!"#$% '()* +%,-)"% .(*/0112 ! "##$$#%'#() $#*#$#+,#( $#-./$,# 0121 !"#$% '()* +%,-)"% .(*/0112 !"#$% '()(*"() +*"%",) !"#$ %&&' %()&*+$ ,&- !"#$%&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&& '()*$%&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&& +#",-%&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&& !"#$%"#& Acutepainafterinjuryorsurgeryremainspoorlytreateddespitean armamentariumofeffectivetreatmentsandtheactivityofacutepain services.Acutepaininitselfisverydistressinghoweveradverse effectsofpainonotherorgansystemscanleadtosignificant complicationsandthegenerationofchronicpain.Effectiveandrapid treatment of pain is vital. Barrierstoeffectivemanagementofacutepainarecurrentlynotwell defined however effective education is a key component. Currently few easilyaccessibleresourcesexistforthepractitionermanagingacute pain. TheAPSHandbookbyKashin,RiaziandSawhneywillbean importantresourceforthemanyinterns,residents,physiciansand nursingstaffdealingwithcommonacutepainproblems.Theauthors aimwastoproducearesourcethatisbothstraightforwardyet comprehensiveenoughtotreatmostacutepainproblemsinatimely andeffectivemanner.BrianKashinMDandMonaSawhneyRNare bothhighlyknowledgeableandexperiencedpainpractitionerswho haveeffectivelytreatedmanypatientsinpain.SheilaRiaziMDisa recently graduated anesthesia resident who has very clear knowledge oftheproblemsandbarriersfacedbymanyresidentswhoarecalled tomanagepatientsinseverepain.Togethertheyhaveproduceda practical and readable handbook. The APS Handbook will be an essential resource leading to better pain management for many patients. commendthe authors for producing this excellent book. Colin J.L. McCartney MBChB FRCA FRCPC Sunnybrook Health Sciences Centre University of Toronto !"#$% Although knowledge regarding the treatment of acute pain is rapidly expanding andthequalityofevidencehasimproved,thisimprovementhasnotledto progressinpatientcare.Thereremainsagapbetweentheadvancesin assessmentandmanagementofacutepainandtheimprovementsinclinical practice Acutepainmanagementhasseenmanychangesintheassessmentandthe available therapies. Acute pain is being identified as a problem in many patient populations.Beyondpostoperative,traumaticandobstetriccausesofpain, patientsexperienceacuteon-chronicpain,acutecancerpainoracutepain from medical conditions. tisourhopethatthishandbookwillprovide,nurses,medicalstudents,and physiciansintrainingsimpleandpracticalinformationthatwouldhelpthem managetheirpatients'paininthemosteffectivemanner.Thishandbook includesinformationregardingconventionalmethodsofanalgesiaforacute painaswellasnewertechniquessuchaspatient-controlledintravenousand epidural analgesia. t also includes information on the management of medical conditions that can cause pain as well as special patient subpopulations. Thepurposeofthisbookistobeapracticalhandbookthereforedetailed informationaboutanatomy,andspecificregionalanesthesiatechniqueshave notbeenincluded.Suggesteddrugs,dosesandtreatmentregimensare guidelines only and may have to be adapted according to different patients and clinicalsituations.Theauthorsofthisbookhaveusedtheirbesteffortsto provideaccurateinformationatthetimeofprintingTheauthorshereby disclaimallresponsibilityforanylosssufferedbyanypersoninthelightof future discoveries in this field, and for any omissions or errors in the text. Special thanks go out to Dr. Mark Friedlander who was the first director of the AcutePainServiceattheTorontoGeneralHospitalandthenNorthYork General Hospital. We are fortunate to have his input and editing skills. would alsoliketothankthecontributionsofthefollowingphysicians:Thomas Engelhardt:UniversityofAberdeen,EdwardMariano:UniversityofCalifornia, San Diego, Paul Tumber: University of Toronto, Dr Basem Naser:Hospital for Sick Children and Anita Sarmah: University of Toronto Brian KashinSheila Riazi Mona Sawhney TabIe of Contents Chapter 1:Pain Pathways, Transmission and Modulation Chapter 2:Pain Assessment Tools and Considerations Chapter 3:Non-Opioids, Opioidsand Adjuvant Agents Chapter 4:Pharmacology of Local Anesthetic Chapter 5:Post-operative Pain Management Chapter 6 :Pain Management in Patient Subpopulations Chapter 7 :Acute Pain Syndromes Appendices: Appendix A:Acute Pain Service nitial Assessment and Daily Flow Sheet Appendix B: Adjuncts Appendix C: Postoperative Nausea and Vomiting (PONV) Appendix D: Common Oral Narcotics Appendix E: NSADS Appendix F: Opioid Equianalgesic Table Appendix G: Pain Glossary !"#$%&' () *#+, *#%"-#./0 %'#,/1+//+2, #,3 12345#%+2, Chaptei 1: Pain pathways, anu mouulationPage | !Chapter 1: Pain pathways, transmission and modulation Tissueinjury,suchasthatinducedbysurgicalincisionresultsinthelocal releaseoInumerouschemicalsthatmediateorIacilitateinIlammation.CollectivelythesechemicalhavebecomeknownasaninIlammatorysoup whichincludesbradykinin,prostaglandin,leukotrienes,serotonin,histamine, substanceP,calcitonin-generelatedpeptide,thromboxanes,platelet-activatingIactor(PAF),adenosine/ATP,cytokinesandneurotrophins(i.e. nervegrowthIactor).ThesesubstancesmaybereleasedIromtissueIactors, suchaslipidsIollowinginjury,Iromnerveendingsthatrespondtoinjury (nociceptors) or Irom immune cells. These agents are generally characterized by their ability to (1) evoke inIlammation (i.e. swelling, redness or increased skin temperature) (2) directly activate and/or sensitize nociceptors. Thoseagentsthatcandirectlyactivatenociceptors,maydosodirectlyor indirectly via inIlammatory cells, which in turn release algogenic agents.For instance, mast cells are the primary source oI histamine and PAF.Histamine contributesdirectlytoinIlammationbyproducingvasodilationandoedema, whilePAFleadstoserotoninreleaseIromplateletswhichcandirectly activateandsensitizenociceptors.TheeIIectoIsensitizationisincreased primaryaIIerentsensitivity(FitzgeraldandLynn1978;SchaibleandGrubb 1993;Pawlaketal.,2001;Chenetal.,2006),whichdecreasesthethreshold IoraIIerentactivationbyanoxiousstimulus.Thisresultsinincreased sensitivitytopainIulstimuli(hyperalgesia)andpaintostimulithatarenot normallypainIul(allodynia).Hyperalgesiaandallodyniaaretheprimary IeaturesoIawiderangeoIchronicpainconditions,includingpostoperative pain. PrimaryaIIerentsthatareactivatedbynoxiousstimulitoperipheraltissues (i.e. viscera and somatic sites) are small-diameter A and C Iibre nociceptive aIIerents.These Iibres send impulses (i.e., action potentials) into the CNS to providesensory-discriminativeinIormationaboutthelocation,quality, intensity and duration oI the noxious stimulus. NociceptiveprimaryaIIerentaxonsterminateexclusivelyinthedorsalhorn oIthespinalcord,anditisthereIorethesiteoItheIirstsynapseinthe ascending pathways that convey (somatosensory cortex), sensory inIormation to the brain that underlies conscious perception oI pain.In addition, neuronal Chaptei 1: Pain pathways, anu mouulationPage | "circuitsinthespinalcordgeneratelocalreIlexes(dorsalrootreIlexes)that sendretrogradeimpulsesintotheperipherythatcancausethereleaseoI inIlammatorymediatorsIromnociceptiveterminals,therebyprolonging inIlammation (Willis and Coggeshall 2004). The dorsal horn oI the spinal cord is also the site where peripheral nociceptive inIormation is modulated by other aIIerent inputs and descending modulatory inputsIromsupraspinal structures(i.e. periaqueductalgrey,raphenucleiand locuscoeruleusinthemidbrain).Dependingonwhichdescending modulatoryinputsareactivated(i.e.,serotonin,noradrenalineversus enkephalin),thetransmissionoInociceptiveinIormationmaybeeither enhanced or attenuated.

Thereare3generalclassesoInociceptors:thermal,mechanical,and polymodal. Thermal(extremetemperatures45Cor5C)andmechanicalnociceptors arethinlymyelinatedAIibreswhereaspolymodalnociceptorsarebothA andunmyelinatedCIibresthatareactivatedbyhighintensitymechanical, chemicalandthermalstimuli(BasbaumandJessell2000;Willisand Coggeshall 2004; Willis 2005).Surgical incision is thought to predominantly activate polymodal A and C Iibre primary aIIerents. NeuronsinthespinalcordthatreceivenociceptiveinIormationreside predominantlyinthemarginallayer(laminaI)andthesubstantiagelatinosa (laminaII)oIthesuperIicialdorsalhorn.ThemajorityoItheseneurons receivedirectconverginginputIromAandCIibres.Neuronsthatrespond exclusively to noxious stimulation are classiIied as nociceptive-speciIic or NS neuronsandprojecttohigherbraincenters,whereassomeneuronsinthis layer,calledwide-dvnamic-range(WDR)neurons,respondinagraded Iashiontobothnon-noxiousandnoxiousstimulation!WDRandsomeNS neuronsarealsoIoundinLaminaVandprojecttothebrainstemandto regions oI the thalamus. Chaptei 1: Pain pathways, anu mouulationPage | # NociceptiveinputtothedorsalhornoIthespinalcordisrelayedtohigher centersinthebrainbyIourmajorascendingpathways:spinothalamictract (STT),spinoreticular(SRT),spinomesencephalic(SMT)anddorsalcolumn-medial lemniscus pathway (DCML).TheSTTisthemostprominentascendingnociceptivepathwayinthespinal cordandoriginatesIromNSandWDRneuronsinlaminaIandV.These projectionscrossthemidlineandascendintheanterolateralquadrantoIthe spinal cord and than travel up the length oI the spinal cord into nuclei in the brainstemandthalamus.NearthethalamustheSTTdividesintoalateral portioncalledtheneospinothalamictract(associatedwith sensory/discriminativeaspectsoIpainperception)andamedialportion, called the paleospinothalamic tract (associated with the aIIective/motivational aspectsoIpainperception).Thelattertracthasnumeroussynapseswiththe reticularIormationoIthebrainstem,themedialthalamus,theperiaqueductal graymatter,andthehypothalamus.Neuronstransmittingnociceptiveand othersensoryinIormationultimatelysynapsewiththird-orderneuronsin several nuclei oI the thalamus -- including the medial dorsal, ventral posterior lateral, and ventral medial posterior nuclei.From there, signals are relayed to Chaptei 1: Pain pathways, anu mouulationPage | $theprimarysomatosensorycortex,whichisresponsibleIorourconscious recognitionoIpain.Thesomatosensorycortexandthethalamusdirectly relay nociceptive inIormation to other brain areas such as the cingulate cortex and insular cortex, which are involved in the evaluative and aIIective aspects oI pain perception. TheSRTplaysacriticalroleinrelayingandintegratingnociceptive inIormation contributing to the motivational, aIIective, and aversive response aspectsoIpain.TheneuronsoItheSRToriginateprimarilyinLaminasVII and VIII oI the spinal cord. They terminate in many sites throughout the brain stemreticularIormation.NeuronsIromthereticularIormationprojectto many areas oI the brain, including the hypothalamus, the thalamus, and both directly and indirectly to the limbic Iorebrain and neocortex; areas associated with the emotional aspect oI pain.The SMT neurons originate in Laminas I, IV, V and VI in the dorsal horn oI thespinalcord.TheyterminateinseveralstructuresoIthemidbrain, especiallytheperiaqueductalgray,the nucleuscuneiIormis,andthesuperior colliculus.TheseconnectionsproduceaIIectiveandaversivebehaviours associated with pain such as Iear. They may also initiate orienting responses. The SMT input to the periaqueductal gray activates the system Ior descending pain modulation which produces endogenous analgesia. TheDCMLpathwaytransmitssensoryinIormationabouttouchand proprioception and has been traditionally viewed as a pathway not involved in painperception.However,thereiscompellingevidencethatimplicatesthe DCMLpathwayinrelayingnociceptiveinIormation.AxonsoItheDCML pathwaytraveluptheipsilateralsideoIthespinalcordandsynapsewith secondorderneuronsatthegracileand cuneatenuclei.Studieshaveshown that Iibres oI the dorsal column that ascend close to the midline are involved inthetransmissionoInociceptiveinIormation.SecondorderaxonsoIthe DCML pathways cross the midline and ascend to the ventral posterior lateral andmedialthalamuswhere theyjoinnociceptiveIibresoItheSTTandthan projecttosamehigherbraincentersinvolvedinpainperception(i.e. somatosensory cortex).Chaptei 1: Pain pathways, anu mouulationPage | %!"#$ &'()*"+#'$ ThetransmissionoInociceptiveinIormationispartoIthebody'sdeIense systemthatproducesarapid-warningresponse,instructingthebodytoreact to damaging stimuli.However, ongoing noxious impulses conveyed Irom the periphery to the spinal cord and brain can result in neuroplastic changes that sensitize several sites oI the pain pathway giving rise to clinical pain.Peripheral modulation. The high threshold oI nociceptors can be reduced by changes in the Iunction or expression oI ion channels, receptors or transducer proteins on peripheral nociceptor terminals.In the case oI tissue damage, the releaseoIinIlammatorymediatorsactivatesnociceptorsandinitiatean intracellularsignalingcascadethatevokessuchchanges.Themajor mechanism responsible Ior these alterations is phosphorylation oI receptor/ion channels and/or changes in the expression oI channels in primary sensory and dorsal horn neurons.This modulation increases the excitability oI nociceptor terminalswhichreducesitsthresholdIoractivation,thusproducing peripheralsensiti:ation.TheclinicalIeatureoIperipheralsensitizationis increasedpainsensitivityatthesiteoIdamagedtissue(i.e.primary hyperalgesia).However,painmayalsoappearoutsidetheareaoIinjury (secondaryhyperalgesia),spontaneouslyorinresponsetolighttouch (allodynia).It is also possible Ior pain to arise without any physical injury at all (migraine, Iibromyalgia or irritable bowel syndrome).In these conditions, painarisesIromcentralampliIicationoIperipheralinputs,central sensiti:ation. Centralmodulation.(1)Spinal.WhenC-Iibrenociceptorsareactivated, theyinducechangesintheCNS.MildnoxiousstimuligeneratesIast excitatoryresponsesinthedorsalhornoIthespinalcord.Theseresponses aremediatedbythesynapticreleaseoIglutamateandactivationoItheN-methyl-D-asparticglutamatergicreceptoronpreandpostsynapticterminals.However,intenseorsustainednoxiousstimuliresultsintheco-releaseoI severalneuromodulators(glutamateandsubstanceP),producingslowlong lastingresponsesintheCNS.BothtypesoIresponsesresultintemporal summationandtheneteIIectisaphenomenomknownaswindup.Windup reIerstotheampliIicationoIexcitatoryresponsesinthedorsalhornoIthe spinalcordandtheclinicalmaniIestationoIthisresponseissecondary Chaptei 1: Pain pathways, anu mouulationPage | &hyperalgesia and allodynia. This change in neuronal Iunction is the result oI activationoIintracellularkinasesbyG-proteincoupledandtyrosinekinase receptorsactivatingproteinkinaseAorproteinkinaseCwhich phosphorylateandalterionchannel(i.e.primarilysodiumandcalcium) Iunction, including activation threshold, rate oI activation/inactivation and the magnitudeoIdepolarization.PhosphorylationoIionchannelsandreceptors is usually a reversible process that returns to normal when the injury heals or disease process is controlled.However, modiIications involving long-lasting alterationsintheexpressionoItransmitters/receptor/ionchannelsorinthe structureandconnectivityoIcentralneuronalcircuitsoItenleadsto permanentneuroplasticchangesandthedevelopmentoIchronicpain conditions.Anotherimportantmechanismthatcontributestocentral sensitizationisareductionininhibitorytransmissioninthedorsalhorn.Inhibitory interneurons in lamina III oI the dorsal horn play an important role indampingdownsensoryprocessing.AIterperipheralinjury,thereisa reductionintheactionoIinhibitorytransmittersandlossoI-aminobutyric acid(GABA)interneurons,resultinginalossoIinhibition(disinhibition) producing pain hypersensitivity. (2) Supraspinal.Supraspinal brain areas that connect back to the spinal cord can modiIy nociceptive inIormation that is coming into the brain. This is one waythatthebraincanreducepain,byamechanismknownassupraspinal (descending)analgesia.ItusesIeedbackloopsthatinvolveseveraldiIIerent nucleiinthebrainstemreticularIormation.TwoimportantareasoIthe brainstemthatareinvolvedinreducingpainaretheperiaqueductalgray (PAG) and the nucleus raphe magnus (NRM).ThePAGcontainsopioid-richneuronsthatexcitetheraphenuclei(RN) and/orloceuscelereus(LC)neuronsbydisinhibitingGABAergic interneurons in the PAG. This allows PAG (anti-nociceptor) neurons to excite theamine-containingcellsintheNRMandLCthatinturnprojectdownto thespinalcordtoblockpaintransmissionbydorsalhorncellsbydiIIerent mechanisms:(1)directpostsynapticinhibitionoIprojectioncellscausing hyperpolarisationoIthemembranepotentialduetoactivationoIGprotein-linked receptors that cause the opening oI potassium channels, (2) presynaptic inhibitionoIneurotransmitterreleaseIromprimaryaIIerentterminals.This Chaptei 1: Pain pathways, anu mouulationPage | 'worksbyactivatingGprotein-linkedreceptorsthatcauseclosingoIcalcium channels, thus reducing transmitter release. A second descending system oI serotonin-containing neurons exists.The cell bodiesoItheseneuronsarelocatedintheNR,likethenoradrenaline-containingneurons,theaxonssynapseoncellsinlaminaII. Theyalso synapseoncellsinlaminaIII. StimulationoItheraphenucleiproducesa powerIulanalgesiaanditisthoughtthattheserotoninreleasedbythis stimulationactivatestheinhibitoryinterneuronsevenmorepowerIullythan the noradrenaline and thus blocks pain transmission.However, serotonin may notbespeciIicallyinvolvedininhibitionoIpaintransmission. Serotonergic agonistsdonothavesigniIicantanalgesiceIIects. Serotoninneuronsappear toinhibitallsomatosensorytransmission,andmayhaveaIunctioninthe initiation oI sleep.A complicating Iactor is that serotonin receptors are Iound inmanyplacesinthedorsalhorn,includingonprimaryaIIerentsIromC Iibres.Serotoninmay act to presynaptically inhibit pain by blocking C Iibre terminals. Some oI the interneurons oI lamina II oI the dorsal horn contain enkephalins.Enkephalinshavebindtothesamereceptorsasopiatedrugslikemorphine and heroin.ThereIore, opiate drugs may act by mimicking the activity oI the interneuronesoIlaminaII. IthasnotyetbeenIullyestablishedhow endogenousenkephalinsworkatthespinallevel. Theymayactastrophic Iactors`,somehowampliIyingtheresponseoIthepost-synapticdendritesto the action oI GABA.Enkephalin-containing neurons have also been Iound in the medulla, mid-brain and hypothalamus. Chapter 2: Pain Assessment Tools and Considerations Chaptei 2: Pain Assessment tools anu consiueiationsPage | !Chapter 2: Pain Assessment Tools and Considerations ByusingavarietyoImeasurementapproaches,itispossibletoobtainan accurate picture oI pain. These approaches include:self-report (what the individual says),behavioural (how the individual behaves) andphysiological indicators (how the individual`s body reacts). ItismostdesirabletoobtainandrelyonselI-reportmeasuresoIpainwhen possible.TheexceptionstothismeasurementapproacharewithinIants, preverbalchildrenandcognitivelyimpairedchildrenandadultsIorwhom behavioural observation should be the primary source Ior pain measurement. The main goals oI pain assessments are to:describe the nature oI pain and Iactors that inIluence it assist in the diagnosis and Iacilitate a pain management plan evaluate the eIIectiveness oI the pain management plan Assessment of Pain!"#$%&' %) *&"%& *+", -./0&"0,10#UnderstandingpastpainexperiencesandpreviouseIIectivetherapieswill help the health care team obtain a clearer picture oI the present experience. 2/01")"1 *+", 3'/0# Nociceptive pain SomaticSharp,hotorstingingpainwhichisusuallylocalizedto the area oI injury VisceralDull, cramping, or colicky pain, oIten poorly localized orreIerred over a wide area There can be associated symptoms such as nausea and sweating Neuropathic Pain Injuryordiseaseleadingtodamagetotheperipheralorcentral nervoussysteme.g.brachialplexusinjury,spinalcordinjury, stroke or shingles Sensoryloss,motorweakness,bowelorbladdersphincter abnormalities Pain in an area oI sensory loss but not conIined to that area Chaptei 2: Pain Assessment tools anu consiueiationsPage | "Increasedsympatheticactivity(skincolor,temperature,texture, sweating) Pain that is burning, shooting, stabbing Pain that is paroxysmal Pain responds poorly to opioids Phantom pain Allodynia: sensation oI pain in response to a stimulus that does not normally produce pain (light touch) Hyperalgesia:Exaggeratedresponsetoastimulusthatisnormally painIul Dysesthesias: Unpleasant abnormal sensations !"#$%&' %) 45&&0,$ *+", There are 12 key Ieatures oI pain which must be elicited in the history: 1.TypeoIpain:e.g.,acuteorpersistent/chronicnon-cancer, cancer,anddisease-relatedpain;nociceptive,neuropathicor mixed2.Timing-onset/duration:Whendidthepainbegin?Whatwas thepersondoingbeIorethepainbegan?Wasthereany initiatinginjury,traumaorstressors?Howlonghasthepain been present? (Eg:minutes, hours, days or months)3.LocationandRadiation:Thiscanbedoneverballyorusinga body map.4.Intensity (at rest and with activity): Ask the patient to rate how severetheirpainisusingapainscaleseg:NRS(010).For thosenotcapableoIselI-reportbehavioralobservational measuresandcompositemeasuresthatcombinebehavioral and physiologic indicators can be used5.Quality oI Pain: Ask the patient to describe their pain by using words such as sharp, dull, achy, stabbing, burning, shooting or throbbing.Thishelpsdeterminewhetherthepainis nociceptive or neuropathic in nature or a combination oI both6.Frequency:HowoItenispainpresent?Isitcontinuousor intermittent?7.PrecipitatingFactors:Whatmakesthepainworse?(e.g., movement, deep breathing and coughing, stress etc.)Chaptei 2: Pain Assessment tools anu consiueiationsPage | #8.RelievingIactors:Whatmakesthepainbetter?Thisshould includebothnon-pharmacologicalandpharmacological interventions.SideeIIectsoIinterventionsshouldbe documented. The degree oI pain relieI or intensity oI pain aIter a pain relieving treatment/intervention should be determined. 9.AssociatedSymptoms:Arethereanyothersymptomsthatgo alongwithoroccurjustbeIoreorimmediatelyaIterthepain, suchasnausea,vomiting,light-headedness,diarrhea,or diIIicultyambulating?Arethereanychangesinthecoloror temperature oI the aIIected extremity or painIul area?10.Temporal or seasonal variations: Does the pain vary with time oI day, changes in seasons or weather? Does the pain occur at certaintimesoItheday,IorexampleaItereatingorgoingto the washroom?11.Impactondaily living:DoesthepaineIIectdailyactivitiesor behaviors(e.g.sleepdisturbances,decreasedappetite, decreased physical activity, changes in mood, or a decrease in social interactions)?12.Culture,ethnic,orreligiousbackground:Elicitculturally determined belieIs about pain that may inIluence care. Ask the patientandIamilyiIthepainhasanyspeciIicmeaningto them,iIthereisaspeciIicwordtheycallthepain,whythey believetheyhavepain,andwhattheythinkwillhelpthem manage their pain. 206)780/%&$ 90+#5&0#SelI-reportapproachtopainassessmentisgenerallyregardedasthegold standardoIpainmeasurement.Theindividual`sownreportoItheirIeelings, imagesorstatementsaboutthepainthattheyperceiveareused.Thereare multiple selI-report rating scales available, 2 which are commonly used are: Numerical Rating ScalesA numerical rating scale oI pain intensity consists oI a range oI numbers (e.g., 010) Respondents are told that the lowest number represents no pain` and thehighestnumberrepresentsanextremeleveloIpain(e.g.,worstpain imaginable`) and are asked to indicate a number or point on this scale. Chaptei 2: Pain Assessment tools anu consiueiationsPage | $ Faces ScalesFacespainscalespresentthepersonwithdrawingsoIIacialexpressions representingincreasinglevelsoIpainintensity.Theindividualisaskedto selectthepictureoIaIacethatbestrepresentstheirpainintensityandtheir score is the number (rank order) oI the expression chosen. 956$":";0,#"%,+6 206)780/%&$ *+", +?"%5&+6 @A#0&?+$"%,#InvolveassessmentoIspeciIic,non-verbalbehaviors.Estimating painIromobservationoIbehaviorsisthemostcommonapproach IorpainassessmentininIants,preverbalchildrenandthosewith cognitive impairments.Thisapproachtopainmeasurementisunobtrusive,andwithout additional burden on the patient. Although some behaviors are more consistent than others across age groups (e.g. Iacial expression), the rangeoIpossibleresponsesiswideandnoparticularsethasbeen shown to be consistent with particular pain experiences.Behavioralobservationsmaynotbeuniquetopain.ThereIore, distinguishingbetweenpainanddistressorotherphenomenasuch as Iear, anxiety or loneliness can be diIIicult. Special Pain Assessment Situations0 B%,7?0&A+6