7.1 Acute Pain Flashcards
Pain is defined
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’
Is pain a simple issue
It is a
multifaceted issue,
having sensory and
affective (emotional) component.
Hence objective assessment of pain is difficult. Therefore, pain rating scores
or questionnaires are often used.
assessing acute pain
Verbal category rating scale
Visual analogue scale
Numerical rating scale
Verbal category rating scale
Verbal category rating scale
None, mild, moderate, severe, unbearable or 1–5
Visual analogue scale
Visual analogue scale
10-cm line with anchor points of
‘no pain’ and ‘worst pain imaginable’ at either end;
most common simple scale used in pain research
Numerical rating scale
Numerical rating scale
Similar to a visual analogue scale,
with the two anchors of ‘no pain’ and ‘worst pain
imaginable’,
but has numbers across the scale from 0 to 10
(making an 11-point scale)
Pain questionnaires:
Pain questionnaires:
multidimensional and
more common in chronic pain settings
McGill Pain Questionnaire, Brief Pain Inventory, The Memorial Pain Assessment Card, Neuropathic Pain Scale, Pain diary and so forth
Simple pain rating scales
Advantages
Simple and easy for the patient
Robust and reproducible
Rapidly recorded
Useful for audit
Simple pain rating scales
Disadvantages
Unable to detect subtle differences
Less suitable for research (semiqualitative)
Not suitable for parametric tests
Non-parametric tests must be used (larger samples)
Response can vary
(in same and among different patients)
Subjective measures (inaccurate)
Nociceptive or pain pathway what type of pathway
Nociceptive or pain pathway is an
afferent pathway involving
Three neurons
Two pathways:
Modulation
Three neurons
First order:
peripheral pain fibres (Aδ and C)
Second order:
nociceptive specific neurons
(Lamina I, II) and
wide dynamic range neurons
(WDR respond to both nociceptive and
innocuous pain; lamina III–VI)
Third order:
thalamic projections to somatosensory cortex.
Two pathways:
Two pathways:
Dorsal column–medial lemniscus pathway
(touch and proprioception)
Anterolateral spinothalamic tract
(pain and temperature).
Modulation
Modulation
Spinal: most common and at dorsal horn of spinal cord
Supraspinal centres.
Pain processing involves:
Pain processing involves:
Transduction
Transmission
Modulation
Perception
Transduction:
Transduction:
conversion of noxious stimuli into action potentials.
Transmission
Transmission:
conduction of action potential through neurons
Modulation:
Modulation:
augmentation or attenuation of afferent transmission.
Perception
Perception:
sensory and affective by integration of inputs in the
somatosensory cortex and limbic system.
FIGURE 7.1 Steps involved in pain processing pathways
FIGURE 7.1 Steps involved in pain processing pathways
Excitatory neurotransmitters
Excitatory neurotransmitters –
glutamate, substance P, calcitonin gene–related peptide, neurokinins, histamine, serotonin, bradykinins, prostaglandins and so forth.
Inhibitory neurotransmitters
Inhibitory neurotransmitters –
in descending modulation system:
Cerebral – GABA, noradrenaline and serotonin
Spinal – GABA and glycine
The gate control theory was presented by
explain
The gate control theory was presented
by Wall and Melzack (1965) to
explain factors
influencing pain perception.
It states that pain is a function of
It states that pain is a function of
It states that pain is a function of
the balance between the
information through
large nerve fibres (Aβ) and
that through small nerve fibres (C).
Gate theory and Ab fibres
how does this affect pain
The collaterals of the large sensory
fibers (Aβ) carrying cutaneous
sensory input
activate inhibitory interneurons,
which inhibit (modulate)
pain-transmission information
carried by the small pain fibres (C)
transcutaneous electrical nerve stimulation is a clinical application of
this theory.
‘gate control’ theory of pain
It explains why local rubbing eases the pain
Descending pain-modulation pathways
most important part
Periaqueductal grey
Descending pain-modulation pathways detail
Neurons from where
alter where
Descending pain-modulation pathways:
pain-modulating neurons
from
1
midbrain periaqueductal grey
and
2
rostral ventral medulla
alter nociception in the
3
dorsal horn of the spinal cord
through inhibition of interneurons
Descending pain
Pathways
+neurochem
what other neurochem involved
This includes the
noradrenergic locus coeruleus pathway
and the
serotoninergic raphe magnus nuclei pathway.
It also involves
endogenous opioid release
What drugs acts at the above descending pathways
this is the site of action for
tramadol,
which inhibits
norepinephrine and
serotonin reuptake inhibition,
mediating analgesia.
Tricyclic antidepressants
are also non-selective reuptake inhibitors,
hence valuable in chronic pain
management.
Intrathecal fentanyl
duration
lipophilic or hydrophilic
pka?
union?
(acts up to 3 hours)
More lipophilic but has high pKa of 8.4,
resulting in 8% unionised fraction.
Fentanyl -
does it undergo ion trapping
Ionised fraction
binds to non-receptor sites
(epidural fat,
myelin and
white matter)
resulting in ‘ion trapping’ there.
Is there much cephalad spread of fentanyl?
what mechanism affects this
Fentanyl undergoes ion trapping by
binding to non-receptor sites,
reducing the unionised fraction
available for diffusion to receptor site
Lower amount of unionised fraction
is available for action by binding
to receptor sites in grey matter
Hence, cerebrospinal fluid (CSF)
concentration falls rapidly, while
epidural and plasma levels rise rapidly.
This limits the cephalad spread,
limiting segmental analgesia,
but offers lower chances of late respiratory depression
Pro and Con of ion trapping
This limits the cephalad spread,
limiting segmental analgesia,
but offers lower chances of late respiratory depression
Intrathecal morphine
duration
lipophilic v hydrophilic?
Intrathecal morphine
(acts up to 12 hours)
More hydrophilic,
hence limited diffusion
to non-receptor-binding sites
Cephalad spread?
why
pro and con
Means more is available
within the CSF for cephalad spread,
hence greater segmental spread
and
more chances of late respiratory depression.
It is unsuitable for day-case surgery
for the same reason,
although it provides considerable
duration of analgesia (12 hours).
Intrathecal diamorphine
duration
Is it like morphine or fentanyl
Intrathecal diamorphine
(acts for 6 hours)
Up to 34% unionised drug
available for binding to receptor sites.
Characteristics intermediate between
fentanyl and morphine.
Diamorphine well suited for which surgery
Ideal for intraoperative and
post-operative analgesia for
lower segment Caesarean section.
It is unlicensed for intrathecal use
but is commonly used.
Ethnic differences in pain perception and response:
Patient ethnicity
Patient ethnicity
affects pain perception
and pain responses to analgesics.
In review of 250 consecutive patients
hospitalised for
open reduction and internal fixation
of a limb fracture,
analgesic consumption was found to be
more in whites than blacks,
while Asians needed the least
Ethnic minorities are at a higher risk of inadequate pain control
Ethnicity of the clinician important role?
Ethnicity of the clinician also has an
important role in both pain
prescriptions and responses to pain relief
Sharing a language with caregivers improves analgesic care.
Stress of surgery leads
what type of response
Stress of surgery leads catabolic response
while suppressing the anabolic response
Stress of surgery leads
suppression of
anabolic mediators is
suppressed (insulin and testosterone).
Stress of surgery leads
release of
Hence all the catabolic mediators are released
cortisol, adrenocorticotropic hormone, catecholamines, growth hormone, antidiuretic hormone, glucagon, aldosterone
Stress of surgery leads to net effect
This leads to
hyperglycaemia,
protein catabolism,
lipolysis
and
ketogenesis,
and water retention by body
Pre-emptive analgesia is
presented and then developed by
delivering analgesics before painful
stimulus (surgical incision).
presented by Crile (1913) and subsequently
developed by
Wall and Woolf.
Pre-emptive analgesia theory
Theoretically was based on the idea
that preventing nociception
early on would
reduce central sensitisation
and receptive-field expansion
Pre-emptive analgesia theory borne out in trials?
However, most trials have
not confirmed the
promising principles of pre-emptive analgesia.
At most, it may reduce
acute post-operative pain,
while others have not found
any benefit for prevention of
development of chronic pain following surgery
Pre-emptive analgesia currently being looked at
‘Anti-hyperalgesics’ like
NMDA antagonists and
gabapentin
are being
evaluated for this role.
Pre-emptive analgesia just pre op meds?
Many have suggested that to be maximally effective, analgesics should be started before surgical incision, continue through the surgery and into the post-operative period until wound healing
Regarding the World Health Organization pain ladder
It is a three-step ladder. (originally)
1
Non-steroidal anti-inflammatory drugs and other non-opioids
(paracetamol) used as first step.
2 Weak opioids (codeine and tramadol) added next.
3 Strong opioids (morphine) are reserved for severe pain.
Regarding the World Health Organization pain ladder
PRN v Reg
Sedatives?
Medications should be given
regularly than on a per-need basis.
Sedatives may be given to reduce pain-related anxiety
Management of perioperative
pain in an opioid-dependent patient
Preoperative
Preoperative
1
Identifying 24-hour opioid dose needed.
2
Liaising with chronic pain services
and planning analgesia.
3
Discussions with patient and reassuring them.
4
Patients should continue their oral opioids in usual doses perioperatively
Management of perioperative
pain in an opioid-dependent patient
Transdermal patches?
Transdermal patches can be left as such unless the surgery is major.
Management of perioperative
pain in an opioid-dependent patient
agonist/antagonist
full antagonist?
Agonist-antagonists
(pentazocine, butorphanol, nalbuphine)
and full antagonists (naloxone and naltrexone)
should be avoided to prevent withdrawal.
Management of perioperative
pain in an opioid-dependent patient
Dose
Higher doses (30%–100%) of opioids used by patients may be needed due to tolerance.
Management of perioperative
pain in an opioid-dependent patient
opioid rotation?
Opioid rotation may reduce
doses needed by 50% in such instances
Management of perioperative
pain in an opioid-dependent patient
Assessing pain towards end of surgery
Neuromuscular reversal
towards the end of the surgery
allows assessment of respiratory rate.
Titration of doses to allow a rate of
12– 14 breaths per minute (in adult)
is an effective way of providing
pain relief.
Management of perioperative
pain in an opioid-dependent patient
immmed px relief
Intravenous opioids on an ‘as per needed’ basis to address initial pain
relief.
Management of perioperative
pain in an opioid-dependent patient
PCA?
PCA subsequently best managed with
basal infusion, with
incremental bolus for breakthrough pain
Management of perioperative
pain in an opioid-dependent patient
how reduce opioid?
Regular non-opioid analgesics
added for opioid sparing if possible.
Regional anaesthesia techniques
help in reducing analgesic
requirements.
Management of perioperative
pain in an opioid-dependent patient
IT + PO
Watch out for risk of respiratory depression in patients receiving
intrathecal and parenteral opioids
