perioperative pain management - download.e-bookshelf.de€¦ · pain perception 15 summary 15 2....

P1: SFK/UKS P2: SFK/UKS QC: SFK/UKS T1: SFK

BLBK046-Cox September 15, 2008 17:9

Perioperative Pain Management

Edited byFelicia Cox MSc (ECP), PGDip, RNSenior Nurse, Pain ManagementRoyal Brompton & Harefield NHS Trust

A John Wiley & Sons, Ltd., Publication

i



This edition first published 2009C© 2009 Blackwell Publishing Ltd

Blackwell Publishing was acquired by John Wiley & Sons in February 2007. Blackwell’s publishingprogramme has been merged with Wiley’s global Scientific, Technical and Medical business to formWiley-Blackwell.

Registered office:John Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, United Kingdom

Editorial offices:9600 Garsington Road, Oxford, OX4 2DQ, United Kingdom

For details of our global editorial offices, for customer services and for information about how to apply forpermission to reuse the copyright material in this book please see our website atwww.wiley.com/wiley-blackwell

The right of the author to be identified as the author of this work has been asserted in accordance with theCopyright, Designs and Patents Act 1988.

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, ortransmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise,except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior permission ofthe publisher.

Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may notbe available in electronic books.

Designations used by companies to distinguish their products are often claimed as trademarks. All brandnames and product names used in this book are trade names, service marks, trademarks or registeredtrademarks of their respective owners. The publisher is not associated with any product or vendormentioned in this book. This publication is designed to provide accurate and authoritative information inregard to the subject matter covered. It is sold on the understanding that the publisher is not engaged inrendering professional services. If professional advice or other expert assistance is required, the services ofa competent professional should be sought.

Library of Congress Cataloging-in-Publication Data

Perioperative pain management / edited by Felicia Cox.p. ; cm.

Includes bibliographical references and index.ISBN 978-1-4051-8077-1 (pbk. : alk. paper)1. Postoperative pain. 2. Analgesia. I. Cox, Felicia.[DNLM: 1. Pain–therapy. 2. Analgesia–methods. 3. Analgesics–therapeutic use.4. Anesthesia–methods. 5. Anesthetics–therapeutic use. 6. Perioperative Care–methods.WL 704 P445 2008]RD98.4.P47 2008617’.9195–dc22

2008015231

A catalogue record for this book is available from the British Library.

Set in 10/12.5 pt Palatino by Aptara R© Inc., New Delhi, IndiaPrinted in Singapore by Markono Print Media Pte Ltd

1 2009

ii



Contents

Dedication xiiiList of contributors xivForeword xviiPreface xviii

1. The Physiology of Pain 1Rohit Juneja and Sian Jaggar

Introduction 1Definitions 1Peripheral mechanisms 2

Peripheral receptors 2Mechanisms of inflammatory pain 5

Central mechanisms 7Spinal cord modulation 7Supraspinal modulation 14

Pain perception 15Summary 15

2. Principles of Acute Pain Assessment 17Donna Brown

Introduction 17Measurement of acute pain 18Unilateral pain-rating scales 19

Verbal rating scale 19Visual analogue scale 20Numerical rating scale 21The faces of pain scale 22The Wong-Baker FACES pain scale 22Limitations 23

Multidimensional pain-rating scales 23The McGill Pain Questionnaire 23The Short-Form McGill Pain Questionnaire 24Royal Brompton and Harefield NHS Trust pain assessment tool 24

iii



Contents

Brief Pain Inventory 27Considerations 27Leeds Assessment of Neuropathic Symptom and SignsPain Score 28

Assessing pain in patients across the age spectrum 28Paediatric pain assessment tools 28

Older people (65 years and over) 31Applying pain assessment tools 31

None-to-mild cognitive impairment 31Moderate-to-severe cognitive impairment 34

When should pain be measured? 35Recovery ward 35Pain assessment at ward level 37

Summary 37

3. Barriers to Effective Pain Management 45Eloise Carr

Introduction 45Patient barriers 46

Anxiety and pain 46Professional barriers 48

Assessing pain 49Communication with other health care professionals 51

Organisational barriers 54Accountability 55Local policies 56Local resources 56

National perspectives – new legislation on prescribing 57Global barriers and policies 58Conclusion 59

4. Psychosocial Perspectives of Acute Pain 64Rachel Hagger-Holt

Introduction 65The medical model: a need for extension 66Biopsychosocial model of pain 68

Gate control theory of pain 69Psychological theories 70

Behavioural theory 71Cognitive theory 72

Application to a specific area 74Preoperative preparation 74Postoperative treatment 76

Summary 77Acknowledgements 77

iv



Contents

5. The Role of Personal Coping Strategies in the Managementof Perioperative Pain 81Dee Burrows and Elaine Taylor

Introduction 81What do we mean by ‘coping strategies’? 82The historical context of personal pain-coping strategies 84From taught to self-generated strategies in acute care 85Engaging patients in their own pain management 86

Findings 89The role of personal coping strategies 90Summary 92

6. How Analgesics Work 95Kirsty Scott

Introduction 95Non-opioid analgesics 96

Anti-inflammatory agents 96Paracetamol 98

Opioid analgesics 99Opioid mode of action 100

Local anaesthetics 103Lidocaine 104Bupivacaine hydrochloride 104Levobupivacaine 105Ropivacaine 105Combining a local anaesthetic with an opioid 106

Other agents 106NMDA receptor antagonists 106�2-Adrenergic agonists 106

Summary 106

7. The Evidence for Acute Perioperative Pain Management 108Jane Quinlan

Introduction 108Randomisation 109Bias 109Double-blind 109Meta-analysis 110Systematic review 110Confidence intervals 110

Levels of evidence 110Pain measurement in research 111

Number needed to treat 113The placebo effect 113

v



Contents

Evidence for effectiveness of specific drugs 116Paracetamol (acetaminophen) 116Non-steroidal anti-inflammatory drugs 117Oral opioids 117Intramuscular opioids 117Patient-controlled analgesia 118Epidural analgesia 119Ketamine 120Gabapentin 120Clonidine 120Magnesium 121

Multimodal analgesia 121Recovery from surgery 122Summary 122

8. Regional Anaesthesia and Analgesia, Part 1: PeripheralNerve Blockade 127Barbora Parizkova and Shane George

Introduction 127General considerations 128Commonly used agents 130Review of evidence in different populations 131Peripheral neural blockade 135Upper limb regional analgesia 135

Brachial plexus blockade 137Lower limb regional analgesia 137

Femoral nerve blockade 138Lumbar plexus blockade 139Sciatic nerve blockade 139

Postoperative care 139Paravertebral blockade 140

Efficacy, indications, contraindications 140Techniques 140PVB nursing care, observations and side effects 141

Other techniques 142Summary 142

9. Regional Anaesthesia and Analgesia, Part 2: Central NeuralBlockade 144Barbora Parizkova and Shane George

Neuraxial techniques – spinals and epidurals 144Anatomy 144Specific contraindications to neuraxial anaesthesia 147Side effects and complications of neuraxial blockade 147

vi



Contents

Epidural blockade 149Epidural techniques 150

Spinal (intrathecal or subarachnoid) anaesthesia 151Technique 152Duration of action 153Continuing care and observation 153Towards safer practice with neuraxial analgesia 154

Summary 156

10. Patient-Controlled Analgesia 161Gillian Chumbley

Introduction 161The evidence for PCA versus conventional analgesia 163What do the systematic reviews tell us about PCA? 164

Opioid consumption 164Patient control 165Satisfaction 165

Standard prescriptions for PCA 166Patient selection and contraindications for using PCA 166PCA programmes and definitions 167

Loading dose 167Bolus dose 167Dose duration 168Lockout interval 168Dose limits 169Background infusion 169

Monitoring and documentation of PCA 170Respiratory rate 170Sedation scores 171Blood pressure 172Pain score 172Location of pain 173Amount of drug used (analgesic consumption) 173Side effects of PCA 173

When to stop PCA? 175Maintaining the patient’s safety when using PCA 177

Patient to press 177Staff education 177Standardisation of PCA solutions 177Dedicated IV access 178Device malfunction 178

Patients’ views of PCA 179Fear of addiction and overdose 179Information about the device 179Opioid side effects 180Other concerns: alarms and attention from nurses 180

vii



Contents

What do patients want to know about PCA? 181Dangers of morphine 181Side effects of morphine 182Alternative pain relief 182Support from staff 182How to use PCA and when to receive information 182

Summary 182

11. Other Routes of Opioid Administration 186Ian McGovern

Introduction 186Intravenous route 187

Intermittent intravenous bolus administration 187Continuous intravenous infusion 188PCA techniques 188

Intramuscular and subcutaneous routes 189Individual agents 190

Enteral routes 190Oral route 190Rectal route 194

Transdermal route (reservoirs and matrix) 194Transdermal fentanyl reservoir patches 195Iontophoretic transdermal delivery systems 195

Transmucosal routes 196Intranasal route 197Sublingual and buccal routes 197

Pulmonary route 198Locally administered opioids 198Summary 198

12. Managing Perioperative Pain in Special Circumstances 203Paediatric Pain Management 203Elizabeth M.C. Ashley

Introduction 203Licensing of analgesic medicines in paediatric practice 204Routes of drug delivery 204Pain management in neonates and children 205

Fetal pain 205Neonatal pain 205Pain in children 206Stress response 206

Pain assessment 206Neonates (up to 1 month; or ex-premature up to60 weeks’-post-conceptual age) 206Infants and toddlers (1 month–3 years) 207

viii



Contents

Children (3–7 years) 207Older children and adolescents (7 years plus) 207

A pain service for children 207A multimodal approach to pain relief in children 208

Local anaesthetic infiltration and peripheral nerve blocks 208Simple analgesics 209

Paracetamol 209Non-steroidal anti-inflammatory drugs 209Codeine phosphate 210

Morphine 210Oral morphine 210Intravenous morphine infusions 210Subcutaneous morphine infusions 211Morphine PCA 211Morphine NCA 211

Epidural analgesia 212Ketamine 213Clonidine 213

Monitoring and complications 213Paediatric day-case surgery 213Pain on the paediatric ICU 214Postoperative nausea and vomiting in children 214Chronic pain development in children 214

The Older Person 216Lesley Bromley

Physiological changes of aging 217Pharmacokinetic changes in the elderly 217

Absorption 217Distribution 217Elimination 218

Pharmacodynamic changes 218Cognitive impairment 218Specific medicines in the older person 218

Opioids 218Paracetamol 219Tramadol 219Local anaesthetics 219NSAIDs 220

Renal Dysfunction 221Lesley Bromley

Specific drugs in renal failure 222Paracetamol 222NSAIDs 222Opioids 222Tramadol 222

ix



Contents

Day Surgery Setting 223Lesley Bromley

The Known or Suspected Substance Misuser 225Brigitta Brandner and Julia Cambitzi

Introduction 225Definition of addiction 225Common treatments for addiction 226

Methadone maintenance 226Buprenorphine 226Naltrexone 227

Perioperative pain management in the substancemisuse patients 227

Preoperative patient assessment 227Perioperative pain management 228Discharge planning 229

The Opioid-dependent Patient 230Brigitta Brandner and Julia Cambitzi

Definitions 231Addiction 231Physical dependence 232Tolerance 232Pseudoaddiction 232Maladaption 232

Opioid rotation 232Treatment plan 233

Satisfactory pain relief 233Suitable techniques 234Withdrawal 235Psychological support 236

Acute Neuropathic Pain 237Ian McGovern

Introduction 237Pathophysiology 238Clinical features 239Chronic post-surgical pain 239Post-surgical neuropathic pain syndromes 240

Post-amputation pain syndromes 240Complex regional pain syndromes 241Treatment 242

Pharmacological treatments 242Other treatment options 245

Prevention 246Summary 246

x



Contents

13. Transcutaneous Electrical Nerve Stimulation inPerioperative Settings 248Mark I. Johnson and Joanne Bagley

Introduction 248Background 249Historical context 250Definition of TENS 251

The standard TENS device 251TENS-like devices 252

The principles of TENS 254TENS techniques 254Mechanism of analgesic action 256

Principles of clinical technique 259Electrode positions 259Electrical characteristics of TENS 261Timing and dosage 261Contraindications 261Precautions and adverse events 262

TENS in the perioperative setting 262Clinical indications 262Merits of TENS 263Perioperative TENS protocol 263

TENS efficacy: clinical research evidence 265TENS for pain 265TENS for post-surgical nausea and vomiting 267TENS for other post-surgical symptoms 268

Summary 269

14. Risk Management in Perioperative Analgesia 277Jeremy Mitchell

Introduction 277Consent to treatment (Department of Health 2004) 278Consent for perioperative analgesia 279Adequate patient information 280Neurological damage associated with neuraxial analgesic

techniques 282Likelihood of neurological damage from neuraxial

analgesic techniques 283Timing of insertion and removal of epidural catheters

in relation to administration of anticoagulants 284Complications associated with peripheral nerve blocks 286

Toxic reactions to local anaesthetic drugs 286Neurological injury following peripheral nerve blocks 287

Perioperative pain management and organisationalrisk management 287Risk assessment 288

xi



Contents

Risk management standards 290Summary 290Notes 293

15. Education 294Angela Cousins

Introduction 294Health professionals’ education 295

Undergraduate education 295Postgraduate education for members of the APS 295Postgraduate tertiary education 296Postgraduate institutional education 297Certification and accreditation 298Educational resources 300Criteria for referral to pain management service 300Safer prescribing 302Safer analgesia administration 304

Patients 304Fear of pain 305Treatment options 306

Patient-related educational material 307Summary 307

Index 310

xii



Dedication

With my heartfelt thanks to Cruisaid Ward staff at St Mary’s Hospital,Paddington, and the haematology team at University College Hospital,London, for the care that I received. Special thanks to my stem celldonor for the gift of life.

iii



List of Contributors

Dr Elizabeth M.C. Ashley, BSc, FRCAConsultant Anaesthetist, Department of Anaesthesia, University CollegeHospitals NHS Trust, The Heart Hospital, London

Joanne Bagley, MSc, RNClinical Nurse Specialist Team Manager, Department of Anaesthetics, LeedsGeneral Infirmary, Leeds

Dr Brigitta Brandner, FRCAConsultant Anaesthetist, Department of Anaesthesia, University CollegeHospitals NHS Trust, London

Dr Lesley Bromley, MBBS, FRCAConsultant Anaesthetist, Department of Anaesthesia, University CollegeHospital NHS Trust, London

Dr Donna Brown, PhD, MA, PGDip (HP), PGCert (LLL), RNSenior Acute Pain Nurse, Acute Pain Service Royal Hospitals, Belfast Trust,Belfast

Dr Dee Burrows, PhD, BSc (Hons), RGN, RNTIndependent Consultant Nurse and Director of Pain Consultants Limited,Painconsultants, Great Missenden, Buckinghamshire

Julia Cambitzi, BSc, RN, CNSPain Management, University College Hospitals NHS Trust, London

Dr Eloise Carr, PhD, MSc, BSc, RNReader in Pain Management and Research, Bournemouth University,Bournemouth

Dr Gillian Chumbley, PhD, BSc (Hons), RNNurse Consultant Pain Service, Imperial College Healthcare NHS Trust,London

xiv




Angela Cousins, RNCNS, Pain Management Service, Royal Brompton & Harefield NHS Trust,Royal Brompton Hospital, London

Felicia Cox, MSc (ECP), PGDip, RNSenior Nurse, Pain Management, Royal Brompton & Harefield NHS Trust,Harefield, Middlesex

Dr Shane George, FRCP, FRCAConsultant Anaesthetist & Intensivist, Department of Anaesthesia, RoyalBrompton & Harefield NHS Trust, Harefield, Middlesex

Dr Rachel Hagger-Holt, MA (Cantab), ClinPsychDClinical Psychologist, Buckinghamshire Primary Care Trust,Buckinghamshire Hospitals NHS Trust, Buckinghamshire

Dr Joan Hester, MBBS, FRCA, LRCP, MRCSConsultant in Pain Medicine, King’s College Hospital, London, President,The British Pain Society, London

Dr Sian Jaggar, MBBS, FRCA, MDConsultant Anaesthetist, Royal Brompton & Harefield NHS Trust RoyalBrompton Hospital, London

Dr Mark I. Johnson, PhD, BSc, PGCHEProfessor of Pain and Analgesia, Faculty of Health, Leeds MetropolitanUniversity, Leeds

Dr Rohit JunejaSpecialist Registrar in Anaesthesia, Royal Brompton & Harefield NHS TrustRoyal Brompton Hospital, London

Dr Ian McGovern, FRCAConsultant Anaesthetist, Harefield Hospital, Royal Brompton & HarefieldNHS Trust, Middlesex

Dr Jeremy Mitchell, FRCA, MScConsultant Anaesthetist & Lead Clinician Clinical Risk, Harefield HospitalRoyal Brompton & Harefield NHS Trust, Harefield, Middlesex

Dr Barbora Parizkova, MUDrConsultant Anaesthetist, Department of Anaesthesia, Papworth Hospital,Cambridge

xv




Dr Jane Quinlan, MB, BS, FRCAConsultant Anaesthetist, Nuffield Department of Anaesthetics, John RadcliffeHospital, Oxford

Kirsty Scott, MRPharmS, Dip Clin Pharm, IPLead Directorate Pharmacist, Critical Care & Accident & Emergency, WestHertfordshire Hospitals NHS Trust, Hemel Hempstead General Hospital,Hertfordshire

Elaine Taylor, MSc, RNPain Service Manager, Stoke Mandeville Hospital, Aylesbury, Bucks

xvi



Foreword

The National Health Service celebrated its 60th birthday in 2008, and the relief ofpain during and after surgery is a fine example of successful and sophisticatedadvances in patient care that have taken place over those 60 years. Gone arethe days of the heavy premedication with a barbiturate, followed by oblivionfor a few hours to awaken with vomiting and immense pain, unrelieved by anopioid because of the fear of respiratory depression.

Postoperative pain management is measured as a hallmark of the qualityof care that is given to hospital patients, and rightly so. Not only does it re-lieve suffering but lessens anxiety, aids early mobilisation, lessens respiratorycomplications and, we now know, lessens the chance of the development ofpersistent pain after surgery.

There have been advances in anaesthesia, too, and the anaesthetist’s skillalso makes an enormous impact on postoperative recovery, well-being andnumber of days spent in hospital. Operations are now performed as day casesthat would have been considered unbelievable 60 years ago. The role of thenurse in managing and educating others about postoperative pain relief ispivotal, and will expand further.

This is a detailed textbook that portrays the state of the art of perioperativepain management in the latter part of the first decade of the new millennium. Itis a comprehensive, evidence-based account that examines psychological andphysical methods of pain management as well as the well-established role ofopioids. Patient-controlled analgesia, nerve blocks and continuous epiduralinfusions have a well-established place, but there is always scope for furtheradvances.

Perhaps in another 60 years it will be possible to decide in advance, for eachindividual, exactly which medicines to use, and in what dose, by genetic testing.At the present time, pain management remains an art, but an art informed byscience and technology.

This is an authoritative book, well-written and -presented. I hope you willenjoy reading it.

Joan HesterConsultant in Pain Medicine, King’s College Hospital, London

President of the British Pain Society

xvii



Preface

Pain is always a subjective experience; therefore, it cannot be quantified byany objective means. The management of pain is considered to be a fundamen-tal human right, yet remains deficient, with the focus on the medical model(Brennan et al. 2007) rather than a biopsychosocial one. Reactions to pain varydue to previous experiences and the emotional response to this current pain.Sex also plays a role as women have lower pain thresholds and tolerance to arange of painful stimuli as compared to men (International Association for theStudy of Pain 2007). Sex differences in pain and analgesia are present on theday of birth.

Comfort after surgery and fear of unrelieved pain remain major concernsfor patients (Royston & Cox 2003). Poorly managed acute pain can impactnegatively on the patient’s recovery from surgery – discouraging the patientfrom mobilising and performing physiotherapy exercises (so-called dynamicanalgesia) due to discomfort. This unrelieved pain may lead to an increase inmorbidity and extend the length of hospital stay.

The evidence base for acute pain management is expanding and access to thisinformation is improving through a combination of Open Access publishing offull-text articles (e.g. Biomed Central), electronic information for professionals(e.g. Bandolier) and patients and databases of peer-reviewed publications.

Perioperative Pain Management is an up-to-date evidence-based guide to theeffective management of perioperative pain even in the most challenging sit-uations. The level of evidence for interventions (National Health and MedicalResearch Council 1999) is provided, where appropriate, within the bracketsnext to the reference. The evidence for acute perioperative pain managementand an explanation of the levels of evidence are provided in Chapter 7.

This text is aimed at all nurses from undergraduate students to experiencedclinical nurse specialists and lecturers as well as pharmacists, operating de-partment practitioners, physiotherapists, psychologists and trainee doctors.It provides readers with an understanding of the physiology, pharmacologyand psychology of acute pain together with key messages for best practice.Examples of assessment documentation and guidelines for specific patient sub-groups are reproduced throughout the text.

The authors of the stand-alone chapters are widely published and are recog-nised as clinical and research experts in their specialist fields. Barriers to

xviii



Preface

effective acute pain management are explored and suggestions for improv-ing practices and removing obstructions are given. The psychosocial impact ofacute pain and personal coping strategies are reviewed in an easy-to-read and-understand format.

This text also tackles questions that are frequently addressed, but in insuf-ficient depth in more general texts. How different medicines produce painrelief (analgesia) and what evidence exists to support different choices of pain-relieving strategies will be addressed. Common routes of administration ofanalgesia are described in detail; regional techniques including epidural, in-travenous patient-controlled analgesia together with less frequent routes andthe management of side effects.

Managing pain in special circumstances describes the diverse challengesfaced by members of the multidisciplinary team and pain management service.Specific sections focus on managing perioperative pain in:� Paediatrics� The older patient� Patients taking opioids for chronic painful conditions� The known or suspected drug misuser� The patient with renal dysfunction� Day-case surgery

The use of transcutaneous electrical nerve stimulation in perioperative set-tings is explored. Examples of specific analgesia-related risks (such as epiduralhaematoma and abscess formation) are explored alongside in depth. Examplesof the varied approaches to enhancing patient and staff education are provided.

I hope this new text provides you with sufficient details for all aspects ofperioperative pain management and provides suggestions and motivates youto improve your practice.

Felicia Cox

References

Brennan, F., Carr, D.B. & Cousins, M. (2007) Pain management: a fundamental humanright. Anesthesia and Analgesia, 105 (1), 205–221.

International Association for the Study of Pain (2007) Differences in Pain Between Womenand Men. International Association for the Study of Pain, Seattle. www.iasp-pain.org.Accessed 23 May 2008.

National Health and Medical Research Council (1999) A Guide to the Development, Imple-mentation and Evaluation of Clinical Practice Guidelines. National Health and MedicalResearch Council, Canberra.

Royston, D. & Cox, F. (2003) Anaesthesia: the patient’s point of view. The Lancet, 362,1648–1658.

xix



1 The Physiology of Pain

Rohit Juneja and Sian Jaggar

Key Messages� Pain is still underdiagnosed and undertreated.� Pain is a subjective experience and may even be present in the absence

of any painful stimulus.� Pain is multifactorial in nature and its management involves

pharmacological, behavioural and psychosocial approaches.� Transmission of nociceptive impulses depends on a balance of inhibitory

and excitatory influences.� With so many and diverse signalling mechanisms, there are numerous

potential targets for analgesic therapies.

Introduction

Pain is an elaborate interaction between sensory, behavioural and emotionalaspects, and past experiences of pain can dictate an individual’s future re-sponse. In evolutionary terms, pain as a sensation serves to prevent ongoingtrauma and to protect the injured area from harm whilst it is healing. However,there are situations where the painful experience far outlasts any tissue damageand does not convey any survival value but does prolong the suffering of theindividual.

Definitions

There are many terms which require clarification in order to fully understandthe processes involved when experiencing pain:� Nociception

The sensory process of detecting tissue damage. Nociceptors are the diversegroup of receptors stimulated in this process.

1



Perioperative Pain Management� PainThe International Association for the Study of Pain defines this as ‘an un-pleasant sensory and emotional experience associated with actual or po-tential tissue damage’ (Merskey & Bogduk 1994, p. 209).

Thus, pain and nociception are not, despite common belief, the same.It is quite possible to experience pain without nociception and vice versa;nociception can occur without any pain being experienced.� TransductionThis is the conversion of one form of energy into another. This occurs atmany stages in the pain pathway.� TransmissionNociceptor excitation is conducted to its target via a combination of elec-trical and chemical transmitters.� ModulationAt all stages along the pain pathway, the transmitted signal is liable toamplification (upregulation) or dampening (downregulation).

In the example shown in Figure 1.1, the above terms are illustrated at variouspoints along the pain pathway.

Nociceptors are excited not only by the physical trauma (such as pressureenergy) to the tissue, but also by the consequent release of a multitude ofchemical mediators (transduction). This information is further transduced intoan electrical signal, which is transmitted along the primary afferent neurone tothe dorsal horn of the spinal cord. The signal is transduced into quantal releaseof chemical neurotransmitters, which transmits the signal across the synapticcleft to the second-order neurone. These events may be subject to presynapticor postsynaptic modulation. Modulating influences may arise from primaryafferent neurones, interneurones or descending pathways.

The majority of second-order neurones decussate at this point, crossing to thecontralateral side of the spinal cord where they synapse again on third-orderneurones, in anterolateral tracts, which ascend to the brainstem and sensorycortex.

Peripheral mechanisms

Peripheral receptors

It was once believed that painful stimuli were detected by the ‘hyperstimula-tion’ of receptors for other sensory modalities. We now know that in somatictissues at least, this is not the case and painful stimuli are detected by spe-cific receptors, called nociceptors. There is even a distinction between the fast‘sharp’ pain transmitted along myelinated A� fibres and the slow ‘dull’ achetransmitted along non-myelinated C fibres.

2



The Physiology of Pain

Nociceptors are activated by pressure,electrical or chemical(exogenous or endogenous) energy. Conversion (or transduction) occurs into chemical mediators and then electrical energy within neurones

Electrical transmission along the primary afferent neurone

Dorsal root ganglion

Spinal nerve

Dorsal root

Ventral root

Transmission up the spinal cord with modulation from supraspinal systems

(1) Electrical chemical Transduction

(2) Chemical Transmission across the synaptic cleft

(3) Chemical electrical Transduction and onward transmission

(4) Modulation at any of these stages

↓↓

Figure 1.1 Transduction, transmission and modulation of a painful stimulus.

3



Perioperative Pain Management� Cutaneous nociceptorsThese are unlike other sensory receptors in that they are free nerve endingsand respond to highly intense stimuli, i.e. those likely to cause injury to thetissue. The stimuli detected may be chemical, thermal or mechanical, hencetheir full title polymodal nociceptors. Information from cutaneous nocicep-tors (transmitted along C-fibre neurones) is responsible for the burningsensation in response to sufficient thermal stimulation (threshold usuallyabout 44◦C in humans).� Deep-tissue nociceptorsThese are located in the deep structures such as joints, bones, muscles andviscera. Compared to their cutaneous counterparts, their receptive fieldsare much larger and pain experienced is more diffuse in nature. Moreover,visceral pain can also be referred to distant parts of the body, as is the casewith cardiac pain referred to the left arm. This may be due to the primaryafferent neurones from the heart entering the dorsal root entry zone at thesame level as those cutaneous nociceptors which serve the left arm. Asthe brain can make no distinction between the two, it interprets the painas coming from the superficial structure. The same mechanism is behinddiaphragmatic pain being experienced in the shoulder tip.

Sensory neurones (primary afferent neurones)

There are numerous types of sensory neurones which are involved in con-veying the information of the peripheral milieu to the central nervous system(CNS). A common classification is according to axon diameter, myelinationand conduction velocity (Table 1.1).

A fibres differ grossly from C fibres in that they are of much larger diameterand are myelinated, hence their faster conduction velocities. A� fibres havea low threshold for activation, are cutaneous mechanoreceptors involved in

Table 1.1 Properties of different nerve fibres.

Fibre Fibre Conductiontype Function diameter (mm) velocity (m/sec) Myelination

A� Motor 12–20 70–120 YesA� Touch, pressure via

cutaneousmechanoreceptors

5–12 30–70 Yes

A� Muscle spindle afferents 3–6 15–30 YesA� ‘Fast’ pain, temperature 2–5 12–30 YesB Autonomic

preganglionic<3 3–15 Yes

C ‘Slow’ pain 0.4–1.2 0.5–2.0 No

4




IIIIII

IV

V

VI

VII

VIIIIX

Lissauer’s tract

Anterior and posterior

spinocerebellar tracts

Lateral spinothalamic

tract

Anterior spinothalamic

tract

Fasciculi cuneatus and

gracilisR

exe

d’s

lam

inae

Figure 1.2 A cross section of the spinal cord, illustrating Rexed’s laminae andthe ascending tracts.

conveying the sensation of touch from somatic tissues and do not contributedirectly to the sensation of pain.

A� fibres in somatic tissues (e.g. skin) transmit the action potentials fromexcited high-threshold thermo/mechanoreceptors which respond to morenoxious stimuli; i.e. they are thermal and mechanical nociceptors. However,in visceral tissues there are no A� fibres and small C and A� fibres must re-spond to all stimuli. A� fibres terminate in laminae I and V of the dorsal horn ofthe spinal cord and, by virtue of their myelination and diameter (compared toC fibres), are responsible for the ‘first’ or ‘fast’ pain that occurs following injury.It allows rapid and fine localisation of the stimulus so that it can be removedswiftly, thus limiting further damage.

C fibres are non-myelinated and relatively thin neurones which convey in-formation from high-threshold polymodal nociceptors. These receptors are freenerve endings which respond to chemical, mechanical and thermal stimuli andare responsible for the ‘second’ or ‘slow’ pain, which is the main area of inter-est in postoperative pain management. C fibres terminate in laminae I and II(the substantia gelatinosa) (see Figure 1.2) but are subject to many modulatingsystems. It is also worth noting that approximately 15% of C-fibre nociceptorsare ‘silent’ and can become active under inflammatory conditions.

Mechanisms of inflammatory pain

The degree of activation of nociceptors in a dynamic state is dependent on thedegree of tissue injury and modulatory factors. For example, in areas of overttrauma or inflammation, nociceptor activity is heightened; i.e. the threshold for

5




nociceptor excitation and action potential generation is reduced. This resultsin a situation in which nociceptors are excited both in greater numbers andat a greater frequency for a given degree of stimulation. This phenomenon isreferred to as hyperalgesia.

This reduced threshold for mechanical and thermal stimuli in the area ofdamage, primary hyperalgesia, manifests as tenderness and ongoing pain. Whenthe reduced threshold extends beyond the area of damage (usually only tomechanical stimuli) and affects undamaged tissue, it is known as secondaryhyperalgesia.

The mechanisms underlying each pathology are different.� Primary hyperalgesiaThis results in part from the natural tissue-healing process. Inflammatorymediators are released from damaged cells and can act directly on noci-ceptors themselves. Examples of these include protons (H+ ions), K+ ions,adenosine triphosphate and bradykinin, which itself recruits mast cells andbasophils to the damaged area.

Mast cell degranulation results in the release of mediators including his-tamine and attracts platelets to the site of injury. Platelets are a rich sourceof serotonin (5-hydroxytryptamine, 5-HT), which is known to sensitise no-ciceptors to further activation via 5-HT2A receptors present on the primaryafferent terminal.

The chemical mediators described are responsible for the classical signsof inflammation, namely:� Calor (warmth)� Tumour (swelling)� Rubor (redness)� Dolor (pain)

Inflammation also brings about the breakdown of the membranephospholipid, arachidonic acid, via the enzymes cyclooxygenase (COX)and lipoxygenase (LOX). The COX metabolites are the numerousprostaglandins, of which PGE2 and PGI2 have been identified as causingperipheral sensitisation of nociceptors afferents. The LOX pathway also pro-duces nociceptor ‘sensitisers’, an area of current investigation. Inhibitionof the COX enzyme is the target for non-steroidal anti-inflammatory drugs(NSAIDs), in a bid to reduce the production of prostaglandin metabolites.

It is because of the huge number of chemical mediators (includingthose yet to be identified) involved in the inflammatory process that theterm ‘inflammatory soup’ has been coined to collectively refer to thesefactors.

A multitude of different receptors exist on the surface of nociceptiveneurones. They include gamma aminobutyric acid (GABA), tachykinin,serotonin, histamine, prostaglandins, substance P (SP), H+ ion, K+ ion opi-oid and cannabinoid receptors, to name just a few. These receptors are

6




intimately involved in the modulation of activity in the peripheral portionof pain pathways.� Secondary hyperalgesiaThis is the phenomenon of reduced nociceptor threshold to mechanicalstimuli in the undamaged tissue surrounding the area of injury.

Unlike primary hyperalgesia, which results from peripheral sensitisationof nociceptor afferents by the ‘inflammatory soup’, secondary hyperalgesiais thought to be mediated by a central mechanism, i.e. central sensitisation.

Peripheral sensitisation, with increased primary afferent activity, resultsin increased frequency of dorsal horn activity in the spinal cord. This is liableto modulation – either amplification or inhibition of the signal before onwardtransmission up the spinal cord to the higher centres of the midbrain andcortex.

Ongoing injury and inflammation will present the dorsal horn with unre-lenting stimulation and can result in the phenomenon called wind-up, whichleads to a state of spinal hyperexcitability. This reduces the threshold of no-ciceptors in surrounding undamaged tissue, by antidromic activation, andincreases their receptive field. These nociceptors may now be excited byusually innocuous stimuli in areas adjacent to the area of injury.� Neurogenic inflammationStimulation of peripheral C fibres results in retrograde transport and localrelease of the neuropeptides calcitonin gene-related peptide (CGRP) andsubstance P (SP), which act on the surrounding vasculature to cause va-sodilatation, mast cell degranulation and increased capillary permeability,which manifests as ‘flare’.

Central mechanisms

Spinal cord modulation

Having established the receptors and neurones involved in the transmission ofnoxious stimuli to the spinal cord, we can now explore the routes which this in-formation takes from entry into the spinal cord to being perceived as a painfulexperience in the higher centres of the brain. The cell body of the first-orderneurone (primary afferent neurone) lies within the dorsal root and is called thedorsal root ganglion. A neurone projects from this cell body to the peripheryand another projects to the dorsal horn where it synapses with a second-orderneurone (see Figure 1.2). These second-order neurones then decussate to thecontralateral side of the spinal cord and ascend in one of two main pathways/tracts. Depending on the ascending pathway, the second-order neuronesynapses once more either in the midbrain or in the thalamus on a third-orderneurone which will project onto higher cortical centres (see Figure 1.3). Eachof these stages shall now be addressed individually.

The ascending pain pathways display evolutionary differences in that the‘older’ spinoreticulodiencephalic tract (see Figure 1.4) is primarily involved in the

7




Brain

Midbrain

Medulla

Spinal cord

Dorsal root ganglion

Free nerve endings

First-order neurone

Second-order neurone

(note the decussation of second-order neurone to the contralateral side)

Third-order neurone

Figure 1.3 Schematic showing first-, second- and third-order neurones.

affective component of pain perception. Its fibres pass via the reticular for-mation, medial thalamic nuclei, and onto the secondary sensory cortex (S2),anterior cingulate gyrus, insula and limbic system.

In comparison, the phylogenetically advanced spinothalamic tract is respon-sible for the localisation of pain. Its fibres are highly organised and pass viathe lateral thalamic nuclei onto the primary sensory cortex (S1), with spe-cific areas of the body corresponding to specific areas of S1 cortex – thebrain homunculus. In essence, the fibres of the spinoreticulodiencephalic tractconvey the sensation that something is ‘painful’, whereas the spinothalamictract conveys the exact location and the discriminatory quality of the painfulstimulus.

8




Highly organised fibres terminate in S1 sensory cortex

•

••

•

•

Spinothalamic tract

Spinoreticulodiencephalic tract

Spinothalamic fibres are highly organised and run in the medial lemniscus

Reticular formation

Spinoreticulodiencephalic fibres are poorly organised, make multiple synapses and decussate along their route

Lateral thalamic nuclei

Reticulodiencephalic fibres terminate on multiple and diverse targets which reflect the emotional component of the pain experience

Anterior spinothalamic tract

Lateral spinothalamic tract

Contralateral spinoreticulodiencephalic

tract

Free nerve endings

Figure 1.4 Ascending pain pathways.

9




Steps to consider include:� Initial spinal connections� Local spinal interneurones� Ascending pathways� Descending pathway – discussed later

The dorsal horn of the spinal cord plays a crucial role in integrating the manyexcitatory and inhibitory neurones, including interneurones and descendinginhibitory pathways. A�- and C-fibre primary afferent neurones enter the dor-sal horn and immediately ascend or descend one or two levels in a thin tractcalled Lissauer’s tract, before synapsing with second-order neurones in thegrey matter. The grey matter of the spinal cord contains the neuronal cell bod-ies and is highly organised into ten laminae.

The important laminae with reference to pain transmission are:� Laminae I and VMany A� fibres terminate here.� Laminae I–VNon-myelinated C fibres terminate here.� Laminae II and III – substantia gelatinosaMany interneurones are present in these laminae and are involved in mod-ulation of the pain signal. In fact, the majority of A� and C fibres synapsein this area.� Gate control theoryIn 1965, Ron Melzack (a psychologist) and Pat Wall (a neuroscientist) pos-tulated that perception of pain was influenced by the pattern of neuronalactivity and proposed two classes of second-order neurones. The first classrespond to non-noxious stimuli (e.g. touch carried via large-diameter, fast,myelinated A� fibres) and intense noxious stimuli (e.g. pain carried viasmall-diameter, slow, non-myelinated C fibres) – they are termed wide dy-namic range (WDR) neurones. The second class respond solely to noxiousstimuli and are termed nociceptive-specific neurones.

They suggested that stimulation of low-threshold, myelinated A� affer-ent fibres would result in activation of an inhibitory interneurone in thesubstantia gelatinosa synapsing on the WDR second-order neurone, thusdecreasing the output from the WDR neurone up the spinal cord. Smaller,non-myelinated C fibres would inhibit the inhibitory interneurone, thusallowing onward transmission of the ‘pain signal’ by the WDR neurone.

They named this the gate control theory because stimulation of A� fibresin the painful area activated inhibitory interneurones and closure of the gateto C-fibre transmission (Figure 1.5). It explains the phenomenon of ‘rubbingit better’, as fast A� touch fibres are stimulated and block WDR neuronaltransmission of the slower C-fibre input. It is also the principle behind tran-scutaneous electrical nerve stimulation, which utilises high-frequency, low-amplitude current to stimulate large peripheral A� fibres.

10

perioperative pain management - download.e-bookshelf.de€¦ · pain perception 15 summary 15 2....

Documents