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Pain Management
and Analgesia
Review
Consequences of Untreated Pain
 Catabolic state, may lead to wasting
 Immune suppression
 Inflammation
 Increased anesthetic risk
 Higher inhalant requirement
 Patient suffering
Physiology of Pain/Types of Pain
 Nociception- Detection by nervous system of
potential for or actual occurrence of tissue injury
 Pain pathway
 Physiologic pain- Minimal or no tissue injury
 Protective sensation of pain
 Pathologic pain- Pain that occurs after tissue injury
 Acute or chronic
 Classification
 Mechanism: inflammation, neuropathic, cancer, idiopathic
 Origin: visceral, somatic
 Severity: none, mild, moderate, or severe
Pain Response
 Mediators- Substances released with peripheral
tissue trauma
 Attract inflammatory cells
 Increase sensitivity of peripheral pain receptors
 Primary hyperalgesia – Peripheral
hypersensitivity
 Painful area close to the site of tissue injury
 Central nervous system hypersensitivity/“wind
up” - Hyperexcitable central neurons that are
sensitive to low-intensity peripheral stimuli
 NMDA receptor activation
Physiologic Signs of Pain
 Cardiovascular
 Hypertension
 Tachycardia/tachyarrhythmia
 Peripheral vasoconstriction (pale
MM)
 Respiratory
 Tachypnea
 Shallow breathing
 Exaggerated abdominal
breathing
 Panting (dogs)
 Open mouth breathing (cats)
 Ophthalmic
 Mydriasis http://www.bellevueanimalhospital.com/services.html
Behavioral Responses to Pain
 Varies with signalment,
temperament
 Changes in gait, activity level
 Lameness, stiffness, reluctance to move
 Exercise intolerance/decreased performance
 Vocalization
 Whining, growling, groaning, purring in SA
 Groaning, grunting, biting, kicking (LA)
 Facial expressions, appearance,
attitude
 Bruxism (LA)
 Poor grooming habits
 Hiding
Pain Assessment
 NO pain
 MILD pain
 MODERATE pain
 SEVERE pain
 Review pages 211-212 of Lerche and
1048-1050 of McCurnin on assessing
pain.
Perioperative Pain Management
 Preemptive analgesia and multimodal therapy are KEY to
successful perioperative analgesia
 Pain medication usually administered preemptively as part
of pre-medication
 Pharmacological agents for analgesia
 Opioids
 Nonsteroidal antiinflammatory drugs (NSAIDs)
 Local anesthetics
 Alpha2-agonists
 Ketamine
 Amantadine
 Corticosteroids
 Tramadol
 Gabapentin
 Tranquilizers
Opioids- Controlled Class
 Can be used for moderate to severe pain
 Can be given IV, CRI, IM, SC, PO, or via
transdermal patch
 Morphine
 Oxymorphone
 Hydromorohone
 Methadone (also NMDA receptor antagonist)
 Meperidine
 Fentanyl
 Buprenorphine
 Butorphanol
 (Nalbuphine – NOT controlled; reversal agent)
Opiods Mechanism
 Opioid receptors in brain and spinal dorsal horn cells
 Opioid receptors
 Mu1, Mu2, Kappa, Delta
 Modulate the pain and its perception
Opioid Classes
 Pure agonists
 Antagonists
 Partial agonists
 Mixed agonists-antagonists
Use of Opioids
 Injectable premedications in combination with
tranquilizer
 Neuroleptanalgesia (higher doses)
 Postoperative pain control with or without other agents
 Short duration of effect, potential for adverse effects
 IV infusion for constant, unremitting pain
 Intraarticular use (elbow, stifle surgery)
 8-12 hours of postoperative analgesia
 Epidural use (after induction, before surgery)
 6-24 hours of analgesia – can prolong with epidural catheter
 Transdermal use (fentanyl) – apply at least 6-12 hours before
procedure
 3-5 days of analgesia
Pure Agonists
 Produce a maximal response
 Pure mu agonist is best analgesia
 Impossible to separate analgesia from respiratory
depression
 e.g., morphine, fentanyl, meperidine, hydromophone,
oxymorphone
Partial Agonists
 Produce a submaximal response
 Dose-response curve
 less steep
 ceiling effect
 bell shaped
 Co-administration of partial + pure Agonists
antagonize the agonist
 Much less analgesia but less respiratory
depression
 Tendency to cause dysphoria so less abused
 e.g., buprenorphine, nalbuphine, diprenorphine
Antagonists
 Competitively reverse (antagonize) agonists
 Low (or no) intrinsic activity
 e.g., naloxone, nalmefene, naltrexone
Mixed Agonists-Antagonists
 Divergent activities on different receptors
 Agonist at one receptor (e.g., kappa + delta)
 Antagonist at another (e.g., mu);
 e.g., pentazocine, butorphanol
NSAIDs
 Analgesics for somatic (musculoskeletal) pain +/-
visceral pain
 Potent anti-inflammatory properties
 Some are antipyretic
 Work by inactivating cyclooxygenase (COX), an
enzyme needed for prostaglandin production
 Prostaglandins are a group of extremely potent chemicals
responsible for pain and inflammation as well as
“housekeeping” functions
 COX-1 and COX-2 isoenzymes
 COX-2 selective or specific NSAIDs less likely to cause GI
ulceration
 Effects on isoenzymes determine potency and severity/type of
adverse effects
NSAIDs
 Significant variation in duration of effect between
species
 Prolonged aspirin half-life (38 hours) in cat due to decreased
glucuronyl transferase levels
 Significant variation in NSAID toxicity between species
 Acetaminophen extremely toxic to cats
 Adverse effects
 Gastrointestinal problems – vomiting, ulceration
 Renal toxicity
 Dehydrated, hypotensive patients
 How do we screen for renal insufficiency?
 Impaired platelet function  prolonged bleeding times
 Liver damage (idiosyncratic reaction to carprofen in Labradors)
Contraindications for NSAIDs
 Presence of renal or hepatic dysfunction
 Coagulopathies
 GI disorders
 Shock
 Hypotension/hypovolemia
 Hypoalbuminemia
 Pregnancy
 Corticosteroids

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Pain Management Review: Untreated Consequences and Treatment Options

  • 2. Consequences of Untreated Pain  Catabolic state, may lead to wasting  Immune suppression  Inflammation  Increased anesthetic risk  Higher inhalant requirement  Patient suffering
  • 3. Physiology of Pain/Types of Pain  Nociception- Detection by nervous system of potential for or actual occurrence of tissue injury  Pain pathway  Physiologic pain- Minimal or no tissue injury  Protective sensation of pain  Pathologic pain- Pain that occurs after tissue injury  Acute or chronic  Classification  Mechanism: inflammation, neuropathic, cancer, idiopathic  Origin: visceral, somatic  Severity: none, mild, moderate, or severe
  • 4.
  • 5. Pain Response  Mediators- Substances released with peripheral tissue trauma  Attract inflammatory cells  Increase sensitivity of peripheral pain receptors  Primary hyperalgesia – Peripheral hypersensitivity  Painful area close to the site of tissue injury  Central nervous system hypersensitivity/“wind up” - Hyperexcitable central neurons that are sensitive to low-intensity peripheral stimuli  NMDA receptor activation
  • 6. Physiologic Signs of Pain  Cardiovascular  Hypertension  Tachycardia/tachyarrhythmia  Peripheral vasoconstriction (pale MM)  Respiratory  Tachypnea  Shallow breathing  Exaggerated abdominal breathing  Panting (dogs)  Open mouth breathing (cats)  Ophthalmic  Mydriasis http://www.bellevueanimalhospital.com/services.html
  • 7. Behavioral Responses to Pain  Varies with signalment, temperament  Changes in gait, activity level  Lameness, stiffness, reluctance to move  Exercise intolerance/decreased performance  Vocalization  Whining, growling, groaning, purring in SA  Groaning, grunting, biting, kicking (LA)  Facial expressions, appearance, attitude  Bruxism (LA)  Poor grooming habits  Hiding
  • 8. Pain Assessment  NO pain  MILD pain  MODERATE pain  SEVERE pain  Review pages 211-212 of Lerche and 1048-1050 of McCurnin on assessing pain.
  • 9. Perioperative Pain Management  Preemptive analgesia and multimodal therapy are KEY to successful perioperative analgesia  Pain medication usually administered preemptively as part of pre-medication  Pharmacological agents for analgesia  Opioids  Nonsteroidal antiinflammatory drugs (NSAIDs)  Local anesthetics  Alpha2-agonists  Ketamine  Amantadine  Corticosteroids  Tramadol  Gabapentin  Tranquilizers
  • 10. Opioids- Controlled Class  Can be used for moderate to severe pain  Can be given IV, CRI, IM, SC, PO, or via transdermal patch  Morphine  Oxymorphone  Hydromorohone  Methadone (also NMDA receptor antagonist)  Meperidine  Fentanyl  Buprenorphine  Butorphanol  (Nalbuphine – NOT controlled; reversal agent)
  • 11. Opiods Mechanism  Opioid receptors in brain and spinal dorsal horn cells  Opioid receptors  Mu1, Mu2, Kappa, Delta  Modulate the pain and its perception
  • 12. Opioid Classes  Pure agonists  Antagonists  Partial agonists  Mixed agonists-antagonists
  • 13. Use of Opioids  Injectable premedications in combination with tranquilizer  Neuroleptanalgesia (higher doses)  Postoperative pain control with or without other agents  Short duration of effect, potential for adverse effects  IV infusion for constant, unremitting pain  Intraarticular use (elbow, stifle surgery)  8-12 hours of postoperative analgesia  Epidural use (after induction, before surgery)  6-24 hours of analgesia – can prolong with epidural catheter  Transdermal use (fentanyl) – apply at least 6-12 hours before procedure  3-5 days of analgesia
  • 14. Pure Agonists  Produce a maximal response  Pure mu agonist is best analgesia  Impossible to separate analgesia from respiratory depression  e.g., morphine, fentanyl, meperidine, hydromophone, oxymorphone
  • 15. Partial Agonists  Produce a submaximal response  Dose-response curve  less steep  ceiling effect  bell shaped  Co-administration of partial + pure Agonists antagonize the agonist  Much less analgesia but less respiratory depression  Tendency to cause dysphoria so less abused  e.g., buprenorphine, nalbuphine, diprenorphine
  • 16. Antagonists  Competitively reverse (antagonize) agonists  Low (or no) intrinsic activity  e.g., naloxone, nalmefene, naltrexone
  • 17. Mixed Agonists-Antagonists  Divergent activities on different receptors  Agonist at one receptor (e.g., kappa + delta)  Antagonist at another (e.g., mu);  e.g., pentazocine, butorphanol
  • 18. NSAIDs  Analgesics for somatic (musculoskeletal) pain +/- visceral pain  Potent anti-inflammatory properties  Some are antipyretic  Work by inactivating cyclooxygenase (COX), an enzyme needed for prostaglandin production  Prostaglandins are a group of extremely potent chemicals responsible for pain and inflammation as well as “housekeeping” functions  COX-1 and COX-2 isoenzymes  COX-2 selective or specific NSAIDs less likely to cause GI ulceration  Effects on isoenzymes determine potency and severity/type of adverse effects
  • 19. NSAIDs  Significant variation in duration of effect between species  Prolonged aspirin half-life (38 hours) in cat due to decreased glucuronyl transferase levels  Significant variation in NSAID toxicity between species  Acetaminophen extremely toxic to cats  Adverse effects  Gastrointestinal problems – vomiting, ulceration  Renal toxicity  Dehydrated, hypotensive patients  How do we screen for renal insufficiency?  Impaired platelet function  prolonged bleeding times  Liver damage (idiosyncratic reaction to carprofen in Labradors)
  • 20. Contraindications for NSAIDs  Presence of renal or hepatic dysfunction  Coagulopathies  GI disorders  Shock  Hypotension/hypovolemia  Hypoalbuminemia  Pregnancy  Corticosteroids

Hinweis der Redaktion

  1. -Immune response suppression: infection, incr hospitalization time and cost -Inflammation – delays wound healing -Anesthetic risk: higher doses of drugs required to maintain stable anesthetic plane -Suffering: inhumane; stress to patient and owner
  2. Transduction- Noxious stimuli transformed into electrical signals Transmission- Conduction of sensory impulses from peripheral pain receptors  spinal cord Modulation- Amplification or suppression of pain impulses by neurons in spinal cord Perception- procession and recognition of impulses in brain
  3. Image: http://www.bellevueanimalhospital.com/services.html
  4. µ1: supraspinal analgesia, euphoria, sedation µ2: respiratory depression, bradycardia, increased gastroinstestinal transmit time, hypothermia, physical dependence kappa : spinal analgesia, sedation, meiosis delta: spinal analgesia, respiratory depression
  5. Avoid butorphanol and buprenorphine – can partially block opioids receptors and thereby decrease analgesic effect
  6. so less abused, ceiling effect
  7. Drugs that target COX-2 isoenzymes and spare the COX-1 isoenzymes do not interfere with gut cytoprotection at therapeutic doses
  8. Differences in hepatic biotransformation Tremendous individual variation among cats Advantages: not controlled/little abuse potential; effective when given orally; negligible CV and resp effects, good for mild to moderate pain; opioids can be used in geriatric/debilitated patients, patients with renal disease
  9. Presence of renal or hepatic dysfunction Coagulopathies, GA hypotentsion Low albumin increased toxicity