Prevent renal necrosis
To prevent renal papillary necrosis with carprofen overdoses, crystalloid fluid administration at twice the maintenance fluid
rate (60 ml/lb/day) is indicated for 48 hours after exposure in dogs to promote diuresis. Carprofen's longer and more variable
half-life in cats may necessitate diuresis for 72 hours. The choice of crystalloid should be dictated by a patient's electrolyte
and acid-base status. If BUN and creatinine concentrations (see "Additional monitoring" below) are normal at 48 hours, the fluids may be tapered over 24 hours and then the renal values reevaluated at 72 hours. Monitor
urine output throughout the diuresis period to ensure that the patient is not oliguric or anuric. Renal damage has been documented
in one case as early as 24 hours after carprofen exposure by the presence of granular casts in the urine (ASPCA APCC Database:
Unpublished data, 2001-2009).
ADDITIONAL SYMPTOMATIC TREATMENT
Antiemetics are indicated in actively vomiting patients (Table 3). If an animal is critically anemic, a whole blood transfusion is warranted. Severe hypoproteinemia or coagulopathy can be
treated with a plasma transfusion (10 to 30 ml/kg intravenously).25 Vitamin K1 may be administered in patients with fulminant liver failure and coagulopathies.26 Diazepam may be given as needed for seizures. Pain due to gastrointestinal ulceration should be treated with opioid analgesia.
Diuretics and dopamine may be necessary to restore urine production in oliguric or anuric animals. Hemodialysis27 or peritoneal dialysis may be an option in patients with acute renal failure if finances are not limited. A more thorough
discussion of acute renal failure treatment is presented elsewhere.28-30 Hepatoprotective agents, such as S-adenosylmethionine (SAMe) or silymarin, can be administered in stable patients long-term
until liver enzyme activities reveal no further hepatocellular damage. Broad-spectrum antibiotics are indicated if ulceration
or hepatic compromise is present.
In patients hospitalized for diuresis, daily assessment of BUN and creatinine concentrations, packed cell volume, liver enzyme
activities, and urine output and character (e.g. presence of casts, urine protein:creatinine ratio) and frequent monitoring of hydration status are indicated. Normal test
results related to renal and hepatic function 72 hours after carprofen exposure are not anticipated to elevate thereafter.
Pain due to gastric ulceration may not become clinically evident until the analgesic effect of carprofen has worn off, so
monitor patients for several days thereafter for melena, anorexia, lethargy, and abdominal pain.
If perforating or bleeding ulcers develop to the point of peritonitis or severe anemia, respectively, the prognosis understandably
worsens. Severe azotemia, oliguria, anuria, and coagulopathy secondary to acute hepatic failure also carry a poorer prognosis.
Even in extreme overdose cases, however, the prognosis with acute carprofen toxicosis is often excellent with prompt decontamination,
diuresis, and gastrointestinal supportive care.
"Toxicology Brief" was contributed by Donna Mensching, DVM, MS, DABVT, DABT, and Petra Volmer, MS, DVM, DABVT, DABT, Department
of Veterinary Biosciences, College of Veterinary Medicine, University of Illinois, Urbana, IL 61802. Dr. Volmer is the editor
of "Toxicology Brief." Dr. Mensching's current address is ASPCA Animal Poison Control Center, 1717 S. Philo Road, Suite 36,
Urbana, IL 61802. Dr. Volmer's current address is Summit VetPharm, 400 Kelby St., Fort Lee, NJ 07024.