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SC WCS > Anaesthesiology SC056: The Pain Is Intolerable: Pain Control > Flashcards

Anaesthesiology SC056: The Pain Is Intolerable: Pain Control Flashcards

1
Q

Pain

A 
Definition:
Unpleasant sensory (i.e. biological component) + emotional experience associated with / resembling that associated with actual / potential ***tissue damage

Biological value:

  • Essential for survival
  • Serves as a warning to avoid / prevent further body injury
  • Enforces rest of injured / diseased parts of body for healing
  • **Fifth vital sign:
  • patients should be assess for pain every time pulse, BP, temp, RR, SaO2 are measured
  • should recognise unrelieved pain is a “red flag”
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2
Q

***Classification of pain

A
  1. Acute pain (<2 weeks)
    - Inflammatory pain
    - Nociceptive pain
    —> Somatic
    —> Visceral
    - Neuropathic pain
  2. Chronic pain (>=3 months)
    - Neuropathic pain
    - Non-neuropathic pain
  3. Cancer pain (Acute / Chronic)
    - Tumour pain
    - Treatment-related pain (e.g. Surgery, Chemotherapy, RT)
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3
Q

Acute pain

A

Characteristics:

  • ***Nociceptive: Sharp + Localised
  • Sudden
  • Intense
  • Self-limiting (usually)
  • May be associated with ***physiologic changes: Sweating, ↑HR, ↑BP
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4
Q

Chronic pain

A

Characteristics:

  • Gnawing, aching, ***diffuse
  • No definite beginning / end
  • ***Temporal variability in intensity; may remit briefly
  • Associated with psychological + social difficulties
  • Acute pain may be superimposed
  • Nerve fibres may become ***pathological —> may extend beyond area of initial injury
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5
Q

Neuropathic pain

A

Characteristics:

  • Pain caused by lesion / disease of ***Somatosensory nervous system (i.e. Nerve fibres affected)
  • Spontaneous pain
  • Burning, tingling, numbness, pinprick, lancinating
  • **Allodynia, **Hyperalgesia

Examples:

  • Zoster
  • Disc prolapse compression on spinal nerves
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6
Q

Pain mechanisms

A

Somatosensory system:
- Ascending + Descending system

Pathophysiology of pain (3 components of nociceptive process):

  • Peripheral nervous system
    1. Periphery (Nociceptors)
    2. Nerve
  • Central nervous system
    3. Spinal Cord + Brain
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7
Q

Nociceptors (Peripheral)

A

Examples:

  • High threshold mechanoreceptors
  • Thermo-mechanoreceptors
  • Polymodal nociceptors
  • Super-high threshold receptors
  • Respond to different stimuli
  • Can be ***“Sensitised” —> after experiencing pain sensation —> more effective in pain transmission —> even when stimuli decrease / normal —> still transmitting pain signal
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8
Q

Sensitisation

A

Following initial stimulation
—> ***Firing threshold of nociceptors is lowered
—> Less stimulus required to be activated / noxious stimulus to be sent to CNS
—> Hyperalgesia, Allodynia

Peripheral sensitisation:
Cell damage / Inflammation / Sympathetic terminals
—> Release of **pain + inflammatory mediators (e.g. Bradykinin, H, Prostaglandin, Substance P, TNFα)
—> **Nociceptor bathed in mediators
—> Keep stimulated
—> Sensitisation

Central sensitisation (occur in **Spinal cord + **Brain):
Prolonged stimulation of **C fibres
—> release **Substance P + **Glutamate in **Dorsal horn
—> cascade of events altering neuro-cellular function
—> development of +ve feedback loop
—> sequential ↑ in spinal cord activity (“wind up” of neuronal excitability), **NMDA receptor activation
—> **Secondary hyperalgesia, allodynia

Progression:
- Peripheral sensitisation —> Central sensitisation at Spinal cord —> Central sensitisation at Brain (poor pain prognosis)

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9
Q

1st order neurons (Periphery)

A

Type Aα:

  • Proprioceptors of skeletal muscle
  • highly myelinated
  • largest diameter

Type Aβ:
- Mechanoreceptors of skin (Touch)
—> ***In pathological condition will also transmit pain

  • **Type Aδ —> Small fibres + Transmit slowly:
  • Mechanoreceptors, ***Nociceptors, Thermoreceptors
  • Pain, temperature
  • **Type C —> Small fibres + Transmit slowly:
  • Mechanoreceptors, ***Nociceptors, Thermoreceptors, Sympathetic post-ganglionic
  • Temperature, pain, itch
  • unmyelinated (much slower conduction speed)
  • smallest diameter
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10
Q

Spinal cord + Brain (Central nervous system)

A

**1st order neurons
—> enter **Dorsal horn
—> synapse with **Interneurons (i.e. 2nd order neurons)
—> **Modulating influences from higher centres in brain (e.g. psychological components)
—> Pain sensation can therefore be modified by **Ascending / **Descending pathways at many levels (usually spinal cord)

Modulating influences:
- can be **inhibiting / **enhancing pain signals
—> drugs targeting modulating influences in chronic pain

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11
Q

Hyperalgesia

A

Response to normal pain signal enhanced

Primary:

  • Sensitisation of primary neurons —> ↓ threshold to noxious stimuli ***within site of injury
  • may include response to innocuous stimuli
  • ↑ pain from suprathreshold stimuli
  • spontaneous pain
Secondary:
- Sensitisation of primary neurons in ***surrounding uninjured areas
- may involve:
—> Peripheral sensitisation
—> Central sensitisation
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12
Q

Allodynia

A
  • Pain evoked by ***innocuous stimuli (e.g. Zoster)
  • Central sensitisation —> pain produced by ***Aβ fibres
  • Possibly mediated by spinal ***NMDA receptors
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13
Q

Pain mediators

A

Examples:

  1. Arachidonic acid —> Prostaglandin
  2. Bradykinin
  3. Substance P

Immune system may also be involved:

  1. Histamine (from mast cell)
  2. Serotonin (from platelets)
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14
Q

Role of Neuropeptides

A

Excitatory:

  • Substance P, Neurokinin A
  • ↑ Ca, induce sensitisation, hyperalgesia
  • Transsynaptic transmitters

Inhibitory:

  • Somatostatin, Enkephalins, Endorphins, Dynorphins
  • Modulate intracellular cAMP, K
  • Act at μ, δ, κ opioid receptors (i.e. Endogenous opioid)
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15
Q

Physiologic consequences of Acute pain

A

General stress response

  1. Endocrine / Metabolic
    - ↑ ACTH, Cortisol, Catecholamines, IL-1
    - ↓ Insulin
    - ↑ BG, Catabolism
  2. Water / Electrolyte flux —> H2O, Na retention

Respiratory effects:

  1. ↓ Tidal volume
  2. ↓ Vital capacity
  3. ↓ FRC —> Atelectasis —> V/Q mismatch
  4. ↓ Alveolar ventilation
  5. ↓ Mobility —> Hypostatic pneumonia
  6. Muscle spasm —> Impaired ventilation —> Muscle splinting (shorten and stiffen) —> Cough suppression —> Sputum accumulation —> Lobular collapse —> Pneumonia / Hypoxaemia

Cardiovascular effects:

  1. ↑ HR, ↑ PVR, ↑ BP, ↑ CO —> Ischaemia
  2. Coronary vasoconstriction —> Ischaemia, Angina, MI —> ↑ Anxiety, Pain —> Coronary vasoconstriction

GI effects:

  1. ↓ Gastric + Bowel motility by pain medications
  2. Ileus

Coagulation + Immune effects:

  1. Hypercoagulability (stress from surgery / pain itself)
  2. Impair cellular + humoral immune function

Pain-signaling systems effects:

  1. ↑ Nerve excitability —> **Hyperalgesia (Primary / Secondary), **Allodynia
  2. ↑ Peripheral nociception —> Prolonged pain —> ***Chronic pain, Damaged spinal pain-signaling systems
Psychological effects (more important for chronic pain):
1. Anxiety —> Depression —> Sleep deprivation —> Anxiety
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16
Q

Assessment of Pain + Pain relief

A

Patient’s perception of pain
- subjective, influenced by: age, gender, culture, communication / language skills, previous experience

Assessment:

  1. Where
  2. Time course
  3. Intensity
  4. Factors relieving / exacerbating pain
  5. Pain on function + life
  6. Investigations for pain
  7. Treatments received
  8. Medical condition + prognosis
  9. Psychological profile (previous psychological disorders)
  10. Social background (poor social support —> more pain)

Pain evaluation tools:

  1. Numerical rating scale (NRS) (0-10) (for adults)
  2. Visual analog scale (VAS)
  3. Graphic pictures
  4. McGill Pain Questionnaire (Multidimensional, good but complex)
  5. Behavioural scores (e.g. CHEOPs) (useful in children / communication problems)
17
Q

Treatment options for Acute pain

A

Analgesic ladder:
Step 1: Non-opioid analgesic (Paracetamol, NSAID) +/- Non-opioid +/- Adjuvant
Step 2: Weak opioid (Codeine, Tramadol) +/- Non-opioid +/- Adjuvant
Step 3: Strong opioid (Morphine, Oxycodone, Fentanyl) +/- Non-opioid +/- Adjuvant

Analgesic options (***Multimodal):

  1. Non-opioid
    - Paracetamol
    - NSAID, COX-2 inhibitors
    - Others: Gabapentanoids
  2. Opioid (most important for acute pain ∵ mostly are post-surgical pain)
  3. Combination analgesic products
  4. Local anaesthetic, Nerve, Neuraxial blocks
18
Q
  1. Opioid
A
  • Binding at μ, δ, κ opioid receptors

Advantages:

  • Highly efficacious
  • ***No ceiling effect (↑ dose —> ↑ effect unlimitedly)
  • May be combined with anti-inflammatory agents
  • May be given via different routes
  • Effects may be reversed (Naloxone)
Disadvantages:
- SE common
—> Respiratory depression
—> ↓ GI motility, N+V
—> CNS depression, sedation, cognitive effects (elderly)
—> Pruritus (esp. spinal opioids)
—> Urinary retention
- Tolerance

Opioid overdose classical signs:

  1. Prolonged unconsciousness
  2. Pinpoint pupils
  3. Slow RR

Methods of opioid delivery:

  1. IM
    - painful, slow onset, variable plasma levels
  2. IV
    - less painful, faster onset, more reliable levels
    - risk of overdose with continuous IV infusion
    - Patient controlled analgesia (PCA)
  3. Epidural / Spinal
  4. Others
    - SC / Oral / Transdermal
19
Q

Epidural / Intrathecal (Spinal) opioid

A
  • Act on Opioid receptors in spinal cord

Advantages:

  • Neuraxial opioids can produce **profound segmental analgesia, with **reduced systemic opioid adverse effects
  • May be combined with LA —> less motor impairment
  • Prolonged effects (up to 1 day)

Disadvantages:
- Potential dangers e.g. late onset respiratory depression (∵ late absorption into circulation)

20
Q

Patient controlled analgesia (PCA)

A
  • Match demand with delivery
  • Button press activation
  • Positive patient psychology
  • Pre-set bolus dose
  • Lock-out interval
  • 1 hour maximum dose
  • Tamper proof machine
  • Patient monitoring

Advantages:
- More stable plasma concentration (than IM bolus)

21
Q

Paracetamol and Tramadol

A

Paracetamol:

  • MOA: ↑ Pain threshold in CNS + COX inhibition
  • SE: Hepatotoxic

Tramadol:

  • MOA: Weak μ binding + Inhibits re-uptake of NE + Serotonin (5HT3) (i.e. also effective for neuropathic pain)
  • SE: Opioid-like effects, **N+V, **Dizziness, Seizures
22
Q

Anti-inflammatory agents

A

For inflammatory component in post-surgical pain

  • Inhibit COX (key enzyme in Prostaglandin synthesis)
  • Conventional anti-inflammatory analgesics inhibit both COX1 + COX2 isoenzymes
  • COX1 inhibition —> Gastrotoxicity, ↓ Platelet aggregation, Renal toxicity, Fluid retention
  • COX2 specific —> Not inhibit COX1 at full therapeutic doses, CVS risk, Fluid retention
MOA of COX in pain:
Arachidonic acid
—> COX
—> Prostanoids (Prostaglandin / Thromboxane)
—> Pain, Inflammation, Fever
COX1:
- Constitutive
- Synthesise prostanoid that mediate ***homeostatic functions
- Esp. important in:
—> Gastric mucosa
—> Kidney
—> Platelet
—> Vascular endothelium

COX2:
- Inducible (in most tissues)
- Synthesise prostanoids that mediate ***inflammation, pain, fever
- Induced mainly at sites of inflammation by cytokines
- Constitutive expression primarily in:
—> Brain
—> Kidney

23
Q

NMDA (N-methyl-D-aspartate) receptor antagonist

A
  • Dorsal horn of spinal cord
  • Inhibition may prevent “wind-up” + central sensitisation
  • ***Ketamine: Non-competitive NMDA antagonist
    —> Analgesia in acute pain
    —> Attenuate opioid tolerance + prevent chronic pain
    —> SE
24
Q

Local anaesthetics, Nerve, Neuraxial blocks

A
  • ***Na channel blockade
  • Possible interaction at pre- + post-synaptic junctions
  • Tachyphylaxis
  • Dose-related CNS, CVS toxicity
LA:
Drugs:
1. Lignocaine 1-2%
2. Bupivacaine 2.5-5% (Levo)
3. Prilocaine 0.5-1%
4. Ropivacaine 0.2-1%

Route of administration:

  • Local infiltration
  • Regional nerve block
  • Spinal block (lower abdominal / lower limb surgery)
  • Epidural block
  • Caudal block

Advantages of LA:

  • Excellent analgesia
  • ***Opioid sparing effect
  • Decreased blood loss
  • ***Localised, no systemic SE (e.g. accumulate in kidney impairment / nephrotoxicity)
  • Ropivacaine and bupivacaine: hepatically eliminated, not usually affected by renal failure

Disadvantages:

  • ***Motor blockade
  • ***Hypotension (in Neuraxial blocks i.e. Epidural, Spinal block) —> Ensure patient not hypovolaemic
  • ***LA toxicity
  • Variable duration (12-24 hours)
  • Require skill (nerve blocks)
  • Malplaced block
  • ***High spinal block
  • Rebound pain after wearing off —> still need oral analgesic
25
Q

Multimodal analgesia

A
  • Acute post-surgical pain
  • Usually >=2 agents with **different but **complementary MOA
  • Reduced doses of each analgesic
  • Improved anti-nociception (∵ synergistic / additive effects)
  • May reduce severity of SE of each drug (esp. opioids)
26
Q

Acute pain services

A

Goals:

  • Improve management of surgical pain
  • Manage **complex pain cases + those with **advanced pain modalities e.g. epidural analgesia, PCA morphine
  • Promote continuing education + training of healthcare providers
Staff:
- Pain physicians, Anaesthetists
- Pain nurses
- Multidisciplinary
—> Twice daily ward rounds
—> Pain consultation service, Pain clinic
—> Therapeutic interventions
27
Q

Chronic pain

A
  • > =3 months
  • Neuropathic / Non-neuropathic pain
  • Cancer / Non-cancer pain
  • Commonly seen: ***Chronic Non-cancer pain
  • Lack of objective signs
  • No longer a symptom
    —> a disease itself (pain signal not useful to body anymore, no organic causes anymore e.g. tissue damage)
    —> ∵ ***severe sensitisation
  • Psychological + Emotional factors
  • Pain behaviour established
  • Responses altered by cultural influences + past experiences
Effects:
1. Psychological
- Depression
- Anxiety
(- PTSD esp. if pain due to accidents)
  1. Functional impairment
    - Work
    - Physical activity
    - Social activity
  2. Reduced QoL
  3. Sleep disturbance
  4. Increased cost + burden to society + healthcare system
28
Q

Treatment options for Chronic pain

A

Non-pharmacological:

  1. Simple measures
    - rest, exercise, heat therapy, vibration therapy
  2. Cognitive-Behavioural (by Psychologists)
    - Relaxation
    - Preparatory information
    - Imagery
    - Hyponosis
    - Biofeedback
  3. Physical agents
    - Superficial heat / cold application
    - Massage
    - Exercise
    - Immobilisation (e.g. to provide rest + maintain alignment after musculoskeletal procedures)
    - Electroanalgesia (e.g. TENS (transcutaneous electrical nerve stimulation))
    - Chiropractic
    - Acupuncture
  4. Multidisciplinary pain programs (a course for patient groups)
  5. Neurolytic procedures
    - Drugs: Phenol, Alcohol
    - Cryoprobe
    - Surgery
  6. TENS (transcutaneous electrical nerve stimulation), Acupuncture
  7. Psychological techniques
  8. Radiofrequency ablation
  9. Implantation techniques: Spinal cord stimulator, Intrathecal / Epidural catheter: LA infusion —> not useful in if brain already sensitised

Pharmacological:

  1. Systemic analgesic drugs
    - Opioids (try not to use ∵ pain not life-threatening), NSAIDs, Paracetamol
  2. Adjuvant drugs (Neuropathic pain medications)
    - Antidepressant (Amitriptyline, Duloxetine), Anticonvulsant (Gabapentin, Pregabalin), Steroids
    - Muscle relaxants e.g. Baclofen
  3. LA nerve block

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