Presentation on theme: "Pathophysiology of Pain Treatment of Acute Postoperative Pain"— Presentation transcript:
1Pathophysiology of Pain Treatment of Acute Postoperative Pain Dr Sajith DamodaranUniversity College of Medical Sciences & GTB Hospital, Delhi
2Objectives: Definition of Pain Anatomy and Physiology of pain perceptionAdverse effects of untreated postoperative painModalities of treating postoperative painSpecial patient populations
3Pain: DefinitionAn unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. [IASP]SubjectiveSensation and emotionUnpleasantPsychological, in absence of any stimulus or pathophysiological causeAn unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. Note: The inability to communicate verbally does not negate the possibility that an individual is experiencing pain and is in need of appropriate pain-relieving treatment. Pain is always subjective. Each individual learns the application of the word through experiences related to injury in early life. Biologists recognize that those stimuli which cause pain are liable to damage tissue. Accordingly, pain is that experience we associate with actual or potential tissue damage. It is unquestionably a sensation in a part or parts of the body, but it is also always unpleasant and therefore also an emotional experience. Experiences which resemble pain but are not unpleasant, e.g., pricking, should not be called pain. Unpleasant abnormal experiences (dysesthesias) may also be pain but are not necessarily so because, subjectively, they may not have the usual sensory qualities of pain. An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. Note: The inability to communicate verbally does not negate the possibility that an individual is experiencing pain and is in need of appropriate pain-relieving treatment. Pain is always subjective. Each individual learns the application of the word through experiences related to injury in early life. Biologists recognize that those stimuli which cause pain are liable to damage tissue. Accordingly, pain is that experience we associate with actual or potential tissue damage. It is unquestionably a sensation in a part or parts of the body, but it is also always unpleasant and therefore also an emotional experience. Experiences which resemble pain but are not unpleasant, e.g., pricking, should not be called pain. Unpleasant abnormal experiences (dysesthesias) may also be pain but are not necessarily so because, subjectively, they may not have the usual sensory qualities of pain. Many people report pain in the absence of tissue damage or any likely pathophysiological cause; usually this happens for psychological reasons. There is usually no way to distinguish their experience from that due to tissue damage if we take the subjective report. If they regard their experience as pain and if they report it in the same ways as pain caused by tissue damage, it should be accepted as pain. This definition avoids tying pain to the stimulus. Activity induced in the nociceptor and nociceptive pathways by a noxious stimulus is not pain, which is always a psychological state, even though we may well appreciate that pain most often has a proximate physical cause.
4Pain: Definition Pain is what the patient says hurts [John Bonica] Affected by the mental and emotional state, preconditioning, past experiences and memories.Always subjective. Varies from person to personPain is the Fifth vital sign [JCAHCO]
5Acute PainNormal predicted physiological response to an adverse chemical, thermal or mechanical stimulus.Generally lasts less than one monthPoorly managed pain leads to chronicityPathophysiological changes in both PNS & CNS
7Anatomy and Physiology of Pain Nociceptive Receptors:Naked Nerve EndingsIn all tissuesSpecific for painStimulus not specificPain is not produced by overstimulation of other receptors
8Anatomy and Physiology of Pain Nociceptive Pathways:AfferentThree neuronFirst order neurons in Dorsal Root GangliaSecond order neurons in Dorsal hornThird order neurons in Thalamic nucleiSecond order neurons include nociceptive specific and WDRDual ascending systemLateral corticospinalDorsal column medial leminiscalDescending modulation by cortex thalamus and brain stemNocicpetive neurons respond only to pain. Invloved in sensory-discriminative aspects of pain. WDR neurons respond to both noxious and non noxious stimuli. Involved in motivational-affective component.
10Anatomy and Physiology of Pain Fast Pain or First Pain:Sharp or stingingwell localisedBy stimulation of thermo-mechanical nociceptorsCarried by A delta fibresTransmitted by the Lateral spinothalamic tractMonosynaptic pathwayUsually disappears when stimulus ends
11Anatomy and Physiology of Pain Slow Pain or Second PainDelayed, DiffuseStimulation of polymodal nociceptorsCarried by C fibresTransmitted by the dorsalcolumn medial leminiscal tractPolysynaptic pathway. Collaterals to midbrain, pontine and medullary RF, PAG, HypothalamusEngage Descending modulatory systemInvolved in the reflex response to pain and emotional and motivational aspectThe paleospinothalamic tract is polysynaptic. Ascends to the medial thalamic nuceli, sends collaterals to the midbrain, pontine an medullary reticaular fromation, periaqueductal gray & hypothalamus. Synapse onto neurons that project to forebrain limbic structures. Primarily involved in refelex response to pain…. Respiratory, circulatory, endocrine. Secondary afferents aslo engage descending modulatory systerm. Reticulospinal and spinomesencephalic tracts also supply afferents. All involved in producing emotoinal and behavioural response to pain.k
12Anatomy and Physiology of Pain Small Myelinated Aδ FibresCarry Fast pain2-5 μm diameter12-30 m/sEnd mainly in lamina I, II & V of dorsal hornSmall unmyelinated C FibresCarry slow painμm diameter0.5-2 m/sEnd in Lamina I & II of dorsal horn
13Anatomy and Physiology of Pain Efferent modulation of pain:Descending inhibitionCortex, thalamus, brain stem PAG, nucleus raphe magnus, locus ceruleusDescend in dorsal column to dorsal horn
15Anatomy and Physiology of Pain Gate Control Theory:Explains the highly variable and non linear relationship between pain and injuryPain is ‘gated’ at the Dorsal HornInvolves WDR neuronExcited by nociceptors and also Aβ fibresInhibitory interneurons, excited by Aβ fibres, inhibited by Aδ and C fibresMOA of TENS, Rubifascients and counterirritants
161.The projection neuron (P) carries both nociceptive stimulation from small fibers (S) and non-nociceptive simulation from large fibers (L) on the way to the brain.2.With no stimulation, the inhibitory neuron (I) keeps the gate "closed," and there is nopainful sensation.3.With painful stimulation, the small fiber (S) blocks the inhibitory neuron (I), "opening" the gatefor the projection neuron (P) to send on the painful stimulus.4.With the addition of non-painful stimulation, the large fiber (L) activates the inhibitoryneuron (I), partially or completely closing the gate depending on the strength of thestimulation, and competes with the painful stimulation for access to the projection neuron (P).
17Anatomy and Physiology of Pain Other Types of Pain:Deep PainPoorly localised, nauseatingeg: periosteal pain, pain from ligamentsMuscle PainDue to ischemiaP factor. ? PotassiumRelieved by restoration of blood supply
18Anatomy and Physiology of Pain Visceral PainPoorly localised and dull – sparse receptor concentrationUsually felt in midlineAssociated with nausea and autonomic disturbancesAfferents carried by ANSSpinal pathways are same as for somatic painReferred to other areas
19Anatomy and Physiology of Pain Referred PainDermatomal RulePain from visceral sites referred to the somatic structure that developed from the same embryonic segment of dermatomeRole of experience:Pain from abdominal structures may be referred to site of previous surgeryRole of convergenceVisceral and somatic sensory input converge on Dorsal Horn.More fibres in the peripheral nerve than the STT
20Anatomy and Physiology of Pain Neuropathic Pain:Direct nerve damage like entrapment, cutting, traction, compression etc.Presents with burning, tingling and other unpleasant sensations in addition to painCommon surgical proceduresLimb amputationsBreast surgeryGall bladder surgeryThoracic surgeryInguinal hernia repairResponds poorly to typical analgesics
21Anatomy and Physiology of Pain Pain Processing - 4 ElementsTransductionNoxious mechanical, chemical and thermal stimuli are converted to action potentialTransmissionAP conducted through nervous systemModulationAlteration of neural transmission along the pain pathway, principally at dorsal hornPerceptionFinal common pathway. Integration of painful input into somatosensory and limbic cortex.Usual analgesic approaches target only perception
22Anatomy and Physiology of Pain Modulation:Augmentation:Sensitisation due to neuronal plasticity (acute pain induced changes in the CNS)Inhibition:GABA, Glycine by intrinsic neuronsNA, serotonin, Endorphins by descending efferent cortical and subcortical input
24Anatomy and Physiology of Pain Chemical Mediators of Pain Processing:Tissue damage and inflammation activate nociceptorsRelease of numerous algogenic substances from the activated macrophages, mast cells, platelets and lymphocytesDirect pain transduction and facilitation of transduction by increasing the excitability of nociceptors
25Neurochemistry of impulse processing at peripheral nerve ending
26Anatomy and Physiology of Pain Neurotransmitters in Spinal Cord:Excitatory Amino AcidsAspartate & GlutamateExcitatory NeuropeptidesSubstance P, Neurokinin AInhibitory Amino AcidsGABA, Glycine
27Anatomy and Physiology of Pain Pain Receptors in Spinal Cord:NMDA (N-methyly-D-Aspartae): Ca++ channel dependentAMPA (alpha-amino-3-hydroxy-5-methylisoxazole-4-propionicacid): Na+ channel dependentKainate: Na+ channel dependentMetabotropicOpioid Receptors: InhibitoryAlpha2 Adrenergic Receptors: InhibitoryThe sodium channel dependent receptors are essential for fast synaptic afferent input. NMDA is only activated following prolonge dedpl of cell mem. Involoved in secondary hyperalgesia.All the peripheral and central neurotransmitters and the receptors are potential targets for modulation of pain processing. However presently very few of these are clinically available.
28Postoperative Pain Management: Why manage postoperative pain?Humanitarian considerationImproved quality of careBetter patient satisfactionLesser morbidity? Economic benefits due to enhanced patient well being and early rehabilitation
29Consequences of poorly managed postoperative pain CardiovasuclarTachycardia, Hypertension, increased cardiac workRespiratorySplinting, Decreased VC, Atelectatsis, Hypoxia, Increased risk of pulmonary infectionGastrointestinalPostoperative IlieusRenalIncreased risk of oliguria and urinary retentionCoagulationIncreased risk of thromboemboliImmunologicalImpaired immune functionMuscularMusce weakness and fatigue, increased risk of DVTPsychologicalAnxiety, Fear, Frustration
30Assessment of pain Background Pain Pain that is persistant May vary over timeBreakthrough PainPain that escalatesabove a persistantBackground painTransitory and IntermittantPain that is episodic inthe absence of background pain
31Assessment of pain Simple Pain Scales: Useful for evaluation of acute painVisual Analouge ScaleValidated for researchSimple to useSensitive to small changesNot useful in visually impaired, cognitively impaired and small childrenNumerical Rating ScaleLess sensitiveRequires patient to be ableto translate pain severity tonumber.Not useful in visually impairedcognitively impaired and childrenVerbal Rating ScaleEasy to UseUseful in mildly cognitivelyimpairedInsensitive to small changesin pain intensity
35Assessment of pain Useful for evaluating chronic pain Include pain intensity as well as mood, behaviour, thoughts and belifes, physiological effects and their interaction with each otherMcGill Pain QuestionnaireBreif Pain InventoryThe Memorial Pain Assessment CardNeuropathic Pain ScaleThe Leeds Assessment of Neurpathic Symptoms and Signs (LANSS)However, the best way to evaluate and assess pain is to ask about it and listen to what the patient says. Pain is a subjective feeling and hence what the patient says has to be taken to face value. Doctors and nurses frequently underassess pain which leads to undertreatment. Drug seeking behaviour is much rarer than undertreated pain.
36Assessment of pain Best assessment: Ask & Listen Features asked for during assessment:OnsetTemporal PatternSite and RadiationCharaceter and IntensityExacerbating and Relieving factorsAssociated symptomsResponse to analgesics, and other interventionsInterference with activities of daily livingPsychological effects
37Strategies of Acute Pain Management ProactivenessAssess, treat, reassessHave predefined pain treatment plan in placePlan should be flexible to include breakthrough painMultimodal ApproachTreat all the possible steps in pain processingBenefits: Synergism, lower side effects, flexibillityEscalating ApproachPatient controlPatient controlled analgesia
39Strategies of Acute Pain Management: Pre-Emptive Analgesia Prevention of Central Sensitisation and hyperexcitability induced amplification, at NMDA receptor.Pre-requisites:Adequate depth to block all nociceptive input during surgeryExtensive enough to cover the whole surgical fieldDuration should include both surgical and post-surgical periodTheoretically can reduce acute postoperative pain/hyperalgesia and chronic pain after surgeryDefinite evidence of clinical benefit lacking.
40Systemic Medications: Opioids Opioid Receptors: μ, κ and δ receptorsLocation of receptors:Periphery following inflammationSpinal cord dorsal hornSupraspinally in the brainstem, thalamus and cortexPAG, nucleus raphe magnus and RVM in descending pathwayPeriaqueductal gray, rostral ventral medulla
42Systemic Medications: Opioids Mechanism of Action:SpinalInhibition of Ca++ influx presynapticallyEnhacing K+ efflux postsynapticallyActivation of descending inhibitory GABAergic circuitPeripheralInhibition of release of proinflammatory and pronociceptive substances
43Systemic Medications: Opioids Adverse Effects & Problems:Respiratory DepressionNausea and VomitingSedationUrinary RetentionEuphoria/DysphoriaConstipationToleranceDependence and AddictionTolerance: A change in dose response relationship due to exposure to drug and manifest as higher dose requirment to achieve a particular effect. Develops at varying rates to different effects: Least for analgesia. Usually tolerance to analgesia is not a clinical problemDependence: development of withdrawal symptoms following drug withdrawal or administration of antagonist.May develop after only a few days of administration. Not a problem if drug is tapered gradually (50%/d)Addiction: Uncontrolled compulsive use despite harm to self and others. Not seen in patients with pain.
44Systemic Medications: Opioids Morphine: Most commonly used opioid forpostoperative analgesiaRoutes of AdministrationIV, IM, SC, PODoseUpto mg/Kg in titrated boluses IV15mg q8-12 hrs (Sustained release)Onset of Action:IV: 5 minutesIM, SC: minDuration of Action4-5 HoursMonitor forRespiratory Depression, Sedation, Nausea & vomiting, Urinary Retention, Biliary spasm
45Systemic Medications: Opioids Transdermal Fentanyl Delivery System (Ionsys)Needle free, patient activated system for in-hospital useIontophoresisLow intensity electrical field used to transport fentanyl across skin into circulationEach double click delivers 40mcg over 10 minFor us in adults > 18 yearsUsed for 24 hours or 80 dosesiontophoresis -- a process in which a low-intensity electric field, which is generally imperceptible to the patient, is used to rapidly transport fentanyl across the skin and into the circulatory system of the body.
46Systemic Medications: Opioids Oral Transmucosal Fentanyl (ACTIQ):To treat breakthrough cancer pain in opioid tolerant patientsTo be sucked by placing in between cheek and lower gumsEach unit to be consumed in 15 minutesSupplied in strengths of 200, 400, 600, 800,1200 & 1600mcg
47Systemic Medications: Opioids Pethidine: Phenylpiperidine derivativeμ and κ receptor agonist.Also has Na+ channel blocking andAtopinergic actionRoutesIM, IV, PODuration of Action2-4 hoursSide effectsCNS excitation- seizures, myoclonus due to nor-pethidine toxicityInteraction with MAO inhibitors, antidepressantsDose100mg IV/IM q 4 hr300 mg PO q 4 hrWatch forNausea,vomiting, euphoria, ventillatory depressionsedation
48Systemic Medications: Opioids Tramadol:Moderate affinity μ receptor agonist.Acts on spinal modulating pathwaysInhibition of neuronal NA and Serotonin uptakeStimulation of presynaptic serotonin releaseAdverse Effects:Nausea & VomitingOndansetron interferes with analgesic effectNon addictive, less sedationDose: 3 mg/kg IM/IV/PO for moderate to severe pain
49Systemic Medications: Opioids Pentazocin:Agonist-Weak antagonistDose mg IV/ 50 mg PO for relief of moderate painSide Effects:DysphoriaSedationTachycardia, Hypertension (catecholamine release)
50Systemic Medications: Opioids Butorphanol:Agonist-AntagonistDose: 2-3 mg IMAlso available as intranasal spraySide Effects:SedationNauseaTachycardia, hypertensionLess dysphoria than other agonist antagonistsAntagonise other opioids if used together
51Systemic Medications: Opioids Buprenorphine:Semisynthetic, Agonist-AntagonistRoutes of administration:IV, IM, Neuraxial, SC, SL, TrasdermalUseful in morphine intolerant patientCeiling effect for respiratory depression, but not for analgesia.Antiflammatory actionUseful in intra-articular injectionsProlongs duration of analgesia in peripheral nerve blocks with LA
53Systemic Medications: Opioids Methadone:Synthetic broad spectrum opioidMu receptor agonistNMDA antagonistInhibitor of monoamine transmittersUseful in treatment of neuropathic painOrally well absorbedNo dose adjustment in renal diseaseDrug most commonly used for opioid rotation
54Systemic Medications: NSAIDs Mechanism of ActionInhibition of Cyclo-oxygenase enzymes (type 1 & 2)Reduce concentrations of PGE2PGE2CentallyIncrease Substance P and GlutamateIncrease sensitivity of second order neuronsDecrease NTs from descending pathwaySensitise peripheral nociceptors to histamine and bradykinin
55Systemic Medications: NSAIDs Benefits:Opioid SparingReduced incidence of opioidside effectsAnti-inflammatory effectsAdverse Effects:Platelet DysfunctionGastrointestinal UlcerationNephrotoxicityImpaired bone healingHypersensitivity
58Systemic Medications: NMDA Antagonists Ketamine:NMDA receptor antagonism theoretically reduces central sensitisation, hyperalgesia and opioid tolreanceCurrently role in postoperative pain relief is uncertainInsignificant difference in painClinically insignificant opioid sparingPsychomimetic side effects – hallucination, nighmares
59Neuraxial Analgesia: Epidural Analgesia Superior to systemic opioidsEfficacy determined byCatheter-incision site congruencyChoice of analgesic drugsLA+OpioidRates of infusionDuration of epidural analgesiaAt least 2-4 daysType of pain assessmentDynamic Vs Rest
60Neuraxial Analgesia: Epidural Analgesia DermatomalGuide to placementOf epidural cathetres
62Neuraxial Analgesia: Epidural Analgesia Opioids:Site of action:Lipophilic: systemicHydrophilic: spinalCathetre-Site congruencynot essentialNo motor blockadeNo hypotensionAnalgesia superior tosystemic opioidsLocal AnaestheticsAct on spinal nerve roots,dorsal root ganglion or spinalcord itself.High incidence of motor blockHypotensionSign\\\ificant failure rate due toregression and inadequateanalgesia
63Neuraxial Analgesia: Epidural Analgesia Differences between lipophilic and hydrophilic opioidsPropertyLipophilic OpioidsHydrophilic OpioidsCommon DrugsFentayl, SufentanylMorphine, HydromorphoneOnset of analgesiaRapid (5-10 min)Delayed (30-60min)Duration of analgesiaShorter (2-4 Hrs)Longer (6-24 hrs)CSF SpreadMinimalExtensiveSite of actionSpinal ± SystemicSpinalSide EffectsLower nausea and vomiting, pruritusEarly respiratory depressionNausea & vomiting, pruritusEarly (<6 Hr) and Delayed (> 6 Hr) respiratory depression
64Neuraxial Analgesia: Epidural Analgesia Local Anaesthetic-Opioid CombinationsAdditive EffectSuperior analgesia, including dynamic pain reliefLimits regression of sensory blockadeDecreased LA dose requirementAnalgesia superior to IV PCA with opioids
65Neuraxial Analgesia: Epidural Analgesia Adjuvants:Clonidine:5-20 μg/HrDose dependent hypotension, bradycardiaEpinephrineconc. Of 2.5 μg/mlKetamineTheoretically useful in attenuatingcentral sensitisation
66Neuraxial Analgesia: Epidural Analgesia Doses of Epidural OpioidsDrugEpidural Single DoseEpidural continuousFentanylμgμg/HrSufentanyl10-50 μg10-20 μg/HrAlfentanyl0.5-1 mg0.2 mg/HrMorphine1-5 mg0.1-1 mg/HrDiamorphine4-6 mg-Pethidine20-60 mg10-60 mg/HrExtended release Morphine5-15 mgNot recommendedDepodur: Extended release morphine. Morphine encapsulated with liposomal delivery system. Upto 48 hrs. only for lumbar.(Controlled releaseUpto 48 hrs)
67Epidural Analgesia: Adverse Effects Hypotension0.7 – 3 % with epidural LAsMotor Block2 – 3 % with epidural LAsMore with cathetre-incision incongruenceResolves within 2 hours of stopping infusionIf persistant, think of Spinal hematoma/abscess, cathetre migrationNausea & vomiting20 – 50 % with single dose neuraxial opioid45 – 80 % with continuous opioid infusionDose depdndent. Due to cephalad migrationLess with fentanyl than morphineTreated with Naloxone, Ondansetrone, Droperidol, Metoclopramide, Dexamethasone
68Epidural Analgesia: Adverse Effects Pruritus60% with Opioids; % with LAsDue to cephalad migration and activation of trigeminal nucleus. ?? Itch centreTreated with Naloxone, DroperidolRespiratory DepressionIncidence 0.1 – 0.9 % with opioidsEquivalent to systemic administration of opioidEarly < 6 hr, Delayed > 6 hrDelayed depression with Morphine. Due to cephalad spreadRisk Factors: Increasing dose, increasing age, concomitant sedatives, prolonged and extensive surgery, thoracic surgeryTreatment: Naloxone 0.5 – 5 μg/kg/hrUrinary RetentionHigher than with systemic opioids10 – 30% with epidural LasHigher with higher infusion rates of LA
69Epidural Analgesia Benefits: (LA based epidurals) Better attenuation of stress response to surgeryEarlier return of GI function without contributing to bowel dehiscenceDecreased postoperative pulmonary complicationsDecreased incidence of postop MI with thoracic epiduralBetter postop analgesiaRisks:Higher incidence of spinal hematoma with LMWHsInfections: Meningitis, Spinal Abscess (1/10000 with catheter < 4 days)Superficial cellulitis: 4-14 %Catheter migration: Intrathecal, Intravascular, subcutaneous
72Peripheral Regional Analgesia Pain control superior to systemic opioidsFewer side effects compared to systemic opioidsFewer neurologic and infectious complications compared to neuraxial blockProlonged durationSingle injection and continuous catheter techniques
73Peripheral Regional Analgesia Indications of peripheral Nerve BlocksPeripheral Nerve BlockadeIndicationsInterscaleneRotator cuff repair, Shoulder arthroplasty, ORIFSupraclavicularAnaesthesia to entire upper limb with single injectionRisk of pneumothoraxInfraclavicularSurgery on distal upper arm, forearm, wrist and handAxillarySurgery distal to elbowSeparate block for musculocutaneous and intercostobrachial nerves requiredMidhumeralSurgery of forearm, wrist and handProvides better block of radial nerve than axillary
74Peripheral Regional Analgesia Indications of peripheral nerve blocksPeripheral Nerve BlockIndicationLumbar plexusSurgery of kneeFemoral NerveTKA, ACL repair, femoral neck fracture, saphenous vein stripping, muscle biopsy of anterior, medial or lateral thighSciatic NerveAK amputation (combined with lumbar plexus blockAnkle replacement, arthrodesisCalcaneal osteotomyAchilles tendon repairPopliteal FossaBK amputation (combined with saphenous nerve block)Ankle surgery: Triple arthrodesis, Achilles tendon repairFoot surgery: Bunion surgery, Transmetatarsal amputation
75Peripheral Regional Analgesia Paravertebral Block:Suited for thoracic, breast surgery, VATS, cholecystectomy, nephrectomy etcUsed to treat rib fracture painPotential space, contains anterior and posterior ramus of the spinal nerve root with white and grey rami communicantesSingle injection or continuous catheter techniqueComparable to thoracic epidural blockadeNo hypotension, PONV, urinary retention
77Peripheral Regional Analgesia Other Techniques:Rectus Sheath BlockTransversus abdominis plane blockPlacement of continuous wound catheterContinuous intra-articular infusion of LAPeriarticular soft tissue injection of LAIntrapleural or Intraperitoneal Analgesia
78Peripheral Regional Analgesia Complications:Intravascular injectionUnintentional neuraxial spreadScalene blockLumbar plexus blockParavertebral blockNerve DamageIncidence 1:10000 – 1:30000Significant nerve damage 1:Direct injury, hematoma, infection, ischemia>90% recover within 1 week92 -97% within 4-6 weeks, 99% within 1 year
79Patient Controlled Analgesia Definition: Any technique of pain management that allows the patients to manage their own analgesia on demand Compensates for interpatient and intrapatient variability in analgesic needs, variability of serum drug levels, administrative delays
80Patient Controlled Analgesia Benefits:Better patient satisfactionBetter analgesiaEquivalent side effectsLess demand on nursing timeVariables programmed with PCA:Bolus DoseIncremental (demand) doseLockout intervalBackground infusion rate
83Patient Controlled Analgesia Risk Factors:Pulmonary diseaseOSARenal or Hepatic dysfunctionCHFClosed head injuryAltered mental statusLactating mothers
84Non Pharmacological Methods: Benefits:Reduce opioid requirement/side effectsAttenuate activation of sympathoadrenal systemMay provide postoperative analgesiaDevoid of any side effectsMethodsTENSAcupuncture/AcupressurePsyhological ApproachesMechanismSpinal cord modulationEndogenous enkephalinsUseful adjuvants to pharmacological therapy
85Special Populations: Pediatric Patients Barriers to effective pain control in children:Myths about pain and children:Children and infants do not feel painPain is not rememberedUnable to tell where it hurtsDon’t tell the truth about painDifficulty in assessmentDevelopmental, emotional and cognitive differencesDifficulty in conceptualising and quantifying painFear of side effects: Respiratory depression, addictiontransmitted by c fibres in neonates. the descending modulatory pathway is less developed and so they might feel more pain. There is less precision of impulse transmission at spinal cord.
86Special Populations: Pediatric Patients Pain Assessment Behavioural Observational Tools: For neonates and children < 3 yrsCRIES scaleCryingO2 requirement for SP)2 > 95%Increased vital signsExpressionsSleeplessnessEach parameter score 0-2Useful for neonatal postoperative painNeonatal-Infant Pain Scale (NIPS)Facial ExpressionCryBreathing PatternArmsLegsState of ArousalObserved for 1 minute before, during & aftera procedure and numeric score applied to eachNIPS > 3 implies painUseful for children < 1 year
87Special Populations: Pediatric Patients Pain Assessment Behavioural Observational Tools: For neonates and children < 3 yrsFLACC ScaleFaceLegsActivityCryingConsolabilityEach component scored 0-2Validated for 2 mo – 7 yrsChildren’s Hospital of Eastern Ontario Scale(CHEOPS)CryFacial ExpressionVerbalisationTouching of affected partTorso movementPosition of legsValidated for children 1-7 yrsScore ≥ 4 implies painSelf report :Children > 3 yrsWong-Baker Faces ScaleVAS
88Special Populations: Pediatric Patients Treatment: Pharmacological interventions similar to adultsPCA/NCANon Pharmacological InterventionsSensoryRocking,cuddling, touching, massaging, dim lighting, pacifiers, heat/cold applicationBehaviouralDistraction toys, music, videosSecurity object: blanket, stuffed animalsPlay therapyImageryCognitivePrayers, humor, relacation techniques
89Special Populations: Elderly Patients Special Considerations:Clinically significant reduction in intensity of pain perceptionCommunication, Affective, Cognitive, Social and Ideological barriersDifficulty in assessing painComorbid conditionsIncreased adverse effects due to untreated pain and interventionsDecreased analgesic requirementIncreased sensitivity and decreased clearanceUntreated pain is an important contributor to postopearive delerium
90SummaryPain is both a sensation and an emotion with wide interpersonal variations and the fifth vital sign.Untreated acute pain leads to many detrimental physiological effects and to chronicity.Treatment should include assessment, intervention and reassessment.A multimodal approach targeting the various elements of pain processing should be tried in all patients.LA based epidural analgesia has many advantages over systemic opioid analgesia.Inspite of the various interventions available, postoperative pain is undertreated in a majority of patients, more so in pediatric and geriatric populations.
91Referrences Barash, Stoelting et al, Clinical Anaesthesia, 6th ed Miller’s anaesthesia, 6th edAnaesthesia and Intensive Care Medicine. Volume 6:1 Jan 2005Recent Advances in Anaesthesia, No. 22. Chapter 74. management of Acute Postoperative PainPractice Guidelines for Acute Pain management in perioperative setting. Report by ASA task force on acute pain management. Anesthesiology 2004; 100:1573–81Pharmacology and Physiology in Anaesthetic practice, Stoelting and Miller, 4th EditionGanong’s Review of Medical Physiology, 22nd edition