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The management of postoperative pain

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The management of postoperative pain Powered By Docstoc
					A New Molecule for
Post Operative Pain
   Management

     Dr.P.Selvakumar M.D.,
       Senior consultant
   Apollo Specialty Hospitals
            Madurai
                   Clinical definition of pain1




     “An unpleasant sensory and emotional experience
    associated with actual or potential tissue damage,
    or described in terms of such damage...




1. IASP Pain Terminology. In Merskey H & Bogduk N eds. Classification of Chronic Pain, Second Edition,
IASP Task Force on Taxonomy. IASP Press, Seattle 1994:209-14.
                 Objectives
   Types of pain
   Pain physiology
   Multimodal analgesia
   Intravenous agents used for postoperative
    pain
   Conclusions
               Pain: Clinical Types
       Nociceptive pain
           Transient pain in response to noxious stimuli

       Inflammatory pain
           Spontaneous pain and hypersensitivity to pain in
            response to tissue damage and inflammation

       Neuropathic pain
           Spontaneous pain and hypersensitivity to pain in
            association with damage to or a lesion of the
            nervous system



Woolf. Ann Intern Med. 2004;140:441-451.
                             Nociceptive Pain
            Is responsive to NSAID’s, coxibs,
                    paracetamol and opiates
           Noxious Peripheral Stimuli

                      Heat                                      Pain-Autonomic Response
                                                                   - Withdrawal Reflex
                       Cold
               Intense
             Mechanical
                                           Nociceptor Sensory
                 Force                     Neuron
                                                                                   Brain
               Chemical
               Irritants

                                                                  Spinal Cord


Woolf. Ann Intern Med. 2004;140:441-451.
                         Inflammatory Pain
               Is responsive to NSAID’s,coxibs,
                     paracetamol, and opiates Pain
                 Inflammation      Spontaneous
 Macrophage
                                                          Pain Hypersensitivity
     Mast Cell                                              -Allodynia
  Neutrophil                                                -Hyperalgesia
 Granulocyte
                                           Nociceptor Sensory
                                           Neuron
                                                                              Brain
 Tissue
 Damage

                                                                Spinal Cord


Woolf. Ann Intern Med. 2004;140:441-451.
                           Neuropathic Pain
                                                 Spontaneous Pain
                                                 Pain Hypersensitivity
•May respond to
  • local anaesthetic
  • anticonvulsants
  • antidepressants
            Peripheral Nerve                                   Brain
                              Damage
                                                               Stroke
•Less responsive to opioids
                                          Spinal Cord Injury

•No response to NSAID’s, coxibs, or
paracetamol   .
Woolf. Ann Intern Med. 2004;140:441-451
               Postoperative pain is nociceptive
                  Perception




Is responsive to NSAID’s,coxibs, paracetamol and
                    Modulation
                     opiates

                                                Transmission



                                                           Transduction


Reuben et al. J Bone Joint Surg. 2000;82:1754-1766.
 Consequences of Unrelieved Pain
                                        Acute Pain

       Increased                       Splinting,      Increased                        Peripheral/
                                                                         Anxiety
       sympathetic      GI effects     shallow         catabolic                        central
                                                                         and fear
       activity                        breathing       demands                          sensitization



      Myocardial                      Atelectasis,   Poor wound
                                                                       Sleeplessness,    Available
      O2               GI motility   hypoxemia,     healing/muscle
                                                     breakdown
                                                                       helplessness      drugs
      consumption                    hypercarbia



                                                      Weakness
        Myocardial       Delayed                                          Psycho-
                                      Pneumonia       and impaired
        ischemia         recovery                     rehabilitation
                                                                          logical


                                                                                        Chronic
                                                                                        pain


Courtesy of Sunil J Panchal, MD
Intensity of Pain After Discharge:
           81% Report Moderate to Extreme Pain

                                   8%         19%
                         21%



                                         52%




     Pain Intensity       Slight        Moderate    Severe   Extreme



Apfelbaum et al. Anesth Analg. 2003;97:534-540.
                             Guidelines for optimising
                              POP management1,2,3,4,5,6

      Adequate and thorough patient information2,3,4,5,6
      Use of written protocols1,3,4,5,6
      Regular assessment of pain intensity1,2,3,4,5,6
      Adequate medical and nursing staff training1,3,4,5,6
   Use of balanced analgesia, PCA, and epidural drug
   administration1,2,3,4,5,6

1. The Royal College of Surgeons of England and the College of Anaesthetists. Commission on the provision
   of surgical services, report of the working party on pain after surgery. London, UK, HMSO.1990.
2. Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services. Acute Pain Management in
Adults: Operative Procedures. Quick Reference Guide for Clinicians. AHCPR Pub. No. 92-0019. Rockville, MD.1992.
3. International Association for the Study of Pain, Management of acute pain: a practical guide. In: Ready LB, Edwards WT, eds. Seattle, 1992.
4. Wulf H et al. Die Behandlung akuter perioperativer und posttraumatischer Schmerzen Empfehlungen einer
   interdisziplinaeren Expertenkommision. G. Thieme, Stuttgart, New York. 1997.
5. EuroPain. European Minimum Standards for the Management of Postoperative Pain.1998.
6. SFAR. Conférence de consensus. Prise en charge de la douleur postopératoire chez l’adulte et l’enfant.
   Ann Fr Anesth Réanim 1998;17:445-61.
Effective pain management may improve
              outcomes1,2,3

                  Effective analgesia included in a comprehensive
                     postoperative rehabilitation programme1,2

                       Improved patient comfort and satisfaction
                          Decreased postoperative morbidity
                                   Faster recovery
                               Shorter hospital stay1,2,3

                                          Very favourable
                                         cost/benefit ratio2

                             Low cost of analgesic techniques
                                        and drugs2
1. Kehlet H. Br J Anaesth 1994;72(4):375-8.
2. Jayr C. In Les Aspects Economiques de l’Anesthésie. JEPU 2000:131-8.
3. D’Amours RH et al. JOSPT 1996;24(4):227-36.
   Physiology &
 pharmacological
 management of
postoperative pain
                Pain pathway and modulation1
                                                                    Descending inhibitory controls /
         Ascending nociceptive pathways
                                                                   Diffuse noxious inhibitory controls

                Interpretation in                                        Activation of serotoninergic
                cerebral cortex:                                          and noradrenergic pathways
                      pain




                                                                          Release of serotonin,
                                                                       noradrenalin and enkephalins
          Stimulation of nociceptors                                         at spinal level
             (A and C fibers) /
                  Release of
            neurotransmitters and
          neuromodulators (i.e. PG)

                       Injury

1. Adapted from: Bonica JJ. Postoperative pain. In Bonica JJ, ed. The management of pain. Philadelphia: Lea
and Febiger;1990:461-80.
             Modes of action of analgesics1,2,3,4
                                                                    Paracetamol
                                                                          
                                                          Inhibition of central Cox-3 (?)
                                                            (Inhibition of PG synthesis)


                                                                      Opioids
                                                                         
                                                                  Activation of
                                                                 opioid receptors

                                                                   Paracetamol
                                                                        
                                                                Interaction with
                                                            serotoninergic descending
                                                               inhibitory pathway

                                                                NSAIDs / Coxibs
                                                                         
                                                           Inhibition of peripheral and
                                                             central Cox-1 / Cox-2
                                                           (Inhibition of PG synthesis)
1. D’Amours RH et al. JOSPT 1996;24(4):227-36.
2. Piguet V et al. Eur J Clin Pharmacol 1998;53:321-4.
3. Pini LA et al. JPET 1997;280(2):934-40.
4. Chandrasekharan NV et al. PNAS 2002;99(21):13926-31.
Multimodal and Preemptive
 Approaches to Managing
    Postoperative Pain
  The concept and benefits of balanced
               analgesia

     “The rationale for multimodal analgesia is
     achievement of sufficient analgesia due to
      additive or synergistic effects between
       different analgesics, with concomitant
    reduction of side effects, due to resulting
   lower doses of analgesics and differences in
               side -effect profiles”


1. Kehlet H et al. Anesth Analg 1993;77:1048-56.
          Patients’ Preferences for
           Acute Pain Treatment
        Patients prefer avoiding side effects
             over complete pain control
                                            Side-Effect Severity
                                                    19%

Pain Control
    41%
                                                                   47%


                                             Side-Effect Type
                                                   28%
                   Setting and Route
                   of Administration
                          12%
Gan et al. Br J Anaesth. 2004;92:681-688.
          Proportion of Patients
       Experiencing Adverse Events
Adverse Event (AE)                      Total %
Constipation                              50
Mental cloudiness/dizziness               82
Itching                                   54
Nightmares/hallucinations                 32
Mood changes/alterations                  34
Nausea                                    70
Sleep disorders                           48
Vomiting                                  32


Gan et al. Br J Anaesth. 2004;92:1-8.
     Preventive Multimodal Analgesia

       Significant improvement in
          Pain reduction
          Opioid use

          Opioid-related AEs

          Recovery or day ward length of stay

          Unplanned admission to the hospital




Reuben et al. Acute Pain. 2004;6:87-93.
“Real World”: Multimodal Analgesia
                                                        Reduced doses
    Opioids
                                                        Improved pain relief

                                                        Reduce severity
                             Potentiation                of AEs

                                                        Earlier discharge
  NSAIDs, coxibs,
  paracetamol,
  nerve blocks                                          Decreased costs



Kehlet et al. Anesth Analg. 1993;77:1048-1056 (B).
Intravenous agents for
 multimodal analgesia
                  IV morphine
   Intermittent IV bolus doses
       Is best method for acute pain
       Optimal doses and dose intervals not established
       2-3 mg doses at 5 minute intervals appears
        effective


   Continuous infusion
       Compared with PCA there is a 5-fold increase in
        respiratory depression
 IV paracetamol - premise


“Is more effective & has a faster onset
         than oral paracetamol”
                Means of pain intensity differences (VAS)




Onset of action is fast and effective – within
                  5 minutes



Sindet-Pedersen S. Br Jr Anesth 2005. 94 (5): 642-8
     Paracetamol:
clinical pharmacology
      Paracetamol: a well known analgesic
                    agent
   First proper account of clinical use in 1894 (Hinsberg                         and Treupel)1



   Analgesic effect formally demonstrated in 1948 (Flinn and Brodie)                              1




   Recommended first-line analgesic therapy:
    - for the treatment of osteoarthritis since 2000                             2,3


    - for musculoskeletal pain in elderly since 2002                         4


    - for patients with renal disease since 1996                        5




1. Prescott LF. Am J Therapeut 2000;7(2):143-7.
2. EULAR recommendations. Pendleton A et al. Ann Rheum Dis 2000;59(12):936-44.
3. American College of Rheumatology Subcommittee on osteoarthritis guidelines.
   Arthritis Rheum 2000;43(9):1905-15.
4. AGS Panel on Persistent Pain in Older Persons. JAGS 2002;50:S205-24.
5. Henrich WL et al. Am J Kidney Dis 1996;27(1):162-5.
          Paracetamol – how does it work?


        Paracetamol is a centrally acting agent

     It selectively inhibits nervous system PG
     synthesis probably via COX-3
                        2,3




     Other central mechanisms of action depend on
     the bulbo-spinal serotoninergic pathway             4,5




1. Piguet V et al. Eur J Clin Pharmacol 1998;53:321-4.
2. Carlsson KH et al. Pain 1988;32:313-26.
3. Flower RJ et al. Nature 1972;240:410-1.
4. Tjølsen A et al. Eur J Pharmacol 1991;193:193-201.
5. Pélissier T et al. JPET 1996;278:8-14.
Objective R-III reflex threshold changes expressed as a percentage of difference
                                  from baseline




      Paracetamol clinically demonstrates
               central activity1



1. Piletta P et al. Clin Pharmacol Ther 1991;49(4):350-4.
        What were the challenges?

1. Making paracetamol soluble
   Use of hydrophilic ingredients   (mannitol and disodium phosphate)



2. Ensuring its stability in solution
 - By   controlling hydrolysis
   Use of a pH buffer (disodium phosphate and sodium hydroxide)

 - By   preventing oxidation
   Addition of cysteine hydrochloride

   Oxygen-free manufacturing process
Indications
   Phase III clinical trials1,2 VS. placebo

      Similar overall incidence of adverse events

      Similar incidence of local adverse events

      No clinically significant changes in vital signs or
       laboratory tests




             IV paracetamol as safe as placebo

1. Lange-Møller P. Anesth Analg 2005;101:90 –6
2. Sinatra RS. Anesthesiology 2005; 102:822–3
India Prescribing Information
    No difference in adverse events vs placebo
                                      Oral surgery




Lange-Møller P. Anesth Analg 2005;101:90 –6.
    No difference in adverse events vs placebo
                              Orthopaedic surgery




                 %




Sinatra RS. Anesthesiology 2005; 102:822–3
    Hepatic safety at therapeutic doses1


   Paracetamol hepatotoxicity was found to be very
   rare (<1 / 2,500)1


      It was always related to misuse and overdose
       (>4g / day)1



                       Good hepatic safety
1. Whitcomb DC et al. JAMA 1994;272(23):1845-50.
                                Renal safety
       Up to 4g / day, paracetamol has an excellent renal
          safety profile1


       No evidence exists for the development of chronic
        nephropathy with paracetamol2

       Recommended by the National Kidney Foundation
        as the non-narcotic analgesic of choice in patients
        with underlying renal disease 3


                           Good renal tolerance
1. Whelton A. Am J Therapeut 2000;7(2):63-74.
2. Blantz RC. Am J Kidney Dis 1996;28(1):S3-6.
3. Henrich WL et al. Am J Kidney Dis 1996;27(1):162-5.
          Paracetamol safety benefits in POP
         No centrally mediated side-effects1
          (e.g. sedation, constipation, nausea, vomiting, respiratory depression)

       No effect on platelet aggregation, bleeding, or uric acid
      excretion2
       No gastrointestinal side effects
                                         3

         Good renal4 and hepatic5 safety
         Few contra-indications and drug interactions




1. Lechat P et al. Thérapie 1989;44:337-54.
2. Insel PA. Analgesic-antipyretic and antiinflammatory agents and drugs employed in the treatment of gout. In: Goodman & Gilman eds.
   The pharmacological basis of therapeutics. McGraw Hill, 9th edition, 1996:617-57.
3. Singh G. Am J Therapeut 2000;7(2):115-21.
4. Whelton A. Am J Therapeut 2000;7(2):63-74.
5. Whitcomb DC et al. JAMA 1994;272(23):1845-50.
How to use Perfalgan
                   Perfalgan is ready-to-use


     •   No reconstitution

                  Saves nurses time1

                  Reduces use of ancillary products1

                  Reduces risk of dosage error1

                  Reduces risk of contamination1




1. Schmitt E et al. Pharm Hosp 2001;36(147):9-18.
1. Take the cap off



2. Link the bottle to a drip
   with an air intake


3. Hook the bottle with the
   built-in calliper
         Perfalgan infusion
   Where ?
        First administration in the OR



   How?
     •   15-minute infusion every 4 to 6 hours


   Dosing schedule:
         - Adolescents and adults weighing more than 50kg:
           1 g / 4 times a day
                    Storage

   Shelf life is 2 years


   Do not store above 30°C


   Do not refrigerate or freeze
Conclusions
       Perfalgan is a fast-acting analgesic, as effective as
        morphine 10mg1

       Perfalgan is a proven opioid-sparing agent2

       Perfalgan is well tolerated in all types of patients

       Perfalgan is ready-to-use and cost-effective3




1. Van Aken H. 1991. Anesth Analg 2004; 98: 159-65
2. Peduto VA et al. Acta Anaesthesiol Scand 1998;42:293-8.
3. Schmitt E et al. Pharm Hosp 2001;36(147):9-18.

				
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