mange of post operative pain

8/9/2019 Mange of Post Operative Pain

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Post operative

PAIN MANAGEMENT

By Dr. Khairy Ehab

MD of Anesthesia & ICU


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PainA physiochemical responsesleading to perception of:An unpleasant sensory&

emotionalexperiencearising from actual or potentialtissue damage.


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Map Of Pain Battle


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Nociception

Processing a noxious stimulusresulting in the perception ofpain by the brain.

I- TransductionConversion of a noxious

stimulus into electrical energyby a peripheral nociceptor.


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II- TransmissionPropagation through first-order

neurons

III- ModulationNeuronal plasticity at the synapse bet1st & 2nd order neurons within the

spinal cord

IV- Perception


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Noxious

StimulationsClick to edit Master text styles

Second level Third level Fourth level Fifth level

Transduction


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Classification Of

Peripheral NervesClick to edit Master text styles



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1st& 2nd-Order

NeuronsClick to edit Master text styles



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Click to edit Master text stylesSecond level Third level Fourth level Fifth level


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Projection OfSpinothalamic TractClick to edit Master text styles



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Categories Of

Postoperative Pain1- Nociceptive Pain Associated withan ongoing noxious stimulus(Somatic)

2- Inflammatory PainDue toongoingtissue inflammation(Somatic& / or Visceral)

3-Neuropathic PainResulting from alesion to P/ or CNSe.g.Damagedperipheral nerve Phantom limb, Stroke, andSpinal cord injury.


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PathophysiologyOf Post operative Pain

A Concept For treatment


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Peripheral And SpinalMechanism Involved In

Pain NeuroplasticityClick to edit Master text stylesSecond level Third level Fourth level Fifth level


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Sensitization OfPeripheral FieldFollowing release of chemical

mediators, nociceptors and theirneurons display sensitization.

Sensitizationmanifestedby:# Enhanced response to noxious

stimulation.# Newly acquired responsiveness

towider ran e of stimuli,


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I- Primary

HyperalgesiaSensitization of nociceptorsresults in:1- Decrease in pain threshold.

2- Increase in the frequencyresponseto the same stimulus intensity.

3- Decrease in response latency.

4-After-discharges: Spontaneousfiring even after cessation of thestimulus.


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II- Secondary

Hyperalgesia OrNeurogenic InflammationManifested byTriple Response

1- Flare red flush around the site ofinjury.

2-Local tissue edema.3-Sensitization to noxious stimuli.

Secondary hyperalgesia is due to antidromic

release of sP and CGRP from collateral axons ofthe primary afferent neuron.


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Central Modulation

Four Main components of the dorsalhorn1. Central terminals of1st order neurons.2. Intrinsic neuronsTheir cell bodies and

terminations within the spinal cord.3. 2nd order neurons with its axons travel in

ascending columns to terminate in the brain.4.Axons of descending systems whose cell

bodies reside in the brain.


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I- Wind-up1- Decreased Threshold of the2nd Order Neuron

Prolonged depolarization of spinalneurons Increase the magnitudeand duration of neuronal firing

Amplification of pain and,increase in the excitability of

spinal neuronsH r l i

Central Sensitization

3 D R L t f th 2 d d


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3- Decrease Response Latencyof the 2nd orderneuron.

4- Prolonged After Discharge of the 2nd Order

neuron even after C fiber input has stopped.II- Expansion Of Receptive FieldDorsal horn neurons increase their receptivefields such that adjacent neurons become

responsive to stimuli (whether noxious or not) towhich they were previously irresponsive.

III- long-Term Potentiation ChronicDue to Changes in dorsal horn neural function

as a result of damage or loss of segmentalinhibitory neurons.

M h i f C l


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Mechanism of CentralSensitizationNeurochemical Mediators

Receptor Major Ligand(s)1- Excitatory IonotropicAMPA GlutamateKainate GlutamateNMDA Aspartate

2- Excitatory MetabotropicNeurokininNK1 Substance P

Prostaglandin PG E2, & PG F2

F t t C t


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Fac tatory CentraModulationIntense and/or chronic noxious

inputMainly C-Fibers

Unplug Mg++from

NMDA The Chief Receptors

Of PainExposing Them To There

Activator - Aspartate

Allowing Ca++ to Surge into the

2nd order neuron


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Facilitatory CentralModulationClick to edit Master text styles


C l i Th C di l I


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Calcium The Cardinal IonOf Pain

High concentration of Ca++into dorsal horn cells

Generated by1- Membrane depolarization.

2- Released from the endoplasmic

reticulum after activation ofmetabotropic receptor.3- NMDA receptors activation.

Click to edit Master text styles


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Click to edit Master text stylesSecond level Third level Fourth level

Fifth level

Calcium Mediated Series

Of Intracellular Events

v


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I-Phospholipa

se C

Phosphat

idylinositol

Biphosph

Inositol

triphosphate

Diacylglyce

rol

Activate

catalyz

e

s

vmetabotr

opicreceptor

Highintracellu

lar Ca++

Di l l l


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DAG+ high intracellular ca++

increase production ofProtein kinase C which,has 2 actions:I- On Cell membrane of the 2nd order neuron

1- Sustains increased Ca++ permeability.

2- Enhances NMDA receptor excitation.3- Uncouples the G protein that activates thepotassium channel from the opioid receptor.

This can lead to opioid tolerance.

Diacylglycerol


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II- Protein Kinase C -Enhances

Intracelluer 3rd MessengerAs, it Activates proto-oncogenes[c-fos and c-jun],which control transcription of genes

encoding a variety of neuropeptidesthat modulate responses to noxiousstimuli.Enkephalins, Dynorphin , Tachykinins


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II- Ca++ Activates

phospholipase A2

tidylcholine

Phospholip

ase A2

Lipoxygenase

CycloxygenaseProstagla

ndin

cascade

Leukotrie

Arachidonicacid

Ca+

+

III C ++ A ti t NOS


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III- Ca++ Activates NOS# In side the 2nd order neuron

NOS catalyzes1- Production of protein kinases PKCand,

2- Alterations in gene expression.3- Increases production ofNO# Diffused NO enhances

1-Neurotransmitters release fromthe primary afferent.2- NMDA receptorresponse of the

Postsynaptic neurons.


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Spinal Reflexes InvolvedIn Pain Modulation



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SpinalModulation

Of Pain


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Segmental Inhibition -Gate theory# Activation of large afferent fiberssub serving epicritic sensationinhibits WDR neuron andspinothalamic tract activity.

# Activation of noxious stimuli innoncontiguous parts of the bodyinhibits WDR neurons at otherlevels; i.e., pain in one part of thebod inhibits ain in other arts.

Segmental Inhibitory


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Segmental InhibitoryNeurotransmittersGABAB Increases K+ conductance across the cell

membrane. Baclofen is an agonist.GABAA Increases Cl conductance across the cell

membrane. Benzodiazepines potentiate thisaction.

Glycine receptors Increases Cl conductanceacross neuronal cell membranes but, also has afacilitatory effect on the NMDA receptor.

AdenosineA1 receptor inhibits adenylcyclasebut, A2 receptor has an opposite effect.

Cli k di M l spinal


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Efferentpathways

involved innociceptiveregulation


spinalModulation


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Descending InhibitoryPathways

It conveys 3 inhibitory systems that,descend in the Dorsolateral funiculus.

1- Noradrenergic System

Originate from the periaqueductalgray area and reticular formation.It activates pre & post-synaptic 2-

G proteins receptors opening K+channels and inhibiting increases inintracellular calcium concentration.

2 Serotonergic System


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2- Serotonergic SystemOriginate from NRM. It provides both

inhibitory and facilitatory control of dorsalhorn nociceptive function depending onthe receptor subtype(s) activated.

Presynaptic Metabotropicreceptors 5- HT

Inhibitory Decreases transmitterrelease.

Presynaptic Ionotropic receptors 5-HT3

Facilitatory Enhance tansmitter

release.


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3- Endogenous Opiate

SystemOriginate from NRM and reticular

formation, acts via methionine, &, leucineenkephalins, and -endorphin.

1- Hyperpolarization of 1st orderneuron , by inhibition of voltage-gated Ca2+channels thus,inhibiting the release of sP. [Unlike exogenous]

2- Hyperpolarization of 2nd order

neuron, as it enhances K+ efflux byactivating G-protein coupled inwardlyrectifying K+ channels.


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Ascending Noxious

Stimulation & MedullaryResponses

1- On Facilitatory ResponseProlonged noxious stimulationactivate descending facilitatory

pathways that enhance dorsal hornnociceptive conduction.

2- Off Inhibitory Response

Provide inhibitory input to dorsalhorn nociceptive circuits but, theyare inhibited by noxious stimuli.

3- Neutral Response


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Adverse PhysiologicSequelae Of Pain

RESPIRATORY


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RESPIRATORY

I-Increased skeletal muscletension HypoxemiaII-Decreased total lung

compliance1- Hypercapnia2- Ventilation-perfusion

3- abnormality4- Atelectasis5- Pneumonitis

ENDOCRINE


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ENDOCRINE Adrenocorticotropic hormone Protein catabolism

Cortisol Lipolysis

Glucagon Hyperglycemia Insulin

Testosterone Protein anabolism Aldosterone Salt and water retention Antidiuretic hormone Cortisol Congestive heart failure

Catecholamines . VasoconstrictionAngiotensin II Myocardial contractility& HR

CARDIOVASCULAR


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CARDIOVASCULAR

Increased myocardial workmediated byCatecholamines,

Angiotensin II

1- Dysrhythmias

2- Angina3- Myocardial infarction4- Congestive heart failure

IMMUNOLOGIC


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IMMUNOLOGIC

1- Lymphopenia ... Decreasedimmune function

2- Depression of reticuloendothelialsystem

3- Leukocytosis

4- Reduced killer T-cell cytotoxicity

COAGULATION


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COAGULATION

EFFECTSIncreased platelet

adhesiveness Increasedincidence of

1- Thromboembolic

2- Diminished fibrinolysis

phenomena

3- Activation of coagulation

GASTROINTESTINAL


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GASTROINTESTINAL

1- Increased sphincter tone Ileus2- Decreased smooth muscle tone

GENITOURINARY1- Increased sphincter tone

2- Decreased smooth muscle toneUrinary retention

General Well Being


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General Well-BeingPain increases skeletal muscle tone

in the area of the surgical field. Thispostoperative impairment of musclefunction may lead to physical

immobility and a delayed return tonormal function. Poorly controlledpain also contributes to insomnia,

anxiety, and a feeling ofhelplessness. These psychologicalfactors, coupled with the

immobilization that occurs because

Inadequately Treated


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Inadequately TreatedInflammatory Models Ultimately

Result in chronic neuropathic pain

I- Peripheral Field


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I- Peripheral Field

Recently it has been shownthat

Wallerian degeneration of

sensory axons can occur withoutany lesion to the nerve axon as aresult, ofongoing inflammation.

i.e. Neuropathic pain is the end

result of in adequately treated Inflammatoryt Wallerian


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DegranulationofMast

cells

NGFGlial &

Schwann cells

InflammatoryMediators

Neutrophils

, &Macrophages

Cytokines

& TNFRelease

MastCells

Relea

se

A

ct

ivat

e

Rec

rui

t

Walleriandegenerati

on

II- Central Glial Cells


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II Central Glial CellsActivation Chronic

Pain - Phantom PainMicroglias initiate the immune

response,

when their toll-like receptors areactivated, they obtains anamoeboid form, and they release

substances that activateAstrocytes andOligodendrocytes.

Both types of cells produce pro-

Click to edit Master text styles


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Eff Of R l d


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Effects Of Released

Cytokines

1- Release of cyclooxygenase.

2- Nitric oxide synthase.3- SP and activate NMDA

receptors.4- Activate chemokines inmacrophages and endothelial

cells, which initiateextravasation of leukocytes

from the blood neuronal

Managements of


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Managements of

Post operative Pain


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Principles of PainAssessment

Assess and reassess Use methods appropriate to cognitive

status and context Assess intensity, relief, mood, and

side effects Visual Analogue Score( VAS ) Use verbal report (VRS) whenever

possible Document in a visible place Include the family

Methods Of Pain


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Methods Of PainControllingII- Pharmacological

1- OpioidsIm, IV infusion or PCA

2- Local anesthetics:Local Infiltration

Nerve BlocksEpidural Blocks

3- NSAIDS & adjuvantIM, IV infusion or PCA

I-Nonpharmacological1- Preoperative2- Counseling TENS3- Acupuncture

I-Non Pharmacologic


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I Non PharmacologicMethods

PRE-OP COUNSELLING:

Well informed patients about: Nature of operation Nature of post operative pain

Methods of analgesia available

Cope better with Post Op Pain

TENS


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TENS

Stimulates afferent myelinated (A-beta) nerve fibers at 70hz

Inhibitory circuits within sp cordactivated

Nerve impulse transmission reduced

Maximum benefit in neurogenic pain

Pharmacologic


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Pharmacologic

MethodsOPIOIDS

1- Activate opioid receptors within theCNS

2- Reduce transmission of nerve

impulses by modulation in the dorsal

horn

Local Anesthetics


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Local Anesthetics

Block conduction of nerveimpulsesCan be given withAdrenaline for

1- Decreases absorption of L.Aallowing larger doses.

NASIDS


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NASIDS

Block the synthesis of PGs

Only suitable for mild pain

In moderate pain it needsadjuvant


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Principle Of PainManagementPre-emptive analgesia

Balanced or combinationanalgesia

Analgesia ladder

Preemptive Analgesia


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Preemptive AnalgesiaPharmacologically induces an

effective analgesic statepriorto thesurgical trauma

This may involve1- Infiltration of the wound with localanesthetic.

2- Central neural blockade.3- Administration of effective doses of

Opioids, NSAIDs, Ketamine,

Al ha-2 A onists or IV infusion of

Danger Of Neuro-axial


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Danger Of Neuro-axialBlock1- Immediately after Spinal

analgesia deafferentationshock

This occur when the neuroendocrine stress response issupporting the hemodynamic.

2- After fid spinal analgesiaSudden sever pain perception

after fid of spinal action can lead

to serous com lications in Postoperative Balanced


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Postoperative BalancedAnalgesia

Co Analgesics Commonly UsedFor Pain

NSAIDSAcetaminophen

Antidepressants

Anticonvulsants

Corticosteroids

AnalepticsBenzodiazepines

Antispasmodics

MusclerelaxantsSystemic local

anestheticsThey Reduce required amount and side

Making PCA Work for


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Making PCA Work foryour Patient

The goal of postoperativepain management is To provideminimum effective analgesic

concentration (MEAC) that issafe, effective and, free side effectscontinuous analgesia.

The AimTo reduce postoperative

morbidity, facilitate recovery, and

PCA Cont


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PCA - Cont.DosingTotal required dose of postoperative opioids

=100 age of the patient/24 Hr.

Basal rates (back ground infusion)produce serumopioid levels around the MEAC as much as possible

BolusTo re-establish analgesia by increasing the serum

opioid concentration from a level slightly less than theMEAC to a level of more than the MEAC but less than thelevel at which side effects become significant.

Modified WHO Analgesic


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Pain

Step 1

Nonopioid Adjuvant

Pain persisting or increasing

Step 2Opioid for mild to moderate pain

Nonopioid Adjuvant



Step 3

Opioid for moderate to severe pain Nonopioid Adjuvant

Invasive treatments

Opioid Delivery

Quality of Life

Modified WHO AnalgesicLadder

Proposed 4th

Step

The WHOLadder

Deer, et al., 1999


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Thank You

mange of post operative pain

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