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

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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 painMILD painMODERATE painSEVERE 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