L.P. was seen by a psychiatrist. She was scheduled for counseling and prenatal classes. L.P. seemed eager to attend the classes,

and she talked enthusiastically about the baby when family members came to visit. Because of L.P.’s pregnancy, the decision was

87Managing Drug Overdoses and Poisonings Chapter 4

made to continue NAC for a full 72-hour course with the goal

of protecting the fetal liver as much as possible. Six weeks later,

she had a normal delivery of a healthy 6-pound, 1-ounce baby

girl.

SUMMARY

Unfortunately, there is no cookbook method to treat all poisoned

patients. Each exposure is unique: the patients, substances, symptoms, time of exposure, and circumstances differ in each case.

Treatment of the poisoned patient often involves controversy

because solid, evidence-based science to support a given decision is frequently lacking. When challenged with a poisoning

exposure, consult with a poison control center. By calling 1-800-

222-1222, the call will be connected to the poison center where

consultation is available 24 hours a day nationwide.

KEY REFERENCES AND WEBSITES

A full list of references for this chapter can be found at

http://thepoint.lww.com/AT10e. Below are the key references

and websites for this chapter, with the corresponding reference number in this chapter found in parentheses after the

reference.

Key References

Boyle JS et al. Management of the critically poisoned patient.

Scand J Trauma Resusc Emerg Med. 2009;17:29. (29)

Bronstein AC et al. 2009 Annual report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 27th Annual Report. Clin Toxicol (Phila). 2010;48:

979. (3)

Chyka PA et al. Position paper: single-dose activated charcoal.

Clin Toxicol (Phila). 2005;43:61. (46)

Committee on Poison Prevention and Control, Board on Health

Promotion and Disease Prevention, Institute of Medicine of the

National Academies. Poison control center activities, personnel,

and quality assurance. Forging a Poison Prevention and Control System. Chapter 5. Washington, DC: The National Academies Press;

2004. (22)

Forsberg S et al. Coma and impaired consciousness in the emergency room: characteristics of poisoning versus other causes.

Emerg Med J. 2009;26:100. (120)

Kociancic T, Reed MD. Acetaminophen intoxication and length

of treatment: how long is long enough. Pharmacotherapy. 2003;23:

1052. (187)

Manoguerra AS et al. Iron ingestion: an evidence-based consensus guideline for out-of-hospital management.Clin Toxicol (Phila).

2005;43:553. (96)

[No authors listed]. Position paper: cathartics [published correction appears in J Toxicol Clin Toxicol. 2004;42:1000]. J Toxicol Clin

Toxicol. 2004;42:243. (47)

[No authors listed]. Position paper: ipecac syrup [published correction appears in J Toxicol Clin Toxicol. 2004;42:1000]. J Toxicol

Clin Toxicol. 2004;42:133. (44)

[No authors listed]. Position paper: whole bowel irrigation [published correction appears in J Toxicol Clin Toxicol.

2004;42:1000; dosage error in article text]. J Toxicol Clin Toxicol.

2004;42:843. (48)

Proudfoot AT et al. Position paper on urine alkalinization.

J Toxicol Clin Toxicol. 2004;42:1. (70)

Rumack BH et al. Acetaminophen overdose: 662 cases with evaluation of oral acetylcysteine treatment. Arch Intern Med. 1981;

141(3 Spec No):380. (166)

Liebelt EL. Targeted management strategies for cardiovascular toxicity from tricyclic antidepressant overdose: the pivotal

role for alkalinization and sodium loading. Pediatr Emerg Care.

1998;14:293. (150)

Temple AR. Pathophysiology of aspirin overdosage toxicity, with

implications for management. Pediatrics. 1978;62(5 Pt 2 Suppl):

873. (81)

Vale JA et al. Position paper: gastric lavage. J Toxicol Clin Toxicol.

2004;42:933. (45)

Key Websites

CDC Injury Prevention and Control: Data and Statistics.

http://www.cdc.gov/injury/wisqars/index.html.

Drug Abuse Warning Network. https://dawninfo.samhsa.

gov/data.

5 End-of-Life Care

Victoria F. Ferraresi

CORE PRINCIPLES

CHAPTER CASES

1 End-of-life care consists of palliative and hospice care. It is ideally introduced early

in the disease progression to provide support to patients of all ages with a serious

chronic or life-threatening illness. Medicare patients who enter a hospice program

agree to relinquish their regular Medicare benefits as they relate to the terminal

illness, and accept the palliative rather than curative approach that will be provided

by hospice. The hospice provides all care related to the hospice diagnosis under a

managed-care model at a fixed reimbursement.

Case 5-1 (Question 1)

2 In 2008, the Hospice Conditions of Participation were updated to include a review

of the medication profile as part of the initial assessment of new patients. The

medication regimens of hospice patients should be continually reviewed and

updated, with unnecessary, ineffective, or duplicative medications discontinued.

Case 5-1 (Question 2)

3 Patients near end of life can experience a number of distressing symptoms. These

should be anticipated and treated in a timely manner that is acceptable to the

patients and their families.

Case 5-1 (Question 3)

4 Well-trained pharmacists can improve medication management for hospice

patients, while helping the hospice manage their drug costs.

Case 5-1 (Question 2)

5 Many barriers exist regarding pain management and the use of opioids. Case 5-1 (Question 4)

6 Effective pain management uses a variety of approaches. Case 5-2 (Question 1)

7 Pain and symptom management may at times require an aggressive approach. Case 5-3 (Questions 1–3)

HOSPICE AND PALLIATIVE CARE

Terminology

Hospice care and palliative care are similar, but distinct, terms

sharing the common belief that the relief of suffering is a longstanding, central, and fully legitimate aim of medicine. End-of-life

carerefers to both hospice care and palliative care. The basic principle of end-of-life care is to optimize the quality of life for the

patient and family in the last weeks and months of life, as well

as to provide support for the family beyond the end of life into

bereavement.

Palliative care, which includes hospice care, is ideally introduced early in the disease progression to provide support to

patients of all ages with a serious chronic or life-threatening illness. It can be provided concurrently with other treatments to

cure or reduce disease, or it can be provided independently. The

word palliation, derived from the Latin word pallium(a cloak), has

been defined as “treatment to reduce the violence of a disease.”

The World Health Organization and the National Consensus

Project define palliative care as an approach that improves the

quality of life of patients and their families who are facing a lifethreatening illness, by preventing and relieving suffering through

early identification and impeccable assessment and treatment of

pain and other physical, psychosocial, and spiritual problems.1–4

Palliative care:

 Affirms life and regards dying as a normal process

 Provides relief from pain and other distressing symptoms

 Intends neither to hasten nor postpone death

 Integrates the psychological and spiritual aspects of patient

care

 Offers a support system to help patients live as actively as

possible until death

 Uses a multidisciplinary team approach to address the needs

of the patient and his or her family during the patient’s illness

and

 Provides bereavement counseling when indicated.3

88

of up to 120 PCA attempts in 24 hours reflects his continued pain. He describes the intensity of his pain as 8 of

10. Before considering palliative sedation, what other therapeutic interventions can be implemented for D.V.?

Before considering palliative sedation, patients should be thoroughly assessed for insomnia and depression. Underlying reasons

for insomnia should be explored and treated. Poor pain management is often the cause. In D.V., lidocaine 0.5 to 1 mg/kg/hour

administered IV or subcutaneously might be useful to assist in

the management of his severe neuropathic pain.89–93 Lidocaine

purportedly interrupts pain transmission by blocking sodium

channels (see Chapter 7, Pain and Its Management).

D.V. was started on lidocaine 1 mg/kg/hour IV. A bolus

dose was not given because of the short half-life of lidocaine.

Overnight, his use of hydromorphone boluses dropped to one.

He now reports his pain as 1 of 10 and that he slept through the

night for the first time in months. During the next 2 days, the

hydromorphone basal rate was tapered to 5 mg/hour. He did

not experience any lidocaine toxicity, such as perioral numbness,

metallic taste, or somnolence. D.V. continued on lidocaine, using

no hydromorphone boluses for the next 2 weeks, until he died

at home surrounded by his family.

KEY REFERENCES AND WEBSITES

A full list of references for this chapter can be found at

http://thepoint.lww.com/AT10e. Below are the key references

and website for this chapter, with the corresponding reference number in this chapter found in parentheses after the

reference.

Key References

Bruera E et al, eds. Textbook of Palliative Medicine. New York, NY:

Oxford University Press; 2006. (2)

National Consensus Project for Quality Palliative Care (2009).

Clinical Practice Guidelines for Quality Palliative Care, Second Edition.

http://www.nationalconsensusproject.org. Accessed March

11, 2011. (4)

Electronic Code of Federal Regulations. Title 42–Public

Health, Chapter IV—Centers for Medicare and Medicaid

Services, Department of Health and Human Services, Part

418—Hospice Care. http://ecfr.gpoaccess.gov/cgi/t/text/

textidx?c=ecfr&sid=6265ddb45c786ea731b66312dcf31d44&

rgn=div5&view=text&node=42:3.0.1.1.5&idno=42. Accessed July 18, 2011. (12)

American Society of Health-System Pharmacists. ASHP statement on the pharmacist’s role in hospice and palliative care. Am

J Health Syst Pharm. 2002;59:1770. (29)

Lycan J et al. Improving efficacy, efficiency and economics of

hospice individualized drug therapy. Am J Hosp Palliat Care.

2002;19:135. (31)

Lee J, McPherson MF. Outcomes of recommendations by hospice

pharmacists. Am J Health Syst Pharm. 2006;63:2235. (33)

Wilson S et al. Impact of pharmacist intervention on clinical

outcomes in the palliative care setting. Am J Hosp Palliat Care.

2010 November 28. [Epub ahead of print] (41)

Victoria Hospice Society. Palliative Performance Scale (PPSv2),

version 2. Medical Care of the Dying. 4th ed. Victoria,

British Columbia, Canada: Victoria Hospice Society; 2006:120.

http://www.victoriahospice.org/sites/default/files/imce/

PPS ENGLISH.pdf. Accessed April 17, 2011. (44)

Qaseem A et al. Evidence-based interventions to improve the

palliative care of pain, dyspnea, and depression at the end of

life: a clinical practice guideline from the American College of

Physicians. Ann Intern Med. 2008;148:141. (56)

U.S. Food and Drug Administration. Code of Federal Regulations Title 21. 21CFR1306.11(g). http://www.accessdata.

fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm?fr=1306.

11. Accessed April 24, 2011. (69)

Fass J, Fass A. Physician-assisted suicide: ongoing challenges for

pharmacists. Am J Health Syst Pharm. 2011;68:846. (81)

Kirk TW et al. National Hospice and Palliative Care Organization

(NHPCO) position statement and commentary on the use of

palliative sedation in imminently dying terminally ill patients.

J Pain Symptom Manage. 2010;39:914. (83)

Key Websites

American Academy of Hospice and Palliative Medicine

(AAHPM). http://www.aahpm.org/

Center to Advance Palliative Care (CAPC). http://www.capc.

org/

Children’s Hospice and Palliative Care Coalition. http://www.

childrenshospice.org

Centers for Medicare & Medicaid Services (CMS). http://www.

cms.gov/center/hospice.asp

End of Life/Palliative Education Resource Center (EPERC).

http://www.eperc.mcw.edu/eperc

Hospice Foundation of America (HFA). http://www.

hospicefoundation.org/

Innovations in End-of-Life Care (an international journal of leaders in end-of-life care). http://www2.edc.org/lastacts/

International Association for Hospice & Palliative Care (IAHPC).

http://www.hospicecare.com/

MedlinePlus. Hospice Care. http://www.nlm.nih.gov/

medlineplus/hospicecare.html

National Hospice and Palliative Care Organization (NHPCO).

http://www.nhpco.org/

The Population-based Palliative Care Research Network

(PoPCRN). http://www.ucdenver.edu/academics/colleges/

medicalschool/departments/medicine/GIM/Popcrn/Pages/

PopcrnHome.aspx

End of Life Online Curriculum. http://endoflife.stanford.edu/

M00 overview/intro lrn overv.html

NHPCO Pediatric Palliative Care and Hospice. http://www.

nhpco.org/pediatrics

American Academy of Pediatrics. Section on Hospice and Palliative Medicine. http://www.aap.org/sections/palliative

The National Consensus Project for Quality Palliative Care.

http://www.nationalconsensusproject.org

6 Nausea and Vomiting

Lisa K. Lohr

CORE PRINCIPLES

CHAPTER CASES

MOTION SICKNESS

1 Motion sickness is caused by discordant information about body position or motion

received from visual, vestibular, or body proprioceptors. Acetylcholine is thought to

be the primary neurotransmitter involved.

Case 6-1 (Question 1)

2 Transdermal scopolamine is recommended for prophylaxis of motion sickness for

moderate to severe stimuli. Dimenhydrinate or promethazine are recommended for

treatment of breakthrough symptoms. The most common adverse effects of these

agents include drowsiness, confusion, and dry mouth.

Case 6-1 (Question 2),

Table 6-1

CHEMOTHERAPY-INDUCED NAUSEA AND VOMITING

1 Nausea and vomiting are initiated by several stimuli, and mediated by several

neurotransmitters in the central nervous system, peripheral nervous system, and

gastrointestinal tract. Because of the multiple neurotransmitter receptors involved,

successful prophylaxis and treatment of chemotherapy-induced nausea and

vomiting will almost always require medications with more than one mechanism of

action.

Case 6-2 (Question 1)

2 The likelihood of nausea and vomiting depends on patient risk factors and most

importantly on the emetogenicity of the chemotherapy agents prescribed. The

antiemetic regimen should be appropriate for the chemotherapy agent with the

highest emetogenicity level.

Case 6-2 (Question 1),

Table 6-2

3 Patients receiving highly emetogenic chemotherapy should receive prophylaxis

with a 5-serotonin receptor type 3 (5-HT3) antagonist, dexamethasone, and

fosaprepitant or aprepitant. Patients receiving moderately emetogenic

chemotherapy should receive prophylaxis with a 5-HT3 antagonist and

dexamethasone (plus fosaprepitant or aprepitant for those chemotherapy agents

posing a high risk of delayed nausea and vomiting).

Case 6-2 (Question 2),

Tables 6-3, 6-4,

Figures 6-2, 6-3

4 For breakthrough symptoms, patients should receive rescue antiemetics with a

different mechanism of action than the prophylactic medications and receive more

aggressive antiemetics before the next cycle of chemotherapy.

Case 6-2 (Question 3),

Tables 6-3, 6-4,

Figures 6-2, 6-3

RADIATION-INDUCED NAUSEA AND VOMITING

1 Radiation can cause nausea and vomiting by the same pathways as chemotherapy.

The risk depends on the area and size of the radiation field as well as the fractional

dose of radiation and whether the patient has had chemotherapy in the past.

Case 6-3 (Question 1),

Table 6-5

2 The recommended prophylaxis for radiation-induced nausea and vomiting includes

a 5-HT3 antagonist with dexamethasone for high-risk patients, and with or without

dexamethasone for patients at moderate risk. Breakthrough symptoms may be

treated with a 5-HT3 antagonist or dopamine antagonist.

Case 6-3 (Question 1),

Table 6-5

continued

98

99Nausea and Vomiting Chapter 6

CHAPTER CASES

POSTOPERATIVE NAUSEA AND VOMITING

1 The risk of postoperative nausea and vomiting depends on several patient, surgical

and anesthetic factors. The antiemetic regimen should be proportional to the risk

factors.

Case 6-4 (Question 1),

Table 6-6

2 The most active agents in preventing postoperative nausea and vomiting are 5-HT3

antagonists. For patients at moderate to high risk, a 5-HT3 antagonist should be

combined with dexamethasone or droperidol. Antiemetics used for rescue therapy

should be of a different class than the prophylaxis agents used.

Case 6-4 (Question 1),

Table 6-6

DEFINITION

Nausea and vomiting are unpleasant symptoms caused by selflimiting disorders or serious conditions such as cancer. These

symptoms can range from mild, short-lived nausea to continuing severe emesis and retching. The emetic response can be

described in three phases: nausea, vomiting, and retching. Nausea is the subjective feeling of the need to vomit. It includes an

unpleasant sensation in the mouth and stomach and can be associated with salivation, sweating, dizziness, and tachycardia. Vomiting is the forceful expulsion of the stomach contents through

the mouth, but is preceded by the relaxation of the esophageal

sphincter, contraction of the abdominal muscles, and temporary

suspension of breathing. Retching is the rhythmic contraction of

the abdominal muscles without actual emesis. It can accompany

nausea, or occur before or after emesis.

EPIDEMIOLOGY AND CLINICAL

PRESENTATION

Nausea and vomiting are caused by many disorders. Central nervous system (CNS) causes include increased intracranial pressure, migraine headaches, brain metastases, vestibular dysfunction, alcohol intoxication, and anxiety. Infectious disease causes

include viral gastroenteritis, food poisoning, peritonitis, meningitis, and urinary tract infections. Metabolic causes include

hypercalcemia, uremia, hyperglycemia, and hyponatremia. Gastrointestinal disorders, such as gastroparesis, bowel obstruction,

distension, and mechanical irritation, can cause nausea and vomiting. Among the many medications that can cause nausea and

vomiting are cancer chemotherapy, antibiotics, antifungals, and

opiate analgesics.

In addition to the suffering involved, uncontrolled vomiting

can lead to dehydration, electrolyte imbalances, malnutrition,

aspiration pneumonia, and esophageal tears. Nausea and vomiting often reduces food intake and can impair a person’s ability

to care for himself or herself. Significant reductions in qualityof-life scores have been demonstrated in cancer patients with

chemotherapy-induced nausea and vomiting compared with

patients who did not have those symptoms.1

PATHOPHYSIOLOGY

The CNS, the peripheral nervous system, and the gastrointestinal

(GI) tract are all involved in initiating and coordinating the emetic

response. In the CNS, the vomiting center (VC) receives incoming signals from other parts of the brain and the GI tract and then

coordinates the emetic response by sending signals to the effector

organs. The VC is located in the medulla oblongata of the brain,

near the nucleus tractus solitarius (NTS). The VC is stimulated

by neurotransmitters released from the chemoreceptor trigger

zone (CTZ), the GI tract, the cerebral cortex, the limbic system,

and the vestibular system (Fig. 6-1). The major neurotransmitter

receptors associated with the emetic response include serotonin (the 5-hydroxytryptamine type 3, [5-HT3]) receptors, neurokinin 1 (NK1) receptors, and dopamine receptors. Other receptors involved include corticosteroid, acetylcholine, histamine,

cannabinoid, gabaminergic, and opiate receptors. Many of these

receptors are targets for antiemetic therapy.

In the CNS, the CTZ is located in the area postrema on the

floor of the fourth ventricle in the brainstem; it lies outside the

blood–brain barrier. When the CTZ senses toxins and noxious

substances in the blood or cerebrospinal fluid, it triggers the

emetic response by releasing neurotransmitters that travel to

the VC and the NTS. The major neurotransmitter receptors