Transcript chronic pain management

CHRONIC PAIN
MANAGEMENT
PRESENTED BY: Dr CHITTRA
MODERATED BY: Dr GIAN CHAUHAN
DEFINITION
IASP defines pain as “an unpleasant sensory and
emotional experience associated with actual or potential
tissue damage, or described in terms of such damage”
pain is always subjective and it is a sensation in part of
the body, is unpleasant and also has an emotional
component
If patients regard their experience as pain or if they report
it in the same way as pain caused by tissue damage, it
should be accepted as pain
ASA defines chronic pain as “pain of any etiology not
directly related to neoplastic involvement, associated
with chronic medical condition or extending in duration
beyond the expected temporal boundary of tissue injury
and normal healing, and adversely affecting the function
or well-being of individual”
IASP defines it as “pain without apparent biological value
that has persisted beyond the normal tissue healing time
usually taken to be 3 months”
PREVALENCE
 20% to 60%
higher prevalence in women and the elderly
CLASSIFICATION
Malignant
nonmalignant
inflammatory musculoskeletal
(arthritic)
(low back pain)
headaches
visceral
neuropathic
post herpetic
phantom limb
CRPS
diabetic
BIOPHYSICAL CONCEPT
Chronic pain patients have in common complex
influences of biologic, cognitive , emotional , and
environmental factors
 patients have limited mobility, lack of motivation,
depression, anger, anxiety, and fear of reinjury, these
hamper return to normal work or recreational
activities
may become preoccupied with pain and somatic
processes, which disrupt sleep ,cause irritability and
social withdrawal
The interplay between these biologic, psychological,
and social factors results in persistence of pain and
illness behavior
Management
of
pain
addresses
physical,
psychological, and social skills and underscores
patients' active responsibility to regain control over
life by improving function and well-being
PATHWAY OF CHRONIC PAIN
CHRONICITY
› Repeated nociceptor stimulation sensitize both
peripheral and central neurons (activity-dependent
plasticity)
› progressive increase in output in response to
persistent nociceptor excitation is known as“windup
› sustained by transcriptional changes in the
expression of genes coding for various
neuropeptides, transmitters, ion channels, receptors,
and signaling molecules in both nociceptors and
spinal neurons
› physical rearrangement of neuronal circuits by
apoptosis, nerve growth, and sprouting occurs in the
peripheral and central nervous systems
PATIENT EVALUATION
HISTORY
Mode of onset
site
chronicity and duration
character and severity(visc pain- dull aching,
neuralgic pain – stabbing, myofascial pain)
investigations, operations, drugs,treatments
done
associated factors ( premonitory symptoms,ppt
factors,environmental factors, family history,pat
medical and surgicl history, psychiatry history,
medications drugs ,alcohol abuse, kinesiophobia
PHYSICAL EVALUATION
1. GPE (Skin lesions, jt deformities etc)
2. PAIN RELATED BEHAVIOUR (facial
expression, emotional)
3. SYSTEMIC EXAMINATION
4. NEUROLOGICAL EXAMINATION
a) cranial nerve fxn
b) msc strength grading
c) DTR
d) Sensation
e) musculoskeletal system
CRANIAL NERVE EXAMINATION
OLFACTORY:
Familiar odors, individual nares
OPTIC:
Vision, fundus, fields of vision
OCULOMOTOR,TROCHLEAR,ABDUCENS
ptosis, light response, nystagmus, fields of gaze,
asymmetric extraocular movements
TRIGEMINAL NERVE
jaw msc strength
superficial pain and touch senation in each
branch
The ophthalmic,
maxillary, and mandibular
nerves provide sensation
to the eye and forehead,
midface and upper jaw,
and lower jaw,
respectively
FACIAL
› Corneal reflex, symmetry
ACOUSTIC
› Sense of hearing, bone and air conduction
GLOSSOPHARYNGEAL
› Gag reflex, ability to swallow
VAGUS
› Palate and uvula inspection, nasal twang
SPINAL ACCESSORY
› Trapezius and SCM strength
HYPOGLOSSAL
› Tongue inspection and strength
MOTOR SYSTEM
CLINICAL FINDING
GRADE
No contractility
Slight flicker
Full movement, gravity eliminated
Full movement with gravity
0
1
2
3
Full movement against gravity some
resistance
Full movement against gravity full
resistance
4
5
DTR SCALE
GRADE
0
1+
2+
3+
4+
RESPONSE
No response
Sluggish
Normal
Brisk
Exaggerated with clonus
SENSORY SYSTEM
› Pain,touch,temperature
› vibration ,proprioception
MUSCULOSKELETAL SYSTEM
1. Inspection
2. Palpation
3. Movement
4. Range of motion
SPECIFIC TESTS
› SLRT
› Spinal flexibility
› Tinel’s test
› Phalen’s test
› Adson’s test
PAIN MEASUREMENT AND
ASSESSMENT
› CATEGORY SCALE
› RUPEE ANALOG SCALE
› NUMERICAL RATING SCALE
› VISUAL ANALOG SCALE
› DESCRIPTOR DIFFERENTIAL SCALE
ASSESSING PAIN IN PRESCHOOLERS
› THE OUCHERS SCALE
› HAPPY-SAD FACE SCALES
› COLOR ANALOG SCALE
› POKER CHIP TOOL
› LADDER SCALE
› LINEAR ANALOGUE SCALE
RADIOGRAPHY AND IMAGING
OPERATING ROOM FLUOROSCOPY:
› Anterior elements
› Posterior elements
› Space components
Procedures performed:
1. Caudal epidural steroids/catheter placement
2. Celiac plexus block
3. Hypogastric plexus block
4. Sympathetic plexus block
5. Trigeminal ganglion block
6. Stellate ganglion block
7. Transforaminal steroid injection
EPIDUROGRAPHY
› Opacification of epidural space with aqueous
contrast medium
SPINAL ENDOSCOPY
› Percutaneous minimally invasive endoscopic
investigation of epidural space to enable color
visualisation anatomical structures inside the
spinal canal
› Direct drug application
› Direct lysis of scarring
› Placement of catheter and electrode system
CT
› Trauma
› Abscess
› Neoplasm
› Metastasis
› LAP
Superior bone detail
MRI
› More contrast resolution
› Better soft tissue detail
BONE SCAN
› Imaging of entire skeleton
› Early detection of abnormal areas
› Metastaic disease
› CRPS
› Joint diseases
MULTIMODAL MODALITY
facilities to evaluate and treat biomedical,
psychosocial, and occupational aspects
Pain physician, psychologist, physical
therapist, and occupational therapist
SINGLE MODALITY MANAGEMENT
used as part of multimodal management
TREATMENT OPTIONS
1)
2)
3)
4)
5)
6)
7)
8)
9)
10)
11)
12)
pharmacologic management
ablative techniques
acupuncture
blocks (i.e., joint and nerve or nerve root)
botulinum toxin injections
electrical nerve stimulation
epidural steroids with or without local anesthetics
intrathecal drug therapies
minimally invasive spinal procedures
physical or restorative therapy
psychologic treatment
trigger point injections
PHARMACOLOGIC MANAGEMENT
1) NSAIDs
2) opioid therapy
3) Serotonergic drugs
4) anticonvulsants
5) anti-depressants
6) benzodiazepines
7) NMDA receptor antagonists
8) skeletal muscle relaxants
9) topical agents
NSAIDS
NSAIDs inhibit COXs
COX-1 and COX-2, are constitutively expressed in
peripheral tissues and in central nervous system
By blocking one or both enzymes prostaglandin formation
diminishes
Less severe pain states ( early arthritis, headache,backache)
are commonly treated with nonselective NSAIDs or
antipyretic analgesics mostly used orally
↓Sensitization of sensory neurons,↑ Inhibition of spinal
neurons
COX-2 expression is constitutive in many tissues,
gastrointestinal epithelium, vascular endothelium, spinal cord
and inhibition of COX-2 may exacerbate inflammation,
impair ulcer healing
Selective COX-2 inhibitors confer an increased risk for
thrombosis, myocardial infarction, renal impairment,
hypertension, stroke, and liver toxicity
OPIOIDS
ASA RECOMMENDS:
controlled or extended release opioid therapy
provides effective pain relief for patients with low
back pain or neuropathic pain for assessment
periods ranging from 1 to 9 weeks, with nausea or
vomiting and constipation as side effects
Tramadol provides effective pain relief for
assessment periods ranging from 4 to 6 weeks
immediate release opioids, transdermal opioids, and
sublingual opioids provide relief for back, neck,
leg, and neuropathic pain for assessment periods
ranging from 2 weeks to 3 months
Dizziness, somnolence, and pruritus are among
reported side effects associated with opioid therapy
All three receptors (µ, δ, κ) mediate analgesia, but
with differing side effects
Tolerance and physical dependence may occur with
prolonged administration of pure agonists, and
abrupt discontinuation or administration of an
antagonist can result in withdrawal syndrome
Proposed
mechanisms
involved
in
pharmacodynamic tolerance include opioid
receptor–G protein uncoupling, decreased receptor
internalization/recycling, and increased sensitivity
of the NMDA receptor
Increased nociceptive stimulation by tumor growth,
inflammation, or neuroma formation are possible
reasons for increased dose requirements
Opioids are effective in periphery ,at neuraxis and
systemically
Systemically and spinally administered opioids can
produce similar side effects, depending on the
dosage and rostral/systemic redistribution
most effective drugs for severe acute and cancerrelated chronic pain
prevalence of addiction is as high as 50% in
patients treated with opioids for chronic
nonmalignant pain
Thus, consistent with the multifactorial nature of
chronic pain, it is highly questionable whether
opioids alone can produce an analgesic response
Thus, the use of opioids as a sole treatment
modality in chronic nonmalignant pain is not
recommended
SEROTONERGIC DRUGS
monoamine neurotransmitter found in sympathetic nervous system,
gastrointestinal tract, and in platelets
Within the dorsal horn of the spinal cord, serotonergic neurons
contribute to endogenous pain inhibition
5-HT1B/1D agonists are effective against neurovascular headaches
Triptans inhibit neurogenic inflammation via 5-HT1D receptors on
trigeminal afferents, with additional sites of action on thalamic
neurons and in the periaqueductal gray matter
Activation of vascular 5-HT1B receptors constricts meningeal and
coronary vessels
Triptans can be applied orally, subcutaneously, or transnasally and
have been used for the treatment of migraine
All triptans narrow coronary arteries via 5-HT1B receptors by up to
20% at clinical doses and should not be administered to patients
with risk factors or coronary, cerebrovascular, or peripheral
vascular disease
ANTIEPILEPTIC DRUGS
used for treatment of neuropathic pain resulting from lesions to
peripheral or central nervous system
cause may be ectopic activity in sensitized nociceptors from
regenerating nerve sprouts, recruitment of previously “silent”
nociceptors, or spontaneous neuronal activity
increased expression and trafficking of ion channels (e.g., Na+,
Ca2+, TRP) and increased activity at glutamate receptor sites
stabilization of neuronal membrane by blockage of pathologically
active voltage-sensitive Na+ channels (carbamazepine, phenytoin,
lamotrigine, topiramate), blockage of voltage-dependent Ca2+
channels (gabapentin, pregabalin), inhibition of presynaptic release
of excitatory neurotransmitters (gabapentin, lamotrigine), and
enhancement of the activity of GABA receptors (topiramate)
Their most common adverse effects are impaired mental and motor
function which limit their clinical use, particularly in elderly
patients
Serious side effects have been reported, including hepatotoxicity,
thrombocytopenia, and life-threatening dermatologic and
hematologic reactions
Carbamazapine:
first line treatment for trigeminal neuralgia
 used in acute onset PDN, post herpetic,central
pain, phantom limb, neural invasion by
tumor,radiation fibrosis
monitor CBC, LFT, every 3 mnths
100mg bd/day ↑by 100 mgbd-tds weekly to
600-800mg/day
OXCARBAZEPINE:
300mg hs weekly ↑ 300mg/day max
1200mg/day
GABAPENTIN
First choice for neuropathic pain in eldrly,
PDN, post herpetic neuralgia and radiculopathy
300mg hs-↑1st week to 300mg bd, ↑3rd week to
300mg tds- ↑ max of 1200-1600mg/d
effect starts in 3 or 4 days and pain relief in 2
weeks
dizziness, seadtion, nausea, rashes
PREGABALIN
ASA recommends:
delta calcium-channel antagonists provide
effective neuropathic pain relief for assessment
periods ranging from 5 to 12 weeks
a meta-analysis found that sodium-channel
antagonists provide effective pain relief for
assessment periods ranging from 2 to 18 weeks
ANTIDEPRESSANTS
 used for treatment of neuropathic pain – post herpetic, PDN- tension
headache migraine,atypical facial pain- 1st line of treatment
 nonselective norepinephrine/5-HT reuptake inhibitors (amitriptyline,
imipramine, clomipramine, venlafaxine), preferential norepinephrine
reuptake inhibitors (desipramine, nortriptyline), and selective 5-HT
reuptake inhibitors (citalopram, paroxetine, fluoxetine)
 The reuptake blockade leads to stimulation of endogenous monoaminergic
pain inhibition in the spinal cord and brain
 In addition, tricyclic antidepressants have NMDA receptor antagonist,
endogenous opioid–enhancing, Na+ channel–blocking, and K+ channel–
opening effects that can suppress peripheral and central sensitization
 require monitoring of plasma drug concentrations to achieve optimal effect
and avoid toxicity, unless sufficient pain relief is obtained with low doses
 Patients with ischemic heart disease may have an increased risk for sudden
arrhythmia, and patients with recent myocardial infarction, arrhythmia, or
cardiac decompensation should not take tricyclic antidepressants at all
 Adverse events include sedation, nausea, dry mouth, constipation,
dizziness, sleep disturbance, and blurred vision
amitryptilline
10mg/d hs-inc 25mg/d after 1 wk, 2-3 wks inc
50mg/d- max 75mg/day
ASA recommends:
tricyclic antidepressants provide effective pain
relief for variety of chronic pain etiologies for
assessment periods ranging from 2 to 8 weeks,
with dry mouth and somnolence or sedation as
reported side effects
selective serotonin–norepinephrine reuptake
inhibitors provide effective pain relief for
variety of chronic pain etiologies for assessment
periods ranging from 3 to 6 months
NMDA RECEPTOR ANTAGONISTS
NMDA receptors involved in central sensitisation
and wind up long term potentiation of pain
ASA RECOMMENDS:
dextromethorphan
and
memantine
are
equivocal regarding pain relief for patients with
diabetic neuropathy, postherpetic neuralgia, or
other neuropathic pain conditions (phantom
limb pain, peripheral nerve injury, and CRPS)
provide pain relief for neuropathic pain for
assessment periods ranging from 2 to 16 weeks
TOPICAL AGENTS
many chronic pain syndromes depend to some
degree on peripheral activation of primary afferent
neurons
Localized administration can potentially optimize
drug concentrations at site of pain generation while
avoiding high plasma levels, systemic side effects,
drug interactions, and need to titrate doses into
therapeutic range
Topical NSAIDs are effective for a limited period
(2 weeks) for chronic musculoskeletal pain
Local adverse effects included rash and pruritus
topical tricyclic antidepressant (doxepin) has
shown efficacy in mixed group of patients with
neuropathic pain and, as a mouthwash, in patients
with chemotherapy-induced oral mucositis
Topically applied capsaicin interacts with
nociceptive neurons via the vanilloid receptor
(TRPV1)
after repeated application depletion of substance
P in sensory neurons, direct neurotoxic effect
that results in degeneration of small-diameter
sensory nerve fibers
supplement for treatment of neuropathic pain in
a small number of patients unresponsive to or
intolerant of other therapeutic approaches
Topical formulations of local anesthetics block Na+
channels in primary afferent neurons,reduces
impulse generation in both normal and damaged
sensory neurons
 Such neurons exhibit spontaneous and ectopic
firing, which possibly contributes to certain
conditions of chronic neuropathic pain
pain relief can be achieved with local anesthetic
concentrations below those that totally block
conduction of impulses
lidocaine patches and gels showed pain reduction
in patients with postherpetic neuralgia and
allodynia
patients with painful diabetic polyneuropathy,
CRPS, postmastectomy syndrome, or postthoracotomy syndrome can achieve relief of pain
Topically applied or locally injected opioids
produce analgesia by activating opioid receptors
on primary afferent neurons
upregulation and accelerated centrifugal
transport of opioid receptors in sensory neurons
and facilitation of access of opioid agonists to
their receptors by disruption of the perineural
barrier
Intra-articular morphine produces analgesia in
chronic rheumatoid and osteoarthritis
OTHER ANALGESICS
Baclofen activates GABAB receptors
presynaptically and postsynaptically, leads to
decrease in excitatory and an increase in inhibitory
neurotransmission
trigeminal neuralgia and central neuropathic pain
 side effects are drowsiness, dizziness, and
gastrointestinal distress
Botulinum toxin is assumed to inhibit release of
acetylcholine at neuromuscular junction ,alleviate
muscle spasticity
Side effects include pain and erythema at the
injection site and unintended paralysis of adjacent
muscles