PAIN PATHWAYS &

PAIN MANAGEMENT

DEFINITION The word pain is derived from the Latin word Peone and the Greek word Poine meaning penalty or punishment

Pain is defined by The International Association for the Study of Pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.

(or)

Pain is an unpleasant subjective experience that is the net effect of a complex interaction of the ascending and descending nervous systems involving biochemical, physiologic, psychological and neocortical processes

HISTORY

ARISTOTLE considered pain a feeling and classified it as a

passion of the soul, where the heart was the source or

processing centre of pain

DESCRATES, GALEN, VESALIUS postulated that pain was a

sensation in which brain played an important role

In 19th century, MUELLER, VAN FREY, GOLDSCHEIDER

hypothesized the concepts of neuroreceptors, nociceptors, and

sensory input

EPIDEMIOLOGY According to The American Pain Foundation, more than 50

million people in the US suffer from chronic pain.

An additional 25%, 20 million experience acute pain from injury or surgery

The annual incidence of moderate – intensity back pain is 10% - 15 % in the adult population with a point prevalence of 15% - 30%

The National Institute for Occupational Safety and health estimated that the cost of low back pain alone was between 50 billions – 100 billions per year

CLASSIFICATION OF PAINBased on source/ location/ referral & duration

ACUTE PAIN / TRAUMATIC PAIN

CHRONIC PAIN

VISCERAL /SPLANCNIC

PAIN

SOMATIC PAIN MALIGNANT PAINOR

CANCER PAIN

NON – MALIGNANT PAINOR

BENIGN PAINSUPERFICIAL PAIN

ORCUTANEOUS PAIN

DEEP SOMATIC PAIN

MUSCULOSKELETAL PAIN

NEUROPATHIC PAIN

ACUTE PAIN

Acute has a sudden onset, usually subsides quickly and is characterized by sharp, localized sensations with an identifiable cause

Lasts > 30 days and occurs after muscle strains and tissue injury such as trauma or surgery and is described as a linear process

A poorly treated pain can cause psychological stress and compromise the immune system due to the release of endogenous corticosteroids

Acute pain is usually characterized by increased autonomic nervous system activity resulting in

Psychological symptoms such as anxiety

Tachypnoea

Tachycardia with hypertension

Pallor

Diaphoresis

Pupil dilation

Visceral pain is a type of nociceptive pain that comes from the internal organs

Unlike somatic pain it is harder to pinpoint

Pain is described as general aching or squeezing pain

It is caused by the activation of pain receptors in the chest, abdomen, or pelvic areas

In cancer patients pain is caused by tumour infiltration, constipation, radiation & chemotherapy

VISCERAL PAIN

SUPERFICIAL PAIN It is also known as

cutaneous pain

It arises from superficial structures such as skin & subcutaneous tissues

It is a sharp, bright pain with a burning quality and may be abrupt or slow in onset

DEEP SOMATIC PAIN It originates in deep body

structures such as periosteum, muscles, tendons, joints & blood vessels

Strong pressure, ischemia, tissue damage act as stimuli for brain damage

Radiation of pain from original site of injury occur

CHRONIC PAIN Chronic pain is arbitrarily defined as pain lasting longer than 3

to 6 months

It begins when pain persists after the initial injury has healed

It is persistent or episodic pain of duration or intensity that adversely affects the function and well being of the patient

It may be nociceptive, inflammatory, neuropathic or functional in origin

It varies from unrelenting extremely severe pain to pain of escalating or non – escalating nature.

CHRONIC PAIN CYCLE

MAIN EFFECTS OF CHRONIC PAIN

Effect on physical function

Psychological changes

Social consequences

Societal consequences

CONTRIBUTING BIOLOGICAL FACTORS

Peripheral mechanisms

Peripheral central mechanisms

Central mechanisms

PERIPHERAL MECHANISMS•Result from peripheral stimulation of nociceptors

• They contribute to pain associated with• Chronic musculoskeletal• Visceral • Vascular disorders

CENTRAL MECHANISMS• Associated with disease or injury of the CNS

• Characterised by burning, aching, hyperalgesia,

dysesthesia. It is associated with

• Thalamic lesions• Spinal cord injury• Surgical interruption of pain pathways

• Multiple sclerosis

PERIPHERAL – CENTRAL MECHANISMS

• These mechanisms involve abnormal function of the peripheral and central portions of the somatosensory system

• Associated with abnormal functions of the peripheral and peripheral portions of SSNS, & loss of descending inhibitory pathways

CHRONIC MALIGNANT PAIN

It occurs in 60-90 % of patients with cancer

Pain can be related to the tumour or cancer therapy or may be idiosyncratic

Pain may also be found at the metastasized regions and treatment interventions may activate peripheral nociceptors

Pain can be somatic/visceral

CHRONIC NONCANCER PAIN

It is also referred to as chronic non – malignant pain

Pain may last for many years and is considered progressive in nature

May be nociceptive, neuropathic or mixed in nature

NEUROPTHIC PAIN Neuropathic pain is a result of an injury or malfunction of the

nervous system

It is described as

Aching

Throbbing

Burning

Shooting

Stinging

Tenderness/ sensitivity of skin

PERIPHERAL PAIN• Acute herpetic neuralgia• Acute shingles outbreak• Distal polyneuropathies• Diabetes• HIV• Chemotherapeutic

agents

CENTRAL PAIN• Central stroke pain• Trigeminal neuralgia• Complex regional pain

syndrome with causalgia & reflex sympathetic dystrophy

MECHANISM OF NEUROPATHIC PAIN

Nerve damage/ persistent stimulation

Rewiring of pain circuits both anatomically & biochemically

Spontaneous nerve stimulation

Autonomic neuronal

stimulation

Increased discharge of dorsal horn neurons

NEUROPATHIC PAIN

Results in

causing

Finally leading to

MUSCULOSKELETAL PAIN This a type of chronic non cancer pain occurring due to

musculoskeletal disorders such as

Rheumatoid arthritis

Osteoarthritis

Fibromyalgia

Peripheral neuropathies

BASED ON TRANSMISSION

FAST PAIN

Felt about 0.1 sec after a pain stimulus is applied

It is described as sharp pain, pricking pain, acute & electric pain

Fast sharp pain is not felt in most deeper tissues of the body

SLOW PAIN

Usually begins after 1 sec or more and may range from seconds to minutes

Described as slow, burning, aching, throbbing, nauseous pain and chronic pain

Associated with tissue destruction

OTHER TYPES OF PAINREFERRED PAIN

Pain that is perceived at the site different from its point of origin but innervated by the same spinal segment

Usually applies to pain that originates from the viscera

Eg. The pain associated with MI commonly is referred to the left arm, neck & chest

BREAKTHROUGH PAIN

Pain is intermittent, transitory & an increase in pain occurs at a greater intensity

Usually lasts from minutes to hours and can interfere with functioning and QOL

Eg. Neuropathic pain

Lower back pain

PAIN RECEPTORS NOCICEPTORS or PAIN RECEPTORS are sensory receptors that are activated by noxious insults to peripheral tissues

The receptive endings of the peripheral pain fibres are free nerve endings

These receptive endings are widely distributed in the

Skin

Dental pulp

Periosteum

Meninges

SKIN RECEPTORS FOR PAIN

HIGH THRESHOLD MECHANORECEPTOR

S( HTMS)

POLYMODAL RECEPTORS

These receptors detect local deformation

Eg: Touch

These receptors detect a variety of stimuli causing injury

Eg: Heat Noxious stimulation These do not have a

specialized and simple nerve endings in the periphery

NERVE FIBRES INVOLVED IN PAIN TRANSMISSION

A FIBRES C FIBRES

A – BETA FIBRES

A – DELTA FIBRES

Large Myelinated Fast conducting Low stimulation

threshold Respond to light

touch

Small Lightly Myelinated Slow conducting Respond to heat,

pressure, cooling & chemicals

sharp sensation of pain

Small & unmyelinated Very slow conducting Respond to all types of

noxious stimuli Transmit prolonged dull

pain Require high intensity

stimuli to trigger a response

SUBSTANCES EXITING NCsHISTAMINEPOTASSIUM

ATP

NEURO TRANSMITTERS INVOLVED IN

PAIN

STIMULATION OF

NOCICEPTORSBRADYKININ

SENSITIZATION OF

NOCICEPTORSPGE2

PGI2

DISCHARGE OF PAIN RELEASING SUBSTANCES BY NOCICEPTORSSUBSTANCE – P

GLUTAMATE

ACTIVATION OF NOCICEPTORS BY

INTERACTING WITH OTHER CHEMICAL

MEDIATORSPGI2

LTs

PATHWAYS OF PAIN SENSATION

The pathways of pain sensation are as follows

Pathway from skin & deeper tissues

Pathway from face – pain sensation is carried by trigeminal nerve

Pathway from viscera – pain sensation from thoracic & abdominal viscera are transmitted by sympathetic nerves & from oesophagus, trachea & pharynx by glossopharyngeal nerves

Pathway from pelvic region – conveyed by sacral parasympathetic nerves

PATHWAY FROM SKIN & DEEPER TISSUES

FIRST ORDER NEURONS• These are the cells in

the posterior nerve root ganglia, receive impulses from pain receptors through dendrites

• These impulses are transmitted through the axons to spinal cord

• Impulses are transmitted by Aδ fibre or C fibres

SECOND ORDER NEURONS

• The neurons of marginal nucleus & substantia gelatinosa form the II order neurons

• Fibres from these neurons ascend in the form of the lateral spinothalamic tract

• Fibres of fast pain arise from neurons of the marginal nucleus

• The fibres of slow pain arise from neurons of substantia gelatinosa

THIRD ORDER NEURONS• The neurons of pain

pathway are the neurons in Thalamic nucleus, reticular formation, tectum, gray matter around the aqueduct of sylvius

• Axons from these neurons reach the sensory area of cerebral cortex or hypothalamus

PAIN PATHWAYS ASCENDING PAIN PATHWAY

DESCENDING INHIBITORY PAIN PATHWAY

ENDOGENOUS ANALGESIC MECHANISMS The endogenous analgesic mechanism comprises of

endogenously synthesized opioid peptides, which are MORPHINE like substances

The opioid like substances are found at different points of the brain which are breakdown products of 3 large protein molecules

Pro – opiomelanocortin: β – endorphin

Pro – encephalin: Met – encephalin & Leu – encephalin

Prodynorphins: Dynorphins

These are found in peripheral processes of 10 afferent neurons, human synovia, many regions of CNS

MECHANISMS OF PAIN Pain sensation involves a series of complex interactions

between peripheral nerves & CNS

Pain sensation is modulated by excitatory and inhibitory NTs released in response to stimuli

Sensation of pain is composed of 4 basic processes

Transduction

Transmission

Modulation

Perception

PAIN THEORIES Pain theories are proposed to offer the possible physiologic

mechanisms involved in pain. They are as follows

Specificity theory

Pattern theory

Neuromatrix theory

Gate control theory

SPECIFICITY THEORY: This theory states pain as separate modality evoked by specific receptors that transmit information to pain centres or regions in the forebrain where pain is experienced.

PATTERN THEORY Pain receptors share endings or pathways with other sensory modalities but different patterns of activity of the same neurons can be used to signal painful and non – painful stimuli

Eg. Light touch applied to skin would produce the sensation of touch and intense pain pressure would produce pain through high frequency firing of the same receptor

NEUROMATRIX THEORY This theory was put forward by MELZACK

This theory explains the role of brain in pain as well as the multiple dimensions and determinants of pain

Acc to this theory the brain contains a widely distributed neural network called the body self Neuromatrix that contains somatosensory, limbic, & Thalamocortical components

The body self Neuromatrix involves multiple input sources such as

Somatosensory inputs

Other impulses/ inputs affecting the interpretation of the situation

Various components of stress regulation systems

Intrinsic neural inhibitory modulatory circuits

GATE CONTROL MECHANISM

Proposed by MELZACK & WALL IN 1965

According to this theory, the pain stimuli transmitted by afferent pain fibres are blocked by GATE MECHANISM located at the posterior gray horn of the spinal cord

If the gate is open pain is felt, and if the gate is closed pain is suppressed

Impulses in A – δ & C – fibres can be blocked by modulated by A – β activity that can selectively block impulses from being transmitted to the transmission cells in the spinal cord and then to CNS resulting in no pain

ROLE OF BRAIN IN GATE CONTROL MECHANISMGates in spinal cord are open

Pain signals reach the thalamus through lateral spinothalamic tract

Signals are processed in thalamus

Signal are sent to sensory cortex & perception of pain occurs in cortex

Signals are sent from cortex back to spinal cord and the gate is closed by releasing pain relievers such as opioid peptides

Minimizing the severity & extent of pain

ASSESSMENT OF PAINMETHOD OF PAIN ASSESSMENT

Comprehensive history intake

Medical history

Physical history

Family history

Physical exam

Questioning on characteristic of pain – onset, duration, location, quality, severity & intensity

Evaluation of psychological status

PAIN ASSESSMENT PNUEMONIC

P – Palliative/ Provocative/ Precipitating

Q – Quality R – Radiation/ Region S – Severity T – Temporal/ Time related

The impact of pain on the patients functional status, behaviour and psychological status should also be assessed

PAIN ASSESSMENT TOOLS Pain may be accompanied by physiologic signs and symptoms

and there are no reliable objective markers of pain

The severity of pain can be assessed by rating scales & multidimensional scales.

RATING SCALES Provide a simple way to classify the intensity of pain and should be selected based on the patients ability to communicate

MULTIDIMENSIONAL SCALESHelpful in obtaining information about the pain and impact on QOL, but are more often time consuming to complete

RATING SCALES SIMPLE DESCRIPTIVE PAIN INTENSITY SCALE

NO PAIN MILD PAIN

MODERATE PAIN

SEVEREPAIN

VERY SEVERE

PAIN

WORST POSSIBLE

PAIN

NUMERIC SCALE

VISUAL ANALOG SCALE (VAS)

FACES SCALE

VERBAL RATING SCALE

PAIN THERMOMETER

MULTIDIMENSIONAL ASSESSMENT SCALES

The following are the types of MAS

Initial pain assessment tools

Brief pain inventory

McGill pain questionnaire

The neuropathic pain scale

The Oswestry disability index

DIAGNOSIS OF CHRONIC PAIN

CLINICAL PRESENTATION OF PAIN General:

Acute distress/ trauma pain No noticeable suffering (Chronic pain)

Symptoms:

Sharp, dull, burning, shock like, tingling, shooting radiating, fluctuating in intensity and varying in location

Non – specific: Anxiety

Depression

Fatigue

Insomnia

Anger and fear

SIGNS OF PAINACUTE PAIN

Hypertension

Tachycardia

Diaphoresis

Mydriasis

Pallor

CHRONIC PAIN

There may be no obvious pain signs in some acute cases and in most chronic/ persistent pain

LABORATORY TESTS Pain is always subjective i.e. there are

no laboratory tests It is diagnosed based on patients

description and history

MANAGEMENT OF PAINGOALS OF THERAPY

To decrease the subjective intensity

To reduce the duration of the pain complaints

To decrease the potential for conversion of acute pain to chronic persistent pain syndromes

To decrease the physiological, psychological, & socioeconomic sequelae associated with under treatment of pain

To minimize ADRs, & Dis intolerance to pain management therapies

Improving the patients QOL and the ability to perform activities of daily living

APPROACHES TO PAIN CONTROL

NON – PHARMACOLOGICAL MANAGEMENT The non – pharmacological management involves the following

approaches

Physiotherapy

Psychological techniques

Stimulation therapies – Acupuncture & Transcutaneous Electrical Nerve Stimulation (TENS)

Palliative care – involves the alleviation of symptoms but does not cure the disease

SURGICAL PROCEDURE FOR THE RELIEF OF PAIN

CORDOTOMY: In the thoracic region , the spinal cord opposite to the side of pain is partially cut to interrupt the anterolateral pathway

THALAMOTOMY: Involves causter ization of specific pain areas in the intrathalamic nuclei in the thalamus, which often relieves suffering type of pain

SYMPATHECTOMY

Excision of the segment of the sympathetic nerve or one or more sympathetic ganglia

RHIZOTOMY

Surgical removal of spinal nerve roots for the relief of pain or spastic paralysis

FRONTAL LOBOTOMY

Surgical process involving division of one or more nerve tracts in a lobe of the cerebrum usually frontal lobe

PHARMACOLOGICAL MANAGEMENT

OPIOID/ NARCOTIC ANALGESICS OPIUM is a raw extract of the poppy plant Papaver

somniferum

During 19th century, MORPHINE was isolated from opium and its pharmacological effects were characterized

OPIOD RECEPTORS TYPE CHARACTERIZATIONµ - MU Highly selective for opioids

δ – DELTA Mixed agonist – antagonist response

K - KAPPA Opioid analgesics selective for these receptors are not

identified

LOCATION OF OPIOID RECPTORS

OPIOID CLASSIFICATION

MECHANISM OF ACTION OF OIPOIDS

MAJOR PHARMACOLOGICAL EFFECTS OF OPIOIDS

ORGAN SYSTEM EFFECTS CENTRAL NERVOUS SYSTEM Analgesia

DysphoriaMiosis

Physical dependenceRespiratory depression

SedationCARDIOVASCULAR SYSTEM Decreased myocardial O2 demand

VasodilationHypotension

GASTROINTESTINAL SYSTEM Constipation Nausea & Vomiting

GENTIOURINARY SYSTEM Increased bladder sphincter toneUrinary retention

ORGAN SYSTEM EFFECTS NEUROENDOCRINE EFFECTS Inhibition of release of leutinizing

hormone (LH)Stimulation of release of ADH & Prolactin

IMMUNE SYSTEM EFFECTS Suppression of function of natural killer cells (NK cells)

DERMAL EFFECTS FlushingPruritusUrticaria

OPIOID ANALGESIC THERAPY IN PAIN

MANAGEMENT OF OPIOID ADVERSE EFFECTS ADVERSE EFFECT MANAGEMENT

EXCESSIVE SEDATION Reduce dose by 25% or increase the dosing intervalCONSTIPATION CASANTHROL – DOCUSATE 1 capsule at bed time/

BD SENNA 1 – 2 tablets at bed time/ BD BISACODYL 5 – 10mg daily + DOCUSATE 100mg BD

NAUSEA & VOMITINGS HYDROXYZINE 25 – 100mg (PO/IM) every 4 – 6 hrs as needed

DIPEHNHYDRAMINE 25 – 50mg (PO/IM) every 6 hours as needed

ONDANSETRON 4mg IV or 16mg PO, 4 – 8mg IV every 8 hours as needed

PROCHLORPERAZINE 5 – 10mg (PO/IM) every 3 – 4 hrs, 25mg/ rectum BD

ADVERSE EFFECT

MANAGEMENT

GASTROPARESIS METOCLOPRAMIDE 10mg (PO/IV) every 6 – 8 hours

VERTIGO MECLIZINE 12.5 – 25mg PO every 6 hours

URTICARIA/ ITCHING HYROXYZINE 25 – 100mg (PO/IM) every 6 hours as needed

DIPHENHYDDRAMINE 25 – 50mg (PO/IM) every 6 hours as needed

RESPIRATORY DEPRESSION MILD: Reduce dose by 25% MODERATE – SEVERE:

NALOXONE 0.4 – 2mg IV every 2 – 3 minutes (up to 10mg)

0.1 – 0.2mg IV every 2 – 3 minutes until desired reversal

CNS IRRITABILITY Discontinue OPIOID, treat with BENZODIAZEPINES

INERTACTING DRUGS EFFECTOPIOIDS + CNS DEPRESSANTS Eg: ALCOHOL ANESTHETICS ANTIDEPRESSANTS ANTIHISTAMINES BARBITURATES BENZODIAZEPINES PHENOTHIAZINES

Additive CNS depressant effects

MEPERIDINE + MAO – I Result in severe reactions such as Excitation, sweating, rigidity, and

hypertension

DRUG INTERACTIONS

NON OPIOID ANALGESICS Nonsteroidal Anti-inflammatory Drugs (NSAIDS) are usually

considered as Non Opioid Analgesics

CHARACTERISTICS FEATURES:

Relieve pain without interacting with opioid receptors

Possess anti – inflammatory properties

Have antiplatelet activities

Do not cause sedation & sleep

Are not addicting

MECHANISM OF ACTION OF NSAIDS

MECHANISM OF ACTION OF COX – 2 INHIBITORS

NON – OPIOID ANALGESIC THERAPY

ADVERSE EFFECTS OF NON NARCOTIC ANALGESICS

ORGAN SYSTEM EFFECTSGASTROINTESTINAL Nausea

Abdominal painDyspepsia

ConstipationVomiting

HaematocheziaIntestinal obductionIntestinal perforation

PancreatitisPeritonitis

PUD Diarrhoea

HEMATOLOGICAL Aplastic anaemiaLeukopeniaNeutropeniaPancytopenia

ThrombocytopeniaMALIGNANCIES Lymphomas

ORGAN SYSTEM EFFECTSRENAL EFFECTS Interstitial nephritis

Impaired renin secretionEnhanced tubular water/ Na+ reabsorption

INFECTIONS Sepsis leading deathMALIGNANCIES & INFECTIONS ARE AS A RESULT OF TNF - INHIBITORS

INTERACTING DRUGS EFFECTASPIRIN – ORAL ANTICOAGULANTS Gastric mucosal bleeding, & increased risk of

bleeding

SALYCYLATES - METHOTREXATE Blockage of METHOTREXATE tubular secretion by SALICYLATES resulting in pancytopenia or hepatotoxicity due to increased METHOTREXATE

NSAIDS – TNF BLOCKING AGENTS Neutropenia

WHO ANALGESIC PAIN LADDER

ALGORITHM FOR ACUTE PAIN MANAGEMENT

ALGORITHM FOR CHRONIC CANCER PAIN MANAGEMENT

THANK U