Anaesthesiology SC056: The Pain Is Intolerable: Pain Control Flashcards
Pain
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”
***Classification of pain
- Acute pain (<2 weeks)
- Inflammatory pain
- Nociceptive pain
—> Somatic
—> Visceral
- Neuropathic pain - Chronic pain (>=3 months)
- Neuropathic pain
- Non-neuropathic pain - Cancer pain (Acute / Chronic)
- Tumour pain
- Treatment-related pain (e.g. Surgery, Chemotherapy, RT)
Acute pain
Characteristics:
- ***Nociceptive: Sharp + Localised
- Sudden
- Intense
- Self-limiting (usually)
- May be associated with ***physiologic changes: Sweating, ↑HR, ↑BP
Chronic pain
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
Neuropathic pain
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
Pain mechanisms
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
Nociceptors (Peripheral)
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
Sensitisation
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)
1st order neurons (Periphery)
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
Spinal cord + Brain (Central nervous system)
**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
Hyperalgesia
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
Allodynia
- Pain evoked by ***innocuous stimuli (e.g. Zoster)
- Central sensitisation —> pain produced by ***Aβ fibres
- Possibly mediated by spinal ***NMDA receptors
Pain mediators
Examples:
- Arachidonic acid —> Prostaglandin
- Bradykinin
- Substance P
Immune system may also be involved:
- Histamine (from mast cell)
- Serotonin (from platelets)
Role of Neuropeptides
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)
Physiologic consequences of Acute pain
General stress response
- Endocrine / Metabolic
- ↑ ACTH, Cortisol, Catecholamines, IL-1
- ↓ Insulin
- ↑ BG, Catabolism - Water / Electrolyte flux —> H2O, Na retention
Respiratory effects:
- ↓ Tidal volume
- ↓ Vital capacity
- ↓ FRC —> Atelectasis —> V/Q mismatch
- ↓ Alveolar ventilation
- ↓ Mobility —> Hypostatic pneumonia
- Muscle spasm —> Impaired ventilation —> Muscle splinting (shorten and stiffen) —> Cough suppression —> Sputum accumulation —> Lobular collapse —> Pneumonia / Hypoxaemia
Cardiovascular effects:
- ↑ HR, ↑ PVR, ↑ BP, ↑ CO —> Ischaemia
- Coronary vasoconstriction —> Ischaemia, Angina, MI —> ↑ Anxiety, Pain —> Coronary vasoconstriction
GI effects:
- ↓ Gastric + Bowel motility by pain medications
- Ileus
Coagulation + Immune effects:
- Hypercoagulability (stress from surgery / pain itself)
- Impair cellular + humoral immune function
Pain-signaling systems effects:
- ↑ Nerve excitability —> **Hyperalgesia (Primary / Secondary), **Allodynia
- ↑ Peripheral nociception —> Prolonged pain —> ***Chronic pain, Damaged spinal pain-signaling systems
Psychological effects (more important for chronic pain): 1. Anxiety —> Depression —> Sleep deprivation —> Anxiety
Assessment of Pain + Pain relief
Patient’s perception of pain
- subjective, influenced by: age, gender, culture, communication / language skills, previous experience
Assessment:
- Where
- Time course
- Intensity
- Factors relieving / exacerbating pain
- Pain on function + life
- Investigations for pain
- Treatments received
- Medical condition + prognosis
- Psychological profile (previous psychological disorders)
- Social background (poor social support —> more pain)
Pain evaluation tools:
- Numerical rating scale (NRS) (0-10) (for adults)
- Visual analog scale (VAS)
- Graphic pictures
- McGill Pain Questionnaire (Multidimensional, good but complex)
- Behavioural scores (e.g. CHEOPs) (useful in children / communication problems)
Treatment options for Acute pain
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):
- Non-opioid
- Paracetamol
- NSAID, COX-2 inhibitors
- Others: Gabapentanoids - Opioid (most important for acute pain ∵ mostly are post-surgical pain)
- Combination analgesic products
- Local anaesthetic, Nerve, Neuraxial blocks
- Opioid
- 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:
- Prolonged unconsciousness
- Pinpoint pupils
- Slow RR
Methods of opioid delivery:
- IM
- painful, slow onset, variable plasma levels - IV
- less painful, faster onset, more reliable levels
- risk of overdose with continuous IV infusion
- Patient controlled analgesia (PCA) - Epidural / Spinal
- Others
- SC / Oral / Transdermal
Epidural / Intrathecal (Spinal) opioid
- 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)
Patient controlled analgesia (PCA)
- 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)
Paracetamol and Tramadol
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
Anti-inflammatory agents
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
NMDA (N-methyl-D-aspartate) receptor antagonist
- 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
Local anaesthetics, Nerve, Neuraxial blocks
- ***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
Multimodal analgesia
- 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)
Acute pain services
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
Chronic pain
- > =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)
- Functional impairment
- Work
- Physical activity
- Social activity - Reduced QoL
- Sleep disturbance
- Increased cost + burden to society + healthcare system
Treatment options for Chronic pain
Non-pharmacological:
- Simple measures
- rest, exercise, heat therapy, vibration therapy - Cognitive-Behavioural (by Psychologists)
- Relaxation
- Preparatory information
- Imagery
- Hyponosis
- Biofeedback - 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 - Multidisciplinary pain programs (a course for patient groups)
- Neurolytic procedures
- Drugs: Phenol, Alcohol
- Cryoprobe
- Surgery - TENS (transcutaneous electrical nerve stimulation), Acupuncture
- Psychological techniques
- Radiofrequency ablation
- Implantation techniques: Spinal cord stimulator, Intrathecal / Epidural catheter: LA infusion —> not useful in if brain already sensitised
Pharmacological:
- Systemic analgesic drugs
- Opioids (try not to use ∵ pain not life-threatening), NSAIDs, Paracetamol - Adjuvant drugs (Neuropathic pain medications)
- Antidepressant (Amitriptyline, Duloxetine), Anticonvulsant (Gabapentin, Pregabalin), Steroids
- Muscle relaxants e.g. Baclofen - LA nerve block
