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2/15/2015

Overview

 What am I treating?
 How do I know if I am being
successful?
 Why are emergency patients
Pain management in the different?
emergency patient  Some ideas and examples
first do no harm!
Louise Clark DiplECVAA MRCVS

Louise Clark Dipl. ECVAA MRCVS


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What is pain? What is pain?

 Important to understand what pain “is” or  It is not a stimulus


“is not”  It is not a defined response from the
animal
 It requires that the animal is conscious
 It is perceived in the higher centres

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What is pain? Pain is always subjective

 Pain is an unpleasant sensory and emotional


experience associated with actual or  It is what the
potential tissue damage or described in patient says
terms of such damage (IASP definition) (expresses) that it
is!
 “The inability to communicate verbally does
not negate the possibility that an individual
is experiencing pain and is in need of
appropriate pain-relieving treatment”

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Perception Why is pain management


perception
•End result of the neuronal activity of pain important?
Transmission occurs in transmission
three stages: •Conscious multidimensional experience
 Ethical considerations
•from the site of
transduction along the  Pain is a physiological stressor
nociceptor fibres to the  → affects health, recovery from illness &
dorsal horn in the spinal Transduction
cord surgery
•from the spinal cord to •Nociceptors of C and
the brain stem A-delta fibres respond  Severe or persistent pain can lead to
•through thalamus to to noxious stimuli maladaptive (pathological) pain
cortex and higher levels •e.g. trauma, surgery,
of the brain •Mechanical thermal
or chemical
•Somatic and visceral
transduction

central sensitisationModulation
transmission
•Changing or inhibiting transmission
•Multiple, complex pathways
•Release of inhibitory neurotransmitters
•E.g. endogenous opioids; serotonin; GABA
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Pain assessment – How do I


What are the aims of pain relief?
know if my patient is painful?
 Reduce neuro-endocrine stress response  Medical benefits
 Attenuate peripheral and central  Moral and ethical obligation
sensitisation reduce chronic pain  Improve animal welfare
 Maintain tissue perfusion  Pain assessment not easy!
 Promote restful sleep  Self report = Gold Standard
 Improve appetite  Surrogate scales with behavioural signs
 Promote early mobilisation  Signs of pain not consistent
 Have a happy patient  Differentiation between pain & anxiety

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Pain assessment – what is


Behaviour
normal?

Changes in specific behaviour can be classified as:


 Get to know the individual
• Posture  Personality
• Gait
 Before surgery
• Activity
• Facial expression  Normal behaviour
• Vocalisation  Difficult when patient
• Mental state presented in distress
• Evoked behaviour  Like and dislikes
• Behaviour patterns
 Questionnaires?
• Response to analgesics

©FAB website

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Practical assessment Pain Scales

 All pain scales are subjective


 Human assessor making a value judgement
 Expression of abnormal behaviours
 Based on previous experience of pain
 Altered posture
 Restlessness
 Hiding (especially cats)
 Inappropriate elimination,
vocalization, aggression/lack of ……
 Decreased interaction (pets/family)
 Altered facial expression

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Factors contributing to restricted


use of analgesic agents
 Poor understanding of pain
pathophysiology
 Poor pain assessment
 ‘Pain helps to limit activity post-
operatively’
 Concern about adverse effects of
analgesic agents
 Dependency on clinical pain as
diagnostic aid

www.gla.ac.uk/faculties/vet/smallanimalhospital/ourservices/p
ainmanagementandacupuncture/

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How do I know if I am being


Pain assessment
successful?
 Vital for effective pain management
 One size does not fit all
 Adjust plan depending upon feedback from
the animal
 Objective assessment
 Subjective assessment

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Are emergency patients any Are emergency patients any


different? different?

 NO  YES
 Requirement for analgesia
 Major surgical procedures e.g. GDV  More vulnerable to negative effects of drugs
 Severe medical conditions e.g. trauma  Care must be given to
 Requirement for pain assessment • drug selection
• method of administration
• patient monitoring

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Drug selection Method of administration

 Knowledge of pharmacology  Parenteral administration → systemic side


 Side effects more pronounced where organ effects
function limited  Titration to effect
• E.g. NSAIDS in renal dysfunction ± hypotension • Intravenous preferable to intramuscular
 Prolonged duration of action route?
• E.g. Compromised liver function in sepsis • More rapid onset
 Increased dosing interval • Less effects of hypo-perfusion
 Inappropriate response/increased sensitivity  Local anaesthetic techniques
• E.g. Opioids in head injury • Avoidance of systemic side effects
• Very effective analgesia

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Patient monitoring Preventive analgesia

 Repeated pain assessment


 May demonstrate only subtle indicators of  Before surgery
pain especially if very obtunded
 Nursing & procedural interventions can
cause pain  During surgery
 More reliance on assessment of physiological
parameters over behavioural signs  After surgery
 More intensive monitoring of efficacy and
side effects

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Pain management Nursing

 Nursing  Tender loving care


 Feeding provides comfort
 Surgical considerations  Support injured limbs
 Medical treatments  Relieve full bladders
 Restful environment
 Promote sleep

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Surgical considerations Analgesic Drugs

 Minimise surgical trauma  Non-steroidal anti-inflammatory agents


 Tissue handling
 Avoid nerve damage  Opioids
 Minimise tension in wound closure
 Local anaesthetics

 Alpha-2 adrenoreceptor agonists

 Miscellaneous drugs with analgesic


properties…
• Ketamine, amantadine
• Gabapentin
• Tricyclic antidepressants...
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Why multimodal?
Local anaesthetics, opioids,
Volatile
α2-agonists, NSAIDs, NMDA
anaesthetics
antagonists  Target multiple sites in pain pathways
opioids,
Modulate  Nociceptive system is “plastic” and
α2-agonists spinal pathways
Inhibit perception
ever changing
(central sensitisation)
 Novel modes of action of many new
and rediscovered drugs
MULTIMODAL ANALGESIA  Target therapy to the problem

Inhibit Inhibit
transmission transduction
(impulse conduction) (peripheral sensitisation)

NSAIDs
local anaesthetics
opioids
α2-agonists
local anaesthetics
opioids
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NSAIDS Opioids

 Extreme care where:  Two types of opioid in clinical use:


 Haemorrhage • full agonists (agonists at the µ/OP3 receptor)
• partial agonists (agonists that do not give a full
 Hypotension effect)
 Liver dysfunction  Pure or full agonists give a predictable effect
 Renal dysfunction which increases as the dose increases
 Coagulation (especially platelet) problems  Partial agonist will have increasing effect up
to a certain dose but after that a ceiling
 Avoid until patient is fully assessed and effect is produced
haemodynamically stable  Side effects follow the same rules and will
increase with the dose

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Opioids Pethidine

 Produce analgesia for inflammatory pain  Full agonist providing analgesia and
 Not very effective for neuropathic pain sedation
 Most cause sedation  Spasmolytic properties - useful for visceral
 Dysphoria occasionally with high doses or in pain
non- painful animals  Short duration limits its use (max. 90
 Potential for respiratory depression but minutes)
unlikely in clinical use  Should not be administered intravenously as
 In non-painful animals nausea can be seen this can lead to massive histamine release
 Vomiting may occur with morphine  Pain on intramuscular injection and also a
large volume of drug to inject

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Morphine Methadone

 Full agonist  Synthetic opioid


 Duration of action is dose  Approximately equipotent to morphine
dependent  Less nausea
 Can be administered by  Ideal for patients where vomiting needs
slow intravenous injection to be avoided after pre-medication
 Safe to use in cats at  Licensed in Europe cats and dogs
relevant doses
 Intra-articular use
(0.1mg/kg)

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Butorphanol Buprenorphine

 κ agonist, can be used for mild pain  Partial µ agonist - ceiling effects well
above clinically applicable doses
 NOT good for severe pain
 Licensed in Europe
 Potent sedative
 Dose 20mcg/kg in cats and dogs
 Excellent sedation combined with
phenothiazines or alpha 2 agonists  Slow onset time and prolonged duration
of action depending on the dose used
 Buccal absorption similar to that of
intravenous injection in cats
 Buccal absorption also in dogs
 Multidose vials STING on injection

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Drug choices – local anaesthetics perception

 Use to reduce opioid


requirements
 Reduce anaesthetic
requirements
 “Perfect analgesics”
 CNS remains naive

transduction

central sensitisation Block transmission

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Drug choices – systemic lidocaine


Local Anaesthetics
 Inhibition of sodium channels
routes of administration sites of action
 Constant rate infusion
•Extra/epidural central  Good analgesia
•Local eg intra-articular peripheral  Some sedation
•Regional techniques  DOGS only
•Specific nerve blocks  NOT CATS
•Systemic bolus/infusion
lidocaine  Mechanism not fully understood
bupivacaine
ropivacaine
Block action potential transmission in all nerve fibres,
including those transmitting nociceptive information
The “perfect analgesic”
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Drug choices – systemic lidocaine Drug choices - Paracetamol

 1mg/kg IV loading dose  Adjunct analgesic


 Followed by 30µg/kg/min CRI  use in conjunction with opioids/steroids/NSAIDS
 Care - metabolism liver blood flow dependent  NOT CATS
 Observe for side effects  Avoid where concerns about liver function
• Nausea (lick face, yawning)  Useful if polyarthritis/meningitis
• Twitching  10 mg/kg bid short term
• Ultimately seizures  NB: check dosing with Pardale
 ONLY lidocaine
 NEVER use bupivacaine
 Observed cases!

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Drug choices - ketamine Drug choices - ketamine

 NMDA receptor antagonist  Useful adjunct analgesic - reduces opioid


 May reduce central sensitisation requirement
 Treatment of neuropathic pain ?  Doses 0.1mg/kg or 0.6mg/kg/hour reducing
to 0.3 mg/kg/hour post-operatively
 Can continue dose for up to 72 hours
 Limited literature!

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Drug choices – α2 agonists Drug choices – α2 agonists

 Potent analgesics  Role for very low doses - post-operative


 Significant CVS effects  1-2 mcg/kg medetomidine as single dose
 Synergism with opioids  Usual dose is 1-2 mcg/kg/hr medetomidine
 Sedation can make pain assessment difficult  Halve this for dexmedetomidine
 Potentiate analgesia and sedation  0.5 -1 mcg/kg/hour dexmedetomidine
 Allows normal sleep  Cats 2-5 µg/kg/hr (anecdotal!)
 Useful for managing difficult recoveries
 Be aware of nursing issues – hypothermia etc.
 Some animals become refractory to sedation
after 24-48 hours

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Gunshot injury to scapula Gunshot injury to scapula

 Presented “flat”  Methadone 0.3mg/kg IM


 Tachycardic – 230 bpm  IV access obtained
 ECG – sinus tachycardia  Fluids bolus 10ml/kg crystalloid x 2
 Minimum database - WNL  Ketamine 0.25mg/kg slow IV
 No CXR  HR decreased to 160bpm
 Received fluids at RVS  Subjectively more comfortable
 Dry mucous membranes  GA for wound assessment and
 Pale ? Vasoconstricted debridement
 Methadone 0.1mg/kg at RVS  Bupivacaine splash block at surgery
 Ketamine CRI 5 → 2 mcg/kg/min
 NSAIDS started following day

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Hindlimb/inguinal crush injury Hindlimb/inguinal crush injury

 Massive blunt trauma  Methadone 0.3mg/kg


 Transfused at RVS  Still agitated and tachycardic
 Surgery at RVS to pack wound  Fentanyl 5mcg/kg prior to GA → relaxed
 H & B – mild anaemia, CK ↑↑↑  Fentanyl 20mcg/kg/hour during GA
 No IV access
 Emergency surgery to assess  Other options:
wound, place central line and IDUC  Ketamine CRI/ Lidocaine CRI
 Methylprednisolone at RVS  Epidural catheter – concern re extent
necrosis
 “splash block” – infected ? efficacy
 NSAIDS – received steroids at RVS

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Thoracotomy for lobectomy Conclusion

 Opioid in pre-medication  Analgesia should be:


 Intercostal nerve block
 NSAIDS at end of procedure  Planned
 Further opioids during and at end of  Preventive
procedure  Multi-modal
 Appropriate for the procedure
 Other options:  Tailored to the needs of the individual
 Epidural morphine?  Based on the results of pain assessment
 CRI ketamine/lidocaine not required
on basis of pain assessment

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