CVC Highlight: Your toolbox for troublesome toxicoses in cats


CVC Highlight: Your toolbox for troublesome toxicoses in cats

For cats, just a little snack in the garden—or the inappropriate treatment of common ailments by well-meaning owners—can result in an emergency situation.
Dec 01, 2011

Dr. Kristy L. Dowers
Cats are a little more finicky than dogs about what they will ingest. But their unique metabolism of xenobiotics makes them particularly sensitive to some substances. In other words, they are not small people or dogs. Here are some toxic substances to watch out for in your feline patients, as well as a quick review of feline metabolism.


We know they're different, but why?

Xenobiotics pass through two phases in the liver during metabolism. Phase one involves oxidation, reduction, and hydrolysis, and phase two involves conjugation. For most species, this means mostly glucuronidation. However, for cats, which have limited glucuronidation capabilities, this phase is accomplished mostly through sulfation. This difference in liver metabolism means that substances that are safe in other species can be deadly in cats and that the toxic dose of many substances may be much lower in this species.


"But I just gave him half of a pill because he wouldn't eat!"

Owners may take it upon themselves to treat their cats' pain or discomfort and will often reach for medications such as acetaminophen formulated for infants or children. This can be a deadly mistake. Just over 10 mg/kg acetaminophen can result in toxicosis and death in cats. The infant's suspension of most acetaminophen formulas contains 100 mg/ml acetaminophen, and most children's suspensions contain 32 mg/ml.

Acetaminophen can produce both hepatotoxicosis and hematotoxicosis in cats. Most acetaminophen ingested is conjugated by sulfation and glucuronidation to form inactive metabolites. However, a small amount of the metabolite N-acetyl-p-benzoquinone imine (NAPQI) is produced and then conjugated with glutathione to an inactive product. In cats, glutathione stores can be quickly depleted, resulting in an accumulation of NAPQI. This metabolite is highly reactive and can cause hepatocellular damage.

A unique feature to this toxicosis in cats (and to a lesser degree in dogs) is the development of methemoglobinemia, which is thought to be caused by another metabolite, para-aminophenol (PAP), also conjugated with glutathione to an inactive product. The enzyme required for these conjugations is deficient in both cats and dogs, resulting in hematotoxicosis.

Clinical signs

  • Tachypnea
  • Pale to muddy (cyanotic) mucous membranes
  • Hypothermia
  • Tachycardia
  • Edema of the face and extremities
  • Central nervous system depression
  • Anorexia
  • Vomiting
  • Salivation
  • Diarrhea
  • Coma
  • Death


  • Clinical signs and history
  • Complete blood count: Heinz body anemia, with or without reticulocytosis, methemoglobin > 15% (a drop of blood on a white paper towel will appear brown)
  • Serum chemistry profile: increased liver enzyme activities
  • Urinalysis: hemoglobinuria


  • Restore oxygenation by providing supplemental oxygen.
  • Administer 5% solution of N-acetylcystine orally or intravenously—loading dose of 140 mg/kg and then 70 mg/kg every four hours for three to five treatments.
  • Administer 30 mg/kg ascorbic acid (intravenously if giving activated charcoal) three or four times daily.
  • Administer 180 mg S-adenosylmethionine orally twice daily for three days and then 90 mg twice daily for 14 days.
  • Do not use methylene blue to treat methemoglobinemia as it has caused Heinz body anemia in cats.