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Review Article
32 (
2
); 120-128
doi:
10.25259/VJIM_16_2022

Basics of Chronic Pain Management

Associate Professor, Department of Anaesthesia, Government Medical College, Nagpur, Maharashtra, India
Corresponding author: Vrishali Ramesh Ankalwar, Associate Professor, Department of Anaesthesia, Government Medical College, Nagpur, Maharashtra, India. vriankalwar@yahoo.com
Licence
This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

How to cite this article: Ankalwar VR. Basics of Chronic Pain Management. Vidarbha J Intern Med 2022;32:120-8.

Abstract

Approximately one in ten people suffer from chronic pain globally with pain being the most common reason to seek medical help. Despite the long-term prevalence of pain, the practice of pain management and the scientific discipline of pain research are relatively new fields. To relieve suffering from chronic pain in the ‘fifth vital sign’ era to date remains a 21st-century dilemma for healthcare providers. In the current review article, numerous articles from various pain journals and books for chronic pain management using medical search engines such as PubMed, Scopus, and Google scholar have been reviewed in an attempt to shed light on the approach, evaluation, and management of chronic pain. Along with the same, recent advances in pharmacotherapy and interventional nerve blocks have been discussed in brief.

Keywords

Chronic non cancer pain
Pharmacotherapy
Nerve blocks
Cancer pain

INTRODUCTION

The International Association for Study of Pain defines pain as ‘An unpleasant sensory and/or emotional experience associated with, or resembling that associated with, actual or potential tissue damage.’ Even if the patient is experiencing pain in the absence of actual tissue damage, it should be accepted as pain. According to a global burden disease study, one in ten adults is diagnosed with chronic pain each year globally.[1]

PAIN PATHWAYS

(1) Transduction, (2) Transmission, (3) Perception, and (4) Modulation. These are the sequence of events that are involved in the neural processing of noxious stimuli [Figure 1].[2-6]

Figure 1:: Afferent pain pathway.

TYPES OF AFFERENT FIBERS THAT CARRY PAIN

  • A-Delta fibre– myelinated and fast, with a conduction velocity of 5–15 m/s, transmits sharp, localised, and fast pain

  • C-fibres – unmyelinated with slow conduction <2 m/s, carry dull, diffuse, aching, and delayed pain.

Gate control theory of pain

Melzak and Wall proposed historical ‘Gate control theory’ in 1965. It states that activating larger diameter A-beta fibres leads to inhibition of pain signals transmitted through smaller diameter A delta and C fibres. An inhibitory interneuron acts as physiological gate which is closed by stimulation of A beta fibres. For example, Spinal cord stimulator and TENS for myofascial pain.[6]

AUTONOMIC NERVOUS SYSTEM

Autonomic nervous system plays an important role in different types of pain. For example, pain signals from thoracic or abdominal viscera and intervertebral disc-or vertebral body are carried by different afferent sympathetic fibres.[1,2-4,7]

SOMATIC SYMPATHETIC COUPLING AND MECHANISM

Somatic and sympathetic nerves are well insulated with no crosstalks in between them. However, with pathological conditions such as peripheral nerve injury/neurolysis and complex regional pain syndrome (CRPS), there is a cross-connection between somatic and sympathetic signals. Sympathetic efferent fibres release catecholamines, which instead of acting on sympathetic receptors may stimulate the nociceptors and generate action which is carried by somatic nerves[2]

SYMPATHETIC BLOCKADE AND ITS SIGNIFICANCE IN PAIN MANAGEMENT

Sympathetic blockade results in interruption of transmission by both the efferent and afferent fibres. It does not result in sensory or motor loss as seen in the somatic blockade.[2]

Examples of sympathetic blockade at various levels:

  1. Stellate ganglion and lumbar sympathetic blockade for CRPS of the upper and lower limbs

  2. Splanchnic and celiac plexus block for the upper abdominal malignancy and chronic benign pain

  3. Superior hypogastric plexus block: Cancer and non-cancer chronic pelvic pain.[8]

TYPES OF PAIN

Based on time

  • Acute pain: Pain lasts <3 months, mostly nociceptive

  • Chronic pain: Pain persisting for more than 3 months, mostly neuropathic.[9,10]

Based on mechanism

  • Nociceptive pain arises from actual or threatened damage to non-neural tissue. For example, acute trauma, postoperative pain, and sickle cell crisis

  • Neuropathic pain is caused by a lesion or disease of somatosensory nervous tissue. For example, post-herpetic neuralgia, trigeminal neuralgia, distal polyneuropathy, and CRPS type

  • Mixed pain is having both nociceptive and neuropathic components. For example, cancer pain and vascular pain syndromes

  • Non-inflammatory/non-nociceptive where the aetiology of the origin of the pain is still confusing. For example, fibromyalgia and irritable bowel syndrome.

ASSESSMENT AND DIAGNOSIS OF PAIN

Pain history

An effective history is vital in making a diagnosis of pain. A pain questionnaire should be based on the following aspects of pain.[9-18]

  1. Onset, location, and radiation of pain

  2. Character or description of pain:

    • Nociceptive pain – Dull aching, cramp, stabbing knife, shooting and throbbing

    • Neuropathic pain – current-like and tingling pain

    • Mixed–burning pain in the chest

  3. Aggravating and relieving factors would explain the possible pathophysiological mechanism.

PAIN ASSESSMENT TOOLS[2,8,18]

  1. Visual Analogue Scale (VAS): This is the most commonly used scale. In this, the patient is asked to place a marker on a 100 mm continuous line between no pain and the worst imaginable pain on every visit [Figure 2]

  2. Numerical Rating Scale (NRS): The patient directly assigns a number between 0 (no pain) and 10 (the worst pain imaginable) [Figure 2]

  3. Verbal Categorical Scale: The patient describes the severity of pain ranging from no pain to ‘mild,’ ‘moderate’ and ‘severe’ [Figure 2].

    • Mild pain: VAS or NRS of 0–3

    • Moderate pain: VAS or NRS of 4–7

    • Severe pain: VAS or NRS of 8–10 or even if the pain is moderate but the patient says I cannot bear it, it can be counted as severe pain.

  4. The faces pain rating scale is used mainly for children and mentally impaired patients. The scale depicts six faces of facial features, each with a numeric value of 0–5, ranging from a smiling and happy face to a sad and teary face.

  5. Comprehensive Pain assessment Questionnaires:

    • McGill pain questionnaires

    • Brief pain inventory

    • Oswestry pain questionnaire

    • Patient health questionnaire-9 scoring is to rule out depression.

Figure 2:: (a) Visual analogue scale (VAS) and (b) Combined pain assessment tool showing numerical rating scale, VAS, Verbal categorical scale, and Wong – Baker fascial pain rating scale.

CLINICAL EXAMINATION

General physical examination

Pain diagram

It is essential to draw a pain diagram for assessment of pain as it provides [Figure 3][8]

Figure 3:: Pain diagram.

  • Visual confirmation of patient’s pain

  • It can be stored as a medical record

  • It helps to note the change in the area of pain especially if the patient’s pain keeps on changing with every visit.

NEUROLOGICAL EXAMINATION

It consists of an examination of all cranial nerves, spinal nerves, and autonomic nervous systems.

Musculoskeletal system examination

It includes:

  • Posture, muscle symmetry, and obvious muscle wasting: Muscle spasm occurs in spinal nerve compression in corresponding myotomes. Straightening of lumbar lordosis or canal stenosis occurs due to spasm of erector spinae muscle. For example, stooped gait or ‘shopping cart’ posture in lumbar canal stenosis

  • Range of motion of joints is noted.

  • Palpation: Done for soft tissues and bones in affected dermatomyotomes to map areas of pain

    • Oedema, clicks, and crepitus in joints

    • Cord like the feel of muscles that are in spasm can be palpated

    • Tenderness, for example, paraspinal tenderness may be felt in facet joint pain

    • The presence of trigger points like trapezius trigger points can cause pain and numbness of the arm or forearm and mimic pain caused by a cervical herniated disc.

SPINE EXAMINATION

It includes sensory and motor examination of spinal nerves.

Spine symmetry and kyphosis or scoliosis should be noted.

Spinal flexibility – Pain on certain movements of the spine could indicate possible diagnosis in spine pain patients like pain in the neck or back on forward bending will indicate discogenic pain. On the contrary; pain on backward bending will point toward facet arthritis or muscular spasm [Table 1].

Table 1:: Spine-specific tests.[8]
Name of the tests Analyse Remarks
SLR or Lasegues test Leg pain at an angle between 40 to70 will be positive Positive means L4, L5, S1, and S2 are having pain on stretching the leg
Reverse SLR Anterior thigh pain on the stretch will be positive reverse SLR Positive meaning L2, 3, 4 could be getting stretched causing pain
Cross SLR Positive leg pain on the affected side will indicate stretch of L4,5, S1nerveroots More specific than SLR
Fabre test for sacroiliac joint pain Pain on the affected side will indicate strain of the SI joint capsule and ligaments Not specific but hints at SI joint pathology

Palpation

Spinous process tenderness might be present in discogenic pain, vertebral body fractures, or spine metastasis.

PHARMACOTHERAPY IN PAIN MANAGEMENT

The most common method of pain management is the use of drugs. Nociceptive pain responds well to simple analgesics such as anti-inflammatory agents, but neuropathic pain responds better to coanalgesics such as anticonvulsants and anti-depressants.[2,8]

Drugs should have

  • Rapid onset, long duration, and effective pain relief

  • Minimal side effects on long-term use

  • Easily self-administered.

WHO STEP LADDER

The World Health Organisation 1986 devised a step-wise approach popularly known as the ‘WHO step ladder’ approach for the management of chronic pain and cancer pain patients. In 2016, with the advent of newer modalities and interventions, this original analgesic ladder was upgraded to the current modified four-stepladder approach [Figure 4].[2]

Figure 4:: Modified four-step ladder.

Drugs used in pain management can be categorised under two broad headings: Analgesics and Coanalgesics.

  • Analgesics are anti-inflammatory, non-selective COX – inhibitors like NSAIDs, and selective COX-2 inhibitors. Acetaminophen/Paracetamol and Opioids

  • Coanalgesics or adjuvant group includes anticonvulsants, antidepressants, local anaesthetics, steroids, muscle relaxants, botulinum toxins, and NMDA receptor antagonists. Others such as Alpha 2, agonists, calcium channel blockers, vitamins, and nutritional supplements.

ANALGESICS

Anti-inflammatory, COX –inhibitors: NSAIDs, COX -2 inhibitors

Commonly used NSAIDs for pain management include Ibuprofen, Diclofenac sodium, Nimesulide, Ketoprofen, Naproxen, Piroxicam, and Mefenamic acid. COX-2 selective inhibitors such as etoricoxib and celecoxib have better gastrointestinal safety profiles and least effect on platelet function.[2,19,20]

These are useful in inflammatory conditions such as rheumatoid arthritis, osteoarthritis, and ankylosing spondylitis where inflammation is the main pathology.

OPIOIDS

Opioids can be classified according to their receptor activity or duration of action (long acting and short acting) or their analgesic and ceiling effects (weak and strong opioids). Opioid receptors are G protein-coupled receptors. mu is the major receptor responsible for analgesia. Pure agonist like morphine is preferred in moderate-to-severe chronic pain like cancer pain. Opioids with agonist-antagonist have a ceiling effect for analgesia. Weak opioids are tramadol, tapentadol, and codeine. Strong opioids are morphine, fentanyl, and buprenorphine. Long-acting opioids are good to treat baseline pain whereas short-acting opioids are useful in breakthrough pain. If a trial of opioids is considered, then: [Table 2][8]

Table 2:: Commonly available opioids in India.[8]
Drug Route Starting dose and frequency Onset of action
Codeine Oral 30 mg 3–6 hrly 30–45 min
Morphine Oral 10 mg 3–6 hrly 30–60 min
Morphine Parenteral SC/IM/IV 5 mg 3–6 hrly Subcutaneous10–30 min.
IM 10–20 min; IV2–5 min
Fentanyl Trandermal Transdermal 25 ug once in 3 days 10–12 hrs
Fentanyl
Parenteral
Transdermal 50 ug 1–4 hrly SC 10–20 min; IM 10–20 min
IV 2–5 min
Fentanyl Lozenges Transmucosal
(Lollipop)
200 ug 5–10 min
Pentazocine SC/IM/IV 30 mg
3–6hrly
SC 10–30 min; IM 10–20 min
IV 2–10 min
Buprenorphine
(Transdermal)
Transdermal 5 mg once in 7 days 12–24 h
Buprenorphine
Parenteral
SC/IM/IV 150 ug
8–12 hrly
SC 10–30 min; IM 10–20 min
IV 2–10 min
Tramadol Oral 50 mg 6–8 hrs 30–60 min
Tramadol SC/IM/IV 50–100 mg
6–8 hrly
10–30 mins
Tapentadol Oral 50 mg, 100 mg
OD to 4 times a day
10–30 min

  • The patient should be explained the benefits and risks of opioids use

  • The WHO analgesic ladder to be followed

  • Strong opioids like morphine should never be used as SOS drug

  • Side effects should be explained and majors to be taken to correct them if possible

  • For elders ‘start low and go slow’, instructions for follow-up and emergency should be provided.

The oral route is the preferred root of administration. Other routes are subcutaneous, IM, IV, transdermal patches, and intrathecal pumps.

Common side effects are nausea, vomiting, itching, drowsiness, euphoria, constipation, urinary retention, respiratory depression, tolerance, dependence, sexual dysfunction, etc.

COMMONLY USED ANTICONVULSANTS IN PAIN PRACTICE

These are mainly either sodium or calcium channel blockers which raise the threshold for nerve depolarisation and thus suppress abnormal neuronal discharge [Table 3].

Table 3:: Commonly used anticonvulsants.
Drug Name Dose Mechanism of Action Side Effects
Gabapentin Starting dose 100–300 HS.
The usual dose is 900–3600 (max) mg in three divided doses
Membrane stabiliser by binding at alpha2delta subunit of L type calcium channel. Dizziness, somnolence, fatigue, Peripheral oedema
Pregabalin Starting dose 50 mg/day
Max dose 300 mg/day
Dizziness, somnolence, fatigue, peripheral oedema, ataxia
Carbamazepine Starting dose 100 mg/day
Max dose1800 mg/day
Sodium channel blocker
Inhibit pain via a central and peripheral mechanism
Aplastic anaemia, Agranulocytosis, leukop enia, sedation, gait alteration.
Oxcarbazepine Starting dose 300 mg/day
Max dose 1200– 2400 mg/day
Maybe modulating voltage-activated calcium current Risk of hyponatremia in first few months
Topiramate Starting dose 50 mg/day
Max dose 200 mg/day
Enhances action of GABA, Inhibit AMPA Type glutamate Sedation, may predispose glaucoma and renal calculi
Lamotrigine Starting dose 20–50 mg/day
Max dose 300–500 mg/day
Prevent the release of glutamate Rash

COMMONLY USED ANTIDEPRESSANTS PAIN PRACTICE

These drugs have a direct analgesic effect at doses much lower than that required for antidepressant action with the added advantage of sedation, diminished anxiety, muscle relaxation, and a restored sleep cycle. These drugs act on descending inhibitory pain pathways. Depending on the mechanism of action antidepressants are-Tricyclic antidepressants, selective serotonin reuptake inhibitors, serotonin norepinephrine re-uptake inhibitors [Table 4].

Table 4:: Commonly used antidepressants in pain practice.
Drug Name Oral dose in mg/duration Clinical consideration
Amitriptyline (TCA) 10–25/12–24 h Caution in elderly male
Urinary retention
Nortriptyline (TCA) 10–25/12–24 h Better tolerated than amitriptyline
Duloxetine (SNRI) 20–60/12–24 h DOC IN diabetic peripheral neuropathy & fibromyalgia.
Milnacipran (SNRI) 50–100/12–24 h FDA-approved drug for fibromyalgia
Venlafaxine (SNRI) 37.5–112.5/12–24 h SNRI better tolerated
Desipramine (TCA) 10–25/24 h Better tolerated TCA in elderly

TCA: Tricyclic antidepressant, SNRI: Serotonin norepinephrine re-uptake inhibitors

COMMONLY USED MUSCLE RELAXANTS IN PAIN PRACTICE

Muscle relaxants are used in addition to rest, physical therapy, and other measures to relieve discomfort. They are typically prescribed for short-term use to treat acute, painful musculoskeletal conditions [Table 5].

Table 5:: Commonly used muscle relaxants in pain practice.
Drug Name Dose (Max) Po Mg/Duration Special Points
Baclofen 5–10 (80)/8–24 h Abrupt withdrawal may predispose to seizures, hallucinations and increased flexor spasm
Tizanidine 4–8 (36)/12–24 h More effective in reducing muscle spasm but less consistent in decreasing muscle tone. Careful administration when used with other antihypertensive
Diazepam 2–4 (20)/12–24 h Concomitant use of other centrally acting drugs may potentiate side effects

Steroids

Glucocorticoids are extensively used in pain management for their anti-inflammatory and possibly analgesic actions. Although epidural and intra-articular steroids are frequently used in pain management, scope of oral steroid is limited. Particulate steroids are preferred over soluble preparations. Commonly used preparations are triamcinolone acetate and methylprednisolone.

NMDA receptor antagonist

NMDA receptors are involved in ‘windup’ phenomenon, modulation of pain pathway and hyperalgesia. Thus, inhibition of these can have potent analgesic effect. Ketamine is popular one but has no oral preparation. Parental ketamine is used in central conditions such as fibromyalgia, CRPS and opioid-induced hyperalgesia.

Alpha agonists

These drugs have sympatholytic effect and they also alter calcium and potassium conductance at spinal cord level. Commonly used is Clonidine (dose 0.1 mg/day orally). It is useful in sympathetically mediated neuropathic pain conditions like CRPS.

Local anaesthetics

Local anaesthetics drugs such as lignocaine and bupivacaine are used to block nerves as a diagnostic or therapeutic procedure. In central desensitisation procedure, it acts as a membrane stabiliser.

Botulinum toxin

Pain associated with spasticity, myofascial pain, cervical dystonia, and some headache well responds to therapeutic botox injection. It acts on the neuromuscular junction, analgesic action probably mediated by blockade of substance P, glutamate, and calcitonin gene-related peptide.

Topical agents

NSAIDs gel, Capsaicin gel, Lignocaine gel, and EMLA cream are found to be useful in pain management.

Interventional pain procedures

An interventional pain procedure is interruption of signals traveling along a nerve by injecting steroids or neurolytic agent on the nerve or using radio-frequency ablation of the nerve [Table 6].

Table 6:: Commonly performed interventions for chronic pain management.
Interventions Indication Special Points Imaging Required
Trigger Point Injection Muscle Spasm, Lignocaine and normal saline injections of steroids may
be added hydrodilatation of
muscles
Blind Or USG Guided
Intraarticular Steroid Injections Osteoarthritis Repeated steroid injections may lead to damage to cartilage,
osteopenia
USG, fluoroscopic guided
Intraarticular platelet-rich plasm
(Prp) Injections
Osteoarthritis Promising results Blind, USG or
fluoroscopic guided
Lumbar and steroid cervical
injections
Lumbar or cervical disc prolapse, nerve rootirritation, sciatica,
lumbar canalstenosis
Very effective in pain relief, can be repeated 3–4 times in a year risk of infection minimal Mostly fluoroscopic guided recently USG guided
Lumbar Transforaminal
injections
Gasserian Neurolysis Trigeminal Neuralgia Radiofrequency ablation is preferred
Effective In Primary Trigeminal
Neuralgia Glycerol Phenol 6% p
Fluoroscopic Or CT guided
Thoracic Epidural Steroid Injection Post-herpetic Neuralgia Intercostal nerve block with steroid need to be combined in a thoracic dermatomal
distribution
Fluoroscopic guided
Ulnar Nerve Or Median Nerve
Hydrodilattion
Cubital Tunnel or Carpal
tunnel Syndrome
Steroid injection or hydro
dilatation
USG guided
Sympatholytic Blocks
Stellate Ganglion Block CRPS Hand Reynauld’s Disease Peripheral Vascular Disease Steroid (Triamicinolone) is preferred
Needs repetition 2-3 Times No Alcohol or Phenol Or Radiofrquency Ablation as it
may lead permanent toHorner’s
Syndrome
Fluoroscopic Or USG guided USG guided blocks has better results
Lumbar Sympathetic Blocks Burgers’ Disease Pvd Diabetic Neuropathy
Phantom Limb
Steroid Injection Alcoho80% Phenol 6%
Radiofrequency Ablation
Fluoroscopy Guided USG Guided for Patient
Who Cannot Lie Prone
Splanchnic Nerve Blocks Celiac Plexus Block Chronic Pancreatitis Upper GI Malignancy
GB Malignancy Irritable
Bowel Syndrome
Steroid Injection Alcohol 80% PHENOL 6%
Radiofrequency ablation
Fluoroscopy guided CT guided
Superior Hypogastric Plexus Block Chronic Pelvic Pain Carcinoma Of Uterus,
Bladder, Vagina, Cervix
Alcohol 80%
Phenol 6% Radiofrequency Ablation
Fluoroscopy guided USG guided patients
who cannot lie prone
Ganglia Impar Coccydynia Ca Anal Canal Ca Vagina Steroid Alcohol 80%
Phenol 6% Radiofrequency Ablation
Fluoroscopy guided

USG: Ultrasonography, CT: Computed tomography

COMMONLY PERFORMED INTERVENTIONS FOR CHRONIC PAIN MANAGEMENT

Regenerative therapy

Is rapidly emerging with extensive biomedical research over the past decade.[2,8,12]

  • Platelet-rich plasma

  • Growth factor

  • Stem cells

  • Prolotherapy.

SPINAL CORD STIMULATOR

Spinal cord stimulation (SCS), also known as neurostimulation, utilises an implant and electrodes to deliver mild electrical pulses to the nerves around the spinal column usually the dorsal column of spinal cord, to stimulate the nerves and block or lessen pain signals that are being sent to the brain [Figure 5].[21,22]

Figure 5:: Spinal cord stimulator.

The major benefit of SCS is that it provides targeted pain relief up to 60% with improved mobility, allowing the patients to return to their daily activities. It minimises the need for invasive surgeries to correct spinal conditions and majority of the times remains the last resort for treating chronic back pain.

CANCER PAIN MANAGEMENT: SPECIAL POINTS

Cancer pain affects more than 9 million people worldwide annually. An estimated one-third (24–60%) and two-thirds (62–86%) of cancer patients suffer from pain, with more than one-third having moderate-to-severe pain. Pharmacotherapy constitutes the mainstay of treatment and approach for pain management as per the WHO analgesic ladder. Indications for interventions are unacceptable side effects and well localised pain syndromes in which pain may get relieved by nerve blocks or a comprehensive trial of pharmacologic therapy fails to provide pain relief. Interventional techniques for pain management include [Figure 6][23-27]

Figure 6:: Cancer pain management continuum: A flexible approach.

  • Regional Infusions

  • Neuraxial analgesia (Intrathecal pump)

  • Neurodestructive procedures

  • Neuromodulation

  • Percutaneous vertebroplasty/kyphoplasty

  • Radiofrequency ablation.

CONCLUSION

Pain treatment goals should include improved functioning and pain reduction. Along with pharmacological treatment, non-pharmacological therapies including integrative medicine therapies such as yoga, physiotherapy, and acupressure which widen the horizon of pain medicine should be routinely considered.

Knowledge of interventional nerve blocks and recent advances such as regenerative therapies and spinal cord stimulators has revolutionised the management of pain in CNCP and cancer patients. Thus, adequate control of chronic pain can be achieved in nearly all patients in a way that adequately balances benefits and potential harms.

Declaration of patient consent

Patient’s consent not required as there are no patients in this study.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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