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2003;23:31-50Crit Care Nurse Kitty Garrett, Kayo Tsuruta, Shirley Walker, Sharon Jackson and Michelle SweatManaging Nausea and Vomiting : Current Strategies

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CURRENT STRATEGIES

CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003 31

The topic of nausea andvomiting is all too familiar to mostnurses. Nausea and vomiting areunpleasant complications or indica-tions of many medical conditions andare adverse effects of hundreds ofmedications. Nausea and vomitingoccur so frequently that they arealmost considered “acceptable,” usu-ally referred to as “minor” and con-sidered more of an inconvenience or anuisance than a medical problem.This duo, however, is not onlyunpleasant but can be debilitatingand can cause unnecessarily pro-longed recovery times and increasedcosts. In critically ill patients, severeor protracted nausea and vomitingcan lead to serious complicationssuch as aspiration pneumonia, dehy-

Managing Nauseaand Vomiting

CoverArticle

Kitty Garrett, RN, MSN, CCRNKayo Tsuruta, RN, MSN, AOCNShirley Walker, RN, MSNSharon Jackson, RN, MSNMichelle Sweat, RN, BSN

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 oncologynurse at Athens Regional Medical Center in Athens, Ga.

Shirley Walker is an instructor in the nursing staff development department at AnMedHealth in Anderson, SC. She has 23 years of nursing experience.

Sharon Jackson has 12 years of experience in medical-surgical nursing and emergencydepartment nursing. She is a major in the US Army Nursing Corps and is stationed atTripler Army Medical Center in Honolulu, Hawaii.

Michelle Sweat is a senior staff nurse in the medical intensive care unit at the MedicalCollege of Georgia Hospital in Augusta. She is currently enrolled in the critical care clinicalnurse 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, [email protected].

Authors

1. Discuss the mechanisms of nausea and vomiting

2. Identify preoperative and postoperativefactors that influence the development of nausea and vomiting

3. Describe treatment options for nausea and vomiting

CE This article has been designated for CE credit. A closed-book, multiple-choice examination follows this article, which tests yourknowledge of the following objectives:

CEContinuing Education



dration, malnutrition, and disruptionof the surgical site.1,2 Metabolic dis-turbances such as metabolic alkalosis,hyponatremia, hypochloremia, andhypokalemia may occur. Vomitingafter craniotomy or any brain injurycauses an increase in intracranialpressure. These complications can belife-threatening. Nausea and vomitingcan also cause patients to experienceincreased anxiety and dissatisfactionwith the hospital experience and cancontribute to future anticipatory nau-sea.2 Also, the increased resourcesand time needed to treat a patientwith nausea and vomiting can have aprofound economic impact.2

Interest in this topic was recentlyrenewed because of an enhancedunderstanding of the physiologicalmechanisms involved in the processof nausea and vomiting. Much hasbeen published about nausea andvomiting as it relates to chemother-apy and postoperative nausea andvomiting, but many correlates can bedrawn to critical care patients. In thisarticle, we present current knowledgeabout the physiological mechanismsof nausea and vomiting and comparetherapeutic agents (pharmacologicaland nonpharmacological) recom-mended for treating and preventingnausea and vomiting. Because it isnow understood that most episodesof nausea and vomiting are preventa-ble, implications for critical care nurs-ing will focus on prevention ratherthan control of nausea and vomiting.

DefinitionsNausea and vomiting are basic

human protective reflexes againstthe absorption of toxins, as well asresponses to certain stimuli.2 Theterms nausea and vomiting are oftenused together, although each phe-

vagal afferent nerves or by the directaction of emetogenic compoundsthat are carried in the blood (anti-cancer drugs, opioids, ipecac).

Specific neurotransmitters andneuromodulators in the CTZ identi-fy substances as potentially harmfuland relay impulses to the vomitingcenter to initiate the vomiting cas-cade so that the harmful substancecan be expelled. These neurotrans-mitters are serotonin, dopamine,acetylcholine (muscarinic choliner-gic), and histamine. A fifth chemore-ceptor, the neurokinin-1neuropeptide, also called substanceP, is currently under study.4,5

Stimulation of these chemore-ceptors triggers activation of thevomiting center. Therefore, anyinterference with the transmissionof these chemoreceptors preventsthe vomiting center from being acti-vated. Many antiemetics act byblocking 1 or more of these recep-tors.3 Dopamine antagonists blockdopamine receptors; muscarinicantagonists block acetylcholinereceptors; histamine blockers blockhistamine receptors; and serotoninreceptor blockers block serotoninreceptors. The adverse effects ofthese drugs are also determined bywhich receptor site is blocked3

(Table 1).

Chemotherapy-InducedNausea and Vomiting

Nausea and vomiting are amongthe most distressing and debilitatingadverse effects of chemotherapy.Even though chemotherapeuticagents are not routinely adminis-tered in critical care, cancer patientswho have had chemotherapy areoften admitted to critical care areas.Hence, a discussion of nausea and

nomenon should be assessed sepa-rately. Nausea is defined as a subjec-tively unpleasant wavelike sensationin the back of the throat or epigastri-um associated with pallor or flush-ing, tachycardia, and an awarenessof the urge to vomit.1 Sweating,excess salivation, and a sensation ofbeing cold or hot may occur.Vomiting, or emesis, is characterizedby contraction of the abdominalmuscles, descent of the diaphragm,and opening of the gastric cardia,resulting in forceful expulsion ofstomach contents from the mouth.1

Retching involves spasmodic con-tractions of the diaphragm and themuscles of the thorax and abdomi-nal wall without expulsion of gastriccontents, the so-called dry heaves.1

Mechanisms of Nausea and Vomiting

The activation of a nucleus ofneurons located in the medullaoblongata, known as the vomitingcenter, initiates the vomiting reflex.The vomiting center can be activateddirectly by signals from the cerebralcortex (anticipation, fear, memory),signals from sensory organs (dis-turbing sights, smells, pain), or sig-nals from the vestibular apparatus ofthe inner ear (motion sickness). Thevomiting center can also be activat-ed indirectly by certain stimuli thatactivate the chemoreceptor triggerzone (CTZ)3 (Figure 1). The CTZ islocated in the highly vascular areapostrema on the surface of the brain.This area lacks a true blood-brainbarrier and is exposed to both bloodand cerebrospinal fluid; thus, theCTZ can react directly to substancesin the blood.2 The CTZ can be acti-vated by signals from the stomachand small intestine traveling along

32 CRITICALCARENURSE Vol 23, No. 1, FEBRUARY 2003



vomiting would not be completewithout a description of the clinicalstudies in this area.

MechanismChemotherapeutic agents stimu-

late enterochromaffin cells in the gas-trointestinal tract to releaseserotonin, which activates serotoninreceptors. Activation of the receptorsactivates the vagal afferent pathway,which activates the vomiting centerand causes an emetic response.10 The

emetic potential of a chemotherapeu-tic agent itself is the major stimulusfor nausea and vomiting inchemotherapy-induced nausea andvomiting (CINV).1 Chemotherapeuticagents are rated according to theiremetic potential; 1 indicates the leastpotential, and 5 indicates the great-est. An example of an agent with thelowest emetic potential (1) is vin-cristine. An example of an agent withthe highest emetic potential (5) is cis-platin. The American Society of

Health System Pharmacists (ASHP)recommends prophylactic antiemetictherapy when drugs with antiemeticpotential of levels 2 to 5 are used1

(Table 2).

Risk FactorsIn addition to the emetic potential

of the chemotherapeutic agents, sever-al other risk factors can be used to pre-dict the likelihood of CINV. Patientsyounger than 50 years have morenausea and vomiting than do olderpatients.1 Women are more suscepti-ble than men, presumably because ofthe influence of hormones.2 A historyof motion sickness, pregnancy-relatednausea and vomiting, or nausea andvomiting with previous chemotherapyare all positive predictors of CINV.1

Patients who use alcohol heavily orwho have done so in the past have areduced risk of emesis.1,11

Patterns of Nausea and VomitingAnticipatory nausea and vomiting

occur before the beginning of a newcycle of chemotherapy, in response toconditioned stimuli such as thesmells, sights, and sounds of thetreatment room or the presence of aspecific person designated to admin-ister the chemotherapy.12 Anticiatorynausea usually occurs 12 hoursbefore administration of chemother-apy in patients who have experiencedfailed control of nausea and vomitingin previous treatments.

Acute nausea and vomiting occurwithin the first 24 hours after theadministration of chemotherapy,usually within the first 1 to 2 hours.This type is initiated by stimulationprimarily of dopamine and sero-tonin receptors in the CTZ, whichtriggers the vomiting cascade.1 Itresolves within 24 hours.


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

CTZ indicates chemoreceptor trigger zone.

Reprinted from Lehne et al,3 with permission.

Receptors: 5HT = SerotoninDA = DopamineM = Muscarinic cholinergicH1 = Histamine1

Stomach and small intestine

Blood-borne emeticsChemotherapy OpioidsIpecac

Sensory inputSightSmellPain

Vestibular apparatus

Higher centersAnticipationFearMemory

5HTDA

Vomitingvia output to stomach,diaphragm, and abdomi-nal muscles

Vomiting center

CTZ

5HTDAM

H1M

Vagala

ffere

nts




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

Site of action

Serotonin receptors

Dopaminereceptors

Drug type

Serotonin (5HT3)receptor antagonists

Dopamine antag-onists

First-line therapy for acute CINV and RINV: use on day ofchemotherapy or radiation therapy only, not more than 24 hourslater

First-line therapy for prevention of PONV and treatment of breakthrough nausea and vomiting

Opioid-induced nausea and vomiting6

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

Prevention of CINV

Prevention and treatment of PONV

PONV

Breakthrough nausea and vomiting in CINV


Acceptable alternative to droperidol in the prevention and treatmentof PONV

Breakthrough nausea and vomiting

Established nausea and vomiting in RINV


Prevention and treatment of established PONV and breakthroughnausea and vomiting in CINV only in patients who do notrespond to other drug8

Can be given in combination with serotonin receptor antagonistsand steroids in patients at high risk for PONV

Indications

Ondansetron(Zofran)

Granisetron(Kytril)

Dolasetron(Anzemet)

Promethazine(Phenergan)

Chlorpromazine(Thorazine)

Prochlorperazine(Compazine)

Droperidol(Inapsine)

Examples

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

Phen

othi

azin

esBu

tyro

phen

ones




Dosage*

CINV prevention: 24 mg by mouth or 8 mg IV 30 minbefore chemotherapy

PONV prevention: 4 mg IV over 2-5 min immediatelybefore or 8 mg by mouth 1 hour before induction ofanesthesia

PONV treatment: 1-4 mg IV

CINV prevention: 2 mg by mouth or 10 µg/kg IV 30 minbefore chemotherapy

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

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

CINV prevention: 100-200 mg by mouth or 1.8 mg/kgIV 30 min before chemotherapy

PONV prevention: 12.5 mg IV intraoperatively or 100mg by mouth 1 hour before induction of anesthesia

PONV treatment: 12.5 mg IV postoperatively

PONV prevention: 25 mg by mouth 1 hour before or12.5-25 mg IV immediately before induction of anesthesia

PONV treatment: 10-25 mg by mouth every 4-6 hours asneeded or 12.5-25 mg intramuscularly or IV every 4 hras needed; 25-mg rectal suppository every 12 hours

PONV treatment: 10-25 mg by mouth every 4-6 hoursas needed; 25- or 100-mg rectal suppository

PONV prevention: 5-15 mg by mouth 1 hour, 5-10 mgintramuscularly 1-2 hours, or 5-10 mg IV 15-30 minbefore 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-mgrectal suppository

CINV treatment: 5-20 mg by mouth, intramuscularly, orIV every 6 hours, 25-mg rectal suppository every 12hours

PONV prevention: 0.625-1.25 mg IV SLOWLY 5 minbefore termination of anesthesia

PONV treatment: 0.625-1.25 mg IV slowly as needed

Maximum dose: 2.5 mg

Mild to moderate and transient;headache most common

IV dolasetron may causechanges in intervals on electrocardiograms; use withcaution in prolonged conduction disorders

Oversedation; lethargy, posturalhypotension; skin sensitivity;dystonic reactions

Extrapyramidal reactions orparadoxical reactions occurmore commonly in children

Sedation, hypotension, tachycardia

Prolonged QT interval leadingto torsade de pointes

Most common adverse effects

Advantages: one-time dosing lasts 24 hours, noknown drug interactions, broad safety profile,may be taken with or without food, nonsedating

Should be administered with steroids to preventdelayed nausea and vomiting

Oral doses recommended over IV doses becauseformer are equally effective, less costly, andmore convenient

Disadvantages: Increased cost; all serotoninreceptor antagonists equally effective atequivalent doses, so cost should be a factorin making a choice

Not first-line drug in breakthrough CINV becauseof cost

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

Widely used because they are inexpensive; moderately effective; available in IV, oral, andsuppository forms

Efficacy generally lower than efficacy of serotonin receptor antagonists

Prochlorperazine more effective than promet-hazine for treating uncomplicated nausea andvomiting in patients in emergency department

7

IV promethazine administered at a rate nogreater than 25 mg/min

IV prochlorperazine administered at a rate nogreater than 5 mg/min

Not available in oral form

Should not be given to patients with long QTintervals

Electrocardiographic monitoring should be donebefore administration and continued for 2-3hours after treatment

Comments

Continued

Society of Clinical Oncology, and Mayo Clinic Clinical Practice Guidelines




Table 1 ContinuedSite of action

Dopamine receptors(continued)

Histaminic receptors

Muscarinic cholin-ergic receptors

Neurokinin-1receptors

Mechanismunknown

Cannabinoid receptor sites(CB-1 and CB-2)exert centralsympathomimeticaction

Limbic systeminhibition

Drug type

Dopamine antago-nists (continued)

Antihistamines

Anticholinergics

Not yet available

Glucocorticoids

Cannabinoids

Benzodiazipines

Primary PONV; breakthrough nausea and vomiting in CINV; opioid-induced nausea and vomiting; nausea and vomiting due tobowel obstruction

Rescue therapy when serotonin receptor antagonists not effective

4

Breakthrough nausea and vomiting in CINV; established nauseaand vomiting in RINV

Prevents nausea and vomiting by stimulating gastric emptying andblocking dopamine receptors


Nausea and vomiting associated with motion sickness or vertigo

First-line drug in prophylaxis of nausea and vomiting associatedwith motion sickness

CINV, sudden onset and delayed

Drug of choice in prevention of delayed nausea and vomiting inCINV

PONV with dolasetron

Modestly effective in CINV; may be used in patients respondingpoorly to other antiemetics

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

Indications

Haloperidol(Haldol)

Metoclopramide(Reglan)

Dimenhydrinate(Dramamine)

Meclizine(Antivert)

Scopolamine

Dexamethasone(Decadron)

Methylprednisolone(Solu-Medrol)

Dronabinol(Marinol)

Lorazepam(Ativan)

Examples

Buty

roph

enon

esBe

nzam

ide

Other sites of action

*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.




Dosage*

CINV treatment: 1-4 mg by mouth, intramuscularly, orIV every 6 hours

CINV treatment: 2 mg/kg by mouth or IV every 2-4hours for 2-5 doses for rescue therapy; for delayednausea and vomiting, 0.5 mg/kg or 30 mg IV or bymouth 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 4-6hours 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 serotoninreceptor 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 beforechemotherapy

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

Nonsedating in lower doses; sedation, hypotension, tachycar-dia, extrapyrimidal effects similarto those of dopamine antagonists

Sedation, restlessness, agitation,diarrhea, drowsiness, sleepless-ness, dystonic reactions withhigher doses

Sedation, dry mouth, constipation,blurred vision

Dry mouth, drowsiness, impairedeye accommodation

Gastrointestinal upset, anxiety,insomnia, hyperglycemia

Drowsiness, dizziness, sedation,hypotension, vision difficulty,vasodilatation, euphoria, dysphoria (especially in olderadults)

Sedation, amnesia, visual disturbances

Most common adverse effects

Cost-effective alternative to serotonin receptorantagonists

At high doses, also inhibits serotonin receptorsUse no longer recommended by Mayo Clinic

guidelines because of adverse effects of restlessness, agitation, and drowsiness

Because of its ability to increase gastric andintestinal motility, contraindicated in patientswith bowel obstruction, gastrointestinal hemorrhage, or perforation

Slightly less effective than serotonin receptorantagonists and droperidol

Used as adjunct to prevent adverse effects inpatients receiving dopamine receptor antagonists; use limited because dopaminereceptors no longer first-line agents

Patch applied behind ear 4 hours before travel;patch should last 3 days

Investigational

Used with serotonin receptor antagonists toenhance their benefit; yields increased protection

Used alone for prevention of level 2 CINV

Inexpensive

Should be used with caution in patients withunstable diabetes mellitus

Other antiemetics more effective, but becausethe mechanism of action differs, cannabinoidsmay be given alone or in combination withother agents

Comments



Delayed nausea and vomitingbegin at least 24 hours after theadministration of chemotherapy andmay last up to 120 hours. Patientswho experience acute CINV are morelikely to also experience delayed eme-sis.12 The causative mechanism indelayed nausea and vomiting is notwell defined, but the metabolites ofthe chemotherapeutic agents arethought to continue to affect the cen-tral nervous system and the gastroin-testinal tract.1,13(p546-549) For example,cisplatin causes delayed nausea andvomiting, up to 48 to 72 hours afteradministration, in more than half ofall patients who receive the drug.1

Other agents that cause delayed nau-sea and vomiting are high-dose carbo-platin, cyclophosphamide, anddoxorubicin.

Breakthrough nausea and vomit-ing occur despite preventive therapy

potential of 3 to 5.1 The SRAs preventemesis by blocking the emeticresponse early in the emeticpathway.10 They are given to patientsbefore chemotherapy to preventCINV. Because the SRAs have noeffect on the histaminergic,dopaminergic, or cholinergic recep-tors, they can provide highly effectiverelief of nausea and vomiting withoutmany 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 TheSRAs used most often areondansetron (Zofran), granisetron(Kytril), and dolasetron (Anzemet).Unfortunately, their high cost mayprevent some patients from benefit-ing from these medications (Table 3).Because SRAs are similarly effectivefor controlling acute nausea and

and require additional therapy.1

Antiemetic treatment administeredto patients who have not respondedto prophylactic regimens is oftenreferred to as rescue therapy.13

TreatmentPrevention of Acute CINV.

Antiemetic therapies have been com-pared in many clinical trials, especial-ly since the advent of the relativelynew class of drugs, the serotoninreceptor antagonists (SRAs). Becausechemotherapeutic agents initiateactivation mainly of serotonin recep-tors, which leads to CINV, the SRAsare among the most effective drugsfor prevention of CINV. These drugshave become the gold standard ofantiemetic therapy,10 and they arerecommended by the ASHP as thedrugs of choice in patients receivingchemotherapeutic agents with emetic


Table 2 Emetogenic potential of chemotherapeutic agents and standard treatments

Level*

5(>90)

4(60-90)

3(30-60)

2(10-30)

1(<10)

CisplatinCyclophosphamide

(>1500 mg/m2)

CarboplatinCyclophosphamide

(>750 mg/m2,<1500 mg/m2)

Doxorubicin (>60 mg/m2)Methotrexate

DoxorubicinIfosfamideIrinotecan

CytarabineDocetaxelEtoposide5-FluorouracilPaclitaxel

BleomycinFludarabineVinblastineVincristine

Agent Prevention

Granisetron, ondansetron,or dolasetron with dexamethasone; ormethylprednisolone

Dexamethasone ormethylprednisolone;prochlorperazine foradults

No treatment

Lorazepan, methyl-prednisolone,prochlorperazine,metoclopramide,dexamethasone,haloperidol, ordronabinol

For children

Chlorpromazine,lorazepam, ormethylpred-nisolone

Breakthrough

High-dose carboplatin:dexamethasone and meto-clopramide or serotoninreceptor antagonists

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

For children

Chlorpromazine, lorazepam, orserotonin receptor antagonists and dexamethasone or methylprednisolone

Delayed

Treatment

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



vomiting, the investigators in severalcomparative medical trials concludedthat the least expensive SRA shouldbe used initially.1,4,12 Also, oral SRAsare less expensive than parenteralSRAs and are as effective as the intra-venous form.1,4,10,12 Wickam11 foundthat because the SRAs are not struc-turally identical, they may have dif-ferences in efficacy, and sherecommends that if an SRA is ineffec-tive, a second SRA should be given.

With less toxic chemotherapeuticagents, combinations of otherantiemetics may be effective.Dexamethasone and prochlorper-azine are recommended forchemotherapeutic agents that havemild to moderate emetic potential.1

The combination of dexamethasonewith metoclopramide, although lesseffective, may also be an option.

Prevention of Delayed CINV. TheSRAs alone are not useful in delayednausea and vomiting. Complete pro-tection from vomiting occurs more

often in patients who are givenondansetron plus dexamethasone.1

Therefore, dexamethasone is thedrug of choice for prevention ofdelayed nausea and vomiting.1,4,9 Itshould be administered with SRAsbefore chemotherapy.

Treatment of Breakthrough CINV. Ifa patient experiences CINV within 24hours despite preventive antiemetictreatment, a combination of differentclasses of antiemetic drugs is given.This intervention is called rescue ther-apy. Drugs of choice for such rescuetherapy include prochlorperazine, thi-ethylperazine, or metoclopramidewith or without diphenhydramine, orlorazepam, haloperidol, or dronabi-nol.1,15 Dronabinol may be indicated inrefractory CINV unresponsive toother classes of drugs. Even thoughthe SRAs may also be effective, theirsuperiority over traditional, lessexpensive agents has not been deter-mined.1 The choice of agent should bebased on patient-specific factors.1 All

patients receiving chemotherapyshould have antiemetics available asneeded for rescue from breakthroughnausea and vomiting.1 If CINV per-sists after the breakthrough treat-ment, these drugs should be given ona scheduled basis rather than on an as-needed basis.

Treatment of Anticipatory CINV.Behavioral interventions are recom-mended for anticipatory emesisbecause they produce physiologicalrelaxation, divert attention awayfrom the conditioned stimulus andtoward relaxing images, andenhance feelings of control.1 Theamnestic and anxiolytic propertiesof lorazepam may also help preventanticipatory nausea and vomiting byblocking the memory of emesis asso-ciated with chemotherapy.1,13

Lorazepam should be given thenight before and the morning ofchemotherapy.13,15

In summary, nausea and vomit-ing are no longer inevitable compli-


Table 3 Comparative costs of antiemetic agents

Ondansetron (Zofran)

Granisetron (Kytril)Dolasetron (Anzemet)

Promethazine (Phenergan)

Chlorpromazine (Thorazine)Prochlorperazine (Compazine)

Droperidol (Inapsine)

Haloperidol (Haldol)Metoclopramide (Reglan)Dimenhydrinate (Dramamine)Scopolamine (Transderm Scop)Methylprednisolone (Solu-Medrol)

Dronabinol (Marinol)Lorazepam (Ativan)

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 applicable10.66 (2 mg/mL, 1-mL vial)

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)

Agent Intravenous form Oral form

Data from Drug Topics Redbook.14

Mean wholesale price, $US



cations of chemotherapy; mostpatients can get complete control ofthese adverse effects. The drugs ofchoice for prevention of acute CINVare the SRAs. Recommended treat-ment for prevention of delayedCINV is dexamethasone. The drugof choice for anticipatory nauseaand vomiting is lorazepam.Breakthrough nausea and vomitingcan be treated with prochlorper-azine, metoclopramide, haloperidol,or dronabinol (Table 1).

PostoperativeNausea and Vomiting

The term acute postoperativenausea and vomiting is defined asany episode of nausea or vomitingthat occurs within 24 hours of

CausesPreoperative Factors. The occur-

rence of postoperative nausea andvomiting is influenced by several fac-tors.1,2,16 The risk is higher in adultsthan in children, in women than inmen, and in patients with a historyof motion sickness or previous post-operative nausea and vomiting.1 Theprevalence is also greater in obesepatients and in patients with delayedgastric emptying disorders such asgastroesophageal reflux disease, gas-trointestinal obstruction, chroniccholecystitis, and neuromusculardisorders.1 A history of smoking isassociated with a decrease in thelikelihood of postoperative nauseaand vomiting.16 Patients’ characteris-tics have a cumulative effect in influ-

receiving anesthesia. Although sig-nificant progress has been made inpreventing this type of nausea andvomiting, it still occurs in 20% to30% of patients after surgery.1,2

MechanismIn postoperative nausea and

vomiting, a wide range of stimulicontribute to the emetic response.Most anesthetic agents and opioidsstimulate the vomiting center indi-rectly through the CTZ. Associatedfactors that directly stimulate thevomiting center include sensoryinput (visual, olfactory, and pain)and the vestibular apparatus.Nitrous oxide directly stimulates thegastrointestinal tract, which acti-vates the vomiting center.2




encing the prevalence of postopera-tive nausea and vomiting.

Intraoperative Factors. The type ofsurgical procedure can also influencethe occurrence of postoperative nau-sea and vomiting. The rate is high inpatients undergoing laparoscopic pro-cedures related to abdominal disten-tion because of the carbon dioxideused for visualization.1,2 The preva-lence of postoperative nausea andvomiting is also greater after plastic,ophthalmic, orthopedic shoulder,gynecologic, and ear, nose, and throatsurgeries than after other proce-dures.1,2 Intubation itself can evokenausea and vomiting. Longer proce-dures with general anesthesia are asso-ciated with more nausea and vomitingthan are shorter procedures.1,2 The

type of anesthetic used is also a factor.General anesthetics vary in theirpropensity to cause postoperativenausea and vomiting. Etomidate, ket-amine, nitrous oxide, and inhaledagents increase the risk of nausea andvomiting.1,2 Gastric distention causedby suction or vigorous positive pres-sure ventilation via face mask mayalso increase the risk of postoperativenausea and vomiting.1,2 Some medica-tions used in association with anesthe-sia decrease the risk of postoperativenausea and vomiting. These includeatropine, which has a vagolytic effect,and propofol (Diprivan).1 Althoughthe exact mechanism of the antiemet-ic effect of propofol is not clear, thedrug may have a weak serotoninantagonistic effect.9

Postoperative Factors. During thepostoperative period, the 2 most com-mon causes of nausea and vomitingare unrelieved pain (especially visceralor pelvic) and the opioids prescribedto control the pain. Adequate painrelief reduces the occurrence of nauseaby 80%.2 Opioids stimulate nauseaand vomiting by a direct action on theCTZ.2 Unrelieved pain directly stimu-lates the vomiting center (Figure 1).Nausea can also be precipitated bysudden motion, changes in body posi-tion, premature oral intake, andhypotension.1,2

PreventionIf postoperative nausea and vom-

iting can be predicted, then theyshould be preventable. However,


Circle number 122 on Reader Service Card



prevention is sometimes difficultbecause of the wide range of stimulithat contribute to the emeticresponse. Also, many of the path-ways involved in the control of post-operative nausea and vomiting arecomplex and are not fully under-stood. The decision to provideantiemetic therapy should be basedon a patient’s risk factors and poten-tial for serious sequelae from vomit-ing. All patients at high risk shouldreceive prophylactic antiemetics,preferably a combined regimen.9

Evidence is conflicting on whetherall surgical patients should receiveroutine prophylactic antiemetics.1,2

Selection of an antiemetic shouldbe based on safety and efficacy, thepatient’s risk factors, the patient’ssatisfaction, and cost. No singleantiemetic is superior in every situa-tion. For the prevention of postopera-tive nausea and vomiting, the ASHPguidelines recommend administra-tion of droperidol (Inapsine) or anSRA.1 Droperidol, a dopamine recep-tor antagonist, is cost-effective andproduces marked tranquilization andsedation. It allays apprehension andprovides a state of mental detach-ment and indifference while main-taining a state of reflex alertness.However, since the ASHP guidelineswere published, studies have indicat-

sea and vomiting. Alternativeantiemetic drugs include metoclo-pramide, chlorpromazine, prochlor-perazine and promethazine.

TreatmentFor established postoperative

nausea and vomiting, the choices ofantiemetic are almost identical tothose used to prevent this type ofnausea and vomiting, with a slightdifference in some of the dosages.The SRAs are considered first-lineagents, and the same alternativedrugs are recommended as thoseused to prevent postoperative nau-sea and vomiting. Dopamine antag-onists, because they are inexpensive,are often used.

Unlike other sedatives used alsofor nausea and vomiting, propofol iscurrently indicated only for seda-tion. Because it has antiemetic prop-erties, several studies have beendone to evaluate subhypnotic dosesin the treatment of postoperativenausea and vomiting. Those studieshad conflicting outcomes. Fujii et al18 found that a small dose (0.5mg/kg) was an effective antiemeticcompared with droperidol andmetoclopramide. Gan et al19 con-cluded that patient-controlled deliv-ery of propofol decreased theprevalence of postoperative nauseaand vomiting compared with placebo. Other studies20,21 in whichpropofol was used postoperativelyindicated that propofol did notdecrease the prevalence of postoper-ative nausea and vomiting.

Pain medication should not bewithheld because of its potential tocause nausea and vomiting.2 Inpatients who do not respond to ini-tial therapy with 1 antiemetic agent,an agent from another pharmacolog-

ed that droperidol can cause a pro-longed QT interval, which can lead topotentially fatal cardiac dysrhyth-mias. The Food and DrugAdministration now requires a black-box warning, and therefore droperi-dol is no longer considered a first-lineagent in postoperative nausea andvomiting.7 Ondansetron (Zofran)and dolasetron (Anzemet) are com-monly used SRAs. Althoughgranisetron (Kytril) prevents postop-erative nausea and vomiting, it is notcurrently approved for this purpose.The cost of using SRAs is thought tobe justified by patients’ satisfactionin avoiding postoperative nausea andvomiting. Dolasetron orondansetron can be given preopera-tively or intraoperatively as a singledose. Combination drugs (eg,dolasetron plus dexamethasone)increase efficacy, especially in high-risk patients. Administration ofintravenous dexamethasone beforeinduction of anesthesia preventspostoperative nausea and vomiting.9

The use of supplemental oxygenhas been shown to decrease theoccurrence of postoperative nauseaand vomiting.17 Also, the restrictionof oral intake until the return ofbowel function after surgery hasbeen used for decades to decreasethe occurrence of postoperative nau-


Table 4 Frequent causes of nausea and vomiting in critical care

SurgeryUnrelieved painPancreatitisDiabetic ketoacidosisIncreased intracranial pressureMeningitisHeart failureHepatobiliary causesCerebrovascular accidentHypotensionBowel obstruction/ileus

Drugs (opioids, antibiotics, drug overdose, nonsteroidal anti-inflammatory drugs, selectiveserotonin reuptake inhibitors, digitalis)

PeritonitisHyponatremiaBrain tumors, vestibular involvementMyocardial infarction, especially inferiorAnxietyGastrointestinal bleedingRenal failure, uremiaHypercalcemia



ical class should be added, the doseof the antiemetic should beincreased to the maximum acceptedrange, or a combination of bothapproaches should be used.1 Inpatients 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 causegastrointestinal irritation and toxiceffects on the kidneys.

In summary, the SRAs are rec-ommended as first-line agents inthe prevention and treatment ofpostoperative nausea and vomiting.Administration of antiemetic med-ications is generally consideredsafe, despite an occasional adversereaction.

Other Causes of NauseaMany medications, medical con-

ditions, and procedures can inducenausea and vomiting. Table 4 lists thecauses most common in critical care.

Drugs that cause gastric irritation(eg, nonsteroidal anti-inflammatorydrugs, selective serotonin reuptakeinhibitors, and antibiotics) can causenausea. Examples of drugs that stim-ulate the vomiting center indirectlythrough the CTZ are digoxin, mor-phine, alcohol, ipecac, and anti-cancer drugs. Motion sickness andinner ear disorders cause nausea bydirectly stimulating the vomitingcenter. Nausea can also be inducedby olfactory, visual, vestibular, andpsychogenic stimuli2 (Figure 1).

Opioids directly stimulate sero-tonin and dopamine receptors in theCTZ, which in turn stimulate thevomiting center. The analgesic effectof opioids is mediated by the activa-tion of both µ1 and µ2 receptors.

Activation of the µ2 receptor unfor-tunately accounts for delayed transittime through the gastrointestinaltract, which contributes to nauseaand vomiting. Currently, no opioidagonists can selectively activate spe-cific µ receptors, and therefore nau-sea and vomiting remain adverseeffects of opioid therapy.6 Toleranceto this opioid-induced nausea andvomiting usually occurs within daysto weeks.6 Although the SRAs dorelieve opioid-induced nausea, theyare not considered first-line drugs inlong-term therapy because of their

cost. Less expensive drugs such asphenothiazines, butyrophenones,anticholinergics, and motility agentsare recommended.21 In the acuteshort-term, however, SRAs may beused as first-line agents for opioid-induced nausea and vomiting.

Pharmacological ManagementThe goal of pharmacological

interventions is to prevent or mini-mize nausea and/or vomiting.Antiemetic agents are more effectiveat preventing emesis than at sup-pressing it.1,3 For prevention,


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

A

B



antiemetics can be administeredorally or parenterally.3 For suppres-sion of ongoing emesis, oral therapyis ineffective; parenteral administra-tion is required. Parenteral therapyincludes intravenous, intramuscular,and rectal routes of administration.Nausea is a complex response. Nosingle pharmacological agent isavailable that blocks all the recep-tors that trigger nausea or elicitvomiting. Also, adverse effects maylimit the use of certain antiemetics.Therefore, the choice of drugsshould be individualized to eachpatient’s needs. Combinationantiemetic therapy using agentswith different mechanisms of actionmay be necessary.1

Antiemetic therapies have beencompared in multiple clinical trials.On the basis of the results, clinicalpractice guidelines for the prophy-laxis and treatment of nausea andvomiting have been developed.These guidelines continue to berefined as more research is complet-ed. Table 1 summarizes currentpharmacological recommendations,emphasizing those from the ASHP,1

the American Society of ClinicalOncology,4 and the Mayo Clinic.8

Table 3 provides a cost comparisonof antiemetic agents.

The pharmacological recommen-dations presented in this article areintended for adults and not for chil-dren. Specifically, the dopamineantagonists such as prochlorperazineand metoclopramide should not beused in children. Data are insufficientto support the use of metoclopramidein children except to facilitate small-bowel intubation in endoscopic pro-cedures. Children are more pronethan adults to extrapyrimidal reac-tions or paradoxical reactions of rest-

and symptoms. The 2 points that areeffective in lessening nausea and vom-iting are P6 and ST36 (Figure 2). Firmand steady pressure applied to thesepoints with the fingers lessens theintensity of chemotherapy-inducednausea.23 Grealish et al24 reported thata 10-minute foot massage was effec-tive in decreasing the intensity of painand nausea and improving relaxationamong cancer patients.

Acupuncture also decreases nau-sea and vomiting; it is based on thesame principles as acupressure.25

Because acupuncture requirestrained and certified personnel, itmay not be a cost-effective methodof treatment. However, Medicare,Medicaid, and some third-party pay-ers now cover acupuncture fees. Alist of certified acupuncturists can befound by visiting the Web site of theAmerican Academy of MedicalAcupuncture at www.med-icalacupuncture.org or that of theNational Acupuncture and OrientalMedicine Alliance at www.acupunc-turealliance.org.

Transcutaneous Electrical NerveStimulation. Recently, a wristband-type device for transcutaneous electri-cal nerve stimulation, the ReliefBand,was approved by the Food and DrugAdministration as an over-the-count-er device. It is also based on the prin-ciples of acupressure and is applied atthe P6 acupressure point. Use of theReliefBand has provided significantrelief from nausea and vomitingamong cancer patients.26,27

Relaxation. In relaxation training,patients are instructed to relax mus-cles in order to decrease the tensionof the muscles. Patients should beencouraged to take slow deepbreaths; the attention to breathingserves as a distraction. In postopera-

lessness and excitement when givenprochlorperazine.1

NonpharmacologicalManagement Dietary Management

The traditional dietary approachto postoperative management is toprovide nothing by mouth and touse a nasogastric tube for gastricdecompression to prevent nausea.Once bowel sounds resume, the tubeis removed, a clear liquid diet isintroduced, and the diet is graduallyadvanced as tolerated. Although thisapproach is commonly practiced,use of this regimen is not supportedby published reports. Jeffrey et al22

challenged this traditionalapproach; they found no differencein postoperative nausea and vomit-ing in patients receiving a clear liq-uid diet compared with patientsreceiving a regular diet as the firstpostoperative meal. Other dietarymodes of decreasing nausea are eat-ing bland foods such as dry toast orcrackers and drinking carbonatedbeverages such as ginger ale.2

Alternative/Complementary and Behavioral Therapy

Although medications are thefirst-line treatment for nausea andvomiting, the use of alternative orcomplementary measures asadjuncts may improve patients’ out-comes and help reduce costs.

Acupressure/Acupuncture.Acupressure originated in China. It isbased on the principle of qi or chi, theenergy present in living organisms.When the flow of qi is stagnant, thephysical condition is affected. Theapplication of pressure to specificpoints on the body unblocks abnor-mal energy flow and relieves signs




tive nausea and vomiting, this tech-nique also helps the body rid itself ofany residual anesthetic agent.2

Imagery training involves using men-tal processes that increase relaxation,such as recalling pleasant memoriesand imaging positive thoughts.Relaxation and imagery can be usedtogether or separately. Therapeutictouch can also be used as a comfortmeasure.2 These techniques are effec-tive for treating nausea and vomiting,pain, and insomnia.28

Music. Ezzone et al29 concludedthat music has a beneficial effect onnausea and vomiting. Musicdecreases the intensity of nauseaand vomiting among cancerpatients, when it is used with phar-macological antiemetic treatment.

Herbs. The use of herbs to treatnausea and vomiting is controver-sial. In one study,2 ginger root wasmore effective than placebo fortreatment of postoperative nauseaand vomiting. However, Ernest andPittler30 reviewed 6 studies on theeffect of ginger to treat nausea andvomiting and concluded that gingermay or may not be effective for post-operative nausea; ginger did appearto reduce the occurrence of nausearelated to seasickness, morning sick-ness, and chemotherapy. Dried gin-ger in capsules has been used totreat car sickness in animals.

Aromatherapy. The use of aro-matherapy is also controversialbecause its scientific effectivenessand safety have not been estab-

lished. Tate31 studied the use of pep-permint oil for postoperative nau-sea. Peppermint oil with a relativelyhigh content of menthol was smelledby an experimental group ofpatients who underwent gynecologicsurgery. Although the results werenot statistically significant, theexperimental group had a lowerprevalence and/or intensity of nau-sea after surgery, less requirementfor antiemetics, and more toleranceto analgesia, which usually causesnausea, than the control group did.

Abdominal Implant. The Foodand Drug Administration recentlygranted humanitarian device exemp-tion approval for an implantable sys-tem (Enterra, Medtronic Inc,Minneapolis, Minn) for the treat-




er intervention in the prophylaxisfor and therefore the control of theseeffects. Even though anesthesiolo-gists routinely screen patients preop-eratively to determine which arehigh-risk patients, this informationmust be communicated to the criti-cal care nurses caring for thepatients in order to optimizepatients’ care. It may be helpful toknow, for example, that patientswith a history of motion sicknessmay be more susceptible to move-ment-induced postoperative nauseaand vomiting.2 Care can then betaken to ensure slow and smoothmovements in transferring and turn-ing a patient who has such a history.Consideration should be given toadministering antiemetics on a

communication, November 7, 2001).The device is externally pro-grammed in a fashion similar to thatused with cardiac pacemakers.32

Implications for Critical Care Nursing

Critical care nurses are responsi-ble for assessing the causes of nauseaand vomiting, administering appro-priate antiemetic agents, evaluatingthe effects of the agents, and provid-ing information to physicians whenchanges in treatment are indicated.Antiemetic agents are most usefulwhen given prophylactically; it ismuch easier to prevent signs andsymptoms than to control them.Identification of patients at high riskfor nausea and vomiting allows earli-

ment of chronic, intractable nauseaand vomiting due to gastroparesis ofdiabetic or idiopathic origin. Thedevice consists of 2 leads with elec-trodes that are implanted in theantrum of the stomach and connect-ed to a pulse generator that is surgi-cally placed in the lower part of theabdomen. The system is pro-grammed to deliver low-frequency,low-amplitude electrical pulses con-tinuously to the stomach muscle.Although the exact mechanism forthe suppression of nausea is notknown, it is thought that the effect isdue to the neurostimulation of cen-tral vagal afferent nerve pathways,not by enhanced gastric emptying aspreviously thought (W. L.Starkebaum, Medtronic, Inc, oral


Circle number 128 on Reader Service Card



Vomiting can also cause dehydra-tion, leading to fluid and electrolyteimbalance. Fluid and electrolyte levelsmust be assessed and the fluids andelectrolytes replaced accordingly.Nausea, headache, and oliguria arecommon indications of hyponatrem-ia, which can cause cerebral edemaand death if untreated. Hypercalcemiacan cause nausea and vomiting.Hypokalemia and life-threatening dys-rhythmias can result from loss of elec-trolytes due to vomiting.

Neurological causes should alsobe considered. Increased intracra-nial pressure can cause refractorynausea, and some brain tumorscause vomiting without nausea.Nausea and vomiting cause anincrease in intracranial pressure andcan be life threatening in a patientwith brain injury. Vomiting must beavoided in patients with suspectedaneurysms in order to prevent sub-arachnoid hemorrhage. In patientswith spinal cord trauma, the move-ments associated with vomiting cancause further injury to the spinalcord. Nausea and vomiting occurfrequently after craniotomy.Antiemetic therapy may cause seda-tion, making postoperative neuro-logical assessment difficult.

Disruption of the surgical siteduring vomiting can cause excessbleeding, a possible need for return tosurgery, increased morbidity,increased scarring, and prolongedrecovery time. Such disruption can beespecially dangerous after eye, neck,or facial surgery. The explosive pres-sure generated during vomiting candislodge indwelling tubes or wires,particularly those that are strategical-ly placed, such as drains used todiminish intracranial pressure, car-diac pacing wires, and chest tubes.


increased in a patient with acutecoronary syndrome exacerbated bynausea and vomiting.

The pulmonary system shouldbe assessed for indications of pul-monary aspiration, especially inpatients receiving tube feedings.Nosocomial pneumonia can becaused by aspiration of oropharyn-geal secretions or gastric contentsinto the lungs. Preventive measuressuch as elevating the head of thebed, ensuring that bowel sounds arepresent, and routinely checking

residual feeding volumes may helpprevent pulmonary aspiration.

The gastrointestinal systemshould be assessed for abdominaldistention, organomegaly, and pres-ence of bowel sounds. Signs of hypo-motility may suggest an increasedrisk for nausea and vomiting.Postprandial nausea and vomitingassociated with bloating and satietysuggest a gastrointestinal cause.6

Nausea and vomiting can be indica-tions of as well as complications ofacute pancreatitis.

Nausea that occurs primarilywith movement can be assumed tobe generated by impulses from thevestibular center.6 Because strongodors can cause or exacerbate nauseaand vomiting, especially postopera-tively, exposure to odors from nearbyfood, strong perfume, and cleaningsolutions should be minimized.2

scheduled basis, rather than as need-ed, for patients at high risk for post-operative nausea and vomiting.2

Causes and AssessmentPatients should be assessed for

pain, including postoperative pain,and should be treated promptly toprevent associated nausea and vom-iting. Suspected opioid-induced nau-sea may be evaluated bydetermining the temporal relation-ship between the time the opioidwas given and the onset of nausea.6

A careful systems assessment shouldbe done, with all possible causesinvestigated before nausea and vom-iting are automatically labeled asopioid induced.6

The cardiovascular system shouldbe assessed for hypotension due tohemodynamic compromise. Nauseamay be the first symptom ofhypotension. Hemodynamic sources(increased or decreased heart rate,decreased preload, increased after-load, or decreased contractility)should be investigated.Postoperatively, hypotension may bedue to the restriction of fluids preop-eratively, intraoperative blood loss,and the use of anesthetics, analgesics,and sedatives.2 Vagal maneuverscaused by retching and vomiting, asoccur in inferior myocardial infarc-tion, can cause bradycardia.Myocardial oxygen demand may be

Although medications are the first-linetreatment for nausea and vomiting, the useof alternative or complementary measures. . . may improve patients’ outcomes. . .



Medications should be evaluatedfor their emetogenic potential.Common offenders are chemothera-peutic agents, opioids, nonsteroidalanti-inflammatory drugs, antibi-otics, and selective serotonin reup-take inhibitors. Assessment ofnausea and vomiting should includedetermination of the severity, dura-tion, and number of episodes. Avisual analog scale can be used tomeasure the severity of nausea, witha scale of 1 to 10, similar to thatused as a pain scale.1,10

Prevention and TreatmentThe prevention and treatment of

nausea and vomiting will becomeeven more of a healthcare concernas hospitals are required to makethe most efficient use of availableresources, decrease the frequency ofcomplications, and decreasepatients’ lengths of stay.1

Traditional, convenient, cost-effec-tive approaches to the preventionand treatment of nausea and vomit-ing in the intensive care unit includethe use of nasogastric tubes for gas-tric decompression and the use ofphenothiazines or metoclopramideas antiemetics. This regimen maystill be effective for most patients.However, the lack of efficacy and theadverse effects (sedation, hypoten-sion) of these drugs may limit theiruse. The most recently publishedMayo Clinic guidelines no longerrecommend metoclopramidebecause of the increased occurrenceof restlessness, agitation, insomnia,and drowsiness associated with useof this drug.4 Also, patients may notrespond to the initially prescribedtherapy. If no response occurs, thenan agent from another pharmaco-logical class should be added, the


Case Study

S.W. is a 68-year-old man whowas brought to the emergencydepartment with a severeheadache, nausea, and right-sidedweakness. A computed tomogramof the head revealed a rupturedcerebral aneurysm that was thensurgically repaired. He returned tothe neurological intensive care unitwith an external ventricular drainin place and an intracranial pres-sure measurement of 5 mm Hg. Hisvital signs, electrocardiographicrhythm, and oxygen saturationwere stable. He has a history ofcolon cancer and had a right hemi-colectomy 4 months ago. This sur-gery was followed by chemotherapywith 5-fluorouracil and leucovorin.His last chemotherapy was 1 weekago. He has had moderate to severenausea and vomiting and has beentaking ondansetron (Zofran) 8 mgby mouth twice a day at home. Healso has been taking prochlorper-azine (Compazine) 10 mg by mouthbefore each meal. Laboratory dataindicate normal liver and kidneyfunction. S.W. has nausea after hisaneurysm surgery. Promethazine(Phenergan) 12.5 mg intravenouslyis ordered to be administered every4 to 6 hours as needed.

Questions1. After S.W. receives 2 doses of

promethazine, he is sleepy but stillhas persistent unrelieved nausea.Which of the following are appro-priate actions for the critical carenurse to take?

a. Give another dose of promet-hazine.

b. Report to the physician thatpromethazine does not relieve thepatient’s nausea and vomiting.

c. Check the external ventriculardrain to ensure proper functioning.

d. Review the patient’s medica-tion administration record to see ifany medication may be contribut-ing to his nausea and vomiting.

e. Assess the patient’s serumlevel of sodium.

2. S.W. is receiving morphineintravenously as needed for pain.His oncologist was consulted for hisuncontrolled nausea and vomiting.The oncologist orderedondansetron on a scheduled basis,and prochlorperazine andlorazepam (Ativan) on an as-need-ed basis. What is the rationale forthis order?

a. Ondansetron is indicated inpostoperative nausea and vomitingwhen other antiemetics are ineffec-tive; it is imperative to keep theintracranial pressure controlledafter craniotomy.

b. Ondansetron can preventopioid-induced nausea.

c. Ondansetron is less sedatingthan promethazine; it will not maskthe neurological assessment.

d. Ondansetron is a serotoninreceptor antagonist, which pre-vents stimulation of the vomitingcenter. Prochlorperazine blocksdopamine receptors in thechemoreceptor trigger zone andalso inhibits stimulation (such as



dose of the antiemetic should beincreased to the maximum withinan acceptable range, or both.1,9 Thisadjustment may require expansionof the use of serotonin receptorantagonists in critical care.

Published views are conflictingabout how much patients’ satisfac-tion should influence the choice ofagent and override the cost con-cerns. If a drug is more expensivebut it prevents complications anddecreases length of stay, it wouldseem to be worth the extra cost inthe final analysis. More studies onthe economics are needed to helpweigh the cost-benefit issue.

Understanding the pathophysi-ology of nausea and vomiting willallow critical care nurses to assist inmaking appropriate decisions toprevent and treat these responses.Nonpharmacological methodsshould be considered as comple-mentary therapy. Complete control,defined as no nausea or vomiting,should be the goal for every patient.

AcknowledgmentsParts of this article were previously published as asynopsis in the Oncology Nursing Society CriticalCare Special Interest Group Newsletter, Vol 10, Issue2, August 2001.We thank Dr Cynthia Chernecky, our faculty andmentor, for her inspiration, guidance, and sup-port in writing this article. We appreciate thecomments of our manuscript reviewers, as well assuggestions from Dr Mark Stewart, anesthesiolo-gist, Dr Sandra Counts and Michael Madden,clinical pharmacists, and Dr Cynthia Chernecky,professor and oncology clinician. We also thankShogo Tsuruta for his expert computer skills incompiling our pharmacology table.

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macological management of nausea andvomiting in adult and pediatric patientsreceiving chemotherapy or radiation thera-py or undergoing surgery. Am J Health SystPharm. 1999;56:729-764. Also available at:www.ashp.org/bestpractices. AccessedDecember 3, 2002.

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caused by odors and pain) to thevomiting center. Lorazepam is indi-cated in anticipatory nausea.

3. On the third postoperativeday, S.W.’s nausea and vomitinghave been well controlled, and hecan tolerate oral intake. However,he complains that he has nauseawhenever a nurse brings a bag ofintravenous solution into his roombecause it reminds him of hischemotherapy. Which antiemeticis the best choice for this type ofnausea?

a. prochlorperazine 10 mg bymouth

b. ondansetron 8 mg by mouthc. lorazepam 1 mg by mouthd. promethazine 12.5 mg intra-

venously

Answers1. b, c, d, and eWhen an antiemetic is ineffec-

tive, other types of drugs should beconsidered. Other possible causesof nausea should be assessed. Theseinclude medical history ofchemotherapy, postoperative con-dition, possible increased intracra-nial pressure, and use of opioids forpain management. Also, nauseacan be a symptom of hyponatrem-ia, which can increase cerebraledema.

2. a, b, c, and dAfter a craniotomy, it is impor-

tant to prevent nausea and vomit-ing that could increase intracranial

pressure. Administration ofantiemetics should therefore bescheduled, not strictly ordered onan as needed basis. Ondansetron iseffective in opioid-induced nauseaand will not cause sedation, whichcould mask the neurological assess-ment. Administration of prochlor-perazine as needed will help inbreakthrough nausea evoked bystimulation of the vomiting centerdirectly. Lorazepam is effective foranticipatory nausea and vomiting.

3. cLorazepam reduces anticipatory

nausea. Oral antiemetics are just aseffective and more cost-effectivethan are parenteral antiemetics.Ondansetron is expensive andshould not be used indiscriminately.



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CE Test Form

Managing Nausea and Vomiting: Current StrategiesObjectives:

1. Discuss the mechanisms of nausea and vomiting2. Identify preoperative and postoperative factors that influence the development of nausea and vomiting3. Describe treatment options for nausea and vomiting

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7. Serotonin receptor antagonists are the drugs ofchoice in patients receiving chemotherapeuticagents with what emetic potential?a. 0 to 1b. 1 to 2c. 2 to 4d. 3 to 5

8. Which antiemetic agent is indicated in refractorychemotherapy-induced nausea and vomitingunresponsive to other classes of agents?’a. Ondansetronb. Granisetronc. Dolasetrond. Dronabinol

9. Postoperative nausea and vomiting occurs inwhat 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 associatedwith increased risk of nausea and vomiting?a. Atropineb. Propofolc. Ketamined. Droperidol

11. Which of the following is associated withdecreased occurrence of postoperative nauseaand vomiting?a. Opioid useb. Supplemental oxygenc. Positive pressure ventilationd. General anesthesia

12. How much does adequate pain relief reduce theoccurrence of nausea?a. 20%b. 40%c. 60%d. 80%

1. Where is the vomiting center located?a. Hypothalamusb. Caudate nucleusc. Medulla oblongatad. Cerebellum

2. Which of the following is not a neurotransmitterthat can relay impulses to the vomiting center?a. Serotoninb. Dopaminec. Histamined. Neurotensin

3. Which antagonist blocks acetylcholine receptors?a. Dopamineb. Muscarinicc. Histamined. Serotonin

4. What emetic potential rating of chemotherapeuticagents indicates the least potential?a. 0b. 1c. 5d. 10

5. What is an example of a chemotherapeutic agentwith the highest emetic potential?a. Cisplatinb. Vincristinec. Carboplatind. Doxorubicin

6. Which of the following chemotherapeutic agentsis not associated with delayed nausea?a. Cisplatinb. Vincristinec. Carboplatind. Cyclophosphamide

CE Test QuestionsManaging Nausea and Vomiting: Current Strategies



Crit Care Nurse 2003 Garrett 31 50

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