7.1 Acute Pain Flashcards

1
Q

Pain is defined

A

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’
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2
Q

Is pain a simple issue

A

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.

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3
Q

assessing acute pain

A

Verbal category rating scale

Visual analogue scale

Numerical rating scale

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4
Q

Verbal category rating scale

A

Verbal category rating scale

None, mild, moderate, severe, unbearable or 1–5

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5
Q

Visual analogue scale

A

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

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6
Q

Numerical rating scale

A

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)

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7
Q

Pain questionnaires:

A

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
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8
Q

Simple pain rating scales

Advantages

A

Simple and easy for the patient
Robust and reproducible
Rapidly recorded
Useful for audit

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9
Q

Simple pain rating scales

Disadvantages

A

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)

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10
Q

Nociceptive or pain pathway what type of pathway

A

Nociceptive or pain pathway is an
afferent pathway involving

Three neurons

Two pathways:

Modulation

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11
Q

Three neurons

A

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.

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12
Q

Two pathways:

A

Two pathways:

Dorsal column–medial lemniscus pathway
(touch and proprioception)

Anterolateral spinothalamic tract
(pain and temperature).

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13
Q

Modulation

A

Modulation

Spinal: most common and at dorsal horn of spinal cord

Supraspinal centres.

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14
Q

Pain processing involves:

A

Pain processing involves:

Transduction

Transmission

Modulation

Perception

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15
Q

Transduction:

A

Transduction:

conversion of noxious stimuli into action potentials.

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16
Q

Transmission

A

Transmission:

conduction of action potential through neurons

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17
Q

Modulation:

A

Modulation:

augmentation or attenuation of afferent transmission.

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18
Q

Perception

A

Perception:
sensory and affective by integration of inputs in the
somatosensory cortex and limbic system.

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19
Q

FIGURE 7.1 Steps involved in pain processing pathways

A

FIGURE 7.1 Steps involved in pain processing pathways

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20
Q

Excitatory neurotransmitters

A

Excitatory neurotransmitters –

glutamate, 
substance P, 
calcitonin gene–related peptide, 
neurokinins, 
histamine, 
serotonin, 
bradykinins,
prostaglandins and so forth.
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21
Q

Inhibitory neurotransmitters

A

Inhibitory neurotransmitters –

in descending modulation system:

Cerebral – GABA, noradrenaline and serotonin

Spinal – GABA and glycine

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22
Q

The gate control theory was presented by

explain

A

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

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23
Q

It states that pain is a function of

A

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).

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24
Q

Gate theory and Ab fibres

how does this affect pain

A

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.

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25
‘gate control’ theory of pain
It explains why local rubbing eases the pain
26
Descending pain-modulation pathways most important part
Periaqueductal grey
27
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
28
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
29
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.
30
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.
31
Fentanyl - | does it undergo ion trapping
Ionised fraction binds to non-receptor sites (epidural fat, myelin and white matter) resulting in ‘ion trapping’ there.
32
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
33
Pro and Con of ion trapping
This limits the cephalad spread, limiting segmental analgesia, but offers lower chances of late respiratory depression
34
Intrathecal morphine duration lipophilic v hydrophilic?
Intrathecal morphine (acts up to 12 hours) More hydrophilic, hence limited diffusion to non-receptor-binding sites
35
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).
36
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.
37
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.
38
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
39
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.
40
Stress of surgery leads what type of response
Stress of surgery leads catabolic response | while suppressing the anabolic response
41
Stress of surgery leads suppression of
anabolic mediators is | suppressed (insulin and testosterone).
42
Stress of surgery leads release of
Hence all the catabolic mediators are released ``` cortisol, adrenocorticotropic hormone, catecholamines, growth hormone, antidiuretic hormone, glucagon, aldosterone ```
43
Stress of surgery leads to net effect
This leads to hyperglycaemia, protein catabolism, lipolysis and ketogenesis, and water retention by body
44
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.
45
Pre-emptive analgesia theory
Theoretically was based on the idea that preventing nociception early on would reduce central sensitisation and receptive-field expansion
46
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
47
Pre-emptive analgesia currently being looked at
‘Anti-hyperalgesics’ like NMDA antagonists and gabapentin are being evaluated for this role.
48
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 ```
49
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. ```
50
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
51
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
52
Management of perioperative pain in an opioid-dependent patient Transdermal patches?
Transdermal patches can be left as such unless the surgery is major.
53
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.
54
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. ```
55
Management of perioperative pain in an opioid-dependent patient opioid rotation?
Opioid rotation may reduce | doses needed by 50% in such instances
56
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.
57
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.
58
Management of perioperative pain in an opioid-dependent patient PCA?
PCA subsequently best managed with basal infusion, with incremental bolus for breakthrough pain
59
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.
60
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