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1050 Xylitol Toxicosis

Xylitol Toxicosis Client Education
Sheet
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• In humans, xylitol does not cause signifi-
BASIC INFORMATION
cant increase in insulin levels, but in dogs, TREATMENT
Definition xylitol causes a rapid and dose-dependent Treatment Overview
Xylitol is a 5-carbon sugar alcohol used as a increase in blood insulin and concomitant Mainstays of therapy are correction of
sweetener in gums, candies, confectionery/ hypoglycemia. hypoglycemia and addressing hepatotoxic-
baked goods, some peanut butters, and in • Mechanism of hepatotoxicosis in dogs ity and coagulopathy. In asymptomatic
some medications. Toxicosis is characterized is unknown. Potential mechanisms animals exposed to a toxic dose, emesis can
by hypoglycemia leading to weakness, ataxia, include necrosis of hepatocytes due to be induced if the exposure occurred within
lethargy, disorientation and seizures within adenosine triphosphate (ATP) deple- a few hours. The clinical presentation and
minutes to hours after ingestion. Hepato- tion, resulting in cell necrosis; or evolution of the case determine treatment
toxicosis can occur in 12-48 hours in some production of reactive oxygen species, needs.
dogs and may be idiosyncratic (individual resulting in damage to cell membranes and
susceptibility). Toxicosis has been fatal in macromolecules. Acute General Treatment
some dogs. • Decontamination of asymptomatic patient
DIAGNOSIS (p. 1087)
Synonyms ○ Induce vomiting (e.g., apomorphine [p.
• Xylite, eutrit, newtol, xyliton Diagnostic Overview 1188]).
• Chemical names: 1,2,3,4,5-pentapentanol Diagnosis rests on history (observed or sus- ○ Do not give activated charcoal, which is
and 1,2,3,4,5-pentahydroxypentane pected ingestion), physical exam, and results not expected to be effective.
• Many sugar-free products contain xylitol as of routine laboratory testing (hypoglycemia • Gastric lavage (p. 1117) is not typically
a sweetener. ± signs of acute liver injury +/− coagu- recommended.
lopathy). No specific confirmatory test • Management of hypoglycemia and associated
Epidemiology exists. signs
SPECIES, AGE, SEX ○ 1-2 mL/kg of 50% dextrose (dilute in
• Toxicosis has been documented in dogs Differential Diagnosis saline) bolus followed by 2 mL/kg/h IV;
only • Rule out other causes of hypoglycemia (p. adjust according to blood glucose level.
• No known age, sex, or breed predisposition 1240). After blood glucose level is stable, continue
○ Toxicologic: insulin overdose, antidiabetic to check q 2-4h.
RISK FACTORS medications overdose (sulfonylureas) ○ Use oral source of dextrose (e.g., Karo
• Animals with pre-existing liver disease may ○ Nontoxicologic: insulinoma, juvenile syrup) to lick if dog is able to swallow;
be at increased risk for hepatotoxicosis. hypoglycemia, sepsis, others give small, frequent meals.
• Young animals may be more prone to • Rule out other causes of acute hepatic injury ○ Seizures initially managed by normalizing
developing hypoglycemia. (p. 442). blood glucose and/or addressing hepatic
○ Toxicologic: acetaminophen, blue-green encephalopathy. Anticonvulsant drugs
Clinical Presentation algae, sago palm, hepatotoxic mushrooms, added if required (p. 903)
DISEASE FORMS/SUBTYPES zinc phosphide, mycotoxin (aflatoxins), • Treat acute hepatic injury (p. 442). Consider
Xylitol toxicosis is an acute syndrome. nonsteroidal antiinflammatory drug S-adenosylmethionine (SAMe) or Denamarin
(NSAID) toxicosis q 8-12h for 24-48 hours. Use of N-acetyl-
HISTORY, CHIEF COMPLAINT ○ Nontoxicologic: bacterial hepatitis, idio- cysteine for 7 treatments may provide some
• Evidence of chewed-up package; gum, or pathic chronic hepatopathy, viral hepatitis, benefits in preventing liver damage (same
wrappers in vomitus/stool leptospirosis, others dose as used for acetaminophen toxicosis
• Vomiting, lethargy, weakness, disorientation, [p. 10]).
ataxia, seizures, typically 30 minutes to 12 Initial Database • Treat bleeding disorders.
hours after ingestion • CBC: ± thrombocytopenia ○ Significant elevations in PT and/or aPTT
• Some dogs develop hypoglycemia and • Serum biochemistry profile (more than double, with or without overt
acute liver failure. Other dogs do not show ○ Hypoglycemia (mild to severe; lowest bleeding): consider frozen or fresh-frozen
evidence of hypoglycemia but develop acute reported is 26 mg/dL [1.5 mmol/L]) plasma transfusion (p. 1169).
hepatic injury (p. 442) in 12-48 hours. ○ Increased liver enzymes (e.g., alanine amino- ○ Hemorrhage addressed as appropriate (p.
transferase [ALT]: 1000 to > 10,000 IU/L; 433)
PHYSICAL EXAM FINDINGS normal < 120 IU/L)
• Nonspecific lethargy, vomiting, weakness ○ Hyperbilirubinemia common (mean, Chronic Treatment
• With marked hypoglycemia: ataxia, disori- 4.1 mg/dL; normal, < 0.6 mg/dL) SAMe 18 mg/kg PO q 24h for 1-3 months if
entation, seizures • Coagulation panel (if elevated liver enzymes) evidence of hepatotoxicosis
• Evidence of bleeding disorder: petechiae, ○ Prothrombin time (PT) often elevated (36
ecchymoses, gastrointestinal (GI) hemor- to > 100 seconds) Nutrition/Diet
rhage, oozing from venipuncture sites ○ Activated partial thromboplastin time • Karo syrup, honey, or corn syrup together
• Vital signs (body temperature, respiratory (aPTT) markedly elevated (>100 seconds) with frequent feeding of small meals may
rate and character, heart rate) are usually be helpful initially for hypoglycemia.
within normal range. Advanced or Confirmatory Testing • Optimal protein diet for liver damage
Necropsy findings include icterus, hepatic
Etiology and Pathophysiology necrosis, peritoneal and GI petechiae, and Drug Interactions
• Toxicosis occurs acutely when dogs eat large ecchymoses. Xylitol is metabolized quickly, Metabolism and pharmacokinetic parameters
amounts of xylitol-containing products. and no residue is expected. of many medications can change due to liver

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