Post on 22-Aug-2015
Pain Process after Surgery & Use of NSAID in Pain Control
Professor Dr. Win KoDepartment of Orthopaedics &
TraumatologyUMM
Prof; Win Ko
Prof; Win Ko
NocioceptorsNocioceptors are free nerve
endingsHigh thresholdUbiquitous distributionChemically activated in
response to tissue damageNocioceptors can be sensitized
Prof; Win Ko
Slow pain◦C fibers, unmyelinated, slow burning
aching pain, Substance P
Fast pain◦A delta fibers, myelinated, sharp
prickly pain, glutaminergic
Prof; Win Ko
How postoperative pain generate?
Prof; Win Ko
A delta fibers project to projection neurons in laminas I and V
C fibers project to projection neurons in lamina II
Both also project to inhibitory and excitatory interneurons
Prof; Win Ko
Dorsal Horn SynapsesNeurotransmitters
◦ Glutamate◦ Substance P◦ CGRP◦ CCK◦ Opiates
Receptors◦ NMDA◦ Neurokinin-1◦ ?◦ ?◦ Endorphin (mu,
kappa, sigma)
Prof; Win Ko
Prof; Win Ko
Prof; Win Ko
Modulation of Pain Information
Gate Control Theory◦ Nocioception arises from activation of
nocioceptors◦ Pain sensation is a product of several
interacting neural systems◦ Afferent transmission relies on a balance in
the activity of both the pain fibers and large proprioceptive/mechanosensory fibers
◦ Inhibitory interneurons are spontaneously active and inhibit projection neurons
Prof; Win Ko
Causes of postop pain1. Incisional- skin and subcutaneous tissue2. Deep- cutting, coagulation, trauma 3. Positional- bed sore, nerve compression &
traction4. IV site- needle trauma, extravasation, venous
irritation5. Tubes- drains, nasogastric tube, ETT6. Respiratory- from ETT, coughing, deep
breathing7. Rehab- physiotherapy, movement, ambulation8. Surgical- complication of surgery9. Others- cast, dressing too tight, urinary
retention
Prof; Win Ko
Factors affecting postop painA. Surgical factors: 1. site of incision and nature of the
surgeryupper abdomen > thoracotomy >
lower abdomen > limbs2. complications, eg wound infection,
intraabdominal sepsis, distension
B. Patient factors:Psychology, genetic, hx of substance
abuse, hx of chronic pain
Prof; Win Ko
Consequences of poorly managed acute post-operative painThe Patient suffers
◦ CVS: MI, dysrhythmias◦ Resp: atelectasis, pneumonia◦ GI: ileus, anastamosis failure◦ Endocrine: “stress hormones”◦ Hypercoagulable state: DVT, PE◦ Impaired immunological state
Infection, cancer, wound healing
◦ Psychological: Anxiety, Depression, Fatigue, Sleep Deprivation
◦ Chronic Pain
Prof; Win Ko
Postsurgical Stress ResponseResults in increased oxygen
consumption, increased carbon dioxide production, hyperglycemia, and generalized catabolic state with negative nitrogen balance
The magnitude of the response correlates with mortality
Prof; Win Ko
Why Treat Pain?Basic human right!↓ pain and suffering↓ complications ↓ likelihood of chronic pain
development↑ patient satisfaction↑ speed of recovery → ↓ length of
stay → ↓ cost↑ productivity and quality of life
Prof; Win Ko
Questions Regarding Pain ControlWhat about the 20% who do not get relief
from the WHO ladder or the 46% of those whose families stated we failed?* ◦ Have the opioids been titrated aggressively?◦ Is the pain neuropathic?◦ Has a true pain assessment been accomplished? ◦ Have invasive techniques been employed?◦ Have you examined the patient?◦ Is the patient receiving their medication?◦ Is the medication schedule and route
appropriate?
*Tolle 2001
Prof; Win Ko
Management of postoperative pain1. Optimal postoperative pain management begins in the
preoperative period
2. Measure pain regularly using a validated assessment tool
3. Ensure all postoperative patients receive safe and effective analgesia
4. Monitor and manage adverse effects
5. Communicate ongoing pain management plan to both patients and primary healthcare professionals at discharge.
Australian and New Zealand College of Anaesthetists Acute Pain Management: Scientific Evidence, 2nd ed, 2005, updated Dec 2007Therapeutic Guidelines: Analgesic, Version 5, 2007
Prof; Win Ko
Pain Assessment
Pain History◦O – Onset ◦P – Provoking / Palliating factors◦Q – Quality / Quantity◦R – Radiation◦S – Severity ◦T – Timing
Prof; Win Ko
Pain Assessment Visual Analogue Scale
Prof; Win Ko
Pain
Step 1±Nonopioid± Adjuvant
Pain persisting or increasing
Step 2Opioid for mild to moderate pain
±Nonopioid ± Adjuvant
Pain persisting or increasing
Pain persisting or increasing
Step 3Opioid for moderate to severe pain
±Nonopioid ±Adjuvant
Invasive treatments
Opioid Delivery
Quality of Life
Modified WHO Analgesic Ladder
Proposed 4th Step
The WHOLadder
Deer, et al., 1999
Prof; Win Ko
Multimodal Analgesia
Using more than one drug for pain control◦Different drugs with different mechanisms/sites of
action along pain pathway◦Each with a lower dose than if used alone◦Can provide additive or synergistic effects◦Provides better analgesia with less side effects
(mainly opiate related S/E)
Always consider multimodal analgesia when treating pain
Prof; Win Ko
Prof; Win Ko
Acute Pain Transmission
Prof; Win Ko
Prof; Win Ko
Prof; Win Ko
NSAIDs Mechanism
◦ Block cyclooxygenase (COX) enzyme → ↓ prostaglandin synthesis Preferential COX-1 inhibitor – aspirin,
indomethacin, piroxicam; Nonselective COX inhibitor – diclofenac,
ibuprofen, naproxen; Preferential COX-2 inhibitor – meloxicam,
nimesulide; Selective COX-2 inhibitor – celecoxib, rofecoxib, valdecoxib, parecoxib, etoricoxib.
Prof; Win Ko
Prof; Win Ko
Cell Membrane Phospholipids
Arachidonic Acid
Phospholipase
Prostaglandins Prostaglandins
Gastric ProtectionPlatelet Hemostasis
Acute PainInflammationFever
COX-2 COX-1
Prof; Win Ko
NSAIDs
- Mild and moderate pain- Opoid sparing- SE: peptic ulcer and bleeding,
platelet aggregation inhibition, bronchospasm, renal impairment, allergy
- Do not use celecoxib is history of anaphylaxis or severe cutaneous reaction (Steven-Johnson sydrome, etc.) with a sulfonamide
Prof; Win Ko
NSAIDs
Warnings: ↓dose / avoid if◦ GI ulceration ◦ Bleeding disorders / Coagulopathy◦ Renal dysfunction◦ High cardiac risk – COXII inhibitors◦ Asthma◦ Allergy◦ hypovolaemia, ◦ pregnancy, breast feeding
?Avoid celecoxib if allergic to Sulpha
Concern for anastomotic leaks?
Prof; Win Ko
Prof; Win Ko
Prof; Win Ko
COX-2 inhibitor
No effects on platelets!
Better GI tolerability◦ Less dyspepsia, less N/V
Equivalent analgesic efficacy with non-selective COX-inhibitors
Prof; Win Ko
Prof; Win Ko
Contra-indications to NSAIDs
Patients with the “ASA triad”◦ Risk of severe asthma, angioedema
precipitated with COX-inhibitor
Renal insufficiency or risk there of ◦ especially if risk of hypovolemia periop◦ Patient on ACE inhibitors or ARBs◦ Vascular patients having aortic cross-clamp
and/or probable angiogram peri-operatively
Prof; Win Ko
Contra-indications to Celecoxib/NSAIDsPoorly controlled hypertension
◦ Especially if pt. is on ACE inhibitor, potent loop diuretics
Congestive heart failure◦Fluid/sodium retention
Active peptic ulcer disease
Prof; Win Ko
Acetaminophen
Typical dose: 650 to 1000 mg PO Q6H
Inhibit prostaglandin synthesis in CNS → analgesia
Max dose: 4 g / 24 hrs from all sources
Warning: ↓ dose / avoid in those with liver damage
Prof; Win Ko
Paracetamol is a centrally acting agent
Action depend on the bulbo-spinal serotoninergic pathway
It selectively inhibits nervous system PG synthesis probably via COX-3
Paracetamol hepatotoxicity was found to be very rare (<1 / 2,500
Prof; Win Ko
KetorolacPotent AnalgesicParenteral (IV or IM)15-30 mg Q 6hrPatients Older than 16 yrsShould not Exceed 5 days
Prof; Win Ko
Cox-2 Inhibitors
Drug Dose
Celecoxib (Celebrex) 100-200mg PO Bid
Rofecoxib (Vioxx)
Valdecoxib (Bextra) 10-20mg PO Qd
Parecoxib 20-40mg IM20-100mg IV
Prof; Win Ko
Prof; Win Ko
Celecoxib OR Diclofenac
□ Celecoxib 200 mg po daily X 3 days
□ Diclofenac 50 mg po q8h X 3 days (may give first dose PR)
□ Diclofenac 50 mg pr q12h X 3 days
Prof; Win Ko
NSAID, Coxibs and Acetaminophen
CONCEPT # 1The foundation of all acute pain Rx
protocols. ”First on last off”
sole agent in mild /moderate pain Analgesic efficacy is limited inherently In contrast, with opioids efficacy is limited by
S/EOpioids added as requiredopioid sparing effect 30-60 %
Prof; Win Ko
COX-INHIBITORS vs. OPIOIDS
EfficacyLimited Inherently Limited by S/E
Inter-patient dose variabilitySmall Large, making dose
titration difficult
Life threatening complicationsUpper GI bleeding Resp. depression
With chronic use Risk is early
Prof; Win Ko
COX-INHIBITORS vs. OPIOIDS
Toxicity, S/ETissue/organ toxic neurologic
dysfunc Drug tolerance
Not evident tolerance is part of
normal response
Abuse potentialNil Yes
Prof; Win Ko
Cyclo-oxygenase inhibitors
Acetaminophen
NaproxenCelecoxib
Ketorolac
Numerous others
Prof; Win Ko
Why a COX-2 inhibitor?
No effects on platelets!
Better GI tolerability◦ Less dyspepsia, less N/V
Equivalent analgesic efficacy with non-selective COX-inhibitors
Prof; Win Ko
Prof; Win Ko
THANK YOU