Toxicology Brief: The 10 most common toxicoses in cats
If the exposure is detected quickly, dilution with milk or water should be performed; do not induce vomiting or administer activated charcoal. Hospitalize symptomatic cats. Sucralfate slurries can be used to coat and protect oral and esophageal lesions while they heal. Pain management with opioids can make the cats more comfortable. Monitor the white blood cell count and begin antibiotics if signs of infection are evident. Give intravenous fluids for hydration. Cats may be anorectic for several days, so forced feeding or alimentation through a feeding tube may be needed until the cats recover. Endoscopy may be required to evaluate esophageal damage, but be sure to avoid further damage to or perforation of a devitalized esophagus. The prognosis with supportive care is good unless esophageal damage has occurred.
7 Nonsteroidal anti-inflammatory drugs
Cats may be exposed to nonsteroidal anti-inflammatory drugs (NSAIDs) either by owner administration or, more rarely, by self-ingestion, often with canine chewable formulations. NSAIDs can cause gastrointestinal upset, including vomiting, diarrhea, ulceration, hemorrhage, and ulcer perforation. Acute renal failure can occur at higher dosages. Some NSAIDs have been associated with CNS signs such as seizures and comas at high doses in cats. The more common drugs that can cause this syndrome include carprofen, ibuprofen, deracoxib, naproxen, etodolac, meloxicam, and indomethacin.10,11In general, cats have a low tolerance for NSAIDs. For example, cats are thought to be at least twice as sensitive to ibuprofen as dogs are.10 Gastrointestinal ulceration can occur in cats exposed to 4 mg/kg of carprofen; acute renal failure can develop at doses greater than 8 mg/kg (ASPCA APCC Database: Unpublished data, 2001-2005). Because of this sensitivity, most exposures require aggressive treatment.
Initial treatment should consist of gastric decontamination. If spontaneous vomiting has not begun and the ingestion was less than four hours earlier, induce emesis. Then administer activated charcoal and give repeated doses when exposure involves an NSAID that undergoes enterohepatic recirculation. To prevent gastrointestinal ulceration, administer an acid reducer such as an H2 blocker (e.g. ranitidine or famotidine) or proton-pump inhibitor (e.g. omeprazole), as well as sucralfate and misoprostol (1 to 3 µg/kg orally b.i.d.)12 for seven to 10 days. Monitor the cat for signs of gastrointestinal hemorrhage, such as melena or a decreased packed cell volume. Initiate fluid diuresis at twice the maintenance rate for at least 48 hours to prevent renal damage, and monitor the results of renal function tests.11
As with NSAIDs, acetaminophen is often administered to sick cats by their owners. Acetaminophen has a narrow margin of safety in cats. One adult tablet (325 to 500 mg) could be lethal. Clinical signs such as depression, vomiting, dyspnea, brown discoloration of the mucous membranes and blood due to methemoglobinemia, respiratory distress, swelling of the face and paws, and hepatic necrosis can develop at almost any level of exposure.11 Signs of methemoglobinemia generally occur within hours of exposure, and liver damage may take a couple of days to manifest.
In asymptomatic cats, emesis may be initiated and activated charcoal administered. If methemoglobinemia is present, start oxygen therapy combined with a blood transfusion or polymerized bovine hemoglobin solution (Oxyglobin—Biopure) administration. Begin N-acetylcysteine (e.g. Mucomyst—Bristol-Myers Squibb) therapy immediately in any case of acetaminophen exposure in a cat. Dilute the N-acetylcysteine solution to a 5% concentration with 5% dextrose or sterile water; this will yield a 50-mg/ml solution. The loading dose is 140 mg/kg followed by 70 mg/kg every six hours for seven additional doses. Administer N-acetylcysteine orally unless either a bacteriostatic filter or a sterile solution of N-acetylcysteine (Acetadote—Cumberland Pharmaceuticals) is available. Adjunctive therapy includes intravenous fluids, cimetidine (to inhibit CP450 liver enzymes that activate acetaminophen to the toxic metabolite), and ascorbic acid, which may be used to help reduce methemoglobin to hemoglobin.11 The prognosis in these cases is fair to guarded.