Page 130 - Problem-Based Feline Medicine

122 PART 2 CAT WITH LOWER RESPIRATORY TRACT OR CARDIAC SIGNS

Most species biotransform acetaminophen by hepatic Finding the pills in stomach contents is confirmatory.
conjugation with glucuronic acid and excrete it in the
Frequent laboratory findings include; methemo-
urine.
globinemia, depletion of erythrocyte-reduced glu-
However, cats have limited ability to conjugate drugs tathione, Heinz bodies and a decreased packed cell
as glucuronides and so they excrete the majority of volume.
acetaminophen as a sulfate conjugate.
Elevated hepatic enzyme levels and total and direct
This pathway is saturated at relatively low drug con- bilirubin levels are evidence of hepatic necrosis.
centrations leading to early oxidative toxicity in the cat.
Hepatocellular injury associated with acute acetamin- Differential diagnosis
ophen toxicity in other species is not seen in cats
Other causes of methemoglobinemia include, benzo-
because cats develop oxidative toxicity at much lower
caine (used as a laryngeal local anesthetic spray to
doses than those required for hepatotoxicity in other
facilitate intubation), DL methionine (used as a uri-
species.
nary acidifier), phenacetin (used as an analgesic in
Accumulation of oxidative metabolites produces humans) and phenazopyridine (used as a urinary anal-
methemoglobin, which reduces oxygenation of blood. gesic drug).
Methemoglobinemia leads to the denaturing of hemo- Methylene blue, a drug previously used to treat cats
globin and Heinz bodies are formed from the precip- with methemoglobinemia may actually cause Heinz
itation of this denatured haemoglobin within the red body formation and hemolytic anemia.
blood cells.
Familial methemoglobin reductase deficiency has
Heinz bodies lead to increased osmotic fragility of red been reported in a family of domestic shorthair cats and
blood cells causing hemolysis and anaemia. is thought to have an autosomal recessive form of
inheritance.
The feline toxic dose of acetaminophen is 50–100
mg/kg, and the average size of a regular tablet is 325
mg (USA) or 250 mg (Europe). Treatment
Induce emesis and administer activated charcoal if the
cat is treated within the first 4 hours post-ingestion.
Clinical signs N-acetylcysteine will provide the cysteine moiety
required for the increased synthesis of gluthathione
Salivation, vomiting and depression progress rapidly
and may increase the concentration of free serum sul-
and cyanosis develops within 4–12 hours of ingestion.
fate. A dose of 140 mg/kg IV should be followed by 70
Hematuria and hemolysis appear when blood levels mg/kg IV every 6 hours for a total of seven treatments.
of methemoglobin reach 20%.
Ascorbic acid provides a reserve system for the non-
Subcutaneous edema of face and extremities may enzymatic reduction of methemoglobin back to
happen and be accompanied by lacrimation and pru- hemoglobin and can be given at a dose of 30 mg/kg IV
ritis. four times a day.
Death may occur. Blood transfusion may provide a lifesaving fraction of
functional hemoglobin until the methemoglobin can
Jaundice is seen 2–7 days post-exposure if the cat sur-
be reduced.
vives.
Cimetidine, which works differently to acetylcysteine
Diagnosis and ascorbic acid in the metabolism of acetaminophen,
has been used in an attempt to reduce hepatotoxicity.
Diagnosis is based on the history of exposure and clin- The suggested dose rate is 15 mg/kg IV every 8 hours
ical signs. or 100 mg/kg orally every 8 hours.