7.3 Chronic Pain Flashcards
Definitions of some chronic pain states
Allodynia
Allodynia
Pain due to a stimulus which
does not normally provoke pain
Dysaesthesia
Dysaesthesia
An unpleasant abnormal sensation,
whether spontaneous or evoked
Hyperaesthesia I
Hyperaesthesia
Increased sensitivity to stimulation, excluding the special senses
Hyperalgesia
Hyperalgesia
An increased response to a stimulus which is normally painful
may be caused by damage to nociceptors or peripheral nerves
Primary hyperalgesia
what is it
how does it occur
Primary hyperalgesia
describes pain sensitivity that occurs
directly in the damaged tissues.
This occurs by peripheral sensitisation whereby
nociceptors exhibit reduction in threshold and an increase in responsiveness
Secondary hyperalgesia
what is it
How does it occur
Secondary hyperalgesia
describes pain sensitivity that occurs in
surrounding or distant undamaged tissues.
This is a result of central sensitisation
wherein there is an increase in the excitability of
neurons within the central nervous system, so that normal inputs begin to produce abnormal responses
Mechanisms involved in hyperalgesia
Peripheral sensitisation
Abnormal nociceptor sensitivity
Spontaneous neuronal activity
and axonal sprouting
Inflammatory mediator-induced
excitation of nociceptors
Sympathetically mediated pain
Mechanisms involved in hyperalgesia
Central sensitisation
Short-term homosynaptic potentiation
(wind-up)
Long-term homosynaptic potentiation
(through NMDA and AMPA receptors)
Changes in synaptic architecture
Loss of inhibition
Pain scales for assessment of chronic pain
Global Impression Of Change Scale
Brief Pain Inventory
Short Form – 36 Physical Function Scale
Roland Morris Questionnaire
Health Assessment Questionnaire
Brief Pain Inventory
Brief Pain Inventory
Worst, best and present pain intensity
Short Form – 36 Physical Function Scale
Short Form – 36 Physical Function Scale
General measure that is
intended to capture quality of life as well as
whether an individual is healthy or not
Global Impression Of Change Scale
Global Impression Of Change Scale
Completed by both the patient
and the
clinician
Roland Morris Questionnaire
Roland Morris Questionnaire
Back/leg pain
Health Assessment Questionnaire
Health Assessment Questionnaire
Difficulty rating of activities
Syndrome-specific pain scales
Galer Neuropathic Pain Score
Oswestry Disability Questionnaire
American College of Rheumatology Response Criteria
Arthritis Impact Measurement Scale
Western Ontario and McMaster Universities (WOMAC) Osteoarthritis Index
Galer Neuropathic Pain Score
Galer Neuropathic Pain Score
For neuropathic pain
Oswestry Disability Questionnaire
Oswestry Disability Questionnaire
For patients with back pain
American College of Rheumatology Response Criteria
American College of Rheumatology Response Criteria
Rheumatoid arthritis
Arthritis Impact Measurement Scale
Arthritis Impact Measurement Scale
Osteoarthritis
Western Ontario and McMaster Universities (WOMAC) Osteoarthritis Index
Western Ontario and McMaster Universities (WOMAC) Osteoarthritis Index
Osteoarthritis
Psychological assessment
McGill Pain Questionnaire
Beck’s Depression Inventory
Sickness Impact Profile
Minnesota Multiphasic Personality Inventory
McGill Pain Questionnaire
Domains: sensory, affective, evaluative and miscellaneous plus a painintensity five-point scale
Beck’s Depression Inventory
A 21-item self-rating scale that measures the severity of key symptoms associated with clinical depression but not with other psychological factors aggravating pain
Sickness Impact Profile
It is a general indicator of health status and health-related dysfunction rather than pain Best studied in the population with chronic back pain
Minnesota Multiphasic Personality Inventory
This is a self-administered true–false test
.
The questionnaire consists of 567 items
and
it places patients in one
of four groups:
hypochondriacal,
reactively depressed,
‘somaticisers’
and manipulators
Glutamate receptors
where
activation
Glutamate receptors
(AMPA and NMDA)
have been
identified in spinal cord.
NMDA role chronic pain
Activation of these receptors by
nociceptive inputs from periphery
is involved in development of chronic pain.
Hence, NMDA antagonists
such as ketamine are used to
treat certain chronic pain states.
Wind up phenomena
Central sensitisation
Persistent nociceptive stimulation
of C fibres produces hyperalgesia and
allodynia through wind-up phenomena
and central sensitisation.
Axonal sprouting and neuroma formation
Axonal sprouting and neuroma formation
subsequent to nerve injury exhibit
altered up- regulation of sodium channels,
and down-regulation of potassium channels.
The net result is increased neuronal excitability.
Is there any phenotypic switching
Lastly, sensory Aβ undergo
phenotypic switching to C fibres
and start conducting pain.
Low-back pain
lumbosacral region
arising from the spinal
or paraspinal structures
Sciatica
(radicular leg pain) may accompany low back
pain but is regarded as a separate entity
Is LBP commong
About 50%–80% of adults experience low-back pain.
Most backaches (85%–90%) are simple low-back pain (mechanical back pain) in which no particular pathology exists
Nonmechanical backaches may be due
Nonmechanical backaches may be
due to more serious conditions like
cancer,
infection
or inflammatory arthritis.
Visceral pathologies may also
lead to low back pain.
Causes of low-back pain
Mechanical
Mechanical
Lumbar strain or sprain Degenerative disease Spondylosis Spondylolysis Spondylolisthesis Disc herniation Facet joint arthropathy Spinal stenosis Osteoporosis
Non-mechanical (spinal pathology)
Non-mechanical (spinal pathology)
Tumours
Infection
Arthritis
Back pain ‘Red flag’ signs
‘Red flag’ signs:
non-mechanical pain,
thoracic pain,
history of cancer,
HIV,
weight loss,
structural deformity,
young (< 20 years) or
old
(> 55 years),
recent trauma,
osteoporosis,
night pain and
bladder/bowel dysfunction.
Back pain Imaging:
Imaging: should be done only if the history or clinical examination is
suggestive of non-mechanical back pain
Back pain Management
Management:
mostly early mobilisation and pain relief.
Physiotherapy may be
needed if progress is slow.
A minority will need
further evaluation and management.
spinal disc herniation
affecting the spine due to
tear in the outer,
fibrous ring (annulus fibrosus)
of an intervertebral disc allowing
nucleus pulposus to bulge
out beyond the damaged outer rings
spinal disc herniation
Is severe pain nerve root compression
This tear causes release of inflammatory
chemical mediators which
may directly cause severe pain,
even in the absence of nerve root compression.
spinal disc herniation
result d/t
Commonest sites x2
rare @
They most often result
due to wear and tear,
and occur most frequently at
L4–L5 or L5–S1 levels.
The second most common site is lower cervical (C5–C6 or C6–C7),
while it is uncommon
at thoracic levels.
spinal disc herniation worsened by what positon
The sitting and bending
forward position
(associated with desk jobs)
cause the highest increases
in intradiscal pressures
predisposing to prolapse.
Neurology in a severe lumbar disc prolapse
L2
L2
Hip flexion (iliopsoas)
Groin
Neurology in a severe lumbar disc prolapse
L3
L3
Knee extension (quadriceps)
Anterolateral thigh
Patellar reflex lost
Neurology in a severe lumbar disc prolapse
L4
L4
Heel walking (ankle dorsiflexors)
Medial ankle
Patellar reflex lost
Neurology in a severe lumbar disc prolapse
L5
L5
First-toe dorsiflexion
Dorsum of foot
Neurology in a severe lumbar disc prolapse
S1
S1
Toe walking
(ankle plantar flexors)
Lateral foot surface
Ankle reflex lost
Neurology in a severe lumbar disc prolapse
Cauda equina
Cauda equina
Ankle weakness
Lax anal sphincter
Paresthesia of leg and perineum
Ankle reflex lost
Neurology in a severe cervical disc prolapse
C5
C5
Arm abduction (deltoid) and elbow flexion (biceps)
Shoulder area and outer
upper arm
Biceps
Neurology in a severe cervical disc prolapse
C6
C6
Elbow flexion (biceps) Wrist extension
Index finger
Brachioradialis
Neurology in a severe cervical disc prolapse
C7
C7
Elbow extension (triceps)
Wrist flexion
Finger extension
Middle finger
Triceps
Neurology in a severe cervical disc prolapse
C8
C8
Finger flexion and adduction
Little finger
Neurology in a severe cervical disc prolapse
T1
T1
Finger abduction
Lateral epicondyle
Regarding lumbar facet arthropathy
causes 15%–40% of cases of low-back pain
due to dysfunction or
inflammation of the facet
(zygapophyseal) joints
facet (zygapophyseal) joints
What makes up the joint
These joints are formed by the articulation
of the articular processes of
the adjacent vertebrae.
They are innervated by
two medial branches of the
dorsal rami of the
corresponding spinal nerves
Facet joint pain
Describe pain
The patient complains of
deep,
achy,
non-specific low-back pain
localised over the affected facet joint.
Facet joint pain
Radiation?
Radiation to the thigh is possible, but radiation
distal to the knee is uncommon.
Facet joint pain
worsened by
The pain is worse with
lumbar extension,
extensive walking
or
sitting for long periods of time.
The bowel and bladder
are not involved.
Facet joint pain
examination
palpation
changes
On examination,
there is pain with deep palpation over
the affected facet joint.
Paraspinal muscle spasm,
loss of lumbar lordosis and
limited extension of spine may be noted.
Facet joint pain
Diagnosis
However,
historic or physical examination findings
cannot reliably diagnose
lumbar zygapophyesal joint pain.
The most accepted method for
diagnosing pain arising from the
lumbar facet joints is
with low-volume intra-articular
injections or medial branch blocks.
Diagnostic blocks
Diagnostic blocks use
only local anaesthetics,
and analgesics (opioids) for
sedation must be avoided.
Lumbar spinal stenosis
mcq bit about walking
Walking uphill is easier than walking on a flat surface
Lumbar spinal stenosis is the
Lumbar spinal stenosis is the
narrowing of the spinal canal
(transforaminal canal),
resulting in nerve compression
of the spinal roots laterally
Lumbar spinal stenosis
Affects usually
symptoms
It usually affects middle-age patients (> 55 years).
Symptom include
leg pain,
weakness,
paraesthesia and
radicular pain
of the involved
spinal root.
Is it the same as intermittent claudication
similar to vascular claudication,
but different in many respects,
hence it is called pseudoclaudication
or neurogenic claudication
Types of claudication and factors affecting them
Neurogenic claudication Vascular claudication
Aggravating factors
Aggravating factors
Neuro - Extension of spine: standing walking hyperextension of spine
IC
Any leg exercise
Types of claudication and factors affecting them
Neurogenic claudication Vascular claudication
Relieving factors
Relieving factors
Neuro Flexion of spine: squatting/sitting bending forward when sitting walking uphill rather than on flat level lying on side rather than on back easier to cycle than to walk
IC
Rest
Types of claudication and factors affecting them
Neurogenic claudication Vascular claudication
Other features
Other features
Pulse:
usually normal
Skin changes:
usually absent
Autonomic disturbances:
rare
IC
Vascular changes:
blood pressure decreased
peripheral pulses weak or absent
bruits or murmurs
Skin changes:
pallor
cyanosis
nail dystrophy
Autonomic:
impotence
sacroiliac joint pain innervation
sacroiliac joint (SIJ) is innervated
posteriorly by lateral branches
of the dorsal primary rami of
L4–S3 and
sacroiliac joint pain innervation
anteriorly by lateral branches
of the dorsal primary rami of
L2–S2.
sacroiliac joint pain
SIJ pain accounts for 16%–30% of
cases of chronic
mechanical low-back pain.
SIJ pain mainly involve
a/w any conditions?
SIJ pain mainly involves the buttocks,
although it may be referred to
the thigh, abdomen, groin or legs.
It may also occur with systemic
conditions such as
ankylosing spondylitis,
Crohn’s disease
and gout
SIJ pain exacerbating / relieving
pain is worse in the morning
and can be
exacerbated by spine flexion,
prolonged sitting and
weight bearing on the painful limb.
Symptoms may be relieved by
flexing the affected leg and weight
bearing on the contralateral leg.
SIJ Pain
Provocative manoeuvre to help distinguise
is it imaged?
Different provocative manoeuvres
help distinguish this condition from
others causing low back pain.
Most commonly used is the FABER
(flexion, abduction, external rotation, and extension of the hip to create a figure of four: elicits pain) Patrick test.
This is used to increase
the predictive value and
establish the diagnosis.
Radiological imaging
is used mainly to exclude red flags.
Lasègue’s sign is not seen in SIJ pain
SIJ Pain
Treatment follows a
multidisciplinary approach.
Conservative treatments include
exercise therapy and manipulation
(address gait and posture imbalance).
Intra-articular SJ infiltrations with local
anaesthetic and corticosteroids
have been found to be effective in most studies.
The piriformis is a muscle where
Function
The piriformis is a muscle
in the gluteal region of the lower limb.
The piriformis muscle is part
of the
lateral rotators of the hip
and
it externally rotates the
extended thigh and
abducts the flexed thigh.
piriformis syndrome causes
In about 15% of patients,
the piriformis muscle is split
and
pierced by the two components of sciatic nerve.
At other times,
overuse injury
(common in cyclists, runners,
tennis players, ballet dancers) of
this muscle may cause symptoms.
Piriformis syndrome symptoms
worsened
This causes sciatic compression
and
consequent sciatica
(pain in the distribution
of sciatic nerve).
Pain worsens on squatting, climbing stairs, walking and
prolonged sitting. It is typically unilateral
Piriformis syndrome eponymous tests
Diagnostic tests include:
Pace sign:
pain and weakness on
resisted abduction of flexed thigh in
seated position.
Lasègue’s sign:
pain on flexion, adduction and
internal rotation of hip
in a supine patient.
Freiberg’s sign:
pain on forced internal rotation
of the extended thigh.
Piriformis syndrome Rx
Conservative management comprises
analgesics, stretching exercises and
deep heat using ultrasound.
Fluoroscopy-guided piriformis injections using
local anaesthetics and corticosteroids are effective.
Botulinum toxin injections have shown more effective pain relief.
Surgical release is the last option
intravenous drug infusion therapy
for treatment of neuropathic pain
1 uses lignocaine (Na+ channel blocker),
2
ketamine (NMDA antagonist),
3
magnesium (NMDA antagonist),
4
adenosine (presynaptic antinociception by preventing release of substance P)
5
alfentanil
(opioid)
Phentolamine infusion used for
Phentolamine (α-blocker) infusion is
used as a diagnostic test for
sympathetic mediated pain.
If positive, the patient is
prescribed oral α-
blocker such as doxazocin
Fibromyalgia syndrome
chronic generalised pain and allodynia,
a heightened and painful response to pressure (tender points)
Fibromyalgia syndrome sy
symptoms may
include fatigue, sleep disturbance, joint stiffness, bowel and bladder abnormalities, paraesthesia, depression and anxiety.
Fibromyalgia syndrome sy prevelance
It is estimated to affect
2%–4% of the population
and is more common in females
FM Diagnosis
The American College of Rheumatology
(ACR 1990)
established criteria for the diagnosis of FMS,
including the presence of
tenderness at 11 or more of 18 preselected sites
(tender points).
Additionally, the
Fibromyalgia Impact Questionnaire
is used to assess the impact of
pain on a patient’s life.
FM rx
A multidisciplinary treatment
programme combining behavioural
modification, education and physical training is effective
Post-herpetic neuralgia is a
what is it?
Post-herpetic neuralgia is a
debilitating neuralgia
following an acute
varicella zoster infection
(usually after 6 weeks).
Post-herpetic neuralgia
where
Easy to Rx?
Typically, it is confined to a
dermatomal distribution of the skin.
It is difficult to treat once established.
Hence both childhood vaccination and early, aggressive treatment of acute
herpes zoster infection are vital.
Post-herpetic neuralgia Rx options
1
Since it is a neuropathic pain,
it is treated first with antidepressants
(tricyclic antidepressants like amitryptyline)
followed by anticonvulsants (gabapentin).
2
Opioids may be needed in some
(NSAIDs are rarely useful).
3
Topical local anaesthetics and
capsaicin may also relieve pain.
4
Intrathecal methylprednisolone
with lignocaine as repeated injection
can help where non-interventional therapies fail.
Diabetic neuropathies are thought to result
Diabetic neuropathies are thought to result from
microvascular injury involving vasa nervorum,
and
macrovascular processes of neuronal ischaemia and infarction.
Incidence increases with age,
duration of diabetes
and degree of hyperglycaemia
Diabetic neuropathies Rx
Treatments include:
tight glycemic control
tricyclic antidepressants: amitryptyline
selective norepinephrine reuptake inhibitors: duloxetine
anticonvulsants: gabapentine and pregabalin
analgesics: opioids
topical agents: capsaicin cream and lignocaine patches
selective serotonin reuptake inhibitors (e.g. fluoxetine) have not been
found to be as efficacious.
The neuropathic pain ladder is different from the World Health
The neuropathic pain ladder is different from the World Health
Organization pain ladder (cancer pain).
First line: tricyclic antidepressant or antiepileptic.
Second line: tricyclic antidepressant and antiepileptic.
Third line: strong opioid plus above, ± invasive procedures.
To make the clinical diagnosis of complex regional pain syndrome
(CRPS),
the following criteria (Budapest) must be met
1
Continuing pain, which is disproportionate to any inciting event.
2
Must report at least one symptom in three of the four following categories:
/Must display at least one sign at time of evaluation in two or more of
the following categories
Sensory:
Vasomotor:
Sudomotor/oedema:
Motor/trophic:
There is no other diagnosis that better explains the signs and
symptoms.
CRPS symptoms
sensory
vasomotor
sudomotor
motor
Sensory:
reports of hyperesthesia
and/or allodynia
Vasomotor:
reports of temperature asymmetry
and/or skin colour changes
and/or skin colour asymmetry
Sudomotor/oedema:
reports of oedema and/or sweating changes
and/or
sweating asymmetry
Motor/trophic:
reports of decreased range of motion
and/or motor
Must display at least one sign at time of evaluation in two or more of
the following categories:
Sensory: evidence of hyperalgesia (to pinprick) and/or allodynia (to
light touch and/or temperature sensation and/or deep somatic pressure
and/or joint movement)
Vasomotor: evidence of temperature asymmetry (> 1°C) and/or skin
colour changes and/or asymmetry
Sudomotor/oedema: evidence of oedema and/or sweating changes
and/or sweating asymmetry
Motor/trophic: evidence of decreased range of motion and/or motor
dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair,
nail, skin).
The International Association for the Study in Pain divides CRPS into two types.
The International Association for the Study in Pain divides CRPS into two types.
Type I: formerly known as reflex sympathetic dystrophy, or Sudeck’s atrophy, it does not have demonstrable nerve lesions.
Type II:
formerly called causalgia,
it has evidence of obvious nerve damage.
pathogenesis of CRPS
peripheral
pathogenesis of CRPS may include
1
peripheral mechanisms
such as
a
upregulation of axonal α2 adrenoceptors,
rendering them sensitive to catecholamines
(hence the term ‘sympathetically mediated pain’)
and
b
denervation hypersensitivity.
pathogenesis of CRPS may include central
Central mechanisms such as wind-up and
central sensitisation play an important role.
Risk factors for the development
of CRPS
include previous trauma, nerve injury, previous surgery, workrelated injury and female sex.
CRPS mainstay of management.
Physical therapy is the mainstay of management.
However, pain precludes this, hence pain relief becomes vital to achieve movement.
CRPS Rx sympathetic pain
Sympatholysis using
intravenous regional anaesthesia
(lignocaine, guanethidine or bretylium)
or sympathetic ganglion blocks are
commonly employed to
address sympathetically mediated pain.
Surgical
resection and radiofrequency ablation of ganglia have also been tried.
Three phenomena occur after amputation
Phantom sensation (non-painful paraesthesias) Stump pain (pain in the stump of the amputated limb) Phantom pain (pain in the amputated limb).
Salient features of phantom pain:
Salient features of phantom pain:
Incidence is up to 75% of amputees.
May start immediately but usually starts within first week after amputation.
Most complain of intermittent pain (few days in a month).
phantom pain type
pathogenesis
Pain may be
shooting, cramping, burning or aching in nature.
Pathogenesis may be related
to spinal and cortical reorganisation of neurons.
phantom pain RF
Risk factors for
development of phantom pain
are pre-amputation pain, persistent stump pain, bilateral amputations and lower-limb amputations.
Gender and age are not known risk factors.
Phantom pain RF
Pharm
Pharmacological treatment
includes
antidepressants,
antiepileptics and
analgesics.
Nonpharmacological Phantom Pain
Nonpharmacological methods
include
TENS,
spinal cord stimulation and
biofeedback.
Recently
‘Ramachandran mirror box’
therapy has been used to
alleviate painful spasms of phantom limb.
Note: pre-emptive regional anaesthesia has not been shown to reduce the
incidence of phantom limb pain
In transcutaneous electrical nerve stimulation (TENS)
Theory
Melzack and Wall proposed
that the transmission of
noxious information (C fibre)
could be inhibited by
activity in large-diameter
peripheral afferents (Aβ fibre)
(gate control theory of pain).
In transcutaneous electrical nerve stimulation (TENS),
In transcutaneous electrical nerve stimulation (TENS),
electric current produced by a
device is used to
stimulate the nerves for therapeutic purposes
(analgesia).
Two types of TENS are used.
Conventional TENS
Pulsed TENS
Conventional TENS
Low intensity, high frequency
Mainly for nociceptive pain
Perceived as a paraesthesia
Relieves pain by a segmental
mechanism
Pulsed TENS
High intensity, low frequency
Mainly for neuropathic pain
Perceived as a muscle twitch
Works by activating
extra segmental descending
inhibitory pain pathways
Indications TENS
Indications include
acute post-operative pain, labour pain, angina, dysmenorrhoea and chronic pain states
Contraindications TENS
Contraindications include
cardiac pacemakers (interference),
pregnancy (can stimulate uterine contractions),
bleeding diathesis and
epilepsy (may induce seizures).
Acupuncture theory
Acupuncture is a
complementary therapy that originated in China.
It assumes that health is achieved by maintaining a ‘balanced state’ of the body, and that disease is the result of an internal imbalance.
This imbalance
leads to blockage in the flow of
qi (vital energy) along pathways known as
meridians.
Acupuncture proposed MOA
Needling increases the
cerebrospinal fluid concentrations of the
endogenous opioids.
This may be the reason for the analgesia obtained.
Acupuncture uses
Acupuncture has been found to be
effective for osteoarthritis,
chronic neck pain,
low-back pain,
and postoperative nausea and vomiting.
However, it is not more
effective than other conventional therapies
Spinal cord stimulation (SCS) what is it
Spinal cord stimulation (SCS) is
the technique of stimulation of large sensory fibres (Aβ) in dorsal column tracts
to mask the pain carried by
spinothalamic tracts
(based on the gate control theory of pain).
However, it may not be the only mechanism.
Spinal cord stimulation (SCS) permanent?
It is not destructive,
unlike cordotomy,
and is reversible
Major indications for SCS
Major indications for SCS are
neuropathic states like failed back surgery
(United States)
and
ischaemic pain (Europe).
Non responsive to SCS
Poor candidates?
Nociceptive pain
does not respond to SCS.
Major psychiatric issues,
drug-seeking behaviour,
cardiac pacemakers and
patients with secondary gain
are poor candidates for
this technique.
Intrathecal drug delivery systems for who
Intrathecal drug delivery systems (IDDSs)
are good options for patients who have
ineffective pain relief at
acceptable oral or transdermal doses,
or
for those who have intolerable side effects.
Intrathecal drug delivery systems commonest indications
1. Cancer pain (most common),
2.
chronic non-malignant pain
- spasticity
are three main
indications for IDDSs.
IDDS Gold standard
also used
Morphine is the gold-standard drug used for this.
Apart from opioids, clonidine (α2 blocker), ziconitide (Ca+ channel blocker) and local anaesthetics (Na+ channel blocker) are also used.
IDDS 1st line
second ine
First-line drugs
include morphine, hydromorphone and ziconitide, whereas fentanyl, clonidine
and local anaesthetics are second-line agents.
Tolerance and opioid-induced hyperalgesia result from
Tolerance and opioid-induced hyperalgesia result
from opioid therapy,
but are caused by
two distinct mechanisms.
Opioid-induced hyperalgesia (OIH)
Opioid-induced hyperalgesia (OIH) is a phenomenon associated with the
long-term use of opioids.
Over time, individuals develop an
increasing sensitivity to noxious stimuli (hyperalgesia),
such that a non-noxious stimulus
evokes a painful response (allodynia).
Mechanisms involved in OIH
Mechanisms involved in OIH are:
spinal NMDA activation,
spinal dynorphin release (KOP agonist)
and facilitation of descending
inhibitory pathways
OIH Rx options
Treatment options include:
reduction of opioid dose
opioid rotation to
methadone or buprenorphine (KOP antagonist)
NMDA antagonists (ketamine).
In tolerance,
In tolerance,
increasing the dose of opioid
can overcome it,
but doing
so in opioid-induced hyperalgesia
may worsen the patient’s condition
by inducing hyperalgesia
while increasing physical dependence.
Tolerance v Pseudotolerance
important to make a
clinical distinction between
1 tolerance (reduction in effect needing an increase of opioid dose to maintain pain relief)
vs
2 pseudotolerance (request of more opioids by patient as the prevalent dose is insufficient for treating the pain).
Difference between opioid tolerance and opioid-induced hyperalgesia
Opioid tolerance
Due to decreased analgesic potency
Down-regulation of anti-nociceptive system Up-regulation of pro-Rightward shift of dose-response curve
Responds to dose increase
Sensory testing reveals no hyperalgesia
Opioid-induced hyperalgesia
Opioid-induced hyperalgesia
Due to increased sensitivity (hyperalgesia)
Up regulation of pro nociceptive system
Downward shift of dose response curve
Sensory testing reveals hyperalgesia
Risk factors for the development of chronic post-surgical pain (CPSP)
are:
1
Age: decreasing incidence with increasing age
2
Preoperative attitude: fear, anxiety or depression
3
Preoperative pain: higher incidence of CPSP
4
Operative technique: invasive and longer surgeries are more associated with CPSP than shorter non-invasive (laparoscopic) procedures
5
Genetic factors
6
Severe acute post-surgical pain
7
Anaesthesia technique:
none shown to be superior, but emphasis is
on multimodal analgesia with good pain relief provision for subacute post-operative pain as well.
