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Cancer-RelatedPain
Cancer-related pain is associated with malignancy and can result from the disease itself, disease
treatments, or damage to secondary tissue. Disease-induced pain may be secondary to direct tumor
involvementofbone,nerves, viscera,or softtissue.Inaddition,muscle spasm,muscleimbalance,and
otherbodystructure/functionchangessecondarytothetumorareconsidereddiseaseinduced.Painmaybe
associatedwithtreatmentofthediseaseandmaybeseenwithbiopsies,surgeries,and/orchemotherapy
andradiationtreatments.Painmaybe presentinsiteswhere cancerhas metastasized(i.e., bonepain).
Cancer treatment interventions may activate peripheral nociceptors, causing somatic and visceral
nociceptive pain. Neuropathic pain involving the sympathetic nervous system may also be seen. In
metastaticcancer,opioidsarethemainstayoftreatmentforseverepain.Nonsteroidalagentsorsteroids
maybeanadditionaloptionforpaincontrol,especiallywhenbonymetastasisarepresent.
BreakthroughPain
Breakthroughpain (BTP) isdefinedas a transitorydiscomfortoftenseeninconjunctionwithcancerrelated pain, where moderate to severe pain occurs in patients with an otherwise well-controlled
analgesic baseline.TrueBTPis characterizedasbrief,lastingminutestohours, andcaninterfere with
functioningandqualityoflife.TrueBTPhashistoricallybeenassociatedwithacancerdiagnosisbutmay
alsobeseeninotherchronicpainconditions,suchasneuropathicpainandchroniclowerbackpain.
Other typesofBTPincludepaincausedbycertainactivities(incidentpain)or whenthedurationof
analgesia is less thanthedosing interval (end-of-dose failure). Giving ananalgesic prior to the event
knowntocausepainwilloftenallowtheactivitytobeperformedwithminimaldiscomforttothepatient.
Shorteningthedosingintervalisrecommendedinpatientswithend-of-dosefailure.
PAINPATHOPHYSIOLOGY
Severaltheoriesexistas tohowinformationresultingfromtissuedamageis perceived bythebrainas
pain.Noxiousstimulifromthepointoftheinitialinjurymovethroughspecializednervefiberswithinthe
CNS,wherethesignalreachesthebrainandisinterpretedaspain.ThistransmissionthroughtheCNSis
termednociception. Freenerve endingsof small myelinatedA-deltafibersandlarger unmyelinated C
fibersarecallednociceptorsandareresponsiblefordeliveringsignalstothebrain.Inthepast,thegate
controltheoryproposedthatthe“closingofthegate”topainsignalswasaccomplishedprimarilythrough
stoppingthetransmissionofthepainsignaltothebrain.However,recentstudiestheorizethatchangesin
thebrain andtheCNS haveamuchlarger role inthe facilitation andperceptionofpain (Woo etal.,
2015).Anxiety,fear,depression,andpreviouspainexperiencesmayinfluenceanindividual’sperception
ofpain,especiallywhenpainbecomeschronic.
A description of nociception can be divided into four main categories: transduction, transmission,
perception,andmodulation(Figure9.1).
Transduction
Transductionreferstoaprocessofnociceptoractivationduetomechanical,thermal,orchemicalinjury.
Nerveendingsareactivatedthroughthereleaseofvariousexcitatorychemicalneurotransmitters,suchas
proinflammatorycytokines,prostaglandins(PGs),substanceP,histamine,bradykinin,andserotonin.
Transmission
Transduction results in an action potential transmitted via the myelinated A-deltaand unmyelinatedC
fibers,bywayofthedorsal rootganglia,synapsinginthedorsalhornofthespinalcord.Second-order
neuronsarethenactivatedandconveypainsignalstothehighercentersoftheCNS.Neurotransmittersin
the dorsal horn directly or indirectly depolarizethesecond-order neurons, facilitatingtransmission of
informationtothebrain,leadingtotheperceptionofpain.Inhibitorysubstancesarealsoreleasedinthe
dorsal horn (see the section titled Modulation that follows) and may decrease the number of signals
reachingthebrain,therebylesseningtransmission.
Perception
Nociceptive information travels through different areas of the CNS to the brain, where the pain is
perceived. Perception is the end result of the nociceptive transmission to the brain; at this point,we
becomeconsciouslyawareofdiscomfort.Painperceptionisnotjustamanifestationofphysicalinjurybut
is affected by psychosocial factors and previous painful experiences. In a chronic pain state, the
perceptionof pain is no longer influenced bythe initial noxiousstimuli. The presence of psychologic
comorbiditiesinmanypatientswithchronicpainmayresultinfearofthepainandpaincatastrophizing,
therebyincreasingitsperception.
FIGURE9-1Acuteandchronicpainpathophysiology.ReprintedwithpermissionfromWhitten,C.E.,
Donovan, M., & Cristobal, K. (2005). Treating chronic pain: New knowledge, more choices. The
PermanenteJournal,9(4),9-18. Retrieved fromhttp://www.thepermanentejournal.org.Copyright2005
ThePermanenteJournal.
Modulation
PainmodulationoccursatvariouslevelsoftheCNS.Endogenousopioidsworkthroughbindingtoopioid
receptors in both the peripheral and CNS. The main central inhibitory neurotransmitters involved in
modulation are serotonin and norepinephrine. These neurotransmitters fight pain by increasing their
concentrationinthespinalcordandbrainstem.
Pain-ModulatingReceptors
Historically,painmodulationwasthoughttobeprimarilyduetodescendinginhibitoryinformationfrom
the brain. Experts now theorize that both descending inhibitory pain pathways and inhibitory
neurotransmittersdecreasetheperceptionofpain.Inhibitorysubstances,suchasendogenousopioids,norepinephrine,andserotoninarereleasedinvariousareasoftheCNSandattenuatethetransmissionofpain
bymodulatingthesignalsinthedorsalhorn(Pasero&McCaffrey,2011).Endogenousopioidsubstances,
primarily beta endorphins, stimulate inhibitory neuronal receptors known as the opioid receptors.
Stimulation of these receptors, particularly the mu opioid receptor, inhibits the transmission of pain
signals to and from the higher brain centers. These receptors are stimulated by morphine-like drugs
(opioids)andaccountforagreatdealofthepainreliefassociatedwiththisclassofanalgesics.
In contrast, neuropathic pain syndromes do not respond as well to conventional analgesic therapy.
Neuropathicpainisoftentheresultofperipheralandcentralsensitizationorfromactualnervedamage.
Sensitization of the N-methyl-D-aspartic acid (NMDA) receptors by various mechanisms is primarily
responsibleforthistypeofpain.Useofcoanalgesicagents,suchasantidepressants,anticonvulsants,and
antiarrhythmicagents,isrecommendedfortreatment.Detailsontheuseofcoanalgesicsarefoundlaterin
thischapter.
Moreinformationis beingassimilatedontheendocannabinoidsystemandpaincontrol.Cannabinoid
receptor activationmayfacilitateanalgesia byinhibitionofexcitatoryneurotransmitters ina retrograde
fashion,therebyattenuatingthehyperalgesicandinflammatorycomponentsofpain.See Chapter11, on
cannabinoidsandpain,formoreinformation.
CHEMICALMEDIATORS
Coupledwiththeneuronalcomponentofpainisthereleaseofchemicalmediatorsinitiatingorcontinuing
the stimulation of pain-conducting fibers. Peripheral chemical mediators include the neurotransmitters
norepinephrine, serotonin, and histamine and polypeptides such as bradykinin, PGs, and substance P.
Neurotransmittersmaybebothexcitatoryandinhibitory,dependingonthesiteofactivityintheCNS.The
role of excitatory neurotransmitters in the pain pathway is activating and sensitizing nociceptors and
increasing neuronal activity. Blocking the production of these mediators, particularly inhibiting the
production of PGs with antiinflammatory medications or similar compounds, minimizes nociceptor
activationandneuronal firing,therebylesseningthetransmissionof painthroughthe CNS.Becauseof
theirroleininitiatingthepainpathway,thesechemicalsaretargetsformanyofthemedicationscurrently
availabletotreatpain.
Bothexcitatory andinhibitoryneurotransmitters canbe found in the dorsal horn of the spinal cord.
Excitatoryaminoacids, glutamateandaspartate,alongwithsubstancePfacilitateactivationofsecondorderneuronsinthedorsalhornprimarilythroughactivationoftheNMDAreceptors.
Natural endocannabinoids may also play a role in inhibition of pain. Anandamide and 2arachidonoylglycerolarethemainnatural endocannabinoidsthatelicitanalgesiathroughmodulationof
painsignaling,perception,andmood(seealsoChapter11).
PERIPHERALANDCENTRALSENSITIZATION
Often,painpersistsdespitehealing,andnobiomedicalexplanationcanbefound.Painpathwaysbecome
“broken,”andpainisexperiencedwithoutanobviouscause.Modificationsoccurringinthenociceptive
conductionpathwaysoftheperipheralnervoussystemandCNS,wherehypersensitivitytoastimulusand
neuronalstructuralchangesresultinchronicpainsyndromes,arereferredtoasperipheralsensitization
andcentralsensitization.
PeripheralSensitization
Whenpainreceptorsintheperipheryarecontinuallystimulated(i.e.,untreatedacutepain),thethreshold
for stimulation becomes lowered and increased nerve firing occurs. Nociceptive neurons become
hypersensitizedthroughactivationofvariousproteinkinasesandmodulationofionchannels.Increased
frequency of nerve impulses result in more pain signals reaching the dorsal horn of the spinal cord.
Release of excitatory neurotransmitters is also increased, producing neuronal hyperexitabiltiy that
contributestothedevelopmentofcentralsensitization.
CentralSensitization
Centralsensitizationisdefinedas“anamplificationofneuralsignalingwithintheCNSthatelicitspain
hypersensitivity”(Woolf,2011,p.4).Whennociceptiveinformationrepeatedlystimulatesnervefibers,
increaseddorsalhornneuronalactivityis seen.Withactualorpotentialnervedamage,asseeninmany
cases ofuncontrolledpain,theincrease infiringleadstoanincreased excitabilityandresponsiveness,
termedcentralsensitization.Neuroinflammationoftheperipheral nervoussystem andtheCNSis now
thought to play a major role in the transition from acute to chronic pain. Characteristics of
neuroinflammationincludeproductionofinflammatorycytocines,infiltrationofleukocytesintotheCNS,
andactivation of various protein kinases andglial cells. The endresult is a decrease ofcentralpain
inhibition,increasedspontaneousneuronalactivityinthedorsalhorn,adecreasedthresholdforneuronal
firing,andspreadofpainsensitivityinareasnotaffectedbytheinitialinsult.SensitizationoftheNMDA
receptorintheareaofthedorsalhornalsocontributestocentralsensitization.Allodynia(painresponse
tosomethingpainless), hyperalgesia(increased responsetopain),persistentpain,orreferredpainmay
result.
Central sensitization can occur in manychronic pain states, especially when associated with nerve
injury or dysfunction. Factors associated with the development of sensitized pain include inadequate
treatmentofacutepain,concomitantpsychologicalcomorbidities,andpoorcopingskills,leadingtothe
developmentofchronicpainthroughthesensitizationoftheCNS.Evidenceisaccumulatingontheroleof
neuroinflammation in patients with chronic overlapping pain conditions, caused by dysregulation of
sensory, inflammatory, and psychological pathways. Examples include but are not limited to patients
sufferingwithfibromyalgia,headache,andirritablebowelsyndrome,wheremultiplefactorscontributeto
thechronicityofpain(Ru-Rongetal.,2018). Painassociatedwithcentralsensitizationoftenresponds
poorlyto traditional therapies.Theadditionofcoanalgesics, reviewed later inthis chapter,should be
consideredforthetreatmentofchronicpainassociatedwithcentralsensitization.
GENERALPRINCIPLESOFPAINMANAGEMENT
Treatment of pain in today’s society rests on three major principles: appropriate assessment of the
severityandintensityofthepain,selectionof themostappropriateagentto relieve painwithminimal
sideeffects,andassessmentforrisksofmisuseorabuse.Painrelief,especiallywithchronicpain,often
requiresamultimodalapproach,usingmultipleagentsthattargetdifferentreceptorsandneurotransmitters
intheCNS.Non-opioid-basedpainmodalitiesshouldbeutilizedinitiallyfortreatment.Additionalmind–
bodyapproachessuchascognitive–behavioraltherapy,massage,acupuncture,andmindfulmeditationare
oftenrecommendedto be usedinadditionto pharmacologic therapyinpatients sufferingfromchronic
nonmalignant pain. Prior to initiation of opioid therapy, assessment for risk of abuse/misuse and
appropriatemonitoringshouldbeestablished.
PainAssessment
Theindividual assessmentofpainisextremelyimportantfor determiningpropertreatmentsas well as
monitoringeffectivenessovertime.AccordingtotheNationalInstitutesofHealth(NIH),self-reportingby
patientsis“themostreliableindicatoroftheexistenceandintensityofpain”(Hootenetal.,2013,p.14).
Along with self-reporting, involving the caregiver’s assessment, especially in the very young or
noncommunicatingolderpatient,maybehelpful.Theself-reportshouldincludeadescriptionofthepain,
location, intensity/severity, aggravating and relieving factors, and effect of pain on quality of life.
Assessment tools are recommended to be brief and easy to use in order to reliably document pain
intensityandpainrelief.Varioustools, especiallythoseused inchronic pain,willalso evaluateother
factors that may facilitate pain perception, such as the presence of psychological comorbidities. One
routineclinicalapproachtopainassessmentandmanagementissummarizedbythemnemonicPQRSTU
(Box 9.2). Assessment tools should be used initially to obtain a baselinelevel of pain and impaired
function.Follow-upassessmentsshould be performedto measuretheprogress towardacceptablepain
reliefbasedontheindividualfunctionalgoalsofthepatient.
Becausepainissubjectiveandisnoteasilyquantifiable,severaltoolsareavailabletodeterminethe
quantity and quality of a patient’s pain. The various pain scales can be classified as single or
multidimensionalandself-reportor observational.Commonsingle-dimensionaltools includethevisual
analogscale(VAS),numericalratingscale(NRS),andverbaldescriptionscale(Figure9.2).Thesingle-
dimensionalscalesevaluatepainintensity.However,single-dimensionalscalesdonottakeintoaccount
function, which may be a more reliable indicator of pain control. Multidimensional scales consider
location, pattern, and affective responses in addition to a severity score alone. Examples of
multidimensionalscalesincludetheBriefPainInventoryandtheInitialPainAssessmentTool(Pasero&
McCaffrey,2011).
FIGURE9-2Visualanalogscaleusedforrankingpain.UsedwithpermissionfromWong-BakerFACES
Foundation(2019).
Box9.2 PQRSTUMnemonicforAssessingPain
P—Presenting,precipitating,palliating.Whenandhowdidthepainstart?Whatmakesthepainbetter?
Whathaveyouusedforpaininthepastthatwasn’teffective?
Q—Qualityofthepain.Whatdoesthepainfeellike?(descriptorssuchassharp,stabbing,burning)
R—Region,radiation.Whereisthepain?Doesthepainstayinonelocationordoesthepainradiate?
S—Severity.Onascaleof0to10,0beingnopain,10beingtheworstpainimaginable,whatisyour
painnow?Inthelast24hours?Afterapainmedication?
T—Temporalpattern.Isthepainconstant,intermittent,associatedwithmovement?
U—Howdoesthepainaffectyou?Quality-of-lifeindicator.
Theinformationobtained,particularlyfromtheNRSandVAS,ishelpfulindeterminingappropriate
treatmentand drug selection. The Institute for ClinicalSystemsImprovement(ICSI), the NIH,and the
CDChavepublishedguidelinesontheappropriateevaluationandtreatmentofacuteandchronicpain.
Acutepainisrecommendedtobeassessedwitha0-to-10scaletodetermineapatient’scurrentlevelof
discomfort.Zerodefinesapain-free state,and a 10 describes themostsevere painimaginable bythe
patient.Painratedat1to3isclassifiedasmild;4to6isclassifiedasmoderate;and7to10isclassified
assevere(Jensenetal.,2001).Othervalidatedscalesareavailableforuseinspecialpopulations,such
asinchildrenandadultsunabletoself-report.
New assessmentscales are being evaluated for assessmentof chronic pain. Acutepain iseasier to
assessviaavailable validatedtools.Chronic painisoftendrivenbymaladaptivethoughtprocesses in
patientswithcomorbidanxietyanddepression.Functionalcapacityisoftenlimited;therefore,inapatient
withchronicpain,functionalimprovementisabetterindicatorofsuccessfultreatmentthanascorefroma
single-dimensionaltool.Anxietyanddepressionareoftenpresentinpatientswithchronicpainandmay
limittheirabilitytocopewithpain,therebyfurtheraffectingfunction.TheIndianaPolyclinicCombined
PainScale,developedin2005,isafour-partassessmenttoolthattakesintoaccountpainscore,function,
depression,andanxietywhenevaluatingchronicpain(Arbuck&Fleming,2019).Eachofthefourscales
offerbothdescriptionsandassociatednumericratingsfortheareaofevaluationandmaybeofvaluefor
use in patients with chronic pain to better determine a successful treatment regimen. Further studyis
neededtovalidatethescalewhencomparedtocurrentlyutilizedassessmenttools.Subsequentmonitoring
should evaluate the effectiveness of the treatment plan. If pain remains uncontrolled, determine if the
reasonforincreasedpainisrelatedtotheprogressionofdisease,diseasetreatments,oranewcause,as
incancerthathasmetastasized.Unrelievedpainmayalsobeduetothedevelopmentofopioidtolerance,
wherethesameamountofpainrequiresincreasingdosesofopioidsinordertoproviderelief.Inchronic
pain,untreatedpsychologicalcomorbiditiesandunrealisticexpectationsareoftenthecauseofpoorpain
control and should be addressed in conjunction with medication management. The assessment of the
patient’s painandtheefficacyof thetreatmentplanshould be ongoing,andthepainreportsshould be
documented. Continueduse of the samepainscale is crucial to the continuedassessmentoftreatment
progressandcommunicationbetweenhealthcareproviders.
PainManagement
Treatmentoptionsforpaincontrolincludenonpharmacologicandpharmacologictherapies.Box9.3lists
treatments that complement medication management of pain. Often, a multimodal, multidisciplinary
approachusinga combinationof bothpharmacologicandnonpharmacologictreatmentsisnecessaryto
reduce pain to an acceptable level and provide an improvement in function, especially when opioid
therapies are used.Maximizingthepatient’squalityoflifeandfunction,while minimizingthe adverse
effectsoftreatments,isthegoalofthetreatmentplan.Individualizationofdrugregimensaccordingtothe
type and severity of pain is essential when using medications tomanage both acuteand chronic pain
states.
Box9.3 AdiunctivePainContro1Options
Acupuncture
Cognitive-behavioraltherapyCopingskillstrainingMassage
Mindfulmeditation
Patienteducation(therapeuticneuroscienceeducation)
Physicalmethods(stretching,exercise,gaittraining,immobilization,hotorcoldapplications)
Transcutaneouselectricalnervestimulation
For mild to moderate pain, acetaminophen, nonsteroidal antiinflammatory agents (NSAIDs), and/or
topicalanalgesicsarerecommendedforinitialtherapy.Acetaminophenisusedformildpainacrossall
agegroups,mainlyduetoitsfavorablesideeffectprofile.NSAIDsareveryeffectiveinpainassociated
withinflammation.However,patientsmaybeatriskforgastrointestinal(GI),cardiac,orrenaltoxicities.
DiscussionofriskversusbenefitsofNSAIDtherapiesarediscussedlaterinthischapter.
For pain assessed as moderate to severe, opioid agonists either alone or in combination with
acetaminophen or ibuprofen can be used. Around the clock (ATC) acetaminophen and NSAIDs can
provide non-opioid choices for persistentpain in conjunction withas-needed opioid therapyandmay
reducetheneedforopioidsasthemaintreatmentoptionwhenpainismoderatetosevere.Combination
opioids,suchasoxycodoneorhydrocodoneinconjunctionwithacetaminophenoribuprofen,canalsobe
usedinpatientswherepainisintermittent.
Morphine, hydromorphone, oxycodone, oxymorphone, andfentanyl are examples of pure mu opioid
agonists. Moderate to severe pain can be treated with low-dose opioids when a patient has
contraindications to NSAIDs or acetaminophen or when these agents arebeing usedaroundtheclock.
Opioidsmaybecombinedwithothercoanalgesicmedicationsbasedonseverity,description,andtypeof
pain.Thecombinationofanopioidandnon-opioid and/or coanalgesic medicationsmayprovidemore
paincontrolthanutilizingasinglemodalityagentforanalgesia.
When developing a treatment plan, members of the health care team should take into account the
preferencesandneedsofpatientswhoseeducationorculturaltraditionsmayimpedeeffectivetreatment.
Certain cultures have strong beliefs about pain and its management. Members of these cultures may
hesitate to report unrelieved pain or may have alternative methods of treatment.Clinicians should be
awareoftheuniqueneedsandcircumstancesofpatientsfromdifferentagegroupsorvariousethnicand
cultural backgrounds. In addition, the current environment of the opioid crisis has increased fear and
stigma surrounding opioid use for persistent pain, especially when not related to cancer. Patient and
provider education may be effective in addressingcultural concerns and alleviatingbiases associated
withopioidtherapies.
Pharmacologic treatmentis themostcommonmodalityinpaincontrol. However,nonpharmacologic
options and therapies have been shown to be effective, especially in patients with chronic pain.
Nonpharmacologic approaches include the use of therapies such as heat,cold, exercise, and physical
therapy.Transcutaneouselectricalnervestimulationtherapyandimplantablespinalcordstimulatorsare
recommendedtobeusedfortreatmentofcertaintypes ofnerve-relatedpain.Complementarytherapies
suchasacupunctureandmassagemayalsobeeffective.
MoredataareemergingonhowCNCPneedstobeseenmoreasabiopsychosocialphenomenonand
notasapurelybiologicalcondition,especiallywhennoobviouscauseispresent.Realisticexpectations
need to be established with the patient early in the treatment plan. Fear of any discomfort and
catastrophizing behaviors are often the main drivers of pain and must be addressed before treatment
strategiescanbeeffective.Behavioraltherapies,includingsystematiccopingapproachesandrelaxation
strategies,havebeenshowntobeessentialinthesepatientsinordertoimprovefunctionandqualityof
life.Cognitive–behavioraltherapy,acceptancetherapy,andmeditationareactivetreatmentstrategiesthat
can help overcome psychological issues central to adequate pain control. Treatment of difficult pain
conditions that cannot be managed by noninvasive and/or pharmacologic treatments may require a
consultationwithapainspecialistorapainpsychologisttoevaluateotheroptionsorinterventions.
DrugTherapybyTypeofPain
The assessment of the source of pain and intensity is important when determining initial analgesic
therapies.Mildtomoderatepaincanbetreatedwithlower-potencymedicationssuchasacetaminophen
andNSAIDs.Theseagentscanalsobepartofamultimodaltherapyplanincombinationwithopioidsfor
severe pain. Historically, aspirin had been used as a pain modality for short-term pain treatment.
However,increasedadverseeffectshavelimiteditschronicuse.Aspirinismostlyusedtodaytoprevent
cardiaceventsandisnotroutinelyusedaspartoffirst-linepainmanagementtherapy.
Combinationopioids,ketorolac,andtramadolarecommonlyusedtotreatmoderatepain.Combination
opioidscontaintheadditionofa“nonopioid,”suchasacetaminophenoribuprofen,creatingatreatment
ceiling dose (maximum dose).Low dosesof strongopioids mayalso be utilized formoderatepainin
patientswhohavecontraindicationstoNSAIDs,acetaminophen,ortramadol.
Opioidsarethemostcommontherapyrecommendedforseverepain.Morphineisthegoldstandardand
themoststudied opioid.Whenusedinequivalentdoses, mostpureopioids(mureceptoragonists) are
equally effective in controlling pain, but individual variation may exist among patients. Morphine,
oxycodone,hydromorphone,oxymorphone, and fentanyl are pure mu opioid agonists indicated for the
treatment of severe pain. Morphine is considered the opioid of first choice unless a contraindication
existsorthepatienthasfailedpriormorphinetherapy.Meperidineisanotheropioidthathashistorically
been utilized for the treatment of severe pain. Use of this agent is no longer recommended due to
neurotoxicityassociatedwithaccumulationoftheactivemetabolitewithroutineuseorinpatientswith
renalinsufficiency.
Inmostcasesinvolvingpersistentcancerpain,analgesicsshouldbeadministeredATC,withas-needed
medications used to treat BTP. This recommendation is based on the finding that regularly scheduled
medicationsmaintainaconstantbaselinelevelofdruginthebodyandhelppreventarecurrenceofpain.
BTPmedicationsareindicatedwhenintermittentpainoccursdespiteATCtherapy.
TABLE9.1
TreatmentStrategyBasedonInitialPainAssessment
APAP,acetaminophen;FLACC,faces,legs,activity,cry,consolability;NRS,numericalratingscale;NSAIDs,nonsteroidalantiinflammatory
agents;VAS,visualanalogscale.
Anessential principlein using medications to manage painis to individualize medicationregimens
accordingto severity(Table9.1). For mild tomoderatepain, acetaminophenor anNSAID isusually
considered initial therapy. Management of moderate to severe pain may require low dose opioids, a
combinationopioid,ortramadol.Severepainistreatedwithhigher-potencyanddosesofopioids,suchas
morphine,hydromorphone,oroxycodone.Variousclasses of coanalgesics,suchas anticonvulsantsand
antidepressants,canalsobeutilizedincombinationwiththeopioids.
AcutePain
Acutepainisoftenaresponsetotissueinjuryortraumaandisusuallynociceptiveinnature.Treatment
includes nonopioids such as NSAIDs and acetaminophen for mild to moderate pain and opioid
medicationsformoderatetoseverepain.Asacutepainincreasesandpersists,itbecomesmoredifficult
tomanage.Therefore,itisimportanttotreatacutepainpromptlyandeffectively.Also,untreatedacute
painisoftenthecatalystinthedevelopmentof chronic painconditionsinwhichpainpersistsdespite
healingoftheoriginalinjury.
Acetaminophenisthedrugofchoicefortreatingminor,noninflammatorypain,especiallyinpatientsat
riskforGIdamage.NSAIDsarealsoeffectiveasmonotherapyinthetreatmentofmildtomoderatepain.
BothacetaminophenandNSAIDsareavailableincombinationwithopioidsformoderatepain.Pureor
multiple-mechanism opioids are used when pain is severe. The opioids, as a class, generally exhibit
equalanalgesiceffectswhengivenatequipotentdoses(adjustedforrouteofadministrationandduration
ofaction).
Variousstrategiesarecurrentlyimplementedinthecontrolofpain.Postoperativepainisoftentreated
withmultimodal therapiesincludingnon-opioid analgesics, opioidmedications,andvariousadjunctive
therapies. Theuseofpreemptiveanalgesia,definedas theadministrationofvariousanalgesicspriorto
procedures, isoftenpartofamultimodal treatmentplanusingtwo or more medicationswith different
mechanisms ofaction.Intra-operative ketamine and lidocaine may be utilized, especially in surgeries
performedonopioid-tolerantpatients(useof60mgormoreoralmorphineorequivalentoveraminimum
oftheprevious7days).PostoperativeATCnon-opioidmedicationswillminimizetheneedforopioids
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