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MANAGEMENT OF PAIN IN
SMALL ANIMALS
PRESENTED BY ,
SWATHI KRISHNA
12 – BVP - 230
PAIN
• “UNPLEASANT SENSORY AND EMOTIONAL EXPERIENCE
ASSOCIATED WITH ACTUAL OR POTENTIAL TISSUE
DAMAGE”.
THE PAIN PATHWAY
Transduction
Transmission
Modulation
Perception
TRANSDUCTION
• Mechanical, chemical and thermal energy are converted into electrical
energy/impulses by specialized nerve endings called “nociceptors”.
• NOCICEPTORS
• Free nerve endings of primary afferent fibers.
• Have high stimulus thresholds for activation.
TRANSMISSION
Occurs along 2 different types of afferent nerve fibers:
A-DELTA FIBERS
• Large diameter
• Myelinated
• Rapid impulse conduction (6-30 m/sec)
• Stimulates immediate reaction
C FIBERS
• Small diameter
• Unmyelinated
• Slow conduction
• (0.5 – 2 m/sec)
• Reinforces the immediate response that is signaled by a-delta
fibers.
Spinothalamic tract
• Most important tract in transmission of nociceptive information.
Spinoreticular tract
Spinohypothalamic tract
MODULATION
• SIGNAL PROCESSING
• Spinal cord
• Dorsal horn
• Endogenous systems
Tissue trauma
Signal enters dorsal horn
Reflex activity
exits ventral
horn
To higher
levels of
CNS
CROSS SECTION OF THE SPINAL CORD
PERCEPTION
• RECEIVING AND INTERPRETATION
• Successful transduction, transmission, &
modulation of a painful stimulus.
Modulation
Perception
TYPES OF PAIN
 PERIPHERAL PAIN
Visceral
• abdominal or thoracic organs
• poorly localized
• referred
Somatic
 superficial
• skin
 deep
• tendons, joints, muscle, periosteum
PHYSIOLOGICAL PAIN
• It is a protective mechanism and causes avoidance.
• Little to no tissue injury.
• Pain stops once the stimulus is removed.
PATHOLOGICAL PAIN
• It results from tissue injury and causes inflammation ,
nerve damage etc.
• Persists after the stimulus is received.
NEUROPATHIC PAIN
• Damage to peripheral nerves or spinal cord.
• Often difficult to treat appropriately.
ACUTE PAIN
• Arises from soft tissue trauma or inflammation.
• Plays a biologically adaptive role by facilitating tissue repair.
CHRONIC PAIN
• Pain that persists beyond the expected time frame for a given
disease, process or injury.
• May be associated with ongoing inflammation.
• May be autonomous with no temporal relation to the inciting
cause.
ADAPTIVE PAIN
• Normal response.
• Protects from further injury.
• Inflammation is a large component.
MALADAPTIVE PAIN
• Abnormal response.
• Stimulus is gone but pain persists.
FACTORS AFFECTING PAIN
• STRESS
• ANXIETY
• WIND-UP
• CENTRAL SENSITIZATION
COMMON BEHAVIORAL RESPONSES TO PAIN
• Dogs arepack animals, theyshareemotions with pack members to receive
support.
 Whine, whimper
 Arched or abnormal posture
 Guarding of injured tissue
 Restlessness
 Behavior change
 Increased heart rate and blood pressure
 Hypersalivation
 Appetite reduction
 Dilated pupils
 Altered voiding behavior
Cats aremore solitary animals, they aregenerally more stoic thandogs; showing pain
highlights a cats vulnerability.
 Over grooming
 Hiding
 Squinting
 Guarding injured tissue
 Desperate attempts to flee
 Reduced grooming
 Appetite reduction
 Pupil dilation
 Salivation
 Restlessness
 Increased heart rate and blood pressure
STRESS RESPONSE MARKERS/PAIN ASSESSMENT
Heart rate
Respiratory rate
Blood pressure
Posture
Attitude
Food and water intake
Patterns of defecation, urination
Change in activity levels
Natural behaviors – inquisitive,
grooming
Provoked behavior
Aggression
Gait-/Posture
Vocalization
Appearance of stereotypical
behaviors
ACTIONS OF ANALGESICS ON PAIN
PROCESSES
TRANSDUCTION:
• Can be blocked by local anesthetics by injection either at the site of
injury/incision or intravenously.
• Can be decreased by use of NSAIDs which decrease the production of
prostaglandins at the site of injury.
TRANSMISSION:
• Can be prevented by local anesthetics by injection along peripheral nerves,
at nerve plexus, or in the epidural or subarachnoid spaces.
MODULATION:
• Can be augmented by injection of local anesthetics or alpha2-adrenergic
agonists; gabapentin may also effect modulation.
PERCEPTION:
• Altered by use of general anesthetics or systemic injection of opioids and/or
alpha2-agonists.
GENERAL APPROACHES TO PAIN
MANAGEMENT
o PRE-EMPTIVE ANALGESIA: Giving analgesics prior to the noxious stimulus
(surgery)
• By blocking or inhibiting the nociceptive process before it begins,
hypersensitivity is prevented.
• May decrease the amount of anesthesia and post-operative analgesia
needed.
o MULTIMODAL OR “BALANCED” ANALGESIA: Using a combination of analgesics
which will impact more than one portion of the nociceptive process.
• for example: buprenorphine and meloxicam pre-surgically, lidocaine block
used prior to incision, and bupivicaine splash prior to closing incision
ANALGESICS
 DIVIDED INTO FIVE MAIN CLASSES BASED ON MODE OF ACTION
• OPIOIDS
• NON-STEROIDAL ANTI-INFLAMMATORY DRUGS
• LOCAL ANESTHETICS
• ALPHA2-ADRENOCEPTOR AGONISTS
• MISCELLANEOUS DRUGS
OPIOID ANALGESICS
OPIOID CLASSIFICATION
AGONISTS
• Stimulate receptor activity
• MU agonists
• most common group of opioid agonists used
• include morphine, meperidine, oxymorphone,
hydromorphone, fentanyl, carfentanil
AGONISTS-ANTAGONISTS
• Stimulate activity at some receptors and antagonize others
• Butorphanol – kappa agonist, mu antagonist
• PARTIAL AGONISTS
• Bind to receptor but only produce a partial effect
• Buprenorphine – partial mu agonist, kappa antagonist
• ANTAGONISTS
• Primary activity is mu receptor antagonism
• Naloxone
• Naltrexone
• Nalmefene
• Diprenorphine
OPIOID RECEPTOR PHARMACOLOGY
• CLASSIFICATION: 4 types μ, κ, ε, σ
MU
• supraspinal, spinal, peripheral and analgesia , respiratory depression ,
euphoria/sedation , physical dependence , bradycardia.
KAPPA
• spinal analgesia , sedation , respiratory depression.
SIGMA
• dysphoria/hallucinations , hypertonia , respiratory stimulation , tachycardia.
OPIOID ADMINISTRATION
• SYSTEMIC: IV, SQ, IM, CRI
• INTRA-ARTICULAR INJECTION
• LOCAL INJECTION
• EPIDURAL INJECTION
• TRANSDERMAL FENTANYL PATCH
GOOD
 GREAT ANALGESIA
 VARIABLE MUSCLE RELAXATION
 SEDATION
BAD
 RESPIRATORY DEPRESSION
 GI EFFECTS
• vomiting
• defecation followed by
constipation
 EXCITEMENT
 DEPRESSION OF THE COUGH
CENTER
OPIOID EFFECTS
OPIOID SPECIES SPECIFIC EFFECTS
Excitement in cats (dose related).
Panting in dogs – resets thermostat.
MISCELLANEOUS ANALGESICS
TRAMADOL
• Synthetic opioid agonist which also inhibits serotonin and norepiniphrine
re-uptake in the spinal cord.
• The main metabolite has moderate opioid activity.
KETAMINE
• NMDA antagonist.
• Used as a cri during surgery at sub-anesthetic doses, it reduces mac and
can help prevent hypersensitivity
• More effective treating somatic pain than visceral pain
• Can be administered via epidural injection
GABAPENTIN
• Analogue of naturally occurring neurotransmitter GABA.
• Believed to increase production of GABA.
• part of endogenous inhibition of nociception
• Used to treat nerve pain.
NON-STEROIDAL ANTI-
INFLAMMATORY DRUGS ( NSAIDS )
• NSAIDS are weak organic acids with anti-inflammatory, analgesic,
and antipyretic properties.
• Inhibit prostaglandin production by inhibiting cox enzymes.
• Are either non-selective (inhibits both cox iso-enzymes) or
selective for cox-2.
• Non-selective NSAIDS have more serious side effects (gastric
ulceration and renal toxicity).
• Decreased renal blood flow during anesthesia makes kidneys more
susceptible to toxic effects.
• Cyclooxygenase inhibition decreased thromboxane decreases
platelet adhesion/clumpingdecreases clot formation and
thromboemboli.
TYPES OF NSAIDS
PHENYLBUTAZONE
COX1 AND 2 INHIBITOR
VERY POTENT
COMMONLY USED IN HORSES
NOT RECOMMENDED IN DOGS
• GI SIDE EFFECTS COMMON
• NEVER IN CATS!
ASPIRIN
• COX1 AND 2 INHIBITOR
• VERY SHORT HALF-LIFE IN HORSES
• COMMONLY USED IN DOGS
• BUFFERED ONLY
• WITH FOOD
• USE WITH CAUTION IN CATS
• CAN’T METABOLIZE WELL
• HALF-LIFE 38 HOURS
• DOSED EVERY 48-72 HOURS
KETOPROFEN
• KETOFEN® (COX1 AND COX2)
• LICENSED IN HORSES
• APPROVED FOR USE IN DOGS AND CATS IN CANADA, EUROPE
• GOOD ANALGESIA, POTENT ANTIPYRETIC
• INJECTABLE
• LIMIT USE
• BLOOD CLOTTING
FLUNIXIN MEGLUMINE
• BANAMINE® (COX1 AND COX2)
• INJECTABLE
• HORSES
• COLIC
• GOOD ANALGESIA
• DOGS
• GI SIDE EFFECTS COMMON, SEVERE
CARPROFEN
• RIMADYL ®
• COX-2 INHIBITOR: “SPARES” “GOOD” PROSTAGLANDINS
• FEWER SIDE EFFECTS
• DOGS ONLY
• BLACK LABS…
• 0.06% OF ALL DOGS DEVELOP HEPATIC PROBLEMS (RARE)
• BID DOSING
ETODOLAC
• ETOGESIC ®
• COX 1 AND 2 INHIBITION
• ONCE DAILY ADMINISTRATION
• DOGS ONLY
DERRAMAX
• USE IN DOGS
• COX 2 SPECIFIC
• SID DOSING
“METACAM” =MELOXICAM
• COX-2 SPECIFIC
• USE IN DOGS AND CATS
• LIQUID
• WELL TOLERATED
ALPHA2-ADRENERGIC AGONISTS
Stimulation of the alpha2 – adrenoceptors result in sedation,
muscle relaxation, and analgesia.
Two alpha-2 agonists (xylazine, medetomidine) and 2 antagonists
(yohimbine, atipamezole) are approved for use in small animals in
canada.
Another alpha-2 agonist, romifidine, is approved for use in
horses, but not in dogs and cats.
LOCAL ANESTHETICS
• LOCAL INFILTRATION OF SURGICAL SITE
• INTRAVENOUS REGIONAL ANESTHESIA
• INTRA-ARTICULAR INJECTION
• NERVE BLOCKS
• EPIDURAL
• TOPICAL ON SKIN/ EYE/ LARYNX
The “-caine” family: Lidocaine, bupivicaine, mepivicaine,
proparicaine, tetracaine, etc.
EPIDURALS
• Administered alone or in combination with other
analgesics.
• If combined, smaller doses can be used, decreasing
risks of adverse effects.
• Can cause motor deficits at higher doses.
MISCELLANEOUS AGENTS
CAPSAICIN
• This medication is used to treat minor aches and pains
of the muscles/joints (e.g., arthritis, backache, sprains).
capsaicin works by decreasing a certain natural
substance in the body (substance p) that helps pass pain
signals to the brain.
ST. JOHNSWORT
• Arthritic pain
• Stimulates neural inhibitory pathways analgesia
CHONDROPROTECTIVE AGENTS
• NUTRACEUTICALS
• chondroitin sulfate
• glucosamine
• hyaluronic acid
• building blocks for cartilage and synovial fluid
• Examples: (oral) synovi, glycoflex (injectable) adequan can be mixed with many
other ingredients (MSM, creatine) to enhance effects.
THANK YOU……….

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Management of pain in smallanimals

  • 1. MANAGEMENT OF PAIN IN SMALL ANIMALS PRESENTED BY , SWATHI KRISHNA 12 – BVP - 230
  • 2. PAIN • “UNPLEASANT SENSORY AND EMOTIONAL EXPERIENCE ASSOCIATED WITH ACTUAL OR POTENTIAL TISSUE DAMAGE”.
  • 4. TRANSDUCTION • Mechanical, chemical and thermal energy are converted into electrical energy/impulses by specialized nerve endings called “nociceptors”. • NOCICEPTORS • Free nerve endings of primary afferent fibers. • Have high stimulus thresholds for activation.
  • 5. TRANSMISSION Occurs along 2 different types of afferent nerve fibers: A-DELTA FIBERS • Large diameter • Myelinated • Rapid impulse conduction (6-30 m/sec) • Stimulates immediate reaction
  • 6. C FIBERS • Small diameter • Unmyelinated • Slow conduction • (0.5 – 2 m/sec) • Reinforces the immediate response that is signaled by a-delta fibers. Spinothalamic tract • Most important tract in transmission of nociceptive information. Spinoreticular tract Spinohypothalamic tract
  • 7. MODULATION • SIGNAL PROCESSING • Spinal cord • Dorsal horn • Endogenous systems Tissue trauma Signal enters dorsal horn Reflex activity exits ventral horn To higher levels of CNS CROSS SECTION OF THE SPINAL CORD
  • 8. PERCEPTION • RECEIVING AND INTERPRETATION • Successful transduction, transmission, & modulation of a painful stimulus. Modulation Perception
  • 9. TYPES OF PAIN  PERIPHERAL PAIN Visceral • abdominal or thoracic organs • poorly localized • referred Somatic  superficial • skin  deep • tendons, joints, muscle, periosteum
  • 10. PHYSIOLOGICAL PAIN • It is a protective mechanism and causes avoidance. • Little to no tissue injury. • Pain stops once the stimulus is removed. PATHOLOGICAL PAIN • It results from tissue injury and causes inflammation , nerve damage etc. • Persists after the stimulus is received.
  • 11. NEUROPATHIC PAIN • Damage to peripheral nerves or spinal cord. • Often difficult to treat appropriately.
  • 12. ACUTE PAIN • Arises from soft tissue trauma or inflammation. • Plays a biologically adaptive role by facilitating tissue repair. CHRONIC PAIN • Pain that persists beyond the expected time frame for a given disease, process or injury. • May be associated with ongoing inflammation. • May be autonomous with no temporal relation to the inciting cause.
  • 13. ADAPTIVE PAIN • Normal response. • Protects from further injury. • Inflammation is a large component. MALADAPTIVE PAIN • Abnormal response. • Stimulus is gone but pain persists.
  • 14. FACTORS AFFECTING PAIN • STRESS • ANXIETY • WIND-UP • CENTRAL SENSITIZATION
  • 15. COMMON BEHAVIORAL RESPONSES TO PAIN • Dogs arepack animals, theyshareemotions with pack members to receive support.  Whine, whimper  Arched or abnormal posture  Guarding of injured tissue  Restlessness  Behavior change  Increased heart rate and blood pressure  Hypersalivation  Appetite reduction  Dilated pupils  Altered voiding behavior
  • 16. Cats aremore solitary animals, they aregenerally more stoic thandogs; showing pain highlights a cats vulnerability.  Over grooming  Hiding  Squinting  Guarding injured tissue  Desperate attempts to flee  Reduced grooming  Appetite reduction  Pupil dilation  Salivation  Restlessness  Increased heart rate and blood pressure
  • 17. STRESS RESPONSE MARKERS/PAIN ASSESSMENT Heart rate Respiratory rate Blood pressure Posture Attitude Food and water intake Patterns of defecation, urination Change in activity levels Natural behaviors – inquisitive, grooming Provoked behavior Aggression Gait-/Posture Vocalization Appearance of stereotypical behaviors
  • 18. ACTIONS OF ANALGESICS ON PAIN PROCESSES TRANSDUCTION: • Can be blocked by local anesthetics by injection either at the site of injury/incision or intravenously. • Can be decreased by use of NSAIDs which decrease the production of prostaglandins at the site of injury. TRANSMISSION: • Can be prevented by local anesthetics by injection along peripheral nerves, at nerve plexus, or in the epidural or subarachnoid spaces. MODULATION: • Can be augmented by injection of local anesthetics or alpha2-adrenergic agonists; gabapentin may also effect modulation. PERCEPTION: • Altered by use of general anesthetics or systemic injection of opioids and/or alpha2-agonists.
  • 19. GENERAL APPROACHES TO PAIN MANAGEMENT o PRE-EMPTIVE ANALGESIA: Giving analgesics prior to the noxious stimulus (surgery) • By blocking or inhibiting the nociceptive process before it begins, hypersensitivity is prevented. • May decrease the amount of anesthesia and post-operative analgesia needed. o MULTIMODAL OR “BALANCED” ANALGESIA: Using a combination of analgesics which will impact more than one portion of the nociceptive process. • for example: buprenorphine and meloxicam pre-surgically, lidocaine block used prior to incision, and bupivicaine splash prior to closing incision
  • 20. ANALGESICS  DIVIDED INTO FIVE MAIN CLASSES BASED ON MODE OF ACTION • OPIOIDS • NON-STEROIDAL ANTI-INFLAMMATORY DRUGS • LOCAL ANESTHETICS • ALPHA2-ADRENOCEPTOR AGONISTS • MISCELLANEOUS DRUGS
  • 22. OPIOID CLASSIFICATION AGONISTS • Stimulate receptor activity • MU agonists • most common group of opioid agonists used • include morphine, meperidine, oxymorphone, hydromorphone, fentanyl, carfentanil AGONISTS-ANTAGONISTS • Stimulate activity at some receptors and antagonize others • Butorphanol – kappa agonist, mu antagonist
  • 23. • PARTIAL AGONISTS • Bind to receptor but only produce a partial effect • Buprenorphine – partial mu agonist, kappa antagonist • ANTAGONISTS • Primary activity is mu receptor antagonism • Naloxone • Naltrexone • Nalmefene • Diprenorphine
  • 24. OPIOID RECEPTOR PHARMACOLOGY • CLASSIFICATION: 4 types μ, κ, ε, σ MU • supraspinal, spinal, peripheral and analgesia , respiratory depression , euphoria/sedation , physical dependence , bradycardia. KAPPA • spinal analgesia , sedation , respiratory depression. SIGMA • dysphoria/hallucinations , hypertonia , respiratory stimulation , tachycardia.
  • 25. OPIOID ADMINISTRATION • SYSTEMIC: IV, SQ, IM, CRI • INTRA-ARTICULAR INJECTION • LOCAL INJECTION • EPIDURAL INJECTION • TRANSDERMAL FENTANYL PATCH
  • 26. GOOD  GREAT ANALGESIA  VARIABLE MUSCLE RELAXATION  SEDATION BAD  RESPIRATORY DEPRESSION  GI EFFECTS • vomiting • defecation followed by constipation  EXCITEMENT  DEPRESSION OF THE COUGH CENTER OPIOID EFFECTS
  • 27. OPIOID SPECIES SPECIFIC EFFECTS Excitement in cats (dose related). Panting in dogs – resets thermostat.
  • 29. TRAMADOL • Synthetic opioid agonist which also inhibits serotonin and norepiniphrine re-uptake in the spinal cord. • The main metabolite has moderate opioid activity. KETAMINE • NMDA antagonist. • Used as a cri during surgery at sub-anesthetic doses, it reduces mac and can help prevent hypersensitivity • More effective treating somatic pain than visceral pain • Can be administered via epidural injection GABAPENTIN • Analogue of naturally occurring neurotransmitter GABA. • Believed to increase production of GABA. • part of endogenous inhibition of nociception • Used to treat nerve pain.
  • 31. • NSAIDS are weak organic acids with anti-inflammatory, analgesic, and antipyretic properties. • Inhibit prostaglandin production by inhibiting cox enzymes. • Are either non-selective (inhibits both cox iso-enzymes) or selective for cox-2. • Non-selective NSAIDS have more serious side effects (gastric ulceration and renal toxicity). • Decreased renal blood flow during anesthesia makes kidneys more susceptible to toxic effects. • Cyclooxygenase inhibition decreased thromboxane decreases platelet adhesion/clumpingdecreases clot formation and thromboemboli.
  • 33. PHENYLBUTAZONE COX1 AND 2 INHIBITOR VERY POTENT COMMONLY USED IN HORSES NOT RECOMMENDED IN DOGS • GI SIDE EFFECTS COMMON • NEVER IN CATS!
  • 34. ASPIRIN • COX1 AND 2 INHIBITOR • VERY SHORT HALF-LIFE IN HORSES • COMMONLY USED IN DOGS • BUFFERED ONLY • WITH FOOD • USE WITH CAUTION IN CATS • CAN’T METABOLIZE WELL • HALF-LIFE 38 HOURS • DOSED EVERY 48-72 HOURS
  • 35. KETOPROFEN • KETOFEN® (COX1 AND COX2) • LICENSED IN HORSES • APPROVED FOR USE IN DOGS AND CATS IN CANADA, EUROPE • GOOD ANALGESIA, POTENT ANTIPYRETIC • INJECTABLE • LIMIT USE • BLOOD CLOTTING
  • 36. FLUNIXIN MEGLUMINE • BANAMINE® (COX1 AND COX2) • INJECTABLE • HORSES • COLIC • GOOD ANALGESIA • DOGS • GI SIDE EFFECTS COMMON, SEVERE
  • 37. CARPROFEN • RIMADYL ® • COX-2 INHIBITOR: “SPARES” “GOOD” PROSTAGLANDINS • FEWER SIDE EFFECTS • DOGS ONLY • BLACK LABS… • 0.06% OF ALL DOGS DEVELOP HEPATIC PROBLEMS (RARE) • BID DOSING
  • 38. ETODOLAC • ETOGESIC ® • COX 1 AND 2 INHIBITION • ONCE DAILY ADMINISTRATION • DOGS ONLY
  • 39. DERRAMAX • USE IN DOGS • COX 2 SPECIFIC • SID DOSING
  • 40. “METACAM” =MELOXICAM • COX-2 SPECIFIC • USE IN DOGS AND CATS • LIQUID • WELL TOLERATED
  • 42. Stimulation of the alpha2 – adrenoceptors result in sedation, muscle relaxation, and analgesia. Two alpha-2 agonists (xylazine, medetomidine) and 2 antagonists (yohimbine, atipamezole) are approved for use in small animals in canada. Another alpha-2 agonist, romifidine, is approved for use in horses, but not in dogs and cats.
  • 44. • LOCAL INFILTRATION OF SURGICAL SITE • INTRAVENOUS REGIONAL ANESTHESIA • INTRA-ARTICULAR INJECTION • NERVE BLOCKS • EPIDURAL • TOPICAL ON SKIN/ EYE/ LARYNX The “-caine” family: Lidocaine, bupivicaine, mepivicaine, proparicaine, tetracaine, etc.
  • 45. EPIDURALS • Administered alone or in combination with other analgesics. • If combined, smaller doses can be used, decreasing risks of adverse effects. • Can cause motor deficits at higher doses.
  • 47. CAPSAICIN • This medication is used to treat minor aches and pains of the muscles/joints (e.g., arthritis, backache, sprains). capsaicin works by decreasing a certain natural substance in the body (substance p) that helps pass pain signals to the brain.
  • 48. ST. JOHNSWORT • Arthritic pain • Stimulates neural inhibitory pathways analgesia
  • 49. CHONDROPROTECTIVE AGENTS • NUTRACEUTICALS • chondroitin sulfate • glucosamine • hyaluronic acid • building blocks for cartilage and synovial fluid • Examples: (oral) synovi, glycoflex (injectable) adequan can be mixed with many other ingredients (MSM, creatine) to enhance effects.