301 Pain Flashcards
Describe the pain pathway and relevant neurotransmitters
Stimulus: Noxious input activates C-fibers
Releases mediators (e.g., BK, 5-HT, PGs), NGF, and neuropeptides (SP, CGRP)
Excites neurons that carry pain signals to the brain
Enkephalins and GABA further inhibit pain transmission
Key Neurotransmitters: 5-HT, NA, enkephalins, GABA
What do opioids do in the pain pathway?
Endogenous/exogenous opioids inhibit pain signals
What happens in descending pain pathway?
Serotonin (5-HT) and noradrenaline (NA) reduce pain perception
Nociceptor structure
Cell body with cross section of spinal cord including peripheral terminal (somatic, visceral) and central terminals (spinal cord dorsal horn, brainstem)
Types of fibers in the peripheral nerves
Aδ Fibers: thin, myelinated fibers; transmit sharp, fast pain (acute pain)
C Fibers: unmyelinated fibers, carry dull, slow pain (chronic pain)
Aβ Fibers: thick, myelinated fibers, transmit touch & pressure, can inhibit pain when stimulated (e.g., rubbing a sore area)
What is the difference between Aδ and C fibers and Aβ fibers?
Aδ and C fibers carry pain while Aβ modulates it
What activates nociceptive neurons, and how is pain signal transmitted?
Activation
Release of mediators
Response pathway
Transmission to CNS
- Heat, cold, pressure, & tissue injury stimulate nociceptive neurons in the periphery
- Injured tissues release substances like bradykinin, prostaglandins, ATP & H+ ions
- Mast cells or neutrophils release histamine & Substance P
CGRP & Substance P cause vasodilation in blood vessels
Nerve Growth Factor (NGF) and serotonin (5-HT) contribute to pain signal - Signals travel to the dorsal root ganglion (DRG), spinal cord & higher brain centres, creating sensation of pain
How is pain transduced from stimulus to action potential in nociceptive fibres?
Overview
Aβ-fiber
Aδ-fiber
C-fiber
- Stimulus activates mechanoreceptors or channels, creating a generator potential, which leads to an action potential
- Mechanoreceptors trigger Na+ influx via voltage-sensitive sodium channel
- Responds to histamine & bradykinin (BK) through H1 & K+ channels
- Responds to noxious stimuli through VR1 receptors, allowing Ca2+ & Na+ influx
What stimuli trigger each of the peripheral nerve fibers?
Aβ - non-noxious mechanical stimuli
Aδ - noxious mechanical stimuli
C - noxious heat and chemical stimuli
What are the main transducers in nociceptors, and how do they relate to pain perception?
Heat (Capsaicin)
Cold (Menthol)
Acidic environments
Mechanical sensitivity (pressure)
Pathway
Result
- Activates TRPV1 receptors
- Activates TRPM8 receptors
- Stimulate ASIC & DRASIC receptors
- Activates MDEG, DRASIC, TREK-1
- Activation of NaV1.7, 1.8, 1.9 channels generates an action potential
- Signal travels through the dorsal root ganglion to the spinal cord & brain, leading to pain sensation & withdrawal or emotional reactions
First and second pain: hand on hotplate example
- Immediate, sharp, localised pain, transmits by A-delta fibers (myelinated), alerts you to move hand preventing further harm
- Slower, duller pain, transmits by C fibers (unmyelinated), sensation lingers with prolonged discomfort, reminder of injury to not re-injure whilst healing
What happens when nociception arrives in spinal cord?
Dorsal horn of spinal cord receives nociceptive signals
Integration & transmits information to CNS regions
Pain modulation mechanism theory of pain: Cartesian model of pain
This does not explain the whole story: things are more complex that this picture shows
Complexity cannot be explained by a simplistic relationship between peripheral and CNS
Pain modulation mechanism theory of pain: gate theory of pain
(Attempted to explain some complexity)
C-fibre nociceptor signal are inhibited at spinal cord level by large nerve fibres (A-alpha, A-beta) before they are transmitted to brain & perceived as pain
Gate theory of pain in practise:
TENS (Transcutaneous Electrical Nerve Stimulator)
Physical therapies (principal of counter-stimulation)
Spinal cord stimulators
- Used for labour or low back pain
- Heat, cold massage, manipulation & acupuncture
- Patients with chronic pain when other methods fail, same principle as TENS
Descending modulatory system
Descending nerve pathways from brainstem, inhibits facilitate nociceptive signals in spine
Implies pain perceived in brain can be decreased or increased
Hence modification of gate theory to include descending nerves
What neurotransmitters are involved in descending modulation?
Opioids
Serotonin (5HT)
Noradrenaline
Gamma amino butyric acid (GABA)
Bidirectional pain network
Noxious signal being modulated at several levels between spinal cord and brain
1. Cognition
2. Mood
3. Experience
4. Attention
Types of nociceptive pain
Somatic - well-localised, pain receptors in soft tissue, skin, skeletal muscle & bone
Visceral - vague, visceral organs
Neuropathic - damaged sensory nerves
What is nociceptive pain?
Response to pathophysiological process occurring in tissues (inflammation)
Pain signal originates in primary afferent nerves signalling noxious events
What are nociceptors?
Pain activated by agents like prostaglandins, bradykinin, serotonin, adenosine & cytokines
What is neuropathic pain?
Signals generated ectopically without ongoing noxious activity from pathologic route in peripheral or CNS
Pain classification
Duration, intensity, presumed pathophysiology (visceral, somatic, sympathetic), opioid sensitivity, pragmatic
Practical pain classification
Neuropathic - disordered sensation - anticonvulsants & antidepressants
Bone - intense & focal - NSAIDS & bisphosphonates
Muscle spasm - muscle relaxants & antispasmodics
Cerebral irritation - caused by brain injury, sign of anxiety - BZDs
Pain control mechanisms
Aspirin and NSAIDS
Morphine and opioids/cannabinoids
TENS
Deep brain stimulation
Placebo
Acupuncture
Hypnosis
Anatomy of pain pathway
Primary afferent neuron –> dorsal root ganglion —> second order neurons –> to brainstem and thalamus
WHO pain ladder and analgesics
Step 1. non opioid (paracetamol)
Step 2. weak opioid (codeine mild/moderate pain) + non opioid
Step 3. strong opioid (morphine for moderate/severe pain) + non opioid
WHO cancer pain ladder for adults
- Non opioid +/- adjuvant (paracetamol & NSAIDS)
- Opioid for mild to moderate pain +/- non-opioid & +/- adjuvant (codeine, dihydrocodeine & tramadol)
- Opioid for moderate to severe pain +/- non-opioid & +/- adjuvant (morphine, diamorphine, buprenorphine, fentanyl & oxycodone)
What is the afferent and efferent neuron?
Afferent - sensory
Efferent - motor
What can anti-inflammatory medication inhibit in the pain pathway and what does it cause?
NSAIDs can inhibit release of mediators like prostaglandins, reducing inflammation & pain
What do the ascending and descending pain pathways do?
A: transmits pain signals to brain
D: modulate and inhibit signals to manage pain perception
What takes place in the ascending pain pathway?
Pain signals travel from C and Aδ fibers in spinal cord brain
Signals pass through medulla, pons & midbrain
They reach the thalamic nuclei and forebrain, processing “early pain” (sharp, initial pain) and “late pain” (dull, prolonged pain)
Reticular formation & periaqueductal gray are involved in pain perception
What takes place in the descending pain pathway?
Pain modulation starts in the frontal cortex, hypothalamus, and periaqueductal gray
These pathways involve locus coeruleus, raphe nuclei, and medulla, releasing inhibitory signals
Signals descend to the spinal cord, reducing pain transmission from skin & other areas
Summary of entire pain pathway:
Site of injury
Spinal cord
Brainstem
Cerebrum
- Pain begins with injury stimulating unmyelinated C-fibers & myelinated Aδ fibers, detect & transmit pain signal
- signal travels along afferent nerves to spinal cord, where synapses & ascends via spinothalamic tract
- Signal moves through brainstem, including reticular formation & midbrain, where modulated
- Signal reaches thalamus & relayed to cerebral cortex for perception, allowing individual to feel & localise pain
Definition of pain
An unpleasant sensory & emotional experience associated with, or resembling that associated with, actual or potential tissue damage
Major features of pain experience
Sensory discriminative
Affective (emotional)
Cognitive
What is nociception?
Nociception is neural process of encoding noxious stimuli, it is triggered when noxious stimuli act on specialised peripheral nerve endings
What can occur in nociception?
It does not necessarily result in individual perceiving pain
It also possible for an individual to perceive pain when there is no nociception, occurs in some chronic pain states
Types of pain
Acute, chronic, malignant vs nociceptive, neuropathic
What are the 3 basic causes of pain?
- Acute trauma or injury
- Chronic painful conditions for which cures were unknown
- Malignant processes (cancer and arthritis)
What 2 types of pain are shown in modern research?
Nociceptive pain
Neuropathic pain
Where is the cell body located in nociceptors
- Dorsal horn of spinal cord
- Vagus nodose ganglion
- Trigeminal ganglia
What is a nociceptor?
Peripheral sensory terminal (part that senses noxious stimulus)
A central termination within spinal cord or brainstem
What activates nociceptors?
- Physical trauma
- Chemicals
- Excessive heat or cold
- Stretching beyond normal range, which can trigger nociception in muscle
- Ischaemia (insufficient blood flow) e.g. angina and inflammation also causes pain
What is capsaicin?
Gives chilli peppers their heat, may help wound healing by reducing inflammation
What are A-alpha/A-beta fibres in nociception?
What type of nociception?
What type of structures are they?
What are the terminals associated with? Transmission speed?
Mechanical & thermal nociception
Innervate somatic structures
Terminals associated with specialised sensory structures
Proprioceptive (skeletal muscle, tendon organs), mechanosensitive (light touch)
Very fast (30-120 m/s)
What are A-delta fibres in nociception?
What type of nociception?
What type of structures are they?
What type of nerve endings?
Transmission speed?
Mechanical, thermal & chemical
Innervate somatic & visceral
Specialised or free
Mechanosensitive (stretch & touch skin, viscera)
Thermosensitive
Fast (4-30m/s)
What are C fibres in nociception?
What type of nociception?
What type of structures are they?
What type of nerve endings?
Transmission speed?
Mechanical, thermal & chemical
Innervate somatic & visceral
Free nerve endings
Mechanosensitive (stretch & touch)
Thermosensitive
Chemically sensitive (itch)
Slower <2.5m/s
Natural products and what can they treat?
Capsicum (TRPV1)
Mentha (TRPM8)
Brassica (TRPA1)
Allium (TRPA1)
- Heat
- Cold
- Pain
- Pain
Cross section of peripheral nerve fibres:
Aβ
Aδ
C
- Large myelinated fibres (response e.g. to light touch, joint movements)
- Small myelinated fibres
- Unmyelinated fibres: these conduct very slowly & most of them are those that are involved in generating pain message
What is the first and second type of pain and what are the signals carried by?
- Sharp & brief, myelinated Aδ neurons
- More delayed & longer lasting, feels more dull, thin & unmyelinated C fibres
What are the 2 possible outcomes when nociception arrives in the spinal cord?
- Can trigger reflex activity like hotplate example - occurs within spinal cord
- Convey information to brain regarding location & intensity of stimulus
Function & contribution to pain perception:
Somatosensory cortex
Limbic system
Prefrontal cortex
- Sensory discrimination & localises site, quality and intensity of stimulus
- Affective-motivational function & emotional aspects of pain, attention to & memory of pain
- Cognitive evaluation of pain & executive control of purposeful behaviour, emotion, memory and decision making
What is somatosensation?
Sense of touch, or the ability to perceive stimuli related to temperature, pressure, pain, body position, and balance
What is proprioception?
Sense of body position and movement
What is nociception?
Process by which the central and peripheral nervous systems (CNS and PNS) process harmful stimuli, such as tissue damage or extreme temperatures
What is acute pain?
Sudden, sharp pain that’s usually caused by an injury, illness, or other environmental stress
What is chronic pain?
Pain that lasts longer than the typical recovery period or occurs along with a chronic health condition
What is neuropathic pain?
Nerve pain that can happen if your nervous system malfunctions or gets damaged
What is allodynia?
A condition where a stimulus that normally wouldn’t cause pain results in pain
What is noxious stimulus?
Physical change that can be internal or external and is strong enough to potentially damage tissue or threaten the body’s integrity
What is sensitisation?
Process that occurs in the nervous system and a type of non-associative learning
What is central sensitisation?
Condition where the central nervous system (CNS) becomes hypersensitive to pain and other sensory stimuli
What is hyperalgesia?
An increased sensitivity to pain or an extreme response to pain
What is the dorsal root ganglion?
Neural structure in the spinal column that plays a key role in processing and developing chronic pain
What are projection neurons?
Neurons in the central nervous system (CNS) that send axons from their cell bodies to other regions of the CNS
What is the spinothalamic tract?
Sensory pathway in the nervous system that carries information about pain, temperature, touch, and pressure from the skin to the brain
What are the spinobulbar tracts?
Pathways that carry information up and down the spinal cord between brain and body
What is the somatosensory cortex?
The part of the brain that receives and processes sensory information from the body, such as touch, temperature, and pain
What is analgesia?
Pain relief or absence of pain
What is musculoskeletal pain?
Conditions
Damage to bones, joints, muscles, tendons, ligaments etc
Osteoarthritis (OA), rheumatoid arthritis, lower back pain
What is osteoarthritis?
Clinical syndrome of joint pain accompanied by varying degrees of functional limitation & reduced QoL
Most common form of arthritis and 1 of leading causes of pain & disability worldwide
NICE guidance for osteoarthritis treatment
- Offer topical NSAIDs to people with knee OA
- Do not routinely offer paracetamol or weak opioids unless used infrequently for pain relief & other treatment C/I
- Explain to OA patients no strong evidence of paracetamol benefit
Osteoarthritis diagnosis
Diagnose clinically without investigations if person is 45+ and has…
- Activity-related joint pain
- Either no morning joint-related stiffness or morning stiffness no longer than 30 mins
- Differential e.g. gout, RA, malignancy
Assessing pain:
Numerical rating scale
Visual analogue scale
- Mark on scale of 0 (no pain) to 10 (worst) how strong it is
- Mark on 10cm line with no pain at one end and worst pain at other
Mild: 3/10
Mild to moderate: 3-6/10
Severe: 6/10
Non-pharmacological management of osteoarthritis
- Exercise: muscle strengthening & aerobic fitness
- Weight loss
- TENS
- Neutraceuticals: no glucosamine/chondroitin
- Acupuncture: no
- Manipulation & stretching
- Aids & devices
WHO pain ladder:
Step 1
Step 2
Step 3
- Simple analgesics e.g. aspirin & paracetamol
- Opioids suitable for mild to moderate pain use & simple analgesics
- Opioids suitable for severe pain use & simple analgesics
Paracetamol pharmacology
- Analgesic & antipyretic
- Little or no anti-inflammatory activity (not considered NSAID)
- MOA unknown (weak inhibitor of COX1 and COX2, possible greater effect in CNS)
- Very minimal GI irritation
- No effect on bleeding time
- No effect on respiration
- Not uricosuric
What are anti-pyretic and uricosuric meanings?
- Reduces fever by tricking hypothalamus into overriding temp caused by prostaglandins
- Drugs that promote uric acid secretion
NSAIDs pharmacology
- Analgesic, antipyretic, anti-inflammatory
- Inhibit peripheral prostaglandin synthesis
- Prostaglandins implicated in pathogenesis of fever & inflammation
- Inhibit cyclo-oxygenases (inhibition of COX2 = therapeutic effect, COX1 = adverse effects)
- COX2 selective/COX2 specific NSAIDs (Coxibs)
- Standard NSAIDs = non selective
NSAIDs indication
- Fever
- Inflammation
- Mild/moderate pain
- Musculoskeletal pain
What do COX1 and 2 do?
Important products
Inhibition
- metabolise arachidonic acid
- Prostaglandins E2, D2, F2, A2 and I2 (prostacyclin)
- Non-selective NSAIDs block both COX1 and 2 enzymes
Selective COX2 inhibitors specifically target COX2 without affecting COX1
Diclofenac and ratio (COX2:COX1 50% inhibition)
Diclofenac is COX2 selective with a ratio of 0.05
Opioid analgesics pharmacology
Opioid - morphine like effects
Opiate - morphine & codeine
Agonists at opioid receptors
- Morphine, diamorphine, oxycodone, codeine
- Pethidine & fentanyl
- Buprenorphine
Opioid analgesics:
Codeine/dihydrocodeine
Tramadol
- Pro-drug - metabolised to morphine (5-10% population lack gene)
MOP agonist (+KOP & DOP)
Mild pain - Weak agonist
Inhibits MAO
Effects of opioid receptor stimulation
Analgesia
Respiratory depression
Pupil constriction
Reduced GI motility
Euphoria
Hallucinations
Sedation
Catatonia
Dependence
Analgesic efficacy in osteoarthritis:
Short term
Moderate term
Long term
- NSAIDs (oral & topical) offer robust relief
- Duloxetine for several months
- Limited (NSAID or opioid use generally avoided due to risks), non-pharmacological approaches
Topical NSAIDs vs placebo efficacy
Topical NSAIDs superior for 1st 2 weeks but not following 2 weeks
Topical NSAIDs and topical capsaicin
- More efficacious than placebo, trial evidence is poor, evidence suggests ineffective after 2 weeks to 1 month use
- More efficacious than placebo
Not tolerated in 1/3 patients
NSAID effectiveness
No important differences in efficacy between NSAIDs
Benefits of NSAIDs increase towards max. value at high dose
No ceiling for adverse effects which increased in approx. linear fashion with dose
(Consider individual response, some patients need to try different NSAIDs)
Tramadol in osteoarthritis
Codeine should be tried first
Profile for tramadol similar to codeine (but more SEs, now a CD)
Some evidence of effectiveness in OA
Paracetamol side effects
- Overdose = liver toxicity due to glucuronide conjugation saturated & mixed function oxidase metabolism (2ndary pathway) produces highly reactive free radicals
- Hepatic necrosis occurs after 10-15g dose, >25 fatal
- Increased hepatotoxicity taken with alcohol or due to alcohol inducing MFO pathway or while fasting (4g/day)
- Nephrotoxicity - renal tubular necrosis, increased risk if lifetime in take >1000 tablets
NSAID ADRs
Upper GI bleed 18 per 100,000
Acute renal failure 10 per 100,000
Congestive heart failure 22 per 100,000
NSAIDs main side effects
GI side effects, dyspepsia, ulceration, bleeding
Indomethacin = more common
Ibuprofen = less common
What 3 drugs have high COX2 selectivity?
- Rofecoxib (Vioxx)
- Etodolac (Ultradol)
- Celacoxib (Celebrex)
GI side effects: influencing factors with NSAIDs
Type of NSAID (COX2 selectivity, half-life, acidity)
Current vs past vs never use
Duration of use
Dose
Hx of PUD
Age of patient
NSAID renal side effects
Renal perfusion depends on prostaglandins (cause vasodilation, opposing vasoconstriction of NA & angiotensin II)
NSAIDs CV side effects
Patients with CHF, chronic renal disease (NSAIDs decrease renal blood flow & GFR, creatinine clearance may fall up to 50%)
Promote salt & water retention (reduce PG inhibition of both chloride re-absorption & ADH action, may cause oedema, oppose anti-hypertensive action)
Promote hyperkalaemia by PG renin secretion suppression, enhance reabsorption of K+ due to decreased availability of Na+ at distal tubular sites
May progress to irreversible renal insufficiency
Other side effects of NSAIDs:
CNS
Ocular
Others
- Dizziness, lightheadedness, headache (indomethacin = severe frontal headache)
- Blurred vision, corneal opacity (indomethacin)
Reversibly prolong bleeding time
Cross hypersensitivity with aspirin (worsening of asthma (CSM warning))
Skin rash
Weight gain
Why do COX2’s have adverse CV effects?
- Within endovascular lumen platelet COX1 dependent prothrombotic (TXA2) & endothelial COX2 dependent antithrombotic (PGI2) are balanced so prevent coagulation
- Selective COX2 inhibitors impair PGI2 synthesis but lack antiplatelet effects, tipping scales in favour of relative increases in TXA2, thrombogenesis & increasing CV event risk
Why do vets want to ban diclofenac?
1.In India Gyps Vulture experience fastest decline in any bed - 95% in 10 yrs
2. Vultures eat dead cattle bodies
3. Diclofenac extensively used in cattle
4. Birds dying from renal failure
NSAID CV adverse effects:
Coxibs
Diclofenac
- Cause small increase of thrombotic effect risk compared to placebo, estimated 3 per 1,000 for one year on average, all coxibs C/I in IHD patients, peripheral arterial disease and/or CV disease
- Diclofenac 150mg has thrombotic risk profile similar to coxibs
Current guidance on coxibs and diclofenac
Both C/I for ischaemic heart disease, peripheral arterial disease, cerebrovascular disease and congestive heart failure
Why worry about 3 in 1000 thrombotic effects when using coxibs and NSAIDs?
Statins (at 20% 10 year CVD risk) reduce rate of events by 5 in 1000 people per year
UK pop. about 65% NSAID plus COX2 prescribing is diclofenac or coxibs
For individual trade off benefits/risks
Paracetamol vs oral NSAID evidence summary:
Efficacy
Safety
- Paracetamol provides less pain reduction than oral NSAIDs
- Oral NSAIDs greater risk of GI adverse effects than paracetamol
COX2 lower GI risk than NSAID (eliminated by low dose aspirin)
PPI reduce GI risk in patients taking NSAIDs & COX2
COX2 & diclofenac increase CV disease risk
NSAID induced GI events: people at high risk have 1 or more risk factors
- Using max. recommended dose of NSAID
- 65+
- Hx gastroduodenal ulcer, GI bleeding or gastroduodenal perforation
- Concomitant use of meds that increase GI events (anticoagulants, aspirin, corticosteroids, SSRIs, venlafaxine or duloxetine)
- Comorbidity (CV disease, hepatic/renal impairment, diabetes, hypertension)
- Requirement for prolonged NSAID use (OA or rheumatoid of any age, chronic low back pain and 45+)
Paracetamol prescribing issues
- Well tolerated and rarely cause ADR when used at recommended dose
- Best avoided in hepatic impairment or alcohol dependence (liver damage risk)
- Pregnant/breastfeeding with OA paracetamol preferred to NSAID
- In GI risk factor patients, use paracetamol (with or without codeine)
NSAID prescribing issues
- If taking OTC aspirin or ibuprofen and need another NSAID, problem
- If C/I to oral NSAIDs (known allergy, severe HF, GI bleed)
- If condition where NSAIDs cautioned (asthma, IBD, renal impairment)
- If increased GI adverse effects - additional gastroprotection needed
- If closer monitoring for GI, CV, renal or hepatic ADRs (elderly, comorbidities)
- If hazardous interactions (thiazide diuretics, SSRIs, warfarin)
NSAIDs in pregnancy/breastfeeding
Paracetamol analgesic, antipyretic of choice during conception but occasional single dose NSAIDs unlikely to affect chances
If NSAID needed, ibuprofen preferred before 30 weeks, NSAIDs NOT used after 30 seeks without fetal monitoring
Codeine and paracetamol
Codeine can cause?
Advice
- Prescribe separately so individually titrated, combo products (co-codamol) not recommended
- GI problems (N + V, constipation) if regular use, prescribe laxative
CNS toxicity (sedation) avoid driving & activities where drowsiness affects - Driving while taking weak opioids
PPIs and liver disease
PPIs undergo extensive hepatic metabolism
With liver disease, do not exceed daily doses
- Omeprazole, pantoprazole & esomeprazole 20mg
- Lansoprazole 30mg
No data on rabeprazole use in severe hepatic impairment but caution advised
Poorly controlled pain can lead to…
Prolonged hospital stay
Increased risk of complications
Transition to chronic pain
Pre-operative assessment
Identify patients at risk for complex pain management
Discuss pain expectations and management strategies
Review medication history for potential interactions
Address chronic pain management preoperatively, if applicable
Assessing postoperative pain
Utilise appropriate pain assessment tools (visual analogue scale, behavioural scales)
Consider holistic assessment beyond just pain intensity
Evaluate functional limitations due to pain
Assessing postoperative pain:
Visual analogue
Numerical pain scales
- Limited in ability to fully understand and describe pain experience, a comprehensive assessment, including indirect measures like opioid usage is crucial
- Not be suitable for patients who are unable to self-report their pain, such as individuals with severe dementia
PAINAD scales (pain assessment in advanced dementia):
Medicine core standards for pain management
Specific assessment tools
Additional assessment
- Emphasise appropriate pain management tools for all patients
Include those with dementia or learning difficulties - CPOT (Critical Care Pain Observation Tool)
PAINAD (Pain Assessment in Advanced Dementia) - 4AT (4 A’s test) for postoperative delirium
What is multimodal analgesia?
Examples?
Combining different medications classes and techniques for pain relief
Opioids (for moderate to severe pain), NSAIDs, paracetamol, ketamine (for specific situations), peripheral nerve blocks, non-pharmacological methods (physiotherapy, heat/cold therapy)
Opioid use in postoperative pain management
Opioids should be reserved for moderate to severe pain
Use immediate-release formulations for better dose control
Minimise opioid use at discharge
Monitor for side effects (constipation, sedation, respiratory depression)
NSAIDs in pain
Effective for pain and inflammation
Consider contraindications (renal impairment, CV risk)
Use lowest effective dose for shortest duration
NSAIDs not recommended after hip fracture surgery
Paracetamol:
Dose, route, frequency
Prescribing risk factors and cautions to consider
- 1g orally TDS
- Low body weight, risk factors for hepatotoxicity
Ibuprofen:
Dose, route, frequency
Prescribing risk factors and cautions to consider
- 200-400mg orally TDS (increased up to 600mg QDS a day if necessary)
- GI bleeding or ulceration, renal impairment, severe heart failure
Morphine 10mg/5ml oral solution:
Dose, route, frequency
Prescribing risk factors and cautions to consider
- 4-10mg orally every 4 hours, dose can be more frequent during titration
- Impaired respiratory function, older age, renal impairment
Ketamine:
Dose, route, frequency
Prescribing risk factors and cautions to consider
- 0.25mg/kg to 1mg/kg IV
- Acute circulatory failure
Ketamine for postoperative pain
May be used for moderate to severe pain or opioid-resistant pain
May reduce the need foropioid
Potential side effects (psychosis, hallucinations)
Non-pharmacological pain management techniques
Physiotherapy
Heat/cold therapy
Relaxation techniques (massage, meditation)
Distraction techniques (music, games)
