- Xylitol Poisoning in Dogs
- Apomorphine to Stimulate Vomiting
- Accidental Poisoning
- N-acetylcysteine as an Antidote for Acetaminophen Toxicosis
- Dimercaptosuccinic Acid for Lead Poisoning in Cats
- Penicillamine for Long-Term Treatment of Lead Poisoning
- 4-Methylpyrazole for Ethylene Glycol (Antifreeze) Poisoning
Compounding pharmacists are now receiving requests from veterinarians to compound oral medications for dogs and cats in vehicles that are known to be free of xylitol. Xylitol is an artificial sweetener commonly used to sweeten human medications, gums, mouthwashes and candies, and while not toxic to humans, can be quite toxic to dogs. Xylitol is not absorbed from the gastrointestinal tract of humans, but is easily absorbed in dogs. Once in the bloodstream, xylitol acts like glucose, stimulating insulin secretion, which causes life-threatening hypoglycemia. Profound hypoglycemia can last for 1-2 hours following xylitol ingestion, and has frequently resulted in death. Many commercially available drugs labeled for humans, such as gabapentin oral suspension, contain xylitol as an inactive ingredient, and all human medications used in dogs should be scrutinized for xylitol content. Compounding pharmacists can play a valuable role for veterinarians and veterinary patients by providing xylitol-free suspensions of medications and by educating clients to avoid all xylitol-containing foods in their pets. It is not currently known if xylitol is toxic in cats, but for the present, xylitol must also be assumed to be toxic to cats. For more information, search "xylitol" at http://www.aspca.org/.
Intl J of Pharm Comp 1997 July/Aug; 1(4): 240
To determine if rectally administered N-acetylcysteine (NAC) is absorbed into the systemic circulation, NAC was administered into the rectal vault (2.0 g/kg) of swine via a balloon-tipped Foley catheter inserted into the animals' rectums. NAC administered via the rectal route resulted in systemic absorption as determined by spectrophotometric methods in 5 of the 7 study animals. This study provides important information regarding the development of a potential alternative route for the administration of NAC to dogs. In dogs and cats, NAC can be administered intravenously or orally, but has a pungent odor. Oral administration of NAC typically causes nausea and vomiting. The oral solution can be compounded as a chicken-flavored preparation to improve palatability. Rapid intravenous administration of NAC can cause hypotension, bronchospasm, and flushing. Reactions can be minimized by slowing the rate of infusion.
Activated charcoal may absorb NAC and reduce its effectiveness, so NAC should not be administered within two hours of giving activated charcoal. "Administration of activated charcoal may exacerbate vomiting and lead to aspiration. A strong antiemetic agent (metoclopramide 0.4 mg/kg IV) may be necessary to prevent emesis."
NAC is currently not approved by the FDA for use in dogs and cats, but is available in human formulations, and upon a prescription order, can be compounded to meet specific veterinary needs.
Compendium 2003 Apr;25(4):276-280
Am J Vet Res 1985 Jul;46(7):1485-9 Comparison of N-acetylcysteine and methylene blue, alone or in combination, for treatment of acetaminophen toxicosis in cats. Click here to access the PubMed abstract of this article.
Vet Hum Toxicol 1997 Dec;39(6):329-31 Rectal administration of N-acetylcysteine in swine: a pilot study. Click here to access the PubMed abstract of this article.
Vet Med 1997;92(2):158-165
The owners of two nine-year-old cats moved to a new house. One week after moving, both cats were vomiting and losing weight so the owners brought the cats to the veterinary clinic. The veterinarian began intravenous hydration. Blood work showed a very high level of nucleated RBC's. The CBC revealed platelet clumps on feathered edge, few macrocytes, moderate anisocytosis, and occasional acanthocytes (54% and 45.1% NRBC). One cat had two seizures on the first day of hospitalization. Based on the initial signs and nucleated red cells, lead poisoning was suspected, although there was no radiographic evidence of lead ingestion. We tested for lead and began treatment with dimercaptosuccinic acid (DMSA) 40mg/cc.
The cats improved clinically within 24 hours. There were no more seizures and the cats began to eat. The blood lead levels were 164.8 and 210 (normal is 0-25). The cats were treated with 40mg (1cc) of DMSA given orally three times per day for a total of 10 days. DMSA is not commercially available in an injectable or liquid form. Therefore, we worked together with our compounding pharmacist to prepare a sterile formulation that would be suitable for intravenous or oral use.
The second day after therapy had begun, the owners informed us that they had been sanding the painted floors in their new house. The cats probably walked through the dust and in grooming themselves licked the lead paint off their paws. There have been no further problems with the cats to our knowledge. The owner declined to come in for a lead level recheck.
Veterinary Drug Handbook, 2nd edition, Donald C. Plumb, Ed.
Am J Vet Res 1995;56:825.