Management of Post Operative Pain 1

8/8/2019 Management of Post Operative Pain 1

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Post operative

PAIN MANAGEMENT

By Dr. Khairy EhabMD of Anesthesia & ICU


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Pain A physiochemical responseseading to perception of:An unpleasant sensory &

motional experience arisingrom actual or potential tissueamage.


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Map Of Pain Battle


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Nociception Processing a noxious stimulusresulting in the perception of pain by the brain.

I- TransductionConversion of a noxious stimulus

into electrical energy by aperipheral nociceptor.


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II- TransmissionPropagation through first-order

neurons

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

spinal cord

IV- Perception


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NoxiousStimulations

Click to edit Master text stylesSecond level

Third level Fourth level

Fifth level

Transduction


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Classification Of Peripheral

NervesClick to edit Master text stylesSecond level


Fifth level


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1st& 2nd-Order NeuronsClick to edit Master text styles

Second level Third level

Fourth level Fifth level


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Fifth level


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Projection Of SpinothalamicTract Click to edit Master text styles




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Categories Of PostoperativePain

1- Nociceptive Pain Associatedwith an ongoing noxious stimulus ( Somatic )

2- Inflammatory Pain Due toongoing tissue inflammation ( Somatic& / or Visceral )

3- Neuropathic Pain Resulting froma lesion to P/ or CNS e.g. Damagedperipheral nerve Phantom limb, Stroke, and

Spinal cord injury.


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Peripheral And Spinal MechanismInvolved In Pain Neuroplasticity



Fifth level


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Sensitization Of PeripheralFieldFollowing release of chemical

mediators, nociceptors and theirneurons display sensitization.

Sensitization manifested by:

# Enhanced response to noxiousstimulation.# Newly acquired responsiveness

to


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I- Primary Hyperalgesia

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

2- Increase in the frequency response tothe same stimulus intensity.3- Decrease in response latency .4- After-discharges : Spontaneous firingeven after cessation of the stimulus.


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II- Secondary Hyperalgesia

OrNeurogenic InflammationManifested by Triple Response

1- Flare red flush around the site of injury.

2- Local tissue edema. 3- Sensitization to noxious stimuli.Secondary hyperalgesia is due to antidromic release of

sP and CGRP from collateral axons of the primary afferent neuron.


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Central Modulat ionFour Main components of the dorsal horn1. Central terminals of 1st order neurons .

2. Intrinsic neurons Their cell bodies andterminations within the spinal cord.3. 2nd order neurons with its axons travel

in ascending columns to terminate in thebrain. 4. Axons of descending systems whosecell bodies reside in the brain.


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I- Wind-up1- Decreased Threshold of the 2nd

Order Neuron

Prolonged depolarization of spinalneurons Increase the magnitude and

duration of neuronal firing Amplification of pain and, increase in

the excitability of spinal neuronsHyperalgesia

-

Central Sensitization

f


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3- Decrease Response Latency of 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 functionas a result of damage or loss of segmental

inhibitory neurons.


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Mechanism of CentralSensitizationNeurochemical Mediators

Receptor Major Ligand(s)1- Excitatory Ionotropic

AMPA Glutamate

Kainate GlutamateNMDA Aspartate

2- Excitatory Metabotropic

Neurokinin NK1 Substance PProstaglandin PG E2, & PG F2


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ac tatory entraModulation

Intense and/or chronic noxious inputMainly C-Fibers

Unplug Mg++from

NMDA The Chief Receptors Of Pain

Exposing 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




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CalciumThe Cardinal Ion Of Pain

High concentration of Ca++ into dorsalhorn cells

Generated by 1- Membrane depolarization .

2- Released from the endoplasmic reticulumafter activation of metabotropic receptor .

3- NMDA receptors activation.

Cli k t dit M t t t t l


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Fifth level

Calcium Mediated SeriesOf Intracellular Events


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DAG + high intracellular ca++increase production of Protein kinase C which,has 2 actions:

I- On Cell membrane of the 2nd orderneuron

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 - EnhancesIntracelluer 3rd Messenger

As, it Activates proto-oncogenes

[c-fos and c-jun

],

which control transcription of genes encoding a variety of

neuropeptides that modulateresponses to noxious stimuli.Enkephalins, Dynorphin , Tachykinins


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II- Ca++ Activates phospholipase A2Phosphati

dyl cholinePhospholipase

A2

Lipoxy genase

CycloxygenaseProstag

landincascade

Leukotrienes

Arachidonic acid

Ca+

+


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

catalyzes1- Production of protein kinases PKC and,

2- Alterations in gene expression .3- Increases production of NO

# Diffused NO enhances

1- Neurotransmitters release from theprimary afferent.

2- NMDA receptor response of the

Postsynaptic neurons.


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Spinal Reflexes Involved InPain Modulation



Fifth level


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Segmental Inhibition - Gatetheory # Activation of large afferent fibers sub

serving epicritic sensation inhibits WDRneuron and spinothalamic tract activity.

# Activation of noxious stimuli innoncontiguous parts of the body inhibitsWDR neurons at other levels; i.e., pain inone part of the body inhibits pain in otherparts.

S g t l I hibit


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Segmental InhibitoryNeurotransmitters

GABAB Increases K+ conductance across the

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

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

Adenosine A1 receptor inhibitsadenylcyclase but, A2 receptor has

an opposite effect.

i l


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Efferent pathways

involved innociceptiveregulation



Fifth level

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-synaptic2- G proteins receptors opening K+channels and inhibiting increases in

intracellular calcium concentration.

2 S i S


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2- Serotonergic SystemOriginate from NRM. It provides both

inhibitory and facilitatory control of dorsalhorn nociceptive function depending on thereceptor subtype(s) activated.

Presynaptic Metabotropic receptors5- HT

Inhibitory Decreases transmitterrelease.

Presynaptic Ionotropic receptors 5-HT3


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3- Endogenous OpiateSystemOriginate from NRM and reticular

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

1- Hyperpolarization of 1st order

neuron , by inhibition of voltage-gated Ca2+channels thus,inhibiting the release of sP. [ Unlikeexogenous ]

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 & MedullaryResponses1- On Facilitatory ResponseProlonged noxious stimulation activatedescending facilitatory pathways that

enhance dorsal horn nociceptiveconduction.2- Off Inhibitory Response Provide

inhibitory input to dorsal horn nociceptivecircuits but, they are inhibited by noxiousstimuli.

3- Neutral Response


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Adverse PhysiologicSequelae Of Pain

RESPIRATORY


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RESPIRATORY I-Increased skeletal muscle

tension HypoxemiaII-Decreased total lung

compliance1- Hypercapnia2- Ventilation-perfusion3- abnormality4- Atelectasis

5- 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 . Vasoconstriction

Angiotensin II Myocardial contractility& HR

CARDIOVASCULAR


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CARDIOVASCULAR

Increased myocardial work mediated by

Catecholamines, Angiotensin II

1- Dysrhythmias

2- Angina3- Myocardial infarction4- Congestive heart failure


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IMMUNOLOGIC

1- Lymphopenia ... Decreased immunefunction

2- Depression of reticuloendothelial system

3- Leukocytosis

4- Reduced killer T-cell cytotoxicity

COAGULATION EFFECTS


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COAGULATION EFFECTS

Increased platelet adhesivenessIncreased incidence of 1- Thromboembolic

2- Diminished fibrinolysis phenomena

3- Activation of coagulation cascade

GASTROINTESTINAL


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GASTROINTESTINAL

1- Increased sphincter tone Ileus2- Decreased smooth muscle tone

GENITOURINARY 1- Increased sphincter tone

2- Decreased smooth muscle tone Urinaryretention

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 to normal function.Poorly controlled pain also contributes toinsomnia, anxiety, and a feeling of helplessness. These psychological factors,coupled with the immobilization thatoccurs because of the increased skeletalmuscle tone, create a perioperative

atmosphere that has been feared by most

I d l T d


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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 shown that Wallerian degeneration of

sensory axons can occur without anylesion to the nerve axon as a result, of ongoing inflammation.

i.e. Neuropathic pain is the endresult of in adequately treated

inflammatory pain . I fle


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Degranulation

of Mast cells

Glial &Schwann cells

InflammatoryMediators

Neutrophils, &Macrophages Cytokines

& TNFRelease

Mast Cells

Release

Activate

Recruit

Walleriandegeneration

II Central Glial Cells Activation


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II- Central Glial Cells ActivationChronic Pain - Phantom

PainMicroglias initiate the immune

response,

when their toll-like receptors areactivated, they obtains an amoeboid form,and they release substances that activateAstrocytes and Oligodendrocytes .

Both types of cells produce pro-inflammatory cytokines, including theinterleukins IL-1 and IL-6 and tumor necrosis factor .

Click to edit Master text styles


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Fifth level


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Effects Of Released

Cytokines1- Release of cyclooxygenase.2- Nitric oxide synthase.3- SP and activate NMDA receptors.

4- Activate chemokines in macrophagesand endothelial cells, which initiateextravasation of leukocytes from the blood

neuronal damage.mainly segmental inhibitory

interneuron

M f


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Managements ofPost operative Pain


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Principles of PainAssessment

Assess and reassessUse methods appropriate to cognitive statusand contextAssess intensity, relief, mood, and sideeffectsVisual Analogue Score( VAS )

Use verbal report (VRS) whenever possibleDocument in a visible placeInclude the family

M th d Of P i


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Methods Of PainControllingII- Pharmacological

1- Opioids

Im, IV infusion or PCA2- Local anesthetics:

Local InfiltrationNerve BlocksEpidural Blocks3- NSAIDS & adjuvan

IM, IV infusion or PCA

iI-Nonpharmacological

1- Preoperative2- Counseling TENS3- Acupuncture


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TENS


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

Inhibitory circuits within sp cordactivated

Nerve impulse transmission reduced

Pharmacologic Methods


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Pharmacologic Methods

OPIOIDS

1- Activate opioid receptors withinthe CNS

2- Reduce transmission of nerveimpulses 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.


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NASIDS

Block the synthesis of PGs

Only suitable for mild pain

In moderate pain it needs

adjuvant


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Principle Of PainManagement Pre-emptive analgesia

Balanced or combinationanalgesia

Analgesia ladder

Preemptive Analgesia


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Preemptive AnalgesiaPharmacologically induces an effective

analgesic state prior to the surgical trauma

This may involve

1- Infiltration of the wound with localanesthetic .

2- Central neural blockade. 3- Administration of effective doses of Opioids , NSAIDs , Ketamine , Alpha-2

Agonists or IV infusion of Lidocain.


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Postoperative Balanced Analgesia


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Postoperative Balanced AnalgesiaCo Analgesics Commonly Used For

PainNSAIDSAcetaminophenAntidepressants

AnticonvulsantsCorticosteroidsNeuroleptics

Antihistamines

AnalepticsBenzodiazepinesAntispasmodics

Muscle relaxantsSystemic localanesthetics

They Reduce required amount and sideeffects of opioids

Making PCA Work for your


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Making PCA Work for yourPatient

The goal of postoperative painmanagement is To provide minimumeffective analgesic concentration (MEAC)that is safe, effective and, free side effectscontinuous analgesia.

The Aim

To reduce postoperative morbidity, facilitaterecovery, and fasten discharge .


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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 4thStep

The WHOLadder

Deer, et al., 1999


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Thank You

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Management of Post Operative Pain 1