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Perioperative pain management Flashcards

1
Q

Define pain

A

Pain is the perception of nociception that occurs in the brain and is determined by memory, emotion, interpretation and genetic influence. Perception of nociception implies a subjective experience and no actual tissue damage needs to be present.

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2
Q

Define nociception

A

The neural process of encoding noxious stimuli

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3
Q

Define acute pain

A

Recent onset and short duration (< 6 weeks)
Trauma | Surgery | Acute illness
Often limited to the area of damage or disease
Resolves with healing

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4
Q

Define chronic pain

A

Pain that is no longer associated with normal tissue healing processes and persists beyond the usual course of an acute illness or injury or beyond normal tissue healing times - inflammatory phase, proliferative phase and remodelling phases usually beyond 3 months.

Chronic pain is not distinguished by its duration but by the inability of the body to achieve normal physiological homeostatic levels.

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5
Q

Compare nociceptive pain, neuropathic pain and nociplastic pain

A

Nociceptive pain: Pain that arises from actual or threatened damage to non-neural tissue and is due to activation of nociceptors

Neuropathic pain: Pain caused by a lesion or disease of the somatosensory nervous system

Nociplastic pain: Pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing activation of peripheral nociceptors or evidence of disease or lesion of the somatosensory system causing the pain

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6
Q

Describe the process of conduction of a pain impulse

A

Potentially harmful thermal | chemical | mechanical stimuli —> free nerve endings (nociceptors) are activated —> A delta (sharp localized pain) and C (delayed, dull, persistent pain) fibres transmit the action potential back to the dorsal horn of the spinal cord.

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7
Q

What are the reflexes involved in neurogenic inflammation. Explain how this process works

A

During AP propagation from the nociceptor along the neuron toward the cell body, the AP is also propagated distally to the dendrites of that branch = axonal reflex

Once the AP reaches the cell body in the dorsal root ganglion, the neuron backfires and send an AP in the reverse direction toward the periheral dendrites = dorsal root reflex

The axon and dorsal root reflexes result in RELEASE of PRO-INFLAMMATORY mediators by the nerve = neurogenic inflammation

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8
Q

List the mediators released by tissue damage and neurogenic inflammation

A

K+ | Substance P | Bradykinin | serotonin |
histamine | Cytokines | Nitric Oxide |
prostaglandins

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9
Q

What clinical neurological symptom related to pain results from tissue and neurogenic inflammation?

A

Primary Hyperalgaesia = Peripheral Sensitization

Hyperalgaesia = Increased pain from a stimulusnthat normally promotes pain

Allodynia = experience of pain from a stimuli that isn’t normally painful

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10
Q

Aside from the Axon reflex and Dorsal root reflex, describe the course of the action potential after passing the cell body

A

Continues up the central process of the axon and terminates on the second order neuron in the dorsal horn. AP then generated in the 2nd order neuron in the dorsal horn of the spinal cord if the AP reaches the threshold potential of the 2nd order neuron.

The impulse then crosses the midline and ascends in the anterior and lateral spinothalamic tracts to the thalamus where the axons synapse with 3rd order neurons in the brain.

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11
Q

What is central sensitization?

A

If nociception is repetitive / large amplitude (significant or recurrent damage) –> central sensitization may occur at the 2nd order neuron.

A sensitized second order neuron has lowered firing threshold and increased receptor field size –> Hyperalgaesia and allodynia.

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12
Q

Why does allodynia occur

A

Large amplitude or repetitive stimulus –> central sensitization of 2nd order neuron –> lowered firing threshold of 2nd order neuron and larger receptor field size –> hyperalgaesia and allodynia

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13
Q

How many areas of the brain are involved in threat evaluation and pain generation

A

3rd order neurons have axonal projections to 200 discreet areas of the brain

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14
Q

What are the excitatory and inhibitory substances that play a role in the CNS pain pathways

A

Excitatory

  • Glutamate
  • Substance P
  • Neurokinin A + B

Inhibitory

  • GABA
  • Glycine
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15
Q

Does the brain initiate a descending inhibitory mechanism or a descending facilitatory mechanism to the 2nd order neuron

A

Either one. This depends on the unconscious evaluation of threat: i.e. how dangerous is the nociceptive message when considered in context of all other information the brain is receiving and has available.

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16
Q

Describe the descending inhibitory mechanism

A
  1. Descending inhibitory mechanism
    - Means of decreasing nociceptive stimulus
    - Efferent neurons from the the Peri-aqueductal Grey (PAG) and the rostro ventromedial medulla (RVM) descend to synapse with 2nd order neurons in the dorsal horn of the SC.
    - endorphins / enkephalins / noradrenalin / serotonin / endogenous opioids / cannabinoids / GABA released —-> these substances dampen nociceptive transmission by making the post synaptic membrane more difficult to depolarize or by impairing the nociceptive neurotransmitters.
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17
Q

Describe descending facilitation

A

Descending facilitation
1, means of increasing nociceptive stimulus
- brain evaluates threat as significant
- Impulses to dorsal horn –> glutamate –> sensitize 2nd order neuron –> increase the amount of nociception reaching the brain

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18
Q

What happens in ‘chronic pain’

A

The resting state should return once the inflammatory and healing process is completed. In chronic (nociplastic) pain, an excited, sensitised state persists beyond the healing period.

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19
Q

What is the aim of Patient Pain Neuroscience Education

A

To ensure that patients understand that pain is not an accurate measure of tissue damage but is an indication of perceived need to protect

All patients should be treated with PNE (Pain Neuroscience Education) prior to the initiation of appropriate non-pharmacological and pharmacological treatment

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20
Q

Give a general approach to the management of pain

A
  1. Understand biopsychosocial context of pain
    - history, previous treatment, stressors etc
  2. Patient PNE (Pain Neuroscience Education)
    - Pain = brains perceived need to protect
  3. Non-pharmacological
    - Diet | Exercise | breathing techniques | Psychosocial interventions (work / relationships/ purpose / mindfulness / sleep / breathing)
  4. Pharmacological
    - Simple analgaesics and NSAIDS
    - Weak oral opioids
    - Strong IV/IM opioids
    - Interventions
    (With neuropathic treatments - adjuvants)
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21
Q

List 6 groups of drugs used for analgaesia

A
  1. Simple analgaesics
  2. NSAIDS
  3. Opioids
  4. Local anaesthetics
  5. Hypnotics (N2O and ketamine)
  6. Secondary analgaesics (chronic pain)
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22
Q

List the ‘secondary analgaesics’ used for neuropathic and chronic pain

A
  1. TCAs
  2. SSRIs
  3. Anticonvulsants
  4. Gabapentin
  5. Alpha 2 agonists (CLonidine and dexmedetomidine)
  6. Steroids

Psychotherapy

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23
Q

What is the mechanism of action of paracetamol

A

Not fully elucidated

  1. Activation of descending inhibitory serotonergic pathways
  2. Antipyresis - inhibition of the heat regulating center in the hypothalamus
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24
Q

What is the maximum dose of paracetamol

A

4 g / 24 hours

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25
Q

What is the dose for paracetamol for paracetamol and ibuprofen in children

A

Paracetamol: 15 mg/kg (max 60 mg/kg/day)

Ibuprofen: 10 mg/kg (max 40 mg/kg/day)

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26
Q

How long does it take for paracetamol to work after oral and rectal administration and what is the duration of action

A

30 minutes

Duration: 2 - 5 hours

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27
Q

What is the onset of IV paracetamol

A

5 - 10 minutes

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28
Q

What is the equivalent morphine dose to 1 g of perfalgan

A

10 mg of morphine

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29
Q

Describe arachidonic acid metabolism and the mechanism of action of NSAIDS

A
  1. Cyclooxygenase pathway

Membrane phospholipids —(Phospholipase A2) –> Arachidonic acid —(Cycloxygenase 1/2)–> Cyclic endoperoxidases

  • -> Platelets (Thromboxane A2)
  • -> Endothelium (PGI2)
  • -> Widespread (PGE2, PGF2alpha, PGD2)

Aspirin: irreversible binding and inhibition of COX
NSAIDS: Reversible binding and inhibition of COX

30
Q

Describe the different COX enzymes and their functions

A

COX 1

  • Maintain normal renal blood flow
  • Maintain normal haemostasis
  • Maintain mucosal integrity

COX 2
- Inducible and is expressed in response to tissue damage

COX 3
- role unclear

31
Q

List the important side effects of NSAIDS

A 
GIT irritation
Bronchospasm
Renal dysfunction
Platelet dysfunction
Hepatotoxicity
Myocardial infarction
32
Q

When should aspirin not be given to children

A

Children recovering from chicken pox or flu-like symptoms due to the association with Reye’s syndrome

33
Q

What is the dose of diclofenac and indomethacin

A

Diclofenac:
Adults: 50 mg PO 8hrly
Kids: 1mg/kg PO 8hrly (1 - 2 mg/kg PR)

Indomethacin
Adults: 50 mg PO 8hrly (100mg PR 12hrly)
Kids: 1 mg/kg PO 8hrly

34
Q

What is the onset of action and duration of action of ibuprofen / diclofenac / indomethacin / Ketorolac

A

Onset: 30 - 60 minutes
Duration: 6 - 8 hours

35
Q

How does route of administration affect ketorolac’s onset

A

PO - 30 - 60 mins
IM - 10 mins
IV - 5 mins

36
Q

What is the dose of ketorolac

A

IM: 60 mg then 30mg 6 hrly
IV: 30 mg 6 hrly

37
Q

What is the dose, onset and duration of action of celecoxib and parecoxib

A

Celecoxib
100mg 12 hrly or 200 mg daily
Onset: 30 - 60 minutes
Duration: 12 hours

Parecoxib
40 mg IV/IM then 20 - 40 mg 6 -12 hrly (max 80mg/day)
Onset: 5 minutes IV and 30 minutes IM
Duration: 8 - 10 hrs

38
Q

What are opiate receptors and where are these found? What endogenous substance stimulate these receptors

A

mew
delta
kappa

Found centrally and peripherally
Endogenous substances: endorphins and enkephalins

39
Q

How do the opiate receptors work

A

They reduce neuronal cell excitability

40
Q

What are the effects of stimulation of opioid receptors in general

A
  1. Analgaesia
  2. Drowsiness (CNS)
  3. Change in mood (CNS)
  4. Nausea (GIT)
  5. Bradycardia (CVS)
  6. Respiratory depression (RSP)
  7. Miosis (ANS)
  8. Pruritis
  9. Constipation and inhibited GIT motility (GIT)
41
Q

What are the common side effects of opiates

A

N,V
Itching
Constipation
Urinary Retention

RSP depression
Reduced LOC
Muscle Rigidity

Physical and psychological dependence

42
Q

What is the dose of codeine and give an example of a common preparation

A

Dose: 30 - 60 mg 4 - 6 hrly

Panadol: Paracetamol 500mg and codeine 8 mg

43
Q

Why is codeine ineffective in some patients

A

10% of codeine is converted in the liver to morphine

Patients with P450 genetic polymorphism have poor metabolism to morphine and less pain relief

44
Q

What is the dose, onset and duration of tramadol

A

50 - 100 mg 4 - 6 hrly (Max 600 mg/day)
Onset: 30 - 60 minutes
Duration: 2 - 5 hours

45
Q

What is the mechanism of action of tramadol

A
  1. Opioid receptor agonist
  2. Noradrenalin and Serotonin Re-uptake inhibitor at pre-synaptic nerve endings and stimulates serotonin release: NB in descending inhibitory pathways

Drug interactions:
- SSRIs and SNRIs can lead to seizures and the serotonin syndrome

46
Q

What is tramacet

A

Tramadol 37.5 mg

Paracetamol 325mg

47
Q

What is the dose of pethidine

A

25 - 50 mg IV 4 hrly
25 - 100 mg IM 4 hrly

Kids: 1 mg/kg 4 hrly

48
Q

What is the mechanism of action of pethidine

A

Opioid receptor agonist in the CNS

Originally designed as an anticholinergic

  • -> dry mouth
  • -> tachycardia
49
Q

Why is pethidine not a good analgaesic

A
  1. Dissociative effects: spaced out patient who still feels the pain
  2. Crosses placenta –> accumulation of less lipid soluble norpethidine in the foetus
  3. ? epileptogenic
50
Q

What is the dose of morphine?

A

0.1 - 0.2 mg/kg 4 - 6 hrly IV and IM

Oral dose is double the parenteral dose

51
Q

How is morphine administered intraoperatively

A

Intraoperative administration

- Titrated to effected with doses of 1 - 5mg IV

52
Q

What is the effect of epidural/intrathecal administration of morphine

A

Enhanced analgaesic effect of the local anaesthetic with increased risk of delayed respiratory depression

53
Q

Describe your approach to PCA

A
  1. Patient selection (capacity)
  2. Counselling, communication, education (surgeon + patient + ward staff) and dedicated IV line.
  3. Preparations

Standard mix
–> Morphine 60 mg + 0.9% N/S ml + 1.25mg droperidol –> 60 ml total volume

OSA mix
–>Ketamine 50mg + Morphine 25mg + droperidol 1.25mg in otal volume 50ml

  1. Prescribe background analgaesia
  2. DO NOT write up opiates (once off rescue only)
  3. Nursing staff must not stop PCA if patient pain free (this means the system is working)
  4. PCA round to follow up the following day.
54
Q

What is the dose, onset and duration of fentanyl

A

1 - 2 mg/kg (adults and kids)
Onset: 3 - 5 minutes
Duration: 30 - 40 minutes (up to 6 hours for high doses)

55
Q

What is the advantage of fentanyl over morphine for neuraxial administration

A

Morphine causes delayed respiratory depression

Fentanyl is 600 times more lipid soluble than morphine and therefore does not cause delayed respiratory depression when administered intrathecal/epidural

56
Q

Which produces more significant histamine release: fentanyl or morphine

A

Morphine

57
Q

What is the problem with high dose fentanyl

A

Chest wall rigidity and bradycardia

58
Q

What are the doses of alfentanil and sufentanil and when are these agents commonly used

A

Alfentanil: 7.5 - 15 ug/kg

Sufentanyl: 8 - 30 ug/kg

Use: Inhibition of intubation response

59
Q

What are the pros and cons of remifentanil

A

Pros

  1. No hepatic or renal metabolism (plasma/tissue cholinesterase
  2. Rapid onset/offset
  3. Significant reduction of ANS reflexes during intubation and surgical stimulation

Cons

  1. Chest wall rigidity with higher doses
  2. Hypotension and bradycardia
  3. Respiratory depression
  4. NO postoperative analgaesia (possible hyperalgaesia)
60
Q

Describe how naloxone is administered. What are the side effects of naloxone

A

0.4 mg per amp
dilute to total volume 10mls –> 40 ug/ml
Give 1 ml bolus every 1 minute and observe for effect
- LOC/BP/HR/RR/movements/breathing effort etc.

Antanalgaesic

  1. Hypertension
  2. Tachycardia/dysrhythmias
  3. Pulmonary oedema
  4. PAIN
61
Q

Ketamine: mechanism of action and effects?

A

Mechanism

  1. Antagonist of glutamate at NMDA receptors
  2. Agonist: kappa and delta opioid receptors
  3. Antagonist of mew opioid receptors

Effects

  1. Airway - reflexes maintained but increased salivation
  2. Breathing - Bronchodilation
  3. Circulation - HPT/^HR (unless adrenal depletion)
  4. Disability - Dissociative anaesthesia / psychotic/emergence phenomena
  5. Exposure - Analgaesia (potent)

NB - tachyphylaxis common.

62
Q

Describe the doses for ketamine for its different clinical uses

A

Analgaesia:
IV: 0.2 - 0.5 mg/kg
IM: 2 - 4 mg/kg
PO: 5 mg/kg

Induction of anaesthesia
IV: 1 -2 mg/kg
IM: 5 - 10 mg/kg

Maintenance of anaesthesia
IV infusion: 10 - 40 ug/kg/min

63
Q

What is the mechanism of action of clonidine and dexmedetomidine and how are these drugs different in term of their mechanism of action.

Describe their clinical effects on each organ system and how these are brought about

A

Alpha 2 receptor agonist

Dexmedetomidine is 8 times more selective for the alpha 1 receptor than is clonidine

CNS
SEDATION/ANXIOLYTIC
- Decreased SNS activity and agitation
- = Stage 2 non-REM sleep without impairing cognition
- sedated but easily aroused and co-operative patient
- minimal respiratory depression
- suppress shivering

ANALGAESIA

  • Multiple analgaesic mechanisms suggested
  • Dorsal horn –> reduction of release of substance P (a nociceptive neurotransmitter)

CVS

  • Initially HPT (activation of alpha 2B receptors –> VC)
  • Then centrally mediated inhibited SNS outflow –> hypotension and bradycardia

RSP
- almost no effect

GIT
- anti-sialogogue

RENAL
- Diuretic (inhibits ADH)

ADRENAL
- no supression

64
Q

What are the benefits of treating postoperative pain

A
  1. Improved patient comfort/satisfaction
  2. Adequate breathing and coughing
  3. Decreased POPC (lung infections)
  4. Early mobilization and reduced VTE
  5. Limited stress response and reduced acute coronary events
65
Q

What is the multi-model approach to pain?

A

Pre-operative

  1. Pharmacological
    - paracetamol/other premedications prescribed to be working maximally in the post-operative period
  2. Non-pharmacological
    - Counselling: advise patients expect some pain which will be treated.

Intraoperative

  1. Perfalgan/Anti-inflammatory/ IV opioid
  2. Regional anaesthesia
  3. Epidural analgaesia (LA + opioids) 24 - 48 hours (High care resources)

Postoperative

  1. Paracetamol/NSAIDS
  2. Tramadol PO or Morphine IM or Tramadol with rescue morphine
66
Q

What medications should be prescribed with morphine/tramadol?

A

Prochlorperazine 12.5 mg 8hrly IM
OR
Ondansetron 4mg IV/IM 8hrly

67
Q

List contraindications to:
Paracetamol
NSAIDs
Opioids

A

Paracetamol - liver failure

NSAIDS - PUD / Renal failure / asthma

Opioids - OSA / neonates

68
Q

What is the STOPBANG score

A 
Snoring
Tiredness
Observed apnoea
Pressure (BP high)
BMI > 35
Age > 50
Neck circ > 40cm
Gender: Male

Interpretation:
0 - 2 low risk
3 - 4 intermediate risk
5 or more: high risk

Intermediate risk patients who are MALE or BMI > 35 or Neck circumference > 40 cm are HIGH risk

69
Q

What is your approach to the treatment of chronic pain

A

Biopsychosocial approach with an interdisciplinary team:

PHYSICIAN
Non-pharmacological
- Pain Neuroscience Education (Burglar alarm metaphor)
- Nociplastic pain is due to changes in the nervous system not actual tissue damage or harm
Pharmacological
- WHO analgaesic stepladder
- Introduce TCA’s earlier
- Carbamazepine (Trigeminal Neuralgia)
- Pregabalin / Gabapentin: Neuropathic pain
- SNRI/SSRI: enhance descending inhibition and Rx co-morbid depression

PHYSIOTHERAPIST

  • Patient education linked to exercise
  • Exercise: prevents nociplastic pain and activates descending inhibitory pathways
  • TENS (transcutaneous electrical nerve stimulation)
  • -> strimulate opioid mechanisms to reduce pain
  • GMI - Graded Motor Imagery. Phantom limb pain and Complex Regional Pain syndrome –> physiotherapists employ the most effective treatment available: Graded Motor Imagery (GMI)

PSYCHIATRIST/PSYCHOLOGIST
- CBT - insight into psychosocial factors contribution to pain.

70
Q

What % of chronic pain will require diagnostic and therapeutic regional blocks and what kind of procedures are available

A

10 % of chronic pain

  1. Radiofrequency ablation (6/12 relief)
  2. Implanted devices
    - -> Spinal Cord Dorsal Column Simulators
    - -> epidural morphine pumps

DA (50 decks)

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