Page 141 - Clinical Small Animal Internal Medicine

13 Hypoglycemia in Patients without Diabetes Mellitus 109

intravenous glucose administration and anticonvulsant has been steadily rising over the last few years, with a
VetBooks.ir therapy. The owners of these dogs chose euthanasia resultant surge in xylitol cases reported to the APCC.
because of poor response to therapy and poor prognosis.
Blood was cultured from one dog using a special enrich­
In laboratory experiments, xylitol directly stimulates
ment PCR media to rule in or rule out an infection Clinical Signs and Laboratory Abnormalities
caused by a fastidious bacteria; Bartonella hensalae insulin synthesis and secretion within 30 minutes after
was amplified and sequenced from this dog’s blood. In ingestion. However, in clinical cases, the onset of clinical
the other dog, Bartonella kohlerae was amplified and signs varies based on the form of xylitol used in the prod­
sequenced retrospectively from paraffin‐embedded uct ingested. The powder used in candies and mints is
tissue. Despite isolating Bartonella spp. from both dogs, absorbed quickly and signs can be seen in 30 minutes.
it is unclear whether B. hensalae and B. kohlerae contrib­ Gum must be chewed to release the xylitol. If the gum is
uted to the pathogenesis of this unusual and rare swallowed whole it leaches into the stomach, and the
hypoglycemic syndrome. That said, persistent hyperin­ onset of clinical signs can be delayed 8–18 hours.
sulinemic hypoglycemic syndrome should be suspected Vomiting is often the first symptom. Clinical signs can
in any young dog with hypoglycemia refractory to intra­ include ataxia, depression, dilated pupils, and seizures
venous glucose. Moreover, until more is known about (related to hypoglycemia), and lethargy, inappetence,
the cause of this syndrome, testing and treating vomiting, and diarrhea (related to liver failure).
for Bartonella should be a diagnostic and therapeutic Laboratory abnormalities initially include hyperinsuline­
consideration. mia, hypoglycemia, hypophosphatemia, hypokalemia,
and increased AST and ALT concentrations. Dogs that
do not exhibit hypoglycemia immediately after ingestion
Xylitol Toxicity
of xylitol may still develop acute liver failure. These dogs
Xylitol exposure, even in small amounts, can cause hypo­ may develop severe signs 24–72 hours later.
glycemia and severe liver damage in dogs. Xylitol is a 5‐
carbon sugar alcohol that is used primarily as an artificial Diagnosis
sweetener that has less than two‐thirds of the calories of The diagnosis of xylitol toxicity is made by history of
most sugars. The two major sources of xylitol exposure exposure, clinical signs, and serum biochemical abnor­
are food and dental or medical products. Initially, expo­ malities consistent with xylitol poisoning. Because the
sure to xylitol in dogs was from “sugar‐free” chewing serum half‐life of xylitol is about two minutes and there
gums. However, with demands from human diabetic is rapid progression of the toxic effect, testing for xylitol
patients, particularly because of the popularity of Atkins‐ in the blood is not realistic.
like “low‐carb” diets, many foods now contain xylitol. A
large number of low‐carbohydrate foods, including Treatment and Monitoring
breads, candies, gums, and deserts, have xylitol as the Blood glucose levels should be determined initially and
sweetener of choice. Xylitol has a wide margin of safety monitored at least every four hours for 24 hours or
in mammals with the exception of dogs. Oral exposures longer, as indicated. Liver enzyme levels and prothrom­
as low as 0.1 mg/kg have induced hypoglycemia in the bin time/partial thromboplastin time (PT/PTT) should
dog, and levels of 0.5 mg/kg have resulted in hepatotoxic­ be monitored every 24 hours for 48–72 hours. It is not
ity in some dogs. For example, one piece of Trident gum uncommon to have a transient elevation in ALT (300–
contains 0.22 g of xylitol and the popular breath mint Ice 800) very quickly after ingestion. Electrolyte status and
Breakers contains 1 g of xylitol per piece and therefore, packed cell volume (PCV) should also be monitored
nine pieces of Trident or two Ice Breaker pieces could regularly.
potentially cause xylitol toxicity in a 20 kg dog. The lit­
erature reports no cases of xylitol toxicity in cats. ● There is no antidote for xylitol toxicity.
Induce emesis if the xylitol ingestion is recent.
●
Prevalence ● Use of activated charcoal is of limited efficacy with
Recently, there has been a rapid increase in the number xylitol because it is not effective at binding xylitol.
of products containing xylitol. According to the ASPCA ● IV fluid support: important to restore or maintain
Animal Poison Control Center (APCC), the number of hydration, treat hypoglycemia, and prevent or treat
reported xylitol exposures in dogs has been increasing disseminated intravascular coagulation (DIC). Patients
steadily and exponentially over the past few years. In with normal blood glucose levels should receive a 2.5%
2007, theAPCC began to log xylitol cases. That year, the dextrose solution.
center received 1764 calls about xylitol. In 2012, the fig­ ● Hypoglycemia caused by xylitol toxicity is usually
ure was 3184. The number of products containing xylitol responsive to IV dextrose solutions. Refractory cases