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*Medicine: Anaesthesia and ITU > Acute Pain Management > Flashcards

Acute Pain Management Flashcards

1
Q

What are implications of inadequate acute pain management?

A
  • CVS → ↑ HR, ↑ BP, ↑ PVR, MI, venous stasis, thrombosis
  • Resp → diaphragmatic splinting, atelectasis, sputum retentions, hypoxaemia
  • GI → delayed gastric emptying, ↓ intestinal motility
  • GU → urinary retention
  • Met/End → ↑ protein breakdown, impaired wound healing, sodium/water retention, ↑ metabolic rate
  • Chronic Pain
  • Psych → anxiety, sleeplessness, fatigue, distress
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2
Q

What is the World Health Organisation Analgesic Ladder?

A
  • Initially → paracetamol / NSAIDs
  • Next → weak opioids
  • Next → strong opioids
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3
Q

How does paracetamol work?

A
  • Number of central mechanisms
  • Effects on PG production, serotonergic, opioid, NO + cannabinoid pathways
  • Analgesic and antipyretic without anti-inflammatory activity
  • Excreted renally, after flucuronide + sulphate conjugation in liver
  • Hepatotoxic metabolite N-acetyl-p-benzoquinoneimine normally inactivated by conjugation with hepatic glutathione
  • In paracetamol OD, pathway is overwhelmed → hepatic cell necrosis
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4
Q

How is paracetamol administered?

A
  • PO or PR
  • Available as IV prep
  • Particularly effective when IV
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5
Q

What is the recommended dose of paracetamol?

A
  • 4 g/d in adults
  • Effective when prescribed regularly rather than PRN
  • MRHA licensed dose of paracetamol is same for all routes of administration in adults 50kg+
  • Dose in children weighing _<_10kg is now 7.5mg/kg (>10kg: 15 mg/kg)
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6
Q

NSAIDs are, in general, more useful for superficial pain arising from the skin, buccal mucosa, joint surfaces and bone. What is the mechanism of action of NSAIDs?

A
  • Analgesic, anti-inflammatory, antiplatelet and antipyretic
  • Due to inhibition of COX → ↓PGs, ↓prostacyclins, ↓Tx A2
  • COX-1: kidney, GI mucosa, platelets (PGs contribute to normal fxn)
  • COX-2: inflammatory mediators following tissue damage
  • NSAID therapeutic effects (COX-2) and adverse effects (COX-1)
  • Selective COX-2 inhibitors developed in attempt to reduce adverse effects of NSAIDs
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7
Q

What are adverse effects of NSAIDs?

A
  • GI toxicity
  • Renal impairment (all)
  • Increased risk of CV events (eg MI / stroke)
  • Lowest GI effects → iboprufen
  • Lowest CV events → naproxen and low-dose iboprufen
  • COX-2 inhibitors have higher CV risk but lower GI effects
  • Other adverse effects: hypersensitivity rxn, fluid retention
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8
Q

What are differences between NSAIDs and COX-2 inhibitors?

A
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9
Q

What are contraindications to NSAIDs?

A

Avoid in severe renal impairment, heart failure, liver failure and known NSAID hypersensitivity

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10
Q

What is the treatment for neuropathic pain?

A

NICE Guidelines:

  1. First line → amitriptyline (or imipramine if untolerated) or pregabalin
  2. Second line → amitriptyline AND pregabalin
  3. Third line → refer to pain specialist, tramadol in interim + avoid morphine
  4. Diabetic neuropathic pain → duloxetine
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11
Q

What are examples of inhaled analgesia?

A
  • Entonox (50/50 N2O, O2) → quick-acting, potent, short duration, self-admin
  • Isonox (isofluorane in entonox) → lower concs of isofluorane produce less drowsiness
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12
Q

What are side-effects of inhaled analgesia?

A
  • Ideal for short procedures (dressings, drain removal, catheter, labour pain, traction)
  • Entonox:
    • Side-effects → drowsiness, nausea, excitability
    • Diffuses rapidly into + increases gas-containing cavities
    • CIs → pneumothorax, decompression sickness, intoxication, bowel obstruction, bullous emphysema + head injury
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13
Q

Opioid drugs act as agonists at opioid receptors, found mainly in brain + spinal cord, but also peripherally.

What are the 3 principal classes of opioid receptor?

A
  • μ (mu) → analgesia, n+v, bradycardia, resp depression, miosis, inhibition of gut motility, pruritus, endogenous agonists are b-endorphins
  • κ (kappa) → analgesia, sedation, dysphoria, diuresis, endogenous agonists are dynorphins
  • δ (delta) → analgesia, endogenous agonists are enkephalins
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14
Q

What are features of morphine?

A
  • Gold standard against which all new analgesics compared
  • Least lipid-soluble opioid in common use
  • Metabolised in liver, excreted by kidney
  • Metabolite morphine-6-flucuronide is more potent than morphine
  • Accumulation can occur after prolonged use in pts w/ impaired renal fxn
  • Dose ranges and dose intervals vary according to route of admin
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15
Q

What are features of diamorphine?

A
  • A prodrug (diacetylmorphine)
  • Rapidly hydrolysed to 6-monoacetylmorphine and then morphine
  • Much more lipid-soluble than morphine
  • More rapid onset of action than morphine when given by epidural or IV
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16
Q

What are features of fentanyl?

A
  • Highly lipid-soluble synthetic opioid
  • Short-acting because of rapid tissue uptake
  • Suitable for transdermal administration
  • Commonly administered IV, epidurally, intrathecally, buccally, or via nasal spray
17
Q

What are features of pethidine?

A
  • Analgesic w/ anticholinergic + some LA activity
  • Metabolised in liver, excreted in kidney
  • Main metabolite is norpethidine (a potent analgesic)
  • High blood conc → CNS excitation
  • Pts with impaired renal fxn are at risk
  • Can be used to treatpost-op shivering associated w/ volatile anaesthetic agents, and epidural + spinal anaesthesia
18
Q

What are features of codeine?

A
  • Prodrug for morphine
  • For mild-mod pain
  • About 10% of dose is converted to morphine
  • Metabolism ⇒ morphine requires CYP2D6 enzyme (part of cytochrome p450 system)
  • 8-10% of caucasians lack this enzyme, obtaining little or no benefit
19
Q

What are features of tramadol?

A
  • Synthetic, centrally acting opioid-like drug
  • < 50% analgesic activity is at μ-receptor
  • Inhibits noradrenaline + serotonin uptake
  • Compared to other opioids → ↓tolerance + abuse, ↓resp depression, ↓constipation
  • Main metabolite more potent, also depends on cytochrome p450 enzyme (same as codeine)
20
Q

All opioids are equianalgesic if adjustments are made for the dose + route of admin. Allowance should be made for long-term opioid therapy, incomplete cross-tolerance between opioids, differing half-lives and interpatient variability.

What are the equianalgesic dosages?

A
21
Q

Opioids have a similar spectrum of side-effects. There is considerable interpatient variability, and some patients may suffer from more side-effects with one particular drug compared to another.

What are side-effects of opioids?

A
  • Resp depression → reduced RR, VT and irregular rhythm
  • Sedation
  • Euphoria + Dysphoria
  • Nausea + Vomiting
  • Muscle rigidity
  • Miosis
  • Bradycardia
  • Myocardiac depression
  • Vasodilatation
  • Delayed gastric emptying
  • Constipation
  • Pruritus
22
Q

What do opioid antagonists do?

A
  • Act at all opioid receptors
  • Naloxone most commonly used
  • Possible to reverse side-effects such as respiratory depression, N+V, sedation
  • Without antagonising the analgesic effects
  • Naloxone effective for ~60 min
23
Q

What are routes of administration for opioids?

A
  • Oral → limited due to first-pass metabolism, immediate-release oral opioids (moprhine syrup, oxycodone) for early management of acute pain, oral fentanyl should be restrictred to treating breakthrough pain in pts receiving opioid therapy for chronic cancer pain
  • SC or IM (intermittent) → 4hrly PRN, titrate for each pt
  • IV (intermittent) → adequate pain relief w/out XS drowsiness + resp depression, suitable for recovery wards. Eg. 1-3mg morphine or 20-60mcg of fentanyl every 5 min, until pt comfortable
  • IV (continuus) → close obs + monitoring essential
  • Intrathecal → good for day-case arthroscopic surgeries, or post-elective C section
  • Intransal → v effective in children (>1yr), for breakthrough pain
  • Transmucosal → fentanyl lollipops for children
  • Transdermal → for lipid-soluble opioids
24
Q

What are recommended doses of transdermal fentanyl, based on morphine doses?

A
25
Q

What is patient-controlled analgesia?

A
  • Pts administer own IV analgesia + titrate dose to own end-point of pan relief using small microprocessor-controlled pump
  • Morphine most common (more pruritus w/ morphine)
  • Others: fentanyl, pethidine, tramadol
  • Equipment malfunction rare
  • Operator error more common
26
Q

How do you manage nausea + vomiting with opioids?

A
  • Add an antiemetic → ondansetron 4mg, cyclizine 50-100mg, haloperidol 2mg
  • Prescribe on a regular basis
  • Change the opioid
27
Q

How do you manage breakthrough pain?

A
  • Add regular NSAID + paracetamol (if not contraindicated)
  • Increase bolus dose
  • Consider background infusion if severe
28
Q

How do you manage respiratory depression, with opioids?

A
  • All opioids have same potential for resp depression
  • Relatively uncommon
  • Early indicator → increasing sedation
  • Opioid doses adjusted so sedation score remains <2
  • Resp depression (RR < 8) is reversed with IV naloxone (100-400 micrograms)
29
Q

For epidural analgesia, an indwelling epidural catheter is inserted used to provide continuous infusion of analgesic agents. Provide excellent analgesia.

What are benefits of epidural analgesia?

A
  • Gold standard for major surgery
  • Prevent postoperative respiratory compromise resulting from pain
  • Post-operative complications reduced → MI, atelectasis, pulmonary infection, DVT, ileus, blood transfusion requirements
  • Improved intestinal motility → permitted earlier feeding
30
Q

What are the disadvantages and contraindications for epidural analgesia?

A
  • No survival benefit in high-risk pts
  • Confine pts to bed (esp if motor block present)
  • Indwelling urinary catheter → infection risk
  • Epidural haematoma
  • Contraindicated with patient refusal and untrained staff
  • Other contraindications → sepsis, hypovolaemia, coagulation disorders, anticoagulants
31
Q

What are complications of epidural analgesia?

A
32
Q

Extreme vigilance is needed for all pts who have epidural analgesia, because of the risk of spinal infection.

What are the clinical features of spinal infection?

A
  • Back pain
  • Fever
  • Leucocytosis
  • ↑ ESR

Epidural catheter should be removed immediately + sent to lab for cultures, Staph aureus most common (90%). MRI w/ gadolinium is investigation of choice - scan early! Once onset of muscle weakness, only 20% of pts regain full function even after surgery.

33
Q

Quality of analgesia is better w/ peripheral nerve blocks, compared with opioids. Incidence of post-operative side-effects is reduced.

What are examples of continuous peripheral nerve blocks?

A
  • Interscalene
  • Axillary
  • Femoral / fascia illiaca
  • Sciatic

Complications → bruising, haematoma, LA toxicity, peripheral nerve damage, infection, catheter kinking, catheter migration

34
Q

Physical opioid dependence is a physiological phenomenon characterised by a withdrawal rxn when the drug is withdrawn or antagonist administered.

What are symptoms of opioid withdrawal?

A
  • Yawning
  • Sweating + Anxiety
  • Rhinorrhoea + Lacrimation
  • Tachycardia, hypertension
  • Diarrhoea, nausea + vomiting
  • Abdo pain + cramps

Symptoms peak 26-72hr after last dose

35
Q

What is buprenorphine?

A
  • Partial opioid agonist
  • Used in treatment of opioid addiction
  • Dose → 8-32mg
36
Q

What are features of ketamine?

A
  • NMDA receptor antagonist in CNS + peripheral NS
  • Major adjuvant analgesic in variety of settings
  • Major side effects uncommon
  • Insufficient evidence to recommend ketamine as routine perioperative analgesic

*Medicine: Anaesthesia and ITU (8 decks)

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