</center class=”full-width-embed”>
In today’s VETgirl continuing education blog, we review NSAID toxicosis in dogs and cats. NSAIDs are competitive inhibitors of prostaglandin synthesis (cyclooxygenase or “COX” inhibitors) and result in decreased prostaglandin, which is important for normal homeostatic function (including maintaining renal blood flow, maintaining mucous production in the stomach, etc.). Common OTC human NSAIDs include active ingredients such as ibuprofen and naproxen sodium. Examples of human NSAIDs include Advil®, Aleve®, certain types of Motrin®, etc. Common prescription veterinary NSAIDs can also result in toxicosis, particularly when available in the chewable, palatable formulation. Examples of veterinary NSAIDs include carprofen, deracoxib, etogesic, previcoxib, etc. With NSAID toxicosis, the GI tract, kidneys, CNS, and platelets can be affected. Cats and certain breeds of dogs (e.g., German shepherds) seem to be more sensitive to NSAIDs, and should be treated aggressively. With cats, severe acute kidney injury (AKI) is often more clinically seen with NSAID toxicosis at lower doses (as compared to dogs). With dogs, signs secondary to GI ulceration (e.g., vomiting, diarrhea, melena, hematemesis, etc.) are more commonly seen initially, followed by secondary AKI.

With NSAID toxicosis, it is important to keep in mind that each NSAID has a different toxic dose, margin of safety, half-life, and route of excretion, and the ASPCA Animal Poison Control Animal Poison Control should be contacted to identify what specific NSAID and toxic dose was ingested. For example, in dogs, ibuprofen results in GI signs at doses as low as 16-50 mg/kg, while severe GI signs may be seen at 50-100 mg/kg.(1) Renal compromise may be seen at doses of 100-250 mg/kg (resulting in potential AKI), and fatalities have been reported at doses > 300 mg/kg.6 This differs tremendously from naproxen sodium (dogs), where severe clinical signs can be seen at doses as low as 5 mg/kg.(1)

Clinical signs of NSAID toxicosis include anorexia, vomiting, hematemesis, diarrhea, melena, abdominal pain, lethargy, malaise, uremic halitosis, dehydration, etc. Treatment includes decontamination, the use of activated charcoal (often multiple doses due to enterohepatic recirculation, if appropriate), GI protectants (e.g., H2 blockers, sucralfate), aggressive IV fluid therapy (to help maintain renal blood flow), anti-emetic therapy, and symptomatic and supportive care. With high doses, anti-convulsants may also be necessary if CNS signs develop.

1. Syring RS. Human NSAIDs. In: Osweiler G, Hovda L, Brutlag A, Lee JA, eds. Blackwell’s Five-Minute Veterinary Consult Clinical Companion: Small Animal Toxicology, 1st Ed. Iowa City: Wiley-Blackwell, 2010, pp.292-299.


Only VETgirl members can leave comments. Sign In or Join VETgirl now!