Xylitol, which is a 5-carbon sugar alcohol, is increasingly being used as a sugar substitute. Initially found in gum and oral care products, it can now be found in some baked goods and candy as well as available in a granular form for cooking (Xylo-Sweet®). Unlike humans, xylitol can cause a rapid increase in blood insulin in dogs causing a precipitous drop in blood glucose levels. Ingestion of larger doses of xylitol can cause hepatic injury.
Doses as low as 0.15g/kg can cause hypoglycemia and doses of >0.5g/kg can lead to hepatic injury, even hepatic necrosis/failure. It is difficult to calculate the amount of xylitol in products like gums because it is not specifically listed on the label. An estimate of 0.3g-0.4g per piece has been used to compute the exposure dose. The powdered bulk product has 190g per cup. This would mean as little as a teaspoon (3.9g) could cause hypoglycemia in a 26kg (57.2 lb) dog or liver issues in a 7.8kg (17lb) dog.
Hypoglycemia can be seen within 30-60 minutes of ingestion but can be delayed. Signs include vomiting, lethargy, disorientation, ataxia, tremors, collapse and seizures. Additional signs that may be seen are weakness, diarrhea, abdominal pain, vocalization, tachypnea, and fasciculation. Signs of hepatic insufficiency can be seen in 8-12 hrs or may be delayed up to 72 hrs. Elevations of hepatic enzymes may be transient or progress to acute liver failure. Not all dogs with liver involvement will show hypoglycemia but will have elevations in ALT, AST, ALP, bilirubin, PT and/or PTT. They may also have hypokalemia and thrombocytopenia. Some dogs will have an initial hypophosphatemia followed by a hyperphosphatemia at death.
Treatment for the asymptomatic dog includes emesis and/or gastrointestinal emptying. It may be followed by activated charcoal but it is not clear how well xylitol adsorbs to it. Due to the signs associated with hypoglycemia beginning so rapidly, care must be taken to avoid aspiration. Small frequent meals along with an IV 2.5% – 5% dextrose solution (+/- potassium supplementation) may be given while monitoring hourly blood glucose levels for at least 6-24 hours. Ingesting larger quantities of xylitol that lead to hepatic damage may require an IV 25% dextrose bolus as well. Liver values should be monitored for 48-72 hours. Hepatic protectants and antioxidants should be administered which may include acetylcysteine, plasma, Vitamin K1, Vitamin E, SAM-E and silymarin. Prognosis depends on the dose of xylitol ingested, the severity of clinical signs and the response to treatment. Hepatic necrosis, coagulopathy and hyperphosphatemia suggest a more guarded to poor prognosis. Xylitol ingestion should be treated aggressively even when there are no clinical signs as delaying treatment may increase the risk of fatal hepatic necrosis.
References: Mason JA et al: Recently recognized animal toxicants. In Bonagura JD, Twedt DC, editors: Kirkâs CVT IV, ed 14, St. Louis, 2009, Elsevier, p. 139
Dunayer EK et al: Acute hepatic failure and coagulopathy associated with xylitol ingestion in eight dogs, JAVMA, 229:1113, 2006Talcott PA: New and used topics in veterinary toxicology. Western Veterinary Conference 2008