New pain management Flashcards
RAT system
Recognise
Assess
Treat
Inflammatory pain presentation
Throbbing, aching, localised to affected area
Inflammatory pain treatment
NSAIDs
Paracetamol
Nociceptive- somatic pain presentation
Sharp pain and localised to affected area
Nociceptive- somatic pain treatment
NSAIDs
Paracetamol
Opioids
Nociceptive- visceral pain presentation
Deep, aching, poorly localised, cramping
Nociceptive- visceral pain treatment
NSAIDs
Paracetamol
Opioids
Neuropathic agents
Neuropathic pain presentation
Shooting, burning, hypersensitive, tingling, numbing
Neuropathic pain treatment
Neuropathic agents
Acute pain
Warning sign of injury
- following injury to body
Well defined onset
- no longer than 6 months
Responds well to treatment
- should be treated promptly and stepped up readily
Generally produces anxiety
Often associated with physical signs
- tachypnoea, tachycardia, decreased immunity, well-being
Chronic pain
Persists behond expected healing time
May or may not have defined onset
Often difficult to treat
Can have physiological element
Pain signals active in nervous system for weeks, months or years
Progressive physical deterioration
Acute pain management
Responds well to conventional analgesics
- paracetamol, NSAIDs, opioids
Non-pharmacological treatments
Chronic pain management
Neuropathic agents
Doesn’t respond well to opioids
Psychological therapies
Pain education
Classification of analgesics
Simple
Opioids
Neuropathic agents
Miscellaneous
Simple analgesics
NSAIDs
Opioid analgesics
Weak/ strong opioids
Neuropathic agents
Anticonvulsants
- gabapentin, pregabalin, carbamazepine
Antidepressants
- amitriptyline, duloxetine
Miscellaneous analgesics
Triptans
Anaesthetic agent
Paracetamol
1g QDS PO/IV
If <50kg 500mg QDS
NSAIDs
Ibuprofen 400mg TDS PO
Naproxen 250-500mg BD PO
Adverse effects of NSAIDs
Renal- prostanoid inhibition
Reduced/ increase platelet aggregation
Reyes syndrome in children
GI side effects
Drug interactions
Hypersensitivity and cross reactivity
Renal protanoid inhibition
Decreased renal blood flow, imbalance in vasodilation mechanism leading to ischaemia
Water/ sodium retention
Reduced/ increase platelet aggregation
Aspirin antiplatelet
NSAIDs and COX-2 thromboembolic
Reyes syndrome
Encephalopathy in children
GI side effects of NSAIDs
Due to inhibition of COX1 of prostaglandins
Decreased blood flow, decreased mucous production, increase acid production
Duration of therapy not good predictor
Weak opioids
Used for: moderate pain and anti-diarrhoeal properties
Dihydrocodeine first line weak opioid- metabolite likely to accumulate
Strong opioids
Used for: effective for moderate to severe acute pain
Usual suspects: morphine, oxycodone, fentanyl
Opioid prescribing
No variable doses or routes of administration on the regular side of the drug chart
No weak opioids plus strong opioids
No systemic opioids with PCA/ epidurals
Adverse effects of opioids
Respiratory depression
- caution elderly patients, COPD, always prescribe prn naloxone 100mcg iv/im
Constipation
- inhibition of peristalsis, increae tone of anal sphincter and reduces the reflex relaxation response to rectal distension
- stimulant laxatives e.g. senna
Nausea and vomiting
Sedation
Pruritis
Nefopam
Non opioid and non NSAID
Mechanism not fully understood, thought to affect serotonin, dopamine and noradrenaline reuptake and glutamine release
Side effects: nausea, dizziness, urinary retention, dry mouth
Can turn urine pink
Contra-indicated in convulsive disorders
Gabapentin
Neuropathic analgesic, used ‘off-label’ in acute post operative pain
Mechanism of action for pain not fully understood
Acts on voltage gated Ca2+ channels, blocking neuronal Ca2+ influx and decreasing glutamate release
Opioid sparing- reduces problematic side effects of opioids (nausea and constipation)
