AAHA offices are closed due to a special staff function from 1-5pm MDT on June 24. We will resume regular business hours on Monday, June 27.


The majority of conditions that cause pain have an inflammatory component. Nonsteroidal anti-inflammatory drugs (NSAIDs) are a mainstay for management of chronic pain as well as for perioperative use. NSAIDs should be used for their central and peripheral effects in both dogs and cats after consideration of risk factors. There is no indication that any one of the veterinary-approved NSAIDs are associated with any greater or lesser incidence or prevalence of adverse events (AEs).19 Canine and feline veterinary-approved NSAIDs have demonstrated acceptable safety profiles, which is in contrast to nonapproved NSAIDs such as aspirin, ibuprofen, naproxen, and meloxicam for human use.20–22 Long-term use of low-dose meloxicam is approved in cats in many countries other than the US.

AEs related to NSAID use in dogs and cats can be minimized by appropriate use as outlined in Figure 3. Although the overall incidence and prevalence of NSAID-related toxicity is unknown, it does appear to be very low relative to the number of doses administered.20

Of the AEs associated with NSAIDs, gastrointestinal (GI) toxicity is the most common. The GI clinical signs associated with NSAID toxicity in dogs include vomiting, diarrhea, and inappetence.20,23–25 In cats, inappetence appears to be the most common AE. Although unlikely, it is possible for erosions and ulcers to be silent and occur prior to any clinical signs.23,26 Studies indicate that NSAIDS that spare cyclooxygenase (COX)-1 produce a lower frequency of GI lesions, although the more highly COX-2-selective inhibitors may actually produce more AEs when underlying gastric damage is already present. 19,27

The leading risk factors for NSAID-associated GI perforations are incorrect dosing, concurrent use with other NSAIDs or corticosteroids, and continued use despite GI signs or anorexia.20,24< Signs of GI toxicity usually emerge within 2–4 wk but can occur at any at any point during administration.28,29 It is critical that veterinarians communicate NSAID toxicity risk factors to pet owners (e.g., providing client information that describes potential side effects, including the commercial circulars provided by drug manufacturers and instruction on when to stop medication and contact a veterinarian). This Task Force strongly encourages implementation of practice systems that ensure communication to clients of appropriate AEs and risk information for any prescribed drug, including NSAIDs.

Another important side effect associated with NSAIDs is nephrotoxicity. When administered before anesthesia in healthy dogs with controlled modest hypotension, no adverse effect on renal function was detected.30,31 However, because some dogs in those studies did develop changes in renal parameters, the importance of maintaining a normotensive state during anesthesia is considered paramount when utilizing preoperative NSAIDs. Preoperative administration in dogs is superior in efficacy to postoperative use, consistent with results of multiple studies performed in humans.32 Similar studies have not been conducted in cats undergoing anesthesia, but one feline study revealed no alteration in glomerular filtration rate measured by iohexol clearance after 5 days of oral meloxicam.27 If IV access is not possible and normotension cannot be achieved with certainty, the Task Force recommends limiting the use of NSAIDs to postsurgical administration.

Idiosyncratic hepatocellular necrosis has been reported with various NSAIDs but remains exceedingly rare, only 1.4 cases/10,000 dogs (0.052%), usually occurring between 2 and 4 wk after starting treatment. Preexisting elevated liver enzymes are not a risk factor.19 Idiosyncratic hepatocellular necrosis is not a true toxicosis but rather an intrinsic, heritable reaction to the molecule being administered.20

Highly COX-2-selective NSAIDs have caused delayed bone healing in rabbit and rodent models, and one study in dogs demonstrated delayed healing of experimental tibial osteotomies following long-term NSAID use.33 The latter study may not be a clinically relevant model, and another study reported that normal tissue healing is rapidly restored once the NSAID is withdrawn.34 Further, of 299 dogs receiving deracoxib, carprofen, and firocoxib in the FDA-approval process, none were reported to have delayed fracture healing or nonunion fractures. Finally, no clinically significant bleeding dyscrasias have been reported with the use of veterinary NSAIDs.20

The information provided on this site is intended for your general knowledge only and is not a substitute for professional medical advice or treatment for specific medical conditions. You should not use this information to diagnose or treat your pet’s health problem or disease without consulting with a veterinarian. Please consult your veterinarian with any questions or concerns you may have regarding your pet’s condition.