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The pain is intolerable!!!

Pain Control

Dr. Cheung Chi WaiMBBS(HK), FHKCA, FHKAM(Anaesthesiology), Dip Pain Mgt(HKCA)

Clinical Assistant ProfessorDepartment of Anaesthesiology

University of Hong Kong

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Learning Outcomes

To define pain and recognize it features

To classify pain and describe its characteristics

To understand pain mechanisms

To understand the physiologic consequences of acute pain

To describe the assessment of pain and pain relief

To know the treatment options for acute pain

To know briefly chronic pain and its psychological effect

To appreciate the treatment options for chronic pain

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Pain

Definition and Features

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Definition

Pain is an unpleasantsensory and emotional

experience associated withactual or potentialtissue damage or described in terms of suchdamage.

International Association for the Study of Pain. Pain. 1979;6:249.

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Dimensions of Pain

Pain is more than nociception

Sensory & discriminative dimension

Emotional & affective dimension

Cognitive & evaluative dimension

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Biological Value of Pain

Pain is essential for survival

Serves as a warning to avoid or prevent

further body injury

Enforces rest of injured or diseased parts

of the body for healing

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Advantages of Effective

Pain Management

Patient comfort and satisfaction1,2,3

Earlier mobilization4

hospital stay3,4

costs4

1. Eisenach JC, et al. Anesthesiology. 1988;68:444448.2. Harrison DM, et al. Anesthesiology. 1988;68:454457.3. Miaskowski C, et al. Pain. 1999;80:2329.

4. Finley RJ, et al. Pain. 1984;2:S397.

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JCAHO and Pain Management

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Joint Commission on

Accreditation of Healthcare Organizations All accredited health care organizations in the USA

required to comply with the standards since January 2001

Record pain as the 5th vital sign

Interdisciplinary management with needs assessment

Patients right to pain assessment

Monitor pain intervention responses

Provide pain management education

Joint Commission on Accreditation of Healthcare Organizations. Jt Comm Perspect. 1999;19(5):68.Sklar DP. Ann Emerg Med. 1996;27:412413.

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Pain: The Fifth Vital Sign

Pain should be considered the fifth vital sign

Patients should be assessed for pain every time

pulse, blood pressure, core temperature, andrespiration are measured

Healthcare professionals should recognize a

report of unrelieved pain as a red flag

American Pain Society Quality Improvement Committee. JAMA. 1995;18471880.

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JCAHO Revised Standards:

The Patients Rights

Patients have the right to appropriateassessment and management of pain

The patients right to painmanagement is respected andsupported

Patients are involved in all aspects oftheir care, including pain management

Joint Commission on Accreditation of Healthcare Organizations. Jt Comm Perspect. 1999;19(5):68.

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Classification of Pain

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Acute Pain Inflammatory Pain

Nociceptive pain

Neuropathic Pain

Chronic Pain

Neuropathic pain

Non-neuropathic pain

Cancer Pain

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Characteristics of

Acute, Chronic,and Neuropathic Pain

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Characteristics of Acute Pain

Sudden, sharp, intense, localized

Usually self-limiting

May be associated with physiologic changes

sweating, HR, BP

Siddall PJ, et al. In: Cousins MJ, Bridenbaugh PO, eds. Neural Blockade in Clinical Anesthesia

and Management of Pain; 1998:675713.

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Characteristics of Chronic Pain

Gnawing, aching, diffuse

No definite beginning or end

Temporal variability in intensity; may remit briefly Associated with psychological and social difficulties

Acute pain may be superimposed

Siddall PJ, et al. In: Cousins MJ, Bridenbaugh PO, eds. Neural Blockade in Clinical Anesthesiaand Management of Pain; 1998:675713.

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Characteristics of

Peripheral Neuropathic Pain Caused by pathologic changes in

peripheral nerves

Spontaneous pain

Burning, tingling, numbness

Allodynia, hyperalgesia

Rathmell JP. Katz JA. In: Benzon H, et al, eds. Essentials of Pain Medicine and Regional Anesthesia;

1999:288

294.

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Pain Mechanisms

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How do we feel pain ?

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The Somatosensory SystemSomatosensory

cortex

Thalamus

Hypothalamus

Ascending tracts

Midbrain

Medulla

Spinalcord

Frontalcortex

Descendingpathway

Periaqueductalgray matter

Dorsal horn area

Noxious stimuli activate receptors in periphery

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The Pathophysiology of Pain

3 components of the nociceptive process

The Periphery

The Nerve

The Spinal Cord & Brain

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The Periphery

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Nociceptors

eg.

High threshold mechano-receptors

Thermo-mechano-receptors

Polymodal nociceptors Super-high threshold receptors

Respond to different stimuli

Can be sensitized

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Sensitization

Following initial stimulation, the firing

thresholdof nociceptors is lowered

THEREFORE LESS STIMULUS REQUIRED

FOR THEM TO BE ACTIVATED AND FOR

A NOXIOUS STIMULUS TO BE SENT TO

THE CNS

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The Sensitizing Soup

Tissue injury cell damage

Cell damage release of pain producing substances

K+ ions, Prostaglandins, Bradykinins, Substance PLeukotrienes, Histamine, Serotonin, Noradrenaline

This chemical soup modifies sensitivity of

nociceptors

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The Nerve

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First Order Neurones

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Peripheral Sensitization

Cell Damage Inflammation Sympathetic

Terminals

Release of pain and inflammatory mediatorseg, bradykinin, H+, prostaglandins

NociceptorCentral

sensitization

Hyperalgesia

Allodynia

High Threshold

Low Threshold

Spinal cord

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First Order Neurones enter Dorsal Horn

Synapse with Interneurones(ie second orderneurones)

Modulating influences come from higher

centres in brain eg psychological components

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Rexed Laminae

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PAIN SENSATION CAN THEREFORE

BE MODIFIED BY ASCENDING OR

DESCENDING PATHWAYS AT MANYLEVELS

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Central Sensitization

Prolonged stimulation ofC fibres release

Substance P + Glutamate in Dorsal Horn

cascade of events altering neuro-cellular function

development ofPOSITIVE FEEDBACK LOOP

sequential increase in spinal cord activity

ie. WIND UP of neuronal excitability

SECONDARY HYPERALGESIA

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Central Sensitization

Peripheral

Sensitization Tissue Injury

C- fibre output Hyperalgesia (1, 2)

Allodynia Activation of NMDAreceptors

Spinal cord

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Hyperalgesia

Primary Sensitization of primary neurons threshold to noxious

stimuli within site of injury

May include response to innocuous stimuli

pain from suprathreshold stimuli

Spontaneous pain

Secondary

Sensitization of primary neurons in surrounding uninjured areas

May involve:Peripheral sensitization

Central sensitization

Raja SN, et al. In: Wall PB, Melzack R, eds. Textbook of Pain. 4th ed; 1999:1157.

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Allodynia

Pain evoked by innocuous stimuli

Central sensitization pain producedby Afibers1

Possibly mediated by spinal NMDAreceptors2

1. Woolf CJ. Drugs. 1994;47(suppl 5):19.

2. Dolan S, Nolan AM. Neuroreport. 1999;10(3):449452.

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Pain Sensitisation

Injury

Pain

Intens

ity

10

8

6

4

2

0

StimulusIntensity

Normal

Pain

Response

Allodynia

Hyperalgesia

Gottschalk and Smith, Am Fam Physician 2001

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Pain Mediators

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Pain Mediators

Aa = arachidonic acid; BK = bradykinin; PG = prostaglandin

Cell Damage

Brain

Spinal cord

Aa K+ BK

PG

Nociceptor

Peptides, eg, SUBSTANCE P

HISTAMINE

SEROTONIN

Mast Cell

Platelet

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Role of Neuropeptides

Excitatory Substance P, neurokinin A

Ca2+, induce sensitization, hyperalgesia

Transsynaptic transmitters

Inhibitory

Somatostatin, enkephalins, endorphins, dynorphins (?)

Modulate intracellular cAMP, K+

Act at , , opioid receptors

cAMP = cyclic adenosine monophosphateDougherty PM, Raja SN. In: Benzon HT, et al, eds. Essentials of Pain Medicine and Regional

Anesthesia; 1999:79.

P id P d i b

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Prostanoid Production by

Cyclooxygenase (COX)

PG = prostaglandin; TX = thromboxane

Arachidonic acid

PGG2

Cyclooxygenase activity of COX

PGH2

Peroxidase activity of COX

PGF2PGD2 PGE2 PGI2 TXA2

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P id d Th i

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Prostanoids and Their

Physiologic Activities

Activities/Properties

Produced in many organs, (eg, kidney,

intestinal tract)

GI mucosal protection/repair

Vasodilates

Diuresis and natriuresis

Inhibits inflammatory/ allergic cells

platelet activation

intravascular platelet aggregation

smooth muscle contraction in arteries and bronchi

platelet aggregation

Vasodilates

renin release in kidney

Prostanoid

PGE2

Thromboxane A2

Prostacyclin (PGI2)

Mechanism of Action of

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Mechanism of Action of

Conventional NSAIDs

Historical Perspective

Arachidonic acid


Prostanoids( Prostaglandins/thromboxane)

Gastrointestinaltoxicity

Renal toxicityImpaired platelet

function

Inflammation,pain, and fever

X ConventionalNSAIDs

T F f

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Two Forms of


Constitutive

Synthesizes prostanoids

that mediate homeostaticfunctions

Especially important in: Gastric mucosa

Kidney

Platelets

Vascular endothelium

COX-1

Inducible (in most tissues)

Synthesizes prostanoids that

mediate inflammation, pain,and fever

Induced mainly at sites ofinflammation by cytokines

Constitutive expressionprimarily in: Brain

Kidney

COX-2

DuBois RN, et al. FASEB J. 1998;12:1063

1073.

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COX in the Human Kidney

COX-1 is widely distributed in the human kidney

Unlike in lower animals, COX-2 expression in the

human kidney is limited

Relative roles and importance of COX-1 and COX-2

in the kidney are not fully understood

Deleterious renal effects of conventional NSAIDs are

well recognized

Renal profile of COX-2 inhibitors is not yet fully

elucidated

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Physiologic Consequences

of Acute Pain

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General stress response/neuroendocrine

Respiratory

Cardiovascular

Gastrointestinal/urinary

Musculoskeletal

Varies with site & extent of tissue damage

Bonica JJ. The Management of Pain. 2nd ed. Vol. 1; 1990.

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General Stress Response

Endocrine/Metabolic ACTH, cortisol, catecholamines, interleukin-1

insulin blood glucose, catabolism

Water/Electrolyte Flux H2O, Na

+ retention

ACTH = adrenocorticotropic hormone

Kehlet H. Reg Anesth.1996;21(6S):3537.

Cousins M, Power I. In: Wall PD, Melzack R, eds. Textbook of Pain. 4th ed; 1999:447

491.

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Respiratory Effects

FRC = functional residual capacity; V/Q = ratio ventilation:perfusion of the lung

Craig DB. Anesth Analg. 1981;60:46.Cousins M, Power I. In: Wall PD, Melzack R, eds. Textbook of Pain. 4th ed; 1999:447491.

Mobility

Hypostatic pneumonia

Tidalvolume

Vitalcapacity

FRC Alveolarventilation

Atelectasis

V/Q inequality

AcutePain

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491.

Impairedventilation

Muscle spasm

Muscle splinting

Cough suppression

Lobular collapse

Infection/pneumonia

AcutePain

Hypoxemia

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Cardiovascular Effects

MI = myocardial infarction; HR = heart rate; PVR = peripheral vascular resistance;

BP = blood pressure

Cousins M, Power I. In: Wall PD, Melzack R, eds. Textbook of Pain. 4th ed; 1999:447491.Bowler DB, et al. In: Cousins MJ, Phillips GD, eds. Acute Pain Management; 1986:187236.

Sympatheticover activity

Coronaryvasoconstriction

Anxiety, painIschaemia

Angina

MI

HR,PVR, BP,cardiacoutput

Ischaemia

AcutePain

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Gastrointestinal System

Decrease gastric and bowel motility

Ileus

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Coagulation and Immune

Hypercoagulability

Impair cellular and humoral immune function

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Effects on Pain-Signaling Systems

Peripheral nociception Nerve excitability

Prolonged pain

Chronic pain Damaged spinal

pain-signaling systems

Cousins M, Power I. In: Wall PD, Melzack R, eds. Textbook of Pain. 4th ed; 1999:447491.

AcutePain

Hyperalgesia (1 + 2)Allodynia

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Psychological Effects


491.

AcutePain

Anxiety

Depression

Sleep deprivation

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Assessment

ofPain and Pain Relief

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Patients Perception of Pain

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Patients Perception of Pain

Pain is subjective and may be influenced by:

Age1,2

Gender1

Culture2

Communication/language skills

Previous experience

1. Burns JW, et al. Anaesthesia. 1989;44:26.2. Preble L, Sinatra R. In: Sinatra RS, et al, eds. Acute Pain Mechanisms and Management. St. Louis:

Mosby-Year Book; 1992:140

150.

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Assessment

History

Physical assessment

Investigations

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Assessment

1. Where2. Time course

3. Intensity

4. Factors relieving or exacebrating pain

5. Pain on function and life

6. Investigations for pain

7. Treatments received

8. Medical condition and prognosis9. Psychological profile

10. Social background

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Example of Measurement Tool

for Assessing Pain

No pain

Carr DB, et al. AHCPR Pub. No. 92

0032. 1992.

Pain as bad as it could

possibly be

Visual Analog Scale (VAS)

Numerical Rating Score (NRS)

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Other Pain Evaluation Tools

Graphic pictures

McGill Pain Questionnaire

Multidimensional, good but complex

Behavioural scores e.g. CHEOPs

Useful in children/communication problems

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"old cart"

Onset

Location

Duration

Characteristics

Aggravating factors

Relieving factors Treatments

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Frequency of

Pain Assessment and Documentation

Preoperatively

Routinely at regular intervalspostoperatively

With each new report of pain

At suitable intervals after each analgesic

intervention

Carr DB, et al. AHCPR Pub. No. 92-0032. 1992.

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Treatment Options for Acute Pain

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WHO Analgesic Ladder

1

2

3

World Health Organization, 1990. Used with permission.

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Analgesic Options for

Acute Pain Management

Opioid analgesics

Non-opioid analgesics

Acetaminophen (paracetamol) Tramadol

Anti-inflammatory agents

others

Combination analgesic products

Local anesthetics, nerve, neuraxial blocks

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Opioid Analgesics

Binding at , , receptors Highly efficacious

May be combined with anti-inflammatory

agents

Effects may be reversed

Side effects common

Pain recurrence

Tolerance

Fishman SM, Borsook D. In: Benzon HT, et al, eds. Essentials of Pain Medicine and Regional

Anesthesia; 1999:51

54.

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Adverse Effects of Opioids

Respiratory depression

GI motility, nausea, vomiting

CNS depression, sedation, cognitiveeffects (elderly)

Pruritus (especially spinal opioids)

Urinary retention

Methods of

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Methods of

Opioid Delivery

1. i.m. - painful, slow onset action, variable plasmalevels

2. i.v.- less painful, faster onset, more reliable levels- risk of overdose with continuous iv infusion

3. PCA

4. Epidural / Spinal

5. Other - S.C. / ORAL / TRANSDERMAL

Epidural /

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Epidural /

Intrathecal Opioids

Opioid receptors in spinal cord

Neuraxial opioids can produce profoundsegmental analgesia, with reduced systemicopioid adverse effects

May be combined with LAs

less motor impairment

Prolonged effects

Potential dangers exist

eg. late onset respiratory depression

P ti t C t ll d A l i

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Patient Controlled Analgesia

PCA

Match demand with delivery

Button press activation

Positive patient psychology

Preset bolus dose

Lock-out interval

1 hour maximum dose

Tamper proof machine Patient monitoring

P ti t t ll d l i

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Patient-controlled analgesia

0

50

100

plasma

conc.

time

PCA

I.M.

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MORPHINE

Gold standard opioid

1) Peak effect 1520 mins i.v.

6090 mins i.m.

2) Duration action 4 - 5 hours

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MORPHINE

Dose

BNF 48 adults 10mg IV / IM every 2-4 hrs

dose in elderly / frail

Better approach- titrate total dose to patient

response

Adult maximum dose ~0.2mg / kg

dose in elderly / frail

PETHIDINE

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PETHIDINE

1. 1:10 as potent as morphine

2. Dose 1 mg/kg

3. Duration action ~3 hours

4. Metabolites can cause - hallucinations

- convulsions

Guideline for Use of Opioids

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for Acute Pain

Opioid Route of

Administration

Recommended

Initial Dose,mg/kg

Frequency

Morphine po

sc, im, iv

0.5

0.15

Q3-4h

Pethidine po

sc, im, iv

2.5-3

1.5-2

Q2-3h

Q3hMethadone po

sc, im, iv

0.2-0.4

0.15

Q6-8h

Codeine po,

sc, im

1.5

1.0

Q3-4h

Tramadol

(?opioid)

po

im, iv

50-100mg/dose

Loading dose up to

250mg

then 50-

100mg/dose

Q4-6h

Nonopioid Analgesics

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Nonopioid Analgesics

Paracetamol Tramadol

Mechanism pain threshold weak bindingof action CNS cox inhibition inhibits re-uptake of

norepinephrine andserotonin (5-HT3)

Adverse effects Hepatotoxic Opioid-like effects,

nausea

dizziness, seizures

Sisson CB. In: Benzon HT, et al, eds. Essentials of Pain Medicine and Regional Anesthesia; 1999:5962.

Anti inflammatory Agents

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Anti-inflammatory Agents

Inhibit cyclooxygenase (COX), key enzyme inprostaglandin synthesis

Conventional anti-inflammatory analgesics

inhibit both COX-1 and COX-2 isoenzymes COX-1 inhibition gastrotoxicity, platelet

aggregation

Some newer agents target COX-2 but do notinhibit COX-1 at full therapeutic doses

Guidelines for Use of

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Guidelines for Use of

NSAIDs for Acute Pain

Drug Routes Recommended dose

Paracetamol Oral, rectal 10-15mg/kg q4h

Ketorolac iv, im, oral 30-60mg im bolus followed by10 mg q6-8h imi or 15-30mg q6h

po

Diclofenac im, oral, rectal 50-100mg q6-12h

Naproxen oral, rectal 500mg initially followed by250mg q8-12h (5mg/kg q12h)

Aspirin oral 10-15mg/kg q4-6h

N methyl D aspartate

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N-methyl-D-aspartate

receptor antagonists

Dorsal horn of the spinal cord

Inhibition may prevent wind-up & central

hypersensitivity Ketamine: non-competitive NMDA receptor antagonist

Analgesia

Possible pre-emptive effects on 2Y hyperalgesia

Attenuates opioid tolerance

Side-effects

Combination Analgesic

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Combination Analgesic

Products

Usually two or more agents with different

yet complementary mechanisms of action

Severity of dose-related side effects may bereduced, since lower doses of each agent are

utilized

Range of side effects increased

Multimodal Analgesia

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Multimodal Analgesia

An Example

Reduced doses of each

analgesic

Improved antinociceptiondue to synergistic/additive

effects

May reduce severity of

side effects of each drug

Kehlet H, Dahl JB. Anesth Analg. 1993;77:10481056.

Morphine

NSAIDs,acetaminophen,

nerve blocks

Potentiation

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Local Anesthetics, Nerve, Neuraxial

Blocks Na+ channel blockade

Possible interaction at pre- and postsynaptic

junctions

Tachyphylaxis

Dose-related CNS, cardiovascular toxicity

Epidural analgesia

Excellent pain relief

LA side-effects

L l th ti (L A )

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Local anaesthetic (L.A.)

Drugs

Lignocaine 1% - 2%

Bupivicaine 2.5% - 5%

Prilocaine 0.5% - 1%

Ropivicaine 0.2% - 1%

Routes ofAdministration

Local infiltration

Regional nerve block

Spinal block

Epidural block

(Caudal block)

L l th ti (L A )

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Local anaesthetic (L.A.)

ADVANTAGES

1. Excellent analgesia

2. Opioid sparing effect

3. Decreased blood loss

DISADVANTAGES

1. Motor blockade

2. Hypotension

3. L.A. toxicity

4. Variable duration

5. Require skill

6. Malplaced block

7. High spinal block

A l i d li

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Analgesia delivery

Chose an appropriate drug

Awareness of pharmacokinetics

Prescribe appropriately Regular administration

Infusion

Patient-controlled delivery

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BNF 48

Analgesics are more effective in

preventing pain than in the relief of

established pain; it is important that they

are given regularly

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Acute Pain Services

f S i l i

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Management of Surgical Pain

The Unmet Needs

Pain is undertreated

Inadequate knowledge of pain management Inadequate pain assessment

Rawal N. Anesth Pain Med. 1999;24(1):6873.Sinatra R. In: Cousins MJ, Bridenbaugh PO. Neural Blockade in Clinical Anesthesia andManagement of Pain; 1998:793835.American Pain Society Quality Improvement Committee. JAMA. 1995;18471880.

Acute Pain Services

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Goals

Improve management of surgical pain Twice daily ward rounds

Pain consultation service, pain clinic

Therapeutic interventions

Promote continuing education and training ofhealthcare providers

Increase awareness of importance of effective pain

management Serve as a clinical research centre

Chin ML. In: Ashburn MA, Rice LJ, eds. The Management of Pain; 1998:537545.

CHRONIC PAIN

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CHRONIC PAIN

1. More than 3 months

2. Lack of objective signs

3. No longer a symptom

4. Psychological and emotional factors

5. Pain behavior established

6. Responses altered by cultural influences and past

experiences


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Chronic Pain

1. Anxiety

2. Depression

3. Psychotic symptoms

4. What pain means to patient

5. Coping mechanisms

6. Family involvement

7. Support networks

8. Patients expectations

Treatment options

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p

CHRONIC PAIN

1. Simple measuresRest, exercise, heat therapy, vibration therapy

2. Systemic analgesic drugsOpioids, NSAIDS, Paracetamol

3. Adjuvant drugsantidepressants, anticonvulsants,steroids

muscle relaxants eg. Baclofen

4. Local anaesthetic nerve block

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5. Neurolytic proceduresDrugsphenol, alcohol

Cryoprobe

Surgery

6. TENS, Acupuncture

7. Psychological techniques

8. Implantation techniques: spinal cordstimulator, intrathecal or epidural cather

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Nonpharmacologic Treatment

O ti f P i

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Options for PainCognitive-Behavioral

Relaxation Preparatory information

Imagery

Hypnosis

Biofeedback

Physical Agents

Application of superficial heat and cold Massage

Exercise

Immobilization (eg, to provide rest and maintainalignment after musculoskeletal procedures)

Electroanalgesia (eg, TENS)

Chiropractic

Acupuncture

Carr DB, et al. AHCPR Pub. No. 92-0032. 1992.

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