Pain Management - Anaesthetics

Pain Management

Pain Physiology

·        Pain is vital to survival, but also an important source of human suffering

·        Subjective response to:

o  Damage to body tissues ® stimulation of somatic and visceral nociceptors (nociceptive pain)

o  Altered function of brain or nerve pathways: neuropathic pain

o  No detectable damage Þ psychological, social or environmental factors – idiopathic pain (diagnosis must include a psychological assessment)

·        Three types of pain:

o  Acute pain: injury, surgery, acute illness

o  Cancer pain

o  Chronic non-cancer pain

·        Nociceptive pain:

o  Nociceptors are free nerve endings stimulated by chemicals (e.g. H+), pressure or hot/cold

o  Sensitivity to noxious stimuli ­ by prostaglandins (long chain fatty acids derived from arachidonic acid), e.g. PGE2 and PGF2

o  Conducted by

§  Fast, myelinated A fibres ® sharp pain

§  Slow, poorly myelinated C fibres ® dull persistent pain

o  Terminate in thalamus. Fast fibres then to sensory area of cortex ® pain localisation. Slow fibres synapse with reticular formation ® general arousal and ® limbic system (autonomic responses and emotion)

·        Facilitation: 

o  Processes that ­ pain sensation 

o  Primary hyperalgesia: sensation heightened in discrete area due to histamine and serotonin sensitising adjacent nociceptors 

o  Windup: hyperalgesia beyond areas actually damaged – due to recruitment of other receptors, mediated by NMDA

o  Cortical factors: facilitate pain in anxiety, stress, absence of other sensory input (e.g. at night) 

o  Long term changes in pain pathways ® pain disorders persisting after tissue damage has resolved

·        Inhibition:

o  Descending fibres activate encephalinergic neurones within dorsal horn

o  Release encephalins which inhibit passage of pain impulses, derived from endorphins (in turn derived from b-lipoprotein). Can be antagonised by naloxone

o  Gate theory: large fibres send inhibitory collaterals to presynaptic C fibres

·        Referred Pain: visceral pain felt in somatic structures.

·        Adverse effects of pain:

o  Psychological effects - adaptive behaviour may become dysfunctional ® stress, dependency, isolation, sleep deprivation, psychiatric illness

o  Neurohumoral reflexes - ­ sympathetic activity, CVS system stimulated, metabolism becomes catabolic (which can inhibit healing), changes in immune system

o  Cardiorespiratory effects: e.g. decreased ventilation, ¯ secretion clearance ® hypoxia (especially given ­cardiac O2 requirements), infection

o  Musculoskeletal spasm

o  Gastro and urinary function - ­secretions, ­sphincter tone, ¯motility ® stasis, urinary retention

Pain Pharmacology

·        Opiod analgesics:

o  Main drugs used in severe pain

o  Act on Mu, kappa and delta receptors in substantia gelatinosa and solitary nuclei in spinal cord, thalamus, periaqueductal grey matter and amygdaloid

o   Different opioids have different affinities for different receptor subtypes ® different effects. E.g. Morphine agonises all receptors giving strong analgesia, respiratory depression (both mediated through M receptor) and dependence. Pentazocine is a weak M-receptor antagonist and strong k-receptor agonist and produces weaker analgesia, low dependence and little respiratory depression

o   Uses of opioids:

§  Relief of pain

§  To supplement regional and general anaesthesia

§  As primary anaesthetic agents

§  Premedication to allay anxiety and sedate

§  Specific indications e.g. pulmonary oedema

o   Alfentanil, fentanyl and remifentanil are opioids used intra-operatively because they are rapid and short acting

o   Side effects: respiratory depression (if dose greater than that necessary for analgesia), addiction (not a problem in severe or post-operative pain), sedation, nausea and vomiting, constipation, cough suppression, histamine release

·        Post-Operative pain relief:

o   Why:

§  Humanitarian reasons

§  Prevent stress and cardiac and endocrine responses

§  Improve ventilation (especially after abdominal surgery) 

§  Hasten mobility ® ¯complications (e.g. DVT)

o   Reasons for poor pain relief: lack of understanding/recognition, poor knowledge of drugs and doses, fear of overdose or addiction, logistic difficulties (e.g. access to controlled drugs), willingness to complain about pain, lack of time, problems with side effects, variation in plasma levels necessary to produce analgesia, wide variations in pharmacokinetics

o   Factors affecting response:

§  Lean body mass

§  Age: neonates sensitive, elderly have slower distribution and metabolism 

§  Liver disease ® slower metabolism, renal disease ® slower elimination 

§  Problems in shock: smaller blood volume, but poorer diffusion. Give little and often and titrate to effect 

§  ¯PaCO2 ® ­plasma concentration

§  Drug interactions (e.g. phenytoin ® ¯ pethidine clearance)

§  Personality type

o   Alternatives to IM opiates: 

§  Continuous iv infusion: morphine 10 – 20 mg loading dose over 45 – 60 minutes followed by 2 – 3 mg/hour

§  PCA

§  Extradural or regional block

§  NSAIDs as adjuncts

§  TENS: transcutaneous electrical nerve stimulation, acupuncture and hypnosis

·        Chronic Non-cancer Pain relief:

o   Opioids: orally (morphine tablets, methadone, codeine), epidural, subcutaneous

o   NSAIDs

o   Chemical or surgical ablation of nerves: e.g. chemical coeliac plexus block for pancreas pain

o   Psychological/emotional support

·        Neuropathic pain (e.g. nerve compression, post herpetic neuralgia, etc):

o   Burning, stabbing, shooting pain

o   Treatment:

§  Amitriptyline: 10- 50 mg nocte, increases descending inhibitory pathways, effect in 48 hours

§  Anticonvulsants (Carbamazepine, Gabapentin)

§  Sympathetic blockade

§  Steroids to reduce inflammation of nerves or adjacent tumour

§  Plus TENS, psychotherapy, rehabilitation, opioids

·        Bone Pain:

o   NSAIDs

o   If bony metastases: bisphosphonates