The document discusses pain management and analgesia. It outlines the consequences of untreated pain such as wasting, immune suppression, and increased risk of complications. It then covers the physiology of pain, types of pain responses, signs of pain, behavioral responses, and methods of pain assessment. Finally, it discusses various pharmacological agents for perioperative pain management including opioids, NSAIDs, local anesthetics, and other drugs, outlining their mechanisms of action, uses, and potential adverse effects.
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
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
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
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
-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
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
Avoid butorphanol and buprenorphine – can partially block opioids receptors and thereby decrease analgesic effect
so less abused, ceiling effect
Drugs that target COX-2 isoenzymes and spare the COX-1 isoenzymes do not interfere with gut cytoprotection at therapeutic doses
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
Presence of renal or hepatic dysfunction Coagulopathies, GA hypotentsion Low albumin increased toxicity