CE

CoverArticle

Continuing Education

Managing Nausea
and Vomiting
CURRENT STRATEGIES
Kitty Garrett, RN, MSN, CCRN
Kayo Tsuruta, RN, MSN, AOCN
Shirley Walker, RN, MSN
Sharon Jackson, RN, MSN
Michelle Sweat, RN, BSN

he topic of nausea and

vomiting is all too familiar to most
nurses. Nausea and vomiting are
unpleasant complications or indications of many medical conditions and
are adverse effects of hundreds of
medications. Nausea and vomiting
occur so frequently that they are
almost considered acceptable, usually referred to as minor and considered more of an inconvenience or a
nuisance than a medical problem.
This duo, however, is not only
unpleasant but can be debilitating
and can cause unnecessarily prolonged recovery times and increased
costs. In critically ill patients, severe
or protracted nausea and vomiting
can lead to serious complications
such as aspiration pneumonia, dehy-

CE

This article has been designated for

CE credit. A closed-book, multiple-choice
examination follows this article, which tests your
knowledge of the following objectives:

1. Discuss the mechanisms of nausea and

vomiting
2. Identify preoperative and postoperative
factors that influence the development
of nausea and vomiting
3. Describe treatment options for nausea
and vomiting

Authors
Kitty Garrett is a critical care clinical nurse specialist at St. Joseph Hospital in Augusta,
Ga. She has worked in critical care and has been CCRN certified for 20 years.
Kayo Tsuruta has 7 years of nursing experience and is currently working as an oncology
nurse at Athens Regional Medical Center in Athens, Ga.
Shirley Walker is an instructor in the nursing staff development department at AnMed
Health in Anderson, SC. She has 23 years of nursing experience.
Sharon Jackson has 12 years of experience in medical-surgical nursing and emergency
department nursing. She is a major in the US Army Nursing Corps and is stationed at
Tripler Army Medical Center in Honolulu, Hawaii.
Michelle Sweat is a senior staff nurse in the medical intensive care unit at the Medical
College of Georgia Hospital in Augusta. She is currently enrolled in the critical care clinical
nurse specialist program at the Medical College of Georgia School of Nursing.
To purchase reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 8092273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints@aacn.org.

CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 31

dration, malnutrition, and disruption

of the surgical site.1,2 Metabolic disturbances such as metabolic alkalosis,
hyponatremia, hypochloremia, and
hypokalemia may occur. Vomiting
after craniotomy or any brain injury
causes an increase in intracranial
pressure. These complications can be
life-threatening. Nausea and vomiting
can also cause patients to experience
increased anxiety and dissatisfaction
with the hospital experience and can
contribute to future anticipatory nausea.2 Also, the increased resources
and time needed to treat a patient
with nausea and vomiting can have a
profound economic impact.2
Interest in this topic was recently
renewed because of an enhanced
understanding of the physiological
mechanisms involved in the process
of nausea and vomiting. Much has
been published about nausea and
vomiting as it relates to chemotherapy and postoperative nausea and
vomiting, but many correlates can be
drawn to critical care patients. In this
article, we present current knowledge
about the physiological mechanisms
of nausea and vomiting and compare
therapeutic agents (pharmacological
and nonpharmacological) recommended for treating and preventing
nausea and vomiting. Because it is
now understood that most episodes
of nausea and vomiting are preventable, implications for critical care nursing will focus on prevention rather
than control of nausea and vomiting.

Definitions
Nausea and vomiting are basic
human protective reflexes against
the absorption of toxins, as well as
responses to certain stimuli.2 The
terms nausea and vomiting are often
used together, although each phe-

nomenon should be assessed separately. Nausea is defined as a subjectively unpleasant wavelike sensation
in the back of the throat or epigastrium associated with pallor or flushing, tachycardia, and an awareness
of the urge to vomit.1 Sweating,
excess salivation, and a sensation of
being cold or hot may occur.
Vomiting, or emesis, is characterized
by contraction of the abdominal
muscles, descent of the diaphragm,
and opening of the gastric cardia,
resulting in forceful expulsion of
stomach contents from the mouth.1
Retching involves spasmodic contractions of the diaphragm and the
muscles of the thorax and abdominal wall without expulsion of gastric
contents, the so-called dry heaves.1

Mechanisms of
Nausea and Vomiting
The activation of a nucleus of
neurons located in the medulla
oblongata, known as the vomiting
center, initiates the vomiting reflex.
The vomiting center can be activated
directly by signals from the cerebral
cortex (anticipation, fear, memory),
signals from sensory organs (disturbing sights, smells, pain), or signals from the vestibular apparatus of
the inner ear (motion sickness). The
vomiting center can also be activated indirectly by certain stimuli that
activate the chemoreceptor trigger
zone (CTZ)3 (Figure 1). The CTZ is
located in the highly vascular area
postrema on the surface of the brain.
This area lacks a true blood-brain
barrier and is exposed to both blood
and cerebrospinal fluid; thus, the
CTZ can react directly to substances
in the blood.2 The CTZ can be activated by signals from the stomach
and small intestine traveling along

32 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003

vagal afferent nerves or by the direct

action of emetogenic compounds
that are carried in the blood (anticancer drugs, opioids, ipecac).
Specific neurotransmitters and
neuromodulators in the CTZ identify substances as potentially harmful
and relay impulses to the vomiting
center to initiate the vomiting cascade so that the harmful substance
can be expelled. These neurotransmitters are serotonin, dopamine,
acetylcholine (muscarinic cholinergic), and histamine. A fifth chemoreceptor, the neurokinin-1
neuropeptide, also called substance
P, is currently under study.4,5
Stimulation of these chemoreceptors triggers activation of the
vomiting center. Therefore, any
interference with the transmission
of these chemoreceptors prevents
the vomiting center from being activated. Many antiemetics act by
blocking 1 or more of these receptors.3 Dopamine antagonists block
dopamine receptors; muscarinic
antagonists block acetylcholine
receptors; histamine blockers block
histamine receptors; and serotonin
receptor blockers block serotonin
receptors. The adverse effects of
these drugs are also determined by
which receptor site is blocked3
(Table 1).

Chemotherapy-Induced
Nausea and Vomiting
Nausea and vomiting are among
the most distressing and debilitating
adverse effects of chemotherapy.
Even though chemotherapeutic
agents are not routinely administered in critical care, cancer patients
who have had chemotherapy are
often admitted to critical care areas.
Hence, a discussion of nausea and

Health System Pharmacists (ASHP)

recommends prophylactic antiemetic
therapy when drugs with antiemetic
potential of levels 2 to 5 are used1
(Table 2).

Stomach and small intestine

5HT
DA

Blood-borne emetics
Chemotherapy
Opioids
Ipecac

Sensory input
Sight
Smell
Pain
Vestibular apparatus

Risk Factors
In addition to the emetic potential
of the chemotherapeutic agents, several other risk factors can be used to predict the likelihood of CINV. Patients
younger than 50 years have more
nausea and vomiting than do older
patients.1 Women are more susceptible than men, presumably because of
the influence of hormones.2 A history
of motion sickness, pregnancy-related
nausea and vomiting, or nausea and
vomiting with previous chemotherapy
are all positive predictors of CINV.1
Patients who use alcohol heavily or
who have done so in the past have a
reduced risk of emesis.1,11

Va

Higher centers
Anticipation
Fear
Memory

ga
la

ff

er

en

ts

5HT
DA
M

CTZ

H1
M

Vomiting center

Vomiting
via output to stomach,
diaphragm, and abdominal muscles

Receptors:
5HT = Serotonin
DA = Dopamine
M = Muscarinic cholinergic
H1 = Histamine1

Figure 1 The emetic response: stimuli, pathways, and receptors.

CTZ indicates chemoreceptor trigger zone.
Reprinted from Lehne et al,3 with permission.

vomiting would not be complete

without a description of the clinical
studies in this area.
Mechanism
Chemotherapeutic agents stimulate enterochromaffin cells in the gastrointestinal tract to release
serotonin, which activates serotonin
receptors. Activation of the receptors
activates the vagal afferent pathway,
which activates the vomiting center
and causes an emetic response.10 The

emetic potential of a chemotherapeutic agent itself is the major stimulus

for nausea and vomiting in
chemotherapy-induced nausea and
vomiting (CINV).1 Chemotherapeutic
agents are rated according to their
emetic potential; 1 indicates the least
potential, and 5 indicates the greatest. An example of an agent with the
lowest emetic potential (1) is vincristine. An example of an agent with
the highest emetic potential (5) is cisplatin. The American Society of

Patterns of Nausea and Vomiting

Anticipatory nausea and vomiting
occur before the beginning of a new
cycle of chemotherapy, in response to
conditioned stimuli such as the
smells, sights, and sounds of the
treatment room or the presence of a
specific person designated to administer the chemotherapy.12 Anticiatory
nausea usually occurs 12 hours
before administration of chemotherapy in patients who have experienced
failed control of nausea and vomiting
in previous treatments.
Acute nausea and vomiting occur
within the first 24 hours after the
administration of chemotherapy,
usually within the first 1 to 2 hours.
This type is initiated by stimulation
primarily of dopamine and serotonin receptors in the CTZ, which
triggers the vomiting cascade.1 It
resolves within 24 hours.

CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 33

Table 1 Summary of antiemetic therapy as recommended by the American Society of Health System Pharmacists, the American
Site of action

Drug type

Indications

Examples

Indirect stimulation of vomiting center through receptor sites (chemoreceptor trigger zone)
Serotonin
receptors

Ondansetron
(Zofran)

Serotonin (5HT3)
receptor
antagonists

First-line therapy for acute CINV and RINV: use on day of

chemotherapy or radiation therapy only, not more than 24 hours
later
First-line therapy for prevention of PONV and treatment of
breakthrough nausea and vomiting
Opioid-induced nausea and vomiting6

Granisetron
(Kytril)

First-line therapy for prevention of acute CINV and RINV

Only effective in acute phase, not useful beyond 24 hours

Not approved for PONV, although clinical trials are under way
Dolasetron
(Anzemet)

Prevention of CINV

Prevention and treatment of PONV

Dopamine
receptors

Promethazine
(Phenergan)

Dopamine antagonists

PONV
Breakthrough nausea and vomiting in CINV
6

Phenothiazines

Opioid-induced nausea and vomiting

Chlorpromazine
(Thorazine)

Acceptable alternative to droperidol in the prevention and treatment

of PONV

Prochlorperazine
(Compazine)

Breakthrough nausea and vomiting

Established nausea and vomiting in RINV
6

Opioid-induced nausea and vomiting

Butyrophenones

Droperidol
(Inapsine)

34 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003

Prevention and treatment of established PONV and breakthrough

nausea and vomiting in CINV only in patients who do not
respond to other drug8
Can be given in combination with serotonin receptor antagonists
and steroids in patients at high risk for PONV

Society of Clinical Oncology, and Mayo Clinic Clinical Practice Guidelines

Dosage*

CINV prevention: 24 mg by mouth or 8 mg IV 30 min

before chemotherapy

Most common adverse effects

Mild to moderate and transient;

headache most common

PONV prevention: 4 mg IV over 2-5 min immediately

before or 8 mg by mouth 1 hour before induction of
anesthesia

Oral doses recommended over IV doses because

former are equally effective, less costly, and
more convenient

CINV prevention: 2 mg by mouth or 10 g/kg IV 30 min

before chemotherapy

Disadvantages: Increased cost; all serotonin

receptor antagonists equally effective at
equivalent doses, so cost should be a factor
in making a choice

In recent trials,4 1 mg as effective as 2 mg and 50% less

expensive
PONV prevention: 20-40 g/kg IV (in clinical trials)

PONV prevention: 12.5 mg IV intraoperatively or 100

mg by mouth 1 hour before induction of anesthesia

Advantages: one-time dosing lasts 24 hours, no

known drug interactions, broad safety profile,
may be taken with or without food, nonsedating
Should be administered with steroids to prevent
delayed nausea and vomiting

PONV treatment: 1-4 mg IV

CINV prevention: 100-200 mg by mouth or 1.8 mg/kg

IV 30 min before chemotherapy

Comments

IV dolasetron may cause

changes in intervals on
electrocardiograms; use with
caution in prolonged
conduction disorders

PONV treatment: 12.5 mg IV postoperatively

PONV prevention: 25 mg by mouth 1 hour before or
12.5-25 mg IV immediately before induction of
anesthesia

Oversedation; lethargy, postural

hypotension; skin sensitivity;
dystonic reactions

PONV treatment: 10-25 mg by mouth every 4-6 hours as

needed or 12.5-25 mg intramuscularly or IV every 4 hr
as needed; 25-mg rectal suppository every 12 hours

Extrapyramidal reactions or
paradoxical reactions occur
more commonly in children

PONV treatment: 10-25 mg by mouth every 4-6 hours

as needed; 25- or 100-mg rectal suppository

Not first-line drug in breakthrough CINV because

of cost
Not first-line drug in chronic opioid-induced
nausea and vomiting because of cost; may be
used as first-line drug in acute episodes of
opioid-induced nausea and vomiting

Widely used because they are inexpensive;

moderately effective; available in IV, oral, and
suppository forms
Efficacy generally lower than efficacy of
serotonin receptor antagonists

PONV prevention: 5-15 mg by mouth 1 hour, 5-10 mg

intramuscularly 1-2 hours, or 5-10 mg IV 15-30 min
before induction of anesthesia

Prochlorperazine more effective than promethazine for treating uncomplicated nausea and
7

vomiting in patients in emergency department

PONV treatment: 5-15 mg by mouth or 5-10 mg intramuscularly or IV every 3-4 hours; 2.5-, 5-, 25-mg
rectal suppository

IV promethazine administered at a rate no

greater than 25 mg/min

CINV treatment: 5-20 mg by mouth, intramuscularly, or

IV every 6 hours, 25-mg rectal suppository every 12
hours

IV prochlorperazine administered at a rate no

greater than 5 mg/min

PONV prevention: 0.625-1.25 mg IV SLOWLY 5 min

before termination of anesthesia

Sedation, hypotension,
tachycardia

PONV treatment: 0.625-1.25 mg IV slowly as needed

Prolonged QT interval leading

to torsade de pointes

Maximum dose: 2.5 mg

Not available in oral form

Should not be given to patients with long QT
intervals
Electrocardiographic monitoring should be done
before administration and continued for 2-3
hours after treatment

Continued

CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 35

Table 1 Continued
Drug type

Dopamine receptors Dopamine antago(continued)

nists
(continued)

Indications

Examples
Butyrophenones

Site of action

Haloperidol
(Haldol)

Primary PONV; breakthrough nausea and vomiting in CINV; opioidinduced nausea and vomiting; nausea and vomiting due to
bowel obstruction
Rescue therapy
when serotonin receptor antagonists not
4
effective

Metoclopramide
(Reglan)

Breakthrough nausea and vomiting in CINV; established nausea

and vomiting in RINV

Benzamide

Prevents nausea and vomiting by stimulating gastric emptying and

blocking dopamine receptors

Histaminic
receptors

Antihistamines

Opioid-induced nausea and vomiting6

Dimenhydrinate
(Dramamine)

Nausea and vomiting associated with motion sickness or vertigo

Meclizine
(Antivert)
Muscarinic cholinergic receptors
Neurokinin-1
receptors

Anticholinergics

Scopolamine

Not yet available

First-line drug in prophylaxis of nausea and vomiting associated

with motion sickness
CINV, sudden onset and delayed

Other sites of action

Mechanism
unknown

Glucocorticoids

Dexamethasone
(Decadron)

Drug of choice in prevention of delayed nausea and vomiting in

CINV
PONV with dolasetron

Methylprednisolone
(Solu-Medrol)
Cannabinoid
Cannabinoids
receptor sites
(CB-1 and CB-2)
exert central
sympathomimetic
action

Dronabinol
(Marinol)

Modestly effective in CINV; may be used in patients responding

poorly to other antiemetics

Limbic system
inhibition

Lorazepam
(Ativan)

Used as adjunct, not primary drug, in anticipatory or delayed nausea and vomiting or breakthrough nausea and vomiting in CINV

Benzodiazipines

*All dosages are from the American Society of Health System Pharmacists Clinical Practice Guidelines unless otherwise noted.
CINV indicates chemotherapy-induced nausea and vomiting; IV, intravenously; PONV, postoperative nausea and vomiting; RINV, radiation-induced nausea and vomiting;
SRA, serotonin receptor antagonist.

36 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003

Comments

Dosage*

Most common adverse effects

CINV treatment: 1-4 mg by mouth, intramuscularly, or

IV every 6 hours

Nonsedating in lower doses;

sedation, hypotension, tachycardia, extrapyrimidal effects similar
to those of dopamine
antagonists

Cost-effective alternative to serotonin receptor

antagonists

CINV treatment: 2 mg/kg by mouth or IV every 2-4

hours for 2-5 doses for rescue therapy; for delayed
nausea and vomiting, 0.5 mg/kg or 30 mg IV or by
mouth every 4-6 hours for 3-5 days

Sedation, restlessness, agitation,

diarrhea, drowsiness, sleeplessness, dystonic reactions with
higher doses

At high doses, also inhibits serotonin receptors

Use no longer recommended by Mayo Clinic
guidelines because of adverse effects of
restlessness, agitation, and drowsiness

PONV prevention: 10-20 mg IV near the end of surgery

Because of its ability to increase gastric and

intestinal motility, contraindicated in patients
with bowel obstruction, gastrointestinal
hemorrhage, or perforation

PONV treatment: 10 mg IV over 1-2 min every 4-6

hours postoperatively

Slightly less effective than serotonin receptor

antagonists and droperidol
Motion sickness and vertigo: 25-50 mg by mouth

Sedation, dry mouth, constipation,

blurred vision

Used as adjunct to prevent adverse effects in

patients receiving dopamine receptor
antagonists; use limited because dopamine
receptors no longer first-line agents

Dry mouth, drowsiness, impaired

eye accommodation

Patch applied behind ear 4 hours before travel;

patch should last 3 days

25-50 mg by mouth6
Motion sickness: patch 0.5 mg/24 hours every 3 days

Investigational

CINV prevention: 20 mg by mouth or IV with serotonin

receptor antagonists before chemotherapy

Gastrointestinal upset, anxiety,

insomnia, hyperglycemia

CINV treatment: 10 mg by mouth or IV every 4-6 hours

Used with serotonin receptor antagonists to

enhance their benefit; yields increased
protection
Used alone for prevention of level 2 CINV

PONV prevention: 10 mg IV before induction of anesthesia9

Inexpensive

CINV prevention: 40-125 mg 1-time dose before

chemotherapy

Should be used with caution in patients with

unstable diabetes mellitus

CINV treatment: 5-20 mg by mouth every 3-6 hours

CINV treatment: 1-2 mg by mouth, sublingually, intramuscularly, or IV every 6 hours

Drowsiness, dizziness, sedation,

hypotension, vision difficulty,
vasodilatation, euphoria,
dysphoria (especially in older
adults)

Other antiemetics more effective, but because

the mechanism of action differs, cannabinoids
may be given alone or in combination with
other agents

Sedation, amnesia, visual

disturbances

CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 37

Table 2 Emetogenic potential of chemotherapeutic agents and standard treatments

Treatment
Level*
5
(>90)

Cisplatin
Cyclophosphamide
(>1500 mg/m2)

4
(60-90)

Carboplatin
Cyclophosphamide
(>750 mg/m2,
<1500 mg/m2)
Doxorubicin (>60 mg/m2)
Methotrexate

3
(30-60)

Doxorubicin
Ifosfamide
Irinotecan

2
(10-30)

1
(<10)

Prevention

Agent

Cytarabine
Docetaxel
Etoposide
5-Fluorouracil
Paclitaxel
Bleomycin
Fludarabine
Vinblastine
Vincristine

Granisetron, ondansetron,
or dolasetron with
dexamethasone; or
methylprednisolone

Dexamethasone or
methylprednisolone;
prochlorperazine for
adults

Delayed

Breakthrough
Lorazepan, methylprednisolone,
prochlorperazine,
metoclopramide,
dexamethasone,
haloperidol, or
dronabinol

High-dose carboplatin:
dexamethasone and metoclopramide or serotonin
receptor antagonists

For children

For children

Chlorpromazine,
lorazepam, or
methylprednisolone

Chlorpromazine, lorazepam, or
serotonin receptor
antagonists and
dexamethasone or
methylprednisolone

High-dose carboplatin,
cyclophosphamide, or doxorubicin:
serotonin receptor
antagonists and
dexamethasone

No treatment

*Numbers in parentheses are percentages of patients who experience nausea and vomiting without effective treatment.

Delayed nausea and vomiting

begin at least 24 hours after the
administration of chemotherapy and
may last up to 120 hours. Patients
who experience acute CINV are more
likely to also experience delayed emesis.12 The causative mechanism in
delayed nausea and vomiting is not
well defined, but the metabolites of
the chemotherapeutic agents are
thought to continue to affect the central nervous system and the gastrointestinal tract.1,13(p546-549) For example,
cisplatin causes delayed nausea and
vomiting, up to 48 to 72 hours after
administration, in more than half of
all patients who receive the drug.1
Other agents that cause delayed nausea and vomiting are high-dose carboplatin, cyclophosphamide, and
doxorubicin.
Breakthrough nausea and vomiting occur despite preventive therapy

and require additional therapy.1

Antiemetic treatment administered
to patients who have not responded
to prophylactic regimens is often
referred to as rescue therapy.13
Treatment
Prevention of Acute CINV.
Antiemetic therapies have been compared in many clinical trials, especially since the advent of the relatively
new class of drugs, the serotonin
receptor antagonists (SRAs). Because
chemotherapeutic agents initiate
activation mainly of serotonin receptors, which leads to CINV, the SRAs
are among the most effective drugs
for prevention of CINV. These drugs
have become the gold standard of
antiemetic therapy,10 and they are
recommended by the ASHP as the
drugs of choice in patients receiving
chemotherapeutic agents with emetic

38 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003

potential of 3 to 5.1 The SRAs prevent

emesis by blocking the emetic
response early in the emetic
pathway.10 They are given to patients
before chemotherapy to prevent
CINV. Because the SRAs have no
effect on the histaminergic,
dopaminergic, or cholinergic receptors, they can provide highly effective
relief of nausea and vomiting without
many of the adverse effects associated with traditional antiemetic agents.
Adverse effects of the SRAs are generally mild to moderate and transient;
headache is the most common.10 The
SRAs used most often are
ondansetron (Zofran), granisetron
(Kytril), and dolasetron (Anzemet).
Unfortunately, their high cost may
prevent some patients from benefiting from these medications (Table 3).
Because SRAs are similarly effective
for controlling acute nausea and

vomiting, the investigators in several

comparative medical trials concluded
that the least expensive SRA should
be used initially.1,4,12 Also, oral SRAs
are less expensive than parenteral
SRAs and are as effective as the intravenous form.1,4,10,12 Wickam11 found
that because the SRAs are not structurally identical, they may have differences in efficacy, and she
recommends that if an SRA is ineffective, a second SRA should be given.
With less toxic chemotherapeutic
agents, combinations of other
antiemetics may be effective.
Dexamethasone and prochlorperazine are recommended for
chemotherapeutic agents that have
mild to moderate emetic potential.1
The combination of dexamethasone
with metoclopramide, although less
effective, may also be an option.
Prevention of Delayed CINV. The
SRAs alone are not useful in delayed
nausea and vomiting. Complete protection from vomiting occurs more

often in patients who are given

ondansetron plus dexamethasone.1
Therefore, dexamethasone is the
drug of choice for prevention of
delayed nausea and vomiting.1,4,9 It
should be administered with SRAs
before chemotherapy.
Treatment of Breakthrough CINV. If
a patient experiences CINV within 24
hours despite preventive antiemetic
treatment, a combination of different
classes of antiemetic drugs is given.
This intervention is called rescue therapy. Drugs of choice for such rescue
therapy include prochlorperazine, thiethylperazine, or metoclopramide
with or without diphenhydramine, or
lorazepam, haloperidol, or dronabinol.1,15 Dronabinol may be indicated in
refractory CINV unresponsive to
other classes of drugs. Even though
the SRAs may also be effective, their
superiority over traditional, less
expensive agents has not been determined.1 The choice of agent should be
based on patient-specific factors.1 All

patients receiving chemotherapy

should have antiemetics available as
needed for rescue from breakthrough
nausea and vomiting.1 If CINV persists after the breakthrough treatment, these drugs should be given on
a scheduled basis rather than on an asneeded basis.
Treatment of Anticipatory CINV.
Behavioral interventions are recommended for anticipatory emesis
because they produce physiological
relaxation, divert attention away
from the conditioned stimulus and
toward relaxing images, and
enhance feelings of control.1 The
amnestic and anxiolytic properties
of lorazepam may also help prevent
anticipatory nausea and vomiting by
blocking the memory of emesis associated with chemotherapy.1,13
Lorazepam should be given the
night before and the morning of
chemotherapy.13,15
In summary, nausea and vomiting are no longer inevitable compli-

Table 3 Comparative costs of antiemetic agents

Agent

Mean wholesale price, $US

Intravenous form

Ondansetron (Zofran)

25.65 (2 mg/mL, 2-mL vial)

Granisetron (Kytril)
Dolasetron (Anzemet)

195.20 (1 mg/mL, 1-mL vial)

166.20 (20 mg/mL, 5-mL vial)

Promethazine (Phenergan)
Chlorpromazine (Thorazine)
Prochlorperazine (Compazine)
Droperidol (Inapsine)
Haloperidol (Haldol)
Metoclopramide (Reglan)
Dimenhydrinate (Dramamine)
Scopolamine (Transderm Sco p)
Methylprednisolone (Solu-Medrol)
Dronabinol (Marinol)
Lorazepam (Ativan)

2.27 (25 mg/mL, 1-mL ampoule)

2.85 (50 mg/mL, 1-mL ampoule)
2.60 (25 mg/mL, 2-mL vial)
4.73 (10-mg ampoule)
5.71 (2.5 mg/mL, 2-mL ampoule)
4.59 (2.5 mg/mL, 1-mL ampoule)
8.15 (5 mg/mL, 1-mL ampoule)
4.56 (5 mg/mL, 2-mL vial)
9.42 (50 mg/mL, 1-mL vial)
2.38 (0.4 mg/mL, 1 mL)
3.51 (40-mg injection)
9.01 (125-mg injection)
Not applicable
10.66 (2 mg/mL, 1-mL vial)

Oral form
27.80 (8-mg tablet)
16.69 (4-mg tablet)
47.05 (1-mg tablet)
55.31 (50-mg tablet)
73.31 (100-mg tablet)
0.04 (25-mg tablet)
0.06 (50-mg tablet)
0.62 (50-mg tablet)
0.54 (5-mg tablet)
0.81 (10-mg tablet)
Not applicable
0.06 (5-mg tablet)
0.25 (10-mg tablet)
0.41 (20-mg tablet)
4.85 (patch)
0.48 (4-mg tablet)
8.06 (5-mg tablet)
0.67 (1-mg tablet)
0.99 (2-mg tablet)

Data from Drug Topics Redbook.14

CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 39

cations of chemotherapy; most

patients can get complete control of
these adverse effects. The drugs of
choice for prevention of acute CINV
are the SRAs. Recommended treatment for prevention of delayed
CINV is dexamethasone. The drug
of choice for anticipatory nausea
and vomiting is lorazepam.
Breakthrough nausea and vomiting
can be treated with prochlorperazine, metoclopramide, haloperidol,
or dronabinol (Table 1).

Postoperative
Nausea and Vomiting
The term acute postoperative
nausea and vomiting is defined as
any episode of nausea or vomiting
that occurs within 24 hours of

receiving anesthesia. Although significant progress has been made in

preventing this type of nausea and
vomiting, it still occurs in 20% to
30% of patients after surgery.1,2
Mechanism
In postoperative nausea and
vomiting, a wide range of stimuli
contribute to the emetic response.
Most anesthetic agents and opioids
stimulate the vomiting center indirectly through the CTZ. Associated
factors that directly stimulate the
vomiting center include sensory
input (visual, olfactory, and pain)
and the vestibular apparatus.
Nitrous oxide directly stimulates the
gastrointestinal tract, which activates the vomiting center.2

40 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003

Causes
Preoperative Factors. The occurrence of postoperative nausea and
vomiting is influenced by several factors.1,2,16 The risk is higher in adults
than in children, in women than in
men, and in patients with a history
of motion sickness or previous postoperative nausea and vomiting.1 The
prevalence is also greater in obese
patients and in patients with delayed
gastric emptying disorders such as
gastroesophageal reflux disease, gastrointestinal obstruction, chronic
cholecystitis, and neuromuscular
disorders.1 A history of smoking is
associated with a decrease in the
likelihood of postoperative nausea
and vomiting.16 Patients characteristics have a cumulative effect in influ-

encing the prevalence of postoperative nausea and vomiting.

Intraoperative Factors. The type of
surgical procedure can also influence
the occurrence of postoperative nausea and vomiting. The rate is high in
patients undergoing laparoscopic procedures related to abdominal distention because of the carbon dioxide
used for visualization.1,2 The prevalence of postoperative nausea and
vomiting is also greater after plastic,
ophthalmic, orthopedic shoulder,
gynecologic, and ear, nose, and throat
surgeries than after other procedures.1,2 Intubation itself can evoke
nausea and vomiting. Longer procedures with general anesthesia are associated with more nausea and vomiting
than are shorter procedures.1,2 The

type of anesthetic used is also a factor.

General anesthetics vary in their
propensity to cause postoperative
nausea and vomiting. Etomidate, ketamine, nitrous oxide, and inhaled
agents increase the risk of nausea and
vomiting.1,2 Gastric distention caused
by suction or vigorous positive pressure ventilation via face mask may
also increase the risk of postoperative
nausea and vomiting.1,2 Some medications used in association with anesthesia decrease the risk of postoperative
nausea and vomiting. These include
atropine, which has a vagolytic effect,
and propofol (Diprivan).1 Although
the exact mechanism of the antiemetic effect of propofol is not clear, the
drug may have a weak serotonin
antagonistic effect.9

Postoperative Factors. During the

postoperative period, the 2 most common causes of nausea and vomiting
are unrelieved pain (especially visceral
or pelvic) and the opioids prescribed
to control the pain. Adequate pain
relief reduces the occurrence of nausea
by 80%.2 Opioids stimulate nausea
and vomiting by a direct action on the
CTZ.2 Unrelieved pain directly stimulates the vomiting center (Figure 1).
Nausea can also be precipitated by
sudden motion, changes in body position, premature oral intake, and
hypotension.1,2
Prevention
If postoperative nausea and vomiting can be predicted, then they
should be preventable. However,

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CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 41

prevention is sometimes difficult

because of the wide range of stimuli
that contribute to the emetic
response. Also, many of the pathways involved in the control of postoperative nausea and vomiting are
complex and are not fully understood. The decision to provide
antiemetic therapy should be based
on a patients risk factors and potential for serious sequelae from vomiting. All patients at high risk should
receive prophylactic antiemetics,
preferably a combined regimen.9
Evidence is conflicting on whether
all surgical patients should receive
routine prophylactic antiemetics.1,2
Selection of an antiemetic should
be based on safety and efficacy, the
patients risk factors, the patients
satisfaction, and cost. No single
antiemetic is superior in every situation. For the prevention of postoperative nausea and vomiting, the ASHP
guidelines recommend administration of droperidol (Inapsine) or an
SRA.1 Droperidol, a dopamine receptor antagonist, is cost-effective and
produces marked tranquilization and
sedation. It allays apprehension and
provides a state of mental detachment and indifference while maintaining a state of reflex alertness.
However, since the ASHP guidelines
were published, studies have indicat-

ed that droperidol can cause a prolonged QT interval, which can lead to

potentially fatal cardiac dysrhythmias. The Food and Drug
Administration now requires a blackbox warning, and therefore droperidol is no longer considered a first-line
agent in postoperative nausea and
vomiting.7 Ondansetron (Zofran)
and dolasetron (Anzemet) are commonly used SRAs. Although
granisetron (Kytril) prevents postoperative nausea and vomiting, it is not
currently approved for this purpose.
The cost of using SRAs is thought to
be justified by patients satisfaction
in avoiding postoperative nausea and
vomiting. Dolasetron or
ondansetron can be given preoperatively or intraoperatively as a single
dose. Combination drugs (eg,
dolasetron plus dexamethasone)
increase efficacy, especially in highrisk patients. Administration of
intravenous dexamethasone before
induction of anesthesia prevents
postoperative nausea and vomiting.9
The use of supplemental oxygen
has been shown to decrease the
occurrence of postoperative nausea
and vomiting.17 Also, the restriction
of oral intake until the return of
bowel function after surgery has
been used for decades to decrease
the occurrence of postoperative nau-

Table 4 Frequent causes of nausea and vomiting in critical care

Surgery
Unrelieved pain
Pancreatitis
Diabetic ketoacidosis
Increased intracranial pressure
Meningitis
Heart failure
Hepatobiliary causes
Cerebrovascular accident
Hypotension
Bowel obstruction/ileus

Drugs (opioids, antibiotics, drug overdose,

nonsteroidal anti-inflammatory drugs, selective
serotonin reuptake inhibitors, digitalis)
Peritonitis
Hyponatremia
Brain tumors, vestibular involvement
Myocardial infarction, especially inferior
Anxiety
Gastrointestinal bleeding
Renal failure, uremia
Hypercalcemia

42 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003

sea and vomiting. Alternative

antiemetic drugs include metoclopramide, chlorpromazine, prochlorperazine and promethazine.
Treatment
For established postoperative
nausea and vomiting, the choices of
antiemetic are almost identical to
those used to prevent this type of
nausea and vomiting, with a slight
difference in some of the dosages.
The SRAs are considered first-line
agents, and the same alternative
drugs are recommended as those
used to prevent postoperative nausea and vomiting. Dopamine antagonists, because they are inexpensive,
are often used.
Unlike other sedatives used also
for nausea and vomiting, propofol is
currently indicated only for sedation. Because it has antiemetic properties, several studies have been
done to evaluate subhypnotic doses
in the treatment of postoperative
nausea and vomiting. Those studies
had conflicting outcomes. Fujii
et al18 found that a small dose (0.5
mg/kg) was an effective antiemetic
compared with droperidol and
metoclopramide. Gan et al19 concluded that patient-controlled delivery of propofol decreased the
prevalence of postoperative nausea
and vomiting compared with
placebo. Other studies20,21 in which
propofol was used postoperatively
indicated that propofol did not
decrease the prevalence of postoperative nausea and vomiting.
Pain medication should not be
withheld because of its potential to
cause nausea and vomiting.2 In
patients who do not respond to initial therapy with 1 antiemetic agent,
an agent from another pharmacolog-

ical class should be added, the dose

of the antiemetic should be
increased to the maximum accepted
range, or a combination of both
approaches should be used.1 In
patients sensitive to opioids, nonopioid analgesics such as ketorolac
(Toradol) can be used as an alternative to control postoperative pain.2
Ketorolac is a nonsteroidal antiinflammatory drug and may cause
gastrointestinal irritation and toxic
effects on the kidneys.
In summary, the SRAs are recommended as first-line agents in
the prevention and treatment of
postoperative nausea and vomiting.
Administration of antiemetic medications is generally considered
safe, despite an occasional adverse
reaction.

Other Causes of Nausea

Many medications, medical conditions, and procedures can induce
nausea and vomiting. Table 4 lists the
causes most common in critical care.
Drugs that cause gastric irritation
(eg, nonsteroidal anti-inflammatory
drugs, selective serotonin reuptake
inhibitors, and antibiotics) can cause
nausea. Examples of drugs that stimulate the vomiting center indirectly
through the CTZ are digoxin, morphine, alcohol, ipecac, and anticancer drugs. Motion sickness and
inner ear disorders cause nausea by
directly stimulating the vomiting
center. Nausea can also be induced
by olfactory, visual, vestibular, and
psychogenic stimuli2 (Figure 1).
Opioids directly stimulate serotonin and dopamine receptors in the
CTZ, which in turn stimulate the
vomiting center. The analgesic effect
of opioids is mediated by the activation of both 1 and 2 receptors.

Figure 2 A, The P6 point is located on the anterior side of the forearm bilaterally
about 3 to 5 cm above the wrist between the tendon of the flexor carpi radialis
and the palmaris longus. B, The ST36 point is located on the anterior side of the
lower extremity bilaterally about 10 cm below the knee.

Activation of the 2 receptor unfortunately accounts for delayed transit

time through the gastrointestinal
tract, which contributes to nausea
and vomiting. Currently, no opioid
agonists can selectively activate specific receptors, and therefore nausea and vomiting remain adverse
effects of opioid therapy.6 Tolerance
to this opioid-induced nausea and
vomiting usually occurs within days
to weeks.6 Although the SRAs do
relieve opioid-induced nausea, they
are not considered first-line drugs in
long-term therapy because of their

cost. Less expensive drugs such as

phenothiazines, butyrophenones,
anticholinergics, and motility agents
are recommended.21 In the acute
short-term, however, SRAs may be
used as first-line agents for opioidinduced nausea and vomiting.

Pharmacological Management
The goal of pharmacological
interventions is to prevent or minimize nausea and/or vomiting.
Antiemetic agents are more effective
at preventing emesis than at suppressing it.1,3 For prevention,

CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 43

antiemetics can be administered

orally or parenterally.3 For suppression of ongoing emesis, oral therapy
is ineffective; parenteral administration is required. Parenteral therapy
includes intravenous, intramuscular,
and rectal routes of administration.
Nausea is a complex response. No
single pharmacological agent is
available that blocks all the receptors that trigger nausea or elicit
vomiting. Also, adverse effects may
limit the use of certain antiemetics.
Therefore, the choice of drugs
should be individualized to each
patients needs. Combination
antiemetic therapy using agents
with different mechanisms of action
may be necessary.1
Antiemetic therapies have been
compared in multiple clinical trials.
On the basis of the results, clinical
practice guidelines for the prophylaxis and treatment of nausea and
vomiting have been developed.
These guidelines continue to be
refined as more research is completed. Table 1 summarizes current
pharmacological recommendations,
emphasizing those from the ASHP,1
the American Society of Clinical
Oncology,4 and the Mayo Clinic.8
Table 3 provides a cost comparison
of antiemetic agents.
The pharmacological recommendations presented in this article are
intended for adults and not for children. Specifically, the dopamine
antagonists such as prochlorperazine
and metoclopramide should not be
used in children. Data are insufficient
to support the use of metoclopramide
in children except to facilitate smallbowel intubation in endoscopic procedures. Children are more prone
than adults to extrapyrimidal reactions or paradoxical reactions of rest-

lessness and excitement when given

prochlorperazine.1

Nonpharmacological
Management
Dietary Management
The traditional dietary approach
to postoperative management is to
provide nothing by mouth and to
use a nasogastric tube for gastric
decompression to prevent nausea.
Once bowel sounds resume, the tube
is removed, a clear liquid diet is
introduced, and the diet is gradually
advanced as tolerated. Although this
approach is commonly practiced,
use of this regimen is not supported
by published reports. Jeffrey et al22
challenged this traditional
approach; they found no difference
in postoperative nausea and vomiting in patients receiving a clear liquid diet compared with patients
receiving a regular diet as the first
postoperative meal. Other dietary
modes of decreasing nausea are eating bland foods such as dry toast or
crackers and drinking carbonated
beverages such as ginger ale.2
Alternative/Complementary
and Behavioral Therapy
Although medications are the
first-line treatment for nausea and
vomiting, the use of alternative or
complementary measures as
adjuncts may improve patients outcomes and help reduce costs.
Acupressure/Acupuncture.
Acupressure originated in China. It is
based on the principle of qi or chi, the
energy present in living organisms.
When the flow of qi is stagnant, the
physical condition is affected. The
application of pressure to specific
points on the body unblocks abnormal energy flow and relieves signs

44 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003

and symptoms. The 2 points that are

effective in lessening nausea and vomiting are P6 and ST36 (Figure 2). Firm
and steady pressure applied to these
points with the fingers lessens the
intensity of chemotherapy-induced
nausea.23 Grealish et al24 reported that
a 10-minute foot massage was effective in decreasing the intensity of pain
and nausea and improving relaxation
among cancer patients.
Acupuncture also decreases nausea and vomiting; it is based on the
same principles as acupressure.25
Because acupuncture requires
trained and certified personnel, it
may not be a cost-effective method
of treatment. However, Medicare,
Medicaid, and some third-party payers now cover acupuncture fees. A
list of certified acupuncturists can be
found by visiting the Web site of the
American Academy of Medical
Acupuncture at www.medicalacupuncture.org or that of the
National Acupuncture and Oriental
Medicine Alliance at www.acupuncturealliance.org.
Transcutaneous Electrical Nerve
Stimulation. Recently, a wristbandtype device for transcutaneous electrical nerve stimulation, the ReliefBand,
was approved by the Food and Drug
Administration as an over-the-counter device. It is also based on the principles of acupressure and is applied at
the P6 acupressure point. Use of the
ReliefBand has provided significant
relief from nausea and vomiting
among cancer patients.26,27
Relaxation. In relaxation training,
patients are instructed to relax muscles in order to decrease the tension
of the muscles. Patients should be
encouraged to take slow deep
breaths; the attention to breathing
serves as a distraction. In postopera-

tive nausea and vomiting, this technique also helps the body rid itself of
any residual anesthetic agent.2
Imagery training involves using mental processes that increase relaxation,
such as recalling pleasant memories
and imaging positive thoughts.
Relaxation and imagery can be used
together or separately. Therapeutic
touch can also be used as a comfort
measure.2 These techniques are effective for treating nausea and vomiting,
pain, and insomnia.28
Music. Ezzone et al29 concluded
that music has a beneficial effect on
nausea and vomiting. Music
decreases the intensity of nausea
and vomiting among cancer
patients, when it is used with pharmacological antiemetic treatment.

Herbs. The use of herbs to treat

nausea and vomiting is controversial. In one study,2 ginger root was
more effective than placebo for
treatment of postoperative nausea
and vomiting. However, Ernest and
Pittler30 reviewed 6 studies on the
effect of ginger to treat nausea and
vomiting and concluded that ginger
may or may not be effective for postoperative nausea; ginger did appear
to reduce the occurrence of nausea
related to seasickness, morning sickness, and chemotherapy. Dried ginger in capsules has been used to
treat car sickness in animals.
Aromatherapy. The use of aromatherapy is also controversial
because its scientific effectiveness
and safety have not been estab-

lished. Tate31 studied the use of peppermint oil for postoperative nausea. Peppermint oil with a relatively
high content of menthol was smelled
by an experimental group of
patients who underwent gynecologic
surgery. Although the results were
not statistically significant, the
experimental group had a lower
prevalence and/or intensity of nausea after surgery, less requirement
for antiemetics, and more tolerance
to analgesia, which usually causes
nausea, than the control group did.
Abdominal Implant. The Food
and Drug Administration recently
granted humanitarian device exemption approval for an implantable system (Enterra, Medtronic Inc,
Minneapolis, Minn) for the treat-

CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 45

ment of chronic, intractable nausea

and vomiting due to gastroparesis of
diabetic or idiopathic origin. The
device consists of 2 leads with electrodes that are implanted in the
antrum of the stomach and connected to a pulse generator that is surgically placed in the lower part of the
abdomen. The system is programmed to deliver low-frequency,
low-amplitude electrical pulses continuously to the stomach muscle.
Although the exact mechanism for
the suppression of nausea is not
known, it is thought that the effect is
due to the neurostimulation of central vagal afferent nerve pathways,
not by enhanced gastric emptying as
previously thought (W. L.
Starkebaum, Medtronic, Inc, oral

communication, November 7, 2001).

The device is externally programmed in a fashion similar to that
used with cardiac pacemakers.32

Implications for
Critical Care Nursing
Critical care nurses are responsible for assessing the causes of nausea
and vomiting, administering appropriate antiemetic agents, evaluating
the effects of the agents, and providing information to physicians when
changes in treatment are indicated.
Antiemetic agents are most useful
when given prophylactically; it is
much easier to prevent signs and
symptoms than to control them.
Identification of patients at high risk
for nausea and vomiting allows earli-

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46 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003

er intervention in the prophylaxis

for and therefore the control of these
effects. Even though anesthesiologists routinely screen patients preoperatively to determine which are
high-risk patients, this information
must be communicated to the critical care nurses caring for the
patients in order to optimize
patients care. It may be helpful to
know, for example, that patients
with a history of motion sickness
may be more susceptible to movement-induced postoperative nausea
and vomiting.2 Care can then be
taken to ensure slow and smooth
movements in transferring and turning a patient who has such a history.
Consideration should be given to
administering antiemetics on a

scheduled basis, rather than as needed, for patients at high risk for postoperative nausea and vomiting.2
Causes and Assessment
Patients should be assessed for
pain, including postoperative pain,
and should be treated promptly to
prevent associated nausea and vomiting. Suspected opioid-induced nausea may be evaluated by
determining the temporal relationship between the time the opioid
was given and the onset of nausea.6

increased in a patient with acute

coronary syndrome exacerbated by
nausea and vomiting.
The pulmonary system should
be assessed for indications of pulmonary aspiration, especially in
patients receiving tube feedings.
Nosocomial pneumonia can be
caused by aspiration of oropharyngeal secretions or gastric contents
into the lungs. Preventive measures
such as elevating the head of the
bed, ensuring that bowel sounds are
present, and routinely checking

Although medications are the first-line

treatment for nausea and vomiting, the use
of alternative or complementary measures
. . . may improve patients outcomes. . .
A careful systems assessment should
be done, with all possible causes
investigated before nausea and vomiting are automatically labeled as
opioid induced.6
The cardiovascular system should
be assessed for hypotension due to
hemodynamic compromise. Nausea
may be the first symptom of
hypotension. Hemodynamic sources
(increased or decreased heart rate,
decreased preload, increased afterload, or decreased contractility)
should be investigated.
Postoperatively, hypotension may be
due to the restriction of fluids preoperatively, intraoperative blood loss,
and the use of anesthetics, analgesics,
and sedatives.2 Vagal maneuvers
caused by retching and vomiting, as
occur in inferior myocardial infarction, can cause bradycardia.
Myocardial oxygen demand may be

residual feeding volumes may help

prevent pulmonary aspiration.
The gastrointestinal system
should be assessed for abdominal
distention, organomegaly, and presence of bowel sounds. Signs of hypomotility may suggest an increased
risk for nausea and vomiting.
Postprandial nausea and vomiting
associated with bloating and satiety
suggest a gastrointestinal cause.6
Nausea and vomiting can be indications of as well as complications of
acute pancreatitis.
Nausea that occurs primarily
with movement can be assumed to
be generated by impulses from the
vestibular center.6 Because strong
odors can cause or exacerbate nausea
and vomiting, especially postoperatively, exposure to odors from nearby
food, strong perfume, and cleaning
solutions should be minimized.2

Vomiting can also cause dehydration, leading to fluid and electrolyte

imbalance. Fluid and electrolyte levels
must be assessed and the fluids and
electrolytes replaced accordingly.
Nausea, headache, and oliguria are
common indications of hyponatremia, which can cause cerebral edema
and death if untreated. Hypercalcemia
can cause nausea and vomiting.
Hypokalemia and life-threatening dysrhythmias can result from loss of electrolytes due to vomiting.
Neurological causes should also
be considered. Increased intracranial pressure can cause refractory
nausea, and some brain tumors
cause vomiting without nausea.
Nausea and vomiting cause an
increase in intracranial pressure and
can be life threatening in a patient
with brain injury. Vomiting must be
avoided in patients with suspected
aneurysms in order to prevent subarachnoid hemorrhage. In patients
with spinal cord trauma, the movements associated with vomiting can
cause further injury to the spinal
cord. Nausea and vomiting occur
frequently after craniotomy.
Antiemetic therapy may cause sedation, making postoperative neurological assessment difficult.
Disruption of the surgical site
during vomiting can cause excess
bleeding, a possible need for return to
surgery, increased morbidity,
increased scarring, and prolonged
recovery time. Such disruption can be
especially dangerous after eye, neck,
or facial surgery. The explosive pressure generated during vomiting can
dislodge indwelling tubes or wires,
particularly those that are strategically placed, such as drains used to
diminish intracranial pressure, cardiac pacing wires, and chest tubes.

CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 47

Medications should be evaluated

for their emetogenic potential.
Common offenders are chemotherapeutic agents, opioids, nonsteroidal
anti-inflammatory drugs, antibiotics, and selective serotonin reuptake inhibitors. Assessment of
nausea and vomiting should include
determination of the severity, duration, and number of episodes. A
visual analog scale can be used to
measure the severity of nausea, with
a scale of 1 to 10, similar to that
used as a pain scale.1,10

Case Study

Prevention and Treatment

The prevention and treatment of
nausea and vomiting will become
even more of a healthcare concern
as hospitals are required to make
the most efficient use of available
resources, decrease the frequency of
complications, and decrease
patients lengths of stay.1
Traditional, convenient, cost-effective approaches to the prevention
and treatment of nausea and vomiting in the intensive care unit include
the use of nasogastric tubes for gastric decompression and the use of
phenothiazines or metoclopramide
as antiemetics. This regimen may
still be effective for most patients.
However, the lack of efficacy and the
adverse effects (sedation, hypotension) of these drugs may limit their
use. The most recently published
Mayo Clinic guidelines no longer
recommend metoclopramide
because of the increased occurrence
of restlessness, agitation, insomnia,
and drowsiness associated with use
of this drug.4 Also, patients may not
respond to the initially prescribed
therapy. If no response occurs, then
an agent from another pharmacological class should be added, the

48 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003

S.W. is a 68-year-old man who

was brought to the emergency
department with a severe
headache, nausea, and right-sided
weakness. A computed tomogram
of the head revealed a ruptured
cerebral aneurysm that was then
surgically repaired. He returned to
the neurological intensive care unit
with an external ventricular drain
in place and an intracranial pressure measurement of 5 mm Hg. His
vital signs, electrocardiographic
rhythm, and oxygen saturation
were stable. He has a history of
colon cancer and had a right hemicolectomy 4 months ago. This surgery was followed by chemotherapy
with 5-fluorouracil and leucovorin.
His last chemotherapy was 1 week
ago. He has had moderate to severe
nausea and vomiting and has been
taking ondansetron (Zofran) 8 mg
by mouth twice a day at home. He
also has been taking prochlorperazine (Compazine) 10 mg by mouth
before each meal. Laboratory data
indicate normal liver and kidney
function. S.W. has nausea after his
aneurysm surgery. Promethazine
(Phenergan) 12.5 mg intravenously
is ordered to be administered every
4 to 6 hours as needed.
Questions
1. After S.W. receives 2 doses of
promethazine, he is sleepy but still
has persistent unrelieved nausea.
Which of the following are appropriate actions for the critical care
nurse to take?

a. Give another dose of promethazine.

b. Report to the physician that
promethazine does not relieve the
patients nausea and vomiting.
c. Check the external ventricular
drain to ensure proper functioning.
d. Review the patients medication administration record to see if
any medication may be contributing to his nausea and vomiting.
e. Assess the patients serum
level of sodium.
2. S.W. is receiving morphine
intravenously as needed for pain.
His oncologist was consulted for his
uncontrolled nausea and vomiting.
The oncologist ordered
ondansetron on a scheduled basis,
and prochlorperazine and
lorazepam (Ativan) on an as-needed basis. What is the rationale for
this order?
a. Ondansetron is indicated in
postoperative nausea and vomiting
when other antiemetics are ineffective; it is imperative to keep the
intracranial pressure controlled
after craniotomy.
b. Ondansetron can prevent
opioid-induced nausea.
c. Ondansetron is less sedating
than promethazine; it will not mask
the neurological assessment.
d. Ondansetron is a serotonin
receptor antagonist, which prevents stimulation of the vomiting
center. Prochlorperazine blocks
dopamine receptors in the
chemoreceptor trigger zone and
also inhibits stimulation (such as

caused by odors and pain) to the

vomiting center. Lorazepam is indicated in anticipatory nausea.
3. On the third postoperative
day, S.W.s nausea and vomiting
have been well controlled, and he
can tolerate oral intake. However,
he complains that he has nausea
whenever a nurse brings a bag of
intravenous solution into his room
because it reminds him of his
chemotherapy. Which antiemetic
is the best choice for this type of
nausea?
a. prochlorperazine 10 mg by
mouth
b. ondansetron 8 mg by mouth
c. lorazepam 1 mg by mouth
d. promethazine 12.5 mg intravenously
Answers
1. b, c, d, and e
When an antiemetic is ineffective, other types of drugs should be
considered. Other possible causes
of nausea should be assessed. These
include medical history of
chemotherapy, postoperative condition, possible increased intracranial pressure, and use of opioids for
pain management. Also, nausea
can be a symptom of hyponatremia, which can increase cerebral
edema.
2. a, b, c, and d
After a craniotomy, it is important to prevent nausea and vomiting that could increase intracranial

pressure. Administration of
antiemetics should therefore be
scheduled, not strictly ordered on
an as needed basis. Ondansetron is
effective in opioid-induced nausea
and will not cause sedation, which
could mask the neurological assessment. Administration of prochlorperazine as needed will help in
breakthrough nausea evoked by
stimulation of the vomiting center
directly. Lorazepam is effective for
anticipatory nausea and vomiting.
3. c
Lorazepam reduces anticipatory
nausea. Oral antiemetics are just as
effective and more cost-effective
than are parenteral antiemetics.
Ondansetron is expensive and
should not be used indiscriminately.

dose of the antiemetic should be

increased to the maximum within
an acceptable range, or both.1,9 This
adjustment may require expansion
of the use of serotonin receptor
antagonists in critical care.
Published views are conflicting
about how much patients satisfaction should influence the choice of
agent and override the cost concerns. If a drug is more expensive
but it prevents complications and
decreases length of stay, it would
seem to be worth the extra cost in
the final analysis. More studies on
the economics are needed to help
weigh the cost-benefit issue.
Understanding the pathophysiology of nausea and vomiting will
allow critical care nurses to assist in
making appropriate decisions to
prevent and treat these responses.
Nonpharmacological methods
should be considered as complementary therapy. Complete control,
defined as no nausea or vomiting,
should be the goal for every patient.
Acknowledgments
Parts of this article were previously published as a
synopsis in the Oncology Nursing Society Critical
Care Special Interest Group Newsletter, Vol 10, Issue
2, August 2001.
We thank Dr Cynthia Chernecky, our faculty and
mentor, for her inspiration, guidance, and support in writing this article. We appreciate the
comments of our manuscript reviewers, as well as
suggestions from Dr Mark Stewart, anesthesiologist, Dr Sandra Counts and Michael Madden,
clinical pharmacists, and Dr Cynthia Chernecky,
professor and oncology clinician. We also thank
Shogo Tsuruta for his expert computer skills in
compiling our pharmacology table.

References
1. ASHP therapeutic guidelines on the pharmacological management of nausea and
vomiting in adult and pediatric patients
receiving chemotherapy or radiation therapy or undergoing surgery. Am J Health Syst
Pharm. 1999;56:729-764. Also available at:
www.ashp.org/bestpractices. Accessed
December 3, 2002.
2. Thompson HJ. The management of postoperative nausea and vomiting. J Adv Nurs.
1999;29:1130-1136.
3. Lehne RA, Moore LA, Crosby LJ, Hamilton
DB. Pharmacology for Nursing Care. 3rd ed.
Philadelphia, Pa: WB Saunders; 1998:794-798.

CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 49

4. Loprinzi CL, Alberts SR, Christensen BJ, et

al. History of the development of antiemetic
guidelines at Mayo Clinic Rochester. Mayo
Clin Proc. 2000;75:303-309.
5. Bleiberg H. A new class of antiemetics: the
NK-1 receptor antagonists. Curr Opin Oncol.
2000;12:284-288.
6. OMahony S, Coyle N, Payne R. Current
management of opioid-related side effects.
Oncology. 2001;15:61-77.
7. Ernst AA, Weiss SJ, Park S, Takakuwa KM,
Diercks DB. Prochlorperazine versus
promethazine for uncomplicated nausea
and vomiting in the emergency department:
a randomized double blind clinical trial.
Ann Emerg Med. 2000;36:89-94.
8. US Food and Drug Administration.
Medwatch: Summary of safety-related drug
labeling changes approved by FDA Center
for Drug Evaluation and Research: inapsine.
November 2001. Available at: www.fda.gov/
medwatch/SAFETY/2001/nov01.htm.
Accessed December 3, 2002.
9. Wang JJ, Ho ST, Tzeng JI, Tang CS. The
effect of timing of dexamethasone administration on its efficacy as a prophylactic
antiemetic for postoperative nausea and
vomiting. Anesth Analg. 2000;91:136-139.
10. Bremerkamp M. Mechanism of action of 5HT3 receptor antagonists: clinical overview
and nursing implications. Clin J Oncol Nurs.
2000;4:201-207.
11. Wickam RS. Ondansetron Versus Granisetron:
Control of Nausea & Emesis, Satisfaction, and
Quality of Life [dissertation]. Chicago, Ill:
University of Illinois at Chicago; 1999.
12. Gralla RJ, Osoba D, Kris MG, et al.
Recommendations for the use of antiemetics:
evidence-based clinical practice guidelines. J
Clin Oncol. 1999;17:2971-2994. Also available
at: asco.org. Accessed December 3, 2002.
13. Yarbro CH, Frogge MH, Goodman M,
Groenwald SL. Cancer Nursing: Principles
and Practice. 5th ed. Boston, Mass: Jones &
Bartlett; 2000.
14. Drug Topics Redbook. Montvale, NJ: Medical
Economics, Thomson Healthcare; 2001.
15. American Cancer Society, National
Comprehensive Cancer Network. Nausea
and Vomiting: Treatment Guidelines for
Patients with Cancer. Atlanta, Ga: American
Cancer Society; 2001.
16. Sinclair DR, Chung F, Mezei G. Can postoperative nausea and vomiting be predicted?
Anesthesiology. 1999;91:109-118.
17. Greif R, Laciny S, Rapf B, Hickle RS, Sessler
DI. Supplemental oxygen reduces the incidence of postoperative nausea and vomiting. Anesthesiology. 1999;91:1246-1252.
18. Fujii Y, Tanaka H, Toyooka H. Preoperative
oral granisetron prevents PONV. Acta
Anaesth Scand. 1998;42:653-657.
19. Gan TJ, El-Molem H, Ray J, Glass PS.
Patient controlled antiemesis: a randomized, double-blind comparison of two doses
of propofol versus placebo. Anesthesiology.
1999;90:1564-1570.
20. Bree SE, West MJ, Taylor, PA, Kestin IG.
Combining propofol with morphine in
patient-controlled analgesia to prevent
postoperative nausea and vomiting. Br J
Anaesth. 1998;80:152-154.
21. Montgomery JE, Sutherland CJ, Kestin IG,
Sneyd JR. Infusions of subhypnotic doses of
propofol for the prevention of postoperative
nausea and vomiting. Anaesthesia.
1996;51:1073-1074.

22. Jeffrey KM, Harkins B, Cresci GA,

Martindale RG. The clear liquid diet is no
longer necessary in the routine postoperative management of surgical patients. Am
Surg. 1996;62:167-171.
23. Dibble SL, Chapman J, Mack KA, Shin, AS.
Acupressure for nausea: results of a pilot
study. Oncol Nurs Forum. 2000;27:41-47.
24. Grealish L, Lomasney A, Whiteman B. Foot
massage: a nursing intervention to modify
the distressing symptoms of pain and nausea in patients hospitalized with cancer.
Cancer Nurs. 2000;23:237-243.
25. Somri M, Vaida SJ, Sabo E, Yassain G,
Gankin I, Gaitini LA. Acupuncture versus
ondansetron in the prevention of postoperative vomiting: a study of children undergoing dental surgery. Anaesthesia. 2001;56:
927-932.
26. Pearl ML, Fischer M, McCauley DL, Valea
FA, Chalas E. Transcutaneous electrical
nerve stimulation as an adjunct for controlling chemotherapy-induced nausea and
vomiting in gynecologic oncology patients.
Cancer Nurs. 1999;22:307-311.
27. Woodside Biomedical. Woodside Biomedical
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28. Fleet SV. Relaxation and imagery for symptom management: improving patient
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Oncol Nurs Forum. 2000;27:501-510.
29. Ezzone S, Baker C, Rosselet R, Terepka E.
Music as an adjunct to antiemetic therapy.
Oncol Nurs Forum. 1998;25:1151-1156.
30. Ernest E, Pittler MH. Efficacy of ginger for
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randomized clinical trials. Br J Anaesth.
2000;84:367-371.
31. Tate S. Peppermint oil: a treatment for postoperative nausea. J Adv Nurs. 997;26:543-549.
32. Henney JE. Implant for chronic nausea [letter]. JAMA. 2000;283:2779.

Bibliography

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Anastasia PJ. Effectiveness of oral 5-HT3 receptor antagonists for emetogenic chemotherapy. Oncol Nurs Forum. 2000;27:483-493.
Epstein O, Perkin GD, deBonon DP, Cookson J.
Clinical Exam. 2nd ed. St Louis, Mo: Mosby
Times Mirror; 1997:185.
Fabling JM, Gan TJ, El-Moalen HE, Warner DS,
Borel CO. A randomized, double blinded
comparison of ondansetron, droperidol,
and placebo for prevention of postoperative
nausea and vomiting after supratentorial
craniotomy. Anesth Analg. 2000;91:358-361.
Faries J. Controlling pain: controlling postoperative nausea. Nursing. August 1998;28:78.
Gralla RJ, Navari RM, Hesketh PJ, et al. Singledose oral granisetron has equivalent
antiemetic efficacy to intravenous
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1998;16:1568-1573.
Granisetron (Kytril tablets) [package insert].
Philadelphia, Pa: SmithKline Beecham;
1998.
Hill RP, Lubarsky DA, Phillips-Bute B, et al.
Cost-effectiveness of prophylactic antiemetic therapy with ondansetron, droperidol or
placebo. Anesthesiology. 2000;92:958-967.
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for prophylaxis of nausea and vomiting in

patients undergoing ambulatory laparoscopic cholecystectomy. Am J Surg.

2000;179:60-62.
Mickle J. The use of haloperidol to treat nausea.
Oncol Nurs Forum. 1998;25:1309.
Potter KL, Schafer SL. Nausea and vomiting.
Am J Nurs. April 1999;99(suppl):2-4, 34-36.
Souney PE. Treatment of severe nausea and
vomiting: an evidence-based approach. Am
J Gastroenterol. 2000;95:2121-2122.
Watson S, Benson J, Joy J. Marijuana and medicine: assessing the science base: a summary
of the 1999 Institute of Medicine Report.
Arch Gen Psychiatry. 2000;57:547-552.
Zarate E, Watcha MF, White PF, Klein KW,
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dolasetron for antiemetic prophylaxis.
Anesth Analg. 2000;90:1352-1358.

CE

Continuing Education

CE Test Instructions
To receive CE credit for this test (ID C031), mark your answers on the form below, complete the enrollment information, and submit it with the $11 processing fee (payable in US funds) to the American
Association of Critical-Care Nurses (AACN). Answer forms must be postmarked by February 1, 2005.
Within 3 to 4 weeks of AACN receiving your test form, you will receive an AACN CE certificate.
This continuing education program is provided by AACN, which is accredited as a provider of continuing education in nursing by the
American Nurses Credentialing Centers Commission on Accreditation. AACN has been approved as a provider of continuing education by the State Boards of Nursing of Alabama (#ABNP0062), California (01036), Florida (#FBN2464), Iowa (#332), Louisiana (#ABN12),
and Nevada. AACN programming meets the standards for most other states requiring mandatory continuing education credit for relicensure.

Test ID: C031

Test writer: Ruth Kleinpell-Nowell, RN, PhD, CS, CCNS
Form expires: February 1, 2005
Contact hours: 1.5
Passing score: 9 correct (75%)
Category: A
Test fee: $11

CE Test Form
Managing Nausea and Vomiting:
Current Strategies
Objectives:

1. Discuss the mechanisms of nausea and vomiting

2. Identify preoperative and postoperative factors that influence the development of nausea and vomiting
3. Describe treatment options for nausea and vomiting
Mark your answers clearly in the appropriate box. There is only 1 correct answer. You may photocopy this form.

1. a 2. a 3. a 4. a
b
b
b
b
c
c
c
c
d
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d
d

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Objective 2 was met
Objective 3 was met
The content was appropriate
My expectations were met
This method of CE is effective
for this content

5. a 6. a
b
b
c
c
d
d

7. a
b
c
d

8. a 9. a 10. a 11. a 12. a

b
b
b
b
b
c
c
c
c
c
d
d
d
d
d
Name

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easy medium difficult
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hours / minutes.

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Mail this entire page to AACN, 101 Columbia, Aliso Viejo, CA 92656, (800) 899-2226

CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 51

CE Test Questions
Managing Nausea and Vomiting: Current Strategies

1.

Where is the vomiting center located?

a. Hypothalamus
b. Caudate nucleus
c. Medulla oblongata
d. Cerebellum

2.

Which of the following is not a neurotransmitter

that can relay impulses to the vomiting center?
a. Serotonin
b. Dopamine
c. Histamine
d. Neurotensin

3.

4.

5.

6.

Which antagonist blocks acetylcholine receptors?

a. Dopamine
b. Muscarinic
c. Histamine
d. Serotonin
What emetic potential rating of chemotherapeutic
agents indicates the least potential?
a. 0
b. 1
c. 5
d. 10
What is an example of a chemotherapeutic agent
with the highest emetic potential?
a. Cisplatin
b. Vincristine
c. Carboplatin
d. Doxorubicin
Which of the following chemotherapeutic agents
is not associated with delayed nausea?
a. Cisplatin
b. Vincristine
c. Carboplatin
d. Cyclophosphamide

52 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003

7.

Serotonin receptor antagonists are the drugs of

choice in patients receiving chemotherapeutic
agents with what emetic potential?
a. 0 to 1
b. 1 to 2
c. 2 to 4
d. 3 to 5

8.

Which antiemetic agent is indicated in refractory

chemotherapy-induced nausea and vomiting
unresponsive to other classes of agents?
a. Ondansetron
b. Granisetron
c. Dolasetron
d. Dronabinol

9.

Postoperative nausea and vomiting occurs in

what percentage of patients after surgery?
a. 10% to 20%
b. 20% t0 30%
c. 30% to 40%
d. 40% to 50%

10. Which of the following medications is associated

with increased risk of nausea and vomiting?
a. Atropine
b. Propofol
c. Ketamine
d. Droperidol
11. Which of the following is associated with
decreased occurrence of postoperative nausea
and vomiting?
a. Opioid use
b. Supplemental oxygen
c. Positive pressure ventilation
d. General anesthesia
12. How much does adequate pain relief reduce the
occurrence of nausea?
a. 20%
b. 40%
c. 60%
d. 80%