Anaesthetics: Pain Flashcards
What is the definition of pain?
Unpleasant sensory & emotional experience associated with actual or potential tissue damage, or described in terms of such damage.
NOTE: new defintion proposed in 2019 (not officially accepted yet): an aversive sensory & emotional experience typically caused by or resembling that caused by, actual or potential tissue injury
Remind yourself of the pain pathway from semester 4: neurology
- Nociceptor detects stimulus
- First order neurone (Adelta or C fibre): periphery to ipsilateral dorsal horn where it synpases with second order neurone in substantia gelatinosa
- Second order neurone: decussates in ventral white commissure to contralateral side and ascends to thalamus where it synpases with third order neurone
- Third order neurone: thalamus to higher cortex (primary somatosensory cortex & OTHERS e.g. insula, anterior cingulate cortex, prefrontal)
- Brain cortex percieves stimulus as pain
Remind yourself of the difference between Adelta and C pain fibres
Idea that A fibres are myelinated & larger diameter and hence send faster signals to brain resulting in us feeling sharp pain. C fibres are thinly myelinated hence their signal transmission is slower so they are responsible for dull, achey, throbbing pains which are of longer duration
Silent nociceptors role in chronic pain.
State, and describe function of, three main pain related ascending tracks in spinal cord
- Spinothalamic tract
- Lateral spinothalamic tract: carries discriminative aspects of pain (location, intensity, duration)
- Medial spinothalamic tract: mediates autonomic and emotional components of pain. Medial spinothalamic tract interacts with many regions such as reticular formation, periaqueductal grey, hypothalamus
- Spino-reticular tract: reaches brainstem reticular formation before projecting onto thalamus & hypothalamus
What is the importance, in terms of understanding symptoms of pain, of the medial spinothalamic tract interacting with/having connections with the reticular formation?
What is the importance, in terms of understanding symptoms of pain, of the medial spinothalamic tract interacting with/having connections with the periaqueductal grey?
Describe the central modulation of pain (descending inhibiton of pain)
- Neurone in periaqueductal grey projects onto another neurone in nucleus raphe magnus- found in reticular formation in the medulla
- Neurone in nucelus raphe magnus desends down cord and stimulates inhibitory interneurones in teh dorsal horn by releasing monoamines such as serotonin, NA etc…
- Activates inhibitiory neurones in dorsal horn which can then inhibit 2nd order sensory neurones by releasing endogenous opiods
- Results in reduction of pain signals being sent ro cortex
Describe the peripheral modulation of pain (peripheral inhbition of pain)
“Gate control theory”
- Stimulate mechanoreceptors
- Signal sent from mechanoreceptor via Abeta fibres
- These stimulate inhibitory interneurones which have an inhibitory effect on the second order neurones in the spinothalamic pathway
- Inhibit second order neurones, decrease pain
Describe the mechanism of action of TENS machines
- The electrical current stimulates mechanoreceptors
- Mechanoreceptors send afferent signal via Abeta fibres
- These can stimulate inhibitory interneurones which can act on second order neurone in spinothalamic pathway and inhibit pain
What is meant by:
- Peripheral sensitisation
- Central sensitiation
… to pain?
- Peripheral sensitization: increased sensitivity of primary sensory neurons in the peripheral nervous system
- Central sensitization: increased sensitivity of spinal dorsal horn and other neurons in the central nervous system
Explain the mechanism of peripheral sensitisation (in relation to pain)
- Inflammatory mediators are released from damaged tissue e.g. histamine, bradykinin, prostaglandins, cytokines, serotonin etc…
- These stimulate nociceptors; they can stimulate silent nociceptors also, which results in an increase in number of functioning nocicpetors
- Furthermore, they decrease the threshold for action potential firing and increase amplitude of action potential
- Resulting in person feeling pain
Discuss central sensitisation to pain, include:
- Two main processes involved
- Components involved in terms of neurochemcial mediators, channels & receptors, final common pathway
Windup & sensitisation of second order neurones: econd order fibres are stimualted with low thresholdand stay activated for longer durations of time
Receptive field expansion in dorsal horn (this is why pts who have chronic pain that starts in knee can start to have pain in thigh etc…)
Components involved:
- Neurochemical mediators: substance P, glutamate & aspartate and inflammatory mediators (IL & TNF-alpha)
- Channels & receptors: Na channels, G-protein coupled receptors, NMDA, AMPA, kainate
- Final common pathway: production NO (stimulates formation of CGMP), increased intracellular calcium, phosphorylation of substrate proteins
Discuss visceral pain, include:
- Which fibres are responsible for visceral pain
- Description of visceral pain e.g. is it sharp or dull?
- What visceral pain can be associated with
- What a viscerosomatic reflex is
- Innervated by C fibres & autonomic fibres
- C fibres therefore typically dull, diffuse, poorly localised pain
- Can be associated with autonomic changes
- A viscerosomatic reflex is formed when a pain signal from an organ enters the dorsal horn of the spinal cord where neurones relating to somatic pain also reside; can result in pain signal being transmitted between the two hence feel somatic pain
Discuss the significance of a pain assessment (i.e. why we do a pain assesment)
- Pain can be extremely debilitating
- Its subjective aswell as being both physical and emotional therefore can be difficult to assess so we need tools to help us
- Precise and systematic pain assessment is required to make the correct diagnosis and determine the most efficacious treatment plan for patients presenting with pain.
State some challenges that you may face when doing a pain asssessment on a pt
- No objective measure
- Sensory/emotional experience
- Is pt able to communicate their pain
- Do environmental factors affect pain e.g. temperature
- Amount of pain does not always correlate with amount of actual tissue damage
- Presentation may be both physical and behavioural
State some tests that can be used to try and assess pain
functional MRI
PET-brain activation
Quantitative sensory testing (specialised & research settings only)
Describe the pain assessment model
Pain assessment should take an extensive history involving:
- SOCRATES
- Medical/surgical history
- Treatment history: effectiveness, side effects
- Red & yellow flags
- Psychology (more important in chronic pain)
- Psychosocial history (impact on every day life, work, family issues/support)
Remind yourself what yellow flags are (in relation to pain)
Yellow flags are pyschosocial factors shown to be indicative of long term chronicity and disability; examples include:
- A negative attitude that back pain is harmful or potentially severely disabling
- Fear avoidance behaviour and reduced activity levels
- An expectation that passive, rather than active, treatment will be beneficial
- A tendency to depression, low morale, and social withdrawal
- Social or financial problems
We’ve already discussed yellow flags for pain; you may often hear of other flags. Briefly describe what is meant by each of the following flags:
- Red
- Orange
- Blue
- Black
State some symptoms and signs of neuropathic pain
- Parasthesia
- Anaesthesia
- Severe pain
- Altered sensory function
- Allodynia: non-painful stimulus causing exagerated painful response
- Hyperalgesia: painful stimulus causing greatly increased pain response
- Hypoalgesia: decreased perception of pain caused by noxious stimulus
What are the key aspects of the examination of someone with pain?
- Gait: assess gait, any walking aids
- Ability to sit and stand up
- General mood
- Further site specific examintion: colour changes, trophic changes, hair loss in painful area, scars
- Palpation: tenderness, swelling, signs of allodynia or hyperalgesia
- Neurological examination if back & neck pain
- Physical changes:
- Physiological: increased Hr, BP, RR, nausea, temperature, sweating, pupil dilation, increased muscle tone
- Physical signs: colour, muscle wasting, muscle spasm
- Visual signs: facial expression, emotional changes, distanced pts
- Specific tests: Carnett’s sign
- Range of movement: active passive
State some pain assessment tools/scales that are used in practice
- Unidimensional pain sclaes
- Multidimensional pain scales
- Diagnostic questionnaires
Which is the most commonly used pain assessment tool/scales
Unidimensional pain scales
For unidimensional pain scales, discuss:
- What they are mainly used for
- What they measure/assess
- How they are completed
- Examples
- Mainly used to assess acute pain.
- These scales assess a single dimension of pain, typically pain intensity, and through patient self-reporting
- Self-reporting scales in which the patient assigns a value to the severity/intensity of pain.
- Examples include:
- Numerical scales (e.g. 1 to 10)
- Verbal scales (e.g. none, mild, severe)
- Visual scales (e.g. visual analogue bar with no pain at one end and severe at other, pt points to intensity of pain, faces pain scale e.g.Wong-Baker scale)
For multidimensional pain scales, discuss:
- What they are mainly used for
- What they measure
- How they work
- Examples
- Usually used in chronic pain
- They measure intensity, nature, and location of pain, as well as, in some cases, the impact that pain is having on a patient’s activity or mood
- Pt or representative completes it
- Examples:
- Brief pain inventory
- McGill Pain Questionnaire
For diagnostic questionnaires, discuss:
- What they are/why used
- How completed
- Examples
- Complex questionnaires mainly used to distinguish between neuropathic and nocicpetive pain
- Generally completed with help of clinician who is completing pain
- Examples:
- LANSS (Leeds assessment of neuropathic symptoms & signs)- 5 pain questions & 2 clinical signs- if score =/>12 indicates neuropathic pain) **COMMONLY USED IN UK
- PainDETECT
- DN4
What pain scale do we commonly use in children, those with learning disabilities and/or poor language skills?
*NOTE: can also used Pieces of Hurt scale, FLACC scale
State some pain scales designed for non-verbal adults
These sclaes focus on observations e.g. is pt comfortable, how they appear (e.g. grimace, tense), behaviour, alterness, observations e.g. BP, breathing etc…
- ABBEY pain scale: useful in dementia
- PAINAD: pain assessment in advanced dementia scale
- COMFORT: can be used in paediatrics aswell
Discuss neuropathic pain, include:
- Definition
- Whether it is central or peripheral or both
*
- Pain due to damage to or disease affecting the somatosensory system
- Can be central (e.g. after stroke, MS) and peripheral (e.g. after injury to nervous system e.g. post surgical)
Remind yourself of the defintions of the following:
- Neuralgia
- Neuritis
- Neuropathy
- Neuralgia: pain in distribution of a nerve or nerves
- Neuritis: inflammation of nerve or nerves
- Neuropathy: disturbance of function or pathological change in a nerve (one nerve= mononeuropathy, several= mononeuropathy multiplex, diffuse & bilateral= polyneuropathy)
State, and describe/define, some pain sensations related to neuropathic pain (7)
- Allodynia: non-painful stimuli causes pain
- Analgesia: absence of pain in response to a stimuli that would usually cause pain
- Anesthesia dolorosa: pain in an area or region which is anaesthetic (numb to touch)
- Dysesthesia: unpleasant abnormal sesnsation whether spontaneous or evoked
- Hyperalgesia: increased pain from a stimulus that normally provokes pain
- Hyperesthesia: increased sensitivity to stimulation, excluding the special senses
- Hyperpathia: painful syndrome characterised by abnormally painful reaction to a stimulus, especially a repetitive stimulus, aswell as increased threshold
The pathophysiology of neuropathic pain is complex; discuss some of the proposed pathophysiology. Consider pathophysiology at different levels e.g:
- Peripheral fibres
- Dorsal root ganglia
- Spinal cord
- Brain
State some common causes of neuropathic pain; split this causes of peripheral lesions and central lesions
Peripheral Lesions
- Post surgical pain (mix of nociceptive & neuropathic pain)
- Post-herpetic neuralgia
- Trigeminal neuralgia
- Complex regional pain syndrome (CRPS) type 1
- Painful diabetic neuropathy
- Phantom limb pain
- Direct nerve injury as a result of e.g. trauma, cancer, HIV, alcohol, chemotherapy etc…
Central Lesions
- Central post-stroke
- Multiple sclerosis
- Spinal cord injury
State some populations in which neuropathic pain is more common
- Women
- People of older age
- People who are unemployed
- People from lower educational background
State some risk factors for post-herpetic neuralgia
- Age
- Female
- Immunosupression
- Severe prodromal perios
- Severe pain during prodrome
- Severity of rash & pain during rash
- Opthalmological involvement
- Depression & anxiety
For post-herpetic neuralgia, discuss:
- What it is
- How many people it affects
- Affect of age on incidence
- Classifications of HZ pain
Discuss the pathophysiology of post-herpetic neuraglia
- NOTES:*
- Peripheral sensitisation of area around the area that was innervated by the damaged nerve
Discuss the clinical presentation of post-herpetic neuralgia
- Shingles history
- Pain:
- Area of shingles rash
- Constant or intermitent
- Intensity increases during day
- Burning, stabbing, shooting, like electric shocks
- Itching in area of shingles rash
- Associated with allodynia, hyperalgesia, hypoaesthesia
- Associated with weithg loss, anorexia, chronic fatigue, sleep disturbance
- Associated with mod & behavioural changes
Discuss the management of post-herpetic neuralgia
- Pt education: wear lose clothing, consider ice packs if don’t cause allodynia, nature of disease (50% show improvemetn at 6 months)
-
Anaglesia:
- Can try paracetamol, codeine
- Can give analgesia for neuropathic pain e.g. amitriptyline, duloxetine, gabapentin, pregabalin, tramadol
- Topical analgesia e.g. capsacin cream, lidocaine plasters
Discuss how we can prevent post-herpetic neuralgia
- Vaccine for primary varicella & for herpes zoster virus (have HZ virus when 72yrs or 78yrs)
- Antiviral medication- e.g. aciclivor for 7 days
Diabetic neuropathy is a common cause of neuropathic pain; state some alternative differentials for someone presenting with what seems like diabetic neuropathy
- Alcohol
- B12
- Thyroid
- Spinal stenosis
- HIV
- Cancer & treatment
Pathophysiology of diabetic neuropathy is complex; summarise the pathophysiology
Multiple processes induce oxidative stress and endothelial damage which cause neuronal ischaemia, neuronal damage and reduce neuronal degeneration
Briefly outline the management of neuropathic pain due to diabetic neuropathy
- Improved glycaemic control
- Manage other risk factors e.g. smoking, BMI, hyperlidaemia
- Pain therapy: anticonvulsants, SNRIs, tricyclic antidepressants
Pts with HIV and AIDS can experience neuropathic pain; true or false?
True!
Summarise commonly used medications in neuropathic pain
Amitriptyline & nortriptyline= TCAs
Duloxetine & venlafaxine= SNRIs
Doses of antidepressants used in neuropathic pain are the same as doses used to treat depression; true or false?
FALSE; doses used for neuropathic pain are lower than doses used in deprssion. ***EXCEPTION: is duloxetine were doses are same
What is discontinuation syndrome?
Discuss the advantages and disadvantages of cannabinoids to terat pain
Why do we manage pain?
*HINT: think about benefits of pain management and consequences of poorly managed pain
- Pain relief is every person’s right
- Pain management improves:
- Physical function
- Mental function
- Quality of life
- If pain is poorly managed:
- Delayed healing
- Decreases appetite
- Increased stress
- Anxiety and depression
- Disrupt sleep
What systematic aproach do we use to manage pain?
Discuss the RAT approach to pain management?
Recognise:
- Does pt have any pain?
- Do other people know pt has pain?
Assess
- How severe is pain?
- What type of pain is it? Acute/chronic, cancer/non-cancer, nocicpetive/neuropathic
- What other factors involved? e.g. physical factors such as activity exacerbates pain, psychological e.g. is pt having anxierty & depression seonceary to pain, social e.g. affecting everyday life
- What is the pain score?
- How is pain affecting the pt?
Treatment
- What non-pharmacological treatments can be use?
- What pharmacological treatments can be used?
What are the 4 main vital signs?
What is the ‘5th vital sign’?
Pain= “5th vital sign”
Compare acute and chonic pain
Compare nocicpetion and pain
- Nocicpetion: how pain signals get from site of injury to the brain
- Pain: how we perceive or feel pain
Discuss some non-pharmacological treatments for pain, include:
- Physical treatments
- Psychological treatments
- Physical treatments:
- Rest, ice, compression, elevation
- Surgery
- Acupuncture, massage, physiotherapy
- Psychological treatments:
- Explanation
- Reassurance
- Counselling e.g. CBT
Discuss some pharmacological treatments for pain
- Simple analgesics:
- Paracetamol
- NSAIDs e.g. ibruprofen
- Opiods:
- Mild: codeine, tramadol, dihydrocodeine
- Strong: morphine, pethidine, oxycodone
- Others:
- TCAs
- Anticonvulsants e.g. carbamezapine, gabapentin
- Local anaesthetics
- Ketamine
- Clonidine
- Adjuvants:
- Capsaicin
- Cannabinoids
- Muscle relaxants e.g. baclofen, benzodiazepines
- Corticosteroids if acute inflammation
What pain treatments work/exert their pain-relieving effects in the periphery?
- RICE
- NSAIDs
- Local anaesthetics
What pain treatments work/exert their pain-relieving effects in the spinal cord?
- Non-pharmacological e.g. acupuncture, massage
- Local anaesthetics
- Opiods
- Ketamine
What pain treatments work/exert their pain-relieving effects in the brain?
- Psychological e.g. CBT
- Paracetamol
- Opiods
- TCAs e.g. amitriptyline
Describe the WHO analgesic ladder
Treats nociceptive pain!
Discuss what is meant by the reverse WHO ladder
- Idea that start at top and step down ladder as pain improves (whereas normally would move up ladder)
- Useful for severe acute nociceptive pain e.g. trauma, post-operative pain
Opiods are usually not helpful for chronic non-cancer pain or neuropathic pain; true or false?
True
Oral dose of morphine is ____ times the IV/IM/SC dose
2-3 times
What are the 3C’s of opiod addiction
After using RAT system to manage pain what should you do?
Use RAT system again to reassess
- Is your treatment working?
- Are other treatments required?
What is PCA?
- Patient controlled analgesia
- Small doses of analgesic drug, usually opiods, are administered (IV) by the patient
- Allows basal infusion and demand boluses
- Overdose is avoided by limiting the amoutn and number of boluses in a set period of time
What does the Oxford Analgesic League table tell you?
Efficacy of pain medications in regards to NNT to give at least 50% pain relief
REVISE ANALGESICS & NSAIDS form CPT
For paracetamol (acetaminophen), discuss:
- Mechanism of action
- Max dose per infusion and per day for >50kg adult
*
- MOA: not fully understood; some proposed mechanisms include prostaglandin inhibition in brain, serotonin pathwy activation, endocannabinoid enhancement
- Max dose per infusion=1g, max daily dose=4g (adult >50kg)
Discuss the metabolism of paracetamol
For tramadol, discuss:
- Mechanism of action
- How it can be given
- Indications
- Advantages
- Disadvantages
- Dual mechanism of action: partial agonist at MOP receptor as well as inhibition of monoamine (serotonin, norepinephrine) re-uptake
- IV, IM
- Indications: nociceptive & neuropathic pain
- Contraindications: epilepsy (reduces seizure threshold), SSRIs & SNRIs- increase risk seizures & serotonin syndrome, warfarin (increases anticoauglation effects of warfarin)
- Advantages: safe, useful for different types of pain, can be used with morphine
- Disadvantages: nausea & vomitting, confusion, convulsions, psychiatric reactions, hyponatramia, hypoglycaemia, constipation (less so than morphine)
*NOTE: can give tramadol & another opiate e.g.morphine as tramadol has weak opiod action and has additional mechanisms of action. In practice will see people are hesitant to give tramadol with morphine
For amitriptyline, discuss:
- Mechanism of action
- Indications
- Advantages
- Disadvantages/side effects
It prevents the re-uptake, and hence the inactivation of noradrenaline and serotonin at nerve terminals
Indications: neuropathic pain
Adavantages: cheap, safe in low doses, also treats depression & poor sleep
Disadvantages/side effects: harmful in overdose, dry mouth, drowsiness, urinary retention
For NSAIDs, discuss:
- Mechanism of action
- Contraindications
- Side effects/ADRs
- Inhibit COX enzymes and therefore inhibit prostaglandin synthesis. Prostaglandins used in transmission of pain therefore inhbiting production inhibits transmission.Prostaglandins sensitise nociceptors to other inflammatory mediators hence why NSAIDs good in inflammatory pain.
- Contraindications:
- High cardiovascular risk
- Poor renal function
- GI disease
- Drug-drug interactions e.g. ACEinhibitors, ARBS, diuretics, sulphonylureas, methorextate, warfarin
- Side effects:
- GI related e.g. dyspepsia, nausea, pepticu ulceration, bleeding, perforation
- Renal ADRs
Opiods can be classified in many ways; discuss these different classifications
- By synthetic process (naturally occuring, semi-synethetic, synthetic)
- By degree of pain relief e.g weak or strong
- By degree of receptor affinity e.g. partial agonist, agonist, antagonist etc…
Opiods can be classified by their synthetic process; state some examples of:
- Naturally occuring compounds
- Semi-synthetic compounds
- Synthetic compounds
Describe the mechanism of action of opiods
- All opiod receptors are inhibitory G-protein coupled receptors. Activation of these receptors causes:
- Closure of voltage gated Ca2+ channels in pre-synaptic neurone resulting in decreased neurotransmitter release
- Activation of K+ channels in the pre-synaptic neurone causing efflux of K+ and therefore hyperpolarisation of post-synaptic neurone which consequenlty decreases action potential firing
- Also get decreased cAMP production which results in decreased neurotransmitter release
Discuss some side effects of opiods
Potential long term:
- Lowered immunity
- Opiod-induced hyperalgesia (nociceptive sensitisation)
- Tolerance/addiction
- Supression hypothalamus-pituitary-adrenal axis
State some contraindications to opiods
- Acute respiratory distress
- Comatose
- Head injuries
- Raised ICP
- Hepatic failure *be cautious
Describe the opioid aware campaign
Discuss the metabolism of codeine
- Metabolised into morphine by CYP2D6 (ultrarapid metabolisers have mutation in CYP2D6 leading to rapid metabolisation of codeine resutling in opiod intoxication)
- Most of codeine converted to gluconoride by liver and excreted by kidneys. Some is metabolised by CYP3A4 into norcodeine (derivative of codeine with little opiate action)
Remind yourself of the metabolism of morphine
Metabolised into M6G (analesica) and M3G (neuroexcitatory/euphoric effect)
Discuss how antidepressants work as analgesics
Antidepressants work as analgesics by increasing levels of serotonin and noradrenaline (if TCA) and noradrenaline only (if SNRI); these monoamines are involved in the central modulation/descending inhibition of pain
State some side effects of TCAs
State some side effects of SSRIs/SNRIs
Discuss how anticonvulsants work as antidepressants
What are neuroaxial blocks?
Neuraxial anesthesia is the administration of medication into the subarachnoid or epidural space to produce anesthesia and analgesia
Remind yourself of the anatomy of the spine, including:
- Spinal cord: where it starts and where it ends
- Cauda equina
- Meninges in spine
- ‘Spaces’ in spine
- Cervical & lumbar enlargements
- Epidural space
- Ligaments
- Spinal cord begins at base of medulla oblongata and extends down to L1/L2
- Cauda equina: L2-S5
- Meninges: pia mater surrounding cord. Filium terminale connects pia mater to sacrococcygeal membrane. Then have subarachnoid space containing CSF. Then have arachnoid layer. Then outermost dura layer. there is a potential space between the dura and arachnoid called the subdural space.
- Subarachnoid space containing CSF. Since spinal cord stops at L1/L2 below this subarachnoid space expands and is referred to as the lumbaar cistern.
- Cervical enlargement: C4-T1, lumbar enlargement: T11-L1
- Epidural space: potential space between the dura mater and the vertebral wall containing fat, small blood vessels, lymphatics etc
- Ligaments: see image
For a spinal anaesthetic, discuss:
- What it involves
- Where it blocks from/what level
- How it is performed
- What layers the needle must pass through
- Inject local anaesthetic (with or without opiates) into the CSF in the subarachnoid. Blocks nerves in that area and then when patient lies supine it spreads following natural curves of spine (lordosis & kyphosis) allowing use to block nerves up to T4 level. Pt will be numb from waist down and will not be able to move their legs
- Insert, usually a 25G needle, between L4/L5. Have pt lie on side with knees curled up or sit on side of bed with feet on low stool
- Feel pop as you go through dura & arachnoid; then CSF should leak out
- Layers: skin, subcutaneous tissue, supraspinous ligament, interspinous ligament, ligamentum flavum, epidural space, dura, subdural space, arachnoid layer and then in subarachnoid sapce
How do we estimate where the L4/L5 intervertebral space is?
Estimate that line between two iliac crests correlates to L4/L5; however, recent studies have shown that this actually correlates to levels ~L2/L3
For an epidural, discuss:
- How it is performed; include two possible techniques
Include the layers the needle must pass through
- 16G/18G epidural needle.
- Most common methos is loss of restistanc method: Pass through interspinsous ligament, once through interspinous ligaments attach a loss of resistance syringe; this syringe is filled with saline. Anaesthetist applies constant pressure to plunger of needle; since liquid is incompressible, as the anaesthetist is passing through the interspinous ligament they will feel extreme resistance. Once needle has passsed through interspinous ligament and ligamentum flavum (this part feels gritty) they will feel the plunger depress (as saline can move into epidural space).
- Hanging drop method where you put autodrop on end of needle and once needle reaches epidrual space that water drop will be sucked in
- In both methods thread an epidural catheter through the needle. Then give drugs via epidural catheter; this can be bolus, infusion or PCA. Can be used for days.
- Layers: skin, subcutaneous tissue, supraspinous ligament, interpspinous ligament, ligamentum flavum
Discuss the differences between spinal and epidural anaesthetics, include:
- Where in spine they are performed
- How long pain relief last for
- Drug volumes required
- Onset
Discuss some indications and benefits of spinals and epidurals
- Surgery below level of umbilics e.g. obstetric, gynaecological, urological, lower abdominal, perineal, orthopaedic
- Avoids complications of GA
- Lower risk of thrombosis
- Lowers risk of bleeding
- Lowers risk of cognitive decline in elderly
State some absolute and relative contraindications to neuroaxial blocks
*fixed cardiac output e.g. aortic stenosis
Discuss some minor, moderate and major complications of spinal anaesthetics & epidurals
State some side effects of general anaesthetics and some side effects of local anaesthetics
What is a nerve block?
Local anesthetic nerve block is a short-term nerve block involving the injection of local anesthetic as close to the nerve as possible for pain relief. The local anesthetic bathes the nerve and numbs the area of the body that is innervated by that nerve. Done under ultrasound.
If someone is on long-term opiods, their PRN dose of opiods should be 1/_ of the total morphine dose (in 24hrs)
PRN dose should be 1/6 of the total opiod dose. PRN dose can be prescribed 4hrly
