Challenges in Pain Assessment Jeffrey A. Katz, MD Associate Professor of Anesthesiology Section of Pain Medicine Feinberg School of Medicine Northwestern University Chicago, Illinois
Dec 29, 2015
Challenges in Pain Assessment
Jeffrey A. Katz, MDAssociate Professor of Anesthesiology
Section of Pain MedicineFeinberg School of Medicine
Northwestern UniversityChicago, Illinois
AssessmentAssessmentPain as a 5th Vital Sign
• Better than VAS: • Verbal Numeric Rating Scale
– 0 = No Pain– 10 = Worst Pain Imaginable– What is your current (or average) pain?
• Also: None-Mild-Moderate-Severe• All have equal validity
VAS = visual analog scale.
Olsen S, et al. Anesthesiol Rev. 1992;19:11-15.
Re-AssessmentRe-Assessment• Obtain Verbal Numeric Rating Scale
– Remember, 0 is NOT always a goal!!!
• Also get Verbal RELIEF Score– 0 = No Relief– 10 = Complete Relief– What is your current (or average) relief?
Consequences of Consequences of Undertreatment of Pain Undertreatment of Pain
Treatment for Chronic Pain Has Not Improved
Louis Harris & Associates Inc. The 1999 National Pain Survey. 1999.Peter D. Hart Research Associates. America Speaks: Pain in America. 2003.Brookoff D. Hosp Pract. 2000;35:45-52, 59.
• Increasing prevalence and incidence of chronic pain
• 1999– 24% of American adults reported chronic pain
• 2002– 57% of adults reported chronic or recurrent pain
• As US population ages more patients will need pain treatment
Pain and Productivity
$0
$10
$20
$30
$40
$50
$60
$70
Cost of Lost ProductiveTime
Job productivity
• 13% reported a loss in productive time due to pain
• $61 billion/year in cost for lost productivity
77% due to reduced work performance
An
nua
l Co
st (
Bill
ion
s)
Stewart WF, et al. JAMA. 2003;290:2443-2454.
23% due to workplace absenteeism
Survey of lost productive time in working adults during a 2-week period (N = 28,902)
Pain and Quality of Life
• Interferes with daily life• Significant emotional impact• Impairs physical, social, and
psychological status• Impairs QoL of family members
and caregivers
QoL = Quality of Life.
Berry PH, et al. Pain: Current Understanding of Assessment, Management, and Treatments. Reston, Va: National Pharmaceutical Council and Joint Commission on Accreditation of Healthcare Organizations; December 2001. Roper Starch Worldwide Inc. Chronic Pain in America: Roadblocks to Relief. 1999.Bair MJ, et al. Arch Intern Med. 2003;163:2433-2445.Ferrell BR, et al. Oncol Nurs Forum. 1995;22:1211-1218.
Pain Management Improves Quality of Life
• Effective multidisciplinary management improves QoL– 84% report feeling happy and upbeat– 89% report feeling positive about life
• Inadequate pain control is unacceptable
Katz N. J Pain Symptom Manage. 2002;24(suppl 1):S38-S47.Roper Starch Worldwide Inc. Chronic Pain in America: Roadblocks to Relief. 1999.
Choosing Choosing PharmacotherapyPharmacotherapy
Nociceptive– Tissue damage– Transmitted
along pain pathways
– eg, Burn
Pain ClassificationNeurophysiologic Origin
Visceral– Visceral
stimulus– Diffuse, dull– Referred pain– eg, Colic
Neuropathic– CNS/PNS injury– Abnormal
sensory function– Spreads– No ongoing
damage– eg, PHN
CNS/PNS = central nervous syste/peripheral nervous system; PHN = postherpetic neuralgia.
Classification of Pain Practical
•Acute•Chronic•Cancer•AIDS
Acute PainAcute Pain• Serves a biologic function
• Resolves with treatment of cause
• Recent onset, short duration
• Goal: Treat symptoms until cause resolves
Chronic PainChronic Pain• Serves no biologic functionServes no biologic function• Persists despite treatment of known or Persists despite treatment of known or
presumed causepresumed cause• Goal: Maximize function independent Goal: Maximize function independent
of health care system constraintsof health care system constraints• As in treating diabetes or asthmaAs in treating diabetes or asthma
– Treat to manage, not cure
Analgesia and the Pain Pathway
NSAIDs = nonsteroidal anti-inflammatory drugs. Adapted from Gottschalk A, et al. Am Fam Physician. 2001;63:1979-1984.
Descending modulation
Dorsal horn
Ascendinginput
Spinothalamic tract
Dorsal root ganglion
Peripheral nerve
Peripheral nociceptors
Pain
Trauma
Local anestheticsOpioids Antiepileptic drugsAnti-inflammatory agents (cox-2 inhibitors, nonspecific NSAIDs)
Centrally acting analgesicsOpioids 2-Agonists TricyclicsAntiepileptic drugsAnti-inflammatory agents
Local anestheticsAnti-inflammatory agents
Local anesthetics Anti-inflammatory agents(cox-2 inhibitors, nonspecific NSAIDs)OpioidsAntiepileptic drugs
Available Pain Medications
Agent Mechanism of Action Typical Uses
Acetaminophen Weak inhibitor of COX-1 and COX-2; may inhibit “unidentified” COX enzyme (ie, COX-3)
Mild to moderate pain states
Nonspecific inhibitors
Inhibition of COX-1 and COX-2 isoenzymes
Mild to moderate pain states
COX-2 specific NSAIDs
Selective inhibition of COX-2 isoenzyme (GI mucosa sparing)
Mild to moderate pain states
Opioids Opioid receptor agonist action, inhibiting pain impulses
Moderate to severe pain states
Tramadol Opioid agonist plus norepinephrine/serotonin reuptake inhibitor
Moderate to moderately severe pain
Available Pain Medications, cont.
Agent Mechanism of Action Typical Uses
Antiepileptics Modulate sodium and calcium channels
Neuropathic pain
Tricyclic antidepressants
Block reuptake of norepinephrine and other amines
Neuropathic pain
Topical treatments
Analgesic/anesthetic action on sensory nerve fibers in skin
Neuropathic pain
Muscle relaxants Inhibition of polysynaptic events in the CNS
Musculoskeletal pain
NMDA receptor antagonists
Inhibition of NMDA-receptor induced neuronal excitation
Neuropathic pain
PKAPKA
PKCPKC
EP EP receptorreceptor
Tissue injuryTissue injury
PGEPGE22
COX-2 expressedCOX-2 expressed
TTx resistantTTx resistantsodium sodium channelchannel
P
COX-2 and Peripheral Mechanisms of Pain
PGE2 = prostaglandin E2; PKA = protein kinase A; PKCε = protein kinase C, TTx = tetrodotoxin.
Samad TA, et al. Nature. 2001;410:471-475.Woolf CJ, et al. Science. 2000;288:1765-1769.Byers MR, Bonica JJ. In: Bonica’s Management of Pain. 2001:27-72.
NociceptorNociceptorResting Resting
membranemembranepotentialpotential
Neuron Neuron firing thresholdfiring threshold
Prostaglandins and Pain
• PGs nociception in nerves and CNS
• PGs sensitize pain nerve endingsMore responsive to touch and pain
• PGs also mediate pain in CNS SP and glutamate release Sensitivity of 2nd order neurons Release inhibitory transmitters
PG = prostaglandis; SP = substance P.
NSAIDs and COX-2s NSAIDs and COX-2s
Are Not AnalgesicsAre Not Analgesics
They Are Anti-Hyperalgesics
NSAIDs and COX-2s Do not NSAIDs and COX-2s Do not Replace OpioidsReplace Opioids
They Greatly Enhance Opioid Analgesia
Central SensitizationCentral Sensitization• Sensitization: Amplification of
signals to CNS after intense pain• Usually the result of touch fibers
cross-circuiting to pain pathways– Touch Pain– Movement Pain– Slight pain Severe Pain
B Fibers: Myelinated Autonomics
C Fibers: Pain and Temperature
A Fibers: Myelinated Large
A-alpha: Motor
A-beta: Touch
A-gamma: Position
A-delta: Pain and
Temperature
Classification of Peripheral Nerve Fibers
Dorsal RootDorsal Root
Dorsal Dorsal RootRoot
GanglionGanglion
To BrainTo Brain
Central Sensitization Causing Allodynia
TO BRAIN
Dorsal HornPain Neuron + +
+
C
ININ
A-delta
+Mediated in part by NMDA receptor on the dorsal horn pain neuron
A-beta
_ _
0
ININ
IN = interneuron; NMDA = N-methyl-D-aspartate.
Woolf CJ, et al. Science. 2000;288:1765-1769.
Guyton’s textbook
A-beta touch fiber
To brain
Guyton’s Textbook of Physiology
Tricyclic AntidepressantsAmitriptylineImipramineNortriptylineDesipramineClomipramineDoxepinTrimipramineAmoxapineProtriptyline
Amitriptyline
• HCl
CH(CH2)2N(CH3)2
‘‘Inappropriate in Elderly’Inappropriate in Elderly’
Baldessarini. In: Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 10th ed.
McGraw-Hill Professional; 2001.
Tricyclic Antidepressants: Pros and Cons
IOP = intraocular pressure; HR = heart rate.
Beers MH, et al. Arch Intern Med. 1997;157:1531-1536.Ray WA, et al. Clin Pharmacol Ther. 2004;75:234-241.
• Anti-Ach effects– Sedation– Constipation, urinary retention IOP, HR, etc
• At doses > 100 mg/day: risk sudden cardiac death– Conduction changes
Track record and inexpensive, but . . .
From body Dorsal horn
spinal cord
To brain
NENE
5-HT5-HT
Tricyclic Antidepressants and Serotonin-Norepinephrine Reuptake Inhibitors: Mechanisms
of Action
NE = Norepinephrine; 5-HT = Serotonin.
Baldessarini. In: Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 10th ed. McGraw-Hill Professional; 2001.
From body Dorsal Horn
Spinal Cord
To Brain
NENE
5-HT5-HT– SSRIs only Act on SSRIs only Act on
serotonin pathwayserotonin pathway
– Ineffective in pain reliefIneffective in pain relief
Selective Serotonin Reuptake inhibitors
CaCa++++
GabapentinGabapentin
Gabapentin: Mechanism of Action
Benefits of Multimodal Analgesia
Kehlet H, et al. Anesth Analg. 1993;77:1048-1056.
• Reduced doses of individual analgesic
• Improved pain reliefdue to synergistic/additive effects
• May reduce severityof side effects ofeach drug
OpioidsOpioids
PotentiationPotentiation
NSAIDs, COX-2s,NSAIDs, COX-2s,acetaminophen,acetaminophen,
nerve blocksnerve blocks