Basics of Pain Management 9789388108072

Table of contents :
Cover
Basics of Pain Management
Copyright
Contributors
Preface
Acknowledgements
Contents
Section I General Consideration
Pain Pathways
Types of Pain
Pharmacotherapy of Pain
Psychological Aspects of Pain
Myths in Pain Management
Section II Back Pain Management
Pain Generators at Back
Management of Back Pain
Myths in Back Pain
Section III Neck Pain Management
Pain Generators at Neck
Examination of Patients with Neck Pain
Management of Neck Pain
Myths in Neck Pain
Section IV Headache Management
Classification and Evaluation of Headache
Tension- type Headache
Migraine
Cervicogenic Headache
Cluster Headache
Myths in Headache
Section V Joint Pain Management
Rheumatoid Arthritis
Spondyloarthropathies
Shoulder Pain
Knee Pain
Nonpharmacological Management of Joint Pain
Management of Joint Pain
Myths in Joint Pain
Section VI Cancer Pain Management
Cancer Pain: What is Special?
Pharmacotherapy in Cancer Pain
Interventions in Cancer Pain
Palliative Care in Cancer
Myths in Cancer Pain
Section VII Management of
Widespread Pain
Widespread Pain
Fibromyalgia
Painful Diabetic Neuropathy
Myths in Widespread Pain
Back Cover

Citation preview

Basics of

Pain Managem ent

Gautam Das _

_ _ Editors R Gurumoorthi Rammurthy Samarjit Dey

~ CBS

CBS Publishers 8c Distributors Pvt ltd

This Page is Intentionally Left Blank

Basics of

Pain Management

Editorial Board

Editors

Dipaari Bhattacharya Kolkata (dipasribhattacharya123 tlgrnall.oom)

Rammurthy Assistant Professor Department of Anesthesiology, Yenepoya Medical College, Mangaluru

Kawtar Sardar

Kam~lndia.

Bangladesh (kawsardrttyahoo.com)

R GurumoGrthi

(dnnou~ldaltaeamaii.ClOm)

Dr Guru's Pain Clinic, Trichy Visiting Consultant, Daradla-The Pain Clinic Kolkata, India

Debjyoti Dutta

Samarjit Dey

Mouftlmi Datta Kollc;u

~ ~ILClOm)

Kanchao Sharma India ~i~l.coml

Chilafat Dalimuthe Indonesia (chac:hajazzttyahoo.com)

Ngurah Ketut Indonesia (ketutngurahOyahoo.com)

Palak Mehta India (pbm_111 Oyahoo.co.ln)

Sunita lawange India (salawangeCigrna.i l.com)

Pankaj Surange India (pank.ajnsurangeOyahoo.co.in)

AshokJadon India

(Jadonaeredlffmall.coml

Mayank Gupta India (dnn_guptaOy~.co.ln)

Karthic Babu Natarajao India (karthicnehDimail.cornl

Department ol Anaestheslology, NEIGRIHMS Shillong, India

Basics of

Pain Management Gautam DaS

MD, RPP

Editor-in-Chief: Journal on Recent Advances in P8in Di~ Daradia-lhe Pain Clinic Cocne Di!Edor: Daradi8 Pain Management Courses and Fellowships, K.olkma

Editors R Gurumoorthl MD, RPP Director: Dr Guru's Pain Care Clinic, Trichy Corditr:x! CUnlcal Methods In Pain ~iclne Vtsiting Con.sultlJnb Dnc:f~The Pain Clinic, K.olblte Rantnurthy ND, FJIM

Assistant Professor Department of Aneslhesiology, Ye:nepoya Medical

Coll~e, Meng~~luru

Vtsiting Consult1fnt: Daradia-The Pain Clinic, K.olkllta

Smi'rjit ll:¥ MD, RPM

Assistant Professor Department of Anesthesiology and Pi!!in Manegernm: NEIGRIHMS, Shlllong Chid Editor. Journal on Recent Advances In Pain Coeditor. Clinical Methods In Pain Medicine Vtsiting Consultant: Daradia-The Pain Clinic, K.olblta

~

CBS

CBS Publishers &Distributors

Pvt Ltd

New Delhi • Bengoluru • Chennol • Koehl • Kolkoto • Mumbol Hydeltlbad • Nagpur • Patna • PUna • \lljayawaaa

Dist:/IUMet

Science and technology are constantly c:b.aDging fields. New resean:h and cxpcrimce broaden the scope of informati011. and knowlcclgc. The authors have tried their best in giviug infonnatioa available to lhczn while piCJllring the material fix this book. Althoush, all efforts have been made to ensure optimum accuracy of tbc material, yet it ie quite poseible some mot$ might have been left uncom:cted. The publisher, tbc printer and the authors will not be held responsible for my inadvertent CIIOI5, omiss:i.lxls or inac:oullmi Ditta

30. Palliative Care in Cancer

151

~Gwpfll

31. Myths in Cancer Pain ~G!qttl

155

Contents

Section VII: Management of Widespread Pain Seclon edllor: Ramml.llhy

32. Widespread Pain

159

33. Fibromyalgia

165

r..._ Jrsmw Bd4y

~,

34. Painful Diabetic Neuropathy

170

s.-jttlky

35. Myths in Widespread Pain li.Mmuutlsy

175

This Page is Intentionally Left Blank

Section

I

General Consideration Kanchan Sha777Ul (Section Editor)

1. Pain Pathways 2. Types of Pain 3. Pharmacotherapy of Pain 4. Psychological Aspects of Pain 5. Myths in Pain Management

This Page is Intentionally Left Blank

1 Pain Pathways Kanchan Sharma, Gautam Das

1. Transduction: It is a process of conversion of a noxious stimulus by the nociceptors into electrical signals or action potentials. Various mechanical, thermal or chemical stimuli are responsible for the generation of these action potentials. 2. Transmission: It is a process by which the action potential generated at the nociceptor is propagated along the axon of the primary afferent neuron.

Pain is produced by the noxious stimuli perceived by specific sensory receptors called nociceptors which are there at the free nerve endings of primary afferent terminals of A5 and C fibres. An action potential is generated at this nociceptor (transduction) which are then further carried by the A5 and C fibres towards the higher centre (transmission) and make us feel pain (perception). There are two important aspects which are unique to pain signal. First, whenever sensory cortex is stimulated, limbic system which controls our emotions are stimulated simultaneously. Thus emotions are the integral components of pain. Second, pain is a unique sensory signal as it is maximally changed on its way towards the higher cortical centres (modulation). The action potential generated in the periphery and the action potential that reaches the somatosensory cortex are not the same. The action potentials are either decreased (mostly in healthy individuals) or increased (anxious and chronic pain patients). Thus, the pain signals generated at the site of tissue damage and the pain we perceived because of that are not the same.

Types of afferent fillres that carries pain:

A8 fibres are lightly myelinated with the conduction velocity of ~15 m/sec which is faster than C fibres. They transmit rapid and sharp pain which is well localised. C fibres are unmyelinated with the slowest conduction velocity of 10 joints (at least 1 small joint)

B. Serology (at least 1 test result is needed for classification): Negative RF and negative anti-CCP antibodies Low-positive RF or low-positive anti-CCP antibodies" High-positive RF or low-positive anti-CCP antibodiesd

3

5

0 2

3

C. Acute phase reactants: Normal CRP level and normal FSR Abnormal CRP level or abnormal ESR

0 1

D. Duration of symptoms: 3 times the upper limit of normal

Treafment

The goals of therapy for RA include relief of pain, reduction of inflammation, protection of articular structures, maintenance of function, and control of systemic involvement. 1 Treatment as such is totally palliative. For symptomatic control of disease, non-steroidal anti-inflammatory drugs [NSAIDs], simple analgesics and steroids [low dose 7.5 mg/day] are used. Considering side effect profile of NSAIDs like gastrointestinal, renal, pulmonary and cardiac damage, cydooxygenase [COX]-2, inhibitors are used. But unfortunately due to sudden cardiac events in COX-2 inhibitors, nowadays lot of drugs are withdrawn from market. Third line of drug belongs to disease modifying anti-rheumatic drugs [DMARDs]. These agents include methotrexate, sulfasalazine, hydroxychloroquine, gold salts and D-penicillamine. Nowadays it had been recommended to start with high dose for rapid control of disease and then tapered slowly. Methotrexate is the anchor drug in RA treatment and is usually given as 7.5--25 mg

Basics of Pain Management

weekly as oral or intramuscular form in order to avoid gastrointestinal side effects. Its main side effect is nausea which usually responds to folic acid. It has onset of action early than other drugs but maximum effect occurs after 6 months. Other drugs like sulfasalazine can be used in mild form of disease. Chloroquine2 can be used as add-on drug to other DMARDs. Patient has to take minimum of 8 weeks of a particular drug to consider its efficacy. When disease is not controlled of DMARDs then biologics are used which include TNF-

neutralizing agents (inflixim.ab, etanercept, and adalimumab), IL-l neutralizing agents (anakinra), those that deplete B cells (rituxim.a.b), and those that interfere with T cell activation (abatacept). These drugs should be administered preferably by rheumatologist who has more experience with these drugs as they have more side effect profiles. Then last group of drugs, immunosuppressive and cytotoxic drugs, including leflunomide, cyclosporine, azathioprine, and cyclophosphamide are used when all drugs fails. 1

REFERENCES 1. Peter El. Rheumatoid arthritis. In: Anthony SF, editor. Harrison's rheumatology. New York: McGraw-Hill; 2010. P. 82-99. 2. Kamran H, Mohammed A. Rheumatoid Arthritis: Clinical Features and Diagnosis. In: Ade Adebajo, editor. ABC of Rheumatoloy. West Sussex: Wiley Blackwell; 2010. P. 71-5.

3. Gary SF. Clinical features of rheumatoid arthritis. Gary SF, Ralph B, Sherine EG, James R, lain BM, editors. Kelleys Textbook of Rheumatology. Philadelphia: Elsevier saunders;2013. P. 1109-36. 4. Daniel A, Tuhina N, Alan JS, Julia F, David TF, Clifton OB, et al. 2010. Rheumatoid Arthritis Classification Criteria. Arthritis and Rheumatism.2010 Sep; 62(9): 2569-81.

21 Spondyloarthropathies Samarjit Dey

The spondyloarthropathies are a diverse group of inflammatory arthritides that share certain genetic predisposinf. factors and clinical features1 (Table 21.1). -3 Their most characteristic feature is inflammatory back pain.4 Enthesitis, another characteristic feature, involves inflammation at sites where tendons, ligaments, or joint capsules attach to bone. Enthesitis is believed to be the primary lesion in the spondyloarthropathies, whereas synovitis is the main lesion in rheumatoid

arthritis. Dactylitis (inflammation of an entire digit), commonly termed"sausage digit," also occurs in the spondyloarthropathies and is thought to arise from joint and tenosynovial inflanunation.These disorders include ankylosing spondylitis, reactive arthritis, psoriatic arthritis and spondylitis, enteropathic arthritis and spondylitis, juvenile-onset spondyloarthritis, and undifferentiated spondyloarthritis. Clinical features of common spondyloarthropathy are listed in Table 21.1.

Table 21.1: Clinical features of common spondytoarthropalhlea

Ankylosing

Features

Rettctioe arthritis (including Reiter's syndrome)

lfrlhritis

IBD-associated spondylotzrthroptlthy

Psorilltic

Prevalence Age at onset

0.1%to0.2%

0.1%

0.2% to 0.4%

Rare

Late teens to early adulthood

Late teens to early adulthood

35 to 45 years

Any age

Male-to-female ratio

3:1

5:1

1:1

1:1

HLA-827

90to95%

80%

40%

30%

Frequency

100%

40to60%

40%

20%

Distribution

Symmetric

Asymmetric

Asymmetric

Symmetric

Syndesmophytes

Delicate, marginal

Bulky, nonmarginal

Bulky, nonmarginal Delicate, marginal

Sarcoilitia

Peripheral arthritis Frequency

Occasional

Common

Common

Common

Distribution

Asymmetric, lower limbs

Asymmetric, lower limbs

Asymmetric, any joint

Asymmetric, lower limbs Contd.

109

Basics of Pain Management

Table 21.1: Clinical features of common spondyloanhropathles (Contd.)

Features

Ankylosing spondylitis

Reactive arthritis (including Reiter's syndrome)

Psoriatic arthritis

IBD-associated spondyloarthropathy

Enthesitis

Common

Very common

Very common

Occasional

Dactylitisq

Uncommon

Common

Common

Uncommon

Skin lesions

None

Circinate balanitis, keratoderma blennorrhagicum

Psoriasis

Erythema nodosum, pyodermagangrenosum

Nail changes

None

Onycholysis

Pitting, onycholysis

Clubbing

Ocular conditions

Acute anterior uveitis

Acute anterior Chronic uveitis liveitis, conjunctivitis

Chronic uveitis Ulcers

Oral conditions

Ulcers

Ulcers

Ulcers

Cardiac conditions

Aorthic regurgitation

Aortic regurgitation, conduction defects

Aortic regurgitation, Aortic conduction defects regurgitation

Puhnonary features

Upper lobe fibrosis

None

None

None

Gastrointestinal conditions

None

Diarrhea

None

None

Renal conditions

Amyloidosis, lgA nephropathy

Amyloidosis

Amyloidosis

Nephrolithiasis

Genitourinary conditions

Prostatitis

Urethritis, cervicitis

None

None

lnvesHgaflon

Investigation is done to confirm diagnosis and assess severity of disease. • Complete blood count, erythrocyte sedimentation rate, c-reactive protein is done to check active inflammatory process. • In case of suspected ankylosing spondylitis, HLA typing usually HLA B-27 is done. • X-ray and MRI of spine is done to confirm sacroilitis and other features like facet joint inflammation, syndesmophytes, etc. In case of peripheral joint, grading of cartilage and bony destruction can be assessed. • In case of joint effusion, fluid tap is done to differentiate from infective pathology. • Scintigraphy can show increased radiotracer uptake in inflamed joints.

• A serum uric acid and urate crystal in joint fluid is done to confirm gouty arthritis. • Colonoscopy can be done in case of suspected bowel related spondyloarthropathy. Diagnostic Criferia As there is no specific sign and investigation

available to confirm spondyloarthropathy, certain criteria are made to confirm different types of spondyloarthropathy. In this section all recent classification criteria for spondyloarthritis are listed, starting with inflammatory back pain criteria sets and mnemonic for assessment of spondyloarthritis international society criteria1 (Table 21.2), 1984 modified New York criteria for ankylosing spondylitis2 (Table 21.3), Amor criteria3 (Table 21. 4) and the European Spondyloarthropathy

Spondyloarthropathies

Table 21.2: Inflammatory back pain criteria set and mnemonic for assessment of spondyloarthritis International society criteria

Calin's criteria

Berlin criteria for IBP

ASAS IBP criteria mnemonic forcriteriaiPAIN

Age at onset < 40 yr

Morning stiffness of >30 min duration

Insidious onset

Duration of back pain >3 mo

Improvement in back pain with exercise but not with rest

Pain at night (with improvement upon gettingup)

Morning stiffness

Nocturnal awakening (second-half of the night only)

Age at onset < 40 yr

Improvement with exercise

Alternating buttock pain

Improvement with exercise

Requires the presence

The sensitivity is 70%, specificity 81% if two of the four criteria are fulfilled

The sensitivity is 77.0% and specificity 91.7% if at least four out of five criteria are fulfilled

Insidious onset

of four of five criteria

IBP: Inflammatory back pain; ASAS: Assessment of spondyloarthritis international society; iPAIN: Inflammatory PAIN.

Study Group (ESSG) criteria4 (Table 21.5) for spondyloarthritis, which cover the whole spectrum of SpA including axial SpA5 (Table 21.6) and peripheral SpA6 (Table 21.7) and psoriatic arthritis study group criteria for the classification of psoriatic arthritis7 (Table 21.8). The most recent ASAS classification criteria for axial spondyloarthritis were developed for early and established cases and include the MRI technique (active inflammation) as an important tool for early diagnosis.

Table 21.4: Amor criteria

Oinical symptoms or history of scoring

Points

Lumbar or dorsal pain at night or morning stiffness of lumbar or dorsal pain

1

Asymmetrical oligoarthritis

2

Buttock pain

1

If alternate buttock pain

2

Sausage like toe or digit

2

Heel pain or other well-defined enthesopathy

2

Iritis

1

Table 21.3: Modified New York criteria for ankylosing spondylitis (1984)

Nongonococcal urethritis or cervicitis 1 within 1 month before the onset of arthritis

• Clinical criteria: - Low back pain and stiffness for more than 3 months that improves with exercise, but is not relieved by rest. - Limitation of motion of the lumbar spine in the sagittal and frontal planes. - Limitation of chest expansion relative to normal values correlated for age and sex. • Radiological criterion: - Sacroilitis grade ~ 2 bilaterally or grade 3-4 unilaterally. Definite AS if the radiological criterion is associated with at least one clinical criterion

Acute diarrhea within one month before the 1 mo onset of arthritis

1

Psoriasis, balanitis, or inflammatory bowel disease (ulcerative colitis or Crohn's disease)

2

Radiological findings Sacroilitis (bilateral grade 2 or unilateral grade 3)

3

Genetic background 2 Presence of HLA-B27 and/or family history of ankylosing spondylitis, reactive Contd.

Basics of Pain Management

Table 21.4: Amor criteria (Cond.) QinicQl sympWm8

or hisrory af scoring

Poinfs

arthritis, uveitis, psoriasis, or inflamma.tmy bowel disease Response to treatment Clear-cut improvement within 48h after NSAIDs intake or Iilpid relapse of the pain after their discontinuation

45 years)

2

Saoconm, oo ;mag;"j

u

Tabla21..5: European Spandyloarttuopathy Study Group (ESSG) crllarla Synovitis • Asymmetric or • Predominantly in the lower limbs

and

Ooe oc moce of the follow;og •ariable" • Positive family history

J

l in patients with 2: 3 months back pain and age at onset