Perioperative pain management Flashcards
Define pain
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.
Define nociception
The neural process of encoding noxious stimuli
Define acute pain
Recent onset and short duration (< 6 weeks)
Trauma | Surgery | Acute illness
Often limited to the area of damage or disease
Resolves with healing
Define chronic pain
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.
Compare nociceptive pain, neuropathic pain and nociplastic pain
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
Describe the process of conduction of a pain impulse
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.
What are the reflexes involved in neurogenic inflammation. Explain how this process works
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
List the mediators released by tissue damage and neurogenic inflammation
K+ | Substance P | Bradykinin | serotonin |
histamine | Cytokines | Nitric Oxide |
prostaglandins
What clinical neurological symptom related to pain results from tissue and neurogenic inflammation?
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
Aside from the Axon reflex and Dorsal root reflex, describe the course of the action potential after passing the cell body
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.
What is central sensitization?
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.
Why does allodynia occur
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
How many areas of the brain are involved in threat evaluation and pain generation
3rd order neurons have axonal projections to 200 discreet areas of the brain
What are the excitatory and inhibitory substances that play a role in the CNS pain pathways
Excitatory
- Glutamate
- Substance P
- Neurokinin A + B
Inhibitory
- GABA
- Glycine
Does the brain initiate a descending inhibitory mechanism or a descending facilitatory mechanism to the 2nd order neuron
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.
Describe the descending inhibitory mechanism
- 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.
Describe descending facilitation
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
What happens in ‘chronic pain’
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.
What is the aim of Patient Pain Neuroscience Education
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
Give a general approach to the management of pain
- Understand biopsychosocial context of pain
- history, previous treatment, stressors etc - Patient PNE (Pain Neuroscience Education)
- Pain = brains perceived need to protect - Non-pharmacological
- Diet | Exercise | breathing techniques | Psychosocial interventions (work / relationships/ purpose / mindfulness / sleep / breathing) - Pharmacological
- Simple analgaesics and NSAIDS
- Weak oral opioids
- Strong IV/IM opioids
- Interventions
(With neuropathic treatments - adjuvants)
List 6 groups of drugs used for analgaesia
- Simple analgaesics
- NSAIDS
- Opioids
- Local anaesthetics
- Hypnotics (N2O and ketamine)
- Secondary analgaesics (chronic pain)
List the ‘secondary analgaesics’ used for neuropathic and chronic pain
- TCAs
- SSRIs
- Anticonvulsants
- Gabapentin
- Alpha 2 agonists (CLonidine and dexmedetomidine)
- Steroids
Psychotherapy
What is the mechanism of action of paracetamol
Not fully elucidated
- Activation of descending inhibitory serotonergic pathways
- Antipyresis - inhibition of the heat regulating center in the hypothalamus
What is the maximum dose of paracetamol
4 g / 24 hours
What is the dose for paracetamol for paracetamol and ibuprofen in children
Paracetamol: 15 mg/kg (max 60 mg/kg/day)
Ibuprofen: 10 mg/kg (max 40 mg/kg/day)
How long does it take for paracetamol to work after oral and rectal administration and what is the duration of action
30 minutes
Duration: 2 - 5 hours
What is the onset of IV paracetamol
5 - 10 minutes
What is the equivalent morphine dose to 1 g of perfalgan
10 mg of morphine
Describe arachidonic acid metabolism and the mechanism of action of NSAIDS
- 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
Describe the different COX enzymes and their functions
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
List the important side effects of NSAIDS
GIT irritation Bronchospasm Renal dysfunction Platelet dysfunction Hepatotoxicity Myocardial infarction
When should aspirin not be given to children
Children recovering from chicken pox or flu-like symptoms due to the association with Reye’s syndrome
What is the dose of diclofenac and indomethacin
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
What is the onset of action and duration of action of ibuprofen / diclofenac / indomethacin / Ketorolac
Onset: 30 - 60 minutes
Duration: 6 - 8 hours
How does route of administration affect ketorolac’s onset
PO - 30 - 60 mins
IM - 10 mins
IV - 5 mins
What is the dose of ketorolac
IM: 60 mg then 30mg 6 hrly
IV: 30 mg 6 hrly
What is the dose, onset and duration of action of celecoxib and parecoxib
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
What are opiate receptors and where are these found? What endogenous substance stimulate these receptors
mew
delta
kappa
Found centrally and peripherally
Endogenous substances: endorphins and enkephalins
How do the opiate receptors work
They reduce neuronal cell excitability
What are the effects of stimulation of opioid receptors in general
- Analgaesia
- Drowsiness (CNS)
- Change in mood (CNS)
- Nausea (GIT)
- Bradycardia (CVS)
- Respiratory depression (RSP)
- Miosis (ANS)
- Pruritis
- Constipation and inhibited GIT motility (GIT)
What are the common side effects of opiates
N,V
Itching
Constipation
Urinary Retention
RSP depression
Reduced LOC
Muscle Rigidity
Physical and psychological dependence
What is the dose of codeine and give an example of a common preparation
Dose: 30 - 60 mg 4 - 6 hrly
Panadol: Paracetamol 500mg and codeine 8 mg
Why is codeine ineffective in some patients
10% of codeine is converted in the liver to morphine
Patients with P450 genetic polymorphism have poor metabolism to morphine and less pain relief
What is the dose, onset and duration of tramadol
50 - 100 mg 4 - 6 hrly (Max 600 mg/day)
Onset: 30 - 60 minutes
Duration: 2 - 5 hours
What is the mechanism of action of tramadol
- Opioid receptor agonist
- 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
What is tramacet
Tramadol 37.5 mg
Paracetamol 325mg
What is the dose of pethidine
25 - 50 mg IV 4 hrly
25 - 100 mg IM 4 hrly
Kids: 1 mg/kg 4 hrly
What is the mechanism of action of pethidine
Opioid receptor agonist in the CNS
Originally designed as an anticholinergic
- -> dry mouth
- -> tachycardia
Why is pethidine not a good analgaesic
- Dissociative effects: spaced out patient who still feels the pain
- Crosses placenta –> accumulation of less lipid soluble norpethidine in the foetus
- ? epileptogenic
What is the dose of morphine?
0.1 - 0.2 mg/kg 4 - 6 hrly IV and IM
Oral dose is double the parenteral dose
How is morphine administered intraoperatively
Intraoperative administration
- Titrated to effected with doses of 1 - 5mg IV
What is the effect of epidural/intrathecal administration of morphine
Enhanced analgaesic effect of the local anaesthetic with increased risk of delayed respiratory depression
Describe your approach to PCA
- Patient selection (capacity)
- Counselling, communication, education (surgeon + patient + ward staff) and dedicated IV line.
- 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
- Prescribe background analgaesia
- DO NOT write up opiates (once off rescue only)
- Nursing staff must not stop PCA if patient pain free (this means the system is working)
- PCA round to follow up the following day.
What is the dose, onset and duration of fentanyl
1 - 2 mg/kg (adults and kids)
Onset: 3 - 5 minutes
Duration: 30 - 40 minutes (up to 6 hours for high doses)
What is the advantage of fentanyl over morphine for neuraxial administration
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
Which produces more significant histamine release: fentanyl or morphine
Morphine
What is the problem with high dose fentanyl
Chest wall rigidity and bradycardia
What are the doses of alfentanil and sufentanil and when are these agents commonly used
Alfentanil: 7.5 - 15 ug/kg
Sufentanyl: 8 - 30 ug/kg
Use: Inhibition of intubation response
What are the pros and cons of remifentanil
Pros
- No hepatic or renal metabolism (plasma/tissue cholinesterase
- Rapid onset/offset
- Significant reduction of ANS reflexes during intubation and surgical stimulation
Cons
- Chest wall rigidity with higher doses
- Hypotension and bradycardia
- Respiratory depression
- NO postoperative analgaesia (possible hyperalgaesia)
Describe how naloxone is administered. What are the side effects of naloxone
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
- Hypertension
- Tachycardia/dysrhythmias
- Pulmonary oedema
- PAIN
Ketamine: mechanism of action and effects?
Mechanism
- Antagonist of glutamate at NMDA receptors
- Agonist: kappa and delta opioid receptors
- Antagonist of mew opioid receptors
Effects
- Airway - reflexes maintained but increased salivation
- Breathing - Bronchodilation
- Circulation - HPT/^HR (unless adrenal depletion)
- Disability - Dissociative anaesthesia / psychotic/emergence phenomena
- Exposure - Analgaesia (potent)
NB - tachyphylaxis common.
Describe the doses for ketamine for its different clinical uses
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
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
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
What are the benefits of treating postoperative pain
- Improved patient comfort/satisfaction
- Adequate breathing and coughing
- Decreased POPC (lung infections)
- Early mobilization and reduced VTE
- Limited stress response and reduced acute coronary events
What is the multi-model approach to pain?
Pre-operative
- Pharmacological
- paracetamol/other premedications prescribed to be working maximally in the post-operative period - Non-pharmacological
- Counselling: advise patients expect some pain which will be treated.
Intraoperative
- Perfalgan/Anti-inflammatory/ IV opioid
- Regional anaesthesia
- Epidural analgaesia (LA + opioids) 24 - 48 hours (High care resources)
Postoperative
- Paracetamol/NSAIDS
- Tramadol PO or Morphine IM or Tramadol with rescue morphine
What medications should be prescribed with morphine/tramadol?
Prochlorperazine 12.5 mg 8hrly IM
OR
Ondansetron 4mg IV/IM 8hrly
List contraindications to:
Paracetamol
NSAIDs
Opioids
Paracetamol - liver failure
NSAIDS - PUD / Renal failure / asthma
Opioids - OSA / neonates
What is the STOPBANG score
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
What is your approach to the treatment of chronic pain
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.
What % of chronic pain will require diagnostic and therapeutic regional blocks and what kind of procedures are available
10 % of chronic pain
- Radiofrequency ablation (6/12 relief)
- Implanted devices
- -> Spinal Cord Dorsal Column Simulators
- -> epidural morphine pumps
