Essential Notes in Pain Medicine

(Oxford Speciality Training-Rev Notes)

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QST OXFO KD SPtC IALTY TRAININ G

ESSENTIAL NOTES
IN PAIN MEDICINE

Edited by
Enrique Col I antes Celador I Jan Rydiger AlifiaTameem
Essential Notes in
Pain Medicine
Essential Notes in Pain
Medicine

EDITED BY

Enrique Collantes Celador BSc (Hons), MBChB, FRCA,

MSc (Med Ed), FFPMRCA, FANZCA, FFPMANZCA
Consultant in Anaesthetics and Pain Medicine
Clinical Lecturer, Northern Clinical School, Faculty of Medicine and Health,
The University of Sydney, Australia
Chris O’Brien Lifehouse Hospital, Sydney, Australia
Royal North Shore Hospital, Sydney, Australia
Concord Hospital, Sydney, Australia
Hornsby Ku-​Ring-​Gai Hospital, Sydney, Australia
Ryde Hospital, Sydney, Australia
Sydney Adventist Hospital, Sydney, Australia

Jan Rudiger Medical State Exam of University Jena in Germany, MD, FRCA,
FFPMRCA
Consultant in Anaesthetics and Pain Management
Clinical Lead in Acute and Chronic Pain Management
Surrey and Sussex Healthcare NHS Trust
Redhill, UK

Alifia Tameem MBBS, MD, DNB, FRCA, FFPMRCA

Consultant in Anaesthetics and Pain Management
Clinical Service Lead in Pain Management
Dudley Group, NHS Foundation Trust
Dudley, UK

1
3
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Oxford University Press in the UK and in certain other countries
Topic 14.5 is an extract of a longer expanded article published in Kapur, S., Dunham, R., Balasubramanian, S. (2021).
Pain and Placebo. J Pain Relief, 10(4): 370. Distributed under the terms of the Creative Commons Attribution License.
© Oxford University Press 2022
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First Edition published in 2022
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DOI: 10.1093/​med/​9780198799443.001.0001
Printed in the UK by
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Oxford University Press makes no representation, express or implied, that the
drug dosages in this book are correct. Readers must therefore always check
the product information and clinical procedures with the most up-​to-​date
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the publishers do not accept responsibility or legal liability for any errors in the
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iv
 Enrique—​Dedicated to my wife Alix, our son Henry, and to our family

Alifia—​To my husband Mustafa and our boys Zuhair and Zayaan; this could not have
been possible without your support

Jan—​Dedicated to my wife Tugba and my sons Deniz, Bernhard, and Albrecht

Foreword

The practice of clinical medicine across its various specialties has much in common. It includes at
its core patient communication to obtain valid information and to optimize compliance with treat-
ment, consideration of diagnostic probabilities through history, examination, and investigations,
and treatment delivery either directly or by referral. These skills are learnt by apprenticeship but,
even in the information age, require a substantial body of knowledge to be drawn upon that is
wide-​ranging. The latter is tested through examination by the governing bodies that regulate post-
graduate medical training, and the relatively new specialty of pain medicine has followed suit with
fellowship examinations across the world. This book on pain management provides a wide-​ranging
and detailed overview of topics that would appeal to the examination candidate in need of a sum-
mary prior to their sitting of fellowship pain examinations.
The book assumes a background knowledge, but in areas where the reader feels they are limited
in this, then references to background sources are provided. The subject is covered in its breadth,
ranging from basic sciences underpinning the subject to clinical matters of assessment tools and
treatment. Being a book for the trainee sitting examinations, it also includes those rarities oft
favoured by examiners to assess clinical acumen and logical thought, but also includes, amongst
these, some that will, on occasion, arise in a long career that follows, for example, serotonin syn-
drome, glossopharyngeal neuralgia, and refractory angina, to name but a few. As such, this book
would also appeal to the pain clinician in practice, especially at the start of their career.
In providing such a broad overview, it allows the reader to not only look up matters for reminder
of detail such as drug prescription, but also be aware of the treatment options, from which they
can consider whether to refer on or obtain further information and apprenticed training to pursue
these themselves.
The book provides a summary of pain as a psychophysical phenomenon by including details on
physiology and psychology. From this flows the philosophy for assessment and management, and
thus this book not only is an aide memoire for examinations, but it also provides an anchor for a
clinician’s ongoing career with the challenges of new information on current treatments, as well as
new treatments to be subsequently appraised in the context of a paradigm for pain management.
The multiauthor book, while drawing predominantly on UK physicians, also includes several from
other countries and, in so doing, provides a broad approach. Furthermore, the authorship includes
those with excellent and innovative practices, some of whose work is not widely appreciated and
whose ideas may offer appealing ways to develop a practice, with some examples being the use
of steroid passports, how to write a patient letter, and examination signs of opioid dependence.
Much of pain practice involves the elderly, rheumatological conditions, and psychological prob-
lems and all of these are addressed in some depth and will serve the pain physician well.
I congratulate the editors on bringing this broad and skilled authorship together and offering a
concise book for the benefit of examination candidates and early career pain physicians.
Jon Raphael
Professor of Pain Science, Birmingham City University

vii
Preface

‘Your pain is the breaking of the shell that encloses your understanding’ –​Khalil Gibran
From The Prophet (Knopf, 1923)

Pain is an unpleasant and emotional experience, but it is not just for the person suffering from it,
but also for loved ones. It remains underestimated and undertreated, and has a major impact in
our society. Treatment for alleviation of pain has been present since the dawn of mankind and has
continued to evolve. Various initiatives have been introduced to make pain a priority, as it is one of
the most common symptoms with which patients present to general practitioners and hospitals.
In 2012, the Faculty of Pain Medicine of the United Kingdom (UK) introduced the exam for the
Fellowship in Pain Medicine (FFPMRCA). We were amongst the first anaesthetists with an interest
in pain medicine, sitting this written and oral exam in the UK. With our collective knowledge, skills,
and experience, we initially decided to write a book with a collection of relevant questions and an-
swers which would have benefitted mainly the pain fellows and trainees sitting the pain exam. The
format of the book was changed to serve as a comprehensive collection of high-​quality resources
written by various health care professionals, with an interest in pain medicine. It is based on the
curriculum of the pain medicine fellowship exam in the UK, including relevant topics, which are vital
for pain clinics, interventional procedures, and allied health therapies.
The book will help all pain doctors and medical and allied health care specialists who treat in-
patient and outpatient chronic non-​cancer and cancer pain patients, as well as pain trainees and
fellows who are subspecializing in pain medicine. It will also be an excellent resource for candidates
preparing for postgraduate examinations in pain medicine in the UK and/​or other countries, as well
as for postgraduate examinations of specialist colleges where pain medicine is in the curriculum
such as rheumatology, neurology, sports medicine, addiction medicine, general practice, psychiatry,
occupational therapy, rehabilitation, surgery, and other specialties.
The chapters have been organized into nine sections, commencing with pain assessment,
through physiology, pharmacology, relevant pain interventions, clinical conditions associated with
pain, psychological impact, and its multidisciplinary management, along with sections on cancer pain
and epidemiology/​evidence-​based medicine.
We are extremely grateful for the expertise and hard work of our contributors and specialists
from all over the world for their continued support and professionalism to make this book a suc-
cess in providing an excellent and concise overview over the whole spectrum of pain medicine.
We hope that the readers of this book find it useful not only for their exams, but also as a com-
prehensive and suitable reference guide in their clinical practice, to improve the quality of care we
provide to our patients.

ix
Acknowledgements

We are very obliged to have had a fantastic team of authors who have contributed towards this
book. Thank you for your precious time, patience, and commitment, while accommodating mul-
tiple requests for changes and amendments along the way. It has been a great pleasure working
collaboratively with you all.
To write and edit a book is a complex task and has been a great educational experience for
us. We could not have achieved this without the invaluable and fantastic support from Rachel
Goldsworthy, Geraldine Jeffers, and Fiona Sutherland, from Oxford University Press, and Helen
Nicholson from Newgen Publishing UK who have tirelessly helped us through this journey.
Last, but not the least, we are particularly grateful to our families for their constant encouragement,
backing, and tolerance during the last few years, thank you!

xi
Contents

Detailed contents xv
Abbreviations xxiii
Contributors xxix

SECTION 1 OVERVIEW OF PAIN 1

1 Types of Pain and Pain Assessment 3

SECTION 2 PAIN PHYSIOLOGY 4 5

2 Pain Pathways 47
3 Neurotransmitters and Receptors 67
4 Neurobiology of Pain 79

SECTION 3 PHARMACOLOGY 9 1
5 Basic Principles of Pharmacology 93
6 Local Anaesthetics 101
7 Opioids 119
8 Non-​steroidal Anti-​inflammatory Drugs and Paracetamol 161
9 Anticonvulsants 173
10 Antidepressants 193
11 Neurolytic Agents 205
12 Corticosteroids 209
13 Miscellaneous 229
14 Clinical Pharmacology 263

xiii
 xiv   Contents

SECTION 4 PAIN INTERVENTIONS 277

15 Overview of Interventions 279
16 Head and Neck 299
17 Thorax and Abdomen 315
18 Lumbar and Pelvis 337
19 Autonomic Nervous System 351
20 Spinal Cord and Neuromodulation 367
21 Surgical Techniques 401
22 Miscellaneous Interventions 409

SECTION 5 CLINICAL 4 4 5
23 Musculoskeletal Pain Conditions 447
24 Neuropathic Pain Conditions 481
25 Rheumatological Conditions 517
26 Visceral Pain Conditions 527
27 Widespread Chronic Pain 547
28 Other Pain Conditions 553

SECTION 6 CANCER AND PAIN 5 8 7

29 Cancer and Pain 589

SECTION 7 PSYCHOLOGY OF PAIN MEDICINE 61 1

30 Psychology and Pain 613

SECTION 8 PHYSIOTHERAPY AND

OCCUPATIONAL THERAPY 6 4 1
31 Physiotherapy and Occupational Therapy 643

SECTION 9 EPIDEMIOLOGY AND STATISTICS 659

32 Epidemiology and Statistics 661

Index 673
Detailed contents

SECTION 1 OVERVIEW OF PAIN 1

1 Types of Pain and Pain Assessment 3
1.1 Acute/​chronic pain and IASP classification of chronic pain for ICD-11 3
1.2 History taking in pain medicine 5
1.3 Examination in the pain clinic 9
1.4 Dermatomes and myotomes 14
1.5 Flags in pain medicine 18
1.6 Mental state exam 20
1.7 Investigations in pain medicine 22
1.8 Quantitative sensory testing 26
1.9 Measurement of pain 27
1.10 Pain assessment in the elderly 32
1.11 Pain assessment in children 36
1.12 Pain letter template 40
1.13 Mnemonics for referrals 42
1.14 Waddell’s signs 43
1.15 IASP classification of chronic pain for ICD-11 44

SECTION 2 PAIN PHYSIOLOGY 4 5

2 Pain Pathways 47
2.1 Peripheral nociceptors 47
2.2 Ascending pain pathways 50
2.3 Descending pain pathways 53
2.4 Theories of pain 55
2.5 Pathophysiology of nociceptive, visceral, and neuropathic pain 57
2.6 Peripheral sensitization 61
2.7 Central sensitization 63
3 Neurotransmitters and Receptors 67
3.1 Neurotransmitters 67
3.2 Opioid receptors 72
3.3 Non-​opioid receptors 75

xv
xvi   Detailed contents

4 Neurobiology of Pain 79
4.1 Immunology, inflammation, glia, and pain 79
4.2 Genetics and pain 82
4.3 Gender and pain 83
4.4 Stress and pain 85
4.5 Tolerance, dependence, addiction, and pseudoaddiction 87
4.6 Neurobiological and physiological changes in response to drug misuse 89

SECTION 3 PHARMACOLOGY 9 1
5 Basic Principles of Pharmacology 93
5.1 Agonists and antagonists 93
5.2 Pharmacokinetics 94
6 Local Anaesthetics 101
6.1 Local anaesthetics 101
6.2 Lidocaine 104
6.3 Bupivacaine 107
6.4 Ametop® 109
6.5 EMLA™ 110
6.6 Cocaine 112
6.7 Mexiletine 114
6.8 Local anaesthetic toxicity 116
7 Opioids 119
7.1 Overview of opioids 119
7.2 Buprenorphine 124
7.3 Codeine 129
7.4 Dihydrocodeine 131
7.5 Fentanyl 133
7.6 Methadone 136
7.7 Morphine 139
7.8 Naloxone 142
7.9 Naltrexone 144
7.10 Oxycodone 146
7.11 Tapentadol 149
7.12 Tramadol 152
7.13 Opioid rotation and conversion 155
8 Non-​steroidal Anti-​inflammatory Drugs and Paracetamol 161
8.1 Overview of non-​steroidal anti-​inflammatory drugs 161
8.2 Cyclo-​oxygenase 2 inhibitors 165
8.3 Diclofenac 166
8.4 Ibuprofen 167
8.5 Naproxen 168
8.6 Paracetamol 169
 Detailed contents   xvii

9 Anticonvulsants 173
9.1 Overview of anticonvulsants 173
9.2 Overview of benzodiazepines 174
9.3 Gabapentin 177
9.4 Pregabalin 179
9.5 Carbamazepine 181
9.6 Oxcarbazepine 182
9.7 Sodium valproate 184
9.8 Phenytoin 186
9.9 Lamotrigine 188
9.10 Topiramate 190
10 Antidepressants 193
10.1 Overview of antidepressants 193
10.2 Tricyclic antidepressants 195
10.3 Serotonin and noradrenaline reuptake inhibitors 197
10.4 Selective serotonin reuptake inhibitors 199
10.5 Mirtazapine 201
11 Neurolytic Agents 205
11.1 Ethyl alcohol 205
11.2 Phenol 207
12 Corticosteroids 209
12.1 Overview of corticosteroids 209
12.2 Triamcinolone acetonide 215
12.3 Methylprednisolone acetate 217
12.4 Dexamethasone 219
12.5 Hydrocortisone 221
12.6 Betamethasone 222
12.7 Steroid passport 224
13 Miscellaneous 229
13.1 Baclofen 229
13.2 Bisphosphonates 231
13.3 Botulinum toxin 234
13.4 Calcitonin 235
13.5 Cannabis 237
13.6 Capsaicin 240
13.7 Clonazepam 242
13.8 Clonidine 244
13.9 Contrast agents 245
13.10 Hyaluronidase 248
13.11 Ketamine 249
13.12 Methocarbamol 251
13.13 Methoxyflurane 253
13.14 Nitrous oxide 255
13.15 Orphenadrine 257
13.16 Vitamin D 259
 xviii   Detailed contents

14 Clinical Pharmacology 263

14.1 Analgesic ladders 263
14.2 Pre-​emptive and preventative analgesia in acute pain 265
14.3 Management of patients with a substance use disorder 267
14.4 Serotonin syndrome 272
14.5 Placebo and nocebo 273

SECTION 4 PAIN INTERVENTIONS 277

15 Overview of Interventions 279
15.1 Overview of pain interventions 279
15.2 Safety in interventional pain procedures 284
15.3 Fluoroscopy, computed tomography, and ultrasound-​guided procedures 287
15.4 Chemical neurolysis 289
15.5 Radiation and Ionising radiation (medical exposure) regulations 291
15.6 Radiofrequency denervation 294
15.7 Pulsed radiofrequency 296
16 Head and Neck 299
16.1 Cranial nerves 299
16.2 Anatomy of the trigeminal nerve and trigeminal ganglion block 301
16.3 Sphenopalatine ganglion block 304
16.4 Greater occipital nerve, minor occipital nerve, and third occipital nerve 307
16.5 Cervical facet joint/​medial branch blocks and radiofrequency denervation 309
17 Thorax and Abdomen 315
17.1 Thoracic facet joint/medial branch blocks and r​ adiofrequency denervation 315
17.2 Intercostal nerve block 318
17.3 Thoracic paravertebral block 320
17.4 Analgesia for rib fractures 324
17.5 Abdominal wall blocks 330
18 Lumbar and Pelvis 337
18.1 Lumbar facet joint/medial branch blocks and radiofrequency denervation 337
18.2 Sacroiliac joint block and radiofrequency denervation 340
18.3 Coccygeal block and ganglion impar block 343
18.4 Caudal epidural 345
18.5 Piriformis injection 347
19 Autonomic Nervous System 351
19.1 Anatomy of the sympathetic and parasympathetic nervous systems 351
19.2 Stellate ganglion block 353
19.3 Splanchnic and coeliac plexus block and neurolysis 356
19.4 Lumbar sympathetic block and sympathectomy 360
19.5 Hypogastric plexus block 364
 Detailed contents   xix

20 Spinal Cord and Neuromodulation 367

20.1 Anatomy of the spinal cord 367
20.2 Anatomy of vertebral bodies 370
20.3 Discography 372
20.4 Dorsal root ganglion 375
20.5 Epidural injections 377
20.6 Lumbar epidural adhesiolysis 380
20.7 Percutaneous cordotomy 382
20.8 Intrathecal drug delivery systems 384
20.9 Percutaneous electrical nerve stimulation 390
20.10 Peripheral nerve stimulation 392
20.11 Spinal cord stimulation 394
20.12 Transcutaneous electrical nerve stimulation 397
21 Surgical Techniques 401
21.1 Spinal decompressive surgery 401
21.2 Spinal fusion surgery 403
21.3 Dorsal root entry zone lesioning 405
21.4 Deep brain stimulation 407
22 Miscellaneous Interventions 409
22.1 Bier’s block 409
22.2 Bursa injection 411
22.3 Ilio-​inguinal nerve, ilio-​hypogastric nerve, and genitofemoral nerve
block 412
22.4 Shoulder, knee, and hip joint—​blocks and denervation procedures 416
22.5 Myofascial trigger point injections 422
22.6 Upper limb blocks 423
22.7 Lower limb blocks 430
22.8 Suprascapular nerve block 436
22.9 Vertebroplasty 438
22.10 Prolotherapy 441

SECTION 5 CLINICAL 4 4 5
23 Musculoskeletal Pain Conditions 447
23.1 Osteoarthritis 447
23.2 Cervicogenic headache 449
23.3 Neck pain 451
23.4 Whiplash injury 456
23.5 Shoulder pain 458
23.6 Carpal tunnel syndrome 462
23.7 Low back pain 463
23.8 Lumbo-​sacral transitional vertebrae 467
23.9 Failed back surgery syndrome 468
23.10 Spondylolysis 469
23.11 Sacroiliac joint pain 471
23.12 Coccygodynia 473
 xx   Detailed contents

23.13 Piriformis syndrome 475

23.14 Greater trochanteric pain syndrome 477
23.15 Plantar fasciitis 478
24 Neuropathic Pain Conditions 481
24.1 Post-​stroke pain 481
24.2 Chronic inflammatory demyelinating polyneuropathy 483
24.3 Multiple sclerosis 484
24.4 Spinal cord injury 486
24.5 Cauda equina syndrome 489
24.6 Trigeminal neuralgia 490
24.7 Glossopharyngeal neuralgia 494
24.8 Occipital neuralgia 495
24.9 Post-​herpetic neuralgia 497
24.10 Meralgia paraesthetica 499
24.11 Complex regional pain syndrome 501
24.12 Phantom limb and stump pain 504
24.13 Diabetic polyneuropathy 509
24.14 Charcot–​Marie–​Tooth syndrome 513
25 Rheumatological Conditions 517
25.1 Biomarkers and investigations in rheumatology 517
25.2 Ankylosing spondylitis 518
25.3 Gout 520
25.4 Joint hypermobility syndrome 521
25.5 Osteoporosis 522
25.6 Rheumatoid arthritis 524
25.7 Systemic lupus erythematosus 525
26 Visceral Pain Conditions 527
26.1 Overview of visceral pain 527
26.2 Chronic abdominal pain 530
26.3 Chronic pancreatitis 534
26.4 Chronic pelvic pain 536
26.5 Vulvodynia 540
26.6 Refractory angina pectoris 543
27 Widespread Chronic Pain 547
27.1 Chronic fatigue syndrome 547
27.2 Fibromyalgia 549
28 Other Pain Conditions 553
28.1 Acute pain 553
28.2 Chronic post-​surgical pain 556
28.3 Erythromelalgia 559
28.4 Headaches 561
28.5 Orofacial pain 564
28.6 Paediatric chronic pain 570
28.7 Pain in the elderly 574
 Detailed contents   xxi

28.8 Human immunodeficiency virus 578

28.9 Sickle cell disease 581
28.10 Vascular insufficiency pain 583

SECTION 6 CANCER AND PAIN 5 87

29 Cancer and Pain 589
29.1 Cancer pain ​mechanisms 589
29.2 Overview of cancer pain management 591
29.3 Cancer pain and psychology 594
29.4 Opioids and adjuvants in cancer pain management 595
29.5 Neurolytic procedures for cancer pain management 598
29.6 Intrathecal drug delivery treatment for cancer pain 602
29.7 Chemotherapy for cancer pain 606
29.8 Radiotherapy for cancer pain 608
29.9 Palliative Surgical Procedures 609

SECTION 7 PSYCHOLOGY OF PAIN MEDICINE 61 1

30 Psychology and Pain 613
30.1 Psychometric assessments 613
30.2 Affective component of pain 614
30.3 Opioid risk assessment tools 616
30.4 Depression, anxiety, and suicidal ideation 618
30.5 Fear avoidance behaviour, catastrophizing, and pain behaviours 620
30.6 Personality disorders 622
30.7 Somatic symptom disorder 623
30.8 Post-​traumatic stress disorder 625
30.9 Compensation issues 626
30.10 Cognitive behavioural therapy 627
30.11 Acceptance and commitment therapy 630
30.12 Mindfulness 632
30.13 Hypnotic therapy 633
30.14 Neurolinguistic programming 635
30.15 Pain management programmes 636

SECTION 8 PHYSIOTHERAPY AND

OCCUPATIONAL THERAPY 6 4 1
31 Physiotherapy and Occupational Therapy 643
31.1 Principles of physiotherapy 643
31.2 Principals of occupational therapy 644
31.3 Graded exercise therapy and therapeutic exercise 646
31.4 Functional restoration programme 648
31.5 Hydrotherapy 650
31.6 Graded motor imagery and mirror box therapy 651
31.7 Acupuncture and electro-​acupuncture 653
31.8 Laser therapy 655
 xxii   Detailed contents

SECTION 9 EPIDEMIOLOGY AND STATISTICS 659

32 Epidemiology and Statistics 661
32.1 Epidemiology of chronic pain 661
32.2 Evidence-​based medicine 663
32.3 Statistics 664
32.4 Clinical trials 670

Index 673
Abbreviations

1st ON first-​order neuron ARDS acute respiratory distress

2nd ON second-​order neuron syndrome
3rd ON third-​order neuron ARR absolute risk reduction
AA arachidonic acid ASA American Society of
AACP Acupuncture Association of Anesthesiologists
Chartered Physiotherapists ASIS anterior superior iliac spine
AAGBI Association of Anaesthetists of ATLS Advanced Trauma Life Support
Great Britain and Ireland ATP adenosine triphosphate
ACDF anterior cervical discectomy AV atrioventicular
and fusion BA bioavailability
ACEI angiotensin-​converting enzyme BAcC British Acupuncture Council
inhibitor BAI Beck Anxiety Inventory
acetyl-​CoA acetyl coenzyme A BASDAI Bath Ankylosing Spondylitis
ACh acetylcholine Disease Activity Index
ACJ acromioclavicular joint BASFI Bath Ankylosing Spondylitis
ACPA anti-​citrullinated protein Functional Index
antibodies BBB blood–​brain barrier
ACT acceptance and commitment BDNF brain-​derived neurotrophic
therapy factor
ACTH adrenocorticotrophic hormone BiPAP bilevel positive airway pressure
ADH antidiuretic hormone BMAS British Medical Acupuncture
ADL activities of daily living Society
ADRB aberrant drug-​related behaviour BMD bone mineral density
AHCPR Agency for Health Care Policy BMI body mass index
and Research BMS burning mouth syndrome
AIDS acquired immunodeficiency BNF British National Formulary
syndrome BP blood pressure
ALARP as low as reasonably practical BPI Brief Pain Inventory
AMPA α-​amino-​3-​hydroxy-​5-​methyl-​ BTX-​A botulinum toxin type A
4-​isoxazole propionic acid BTX-​B botulinum toxin type B
receptor BZD benzodiazepine
ANA anti-​nuclear antibodies Ca+​+​ calcium
ANCA anti-​neutrophil cytoplasmic CABG coronary artery bypass grafting
antibodies cAMP cyclic adenosine
ANOVA analysis of variance monophosphate
ANS autonomic nervous system CBD cannabidiol
AP action potential; CBG corticosteroid-​binding globulin
anteroposterior CBN cannabinol

xxiii
 xxiv   Abbreviations

CBR cannabinoid receptor Css plasma concentration at steady

CBT cognitive behavioural therapy state (mg/​mL)
CCP cyclic citrullinated peptide CT computed tomography
CDA cervical disc arthroplasty CVS cardiovascular system
cDMARD conventional disease-​modifying CXR chest X-​ray
anti-​rheumatic medication CYP cytochrome peroxidase
CFS chronic fatigue syndrome CYP450 cytochrome P450 isoenzymes
CFT compassion focused therapy CYP2C9 cytochrome P450 2C9
CGRP calcitonin gene-​related peptide CYP3A4 cytochrome P450 3A4
CHEOPS Children’s Hospital of Eastern DAG diacylglycerol
Ontario Pain Scale DAP dose–​area product
CI confidence interval DASS Depression, Anxiety, and Stress
CINV chemotherapy-​induced nausea Scale-​21
and vomiting DBS deep brain stimulation
CK creatinine kinase; creatine DBT dialectical behaviour therapy
kinase DCT distal convoluted tubule
Cl clearance DEXA dual-​energy X-​ray
CMT Charcot–​Marie–​Tooth absorptiometry
CMV cytomegalovirus DH dorsal horn
CN cranial nerve DLPFC dorsolateral prefrontal cortex
CNCP chronic non-​cancer pain DMSO dimethylsulfoxide
CNMP chronic non-​malignant pain DMT disease-​modifying therapy
CNS central nervous system DN4 douleur neuropathique 4
CO2 carbon dioxide DNA deoxyribonucleic acid
COMT catechol-​O-​methyltransferase DOP delta opioid
CONSORT Consolidated Standards of DRG dorsal root ganglion
Reporting Trials DSA digital subtraction angiography
COPD chronic obstructive pulmonary dsDNA double-​stranded DNA
disease DSM-​5 Diagnostic and Statistical
COX cyclo-​oxygenase Manual of Mental Disorders,
CPAP continuous positive airway fifth edition
pressure DS-​SAT Discomfort Scale-​Dementia of
CPAQ Chronic Pain Acceptance Alzheimer Type
Questionnaire DVLA Driver and Vehicle Licensing
CPB coeliac plexus block Agency
CPM conditioned pain modulation DVT deep vein thrombosis
CPR cardiopulmonary resuscitation EAR estimated average requirement
CPSP chronic post-​surgical pain EBM evidence-​based medicine
CRF corticotropin-​releasing factor ECG electrocardiogram
CRH corticotrophin-​releasing ECSWT extracorporeal shockwave
hormone therapy
CRP C-​reactive protein ED50 effective dose 50
CRPS complex regional pain EDS Ehlers–​Danlos syndrome
syndrome EDTA ethylenediaminetetraacetate
CSCI continuous subcutaneous EEG electroencephalogram
infusion EF ejection fraction
CSF cerebrospinal fluid eGFR estimated glomerular filtration
CSP Chartered Society of rate
Physiotherapy EMG electromyography,
CSQ Coping Strategies electromyelogram
Questionnaire
 Abbreviations   xxv

EN-​PNS external peripheral nerve GHQ General Health Questionnaire

stimulation GI gastrointestinal
ENT ear, nose, and throat GMI graded motor imagery
EO external oblique GON greater occipital nerve
EPSP excitatory post-​synaptic GP general practitioner
potential GPCR G-​protein coupled receptor
EQ-​5D EuroQol-​5D GPM Geriatric Pain Measure
ERCP endoscopic retrograde GWAS genome-​wide association
pancreaticocholangiography studies
ESI epidural steroid injection H+​ proton
ESR erythrocyte sedimentation rate HADS Hospital Anxiety and
EULAR European League against Depression Scale
Rheumatism Hb haemoglobin
FABQ Fear Avoidance Beliefs HDU high dependency unit
Questionnaire 5-​HIAA 5-​hydroxyindoleacetic acid
FAIR flexion, adduction, and internal HIV human immunodeficiency virus
rotation HLA human leucocyte antigen
FBC full blood count H2O PET water-​based positron emission
FBSS failed back surgery syndrome tomography
FDA Food and Drug Administration HPA hypothalamic–​pituitary–​adrenal
of the United States HPPH 5-​(p-​hydroxyphenyl)-​5-​
FDG-​PET fluorodeoxyglucose positron phenylhydantoin
emission tomography HR heart rate
FHR fetal heart rate 5-​HT 5-​hydroxytryptamine
FLACC Face, Legs, Activity, Cry, and (serotonin)
Consolability (Scale) IA intrinsic activity
FLAIR fluid-​attenuated inversion IAPT Improving Access to
recovery Psychological Therapies
fMRI functional magnetic resonance IASP International Association for the
imaging Study of Pain
FN false negative IBS irritable bowel syndrome
FP false positive ICP intracranial pressure
FPS-​R Faces Pain Scale-​Revised ICD-​11 International Classification of
FRP functional restoration Diseases, 11th Revision
programme ICU intensive care unit
FSH follicle-​stimulating hormone IFN-​γ interferon gamma
G Gauge Ig immunoglobulin
G-​6-​PD glucose-​6-​phosphate IgA immunoglobulin A
dehydrogenase IHD ischaemic heart disease
GABA gamma aminobutyric acid IHN ilio-​hypogastric nerve
GABA-​T GABA-​transaminases IIm internal intercostal membrane
GAD glutamic acid decarboxylase IIN ilio-​inguinal nerve
GAD-​7 Generalized Anxiety Disorder-​7 IL interleukin
GAT GABA transporter IM intramuscular
GC glucocorticoid; grey commissure IMMPACT Initiative on Methods,
GDNF glial cell line-​derived Measurement, and Pain
neurotrophic factor Assessment in Clinical Trials
GDS Geriatric Depression Scale IN-​PNS internal peripheral nerve
GET graded exercise therapy stimulation
GFN genitofemoral nerve INR international normalized ratio
GFR glomerular filtration rate IO internal oblique
 xxvi   Abbreviations

IP3 inositol triphosphate Mg+​+​ magnesium

IPT inpatient pain team MHD monohydroxy derivative
IQ intelligence quotient MHRA Medicines and Healthcare
IQR interquartile range products Regulatory Agency
IR immediate release MI myocardial infarction; motor
IRAS Integrated Research Application imagery
System MMPI-​2 Minnesota Multiphasic
IRMER Ionising Radiation (Medical Personality Inventory-​2
Exposure) Regulations MOP mu opioid
ISSVD International Society for the MPQ McGill Pain Questionnaire
Study of Vulvovaginal Disease MR modified release
IT intrathecal MRI magnetic resonance imaging
ITDD intrathecal drug delivery mRNA messenger ribonucleic acid
IV intravenous MRSA methicillin-​resistant
JIH joint hypermobility syndrome Staphylococcus aureus
K+​ potassium MS multiple sclerosis
Ke elimination rate constant MSE mental state exam
(min−1) MSK musculoskeletal
KOP kappa opioid MSU monosodium urate
LA local anaesthetic(s) MTP metatarsophalangeal
LANSS Leeds Assessment of MTrP myofascial trigger point
Neuropathic Symptoms and Na+​ sodium
Signs NAPQI N-​acetyl-​p-​benzo-​quinone
LASER light amplification by stimulated imine
emission of radiation NASS National Ankylosing Spondylitis
LET linear energy transfer Society
LFT liver function test NCS nerve conduction study
LH lateral horn; luteinizing NGF nerve growth factor
hormone NHS National Health Service
LLLT low-​level laser therapy NICE National Institute for Health
LON lesser occipital nerve and Care Excellence
LSD lysergic acid diethylamide NIPS Neonatal/​Infant Pain Scale
LTP long-​term potentiation NIRS near infra-​red spectroscopy
MAC minimum alveolar concentration NK1 neurokinin-​1
MAO monoamine oxidase NK2 neurokinin-​2
MAOI monoamine oxidase inhibitors NLP neurolinguistic programming
MAPK mitogen-​activated protein NMDA N-​methyl-​D-​aspartic acid
kinases NMJ neuromuscular junction
MBB medial branch block NNH number needed to harm
MBSR mindfulness-​based stress NNT number needed to treat
reduction NO nitric oxide
MCBT mindfulness-​based CBT N2O nitrous oxide
mcg microgram (μg) NOP nociceptin opioid peptide
MCP metacarpophalangeal NPQ Neuropathic Pain Questionnaire
MCS motor cortex stimulation NPS Neuropathic Pain Score
MD-​2 myeloid differentiation protein 2 NPV negative predictive value
MDMA 3,4-​methylenedioxy-​ nr-​ax SpA non-​radiographic axial
methamphetamine spondyloarthritis
MDT multidisciplinary treatment NRS Numeric Rating Scale
ME myalgic encephalomyelitis NRTI nucleoside reverse transcriptase
MEG magnetoencephalography inhibitor
 Abbreviations   xxvii

NSAID non-​steroidal anti-​inflammatory PIPP Premature Infant Pain Profile

drug PMMA polymethylmethacrylate
NSC non-​selective cation channel PMP pain management programme
nsNSAID non-​selective NSAID PNFS peripheral nerve field
NT neurotransmitter stimulation
OA osteoarthritis PNS peripheral nerve stimulation
OCD obsessive–​compulsive disorder PO per oral
OCF osteoporotic compression POMS Profile of Mood States
fracture PPV positive predictive value
ODI Oswestry Disability Index PRF pulsed radiofrequency
OH hydroxyl group PRN as needed (Latin: pro re nata)
OIH opioid-​induced hyperalgesia PROSPECT PROcedure-​SPECific post-​
OLP open-​label placebo operative pain managemenT
OMEDD oral morphine equivalent daily PRP platelet-​rich plasma
dose PSEQ Pain Self-​Efficacy Questionnaire
ONS occipital nerve stimulation Psi pound per square inch
OR odds ratio PSIS posterior superior iliac spine
ORT Opioid Risk Tool PTNS percutaneous Posterior Tibial
OST opioid substitution therapy Nerve Stimulation
OT occupational therapy PTSD post-​traumatic stress disorder
OXC oxcarbazepine QLB quadratus lumborum block
PA posteroanterior QLM quadratus lumborum muscle
PaCO2 Partial pressure of carbon QoL quality of life
dioxide QST quantitative sensory testing
PACSLAC Pain Assessment Checklist for RA rheumatoid arthritis; rectus
Seniors with Limited Ability to abdominis
Communicate rACC rostral anterior cingulate cortex
PACU Post-​anaesthesia care unit RAD radiation absorbed dose
PAG periaqueductal grey area RBC red blood cell
PAINAD Pain Assessment in Advanced RCT randomized controlled trial
Dementia (scale) RDA recommended daily allowance
PaO2 Partial pressure of oxygen Relim rate of drug elimination
PBCL Procedure Behaviour Checklist REM radiation equivalent in man
PCA patient-​controlled analgesia RF radiofrequency
PCR polymerase chain reaction RFS Risk Fracture Score
PCS Pain Catastrophizing Scale RMP resting membrane potential
PCT proximal convoluted tubule RNA ribonucleic acid
PD personality disorder RNP ribonucleoprotein
PDUQ Prescription Drug Use ROM range of movement
Questionnaire RR respiratory rate; risk reduction;
PE pulmonary embolus relative risk
PEG polyethylene glycol RS respiratory system
PENS percutaneous electrical nerve rTMS repetitive transcranial magnetic
stimulation stimulation
PET positron emission tomography RVM rostroventral medulla
PG prostaglandin SA sinoatrial
PGI2 prostacyclin SC subcutaneous
PHN post-​herpetic neuralgia SCI spinal cord injury
PHQ Patient Health Questionnaire SCJ sternoclavicular joint
PIP psychologically informed SCL superior costotransverse
physiotherapist ligament
 xxviii   Abbreviations

SCS spinal cord stimulation TB tuberculosis

SD standard deviation TC therapeutic community
SDS Severity of Dependence Scale TCA tricyclic antidepressant
S/​E side effect TCM traditional Chinese medicine
SEM standard error of the mean TEN toxic epidermal necrolysis
SENS subcutaneous peripheral nerve TENS transcutaneous electrical nerve
stimulation stimulation
SEP sensory evoked potential TFESI transforaminal epidural steroid
SG substantia gelatinosa injection
SIADH syndrome of inappropriate TFT thyroid function test
antidiuretic hormone THC delta-​9-​tetrahydrocannabinol
SIGN Scottish Intercollegiate THCV tetrahydrocannabivarin
Guidelines Network TLR Toll-​like receptor
SIJ sacroiliac joint TLR4 Toll-​like receptor
SIS Spine Intervention Society TMD temporomandibular disorder
SISAP Screening Instrument for TN trigeminal neuralgia; true
Substance Abuse Potential negative
SJS Stevens–​Johnson syndrome TNF tumour necrosis factor
SLE systemic lupus erythematosus TON third occipital nerve
SNAP sensory nerve action potential TP transverse process; true
SNP single nucleotide polymorphism positive
SNRI serotonin and noradrenaline TPI trigger point injection
reuptake inhibitor TRP transient receptor potential
SNS sympathetic nervous system TRPV transient receptor potential
SOAPP Screener and Opioid vanilloid
Assessment for Patients with TSH thyroid-​stimulating hormone
Pain TV tidal volume
SP substance P TXA2 thromboxane
SPECT single-​photon emission UGT uridine 5′-​diphospho-​
computed tomography glucurosyltransferase
SPG sphenopalatine ganglion UMN upper motor neuron
SpO2 oxygen saturation US ultrasound
SSCS Stress Symptoms Checklist USS ultrasound scan
SSD somatic symptom disorder UV ultraviolet
SSN suprascapular nerve VAS Visual Analogue Scale
SSNRI selective serotonin–​ Vd volume of distribution
noradrenaline reuptake inhibitor VGAT vesicular GABA transporter
SSRI selective serotonin reuptake VH ventral horn
inhibitor VMAT vesicular monoamine
STIR short tau inversion recovery transporter
SUA serum uric acid VNS vagus nerve stimulation
SUNA short-​lasting unilateral VRS Verbal Rating Scale
neuralgiform headaches with VZV varicella zoster virus
cranial autonomic symptoms WAD whiplash-​associated disorder
SUNCT short-​lasting unilateral WC white commissure
neuralgiform headaches with WDR wide dynamic range
conjunctival tearing WHO World Health Organization
t1/​2 half-​life w/​v weight by volume
TA transverse abdominis
TAC trigeminal autonomic cephalgia
TAP transverse abdominis plane
Contributors

Adnan Al-​Kaisy, MBChB, FRCA, FPMRCA, FIPP, Consultant in Pain Medicine and
Neuromodulation, Clinical Lead, Guy’s and St Thomas’ Pain Management and Neuromodulation
Centre, London, UK Topic 15.2
Sabina Bachtold, EDAIC, FRCA, FFPMRCA, Consultant in Anaesthesia and Pain Medicine,
Frimley Park Hospital, Camberley, UK Topics 1.1, 14.1, 30.1, 32.3, 32.4, 24.1
Shyam Balasubramanian, MBBS, MD, MSc, FRCA, FFPMRCA Consultant in Pain Medicine
and Anaesthesia, Associate Medical director, University Hospitals Coventry & Warwickshire NHS
Trust, Coventry, UK Topics 14.5, 17.2, 17.3
Laura Beard, MBChB, FRCA, PGCME, EDRA, Regional Anaesthesia Reseach Fellow, University
Hospital Birmingham, Birmingham, UK Topics 17.2, 17.3, 17.4
Hadi Bedran, MD, FCARCSI, FFPMRCA, Consultant in Anaesthetics and Pain Medicine, St
George’s University Hospital, London, UK Topics 10.2, 10.5, 11.1, 11.2, 13.1, 22.5, 22.6,
22.7, 22.8
Sadiq Bhayani, MBBS, FRCA, EDRA, FFPMRCA, CIPS, FIPP, Consultant in Pain Medicine and
Anaesthesia, Lead Physician Department of Pain Medicine, University Hospitals Leicester NHS
Trust, Leicester General Hospital, Leicester, UK Topics 14.5, 17.2, 17.3
Owen Bodycombe, MBChB, FRCA, FFPMRCA, Consultant in Anaesthetics and Pain Medicine,
Gloucestershire Hospitals NHS Foundation Trust, Gloucester, UK Topics 23.1, 24.3
Simon Braude, BMedSc, MBChB, FRCA, FFPMRCA, Consultant in Anaesthetics and Pain
Medicine, Northwick Park Hospital, Harrow, UK Topics 15.1, 15.3, 15.4
Caroline Burrow, BSc, PhD, Cpsychol, ClinPsyD, Clinical Psychologist, Northern Meadow
Therapy, Cooneen, Brookeborough, Northern Ireland Topics 30.2, 30.5, 30.9, 30.10, 30.11,
30.12, 30.13, 30.14
Udaya Chakka, MBBS, MD, FCAI, EDRA, FFPMRCA, Consultant in Anaesthesia and Pain
Management, University Hospitals Coventry & Warwickshire NHS Trust, Coventry, UK Topics
13.2, 13.9, 13.11, 13.16
Kasia Chmiel, BSc i(Adv), MBBS, FRACP (Med Onc), FAChPM, Head of Palliative Care
Department, Chris O’Brien Lifehouse Hospital, Sydney, Australia Topic 29.7
Mahesh Choudhari, MBBS, MD, FRCA, FFPMRCA, Consultant in Anaesthesia and Pain
Management, Worcester Royal Hospital, Worcester, UK Topic 29.5
Bill Clark, FRANZCR, EBIR, Consultant in Radiology, Director Interventional Radiology,
Department of Radiology, St George Private Hospital, Sydney, Australia Topic 22.9

xxix
 xxx   Contributors

Enrique Collantes, BSc (Hons), MBChB, FRCA, MSc (Med Ed), FFPMRCA, FANZCA,
FFPMANZCA, Consultant in Anaesthesia and Pain Management, Clinical Lecturer, Northern
Clinical School, Faculty of Medicine and Health, The University of Sydney, Department of
Anaesthesia and Pain Medicine, Royal North Shore Hospital, Sydney, Concord Hospital, Sydney,
Hornsby Ku-​Ring-​Gai Hospital, Ryde Hospital, Sydney Adventist Hospital, Sydney, Australia Topics
1.6, 2.2, 2.3, 2.5, 2.7, 3.2, 6.1, 6.2, 6.3, 6.4, 6.5, 6.7, 6.8 7.2, 7.13, 8.1, 8.2, 8.3, 8.4, 8.5, 8.6,
10.1, 10.5, 13.3, 13.5, 15.1, 15.3, 15.4, 22.5, 22.6, 22.7, 22.8, 23.5, 23.8, 23.9, 23.14, 24.2,
24.4, 24.7, 24.14, 26.1, 27.1, 27.2, 28.1, 28.8, 28.10
Sangeeta Das, MBBS, DA, FRCA, FFPMRCA, Assistant Professor Anaesthesia and Pain,
Department of Anaesthesia and Pain Management, St John’s National Academy of Health
Sciences, Bengaluru, India Topic 20.8
Mohamed Dorgham, MD, FFPMRCA, FIPP, Consultant in Pain Management and Anaesthesia,
University Hospital Birmingham, Birmingham, UK, Lecturer of Anaesthesiology, Critical care and
Pain medicine, Ain-Shams University, Egypt Topics 17.2, 17.3, 23.15
Alix Dumitrescu, BSc (Med), MBBS, FRACP, FFPMANZCA, FRACP, FAChPM, Consultant in
Palliative Care and Pain Management, Department of Pain Medicine and Palliative Care, Royal
Prince Alfred Hospital, Sydney, Australia Topice 29.9
Rebecca Elijah-​Smith, BSc, MSc, PG Cert Pain Management, Lead Physiotherapist in Pain
Management, Sandwell and West Birmingham NHS Trust, Birmingham, UK Topics 31.1, 31.3,
31.4, 31.5, 31.6, 31.7, 31.8
Bethany Fitzmaurice, MBChB, FRCA, Advance Trainee in Pain Medicine, Sandwell & West
Birmingham NHS Trust, Birmingham, UK Topics 4.5, 12.1, 12.2, 12.3, 12.4, 12.5, 12.6,
13.13, 23.3
Ann-​Katrin Fritz, Medical State Exam Heidelberg University in Germany, FRCA, FFPMRCA,
FIPP, CIPS, Consultant in Anaesthetics and Pain Medicine, Norfolk & Norwich University
Hospital, Norwich, UK Topics 16.1, 16.2, 16.3, 16.4, 16.5, 19.2
Praveen Ganty, MBBS, DA, FRCA, FCARCSI, FFPMRCA, FRCPC, Consultant in Pain Medicine
and Anesthesiology, Toronto Rehabilitation Institute, University Health Network, Toronto,
Canada Topics 1.8, 7.13, 13.6
Sian Griffith, MBChB, MD, MRCP, FRCP, Consultant Rheumatologist, Rheumatology Audit
Lead, and Trust Lead for Osteoporosis, Surrey and Sussex Healthcare NHS Trust, Redhill, UK
Topics 25.1, 25.2, 25.3, 25.4, 25.5, 25.6., 25.7
Anthony Gubbay, MBChB, BSc, FRCA, Consultant in Anaesthesia and Pain Management, Royal
Free Hospital, Department of Anaesthesia & Pain Medicine, London, UK Topic 28.7
Sumit Gulati, MD, FRCA, FFPMRCA, EDRA, Consultant in Pain Medicine and Anaesthesia, The
Walton Centre NHS Foundation Trust, Liverpool, UK Topics 15.6, 15.7, 24.6, 28.4
Rajesh Gupta, MBBS, BSc, FRCA, FFPMRCA, Consultant in Pain Medicine and Anaesthesia,
Whipps Cross University Hospital, London, UK Topic 24.4
Rahul Guru, MBBS, MD, FCARCSI, DPMCAI, Consultant in Pain Medicine and Anaesthesia,
University Hospital of Wales, Cardiff, UK Topic 14.3, 17.1, 19.3, 23.13, 24.12, 30.3
Sarah Harper, MBChB, FRCA, FFPMRCOA, Consultant in Pain Medicine and Anaesthesia,
Gloucestershire Hospitals NHS Foundation Trust, Gloucester, UK Topics 28.5, 28.9
Katharine Howells, MBBS, BSc, FRCA, FFPMRCA, Consultant in Anaesthesia and Pain
Management, Royal United Hospital Bath NHS Foundation Trust, Bath, UK Topic 14.2
 Contributors   xxxi

James Jack, MBBS, BSc (Hons), Specialty Registrar in Anaesthetics, Surrey and Sussex
Healthcare NHS Trust, Redhill, UK Topics 7.3, 7.4, 7.5, 7.7, 7.8, 7.10, 7.12, 13.10, 14.4
Senthil Jayaseelan, FRCA, FCARCSI, FFPMRCA, FIPP, Consultant in Anaesthesia and Pain
Management, St Helens and Knowsley Teaching Hospitals NHS Trust, Prescot, UK Topics 4.2, 4.3
Gustav Jirikowski, Prof Dr phil med habil Professor in Anatomy and Neuroanatomy,
Department Vorklinische Medizin, Medical School Hamburg MSH, Hamburg, Germany Topics 1.4,
2.1, 4.4, 19.1, 20.1, 20.4
Yehia Kamel, MBBCh, MSc, FRCA, FFPMRCA, FIPP, EDRA, CIPS, Consultant in Anaesthesia
and Pain Management, University Hospital of Leicester, Leicester, UK Topics 1.5, 18.2, 20.12,
23.8, 23.10, 29.4, 29.6, 29.8
Ilya Kantsedikas, MBBS, BMedSci (Hons), MRCP, FRCA, Specialist Registrar in Anaesthesia,
St Mary’s Hospital, London, UK Topics 22.2, 22.1
Sandeep Kapur, MBBS, MD, FRCA, FFPMRCA, Consultant in Pain Medicine and Anaesthesia,
University Hospital Birmingham, Birmingham, UK Topics 4.6, 14.5, 23.4
Peter Keogh, MB ChB, FRCA, FANZCA, FFPMANZCA, MAcadMEd, Specialist Pain Medicine
Physician and Specislist Anaesthetist, Melbourne, Australia Topics 8.1, 8.2, 8.3, 8.4, 8.5, 8.6, 10.3,
10.4, 13.5
Andrzej Krol, MD, DEAA, FRCA, FFPMRCA, EDPM-​ESRA, Consultant in Pain Management
and Anaesthesia, Pain Clinic, Atkinson Morley Wing, St George’s Hospital, London, UK Topics
22.6, 22.7
Karen LeMarchand, BSc, MSc, MScDip, CPsychol, AFBPsS, Lead Clinical Psychologist—​Pain
Management at the Dudley Group of Hospitals, Black Country Partnership Foundation Trust,
Dudley, UK Topics 30.4, 30.6, 30.7, 30.8, 30.15
Tommy Lwin, MBBS, BSc, Anaesthetic Trainee CT2, Surrey and Sussex Healthcare NHS Trust,
Redhill, UK Topic 28.2
Deepak Malik, DFPMRCA, EDRA, MRCA, FCARCSI, DA, MBBS, Consultant in Anaesthesia
and Pain Management, Queen Elizabeth Hospital Birmingham, Birmingham, UK Topic 20.9
Manish Mittal, MBBS, DA, FRCA, EDAIC, FFPMRCA, Consultant Anaesthesia and Chronic
Pain, Russell’s Hall Hospital, Dudley Foundation trust, Dudley, UK Topics 4.1, 20.3
Ramy Mottaleb, MBBS, BSc, FRCA, FFPMRCA, Consultant in Pain Medicine and Anaesthesia,
Kingston NHS Foundation Trust, Kingston Upon Thames, UK Topic 3.3
Nofil Mulla, MBBS, MD, FRCA, FFPMRCA, NBME (USA), Consultant in Pain Medicine and
Anaesthesia, Luton and Dunstable University Hospital, UK Topics 3.2, 23.2, 23.9, 24.2, 24.7,
24.8, 24.14, 27.1, 28.1
Yin Yee Ng, BMBS, FRCA, FFPMRCA, Consultant in Anaesthetics and Pain Medicine, North
Bristol NHS Trust, Bristol, UK Topics 18.4, 20.2
Jonathan Norman, MBBS, MRCP, FRCA, FFPMRCA, Consultant in Pain Medicine and
Anaesthetics, DMRC Stanford Hall, Stanford on Soar, UK Topics 7.1, 7.2, 7.6, 7.9, 7.11, 7.13
Paolo Pais, MD, Consultant in Anaesthesia and Pain Medicine, Chivasso Civil Hospital, Chivasso,
Italy Topics 2.5, 23.14, 26.1, 28.8
Stefano Palmisani, MD, Consultant in Pain Medicine, Guy’s and St Thomas’ Pain Management
and Neuromodulation Centre, London, UK Topic 20.6
 xxxii   Contributors

David Pang, MRCPCH, FRCA, FFPMRCA, FIPP, Consultant in Pain Management, Guy’s and St
Thomas’ Pain Management and Neuromodulation Centre, London, UK Topics 20.5, 20.7, 20.11,
28.6, 32.1
Nishi Patel, MBBS, BSc, FRCA, FFPMRCA, Consultant in Pain Medicine and Anaesthesia,
Gloucestershire Hospitals NHS Foundation Trust, Gloucester, UK Topics 5.1, 5.2
Erlick Pereira, MA(Camb), BM BCh DM(Oxf ), FRCS(SN), SFHEA, Reader in Neurosurgery
and Consultant Neurosurgeon, Department of Neurosurgery, Atkinson Morley Wing, St
George’s Hospital, London, UK Topic 21.1, 21.2, 21.3, 21.4, 24.5
Arumugam Pitchiah, MBBS, MD, FRCA, FFPMRCA, Consultant in Anaesthesia and Pain
Management, Department of Anaesthetics, Royal Preston Hospital, Preston Topic 13.4, 13.8,
23.6
Kavita Poply, FRCA, DA, FCA RCSI, FFPMRCA, Consultant in Anaesthesia and Pain
Management, Clinical Lecturer, Queen Mary University London, and Consultant in Barts Health
NHS Trust, London, UK Topics 6.1, 6.2, 6.3, 6.4, 6.5, 6.7, 6.8, 13.7, 27.2
Ashok Puttapa, MD, FCAI, AFRCA, DIFPMCAI, EDPM, MSC, DESRA, Consultant in
Anaesthesia and Pain Management, Royal Stoke University Hospital, Stoke-​on-​Trent, UK Topics
15.5, 24.1,29.1, 29.2, 29.3
Bhavesh Raithatha, MBChB, FRCA, FFPMRCA, Consultant in Anaesthesia and Pain
Management, Leicester General Hospital, Leicester, UK Topics 18.3, 19.5
Subramanian Ramani, MBBS, FRCA, FFPMRCA, PGA-​MedEd, Consultant in Anaesthesia and
Pain Management, Northampton General Hospital, Northampton, UK Topic 19.4
Shankar Ramaswamy, MBBS, MD, FRCA, FFPMRCA, EDRA, Cer Cli res Consultant in Pain
Medicine and Anaesthesia, Bart’s Health NHS Trust, The Royal London Hospital, London, UK
Topics 23.5, 23.14, 28.10
Manamohan Rangaiah, MD, DNB, FCAI, FRCA, DIPCAI, EDAIC, EDRA, Consultant in
Anaesthesia and Pain Management, Walsall Manor Hospital, Walsall, UK Topics 13.12, 13.14
Deepak Ravindran, MD, FRCA, FFPMRCA, FIPP, EDRA, DMSKMed, BSLM Consultant and
Clinical Lead for Pain Medicine, Royal Berkshire NHS Foundation Trust, Reading, UK Topics 1.2,
1.7, 1.9, 1.10, 1.11, 2.1, 2.2, 2.6
Jan Rudiger, Medical State Exam of University Jena in Germany, PhD, FRCA, FFPMRCA,
Consultant in Anaesthetics and Pain Management, Pain Lead, Surrey and Sussex Healthcare NHS
Trust, Redhill, UK Topics 1.2, 1.4, 1.5, 1.7, 1.9, 1.12, 1.13, 1.14, 2.1, 2.2, 6.6, 6.7,7.1, 7.2, 7.6,
7.11, 7.13, 13.6, 13.10, 13.15, 14.4, 15.1, 15.3, 15.4, 16.1, 16.2, 16.3, 16.4, 16.5, 18.1, 19.1,
19.2, 20.1, 23.12, 24.9, 24.11, 24.13, 26.2, 28.2, 28.3
Mohammed Sajad, MBChB, FRCA, FCAI, PGDip, Consultant in Anaesthesia and Pain
Management, Russells Hall Hospital, Dudley Group of Hospitals, Dudley, UK Topics 9.2, 9.3, 9.4,
9.5, 9.6, 9.7, 9.8, 9.9, 9.10
Haggai Sharon, MD, PhD, FIPP, Consultant in Pain Management, Institute of Pain Medicine, Tel
Aviv Medical Center, Tel Aviv, Israel Topic 15.2
Kathleen Shelley, BSc (Hons), BM, FRCA, Specialist Registrar in Anaesthesia, Welsh School of
Anaesthesia, Cardiff, Wales, UK Topics 5.1, 5.2
Attam Jeet Singh, MBBS, FRCA, FFPMRCA, Consultant in Anaesthesia and Pain Management,
West Herfordshire NHS Trust, Watford, UK Topics 22.1, 22.2
 Contributors   xxxiii

Thomas E Smith, MBBS, MD, FRCA, FFPMRCA, Consultant in Pain Management and
Neuromodulation, Guy’s and St Thomas’ Pain Management and Neuromodulation Centre,
London, UK Topics 18.1, 23.7, 23.11, 24.10
Doug Stangoe, BSc, BM, FRCA, Speciality Registrar in Anaesthetics and Intensive Care, Surrey
and Sussex Healthcare NHS Trust, Redhill, UK Topic 17.5
Maria Stasiowska, MBBS, BSc, FRCA, FFPMRCA, Consultant in Anaesthetics and Pain
Medicine, The National Hospital for Neurology and Neurosurgery, London, UK Topics 2.2, 2.3,
2.4, 2.7, 3.1, 13.3
Kantharuby Tambirajoo, MB BCh, BAO, BA, Senior Clinical Fellow in Functional
Neurosurgery, King’s College Hospital, London, UK Topics 24.6, 28.4
Alifia Tameem, MBBS, MD, DNB, FRCA, FFPMRCA, Consultant in Anaesthetics and Pain
Management, Clinical Service Lead in Pain Management, Russells Hall Hospital, Dudley Group of
Hospitals, Dudley, UK Topics 1.1, 9.1, 9.2, 12.1, 12.4, 13.9, 13.13, 14.1, 15.1, 15.3, 15.4, 15.5,
17.2, 17.3, 24.1, 24.8, 24.12, 29.1, 32.2, 32.3, 32.4, 4.5, 9.10, 12.3, 13.11, 13.12, 13.16, 17.4,
23.1, 23.15, 24.3, 29.2, 29.3, 29.5
John Tanner, BSc, MBBS, FFSEM, D M-​S M DSMSA, Musculoskeletal and Sports Medicine, BASEM
Education Committee, Past President of British Institute of Musculoskeletal Medicine, European
Faculty of Spine Intervention Society, Hon Lecturer Queen Mary University London, St Bartholomew
and Royal London Medical School, External Lecturer MS Ultrasonography Bournemouth University
(AECC University College), Registered Osteopath, Oving Clinic, Oving, UK Topics 1.3, 22.10
Fiona Thomas, BAppSc, OT Occupational Therapist, The Caulfield Pain Management and
Research Centre, Melbourne, Australia Topic 31.2
Athmaja Thottungal, MBBS, FRCA, FFPMRCA, EDRA, FIPP, CIPS, Consultant in Pain
Medicine and Anaesthesia, Chronic Pain Lead, Kent and Canterbury Hospital, East Kent Hospitals
University Foundation NHS Trust, Canterbury, UK Topic 20.10, 23.12, 24.11, 26.3, 26.4., 26.5,
26.6
Victoria Winter, BMBCh BA (Hons Oxon), MA (Oxon), FRCA, Specialist Registrar
in Anaesthesia, North Central London School of Anaesthesia, Royal Free London NHS,
Department of Anaesthesia & Pain Medicine, London, UK Topic 28.7
Ivan Wong, MBChB, FRCA, FFPMRCA, Consultant in Pain Medicine and Anaesthesia, The Royal
London Hospital, London, UK Topics 23.5, 28.10
Matthew Wong, BAppSc, MD, Specialty Registrar in Anaesthesia, Hornsby Ku-Ring-Gai
Hospital, Hornsby, NSW, Australia Topics 3.2, 10.1, 13.1
SECTI ON 1

OVERVIEW O F PA I N
 CH A PTE R 1

Types of Pain and

Pain Assessment
Sabina Bachtold, Enrique Collantes, Praveen Ganty, Yehia Kamel, Gustav
Jirikowski, Deepak Ravindran, Jan Rudiger, Alifia Tameem, and John Tanner

CO NT ENTS
1.1 Acute/​chronic pain and IASP classi cation 1.8   Quantitative sensory testing 26
of chronic pain for ICD-11 3 1.9   Measurement of pain 27
1.2 History taking in pain medicine 5 1.10 Pain assessment in the elderly 32
1.3 Examination in the pain clinic 9 1.11 Pain assessment in children 36
1.4 Dermatomes and myotomes 14 1.12 Pain letter template 40
1.5 Flags in pain medicine 18 1.13 Mnemonics for referrals 42
1.6 Mental state exam 20 1.14 Waddell’s signs 43
1.7 Investigations in pain medicine 22 1.15 IASP classi cation of chronic pain for ICD-11 44

1.1 Acute/​chronic pain and IASP classi cation of chronic pain for
ICD-11

De nition
w)denit(vsofpa R
‘An unpleasant sensory and emotional experience associated with, or resembling that associated with,
actualorpotentialtissuedamage’ 1

ousdenitvPrfpa
‘An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or
describedintermsof suchdamage’ 2

etpaincovN
‘Pain that arises from actual or threatened damage to non-neural tissue and is due to the activation of
nociceptors’3

euroainNptcPh
‘Paincausedbyalesionordiseaseof thesomatosensorynervoussystem’ 3

1. Reproduced with permission from Raja, S., N., etal.(2020). The revised International Association for the
Study of Pain de nition of pain: concepts, challenges, and compromises, Pain. 161(9): 1976–​1982. doi: 10.1097/​
j.pain.0000000000001939.
2. Reproduced with permission from The need of a taxonomy. Pain, 6(3). 247–​252, 1979. DOI: 10.1016/​
0304-​3959(79)90046-​0
3. Reproduced from Kosek E, et al. Do we need a third mechanistic descriptor for chronic pain states?, Pain, 157(7):
1382–1386, copyright 2016, International Association for the Study of Pain.

3
 4   Chapter 1 Types of Pain and Pain Assessment

Table 1.1.1 Di erence between acute and chronic pain

Acute pain Chronic pain

At the same time with an acute illness/​injury
Warning system to alert the body to a problem
Predominantly nociceptive
Usually resolves with complete tissue healing
Inadequate treatment can lead to chronic pain
states
Persists beyond the expected time of
healing (3 months)
Serves no physiological purpose
Frequently neuropathic in nature
Persistent
Negative impact on quality of life.
High costs to society

ociplastNn
‘Painthatarisesfromalterednociceptiondespitenoclearevidenceof actualorthreatenedtissuedamage
causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory
systemcausingthepain’ 3

The di erence between acute and chronic pain

(See Table 1.1.1.)

Transition from acute to chronic pain

The mechanisms that might underlie the transition are not yet fully understood but may be
minimized by early recognition of risk factors (see Table 1.1.2) and early biopsychosocial pain
management

aleriphyP
Continuous and prolonged in ammatory reaction releases pro-​nociceptive factors, such as
cytokines, prostaglandins (PGs), substance P (SP), tumour necrosis factor (TNF) alpha, and
interleukins (ILs), resulting in decreased activation thresholds and spontaneous discharge
Peripheral sensitization occurs, causing allodynia and hyperalgesia within an area of
in amed skin

Table 1.1.2 Risk factors for transition from acute to chronic pain

Pre-​existing At the time of injury/​surgery Post-​injury/​surgery

Pre-​existing pain in the area Type of surgery (amputation, Severe post-​operative pain
High opioid use breast surgery, thoracotomy, Poorly treated acute pain
Female—​higher scores hernia repair, coronary artery Catastrophizing
Age (children < elderly < young) bypass, Caesarean section)
Raised BMI Operations >3 hours
Genetic polymorphism Surgical technique
Radiation therapy Repeat surgery
Psychological vulnerability
Psychosocial issues
Yellow ags
Blue ags
Black ags
Other chronic conditions
 History taking in pain medicine    5

ordalcSpin
Intense nociceptive activation leads to changes in the dorsal root ganglion (DRG) and dorsal
horn (DH) neurons, increasing sodium (Na+​) and transient receptor potential vanilloid (TRPV)
1 receptor and activation of the N-​methyl-​D-​aspartic acid (NMDA) receptor
There is a phenotypic switch, cross-​sprouting with receptive elds on the DH being widened
Central sensitization arises in undamaged tissue away from the site of injury, with
secondary allodynia or hyperalgesia. The application of noxious heat and capsaicin has been
shown to produce secondary hyperalgesia and reversible changes in the brainstem of human
volunteers. This reversible form of central sensitization has been termed ‘wind-​up’
Transcription-​dependent central sensitization is more permanent and occurs if the stimuli
triggering central sensitization continue causing new synaptic connections to be made and there
may even be death of certain cells. This more permanent form of sensitization may even result in
structural changes in the brain that are visible on magnetic resonance imaging (MRI) scanning

ainBr
Functional MRI (fMRI) and positron emission tomography (PET) scans con rmed changes
that occur in the pain matrix (thalamus, mid/​anterior insula, anterior cingulate and prefrontal
cortex, periaqueductal grey area (PAG) and rostroventral medulla (RVM), reticular formation,
and amygdala) with increased functional connectivity between the medial prefrontal cortex and
nucleus accumbens (the brain’s emotion learning circuits) being highly predictive of chronicity
Strong correlation between mental health of the patient and chronic pain leading to
maladaptive coping habits

Further reading

1. Nicholas M, Vlaeyen JWS, Rief W et al. The IASP Taskforce for the Classi cation of Chronic Pain
The IASP classi cation of chronic pain for ICD-11: chronic primary pain, PAIN. 2019;160(1):28–37
2. Raja SN, Carr DB, Cohen M, et al. The revised International Association for the Study
of Pain de nition of pain: concepts, challenges, and compromises. Narrative review. Pain
2020;161(9):1976–​82 https://​journals.lww.com/​pain/ https://www.iasp-pain.org/resources/
terminology/#pain​
3. Feizerfan, A, Sheh, G. Transition from acute to chronic pain. Contin Educ Anaesth Crit Care Pain
2014;15(2):98–​102
4. Macrae WA, Davies HTO. Chronic postsurgical pain. In: Crombie IK (ed). Epidemiology of Pain.
1999; pp. 125–​42. Seattle, WA: IASP Press
5. Apkarian AV, Baliki MN, Farmer MA. Predicting transition to chronic pain. Curr Opin Neurol.
2013 Aug;26(4):360–7

1.2 History taking in pain medicine

Principles
A thorough, comprehensive history helps in establishing a good relationship with the patient
and to formulate a comprehensive multimodal treatment plan
Follow the principles of VEMA—​Validate their symptoms, Educate the patient, Motivate them,
and provide them the tools for Activation
Screen all patients for pain and perform a comprehensive pain assessment
Common elements of a thorough, semi-​structured interview include:
Experience of pain and related symptoms and factors in uencing it
Treatments received and ongoing
 6   Chapter 1 Types of Pain and Pain Assessment

Current litigation status, if any

Coping abilities
Educational/​vocational/​work/​employment status
Any relevant psychosocial history, including adversity in childhood, if relevant
Alcohol and any substance misuse
Ongoing psychological issues, if any
Concerns and explanations for pain
Treatment goals

Set the stage

Reassure patients that you take their pain seriously, and understand its impact and the need for
treatment
Maintain a respectful and professional attitude
It is important to believe the patient’s reports of pain and distress, particularly in the case of
patients with chronic non-​cancer pain (CNCP) who may have had di cult encounters with
previous health care professionals
Even if psychological issues or addiction are present, respectful validation of the patient’s
su ering is invaluable to assessment and will lead to more e ective treatment planning
Pain is a multi-​dimensional phenomenon that can produce strong emotional reactions that impact
on function, quality of life (QoL), emotional state, social and job status, and general well-​being
Pain assessment should also be multi-​dimensional: evaluate these various elements during the
interview and examination, and include them in the diagnostic formulation
A thorough history and physical examination are essential for the medical and pain diagnosis
and treatment planning
Careful attention to the patient’s reported symptoms will help direct the physical examination
and narrow the pain di erential diagnosis
Perform complete neurological and musculoskeletal (MSK) examinations
Additional testing, such as imaging and laboratory studies or electrophysiological testing
(electromyography (EMG)/nerve conduction studies), may be ordered as needed, based on
the results of the history and examinations

The RAT model

(See Table 1.2.1.)

Table 1.2.1 The RAT model

Recognize pain Does the patient have pain?

Do other people (carers/​family) know that the patient is in pain?
Assess pain Measure the severity
What is the pain score at rest? With movement?
How is the pain a ecting the patient?
What scales would you use?
Make a diagnosis
Acute or chronic
Cancer or non-​cancer
Nociceptive/​neuropathic or mixed or nociplastic
Are there other factors?
Psychological factors
Physical factors (other illnesses)
Treat Non-​drug and drug strategies
 History taking in pain medicine    7

Table 1.2.2 Simple steps to make a provisional pain diagnosis

What is the duration of pain? Acute

Chronic
Acute-​on-​chronic
What is the main cause of pain? Cancer
Non-​cancer
What is the suspected mechanism? Nociceptive. Neuropathic
Mixed (nociceptive and neuropathic)
Nociplastic

The Faculty of Pain Medicine (UK) advises all health care professionals to consider using the
RAT model as a simple framework for patients with pain:
R for ‘Recognize pain’
A for ‘Assessment of pain’
T for ‘Treat the pain using non-​drug and drug strategies’
Another simple way to assess pain is shown in Table 1.2.2

Pain scales
Pain is a subjective experience with a di erent meaning to each person
Changes in pain intensity are valuable when measured for single individuals (e.g. before and
after a treatment)
Pain intensity measures should not be used to compare pain between di erent individuals.
One person’s 4/​10 might be another’s 10/​10
A numeric pain rating scale for most clinical settings. The most common one is the 11-​point
Likert scale where 0 =​no pain and 10 =​worst pain imaginable
For children, consider using the 0–​5 Wong-​Baker Faces scale (see Table 1.2.3)
Non-​verbal patients (e.g. those in coma or with dementia or other cognitive impairments)
must be assessed for pain by the Abbey Pain scale and by other observational means
(e.g. body language, movement, autonomic arousal, and non-​verbal pain behaviour)

The pain history interview

A number of mnemonic-​based, structured history taking approaches are available such as
SOCRATES (see 1.13 Mnemonics for referrals p. 42) or PAIN FRAME
The mnemonic ‘QISS TAPED’ is a comprehensive tool to help ensure all information is sought
(see Table 1.2.4)
Table 1.2.3 Types of pain assessment tools

Uni-​dimensional tools Verbal Rating Scale

Multi-​dimensional tools
Screening tools for
neuropathic pain
Numerical Rating Scale
Visual Analogue Scale
Faces scale (Wong-​Baker scale)
McGill Pain Questionnaire
Brief Pain Inventory
West Haven-​Yale Multi-​dimensional Pain Inventory (WHYMPI)
Medical Outcome Study 36-​item Short-​form Health Survey (SF-​36)
Leeds Assessment of Neuropathic Symptoms and Signs (LANSS)
Neuropathic Pain Questionnaire (NPQ)
DN4
PainDETECT
 8   Chapter 1 Types of Pain and Pain Assessment

Table 1.2.4 Pain assessment mnemonic (QISS TAPED)

Q Quality What were your rst symptoms? What words would you use to
describe the pain (aching, sharp, burning, squeezing, dull, icy, etc.)?
I Impact How does the pain a ect you?
What does the pain prevent you from doing?
(Depression screen) Do you feel sad or blue? Do you cry often? Is
there loss of interest in life? Decreased or increased appetite?
(Anxiety screen) Do you feel stressed or nervous? Have you been
particularly anxious about anything? Do you startle easily?
S Site Show me where you feel the pain. Can you put your nger/​hand on it?
Or show me on a body map?
Does the pain move/​radiate anywhere? Has the location changed
over time?
S Severity On a 0–​10 scale, with 0 =​no pain and 10 =​the worst pain imaginable,
how much pain are you in right now?
What is the least pain you have had in the past (24 hours, 1 week,
1 month)?
What is the worst pain you have had in the past (24 hours, 1 week,
1 month)?
How often are you in severe pain (hours in a day, days in a week you
have pain)?
Consider using Brief Pain Inventory if possible
T Temporal When did the pain start? Was it sudden? Gradual? Was there a clear
characteristics triggering event?
Is the pain constant or intermittent? Does it come spontaneously or is
it provoked?
Is there a predictable pattern? (e.g. always worst in the morning or in
the evening? Does it suddenly are up?)
A Aggravating and What makes the pain better?
alleviating What makes the pain worse? When do you get the best relief? How
factors much relief do you get? How long does it last?

P Past response, How have you managed your pain in the past? (Ask about both drug
preferences and non-​drug methods)
What helped? What did not help? (Be speci c about drug trials—​how
much and for how long?)
What medications have you tried? Was the dose increased until you
had pain relief or side e ects? How long did you take the drug?
Are there any pain medicines that have caused you an allergic or other
bad reaction?
How do you feel about taking medications?
Have you tried physical or occupational therapy? What was done?
Was it helpful?
Have you tried spinal or other injections for pain treatment? What
was done? Was it helpful?
E Expectations, What do you think is causing the pain?
goals, meaning How may we help you? What do you think we should do to treat
your pain?
What do you hope the treatment will accomplish?
What do you want to do that the pain keeps you from doing?
What are you most afraid of? (Uncover speci c fears, such as fear of
cancer, which should be acknowledged and addressed)
D Diagnostics Examine and inspect the site
and physical Perform a systems assessment and examination as indicated
examination Review imaging, laboratory, and/​or other test results as indicated
 Examination in the pain clinic    9

A pain history should include location, quality, intensity, temporal characteristics, aggravating
and alleviating factors, impact of pain on function and QoL, past treatment and response,
and patient expectations and goals. Table 1.2.4 summarizes the general categories that should
be addressed during a pain assessment, along with examples of questions that may be useful
during the interview

Further reading

1. Day MA. Mindfulness-​Based Cognitive Therapy for Chronic Pain: A Clinical Manual and Guide.
1st edition, 2017. Chichester, West Sussex: Wiley and Sons
2. Faculty of Pain Medicine (UK). Essential Pain Management UK. Roger Goucke, Wayne Morriss
(Australia), Linda Huggins (NZ). 2016
3. Faculty of Pain Medicine ANZCA. How EPM works. 2016. https://​www.anzca.edu.au/​
getattachment/​5647be92-​3387-​4983-​807f-​06da768f99b1/​1-​EPM-​participant-​manual-​(English)
4. Gurumoorthi R, Das G, Gupta M, et al. The art of history taking in patient with pain: an ignored
but very important component in making diagnosis. Indian J Pain 2013;27:59–​66
5. Powell RA, Downing J, Ddungu H, Mwangi-​Powell FN. Pain History and Pain Assessment. In: Kopf
A, Patel NB (eds). Guide to pain measurement in low-​resource settings. 2010. ASP, Seattle
https://​www.cfpc.ca/​CFPC/​media/​Resources/​Pain-​Management/​Pain-​assessment.pdf
6. Medistudents, Other skills –​History taking. 2018. London, UK https://​www.medistudents.
com/​osce-​skills/​patient-​history-​taking

1.3 Examination in the pain clinic

Introduction
Pain clinic examination needs to be as broad and deep as the history taking aspect
Examination is a good opportunity to re-​evaluate the entire clinical presentation
Do not assume that your colleague’s referral and examination are correct
One commonly hears from the patient, after a thorough clinical examination, that ‘this is the
rst time someone has actually taken the trouble to examine me in detail’ despite having seen
several other clinicians
Patients appreciate attention to detail, and trust and con dence will be established early
The history is 80–​90% of the diagnosis, but the examination needs to be thorough and
detailed to support or refute the diagnostic label (already supplied in most cases) and to
provide further speci c information regarding the degree of physical impairment, disability, and
pain characteristics
The examination can be divided into generalhealthandsystemexamination, and regional
examination

General health and system examination

Clinicians are generally good at recognizing unwellness through pallor, breathlessness, ushed
skin, unusual discoloration, grey or sallow complexions, and rapid pulse
The opioid-​dependent patient may have a faint layer of sweat, glassy eyes, tremor, and
at a ect
Unexplained features need to be evaluated carefully from a medical point of view, looking
at the skin, hands, and nails, with a brief assessment of the cardiovascular system (CVS),
abdominal palpation, and other systems, and reviewing medication
 10   Chapter 1 Types of Pain and Pain Assessment

Unexplained rash, itching, or excoriation need to be identi ed

Signs of self-​harm, whether recent or old, indicate previous mental health problems
Assessment of posture, gait, and mobility is essential (do not commence the examination on
the couch)
MSK issues: osteoarthritic knees or hips, e usions, muscle wasting, deformities
Screen all widespread pain patients for hypermobility according to the Brighton criteria
Obesity and metabolic issues complicate many aspects of management
General demeanour: a ect, responsiveness, ability to communicate (assessment via an
interpreter is an unfortunate compromise)
Pain patients may simply have a nociceptive source such as a speci c nerve entrapment
Peripheral and central sensitization features of neuropathic pain: hyperalgesia or allodynia,
cutaneous hyperaesthesia, and possible sensory or motor impairment
Patients may have a host of psychosocial issues: depression, anxiety, and unhelpful beliefs
about the nature of their pain which a ect their communication and expression of the pain
(identi ed in their painbehaviour)
Fear of pain and pain avoidance are common (secondary gain factors may drive this)
Subconscious post-​traumatic stress can cause fear and anxiety about their pain condition
Complex regional pain syndrome (CRPS) in a limb extremity: patients show disa ectation or
dissociation from the painful part (lack of voluntary movement is common)
Faulty movement patterns as a result of inhibition, weakness, or pain avoidance
Cooperation and consent for a thorough examination of all these aspects must be sought with
a statement like ‘I would now like to examine you very carefully . . .’
Undressing must be su cient to inspect, assess range of motion, and palpate adequately
Before any examination, ask the patient to indicate where the pain is or, if absent, at what
point the movement provokes it and where
Depending on the presentation, a neurological examination of the cranial nerves (CNs)
and/​or peripheral nervous system is needed. Examination of CNs is covered in 16.1
Cranial nerves, p. 299. Upper and lower limb neurological examination includes an
assessment of muscle tone, power, re exes, coordination and sensation (temperature,
pinprick, proprioception, light touch, deep touch, brush, sensory mapping) which is covered
subsequently in this chapter

Regional examination
e’adch,nkpirm‘wlsCofv
Patient standing or sitting (examiner behind)
Assess posture (forward head?)
Muscle wasting or hypertrophy—​trapezii muscles
Active range of motion assesses willingness
Passive range of motion (to assess end-​range feel)
Foraminal closing test for radicular symptoms (Spurling’s test combining extension, ipsilateral
rotation, and side-​bending sustained, but without axial compression)
Shoulder: active range of elevation and controlled descent
Examine upper limbs for referred pain or if neurological de cit for radicular symptoms

Patient supine
Palpate suboccipital muscles for tender points (localized pain on one side increased by
passive exion may indicate greater occipital nerve entrapment) and other paraspinal
muscles (e.g. scalenus muscles)
 Examination in the pain clinic    11

Figure 1.3.1 Palpation points on cervical articular column

Passive range of nutation at atlanto-​occipital joint (usually restricted with cervical extensor
muscle shortening or tension)
Passive rotation at atlanto-​axial joints (painful restriction of rotation in one direction indicates
C1–​2 arthropathy)
Segmental side gliding for tenderness or localized restriction ( ngertips placed at 4 and 8 o’clock
over the articular column) identi es dysfunctional level for treatment (see Figs. 1.3.1 and 1.3.2)

Patient prone
Palpate the medial scapular muscles and trapezii for tender/​trigger points and upper thoracic
spine segments
Note: A subroute if thoracic outlet syndrome is suspected: Roos test (hands up), Lindgren’s
rst rib assessment, palpate the supraclavicular fossa and scalenus muscles, neurological
assessment of the upper limb

alestwdchnpiorT
Benign pain is common, but referred pain or metastases from malignancy or viscera are not
uncommon (in the elderly, compression fractures are often missed)
Patient stripped to waist (with bra). Note deformities and scoliosis, angular kyphosis on
standing

Patient sitting
Observe chest movement with breathing and abnormal pattern (breath holding or hyperventilation)
Measure chest expansion in suspected ankylosing spondylitis
 12   Chapter 1 Types of Pain and Pain Assessment

Figure 1.3.2 Fingertips placed at 4 and 8 o’clock over the articular column

Observe active rotation, side-​bending, exion, and extension in sitting, inspecting from behind
(symmetric limitation suggests spondyloarthropathy, whereas asymmetric limitation suggests
dysfunction)
Localized percussion of segments for exquisite pain

Patient prone
Palpate spinous processes with posterior–​anterior and lateral pressures to identify segmental
dysfunction
Repeat localized percussion if indicated
Palpate paravertebral gutters for muscle tenderness, trigger points, and deeper facet joint
tenderness. Palpate costo-​transverse joints and rib movements and intercostal muscles with
inspiration and expiration

Patient supine
Palpate costo-​chondral junctions for swelling or tenderness

toinsacrljdLeumbp
Patient standing
Assess stance from behind—​is the pelvis level and the spine straight?
Is there an antalgic position, e.g. deviation to one side?
Inspect for scoliosis in full exion and extension (i.e. rib hump)
Active side-​bending (rotation not necessary unless combined with side-​bending for possible
facetal pain and stress fracture)
Extension with side-​bending may elicit radicular pain in foraminal stenosis
 Examination in the pain clinic    13

Figure 1.3.3 The slump test identi es dural in ammation usually related to disc herniation

Forward exion—​is the spine exing (consider modi ed Schober’s test) or are the hips?
Consider uency and cadence—​catch pains and deviatory arcs of movement, as well as
ngertip-​to-​ oor distance
Modi ed Schober’s test: while the patient is in full forward exion, place your outstretched
thumb and index in the midline to span the patient’s lumbo-​sacral area, with your thumb at
the level of the posterior superior iliac spines and your index as high as you can reach on the
spine. The span between these digits will be about 15 cm. Ask the patient to extend up to a
neutral erect position. The span between your thumb and index should decrease by around
5 cm. Less than 3 cm will indicate signi cantly decreased lumbar spinal exion
Ask to squat: competence of lower limb joints and muscles
Trendelenburg’s test for hip dysfunction
Ask the patient to raise each heel o the ground as far as possible (supporting them with the
hands if necessary) to test S1 myotome
Ask them to rock back on the heels, looking for signs of a partial foot drop

Patient sitting
Slump test for dural tension (more sensitive than straight leg raise test) (see Fig. 1.3.3)
Are iliac crests level? (consider leg length di erence or scoliosis)

Patient supine
Log roll each leg rmly, observing rebound if normal laxity, and whether pain is provoked in
the hip at either extreme of internal or external rotation
Measure leg length (anterior superior iliac spines (ASIS) to medial malleoli)
 14   Chapter 1 Types of Pain and Pain Assessment

Passive knee and hip range of motion testing before straight leg raise test
Sacroiliac pain provocation tests:
Anterior compression and distraction
Axial thigh thrust or P4 test ( ex one hip to 90° and align the knee vertically over
the sacroiliac joint (SIJ); apply rm impulse pressure through the axis of the femur to
provoke pain in the posterior SIJ region. Compare both sides. Caution: lumbar pain may
also be provoked by this test if lordosis is not supported (use the patient’s hand). The
same false positive may occur with anterior compression or distraction tests.
Gaenslen’s test (move the patient to one side of the couch and bring one hip and knee
into full exion; then drop the other hip and knee into full extension o the side of the
couch to provoke pain in either joint. Repeat on other side)
Faber’s test (Flexion—​Abduction—​External Rotation) of one hip—​apply overpressure
to the ipsilateral knee (pain must be provoked in the posterior SIJ region. Test is not valid
with any associated hip or adductor/​symphysis problem)
Perform sensory, re ex, and motor tests for lumbar radiculopathy, including plantar responses
for upper motor neuron (UMN) lesion

Patient prone
Femoral nerve stretch test
Post-​sacral spring test (for SIJ)
Buttock clench test for S1 myotome
Spring in a postero-​anterior direction the lumbar spinous processes, rst gently, then deeply
for segmental pain
Palpate the SIJ sulcus and paravertebral muscles and facetal areas for tenderness

Patient side-​lying or in decubitus position

Lateral compression (for SIJ)
Palpate the trochanteric area for tenderness over the trochanter or gluteus medius/​minimus
tendons and piriformis and hip external rotators
Palpation over the sciatic foramen is unreliable for piriformis syndrome diagnosis. Test
shortening of external hip rotators in supine position by laterally rotating the hip; maintain
while slowly bringing towards greater exion. Pain and reproduction of symptoms occur
earlier than on the normal side

Further reading

1. Hutson M, Ward A. Textbook of Musculoskeletal Medicine. 2nd edition, 2015. Oxford: Oxford
University Press

1.4 Dermatomes and myotomes

De nitions
esomatDr
Areas of skin that receive sensory innervation from a speci c cranial or spinal nerve
Sensory neurons are located either in the DRGs or in the trigeminal ganglia (ganglion Gasseri
or nucleus spinalis V)
 D er m at o m es a n d m y ot o m es 15

● E a c h of t h es e n er v es r el a ys s e ns ati o ns (i n cl u di n g p ai n) fr o m a p arti c ul ar s ki n r e gi o n t o t h e
d ors al h or n of t h e s pi n al c or d or t o t h e br ai n

M y ot o m es
● Gr o u ps of s k el et al m us cl es t h at r e c ei v e m ot or i n n er v ati o n fr o m t h e v e ntr al r o ot of a si n gl e
cr a ni al or s pi n al n er v e
● M o t or n e ur o ns ar e l o c at e d i n t h e m ot or n u cl ei of t h e br ai nst e m or i n t h e v e ntr al h or n of t h e
s pi n al c or d

A n at o m y
D er m at o m es
( S e e Fi g. 1. 4. 1.)
Tri g e mi n al n er v e:
V 1: f or e h e a d, e y e
V 2: u p p er f a c e, n os e
V 3: l o w er f a c e, c hi n

V C2
VII
V2
V3 C3
C2 VII
C3
C4 C5
C4 C5
T2 T3 C5 C6
T4 C6
T3 C8
C5 T5
T4 T6 T3
T5 T7 T2 T4 C7
T2 T6 T8 T5
T7 T9 C6 T6
T9 T8 T 0 T7
T
T 0 T 2 T8
T L T T 0 T9 C7
T L
L2
T 2 L3 T L2
C8
C8
C7 L1 S5 S3 C6 T 2 L3
S3
C8 S2 S4 C8 S

L2
L2

S2
L3 L4 S
L3 S

L5
L5 S2
S2

L4 L5
L4
S

S1
S

D e r m at o m es M y ot o m es

Fi g ur e 1. 4. 1 H u m a n d er m at o m es a n d m y ot o m es, a n d i n n er v ati o n of b o n es a n d ot h er s k el et al
tiss u es (s cl er ot o m es)
 16   Chapter 1 Types of Pain and Pain Assessment

Cervical nerves:
C2: base of the skull
C3: supraclavicular and mid-​clavicular line
C4: acromion
C5: cubital fossa and elbow
C6, C7, C8: upper arm, forearm, and hands
Thoracic nerves:
T1: medial aspect of the forearms
T2: axilla and medial aspect of upper arms
T3–​T8: corresponding intercostal spaces
T9: area between xiphoid process and umbilicus
T10: umbilical region
T11: lower abdomen
T12: inguinal region
Lumbar nerves:
L1: inguinal region and upper anterior thigh above L2
L2: antero-​medial thigh
L3: antero-​medial aspect of the knee
L4: medial aspect of the lower leg and medial ankle
L5: lateral aspect of the leg, dorsal aspect of the foot and heel
Sacral segments:
S1: postero-​lateral leg, lateral aspect of the foot and sole of the foot ± heel
S2: postero-​medial leg, popliteal fossa
S3: ischium and infra-​gluteal fold
S4–​S5: perianal area

esomtMy
(See Fig. 1.4.2.)
Trigeminal nerve: V1: jaw muscles, tensor tympani
Facial nerve: mimics muscles, M. stapedius
Vagus nerve: larynx
Cervical segments:
C1/​2/​3: neck exion/​extension
C4: shoulder elevation, diaphragm (phrenic nerve)
C5: shoulder abduction (axillary nerve)
C6/​7/​8: shoulder adduction
C5: elbow exion (musculocutaneous nerve)
C7: elbow extension (radial nerve)
C6/​7: wrist exion and extension
C7: nger extension (radial nerve)
C8: nger exion (median nerve)
Thoracic segments:
T1: nger abduction (ulnar nerve), thumb abduction (median nerve)
T1–​T12: intercostal muscles, abdominal muscles, paravertebral back muscles
 D er m at o m es a n d m y ot o m es 17

C5

C4 C4
C6
C5
C6
C5
C6
C6
C7

L2 C7
C7 C8
C6
C8
C8 L5

C8 C8
L5
C7 L4
L2
S
L4 L3

S2 L4
L5 L5
L5

S
S2

( M y ot o m e) ( S cl er ot o m e)

Fi g ur e 1. 4. 2 M y ot o m es, i n n er v ati o n of b o n es a n d ot h er s k el et al tiss u es (s cl er ot o m es)

L u m b ar s e g m e nts:
L 2: hi p fl e xi o n (f e m or al n er v e); L 5: hi p e xt e nsi o n (i nf eri or gl ut e al n er v e)
L 3 / 4: k n e e e xt e nsi o n ( f e m or al n er v e)
L 4: a n kl e d orsi fl e xi o n ( d e e p p er o n e al n er v e)
L 5: bi g t o e d orsi fl e xi o n ( d e e p p er o n e al n er v e)
S a cr al s e g m e nts:
S 1: a n kl e pl a nt ar fl e xi o n, f o ot e v ersi o n, hi p e xt e nsi o n
S 2: k n e e fl e xi o n
S 3 – S 4: p eri n e al r e gi o n a n d a n al s p hi n ct er

Cli ni c al r el e v a n c e
● D er m at o m e t esti n g ass ess es distri b uti o n of p ai n s y m pt o ms a n d r e d u c e d s e ns ati o n t o
d et er mi n e t h e l e v el of a s pi n al n er v e l esi o n ( e. g. aft er dis c pr ol a ps e). H o w e v er, t h er e c a n b e
o v erl a p pi n g s u p pl y of s pi n al n er v es t o d er m at o m es
● Vis c er al s e ns ati o ns c a n m a p t o s p e ci fi c d er m at o m es. S o m e s e ns ati o ns ar e f elt l o c all y, w h er e as
ot h ers ar e p er c ei v e d o v er ar e as t h at ar e m or e dist a nt fr o m t h e i n v ol v e d or g a n (‘r ef err e d
p ai n’). P ai n i n t h e l eft s h o ul d er c a n i n di c at e a n gi n a p e ct oris. T h es e d er m at o m es ar e r ef err e d t o
as ‘ h e a d z o n es’
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phosgene and chloropicrin, phosgene and superpalite, and
phosgene and diphenylchloroarsine have been found.

Fig. 26.—Interior of a Shell Dump.

The English introduced the use of projectors in the Spring of

1917. They have a decided advantage over shell in that they hold a
larger volume of gas and readily lend themselves to surprise attacks.
As the Germans say, “the projector combines the advantages of gas
clouds and gas shell. The density is equal to that of gas clouds and
the surprise effect of shell fire is also obtained.”
Toward the close of the war, the Germans made use of a mixture
of phosgene and pumice stone. A captured projector contained
about 13 pounds of phosgene and 5½ pounds of pumice. There
seems to be some question as to the value of such a procedure.
Lower initial concentrations are secured; this is due, in part of
course, to the smaller volume of phosgene in the shell containing
pumice. Pumice does seem to keep the booster from scattering the
phosgene so high into the air, and at the same time does not prevent
the phosgene from being liberated in a gaseous condition. This
would indicate that pumice gives a more even and uniform
dispersion and a more economical use of the gas actually used.
Owing to its non-persistent nature (the odor disappears in from
one and a half to two hours) and to its general properties, phosgene
really forms an ideal gas to produce casualties.

Action on Man
Phosgene acts both as a direct poison and as a strong lung
irritant, causing rapid filling of the lungs with liquid. The majority of
deaths are ascribed to the filling up of the lungs and consequently to
the suffocation of the patients through lack of air. This filling up of the
lungs is greatly hastened by exercise. Accordingly, all rules for the
treatment of patients gassed with phosgene require that they
immediately lie down and remain in that position. They are not even
allowed to walk to a dressing station. The necessity of absolute quiet
for gassed patients undoubtedly partly accounts for the later habit of
carrying out a prolonged bombardment after a heavy phosgene gas
attack. The high explosive causes confusion, forcing the men to
move about more or less and practically prevents the evacuation of
the gassed. In the early days of phosgene the death rate was unduly
high because of lack of knowledge of this action of the gas. Due to
the decreased lung area for oxygenizing the air, a fearful burden is
thrown on the heart, and accordingly, those with a heart at all weak
are apt to expire suddenly when exercising after being gassed.
As an illustration of the delayed action of phosgene, a large scale
raid made by one of the American divisions during its training is
highly illuminating.
This division decided to make a raid on enemy trenches which
were situated on the opposite slope of a hill across a small valley. Up
stream from both of the lines of trenches was a French village in the
hands of the Germans. When the attack was launched the wind was
blowing probably six or seven miles per hour directly down stream
from the village, i.e., directly toward the trenches to be attacked. The
usual high explosive box barrage was put around the trenches it was
intended to capture.
Three hundred Americans made the attack. During the attack a
little more than three tons of liquid phosgene was thrown into the
village in 75- and 155-millimeter shells. The nearest edge of the
village shelled with phosgene was less than 700 yards from the
nearest attacking troops. None of the troops noticed the smell of
phosgene, although the fumes from high explosive were so bad that
a few of the men adjusted their respirators. The attack was made
about 3 a.m., the men remaining about 45 minutes in the vicinity of
the German trenches. The men then returned to their billets, some
five or six kilometers back of the line. Soon after arriving there, that
is in the neighborhood of 9 a.m., the men began to drop, and it was
soon discovered that they were suffering from gas poisoning. Out of
the 300 men making the attack 236 were gassed, four or five of
whom died.
The Medical Department was exceedingly prompt and vigorous in
the treatment of these cases, which probably accounted for the very
low mortality.
This is one of the most interesting cases of the delayed action
that may occur in gassing from phosgene. Here the concentration
was slight and there is no doubt its effectiveness was largely due to
the severe exercise taken by the men during and after the gassing.
It should be remarked in closing that while gas officers were not
consulted in the planning of this attack, a general order was shortly
thereafter issued requiring that gas officers be consulted whenever
gas was to be used.
 CHAPTER VII
LACHRYMATORS

Without question the eyes are the most sensitive part of the body
so far as chemical warfare is concerned. Lachrymators are
substances which affect the eyes, causing involuntary weeping.
These substances can produce an intolerable atmosphere in
concentrations one thousand times as dilute as that required for the
most effective lethal agent. The great military value of these gases
has already been mentioned and will be discussed more fully later.
There are a number of compounds which have some value as
lachrymators, though a few are very much better than all the others.
Practically all of them have no lethal properties in the concentrations
in which they are efficient lachrymators, though we must not lose
sight of the fact that many of them have a high lethal value if the
concentration is of the order of the usual poison gas. The
lachrymators are used alone when it is desired to neutralize a given
territory or simply to harrass the enemy. At other times they are used
with lethal gases to force the immediate or to prolong the wearing of
the mask.
A large number of the lachrymators contain bromine. In order to
maintain the gas warfare requirements, it was early decided that the
bromine supply would have to be considerably increased. The most
favorable source of bromine is the subterranean basin found in the
vicinity of Midland, Michigan. Because of the extensive experience of
the Dow Chemical Co. in all matters pertaining to the production of
bromine, they were given charge of the sinking of seventeen
government wells, capable of producing 650,000 pounds of bromine
per year. While the plant was not operated during the War, it was
later operated to complete a contract for 500,000 pounds of bromine
salts. They will be held as a future war asset of the United States.
 The principal lachrymators used during the War were:

Bromoacetone,
Bromomethylethylketone,
Benzyl bromide,
Ethyl iodoacetate,
Bromobenzyl cyanide,
Phenyl carbylamine chloride.

Chloropicrin is something of a lachrymator, but it has greater

value as a toxic gas.

Halogenated Ketones
One of the earliest lachrymators used was bromoacetone.
Because of the difficulty of obtaining pure material, the commercial
product, containing considerable dibromoacetone and probably
higher halogenated bodies, was used. The presence of these higher
bromine derivatives considerably decreased its efficiency as a
lachrymator. The preparation of bromoacetone involved the loss of
considerable bromine in the form of hydrobromic acid. This led the
French to study various methods of preparation, and they finally
obtained a product containing 80 per cent bromoacetone and 20 per
cent chloroacetone, which they called “martonite.” As the war
progressed, acetone became scarce, and the Germans substituted
methylethylketone, for which there was little use in other war
activities. This led to the French “homomartonite.”
Various other halogen derivatives of ketones have been studied
in the laboratory, but none have proven of as great value as
bromoacetone, either from the standpoint of toxicity or lachrymatory
power.
Bromoacetone may be prepared by the action of bromine (liquid
or vapor) upon acetone (with or without a solvent). Aqueous
solutions of acetone, or potassium bromide solutions of bromine,
have also been used.
 Pure bromoacetone is a water clear liquid. There are great
differences in the properties ascribed to this body by different
investigators. This probably is due to the fact that the monobromo
derivative is mixed with those containing two or more atoms of
bromine. A sample boiling at 126-127° and melting at -54°, had a
specific gravity of 1.631 at 0°. It has a vapor pressure of 9 mm. of
mercury at 20°.
While bromoacetone is a good lachrymator, it possesses the
disadvantage that it is not very stable. Special shell linings are
necessary, and even then the material may be decomposed before
the shell is fired. The Germans used a lead-lined shell, while
considerable work has been carried out in this country with enamel
lined shell. Glass lined shell may also be used. It is interesting to
note that, while bromoacetone decomposes upon standing in the
shell, it is stable upon detonation. No decomposition products are
found after the explosion, and even unchanged liquid is found in the
shell. It may be considered as having a low persistency, since the
odor entirely disappears from the surface of the ground in twenty-
four hours.
Bromoacetone was also used by the Germans in glass hand
grenades (Hand-a-Stink Kugel) and later in metal grenades. The
metal grenades weighed about two pounds and contained about a
pound and a half of the liquid.
Martonite was prepared by the French in an attempt more
completely to utilize the bromine in the preparation of bromoacetone.
They regenerated the bromine by the use of sodium chlorate:

NaClO₃ + 6HBr = NaCl + 3Br₂ + 3H₂O

In practice sulfuric acid is used with the sodium chlorate, so that
the final products are sodium acid sulfate and a mixture of 20 per
cent chloroacetone and 80 per cent bromoacetone, according to the
reaction:

5(CH₃)₂CO + 4Br + H₂SO₄ + NaClO₃ =

4CH₂BrCOCH₃ + CH₂ClCO CH₃ + NaHSO₄ + 3H₂O.
 This product is equally as effective as bromoacetone alone and is
very much cheaper to manufacture. In general its properties
resemble very closely those of bromoacetone.

German Manufacture of Bromoacetone

and Bromomethylethyl ketone[17]
These two products were prepared by identical methods. About
two-thirds of the product produced by the factory was prepared from
methylethyl ketone which was obtained from the product resulting
from the distillation of wood. The method employed was to treat an
aqueous solution of potassium or sodium chlorate with acetone or
methylethyl ketone, and then add slowly the required amount of
bromine. The equation for the reaction in the case of acetone is as
follows:

CH₃COCH₃ + Br₂ = CH₂BrCOCH₃ + HBr

Ten kg.-mols of acetone or methylethyl ketone were used in a
single operation. About 10 per cent excess of chlorate over that
required to oxidize the hydrobromic acid formed in the reaction was
used. The relation between the water and the ketone was in the
proportion of 2 parts by weight of the former to 1 part by weight of
the latter. For 1 kg.-mol. wt. of the ketone, 10 per cent excess over 1
kg. atomic-weight of bromine was used.
The reaction was carried out either in earthenware vessels or in
iron kettles lined with earthenware. The kettles were furnished with a
stirrer made of wood, and varied in capacity from 4,000 to 5,000
liters. They were set in wooden tanks and cooled by circulating
water. The chlorate was first dissolved in the water and then the
ketone added. Into this mixture the bromine was allowed to run
slowly while the solution was stirred and kept at a temperature of
from 30° to 40° C. The time required for the addition of the bromine
was about 48 hrs. When the reaction was complete, the oil was
drawn off into an iron vessel and stirred with magnesium oxide in the
presence of a small amount of water in order to neutralize the free
acid. It was then separated and dried with calcium chloride. At this
point a sample of the material was taken and tested. The product
was distilled to tell how much of it boiled over below 130° when
methylethyl ketone had been used. If less than 10 per cent distilled
over, the bromination was considered to be satisfactory. If, however,
a larger percentage of low boiling material was obtained, the product
was submitted to further bromination. The material obtained in this
way was found on analysis to contain slightly less than the
theoretical amount of monobromoketone.
It was finally transferred by suction or by pressure into tank-
wagons. At first lead-lined tanks were used, but later it was found
that tanks made of iron could be substituted. In order to take care of
the small amount of hydrobromic acid, which is slowly formed, a
small amount of magnesium oxide was added to the material. The
amount of the oxide used was approximately in the proportion of 1
part to 1000 parts of ketone. When the magnesium oxide was used,
it was found that the bromoketone kept without appreciable
decomposition for about 2 months. The yield of the product from 580
kg. of acetone (10 kg.-mol. wts.) was 1,100 kg. The yield from 720
kg. of methylethyl ketone (10 kg.-mol. wts.) was 1,250 kg.

Halogenated Esters
The use of ethyl iodoacetate was advocated at a time when the
price of bromine seemed prohibitive. Because of the relative price of
bromine and iodine under ordinary conditions, it is not likely that it
would be commonly used. However, it is an efficient lachrymator and
is more stable than the halogenated ketones, so that on a smaller
scale it might be advisable to use it.
It is prepared by the reaction of sodium iodide upon an alcoholic
solution of ethyl chloroacetate. It is a colorless oil, boiling at 178-
180° C. (69° C. at 12 mm.) and having a density of about 1.8. It is
very much less volatile than bromoacetone, having a vapor pressure
of 0.54 mm. of mercury at 20° C. Ethyl iodoacetate is about one-third
as toxic as bromoacetone, but has about the same lachrymatory
value.
 Aromatic Halides
“Benzyl bromide” was also used during the early part of the war,
usually mixed with bromoacetone. The material was not pure benzyl
bromide, but the reaction product of bromine upon xylene, and
should perhaps be referred to as “xylyl bromide.”
Pure benzyl bromide is a colorless liquid, boiling at 198-199° C.,
and having an odor reminiscent of water cress and then of mustard
oil. The war gas is probably a mixture of mono- and dibromo
derivatives, boiling at 210-220° C., and having a density at 20° C. of
1.3. The mixture of benzyl and xylyl bromides used by the Germans
was known as “T-Stoff,” while the mixture of 88 per cent xylyl
bromide and 12 per cent bromoacetone was called “Green T-Stoff.”
As in the case of the halogenated acetones, it is necessary to
use lead lined shell for these compounds. Enamel and glass lined
shell may be used and give good results. While they are difficult of
manufacture, satisfactory methods were being developed at the
close of the war.
“T-Stoff” may be detected by the nose in concentrations of one
part in one hundred million of air, and will cause profuse
lachrymation with one part in a million. It is a highly persistent
material and may last, under favorable circumstances, for several
days. While it is relatively non-toxic, French troops were rendered
unconscious by it during certain bombardments in the Argonne in the
summer of 1915.
A number of derivatives of the benzyl halides have been tested
and some have proven to be very good lachrymators. The difficulty
of their preparation on a commercial scale has made it inadvisable to
use them, and especially inasmuch as bromobenzyl cyanide has
proven to be such a valuable compound.

Bromobenzyl Cyanide
 Bromobenzyl cyanide is, chemically, α-bromo-α-tolunitrile, or
phenyl-bromo-acetonitrile, C₆H₅CHBrCN. It is prepared by the
action of bromine upon benzyl cyanide.
Benzyl cyanide is prepared by the action of sodium cyanide upon
a mixture of equal parts of 95 per cent alcohol and benzyl chloride.
The benzyl chloride in turn is obtained by the chlorination of toluene
at 100°. The material must be fairly pure in order that the benzyl
cyanide reaction may proceed smoothly. The cyanide is subjected to
a fractional distillation and that part boiling within 3 degrees (the pure
product boils at 231.7° C.) is treated with bromine vapor mixed with
air. It has been found necessary to catalyze the reaction by sunlight,
artificial light or the addition of a small amount of bromobenzyl
cyanide.
The product obtained from this reaction, if the hydrobromic acid
which is formed is carefully removed by a stream of air, is sufficiently
pure for use as a lachrymator. It melts from 16 to 22° C., while the
pure product melts at 29° C. It cannot be distilled, even in a high
vacuum. It has a low vapor pressure and thus is a highly persistent
lachrymator.
Bromobenzyl cyanide is about as toxic as chlorine, but is many
times as effective a lachrymator as any of the halogenated ketones
or aromatic halides studied. It has a pleasant odor and produces a
burning sensation on the mucous membrane.
Like the other halogen containing compounds, lead or enamel
lined shell are necessary for preserving the material any length of
time. In all of this work the United States was at a very marked
disadvantage. While the Allies and the Germans could prepare
substances of this nature and use them in shell within a month, the
United States was sure that shell filled at Edgewood Arsenal
probably would not be fired within three months. This means that
much greater precautions were necessary, both as to the nature of
the shell lining and as to the purity of the “war gas.”
The question of protection against lachrymatory gases was never
a serious one. During the first part of the war this was amply
supplied by goggles. Later, when the Standard Respirator was
introduced, it was found that ample protection was afforded against
all the lachrymators. Their principal value is against unprotected
troops and in causing men to wear their masks for long periods of
time.
The comparative value of the various lachrymators mentioned
above is shown in the following table:
Bromobenzyl cyanide 0.0003
Martonite 0.0012
Ethyl iodoacetate 0.0014
Bromoacetone 0.0015
Xylyl bromide 0.0018
Benzyl bromide 0.0040
Bromo ketone 0.011
Choroacetone 0.018
Chloropicrin 0.019
The figures give the concentration (milligram per liter of air)
necessary to produce lachrymation. The method used in obtaining
these figures is given in Chapter XXI.
 CHAPTER VIII
CHLOROPICRIN

During the spring of 1917, strange reports came from the Italian
front that the Germans were using a new war gas. This gas, while it
did not seem to be very poisonous, had the combined property of
being a lachrymator and also of causing vomiting. Large number of
casualties resulted through the men being forced to remove their
masks in an atmosphere filled with lethal gases. The gas had the
additional and serious disadvantage of being a very difficult one to
remove completely in the gas mask. The first American masks were
very good when chlorine or phosgene was considered but were of no
value when chloropicrin was used.
One of the interesting facts of chemical warfare is that few if any
new substances were discovered and utilized during the three years
of this form of fighting. Chlorine and phosgene were well known
compounds. And likewise, chloropicrin was an old friend of the
organic chemist. So much so, indeed, that several organic
laboratories prepared the compound in their elementary courses.
Chloropicrin was first prepared by the English chemist,
Stenhouse, in 1848, by the action of bleaching powder upon a
solution of picric acid. This was followed by a careful study of its
physical and chemical properties, few of which have any connection
with its use as a poison gas. The use of picric acid as an explosive
made it very desirable that other raw materials should be used.
Chloroform, which is the ideal source theoretically (since chloropicrin
is nitro-chloroform, Cl₃CNO₂), gave very poor yields. While it may be
prepared from acetone, in fair yields, acetone was about as valuable
during the war as was picric acid. Practically all the chloropicrin used
was prepared from this acid as the raw material.
 Manufacture
In the manufacture of chloropicrin the laboratory method was
adopted. This consisted simply in passing live steam through a
mixture of picric acid and bleaching powder. The resulting
chloropicrin passes out of the still with the steam. There was a
question at first whether a steam jacketed reaction vessel should be
used, and whether stirrers should be introduced. Both types were
tested, of which the simpler form, without steam jacket or stirrer,
proved the more efficient.

Fig. 27.—Interior of Chloropicrin Plant.

The early work was undertaken at the plant of the American

Synthetic Color Company at Stamford, Connecticut. Later a large
plant was constructed at Edgewood Arsenal. At the latter place ten
stills, 8 by 18 feet, were erected, together with the necessary
accessory equipment. The following method of operation was used:
The bleach is mixed with water and stirred until a cream is
formed. This cream is then pumped into the still along with a solution
of calcium picrate (picric acid neutralized with lime). When the
current of live steam is admitted at the bottom of the still, the
temperature gradually rises, until at 85° C. the reaction begins. The
chloropicrin passes over with the steam and is condensed. Upon
standing, the chloropicrin settles out, and may be drawn off and is
then ready for filling into the shell. The yield was about 1.6 times the
weight of picric acid used.

Properties
Chloropicrin is a colorless oil, which is insoluble in water, and
which can be removed from the reaction by distillation with steam. It
boils at 112° C. and will solidify at -69° C. At room temperature it has
a density of 1.69 and is thus higher than chloroform (1.5) or carbon
tetrachloride (1.59). At room temperature it has a vapor pressure of
24 mm. of mercury. It thus lies, in persistency, between such gases
as phosgene on the one hand, and mustard gas on the other, but so
much closer to phosgene that it is placed in the phosgene group.
Chloropicrin is a very stable compound and is not decomposed
by water, acids or dilute alkalies. The reaction with potassium or
sodium sulfite, in which all the chlorine is found as potassium or
sodium chloride, has been used as an analytical method for its
quantitative determination. The qualitative test usually used consists
in passing the gas-air mixture through a heated quartz tube, which
liberates free chlorine. The chlorine may be detected by passing
through a potassium iodide solution containing starch, or by the use
of a heated copper wire gauze, when the characteristic green color is
obtained.
An interesting physiological test has also been developed. The
eye has been found to be very sensitive to chloropicrin. The gas
affects the eye in such a way that its closing is practically involuntary.
A measurable time elapses between the instant of exposure and the
time when the eye closes. Below 1 or 2 parts per million, the average
eye withstands the gas without being closed, though considerable
blinking may be caused. Above 25 parts, the reaction is so rapid as
to render proper timing out of the question. But with concentrations
between 2 and 25 parts, the subject will have an overpowering
impulse to close his eye within 3 to 30 seconds. The time may be
recorded by a stop watch and from the values thus determined a
calibration curve may be plotted, using the concentration in parts per
million and the time to zero eye reaction. Typical figures are given
below. It will be noted that different individuals will vary in their
sensitivity, though the order is the same.

Conc. A B
p.p.m. Seconds Seconds
20.0 4.0 5.0
15.0 5.4 5.4
10.0 7.5 7.5
7.5 9.0 10.0
5.0 13.0 15.0
2.5 18.0 30.0
Fig. 28.—Calibration Curve of Eyes for Chloropicrin.

Protection
Because of the stability of chloropicrin, the question of protection
resolves itself into finding an absorbent which is very efficient in
removing the gas from air mixtures. Fortunately such an agent was
found in the activated charcoal used in the American gas mask. The
removal of the gas appears to take place in two stages. In the first,
the gas is adsorbed in such a way that the long-continued passage
of air does not remove it. In the second, the gas is absorbed, and
this, really excess gas, is removed by pure air passing over the
charcoal. The relation of these two factors has an important bearing
on the quality of charcoal to be used in gas masks. It appears that up
to a certain point an increase of the quality is desirable: beyond this,
it is of doubtful value.
Unlike phosgene, chloropicrin is absorbed equally well at all
temperatures. Moisture on the other hand has a very decided effect.
It appears that charcoal absorbs roughly equivalent weights of
chloropicrin and of water; the presence of water in the charcoal thus
displaces an approximately equal amount of chloropicrin.
In the study of canisters it has been found that the efficiency time
is approximately inversely proportional to the concentration.
Formulas have been calculated to express the relation existing
between concentration and life of the canister, and also between the
rate of flow of the gas and the life.
While water seems to have a decidedly marked effect upon the
life of a canister, this is not true of other gases, and the efficiency of
the canister for each gas is not decreased when used in a binary
mixture.

Tactical Uses
Because of the high boiling point of chloropicrin it can only be
used in shell. The German shell usually contained a mixture of
superpalite (trichloromethyl chloroformate) and chloropicrin, the
relative proportions being about 75 to 25. These were called Green
Cross Shell, from the peculiar marking on the outside of the shell.
Mixtures of phosgene and chloropicrin (50-50) have also been used.
The Allies have used a mixture of 80 per cent chloropicrin and 20
per cent stannic chloride (so-called N. C.). This mixture combines
the advantages of a gas shell with those of a smoke shell, since the
percentage of stannic chloride is sufficiently high to form a very good
cloud. In addition to this, it is believed that the presence of the
chloride increases the rate of evaporation of the chloropicrin. It has
been claimed that the chloride decreases the amount of
decomposition of the chloropicrin upon the bursting of the shell, but
careful experiments appear to show that this decomposition is
negligible and that the stannic chloride plays no part in it. This
mixture was being abandoned at the close of the war.
This N. C. mixture has also been used in Liven’s projectors and
in hand grenades. The material is particularly fitted for hand
grenades, owing to the low vapor pressure of the chloropicrin, and
the consequent absence of pressures even on warm days. As a
matter of fact, it was the only filling used for this purpose, though
later the stannic chloride was changed, owing to the shortage of tin,
to a mixture of silicon and titanium chlorides.
While chloropicrin is sufficiently volatile to keep the strata of air
above it thoroughly poisonous, it is still persistent enough to be
dangerous after five or six hours.
 CHAPTER IX
DICHLOROETHYLSULFIDE
“MUSTARD GAS”

The early idea of gas warfare was that a material, to be of value as

a war gas, should have a relatively high vapor pressure. This would, of
course, provide a concentration sufficiently high to cause casualties
through inhalation of the gas-ladened air. The introduction of “mustard
gas” (dichloroethylsulfide) was probably the greatest single
development of gas warfare, in that it marked a departure from this
early idea, for mustard gas is a liquid boiling at about 220° C., and
having a very low vapor pressure. But mustard gas has, in addition, a
characteristic property which, combined with its high persistency,
makes it the most valuable war gas known at the present time. This
peculiar property is its blistering effect upon the skin. Very low
concentrations of vapor are capable of “burning” the skin and of
producing casualties which require from three weeks to three months
for recovery. The combination of these properties removed the
necessity for a surprise attack, or the building up of a high
concentration in the first few bursts of fire. A few shell, fired over a
given area, were sufficient to produce casualties hours and even days
afterwards.
Mustard gas, chemically, is dichloroethylsulfide (ClCH₂CH₂)₂S.
The name originated with the British Tommy because the crude
material first used by the Germans was suggestive of mustard or
garlic. Various other names were given the compound, such as
“Yellow Cross,” from the shell markings of the Germans; “Yperite,” a
name used by the French, because the compound was first used at
Ypres; and “blistering gas,” because of its peculiar effect upon the
skin.

Historical
 It seems probable that an impure form of mustard gas was
obtained by Richie (1854) by the action of chlorine upon ethyl sulfide.
The substance was first described by Guthrie (1860), who recognized
its peculiar and powerful physiological effects. It is interesting in this
connection to note that Guthrie studied the effect of ethylene upon the
sulfur chlorides, since this reaction was the basis of the method finally
adopted by the Allies.
The first careful investigation of mustard gas, which was then only
known as dichloroethylsulfide, was carried out by Victor Meyer (1886).
Meyer used the reaction between ethylene chlorhydrin and sodium
sulfide, with the subsequent treatment with hydrochloric acid. All the
German mustard gas used during 1917 and 1918 was apparently
made by the use of these reactions, and all the early experimental
work of the Allies was in this direction.
Mustard gas was first used as an offensive agent by the Germans
on July 12-13, 1917, at Ypres. According to an English report, the
physiological properties of mustard gas had been tested by them
during the summer of 1916. The Anti-Gas Department put forward the
suggestion that it should be used for chemical warfare, but at that time
its adoption was not approved. This fact enabled the English to quickly
and correctly identify the contents of the first Yellow Cross dud
received. It is not true, as reported by the Germans, that the material
was first diagnosed as diethylsulfide.
The tactical value of mustard gas was immediately recognized by
the Germans and they used tremendous quantities of it. During ten
days of the Fall of 1917, it is calculated that over 1,000,000 shell were
fired, containing about 2,500 tons of mustard gas. Zanetti states that
the British gas casualties during the month following the introduction of
mustard gas were almost as numerous as all gas casualties incurred
during the previous years of the war. Pope says that the effects of
mustard gas as a military weapon were indeed so devastating that by
the early autumn of 1917 the technical advisers of the British, French,
and American Governments were occupied upon large scale
installations for the manufacture of this material.

Preparation and Manufacture