Nonsteroidal Antiinflammatory Drug Toxicosis
Basic Information
Definition
• Adverse effects of the nonsteroidal antiinflammatory drugs (NSAIDs) are caused by cyclooxygenase (COX) inhibition in tissues where prostaglandins are beneficial and protective.
• Renal papillary necrosis (medullary crest necrosis), oral and gastrointestinal (GI) ulceration, and right dorsal colitis are common signs of NSAID toxicity in horses.
• Platelet aggregation is classically inhibited by NSAIDs that prevent thromboxane production via the COX-1 pathway.
Clinical Presentation
History, Chief Complaint
• Amount administered: Phenylbutazone may cause toxicity when administered according to the label dose. Other NSAIDs usually require an overdose to cause toxicity.
Etiology and Pathophysiology
• Nephrotoxicity: NSAIDs typically have little effect on renal function in normal adult animals, but they decrease renal blood flow and glomerular filtration rate in patients with congestive heart failure, those that are hypotensive or hypovolemic (especially during anesthesia and surgery), and those that have chronic renal disease. Renal papillary necrosis is a severe dose-dependent toxicity most commonly associated with phenylbutazone. Although attributed to impaired renal blood flow, other mechanisms such as direct nephrotoxicity of the drug or its metabolites may be involved.
• GI toxicity: Reduced prostaglandin (PG) concentrations in the large colon may decrease colonic blood flow, resulting in mucosal atrophy, protein loss, ulceration, and inflammation.
Diagnosis
Initial Database
• In asymptomatic horses, consider obtaining baseline renal and hepatic function tests.
• In symptomatic horses, monitor: