9/10/2015pain1 pain!! definition, assessment, physiology and treatment dr simon holbrook
TRANSCRIPT
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PAIN!! PAIN!! Definition, assessment, Definition, assessment,
physiology and treatmentphysiology and treatment
Dr Simon HolbrookDr Simon Holbrook
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Aims & ObjectivesAims & Objectives AimAim
– To improve overall understanding of pain managementTo improve overall understanding of pain management Learning ObjectivesLearning Objectives
– To define painTo define pain– To describe methods of pain assessmentTo describe methods of pain assessment– To illustrate pain pathwaysTo illustrate pain pathways– To describe commonly used drugs & methods of To describe commonly used drugs & methods of
administration administration – To define the analgesic ladderTo define the analgesic ladder– To calculate safe doses of local anaesthetic agentsTo calculate safe doses of local anaesthetic agents– To define chronic pain To define chronic pain – To illustrate briefly the management of chronic painTo illustrate briefly the management of chronic pain
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Definition of painDefinition of pain
““An unpleasant sensory and emotional An unpleasant sensory and emotional experience associated with actual or experience associated with actual or potential tissue damage, or described potential tissue damage, or described in terms of such damage”in terms of such damage”
International Association for the Study of International Association for the Study of PainPain
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AssessmentAssessment
An objective estimate of a subjective An objective estimate of a subjective perception (i.e. it’s difficult!)perception (i.e. it’s difficult!)
ScalesScales– Pictures for childrenPictures for children– Numerical for adultsNumerical for adults
Clouded by personality and cultureClouded by personality and culture
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Pain PathwaysPain Pathways
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POSTOPERATIVE PAINPOSTOPERATIVE PAINWhy bother?Why bother?
CVSCVS– TachycardiaTachycardia– HypertensionHypertension– Increased Increased
myocardial Omyocardial O2 2
demanddemand GIGI
– Nausea and Nausea and vomitingvomiting
– IleusIleus
RSRS– ↓ ↓ Vital CapacityVital Capacity– ↓ ↓ FRCFRC– Basal atelectasisBasal atelectasis– Respiratory Respiratory
infectioninfection
OtherOther– Urinary retentionUrinary retention– DVT + PEDVT + PE
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ANALGESICS ANALGESICS Site of ActionSite of Action
They may act at site of injury – They may act at site of injury – decrease pain associated with nerve decrease pain associated with nerve conductionconduction
They may alter nerve conductionThey may alter nerve conduction They may modify nerve transmission They may modify nerve transmission
in dorsal hornin dorsal horn They may affect the central They may affect the central
component component
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ORAL ANALGESICS 1ORAL ANALGESICS 1
Paracetamol Paracetamol – Inhibits prostaglandin productionInhibits prostaglandin production– Central action – COX 3Central action – COX 3– Dose = 10-20mg/kg up to 1gDose = 10-20mg/kg up to 1g– Repeat 4 times a day (max 4g/day)Repeat 4 times a day (max 4g/day)– Good opioid sparing effect if given Good opioid sparing effect if given
regularlyregularly– Good antipyreticGood antipyretic– Poor anti-inflammatoryPoor anti-inflammatory
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ORAL ANALGESICS ORAL ANALGESICS
ParacetamolParacetamol– Side-effects extremely rare unless taken in Side-effects extremely rare unless taken in
overdoseoverdose– 1% is metabolised to toxic metabolite and 1% is metabolised to toxic metabolite and
normally inactivated by conjugation normally inactivated by conjugation – In overdose glutathione groups depleted In overdose glutathione groups depleted – Excess metabolite binds to SH groups on liver Excess metabolite binds to SH groups on liver
macromolecules –hepatic necrosismacromolecules –hepatic necrosis– RRxx N-acetylcysteine (-SH donor) N-acetylcysteine (-SH donor)
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ORAL ANALGESICS ORAL ANALGESICS NSAIDsNSAIDs
Cyclo-oxygenase inhibitorsCyclo-oxygenase inhibitors Blocks prostaglandin and Blocks prostaglandin and
thromboxane productionthromboxane production Prostaglandins potentiate action of Prostaglandins potentiate action of
bradykinin & other polypeptides at bradykinin & other polypeptides at pain receptorspain receptors
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ORAL ANALGESICS ORAL ANALGESICS NSAIDsNSAIDs
COX 1 constitutive isoenzyme COX 1 constitutive isoenzyme responsible for homeostatic responsible for homeostatic mechanisms (renal and gastric mucosa)mechanisms (renal and gastric mucosa)
COX 2 inducible form in response to COX 2 inducible form in response to inflammation inflammation
Selective COX 2 inhibitors with fewer Selective COX 2 inhibitors with fewer side effectsside effects
Side effects: Bronchospasm, GI effects, Side effects: Bronchospasm, GI effects, renal, plateletsrenal, platelets
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ORAL ANALGESICS ORAL ANALGESICS
Compound analgesicsCompound analgesics– Paracetamol plus weak opioidParacetamol plus weak opioid– Codeine, DihydrocodeineCodeine, Dihydrocodeine– E.g. Co-codamol, Co-dydramolE.g. Co-codamol, Co-dydramol– Mild to moderate painMild to moderate pain– Beware overdoseBeware overdose
Oral opioidsOral opioids– Codeine, dihydrocodeine (weak)Codeine, dihydrocodeine (weak)– Morphine (strong)Morphine (strong)
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OPIOID RECEPTORSOPIOID RECEPTORS
Mu – OP3 – analgesia, respiratory Mu – OP3 – analgesia, respiratory depression, euphoria, miosis, depression, euphoria, miosis, bradycardia, physical dependencebradycardia, physical dependence
Delta – OP1 – unclearDelta – OP1 – unclear Kappa – OP2 - analgesia, respiratory Kappa – OP2 - analgesia, respiratory
depression, miosis, sedation, depression, miosis, sedation, dysphoria dysphoria
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ORAL ANALAGESICS ORAL ANALAGESICS
TramadolTramadol– mu receptor agonistmu receptor agonist– Increases inhibitory descending activity Increases inhibitory descending activity
(5HT & noradrenaline)(5HT & noradrenaline)– PO / IM / IV 50 – 100mg/ 4-6 hourlyPO / IM / IV 50 – 100mg/ 4-6 hourly– Not controlled drugNot controlled drug– Lower incidence of some side effectsLower incidence of some side effects
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INTRAVENOUS INTRAVENOUS ANALGESICS ANALGESICS
OPIOIDSOPIOIDS IV opioids for severe pain e.g. IV opioids for severe pain e.g.
morphine, diamorphine, oxycodonemorphine, diamorphine, oxycodone Strong OP3 receptor agonistsStrong OP3 receptor agonists Can be given po / im / Can be given po / im /
transcutaneous /spinal / epiduraltranscutaneous /spinal / epidural PCASPCAS Effective for C-fibre painEffective for C-fibre pain Ineffective for AIneffective for Aδ-fibre painδ-fibre pain
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INTRAVENOUS INTRAVENOUS ANALGESIA OPIOIDSANALGESIA OPIOIDS
Opioid side-effectsOpioid side-effects– Respiratory depression: Tidal Volume Respiratory depression: Tidal Volume ↑, ↑,
Respiratory Rate ↓: Overall MV ↓Respiratory Rate ↓: Overall MV ↓– Hypotension: Sympathetic tone Hypotension: Sympathetic tone ↓, ↓, vagal vagal
tone tone ↑↑, histamine release * , histamine release * – Euphoria, decreased conscious levelEuphoria, decreased conscious level– ConstipationConstipation– Tolerance and dependenceTolerance and dependence
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LOCAL ANAESTHETICS LOCAL ANAESTHETICS (LA)(LA)
Prevent pain by causing a reversible Prevent pain by causing a reversible block of conduction along nerve block of conduction along nerve fibres.fibres.
Inhibition of Sodium channel in axon Inhibition of Sodium channel in axon preventing K/Na exchangepreventing K/Na exchange
Membrane stabilisation affectMembrane stabilisation affect
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LA - HistoryLA - History
Cocaine isolated from Erythroxylon Cocaine isolated from Erythroxylon cocacoca
Eye surgery - Koller 1884Eye surgery - Koller 1884 Nerve blocks – Hall & HalstedNerve blocks – Hall & Halsted Epidural / spinal? - Corning 1885Epidural / spinal? - Corning 1885 Spinal - Bier 1899Spinal - Bier 1899 Caudal Epidural 1901Caudal Epidural 1901 Procaine – Einhorn -1904Procaine – Einhorn -1904 Lumbar epidural – Pages 1921Lumbar epidural – Pages 1921
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StructureStructure
Two groups - Esters and AmidesTwo groups - Esters and Amides Difference is in the link Difference is in the link Esters include cocaine, Esters include cocaine,
amethocaineamethocaine Amides include lidocaine, Amides include lidocaine,
bupivacaine, prilocaine, bupivacaine, prilocaine, mepivacaine, etidocainemepivacaine, etidocaine
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Mechanism of ActionMechanism of Action
LA in 2 forms - hydrochloride salt LA in 2 forms - hydrochloride salt (acid) and free base(acid) and free base
Only free base can penetrate lipid to Only free base can penetrate lipid to get to Na channelget to Na channel
Free base concentration depends on Free base concentration depends on dissociation which depends on pH dissociation which depends on pH tissuetissue
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Types of Nerves BlockedTypes of Nerves Blocked
Sensory – anaesthesia – primarily Sensory – anaesthesia – primarily pain fibrespain fibres
Autonomic - mainly loss of Autonomic - mainly loss of sympathetic tonesympathetic tone
Motor - paralysis/ weaknessMotor - paralysis/ weakness i.e. all nerves!!!i.e. all nerves!!!
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Side EffectsSide Effects
Sympathetic blockade after epidural Sympathetic blockade after epidural and spinal anaesthetic causing and spinal anaesthetic causing hypotension = commonhypotension = common
Dural puncture headache 1/200Dural puncture headache 1/200 Rarely epidural haematoma, Rarely epidural haematoma,
abscess, nerve / spinal cord damaheabscess, nerve / spinal cord damahe Allergy very rare - dentistsAllergy very rare - dentists SYSTEMIC TOXICITYSYSTEMIC TOXICITY
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Systemic ToxicitySystemic Toxicity
LA leaks into circulation and acts on brain LA leaks into circulation and acts on brain and heartand heart
Changes seen due to membrane Changes seen due to membrane stabilising effectstabilising effect
Effects depend on dose of LA, injection site Effects depend on dose of LA, injection site and speed, vasoconstrictor, metabolismand speed, vasoconstrictor, metabolism
Worst if large dose of poorly metabolised Worst if large dose of poorly metabolised LA injected into very vascular areaLA injected into very vascular area
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Signs and SymptomsSigns and Symptoms
Tingling - mouth and noseTingling - mouth and nose TinnitusTinnitus Light-headedness, anxiety, Light-headedness, anxiety,
drowsinessdrowsiness Convulsions and loss of Convulsions and loss of
consciousnessconsciousness Respiratory depressionRespiratory depression Cardiovascular collapseCardiovascular collapse
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Treatment of Treatment of ToxicityToxicity
Stop injection of drugStop injection of drugGive oxygenGive oxygenABCABC
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Safe DosesSafe Doses
All have published safe doses All have published safe doses based on mg per kg based on mg per kg
A 1% solution has 10 mg per mlA 1% solution has 10 mg per ml Bupivacaine max. dose 2mg/kgBupivacaine max. dose 2mg/kg Lignocaine max. dosesLignocaine max. doses
– 3mg/kg3mg/kg– 7mg/kg with adrenaline7mg/kg with adrenaline
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Toxic Dose CalculationToxic Dose Calculation
Look at the back page Look at the back page now and work in groups now and work in groups through the questionsthrough the questions
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Routes of AdministrationRoutes of Administration
Topical - EMLA, AmetopTopical - EMLA, Ametop Mucosal - ENT proceduresMucosal - ENT procedures Tissue infiltration - around incisionTissue infiltration - around incision Peripheral nerve block – e.g. femoralPeripheral nerve block – e.g. femoral Plexus block – e.g. brachialPlexus block – e.g. brachial EpiduralEpidural SpinalSpinal
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Epidural Analgesia 1Epidural Analgesia 1
Local anaesthetic & opioid mixtureLocal anaesthetic & opioid mixture Concentration of LA sufficient to Concentration of LA sufficient to
block C- and Ablock C- and Aδ-fibres but not the δ-fibres but not the larger fine touch, proprioception and larger fine touch, proprioception and motor fibresmotor fibres
Only way to prevent fast pain on Only way to prevent fast pain on moving and coughing moving and coughing
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Epidural Analgesia 2Epidural Analgesia 2
Side-effects Side-effects – Hypotension related to sympathetic blockade. Hypotension related to sympathetic blockade. – Epidural abscess, haematoma, spinal Epidural abscess, haematoma, spinal
cord/nerve damage is rarecord/nerve damage is rare Added opioids allows high concentration at Added opioids allows high concentration at
spinal mu receptors keeping systemic spinal mu receptors keeping systemic levels low, limiting side-effects.levels low, limiting side-effects.
Also adding opioids decreases required Also adding opioids decreases required concentration of local anaesthetic – aids concentration of local anaesthetic – aids patient mobilitypatient mobility
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Epidural Analgesia 3Epidural Analgesia 3
Do not remove – leave it to the pain teamDo not remove – leave it to the pain team Hypotension and pain free => reduce rateHypotension and pain free => reduce rate Hypotension and in pain => fluid bolus & Hypotension and in pain => fluid bolus &
discuss with anaesthetist / pain teamdiscuss with anaesthetist / pain team Only stop it if severe hypotension presentOnly stop it if severe hypotension present
– Call pain team or on-call anaesthetist Call pain team or on-call anaesthetist immediately immediately
– Ephedrine 3mg bolus iv (only if you have to, Ephedrine 3mg bolus iv (only if you have to, comes as 30mg in 1ml vials)comes as 30mg in 1ml vials)
Never inject down itNever inject down it– Make sure you know which is the iv lineMake sure you know which is the iv line
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OTHERSOTHERS Good communication because of Good communication because of
unrealistic expectationsunrealistic expectations AlternativesAlternatives
– Local anaesthetic infiltration/nerve Local anaesthetic infiltration/nerve blocksblocks
– Heat pads/ massageHeat pads/ massage– TENS / acupunctureTENS / acupuncture– +/- visitors+/- visitors
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CHRONIC PAIN CHRONIC PAIN DefinitionDefinition
““Persistent and intractable pain lasting Persistent and intractable pain lasting more than 6 months”more than 6 months”
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CHRONIC PAIN CHRONIC PAIN
Often neuropathic in originOften neuropathic in origin 2 characteristic types of pain2 characteristic types of pain
– Sharp, shootingSharp, shooting– burningburning
ExamplesExamples– Nerve root compression, pancreatitis, ischaemic Nerve root compression, pancreatitis, ischaemic
painpain Pain experienced beyond area of original Pain experienced beyond area of original
injury (neural plasticity)injury (neural plasticity) Allodynia – light touch feels unpleasantAllodynia – light touch feels unpleasant
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CHRONIC PAINCHRONIC PAIN MultidisciplinaryMultidisciplinary
– Anaesthetist (coordinates)Anaesthetist (coordinates)– Pain nurses, psychologist, physiotherapist, Pain nurses, psychologist, physiotherapist,
pharmacistpharmacist Patient must understand there is no Patient must understand there is no
curecure Treatment is aimed at symptom control Treatment is aimed at symptom control
& minimizing lifestyle restrictions& minimizing lifestyle restrictions
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Drugs Used in Chronic PainDrugs Used in Chronic Pain
Conventional analgesicsConventional analgesics Antidepressants e.g. amitriptylineAntidepressants e.g. amitriptyline AntiepilepticsAntiepileptics
– Phenytoin, carbamazepine, sodium valproatePhenytoin, carbamazepine, sodium valproate– Gabapentin Gabapentin
Clonidine – alpha 2 agonistClonidine – alpha 2 agonist KetamineKetamine CorticosteroidsCorticosteroids Capsaicin Capsaicin
– C fibresC fibres– Depletes substance PDepletes substance P
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APPLY THIS APPLY THIS KNOWLEDGEKNOWLEDGE
TO THE PAPERMAN!!TO THE PAPERMAN!!
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04/19/2304/19/23 PAINPAIN 5656
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Local anaestheticsNSAID’s
TENSHeatMassage
Nerve blocks
Sympathetic block
Epidural
Spinal
Opioids
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QuestionsQuestions