Perioperative pain management Flashcards
(70 cards)
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
