7.3 Chronic Pain Flashcards
(136 cards)
1
Q
Definitions of some chronic pain states
Allodynia
A
Allodynia
Pain due to a stimulus which
does not normally provoke pain
2
Q
Dysaesthesia
A
Dysaesthesia
An unpleasant abnormal sensation,
whether spontaneous or evoked
3
Q
Hyperaesthesia I
A
Hyperaesthesia
Increased sensitivity to stimulation, excluding the special senses
4
Q
Hyperalgesia
A
Hyperalgesia
An increased response to a stimulus which is normally painful
may be caused by damage to nociceptors or peripheral nerves
5
Q
Primary hyperalgesia
what is it
how does it occur
A
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
6
Q
Secondary hyperalgesia
what is it
How does it occur
A
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
7
Q
Mechanisms involved in hyperalgesia
Peripheral sensitisation
A
Abnormal nociceptor sensitivity
Spontaneous neuronal activity
and axonal sprouting
Inflammatory mediator-induced
excitation of nociceptors
Sympathetically mediated pain
8
Q
Mechanisms involved in hyperalgesia
Central sensitisation
A
Short-term homosynaptic potentiation
(wind-up)
Long-term homosynaptic potentiation
(through NMDA and AMPA receptors)
Changes in synaptic architecture
Loss of inhibition
9
Q
Pain scales for assessment of chronic pain
A
Global Impression Of Change Scale
Brief Pain Inventory
Short Form – 36 Physical Function Scale
Roland Morris Questionnaire
Health Assessment Questionnaire
10
Q
Brief Pain Inventory
A
Brief Pain Inventory
Worst, best and present pain intensity
11
Q
Short Form – 36 Physical Function Scale
A
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
12
Q
Global Impression Of Change Scale
A
Global Impression Of Change Scale
Completed by both the patient
and the
clinician
13
Q
Roland Morris Questionnaire
A
Roland Morris Questionnaire
Back/leg pain
14
Q
Health Assessment Questionnaire
A
Health Assessment Questionnaire
Difficulty rating of activities
15
Q
Syndrome-specific pain scales
A
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
16
Q
Galer Neuropathic Pain Score
A
Galer Neuropathic Pain Score
For neuropathic pain
17
Q
Oswestry Disability Questionnaire
A
Oswestry Disability Questionnaire
For patients with back pain
18
Q
American College of Rheumatology Response Criteria
A
American College of Rheumatology Response Criteria
Rheumatoid arthritis
19
Q
Arthritis Impact Measurement Scale
A
Arthritis Impact Measurement Scale
Osteoarthritis
20
Q
Western Ontario and McMaster Universities (WOMAC) Osteoarthritis Index
A
Western Ontario and McMaster Universities (WOMAC) Osteoarthritis Index
Osteoarthritis
21
Q
Psychological assessment
A
McGill Pain Questionnaire
Beck’s Depression Inventory
Sickness Impact Profile
Minnesota Multiphasic Personality Inventory
22
Q
McGill Pain Questionnaire
A
Domains: sensory, affective, evaluative and miscellaneous plus a painintensity five-point scale
23
Q
Beck’s Depression Inventory
A
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
24
Q
Sickness Impact Profile
A
It is a general indicator of health status and health-related dysfunction rather than pain Best studied in the population with chronic back pain
25
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
26
Glutamate receptors
where
activation
Glutamate receptors
(AMPA and NMDA)
have been
identified in spinal cord.
27
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.
28
Wind up phenomena
| Central sensitisation
Persistent nociceptive stimulation
of C fibres produces hyperalgesia and
allodynia through wind-up phenomena
and central sensitisation.
29
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.
30
Is there any phenotypic switching
Lastly, sensory Aβ undergo
phenotypic switching to C fibres
and start conducting pain.
31
Low-back pain
lumbosacral region
arising from the spinal
or paraspinal structures
32
Sciatica
(radicular leg pain) may accompany low back
| pain but is regarded as a separate entity
33
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
```
34
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.
35
Causes of low-back pain
Mechanical
Mechanical
```
Lumbar strain or sprain
Degenerative disease
Spondylosis
Spondylolysis
Spondylolisthesis
Disc herniation
Facet joint arthropathy
Spinal stenosis
Osteoporosis
```
36
Non-mechanical (spinal pathology)
Non-mechanical (spinal pathology)
Tumours
Infection
Arthritis
37
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.
38
Back pain Imaging:
Imaging: should be done only if the history or clinical examination is
suggestive of non-mechanical back pain
39
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.
40
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
41
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.
42
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.
43
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.
44
Neurology in a severe lumbar disc prolapse
L2
L2
Hip flexion (iliopsoas)
Groin
45
Neurology in a severe lumbar disc prolapse
L3
L3
Knee extension (quadriceps)
Anterolateral thigh
Patellar reflex lost
46
Neurology in a severe lumbar disc prolapse
L4
L4
```
Heel walking
(ankle dorsiflexors)
```
Medial ankle
Patellar reflex lost
47
Neurology in a severe lumbar disc prolapse
L5
L5
First-toe dorsiflexion
Dorsum of foot
48
Neurology in a severe lumbar disc prolapse
S1
S1
Toe walking
(ankle plantar flexors)
Lateral foot surface
Ankle reflex lost
49
Neurology in a severe lumbar disc prolapse
Cauda equina
Cauda equina
Ankle weakness
Lax anal sphincter
Paresthesia of leg and perineum
Ankle reflex lost
50
Neurology in a severe cervical disc prolapse
C5
C5
```
Arm abduction (deltoid)
and elbow flexion (biceps)
```
Shoulder area and outer
upper arm
Biceps
51
Neurology in a severe cervical disc prolapse
C6
C6
```
Elbow flexion (biceps)
Wrist extension
```
Index finger
Brachioradialis
52
Neurology in a severe cervical disc prolapse
C7
C7
Elbow extension (triceps)
Wrist flexion
Finger extension
Middle finger
Triceps
53
Neurology in a severe cervical disc prolapse
C8
C8
Finger flexion and adduction
Little finger
54
Neurology in a severe cervical disc prolapse
T1
T1
Finger abduction
Lateral epicondyle
55
Regarding lumbar facet arthropathy
causes 15%–40% of cases of low-back pain
due to dysfunction or
inflammation of the facet
(zygapophyseal) joints
56
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
57
Facet joint pain
Describe pain
The patient complains of
deep,
achy,
non-specific low-back pain
localised over the affected facet joint.
58
Facet joint pain
Radiation?
Radiation to the thigh is possible, but radiation
| distal to the knee is uncommon.
59
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.
60
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.
61
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.
62
Diagnostic blocks
Diagnostic blocks use
only local anaesthetics,
and analgesics (opioids) for
sedation must be avoided.
63
Lumbar spinal stenosis
mcq bit about walking
Walking uphill is easier than walking on a flat surface
64
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
65
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.
66
Is it the same as intermittent claudication
similar to vascular claudication,
but different in many respects,
hence it is called pseudoclaudication
or neurogenic claudication
67
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
68
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
69
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
70
sacroiliac joint pain innervation
sacroiliac joint (SIJ) is innervated
posteriorly by lateral branches
of the dorsal primary rami of
L4–S3 and
71
sacroiliac joint pain innervation
anteriorly by lateral branches
of the dorsal primary rami of
L2–S2.
72
sacroiliac joint pain
SIJ pain accounts for 16%–30% of
cases of chronic
mechanical low-back pain.
73
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
74
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.
75
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
76
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.
77
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.
78
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.
79
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
80
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.
81
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
82
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)
83
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
84
Fibromyalgia syndrome
chronic generalised pain and allodynia,
```
a heightened and painful response
to pressure (tender points)
```
85
Fibromyalgia syndrome sy
symptoms may
```
include fatigue,
sleep disturbance,
joint stiffness,
bowel and bladder abnormalities,
paraesthesia,
depression and anxiety.
```
86
Fibromyalgia syndrome sy prevelance
It is estimated to affect
2%–4% of the population
and is more common in females
87
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.
88
FM rx
A multidisciplinary treatment
programme combining behavioural
modification, education and physical training is effective
89
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).
90
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.
91
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.
92
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
93
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.
94
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.
95
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.
96
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
97
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).
98
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.
99
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.
100
pathogenesis of CRPS may include central
Central mechanisms such as wind-up and
| central sensitisation play an important role.
101
Risk factors for the development
| of CRPS
```
include previous trauma,
nerve injury,
previous surgery,
workrelated injury and
female sex.
```
102
CRPS mainstay of management.
Physical therapy is the mainstay of management.
However, pain precludes this, hence pain relief becomes vital to achieve movement.
103
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.
104
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).
```
105
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).
106
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.
107
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.
108
Phantom pain RF
Pharm
Pharmacological treatment
includes
antidepressants,
antiepileptics and
analgesics.
109
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
110
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).
111
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).
112
Two types of TENS are used.
Conventional TENS
Pulsed TENS
113
Conventional TENS
Low intensity, high frequency
Mainly for nociceptive pain
Perceived as a paraesthesia
Relieves pain by a segmental
mechanism
114
Pulsed TENS
High intensity, low frequency
Mainly for neuropathic pain
Perceived as a muscle twitch
Works by activating
extra segmental descending
inhibitory pain pathways
115
Indications TENS
Indications include
```
acute post-operative pain,
labour pain,
angina,
dysmenorrhoea
and chronic pain states
```
116
Contraindications TENS
Contraindications include
cardiac pacemakers (interference),
pregnancy (can stimulate uterine contractions),
bleeding diathesis and
epilepsy (may induce seizures).
117
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.
118
Acupuncture proposed MOA
Needling increases the
cerebrospinal fluid concentrations of the
endogenous opioids.
This may be the reason for the analgesia obtained.
119
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
120
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.
121
Spinal cord stimulation (SCS) permanent?
It is not destructive,
unlike cordotomy,
and is reversible
122
Major indications for SCS
Major indications for SCS are
neuropathic states like failed back surgery
(United States)
and
ischaemic pain (Europe).
123
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.
124
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.
125
Intrathecal drug delivery systems commonest indications
```
1.
Cancer pain (most common),
```
2.
chronic non-malignant pain
3. spasticity
are three main
indications for IDDSs.
126
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.
```
127
IDDS 1st line
second ine
First-line drugs
include morphine, hydromorphone and ziconitide, whereas fentanyl, clonidine
and local anaesthetics are second-line agents.
128
Tolerance and opioid-induced hyperalgesia result from
Tolerance and opioid-induced hyperalgesia result
from opioid therapy,
but are caused by
two distinct mechanisms.
129
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).
130
Mechanisms involved in OIH
Mechanisms involved in OIH are:
spinal NMDA activation,
spinal dynorphin release (KOP agonist)
and facilitation of descending
inhibitory pathways
131
OIH Rx options
Treatment options include:
reduction of opioid dose
opioid rotation to
methadone or buprenorphine (KOP antagonist)
NMDA antagonists (ketamine).
132
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.
133
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).
```
134
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
135
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
136
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.
