Megestrol (Megace), 200 mg taken orally every 6 to 8 hours; titrate dosage to achieve and maintain desired effect.

Dronabinol (Marinol), 2.5 mg taken orally two or three times daily; titrate dosage to patient tolerance and to achieve and maintain desired effect.

Androgens (e.g., oxandrolone [Oxandrin], nandrolone [Durabolin]) are currently under investigation for their effects on appetite and weight.


*— Pharmacologic therapy should be considered an adjunct to general nonpharmacologic measures; a drug should be discontinued if no benefit occurs after two to six weeks of treatment.

Information from Module 10: Common physical symptoms. In: Education for physicians on end-of-life care. Chicago: EPEC Project, The Robert Wood Johnson Foundation, 1999.

The common causes, pathophysiology and treatments of nausea and vomiting in terminally ill patients are summarized in Table 3.14  Medications frequently used in the treatment of these symptoms are listed in Table 4,14 along with typical dosage schedules.

TABLE 3

Management of Nausea and Vomiting—the 11 M's

Etiology Pathophysiology Treatment

Metastases

Cerebral

Increased intracranial pressure, direct chemoreceptor trigger zone effect

Corticosteroids, mannitol, dopamine antagonists, histamine antagonists

Liver

Toxin buildup

Dopamine antagonists, histamine antagonists

Meningeal irritation

Increased intracranial pressure

Corticosteroids

Movement

Vestibular stimulation (may be worse with morphine)

Acetylcholine antagonists

Mentation (e.g., anxiety)

Cerebral cortex

Anxiolytics (e.g., benzodiazepines, dronabinol [Marinol])

Medications

Opioids

Chemoreceptor trigger zone, vestibular effect, gastrointestinal tract

Dopamine antagonists, histamine antagonists, acetylcholine antagonists, prokinetic agent, stimulant laxatives

Chemotherapy

Chemoreceptor trigger zone, gastrointestinal tract

Serotonin antagonists, dopamine antagonists, corticosteroids

Others (e.g., NSAIDs)*

Chemoreceptor trigger zone

Dopamine antagonists, histamine antagonists

Mucosal irritation

NSAIDs

Gastrointestinal tract, gastritis

Cytoprotective agents

Hyperacidity, gastroesophageal reflux

Gastrointestinal tract, gastritis, esophagitis, duodenitis

Antacids

Mechanical obstruction

Intraluminal

Constipation, obstipation

Manage with laxatives, stool softeners, lubricants, etc.

Extraluminal

Tumor, fibrotic stricture

Reversible: surgery

Irreversible: manage fluids, administer corticosteroids, inhibit secretions with octreotide (Sandostatin) or scopolamine (Transderm Scop)

Motility

Ileus, opioids and other medications

Gastrointestinal tract, central nervous system

Prokinetic agent, stimulant laxatives

Metabolic imbalance

Hypercalcemia, hyponatremia, hepatic or renal failure

Chemoreceptor trigger zone

Dopamine antagonists, histamine antagonists, corticosteroids; correct electrolyte imbalance

Microbes

Local irritation (e.g., esophagitis, gastritis caused by infection with Candida species, Helicobacter pylori, herpesvirus, cytomegalovirus)

Gastrointestinal tract

Antibacterials, antivirals, antifungals, antacids

Systemic sepsis

Chemoreceptor trigger zone

Dopamine antagonists, histamine antagonists, antibacterials, antivirals, antifungals

Myocardial dysfunction

Ischemia, congestive heart failure

Vagal stimulation, cerebral cortex, chemoreceptor trigger zone

Oxygen, opioids, dopamine antagonists, histamine antagonists, anxiolytics


NSAIDs = nonsteroidal anti-inflammatory drugs.

*—See mucosal irritation.

TABLE 3   Management of Nausea and Vomiting—the 11 M's

View Table

TABLE 3

Management of Nausea and Vomiting—the 11 M's

Etiology Pathophysiology Treatment

Metastases

Cerebral

Increased intracranial pressure, direct chemoreceptor trigger zone effect

Corticosteroids, mannitol, dopamine antagonists, histamine antagonists

Liver

Toxin buildup

Dopamine antagonists, histamine antagonists

Meningeal irritation

Increased intracranial pressure

Corticosteroids

Movement

Vestibular stimulation (may be worse with morphine)

Acetylcholine antagonists

Mentation (e.g., anxiety)

Cerebral cortex

Anxiolytics (e.g., benzodiazepines, dronabinol [Marinol])

Medications

Opioids

Chemoreceptor trigger zone, vestibular effect, gastrointestinal tract

Dopamine antagonists, histamine antagonists, acetylcholine antagonists, prokinetic agent, stimulant laxatives

Chemotherapy

Chemoreceptor trigger zone, gastrointestinal tract

Serotonin antagonists, dopamine antagonists, corticosteroids

Others (e.g., NSAIDs)*

Chemoreceptor trigger zone

Dopamine antagonists, histamine antagonists

Mucosal irritation

NSAIDs

Gastrointestinal tract, gastritis

Cytoprotective agents

Hyperacidity, gastroesophageal reflux

Gastrointestinal tract, gastritis, esophagitis, duodenitis

Antacids

Mechanical obstruction

Intraluminal

Constipation, obstipation

Manage with laxatives, stool softeners, lubricants, etc.

Extraluminal

Tumor, fibrotic stricture

Reversible: surgery

Irreversible: manage fluids, administer corticosteroids, inhibit secretions with octreotide (Sandostatin) or scopolamine (Transderm Scop)

Motility

Ileus, opioids and other medications

Gastrointestinal tract, central nervous system

Prokinetic agent, stimulant laxatives

Metabolic imbalance

Hypercalcemia, hyponatremia, hepatic or renal failure

Chemoreceptor trigger zone

Dopamine antagonists, histamine antagonists, corticosteroids; correct electrolyte imbalance

Microbes

Local irritation (e.g., esophagitis, gastritis caused by infection with Candida species, Helicobacter pylori, herpesvirus, cytomegalovirus)

Gastrointestinal tract

Antibacterials, antivirals, antifungals, antacids

Systemic sepsis

Chemoreceptor trigger zone

Dopamine antagonists, histamine antagonists, antibacterials, antivirals, antifungals

Myocardial dysfunction

Ischemia, congestive heart failure

Vagal stimulation, cerebral cortex, chemoreceptor trigger zone

Oxygen, opioids, dopamine antagonists, histamine antagonists, anxiolytics


NSAIDs = nonsteroidal anti-inflammatory drugs.

*—See mucosal irritation.

TABLE 4

Medications Commonly Used in the Treatment of Nausea and Vomiting

Medication Dosage and usual routes of administration

Dopamine antagonists

Haloperidol (Haldol)

0.5 to 2 mg orally, IV or SC every 6 hours; then titrate the dosage

Prochlorperazine (Compazine)

10 to 20 mg orally every 6 hours, 25 mg rectally every 12 hours, or 5 to10 mg IV every 6 hours

Droperidol (Inapsine)

2.5 to 5 mg IV every 6 hours

Thiethylperazine (Torecan)

10 to 20 mg orally every 6 hours

Perphenazine (Trilafon)

2 to 8 mg orally or IV every 6 hours

Histamine H1 receptor blockers (antihistamines)

Diphenhydramine (Benadryl)

25 to 50 mg orally every 6 hours

Meclizine (Antivert)

25 to 50 mg orally every 6 hours

Hydroxyzine hydrochloride (Atarax), hydroxyzine pamoate (Vistaril)

25 to 50 mg orally every 6 hours

Promethazine (Phenergan)

12.5 to 25 mg IV or IM every 4 to 6 hours, or 25 mg orally or rectally every 4 to 6 hours

Acetylcholine antagonist (anticholinergic)

Scopolamine (Transderm Scop)

1 to 3 transdermal patches every 72 hours

Serotonin antagonists

Ondansetron (Zofran)

8 mg orally three times daily

Granisetron (Kytril)

1 mg orally once or twice daily

Dolasetron (Anzemet)

100 mg orally once daily

Prokinetic agent

Metoclopramide (Reglan)

10 to 20 mg orally every 6 hours

Antacids

Liquid antacids (various)

1 to 2 tablespoons every 2 hours as needed

Histamine H2 receptor blockers

800 mg orally at bedtime for ulcers; 800 mg orally twice daily for gastroesophageal reflux

Cimetidine (Tagamet)*

Ranitidine (Zantac)

150 mg orally twice daily or 300 mg orally at bedtime; decrease dosage by 50% if creatinine clearance is less than 50 mL per minute (0.84 mL per second)

Famotidine (Pepcid)

20 to 40 mg orally at bedtime for ulcers; 20 to 40 mg orally twice daily for gastroesophageal reflux

Proton pump inhibitors

Omeprazole (Prilosec)

20 mg orally once daily; dosage should be reduced in Asian patients

Lansoprazole (Prevacid)

15 mg orally once daily

Cytoprotective agents

Misoprostol (Cytotec)

200 μg orally two to four times daily

Proton pump inhibitors

Same as above

Other medications

Dexamethasone (Decadron)

6 to 20 mg orally once daily

Dronabinol (Marinol)l

2.5 to 5 mg orally three times daily

Lorazepam (Ativan, Intensol)

0.5 to 2 mg orally, sublingually or SC every 4 to 6 hours

Octreotide (Sandostatin)

50 to 150 μ g IV or SC every 8 to12 hours; titrate dosage every 24 to 48 hours to achieve and maintain desired effect


IV = intravenous; SC = subcutaneous; IM = intramuscular.

*— Note that liquid antacids impair the absorption of cimetidine.

Adapted with permission from Module 10: Common physical symptoms. In: Education for physicians on end-of-life care. Chicago: EPEC Project, The Robert Wood

TABLE 4   Medications Commonly Used in the Treatment of Nausea and Vomiting

View Table

TABLE 4

Medications Commonly Used in the Treatment of Nausea and Vomiting

Medication Dosage and usual routes of administration

Dopamine antagonists

Haloperidol (Haldol)

0.5 to 2 mg orally, IV or SC every 6 hours; then titrate the dosage

Prochlorperazine (Compazine)

10 to 20 mg orally every 6 hours, 25 mg rectally every 12 hours, or 5 to10 mg IV every 6 hours

Droperidol (Inapsine)

2.5 to 5 mg IV every 6 hours

Thiethylperazine (Torecan)

10 to 20 mg orally every 6 hours

Perphenazine (Trilafon)

2 to 8 mg orally or IV every 6 hours

Histamine H1 receptor blockers (antihistamines)

Diphenhydramine (Benadryl)

25 to 50 mg orally every 6 hours

Meclizine (Antivert)

25 to 50 mg orally every 6 hours

Hydroxyzine hydrochloride (Atarax), hydroxyzine pamoate (Vistaril)

25 to 50 mg orally every 6 hours

Promethazine (Phenergan)

12.5 to 25 mg IV or IM every 4 to 6 hours, or 25 mg orally or rectally every 4 to 6 hours

Acetylcholine antagonist (anticholinergic)

Scopolamine (Transderm Scop)

1 to 3 transdermal patches every 72 hours

Serotonin antagonists

Ondansetron (Zofran)

8 mg orally three times daily

Granisetron (Kytril)

1 mg orally once or twice daily

Dolasetron (Anzemet)

100 mg orally once daily

Prokinetic agent

Metoclopramide (Reglan)

10 to 20 mg orally every 6 hours

Antacids

Liquid antacids (various)

1 to 2 tablespoons every 2 hours as needed

Histamine H2 receptor blockers

800 mg orally at bedtime for ulcers; 800 mg orally twice daily for gastroesophageal reflux

Cimetidine (Tagamet)*

Ranitidine (Zantac)

150 mg orally twice daily or 300 mg orally at bedtime; decrease dosage by 50% if creatinine clearance is less than 50 mL per minute (0.84 mL per second)

Famotidine (Pepcid)

20 to 40 mg orally at bedtime for ulcers; 20 to 40 mg orally twice daily for gastroesophageal reflux

Proton pump inhibitors

Omeprazole (Prilosec)

20 mg orally once daily; dosage should be reduced in Asian patients

Lansoprazole (Prevacid)

15 mg orally once daily

Cytoprotective agents

Misoprostol (Cytotec)

200 μg orally two to four times daily

Proton pump inhibitors

Same as above

Other medications

Dexamethasone (Decadron)

6 to 20 mg orally once daily

Dronabinol (Marinol)l

2.5 to 5 mg orally three times daily

Lorazepam (Ativan, Intensol)

0.5 to 2 mg orally, sublingually or SC every 4 to 6 hours

Octreotide (Sandostatin)

50 to 150 μ g IV or SC every 8 to12 hours; titrate dosage every 24 to 48 hours to achieve and maintain desired effect


IV = intravenous; SC = subcutaneous; IM = intramuscular.

*— Note that liquid antacids impair the absorption of cimetidine.

Adapted with permission from Module 10: Common physical symptoms. In: Education for physicians on end-of-life care. Chicago: EPEC Project, The Robert Wood

If patients have persistent nausea and treatable causes have been ruled out, haloperidol (Haldol), 0.5 to 2 mg given orally, intravenously or subcutaneously every six hours, can be very effective. The dosage can be titrated, if necessary, to a total of 10 to 15 mg daily. If needed, an antihistamine or a prokinetic agent may provide additional benefit.24 Severe symptoms may require a judicious combination of agents, based on mechanism of action.

Note that health care providers should use clinical judgment and consult official prescribing information before any pharmaceutical product mentioned in this article is used.

The Authors

DOUGLAS D. ROSS, M.D., PH.D., is professor of medicine at the University of Maryland School of Medicine, Baltimore, and director of the Program in Experimental Therapeutics at the University of Maryland Greenebaum Cancer Center, also in Baltimore. As the principal investigator of an educational grant from the National Cancer Institute, Dr. Ross recently led a team that integrated approximately 20 hours of required classroom and experiential training in hospice and palliative care into the curriculum of the University of Maryland School of Medicine.

CARLA S. ALEXANDER, M.D., is clinical assistant professor of medicine at the University of Maryland School of Medicine, where she is also director of palliative care for the Institute of Human Virology. In addition, Dr. Alexander is medical director of the National Hospice and Palliative Care Organization and vice president of medical services for Hospice and Palliative Care of Metropolitan Washington, in Washington, D.C.

Address correspondence to Douglas D. Ross, M.D., Ph.D., University of Maryland Greenebaum Cancer Center, Bressler Research Bldg., Room 9–015, 655 W. Baltimore St., Baltimore, MD 21201 (e-mail: dross@som.umaryland.edu). Reprints are not available from the authors.

The authors indicate that they do not have any conflicts of interest. Sources of funding: Dr. Ross's work was supported in part by grant R25-CA66940 from the National Institutes of Health, National Cancer Institute. Dr. Alexander's work is supported in part by the Ryan White Care Act Special Projects of National Significance, from the Health Resources and Services Administration.

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24. Storey P. Primer of palliative care. 2d ed. rev. Gainesville, Fla.: American Academy of Hospice and Palliative Medicine, 1996.

This is part of a series of articles and features on issues in end-of-life care. Coordinator of this series is Caroline Wellbery, M.D., assistant deputy editor of AFP.


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