CoverArticle
CE 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
T he topic of nausea and
vomiting is all too familiar to most
nurses. Nausea and vomiting are
unpleasant complications or indica-
tions of many medical conditions and
are adverse effects of hundreds of
medications. Nausea and vomiting
occur so frequently that they are
almost considered “acceptable,” usu-
ally referred to as “minor” and con-
sidered 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 pro-
longed 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) 809-
2273 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 dis-
turbances 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 nau-
sea.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 chemother-
apy 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) recom-
mended for treating and preventing
nausea and vomiting. Because it is
now understood that most episodes
of nausea and vomiting are preventa-
ble, implications for critical care nurs-
ing 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-
32 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003
nomenon should be assessed sepa-
rately. Nausea is defined as a subjec-
tively unpleasant wavelike sensation
in the back of the throat or epigastri-
um associated with pallor or flush-
ing, 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 con-
tractions of the diaphragm and the
muscles of the thorax and abdomi-
nal 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 (dis-
turbing sights, smells, pain), or sig-
nals from the vestibular apparatus of
the inner ear (motion sickness). The
vomiting center can also be activat-
ed 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 acti-
vated by signals from the stomach
and small intestine traveling along
vagal afferent nerves or by the direct
action of emetogenic compounds
that are carried in the blood (anti-
cancer drugs, opioids, ipecac).
Specific neurotransmitters and
neuromodulators in the CTZ identi-
fy substances as potentially harmful
and relay impulses to the vomiting
center to initiate the vomiting cas-
cade so that the harmful substance
can be expelled. These neurotrans-
mitters are serotonin, dopamine,
acetylcholine (muscarinic choliner-
gic), and histamine. A fifth chemore-
ceptor, the neurokinin-1
neuropeptide, also called substance
P, is currently under study.4,5
Stimulation of these chemore-
ceptors triggers activation of the
vomiting center. Therefore, any
interference with the transmission
of these chemoreceptors prevents
the vomiting center from being acti-
vated. Many antiemetics act by
blocking 1 or more of these recep-
tors.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 adminis-
tered 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)
Stomach and small intestine
recommends prophylactic antiemetic
Sensory input
Sight therapy when drugs with antiemetic
5HT Smell potential of levels 2 to 5 are used1
DA Pain
Blood-borne emetics (Table 2).
Chemotherapy Vestibular apparatus
Opioids
Ipecac Risk Factors
In addition to the emetic potential
of the chemotherapeutic agents, sever-
Higher centers
al other risk factors can be used to pre-
Anticipation dict the likelihood of CINV. Patients
Fear younger than 50 years have more
Va

Memory
nausea and vomiting than do older
ga
la

ff
er patients.1 Women are more suscepti-
en
ts ble than men, presumably because of
5HT the influence of hormones.2 A history
DA
M of motion sickness, pregnancy-related
nausea and vomiting, or nausea and
vomiting with previous chemotherapy
H1
CTZ
are all positive predictors of CINV.1
M
Patients who use alcohol heavily or
Vomiting center
who have done so in the past have a
reduced risk of emesis.1,11

Vomiting
via output to stomach,
diaphragm, and abdomi-
nal muscles
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 stimu-
late enterochromaffin cells in the gas-
trointestinal 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
Receptors:
5HT = Serotonin
DA = Dopamine
M = Muscarinic cholinergic
H1 = Histamine1
emetic potential of a chemotherapeu-
tic 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 great-
est. An example of an agent with the
lowest emetic potential (1) is vin-
cristine. An example of an agent with
the highest emetic potential (5) is cis-
platin. 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 admin-
ister the chemotherapy.12 Anticiatory
nausea usually occurs 12 hours
before administration of chemother-
apy 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 sero-
tonin 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 Examples Indications

Indirect stimulation of vomiting center through receptor sites (chemoreceptor trigger zone)
Serotonin Serotonin (5HT3) Ondansetron First-line therapy for acute CINV and RINV: use on day of
receptors receptor (Zofran) chemotherapy or radiation therapy only, not more than 24 hours
antagonists later

First-line therapy for prevention of PONV and treatment of

breakthrough nausea and vomiting

Opioid-induced nausea and vomiting6

Granisetron First-line therapy for prevention of acute CINV and RINV
(Kytril)

Only effective in acute phase, not useful beyond 24 hours

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

Prevention and treatment of PONV

Dopamine Dopamine antag- Promethazine PONV

receptors onists (Phenergan)
Breakthrough nausea and vomiting in CINV
6
Opioid-induced nausea and vomiting

Chlorpromazine Acceptable alternative to droperidol in the prevention and treatment

Phenothiazines

(Thorazine) of PONV
Prochlorperazine Breakthrough nausea and vomiting
(Compazine)
Established nausea and vomiting in RINV
6
Opioid-induced nausea and vomiting

Droperidol Prevention and treatment of established PONV and breakthrough

(Inapsine) nausea and vomiting in CINV only in patients who do not
respond to other drug8
Butyrophenones

Can be given in combination with serotonin receptor antagonists

and steroids in patients at high risk for PONV

34 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003

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
PONV prevention: 4 mg IV over 2-5 min immediately
before or 8 mg by mouth 1 hour before induction of
anesthesia
PONV treatment: 1-4 mg IV
CINV prevention: 2 mg by mouth or 10 µg/kg IV 30 min
before chemotherapy
In recent trials,4 1 mg as effective as 2 mg and 50% less
expensive
PONV prevention: 20-40 µg/kg IV (in clinical trials)
CINV prevention: 100-200 mg by mouth or 1.8 mg/kg
IV 30 min before chemotherapy
PONV prevention: 12.5 mg IV intraoperatively or 100
mg by mouth 1 hour before induction of anesthesia
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
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
PONV treatment: 10-25 mg by mouth every 4-6 hours
as needed; 25- or 100-mg rectal suppository
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
PONV treatment: 5-15 mg by mouth or 5-10 mg intra-
muscularly or IV every 3-4 hours; 2.5-, 5-, 25-mg
rectal suppository
CINV treatment: 5-20 mg by mouth, intramuscularly, or
IV every 6 hours, 25-mg rectal suppository every 12
hours
PONV prevention: 0.625-1.25 mg IV SLOWLY 5 min
before termination of anesthesia
PONV treatment: 0.625-1.25 mg IV slowly as needed
Maximum dose: 2.5 mg
Most common adverse effects
Mild to moderate and transient;
headache most common
IV dolasetron may cause
changes in intervals on
electrocardiograms; use with
caution in prolonged
conduction disorders
Oversedation; lethargy, postural
hypotension; skin sensitivity;
dystonic reactions
Extrapyramidal reactions or
paradoxical reactions occur
more commonly in children
Sedation, hypotension,
tachycardia
Prolonged QT interval leading
to torsade de pointes
CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 35
Comments
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
Oral doses recommended over IV doses because
former are equally effective, less costly, and
more convenient
Disadvantages: Increased cost; all serotonin
receptor antagonists equally effective at
equivalent doses, so cost should be a factor
in making a choice
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
Prochlorperazine more effective than promet-
hazine for treating uncomplicated nausea and
7
vomiting in patients in emergency department
IV promethazine administered at a rate no
greater than 25 mg/min
IV prochlorperazine administered at a rate no
greater than 5 mg/min
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
 Table 1 Continued
Site of action Drug type Examples Indications

Dopamine receptors Dopamine antago- Haloperidol Primary PONV; breakthrough nausea and vomiting in CINV; opioid-

Butyrophenones
(continued) nists (Haldol) induced nausea and vomiting; nausea and vomiting due to
(continued) bowel obstruction

Rescue therapy
4
when serotonin receptor antagonists not
effective
Metoclopramide Breakthrough nausea and vomiting in CINV; established nausea
(Reglan) and vomiting in RINV

Prevents nausea and vomiting by stimulating gastric emptying and

blocking dopamine receptors
Benzamide
Opioid-induced nausea and vomiting6

Histaminic Antihistamines Dimenhydrinate Nausea and vomiting associated with motion sickness or vertigo
receptors (Dramamine)

Meclizine
(Antivert)
Muscarinic cholin- Anticholinergics Scopolamine First-line drug in prophylaxis of nausea and vomiting associated
ergic receptors with motion sickness
Neurokinin-1
receptors Not yet available CINV, sudden onset and delayed

Other sites of action

Mechanism Glucocorticoids Dexamethasone Drug of choice in prevention of delayed nausea and vomiting in
unknown (Decadron) CINV

PONV with dolasetron

Methylprednisolone
(Solu-Medrol)
Cannabinoid Cannabinoids Dronabinol Modestly effective in CINV; may be used in patients responding
receptor sites (Marinol) poorly to other antiemetics
(CB-1 and CB-2)
exert central
sympathomimetic
action

Limbic system Benzodiazipines Lorazepam Used as adjunct, not primary drug, in anticipatory or delayed nau-
inhibition (Ativan) sea and vomiting or breakthrough nausea and vomiting in CINV

*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

 Dosage*
CINV treatment: 1-4 mg by mouth, intramuscularly, or
IV every 6 hours
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
PONV prevention: 10-20 mg IV near the end of surgery
PONV treatment: 10 mg IV over 1-2 min every 4-6
hours postoperatively
Motion sickness and vertigo: 25-50 mg by mouth
25-50 mg by mouth6
Motion sickness: patch 0.5 mg/24 hours every 3 days
CINV prevention: 20 mg by mouth or IV with serotonin
receptor antagonists before chemotherapy
CINV treatment: 10 mg by mouth or IV every 4-6 hours
PONV prevention: 10 mg IV before induction of anes-
thesia9
CINV prevention: 40-125 mg 1-time dose before
chemotherapy
CINV treatment: 5-20 mg by mouth every 3-6 hours
CINV treatment: 1-2 mg by mouth, sublingually, intra-
muscularly, or IV every 6 hours
Most common adverse effects
Nonsedating in lower doses;
sedation, hypotension, tachycar-
dia, extrapyrimidal effects similar
to those of dopamine
antagonists
Sedation, restlessness, agitation,
diarrhea, drowsiness, sleepless-
ness, dystonic reactions with
higher doses
Sedation, dry mouth, constipation,
blurred vision
Dry mouth, drowsiness, impaired
eye accommodation
Gastrointestinal upset, anxiety,
insomnia, hyperglycemia
Drowsiness, dizziness, sedation,
hypotension, vision difficulty,
vasodilatation, euphoria,
dysphoria (especially in older
adults)
Sedation, amnesia, visual
disturbances
CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 37
Comments
Cost-effective alternative to serotonin receptor
antagonists
At high doses, also inhibits serotonin receptors
Use no longer recommended by Mayo Clinic
guidelines because of adverse effects of
restlessness, agitation, and drowsiness
Because of its ability to increase gastric and
intestinal motility, contraindicated in patients
with bowel obstruction, gastrointestinal
hemorrhage, or perforation
Slightly less effective than serotonin receptor
antagonists and droperidol
Used as adjunct to prevent adverse effects in
patients receiving dopamine receptor
antagonists; use limited because dopamine
receptors no longer first-line agents
Patch applied behind ear 4 hours before travel;
patch should last 3 days
Investigational
Used with serotonin receptor antagonists to
enhance their benefit; yields increased
protection
Used alone for prevention of level 2 CINV
Inexpensive
Should be used with caution in patients with
unstable diabetes mellitus
Other antiemetics more effective, but because
the mechanism of action differs, cannabinoids
may be given alone or in combination with
other agents
 Table 2 Emetogenic potential of chemotherapeutic agents and standard treatments
Treatment

Level* Agent Prevention Breakthrough Delayed

5 Cisplatin Granisetron, ondansetron, Lorazepan, methyl- High-dose carboplatin:
(>90) Cyclophosphamide or dolasetron with prednisolone, dexamethasone and meto-
(>1500 mg/m2) dexamethasone; or prochlorperazine, clopramide or serotonin
methylprednisolone metoclopramide, receptor antagonists
4 Carboplatin dexamethasone,
(60-90) Cyclophosphamide haloperidol, or High-dose carboplatin,
(>750 mg/m2, dronabinol cyclophosphamide, or dox-
<1500 mg/m2) orubicin:
Doxorubicin (>60 mg/m2) serotonin receptor
Methotrexate antagonists and
dexamethasone
3 Doxorubicin
(30-60) Ifosfamide
Irinotecan For children For children

2 Cytarabine Dexamethasone or Chlorpromazine, Chlorpromazine, lorazepam, or

(10-30) Docetaxel methylprednisolone; lorazepam, or serotonin receptor
Etoposide prochlorperazine for methylpred- antagonists and
5-Fluorouracil adults nisolone dexamethasone or
Paclitaxel methylprednisolone

1 Bleomycin
(<10) Fludarabine No treatment
Vinblastine
Vincristine
*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 eme-
sis.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 cen-
tral nervous system and the gastroin-
testinal 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 nau-
sea and vomiting are high-dose carbo-
platin, cyclophosphamide, and
doxorubicin.
Breakthrough nausea and vomit-
ing 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 com-
pared in many clinical trials, especial-
ly since the advent of the relatively
new class of drugs, the serotonin
receptor antagonists (SRAs). Because
chemotherapeutic agents initiate
activation mainly of serotonin recep-
tors, 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
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 recep-
tors, they can provide highly effective
relief of nausea and vomiting without
many of the adverse effects associat-
ed with traditional antiemetic agents.
Adverse effects of the SRAs are gener-
ally 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 benefit-
ing from these medications (Table 3).
Because SRAs are similarly effective
for controlling acute nausea and

38 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003

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 intra-
venous form.1,4,10,12 Wickam11 found
that because the SRAs are not struc-
turally identical, they may have dif-
ferences in efficacy, and she
recommends that if an SRA is ineffec-
tive, a second SRA should be given.
With less toxic chemotherapeutic
agents, combinations of other
antiemetics may be effective.
Dexamethasone and prochlorper-
azine 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 pro-
tection from vomiting occurs more
Table 3 Comparative costs of antiemetic agents
Agent
Ondansetron (Zofran)
Granisetron (Kytril)
Dolasetron (Anzemet)
Promethazine (Phenergan)
Chlorpromazine (Thorazine)
Prochlorperazine (Compazine)
Droperidol (Inapsine)
Haloperidol (Haldol)
Metoclopramide (Reglan)
Dimenhydrinate (Dramamine)
Scopolamine (Transderm Scōp)
Methylprednisolone (Solu-Medrol)
Dronabinol (Marinol)
Lorazepam (Ativan)
Data from Drug Topics Redbook.14
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 ther-
apy. Drugs of choice for such rescue
therapy include prochlorperazine, thi-
ethylperazine, or metoclopramide
with or without diphenhydramine, or
lorazepam, haloperidol, or dronabi-
nol.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 deter-
mined.1 The choice of agent should be
based on patient-specific factors.1 All
Mean wholesale price, $US
Intravenous form
25.65 (2 mg/mL, 2-mL vial)
195.20 (1 mg/mL, 1-mL vial)
166.20 (20 mg/mL, 5-mL vial)
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)
CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 39
patients receiving chemotherapy
should have antiemetics available as
needed for rescue from breakthrough
nausea and vomiting.1 If CINV per-
sists after the breakthrough treat-
ment, these drugs should be given on
a scheduled basis rather than on an as-
needed basis.
Treatment of Anticipatory CINV.
Behavioral interventions are recom-
mended 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 asso-
ciated with chemotherapy.1,13
Lorazepam should be given the
night before and the morning of
chemotherapy.13,15
In summary, nausea and vomit-
ing are no longer inevitable compli-
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)
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 treat-
ment 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 prochlorper-
azine, 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
40 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003
receiving anesthesia. Although sig-
nificant 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 indi-
rectly 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 acti-
vates the vomiting center.2
Causes
Preoperative Factors. The occur-
rence of postoperative nausea and
vomiting is influenced by several fac-
tors.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 post-
operative 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, gas-
trointestinal 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’ characteris-
tics have a cumulative effect in influ-
encing the prevalence of postopera-
tive nausea and vomiting.
Intraoperative Factors. The type of
surgical procedure can also influence
the occurrence of postoperative nau-
sea and vomiting. The rate is high in
patients undergoing laparoscopic pro-
cedures related to abdominal disten-
tion because of the carbon dioxide
used for visualization.1,2 The preva-
lence of postoperative nausea and
vomiting is also greater after plastic,
ophthalmic, orthopedic shoulder,
gynecologic, and ear, nose, and throat
surgeries than after other proce-
dures.1,2 Intubation itself can evoke
nausea and vomiting. Longer proce-
dures with general anesthesia are asso-
ciated with more nausea and vomiting
than are shorter procedures.1,2 The
Circle number 122 on Reader Service Card
type of anesthetic used is also a factor.
General anesthetics vary in their
propensity to cause postoperative
nausea and vomiting. Etomidate, ket-
amine, nitrous oxide, and inhaled
agents increase the risk of nausea and
vomiting.1,2 Gastric distention caused
by suction or vigorous positive pres-
sure ventilation via face mask may
also increase the risk of postoperative
nausea and vomiting.1,2 Some medica-
tions used in association with anesthe-
sia 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 antiemet-
ic effect of propofol is not clear, the
drug may have a weak serotonin
antagonistic effect.9
CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 41
Postoperative Factors. During the
postoperative period, the 2 most com-
mon 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 stimu-
lates the vomiting center (Figure 1).
Nausea can also be precipitated by
sudden motion, changes in body posi-
tion, premature oral intake, and
hypotension.1,2
Prevention
If postoperative nausea and vom-
iting can be predicted, then they
should be preventable. However,
prevention is sometimes difficult ed that droperidol can cause a pro- sea and vomiting. Alternative
because of the wide range of stimuli longed QT interval, which can lead to antiemetic drugs include metoclo-
that contribute to the emetic potentially fatal cardiac dysrhyth- pramide, chlorpromazine, prochlor-
response. Also, many of the path- mias. The Food and Drug perazine and promethazine.
ways involved in the control of post- Administration now requires a black-
operative nausea and vomiting are box warning, and therefore droperi- Treatment
complex and are not fully under- dol is no longer considered a first-line For established postoperative
stood. The decision to provide agent in postoperative nausea and nausea and vomiting, the choices of
antiemetic therapy should be based vomiting.7 Ondansetron (Zofran) antiemetic are almost identical to
on a patient’s risk factors and poten- and dolasetron (Anzemet) are com- those used to prevent this type of
tial for serious sequelae from vomit- monly used SRAs. Although nausea and vomiting, with a slight
ing. All patients at high risk should granisetron (Kytril) prevents postop- difference in some of the dosages.
receive prophylactic antiemetics, erative nausea and vomiting, it is not The SRAs are considered first-line
preferably a combined regimen.9 currently approved for this purpose. agents, and the same alternative
Evidence is conflicting on whether The cost of using SRAs is thought to drugs are recommended as those
all surgical patients should receive be justified by patients’ satisfaction used to prevent postoperative nau-
routine prophylactic antiemetics.1,2 in avoiding postoperative nausea and sea and vomiting. Dopamine antag-
Selection of an antiemetic should vomiting. Dolasetron or onists, because they are inexpensive,
be based on safety and efficacy, the ondansetron can be given preopera- are often used.
patient’s risk factors, the patient’s tively or intraoperatively as a single Unlike other sedatives used also
satisfaction, and cost. No single dose. Combination drugs (eg, for nausea and vomiting, propofol is
antiemetic is superior in every situa- dolasetron plus dexamethasone) currently indicated only for seda-
tion. For the prevention of postopera- increase efficacy, especially in high- tion. Because it has antiemetic prop-
tive nausea and vomiting, the ASHP risk patients. Administration of erties, several studies have been
guidelines recommend administra- intravenous dexamethasone before done to evaluate subhypnotic doses
tion of droperidol (Inapsine) or an induction of anesthesia prevents in the treatment of postoperative
SRA.1 Droperidol, a dopamine recep- postoperative nausea and vomiting.9 nausea and vomiting. Those studies
tor antagonist, is cost-effective and The use of supplemental oxygen had conflicting outcomes. Fujii
produces marked tranquilization and has been shown to decrease the et al18 found that a small dose (0.5
sedation. It allays apprehension and occurrence of postoperative nausea mg/kg) was an effective antiemetic
provides a state of mental detach- and vomiting.17 Also, the restriction compared with droperidol and
ment and indifference while main- of oral intake until the return of metoclopramide. Gan et al19 con-
taining a state of reflex alertness. bowel function after surgery has cluded that patient-controlled deliv-
However, since the ASHP guidelines been used for decades to decrease ery of propofol decreased the
were published, studies have indicat- the occurrence of postoperative nau- prevalence of postoperative nausea
and vomiting compared with
placebo. Other studies20,21 in which
Table 4 Frequent causes of nausea and vomiting in critical care
propofol was used postoperatively
Surgery Drugs (opioids, antibiotics, drug overdose,
indicated that propofol did not
Unrelieved pain nonsteroidal anti-inflammatory drugs, selective decrease the prevalence of postoper-
Pancreatitis serotonin reuptake inhibitors, digitalis) ative nausea and vomiting.
Diabetic ketoacidosis Peritonitis
Increased intracranial pressure Hyponatremia Pain medication should not be
Meningitis Brain tumors, vestibular involvement withheld because of its potential to
Heart failure Myocardial infarction, especially inferior
Hepatobiliary causes Anxiety
cause nausea and vomiting.2 In
Cerebrovascular accident Gastrointestinal bleeding patients who do not respond to ini-
Hypotension Renal failure, uremia tial therapy with 1 antiemetic agent,
Bowel obstruction/ileus Hypercalcemia
an agent from another pharmacolog-

42 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003

ical class should be added, the dose
A
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, nonopi-
oid analgesics such as ketorolac
(Toradol) can be used as an alterna-
tive to control postoperative pain.2
Ketorolac is a nonsteroidal anti-
inflammatory drug and may cause
gastrointestinal irritation and toxic
effects on the kidneys.
In summary, the SRAs are rec-
B
ommended as first-line agents in
the prevention and treatment of
postoperative nausea and vomiting.
Administration of antiemetic med-
ications is generally considered
safe, despite an occasional adverse
reaction.

Other Causes of Nausea

Many medications, medical con-
ditions, 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 stim-
ulate the vomiting center indirectly
through the CTZ are digoxin, mor-
phine, alcohol, ipecac, and anti-
cancer 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 sero-
tonin and dopamine receptors in the
CTZ, which in turn stimulate the
vomiting center. The analgesic effect
of opioids is mediated by the activa-
tion of both µ1 and µ2 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 µ2 receptor unfor- cost. Less expensive drugs such as
tunately accounts for delayed transit phenothiazines, butyrophenones,
time through the gastrointestinal anticholinergics, and motility agents
tract, which contributes to nausea are recommended.21 In the acute
and vomiting. Currently, no opioid short-term, however, SRAs may be
agonists can selectively activate spe- used as first-line agents for opioid-
cific µ receptors, and therefore nau- induced nausea and vomiting.
sea and vomiting remain adverse
effects of opioid therapy.6 Tolerance Pharmacological Management
to this opioid-induced nausea and The goal of pharmacological
vomiting usually occurs within days interventions is to prevent or mini-
to weeks.6 Although the SRAs do mize nausea and/or vomiting.
relieve opioid-induced nausea, they Antiemetic agents are more effective
are not considered first-line drugs in at preventing emesis than at sup-
long-term therapy because of their pressing it.1,3 For prevention,

CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 43

antiemetics can be administered
orally or parenterally.3 For suppres-
sion of ongoing emesis, oral therapy
is ineffective; parenteral administra-
tion 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 recep-
tors 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
patient’s 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 prophy-
laxis and treatment of nausea and
vomiting have been developed.
These guidelines continue to be
refined as more research is complet-
ed. 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 recommen-
dations presented in this article are
intended for adults and not for chil-
dren. 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 small-
bowel intubation in endoscopic pro-
cedures. Children are more prone
than adults to extrapyrimidal reac-
tions or paradoxical reactions of rest-
44 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003
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 vomit-
ing in patients receiving a clear liq-
uid diet compared with patients
receiving a regular diet as the first
postoperative meal. Other dietary
modes of decreasing nausea are eat-
ing 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’ out-
comes 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 abnor-
mal energy flow and relieves signs
and symptoms. The 2 points that are
effective in lessening nausea and vom-
iting 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 effec-
tive in decreasing the intensity of pain
and nausea and improving relaxation
among cancer patients.
Acupuncture also decreases nau-
sea 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 pay-
ers 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.med-
icalacupuncture.org or that of the
National Acupuncture and Oriental
Medicine Alliance at www.acupunc-
turealliance.org.
Transcutaneous Electrical Nerve
Stimulation. Recently, a wristband-
type device for transcutaneous electri-
cal nerve stimulation, the ReliefBand,
was approved by the Food and Drug
Administration as an over-the-count-
er device. It is also based on the prin-
ciples 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 mus-
cles 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 tech-
nique also helps the body rid itself of
any residual anesthetic agent.2
Imagery training involves using men-
tal 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 effec-
tive 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 phar-
macological antiemetic treatment.
Herbs. The use of herbs to treat
nausea and vomiting is controver-
sial. 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 post-
operative nausea; ginger did appear
to reduce the occurrence of nausea
related to seasickness, morning sick-
ness, and chemotherapy. Dried gin-
ger in capsules has been used to
treat car sickness in animals.
Aromatherapy. The use of aro-
matherapy is also controversial
because its scientific effectiveness
and safety have not been estab-
CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 45
lished. Tate31 studied the use of pep-
permint oil for postoperative nau-
sea. 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 nau-
sea 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 exemp-
tion approval for an implantable sys-
tem (Enterra, Medtronic Inc,
Minneapolis, Minn) for the treat-
ment of chronic, intractable nausea
and vomiting due to gastroparesis of
diabetic or idiopathic origin. The
device consists of 2 leads with elec-
trodes that are implanted in the
antrum of the stomach and connect-
ed to a pulse generator that is surgi-
cally placed in the lower part of the
abdomen. The system is pro-
grammed to deliver low-frequency,
low-amplitude electrical pulses con-
tinuously 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 cen-
tral vagal afferent nerve pathways,
not by enhanced gastric emptying as
previously thought (W. L.
Starkebaum, Medtronic, Inc, oral
46 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003
communication, November 7, 2001).
The device is externally pro-
grammed in a fashion similar to that
used with cardiac pacemakers.32
Implications for
Critical Care Nursing
Critical care nurses are responsi-
ble for assessing the causes of nausea
and vomiting, administering appro-
priate antiemetic agents, evaluating
the effects of the agents, and provid-
ing 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-
Circle number 128 on Reader Service Card
er intervention in the prophylaxis
for and therefore the control of these
effects. Even though anesthesiolo-
gists routinely screen patients preop-
eratively to determine which are
high-risk patients, this information
must be communicated to the criti-
cal 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 move-
ment-induced postoperative nausea
and vomiting.2 Care can then be
taken to ensure slow and smooth
movements in transferring and turn-
ing a patient who has such a history.
Consideration should be given to
administering antiemetics on a
scheduled basis, rather than as need-
ed, for patients at high risk for post-
operative 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 vom-
iting. Suspected opioid-induced nau-
sea may be evaluated by
determining the temporal relation-
ship between the time the opioid
was given and the onset of nausea.6
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 vom-
iting 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 after-
load, or decreased contractility)
should be investigated.
Postoperatively, hypotension may be
due to the restriction of fluids preop-
eratively, intraoperative blood loss,
and the use of anesthetics, analgesics,
and sedatives.2 Vagal maneuvers
caused by retching and vomiting, as
occur in inferior myocardial infarc-
tion, can cause bradycardia.
Myocardial oxygen demand may be
increased in a patient with acute
coronary syndrome exacerbated by
nausea and vomiting.
The pulmonary system should
be assessed for indications of pul-
monary aspiration, especially in
patients receiving tube feedings.
Nosocomial pneumonia can be
caused by aspiration of oropharyn-
geal 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
residual feeding volumes may help
prevent pulmonary aspiration.
The gastrointestinal system
should be assessed for abdominal
distention, organomegaly, and pres-
ence of bowel sounds. Signs of hypo-
motility 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 indica-
tions 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 postopera-
tively, exposure to odors from nearby
food, strong perfume, and cleaning
solutions should be minimized.2
CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 47
Vomiting can also cause dehydra-
tion, 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 hyponatrem-
ia, which can cause cerebral edema
and death if untreated. Hypercalcemia
can cause nausea and vomiting.
Hypokalemia and life-threatening dys-
rhythmias can result from loss of elec-
trolytes due to vomiting.
Neurological causes should also
be considered. Increased intracra-
nial 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 sub-
arachnoid hemorrhage. In patients
with spinal cord trauma, the move-
ments associated with vomiting can
cause further injury to the spinal
cord. Nausea and vomiting occur
frequently after craniotomy.
Antiemetic therapy may cause seda-
tion, making postoperative neuro-
logical 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 pres-
sure generated during vomiting can
dislodge indwelling tubes or wires,
particularly those that are strategical-
ly placed, such as drains used to
diminish intracranial pressure, car-
diac pacing wires, and chest tubes.
 Medications should be evaluated
for their emetogenic potential.
Common offenders are chemothera-
peutic agents, opioids, nonsteroidal
anti-inflammatory drugs, antibi-
otics, and selective serotonin reup-
take inhibitors. Assessment of
nausea and vomiting should include
determination of the severity, dura-
tion, 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
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-effec-
tive approaches to the prevention
and treatment of nausea and vomit-
ing in the intensive care unit include
the use of nasogastric tubes for gas-
tric 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, hypoten-
sion) 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 pharmaco-
logical class should be added, the
48 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003
Case Study
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 pres-
sure 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 hemi-
colectomy 4 months ago. This sur-
gery 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 prochlorper-
azine (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 appro-
priate actions for the critical care
nurse to take?
a. Give another dose of promet-
hazine.
b. Report to the physician that
promethazine does not relieve the
patient’s nausea and vomiting.
c. Check the external ventricular
drain to ensure proper functioning.
d. Review the patient’s medica-
tion administration record to see if
any medication may be contribut-
ing to his nausea and vomiting.
e. Assess the patient’s 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-need-
ed basis. What is the rationale for
this order?
a. Ondansetron is indicated in
postoperative nausea and vomiting
when other antiemetics are ineffec-
tive; 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 pre-
vents 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 indi-
cated 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 intra-
venously
Answers
1. b, c, d, and e
When an antiemetic is ineffec-
tive, other types of drugs should be
considered. Other possible causes
of nausea should be assessed. These
include medical history of
chemotherapy, postoperative con-
dition, possible increased intracra-
nial pressure, and use of opioids for
pain management. Also, nausea
can be a symptom of hyponatrem-
ia, which can increase cerebral
edema.
2. a, b, c, and d
After a craniotomy, it is impor-
tant to prevent nausea and vomit-
ing 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 assess-
ment. Administration of prochlor-
perazine 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.
CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 49
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’ satisfac-
tion should influence the choice of
agent and override the cost con-
cerns. 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 pathophysi-
ology 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 comple-
mentary 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 sup-
port in writing this article. We appreciate the
comments of our manuscript reviewers, as well as
suggestions from Dr Mark Stewart, anesthesiolo-
gist, 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.
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 CE Continuing Education

CE Test Instructions
To receive CE credit for this test (ID C031), mark your answers on the form below, complete the enroll-
ment 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
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censure.

Test ID: C031

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

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❑b ❑b ❑b ❑b ❑b ❑b ❑b ❑b ❑b ❑b ❑b ❑b
❑c ❑c ❑c ❑c ❑c ❑c ❑c ❑c ❑c ❑c ❑c ❑c
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CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 51

CE Test Questions
Managing Nausea and Vomiting: Current Strategies

1. Where is the vomiting center located? 7. Serotonin receptor antagonists are the drugs of
a. Hypothalamus choice in patients receiving chemotherapeutic
b. Caudate nucleus agents with what emetic potential?
c. Medulla oblongata a. 0 to 1
d. Cerebellum b. 1 to 2
c. 2 to 4
2. Which of the following is not a neurotransmitter d. 3 to 5
that can relay impulses to the vomiting center?
a. Serotonin 8. Which antiemetic agent is indicated in refractory
b. Dopamine chemotherapy-induced nausea and vomiting
c. Histamine unresponsive to other classes of agents?’
d. Neurotensin a. Ondansetron
b. Granisetron
3. Which antagonist blocks acetylcholine receptors? c. Dolasetron
a. Dopamine d. Dronabinol
b. Muscarinic
c. Histamine 9. Postoperative nausea and vomiting occurs in
d. Serotonin what percentage of patients after surgery?
a. 10% to 20%
4. What emetic potential rating of chemotherapeutic b. 20% t0 30%
agents indicates the least potential? c. 30% to 40%
a. 0 d. 40% to 50%
b. 1
c. 5 10. Which of the following medications is associated
d. 10 with increased risk of nausea and vomiting?
a. Atropine
5. What is an example of a chemotherapeutic agent b. Propofol
with the highest emetic potential? c. Ketamine
a. Cisplatin d. Droperidol
b. Vincristine
c. Carboplatin 11. Which of the following is associated with
d. Doxorubicin decreased occurrence of postoperative nausea
and vomiting?
6. Which of the following chemotherapeutic agents a. Opioid use
is not associated with delayed nausea? b. Supplemental oxygen
a. Cisplatin c. Positive pressure ventilation
b. Vincristine d. General anesthesia
c. Carboplatin
d. Cyclophosphamide 12. How much does adequate pain relief reduce the
occurrence of nausea?
a. 20%
b. 40%
c. 60%
d. 80%

52 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003