Acute Pain: Mechanisms, Management, And Treatment Options

Acute Pain: Mechanisms, Management, and Treatment Options

ACUTE PAINIT WILL BE POTENTIAL TO KILL YOUR

PATIENTSMulyono Soedirman

FK UNHAS / RSPAD GATOT SOEBROTOJAKARTA

ACUTE PAINIT WILL BE POTENTIAL TO KILL YOUR

PATIENTSMulyono Soedirman

FK UNHAS / RSPAD GATOT SOEBROTOJAKARTA


OverviewOverviewPain: Definition and Features

Physiologic Consequences of Acute Pain

JCAHO and Pain Management

Characteristics of Acute, Chronic, Peripheral Neuropathic Pain

Assessment of Pain and Pain Relief

Pain Mechanisms

Role of Prostanoids in Pain

Treatment Options for Acute Pain

Other Approaches

Acute Pain Services


Pain

Definition and Features

Pain

Definition and Features


DefinitionDefinition

“Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.”

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


Features of Acute PainFeatures of Acute Pain

Onset

Intensity

Somatic vs visceral

May be referred

Siddall PJ, Cousins MJ. In: Cousins MJ, Bridenbaugh PO, eds. Neural Blockade in Clinical Anesthesia and Management of Pain. 3rd ed; 1998:675–713.


Physiologic Consequences of Acute PainPhysiologic Consequences of Acute Pain


Physiologic Consequences of Acute PainPhysiologic Consequences of Acute Pain

General stress response/neuroendocrine Respiratory Cardiovascular Gastrointestinal/urinary Musculoskeletal

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


General Stress ResponseGeneral Stress Response

Endocrine/Metabolic

ACTH, cortison, catecholamines, interleukin-1

insulin

Water/Electrolyte Flux

H2O, Na+ retention

ACTH = adrenocorticotropic horrmone

Kehlet H. Reg Anesth.1996;21(6S):35–37.Cousins M, Power I. In: Wall PD, Melzack R, eds. Textbook of Pain. 4th ed; 1999:447–491.


Respiratory EffectsRespiratory 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; 1999:447–491.

Mobility

Hypostatic pneumonia

Tidal volume

Vital capacity

FRC Alveolar ventilation

Atelectasis

V/Q inequality

Acute Pain

Acute Pain


Respiratory Effects (Cont’d)Respiratory Effects (Cont’d)

Cousins M, Power I. In: Wall PD, Melzack R, eds. Textbook of Pain. 4th ed; 1999:447–491.

Impaired ventilation

Muscle spasm

Muscle splinting

Cough suppression

Lobular collapse

Infection/pneumonia

Acute Pain

Acute Pain

Hypoxemia


Cardiovascular EffectsCardiovascular Effects

MI = myocardial infarction; HR = heart rate; PVR = peripheral vascular resistance; BP = blood pressureCousins M, Power I. In: Wall PD, Melzack R, eds. Textbook of Pain. 4th ed; 1999:447–491.Bowler DB, et al. In: Cousins MJ, Phillips GD, eds. Acute Pain Management; 1986:187–236.

Sympatheticoveractivity

Coronaryvasoconstriction

Anxiety, pain Ischemia

Angina

MI

HR, PVR, BP, cardiac output

Ischemia

Acute Pain

Acute Pain


Effects on Peripheral CirculationEffects on Peripheral Circulation

Limb blood flow1

Venous emptying2

Venous thrombosis/embolism3

1. Cousins M, Power I. In: Wall PD, Melzack R, eds. Textbook of Pain. 4th ed; 1999:447–491.2. Modig J, et al. Acta Anaesth Scand. 1980;24:305–309.3. Modig J, et al. Anesth Analg. 1983;62:174–180.

Acute Pain

Acute Pain


Gastrointestinal and Urinary EffectsGastrointestinal and Urinary Effects

UrinaryGastrointestinal


Urinary sphincter activity

Urinary retention

Intestinal secretions

Smooth musclesphincter tone

Intestinal motility

Cousins M, Power I. In: Wall PD, Melzack R, eds. Textbook of Pain. 4th ed; 1999:447–491.Nimmo WS. Br J Anaesth. 1984.56:29–37.

Acute Pain

Acute Pain


Musculoskeletal EffectsMusculoskeletal Effects


Sensitivity of peripheral nociceptors

Musclespasm


Acute Pain

Acute Pain


Musculoskeletal Effects (Cont’d)Musculoskeletal Effects (Cont’d)

Mobility

Impaired muscle metabolism

Muscle atrophy Delayed normal

muscle function

Reflex vasoconstriction


Acute Pain

Acute Pain


Effects on Pain-Signaling SystemsEffects on Pain-Signaling Systems

Peripheral nociception Nerve excitability

Prolonged pain

Chronic pain Damaged spinal pain-signaling systems


Acute Pain

Acute Pain

Hyperalgesia (1 + 2)

Allodynia


Psychologic EffectsPsychologic Effects


Acute Pain

Acute Pain

Anxiety

Depression

Sleep deprivation


Other Effects of Acute PainOther Effects of Acute Pain

Wound repair

Impaired immunocompetence

Hypercoagulable state

Drucker W, et al. J Trauma. 1996;40(3):S116–122.Cousins M, Power I. In: Wall PD, Melzack R, eds. Textbook of Pain. 4th ed; 1999:447–491.Jorgensen L, et al. Br J Anaesth. 1991;66:8–12.


Advantages of Effective Pain ManagementAdvantages of Effective Pain Management

Patient comfort and satisfaction1,2,3

Earlier mobilization4

hospital stay3,4

costs4

1. Eisenach JC, et al. Anesthesiology. 1988;68:444–448.2. Harrison DM, et al. Anesthesiology. 1988;68:454–457.3. Miaskowski C, et al. Pain. 1999;80:23–29.4. Finley RJ, et al. Pain. 1984;2:S397.


JCAHO and Pain ManagementJCAHO and Pain Management


Joint Commission on Accreditation of Healthcare Organizations

Joint Commission on Accreditation of Healthcare Organizations

New standards in 2000–2001; scoring begins in 2001

Record pain as the 5th vital sign

Interdisciplinary management with needs assessment

Patient’s 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):6–8.Sklar DP. Ann Emerg Med. 1996;27:412–413.


Pain: The Fifth Vital SignPain: 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, and respiration are measured

Healthcare professionals should recognize a report of unrelieved pain as a “red flag”

American Pain Society Quality Improvement Committee. JAMA. 1995;1847–1880.


JCAHO Revised Standards: The Patient’s RightsJCAHO Revised Standards: The Patient’s Rights

Patients have the right to appropriate assessment and management of pain

The patient’s right to pain management is respected and supported

Patients are involved in all aspects of their care, including pain management

Joint Commission on Accreditation of Healthcare Organizations. Jt Comm Perspect. 1999;19(5):6–8.


A Team Approach to Implementing the JCAHO Revised Standards for Pain Management

A Team Approach to Implementing the JCAHO Revised Standards for Pain Management

Medical

Pharmacy

Dietetic

Rehabilitation

Managers

Nursing

Others

Joint Commission on Accreditation of Healthcare Organizations. Jt Comm Perspect. 1999;19(5):6–8.


Characteristics of Acute, Chronic,and Peripheral Neuropathic Pain

Characteristics of Acute, Chronic,and Peripheral Neuropathic Pain


Characteristics of Acute PainCharacteristics of Acute Pain

Sudden, sharp, intense, localized

Usually self-limited

May be associated with physiologic changes, eg, sweating, HR, BP

Siddall PJ, et al. In: Cousins MJ, Bridenbaugh PO, eds. Neural Blockade in Clinical Anesthesia and Management of Pain; 1998:675–713.


Characteristics of Chronic PainCharacteristics of Chronic Pain

Gnawing, aching, diffuse

No definite beginning or end

Varies 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 Anesthesia and Management of Pain; 1998:675–713.


Characteristics of Peripheral Neuropathic PainCharacteristics 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.


Assessment of Pain and Pain ReliefAssessment of Pain and Pain Relief


Patient’s Perception of PainPatient’s 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;44:2–6.2. Preble L, Sinatra R. In: Sinatra RS, et al, eds. Acute Pain Mechanisms and Management. St. Louis: Mosby-Year Book; 1992:140–150.


Benefits of Patient PreparationBenefits of Patient Preparation

Less postoperative pain1

Fewer postoperative analgesic medications

Reduced hospitalization2

1. Croog SH, et al. J Am Dent Assoc. 1994;125:1353–1359.2. Boeke S, et al. Pain. 1991;45:293–297.


Example of Measurement Tool for Assessing PainVisual Analog Scale (VAS)

Example of Measurement Tool for Assessing PainVisual Analog Scale (VAS)

No pain Pain as bad as it could possibly be

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


Frequency of Pain Assessment and Documentation

Frequency of Pain Assessment and Documentation

Preoperatively

Routinely at regular intervals postoperatively

With each new report of pain

At suitable intervals after each analgesic intervention

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


Pain MechanismsPain Mechanisms


The Somatosensory SystemThe Somatosensory SystemSomatosensory cortex

Thalamus

Hypothalamus

Ascending tracts

Midbrain

Medulla

Spinal cord

Frontal cortex

Descending pathway

Periaqueductal gray matter

Dorsal horn area

Noxious stimuli activate receptors in periphery


Peripheral SensitizationPeripheral Sensitization

Cell Damage Inflammation Sympathetic Terminals

Release of pain and inflammatory mediators eg, bradykinin, H+, prostaglandins

Nociceptor Central sensitization

Hyperalgesia Allodynia

High Threshold

Low Threshold

Spinal cord


Central SensitizationCentral Sensitization

Peripheral Sensitization Tissue Injury

C-fiber output Hyperalgesia (1, 2)

Allodynia Activation of NMDA

receptors

Spinal cord


HyperalgesiaHyperalgesiaPrimary

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; 1999:11–57.


AllodyniaAllodynia

Pain evoked by innocuous stimuli

Central sensitization pain produced by A fibers1

Possibly mediated by spinal NMDA receptors2

1. Woolf CJ. Drugs. 1994;47(suppl 5):1–9.2. Dolan S, Nolan AM. Neuroreport. 1999;10(3):449–452.


Pain MediatorsPain 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


Role of NeurotransmittersRole of Neurotransmitters

Excitatory

Glutamate, aspartate, ATP

Mediate afferent synaptic transmission

Inhibitory

GABA, glycine, norepinephrine, 5-HT, adenosine, Ach

Analgesia at spinal and higher levels

Altered function hyperalgesia, neuropathic or chronic pain

GABA = -aminobutyric acid; 5-HT = 5-hydroxytryptamine (serotonin); Ach = acetylcholineDougherty PM, Raja SN. In: Benzon HT, et al, eds. Essentials of Pain Medicine and Regional Anesthesia; 1999:7–9.


Role of NeuropeptidesRole 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; 1999:7–9.


Role of Prostanoids in PainRole of Prostanoids in Pain


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


Prostanoids and Their Physiologic ActivitiesProstanoids 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)


Treatment Options for Acute PainTreatment Options for Acute Pain


WHO Analgesic LadderWHO Analgesic Ladder

1

2

3

Freedom from cancer pain

Opioid for moderate

to severe pain Non-opioid Adjuvant

Opioid for mild to

moderate pain

Non-opioid Adjuvant

Pain persisting

or increasing

Non-opioid Adjuvant

World Health Organization, 1990. Used with permission.

Pain persisting

or increasing


Analgesic Options for Acute Pain ManagementAnalgesic Options for Acute Pain Management

Opioid analgesics

Nonopioid analgesics

– acetaminophen

– tramadol

– anti-inflammatory agents

Combination analgesic products

Local anesthetics, nerve, neuraxial blocks


Opioid AnalgesicsOpioid Analgesics

Binding at , , receptors

Highly efficacious

May be combined with anti-inflammatory agents

Effects may be reversed

Side effects common

Pain recurrence

Fishman SM, Borsook D. In: Benzon HT, et al, eds. Essentials of Pain Medicine and Regional Anesthesia; 1999:51–54.


Adverse Effects of OpioidsAdverse Effects of Opioids

CNS depression, sedation

Respiratory depression

GI motility, nausea, vomiting

Urinary retention

Pruritus


Nonopioid AnalgesicsNonopioid Analgesics

Acetaminophen Tramadol

Mechanism pain threshold -receptor bindingof action inhibits re-uptake of

norepinephrine and serotonin (5-HT3)

Adverse effects Hepatotoxic Opioid-like effects

Sisson CB. In: Benzon HT, et al, eds. Essentials of Pain Medicine and Regional Anesthesia; 1999:59–62.


Anti-inflammatory AgentsAnti-inflammatory Agents

Inhibit cyclooxygenase (COX), key enzyme in prostaglandin 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 not inhibit COX-1 at full therapeutic doses (specific cox-2 inhibitor, the COXIBS, e.g. Celecoxib, the savest anti inflamatory agents in this decade, that effective also as pain killer).


Combination Analgesic ProductsCombination Analgesic Products

Usually two or more agents with different yet complementary mechanisms of action

Severity of dose-related side effects may be reduced, since lower doses of each agent are utilized

Range of side effects increased


Local Anesthetics, Nerve, Neuraxial BlocksLocal Anesthetics, Nerve, Neuraxial Blocks

Na+ channel blockade

Possible interaction at pre- and postsynaptic junctions

Tachyphylaxis

Dose-related CNS, cardiovascular toxicity


Nonpharmacologic Treatment Options for PainNonpharmacologic Treatment 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 maintain

alignment after musculoskeletal procedures) Electroanalgesia (eg, TENS) Chiropractic Acupuncture

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


Other ApproachesOther Approaches


Multimodal AnalgesiaAn Example

Multimodal AnalgesiaAn Example

Kehlet H, Dahl JB. Anesth Analg. 1993;77:1048–1056.

Reduced doses of each analgesic

Improved antinociception due to synergistic/additive effects

May reduce severity of side effects of each drug

MorphineMorphine

NSAID,acetaminophen,

nerve blocks

NSAID,acetaminophen,

nerve blocks

PotentiationPotentiation


New Approaches to Treatment of Acute PainNew Approaches to Treatment of Acute Pain

Bradykinin receptor antagonist

COX-2 specific inhibition

Cytokine suppressive anti-inflammatory agents (CSAIDs)

Neuropeptide inhibitors

Epibatidine analogues

Rang HP, Urban L. Br J Anaesth. 1995;75(2):145–156.


Acute Pain ServicesAcute Pain Services


Management of Surgical PainThe Unmet Needs

Management of Surgical PainThe Unmet Needs

Pain is undertreated

Inadequate knowledge of pain management

Inadequate pain assessment

Rawal N. Anesth Pain Med. 1999;24(1):68–73.Sinatra R. In: Cousins MJ, Bridenbaugh PO. Neural Blockade in Clinical Anesthesia and Management of Pain; 1998:793–835.American Pain Society Quality Improvement Committee. JAMA. 1995;1847–1880.


Acute Pain ServicesGoals

Acute Pain ServicesGoals

Improve management of surgical pain

Promote continuing education and training of healthcare providers

Increase awareness of importance of effective pain management

Serve as clinical research center

Chin ML. In: Ashburn MA, Rice LJ, eds. The Management of Pain; 1998:537–545.

Acute Pain: Mechanisms, Management, And Treatment Options

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