NSAIDs-1
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)
Presenter: Dr. André Escobar, DVM, Ms, PhD, DACVAA
Associate Professor of Anesthesiology
Content adapted and delivered by Dr. Miguel Martinez, Dip ECVAA
Objectives
Understand the mechanism of action of NSAIDs
Learn about the classification of NSAIDs
Discuss indications and clinical effects
Identify adverse effects and contraindications
Review commonly used NSAIDs
Historical Perspective
Willow Bark: Traditional NSAID; its use dates back thousands of years
Ancient Civilizations: Used by Egyptians and Sumerians (3.5k years ago)
Hippocrates: Known as the "father of medicine" (2.5k years ago)
Salicylic Acid: Isolated in Germany, 1878
Acetylsalicylic Acid (Aspirin): Developed by Bayer in 1899
Post WWI: Bayer lost trademark rights due to war reparations
COX Inhibition Theory: Proposed 40 years ago
Mechanism of Action
Competitive Inhibition: NSAIDs inhibit cyclo-oxygenase (COX) pathways
COX Isoforms:
COX-1: Constitutive enzyme, present in most tissues (e.g., platelets, liver, kidney, gastric mucosa); involved in normal physiological functions
COX-2: Inducible enzyme, produced by inflammatory cells and activated by cytokines
COX-3: Variant of COX-1, primarily in brain and heart
Arachidonic Acid Pathway
Source: Predominant fatty acid in cell membranes
Biotransformation: Arachidonic acid is transformed into eicosanoids, influencing inflammation and physiology
Products:
Prostaglandins (PGE2, PGF2, PGD2)
Prostacyclin (PGI2)
Thromboxane (TXA2)
Role of Prostaglandins
Sensitization: Prostaglandins sensitize nociceptors to inflammatory mediators
Biological Functions:
GI: Increase mucosal blood flow, bicarbonate and mucus secretion, decrease acid production
Kidneys: Induce renal vasodilation and diuresis
Uterus: Increase blood flow and contractions
Brain: Induce fever
Blood Vessels: Cause vasodilation
Platelets: Inhibit (PGI2) or promote (TXA2) aggregation
COX Isoforms and Their Effects
COX-1: Generally considered "good"; inhibition leads to side effects but plays roles in homeostasis
COX-2: Considered "bad"; inhibition helps alleviate pain and fever, primarily acts in inflammatory process
NSAIDs Classification
COX-1: COX-2 Inhibitory Ratio (IC50):
Determines the selectivity of NSAIDs towards COX enzymes
Higher ratios indicate greater action on COX-2
Common NSAIDs and Their Ratios
Aspirin: 0.3 – 0.4
Ketoprofen: 0.1 – 0.6
Meloxicam: 2.7 – 10.0
Carprofen: 1.8 - 65
Firocoxib: 384 - 427
Deracoxib: 12 - 1275
Clinical Effects
Analgesic: Provides pain relief both centrally and peripherally
Anti-inflammatory: Inhibits mediators of inflammation, acts as a free radical scavenger, stabilizes membranes, and reduces leukocyte accumulation
Anti-pyretic: Reduces fever associated with endotoxemia
Indications for Use
Used for chronic pain, osteoarthritis, neoplasia, and otitis
Commonly prescribed post-operatively for acute surgical pain
Ideal candidates: Well-hydrated, normotensive, young to middle-aged animals with normal renal function
Compared to opioids: NSAIDs are usually longer acting, more effective for inflammatory conditions, easier for at-home use, and cost-effective
Contraindications
Avoid use in cases of:
GI disorders
Dehydration
Hypotension
Shock or unstable cases
Azotemia
Thrombocytopenia
Hepatic insufficiency
Concurrent corticosteroid therapy
Routes of Administration
Common Routes:
Oral, Subcutaneous (SC)
Less Common (In hospital use):
Intravenous (IV)
Oral Medications: Well absorbed (>90% protein binding, weak acids with high lipophilicity)
Topical Formulations: Creams
Adverse Effects
Gastrointestinal: Potential for vomiting, diarrhea, inappetence; gastric ulceration/perforation is a major concern
Risk Management: Use of gastric protectors (sucralfate, omeprazole, famotidine)
Renal Function: NSAIDs are not inherently nephrotoxic but can cause damage under certain risk factors
Associated with dehydration, pre-existing renal disease, concurrent corticosteroid usage
Coagulation: Impaired by TXA2 inhibition; increases the risk of perioperative bleeding
Example: Aspirin causes irreversible COX-1 inhibition
Cardiovascular Risks: Potential for creating a prothrombotic state leading to thrombosis
Historical Context: Rofecoxib and valdecoxib withdrawn from market due to safety concerns
Hepatic Injury: NSAIDs metabolized in the liver can have predictable reactions or idiosyncratic reactions
Cats show higher susceptibility due to metabolic pathways
Special Considerations
Pregnant Animals: Caution due to COX-2's role in reproduction and nephrogenesis
Pediatric Patients: Avoid NSAIDs before 4 weeks of age due to nephrogenesis completion
Fracture Healing: COX-2 importance in bone healing; NSAIDs to be used sparingly
Felines: Slow metabolic clearance; under dosing is crucial due to toxicity risks associated with overdose from common analgesics
Precautionary Measures
Ensure access to food and water
Monitor blood pressure and maintain normal blood volume
Regular monitoring of BUN and creatinine levels
Washout period of 4-10 days is necessary for most NSAIDs
Specific NSAIDs
Robenacoxib (Onsior, Novartis)
Routes: SC and oral
Approved for use in cats and dogs for up to 3 days
COX-2 selective inhibitor with minimal adverse effects
Other Coxibs
Deracoxib (Deramaxx): Approved for dogs
Firocoxib (Previcox): Special caution is required for use according to veterinarian's guidance
Carprofen
Available as injectable (SC and IV) and oral formulation
Generally approved for dogs; limited use in cats (only single use)
Considered a COX-2 preferential inhibitor with few side effects
Meloxicam
Available as injectable and oral (liquid) formulation
Approved for various species including cats, dogs, cattle, and pigs
Phenylbutazone
Administered both orally and via injection
Used for musculoskeletal inflammation and pain but poses higher risks for GI and renal toxicity
Ketoprofen
Non-selective COX inhibitor used in various species; carries risk of adverse effects
Flunixin Meglumine
Utilized in dogs, cats, horses, and cattle; only FDA approved for inflammation and fever in food animals
Acetylsalicylic Acid (Aspirin)
Non-specific COX inhibitor not approved for veterinary use; serious risks of GI bleeding
Acetaminophen (Tylenol)
Not approved for veterinary use; highly toxic to cats
Death in cats can occur from overdose or accidental ingestion
Common signs of toxicity include vomiting and cyanosis
Grapiprant (Galliprant)
Latest development approved for dogs
Works as an antagonist of EP4 receptors to relieve osteoarthritis pain without liver or GI effects
Questions?
Open floor for questions on content.