TOXICOLOGY

CPD article

Xylitol toxicosis in dogs

Xylitol is toxic to dogs, causing hypoglycaemia and, in some cases, liver failure. This sweetener is found in
many foods, medicines and confectionary, particularly chewing gums, because it has anticaries properties and
a low glycaemic index. The most common source of xylitol poisoning in dogs is chewing gum, in which the
xylitol content can vary enormously. In addition, granulated xylitol is available as a sugar substitute for baking.
Xylitol-induced hypoglycaemia may be rapid in onset or, as is often the case with chewing gums, delayed for
several hours. Elevated liver enzymes may be apparent within a few hours in some cases. Treatment is aimed at
monitoring blood glucose and correcting hypoglycaemia, and protecting the liver. Dogs can survive high doses of
xylitol with prompt aggressive treatment. In contrast, xylitol-induced hypoglycaemia and liver failure is not seen in
cats, rabbits or rodents, but poisoning has been reported in birds. 10.12968/coan.2019.24.4.182

Nicola Bates BSc (Brunel), BSc (Open) MSc MA. Senior Information Scientist, Veterinary Poisons Information Service (VPIS),
2nd Floor, Godfree Court, 29-35 Long Lane, London SE1 4PL. nicola.bates@vpisglobal.com

Key words: poisoning | toxicology | xylitol | hypoglycaemia | hepatotoxicity

X
ylitol is a 5-carbon sugar alcohol. Although often
described as an artificial sweetener this is not the
case, as xylitol occurs naturally in low concentrations
in fruit and vegetables and is a normal intermediary
metabolite in glucose metabolism. It was originally made by
extracting a precursor from hardwoods but is now produced from
other, cheaper sources, and is most commonly encountered as a
sweetener in a wide variety of foods.
Sources of xylitol
Xylitol is found in numerous products (Box  1). It is used as a
sweetener and is frequently found in sugar-free chewing gums
(Figure 1) and confectionary, where it protects against tooth decay.
It is also present in some toothpastes. It has multiple effects on
oral hygiene, including the inability of oral bacteria to use it as
an energy source (Nayak et al, 2014). Although xylitol is found in
some drinking water additives for animals at low concentrations
to decrease dental plaque and calculus formation by inhibiting
growth of oral bacteria (Clarke, 2006), this is generally not a source
of poisoning in pets (Murphy and Coleman, 2012). Xylitol is also
found as an excipient in some human and veterinary medicines,
particularly in chewable medicines including supplements,
nicotine gums and lozenges for smoking cessation. The ingredients
of any medicine or product labelled as ‘sugar-free’ should also
be checked, as it may contain xylitol. Other sweeteners such as
sucralose, maltitol, sorbitol, saccharin, aspartame and acesulfame
K may also be present in sugar-free products; these sweeteners do
not have the same effect as xylitol and generally only cause mild
gastrointestinal upset if eaten in excess.
baking, so home-baked cakes (Figure 2b), muffins and biscuits are
also potential sources of xylitol exposure.
It is important to note that on some food packaging xylitol may
only be listed by its food additive code, E967.
In America, xylitol has also been used to lace baits for the control
of predators such as wolves and coyotes (Talcott et al, 2015).
Owners are often unaware of the risk of xylitol poisoning, and
xylitol-containing products may be readily accessible to dogs, e.g.
left in handbags, baked goods left out to cool, etc.
Species differences in effects of xylitol
There are important species differences in the effect of xylitol but the
reasons for these differences are unknown.
Cats
Xylitol-induced hypoglycaemia and liver damage is not seen in
cats. In an experimental study, oral doses of 100, 500 or 1000 mg/kg
given to cats did not cause significant changes in haematological or
biochemical parameters up to 72 hours after ingestion. All the cats
remained well, with only transient salivation reported (Jerzsele et
al, 2018).
Rabbits and rodents
Xylitol is also well tolerated in rabbits and rodents. Acute oral
administration does not cause hypoglycaemia or severe liver damage
in rabbits (Wang et al, 1973) or rodents (Truhaut et al, 1977; Ellwood
et al, 1999). The oral LD50 of xylitol in rabbits is >2 g/kg (Pool
and Hane, 1970) and in mice is 21–25.7 g/kg (Kieckebuch et
al, 1961; Salminen, 1982). Xylitol given to rats at a dose of
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Xylitol lowers the calories in products, and the glycaemic
index, and is found in some ice creams and peanut butters
(usually speciality brands). Xylitol is not broken down, denatured
or modified in baking or cooking processes and is available as a
granulated powder (Figure 2a) for use as a sugar replacement in
1.25–10 g/kg/day for 14 days did not cause hepatotoxicity or any
histopathological changes (Truhaut et al, 1977).
Birds
There are no studies on the effects of xylitol in birds, but they appear

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TOXICOLOGY
to be particularly susceptible. In the only case reported in the
literature, wild Cape sugarbirds (Promerops cafer) in South Africa
became unwell after drinking a homemade xylitol nectar solution
from a bird feeder. Within 15–30 minutes the birds developed ataxia
and lethargy, and some were seen to fall from their perches. Within
Figure 1. Chewing gum is a common source of xylitol in dogs.
Figure 2. Xylitol is available as granulated powered for baking (a, b) and may be
found in home-baked cakes, cookies, muffins or cupcakes (b).
184
45 minutes of feeding, 29 dead birds were found near the feeder.
Approximately 15 other birds showed mild to moderate signs
and recovered. These birds flew away and it is not known if they
survived. Although no blood glucose measurements were made,
post-mortem findings supported the diagnosis of death from acute
hypoglycaemia. At post-mortem examination there was cardiac
and pulmonary congestion, severe hepatic necrosis and pancreatic
necrosis, with acute tissue congestion on histological examination
(Gardner et al, 2017).
Toxic effects in dogs
In dogs, xylitol has two main effects: hypoglycaemia and
liver damage.
Hypoglycaemia
Xylitol is a potent stimulator of insulin release in dogs, and this causes
a decrease in blood glucose. Experimental studies have shown that
oral or intravenous (IV) administration of xylitol can cause a dose-
dependent and rapid increase in insulin concentrations, resulting
in a decrease in blood glucose concentrations in dogs (Hirata et al,
1966; Kuzuya and Kanazawa, 1969; Kuzuya et al, 1969; Asano et al,
1977). In dogs, xylitol is more effective than glucose in stimulating
insulin release (Asano et al, 1977), particularly at high doses
(Kuzuya et al, 1969) but is thought to act on the pancreas in a similar
way to glucose. It is thought that xylitol is metabolised in the liver
to metabolites that interfere with the normal pentose phosphate
pathways affecting the synthesis and release of insulin (Kuzuya et al,
1969). In addition, dogs appear to absorb xylitol at a faster rate and
more extensively than humans (Kuzuya et al, 1969).
In an experimental study in dogs, the insulin concentration
increased from 20 minutes after oral administration of xylitol (1 or
4 g/kg) and the blood glucose concentration started to fall from 30
minutes. There were also falls in blood potassium and phosphorous
concentrations from 30–60 minutes and an increase in liver enzymes,
which was dose-related and noted by 4 hours (Xia et al, 2009).
The electrolyte changes seen with xylitol toxicosis are due to
the effect of insulin shifting magnesium and potassium into cells
resulting in low blood concentrations.
Based on first principles, xylitol is likely to have a minimal effect
on the blood glucose in diabetic dogs, since diabetes is usually due to
insulin deficiency or interference with the action of insulin.
Liver failure
The mechanism of xylitol-induced liver damage is unknown. It
may be due to prolonged adenosine triphosphate (ATP) depletion
from xylitol metabolism resulting in cellular necrosis, or production
of reactive oxygen species that damage cell membranes and
macromolecules (Dunayer and Gwaltney-Brant, 2006).
Toxic dose
A dose of 0.05 g/kg (50 mg/kg) xylitol can cause hypoglycaemia in
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dogs (Box 2). A dose of more than 0.5 g/kg (500 mg/kg) can cause
liver failure (Dunayer, 2006), although this may be an idiosyncratic
reaction rather that a dose-related effect (Dunayer, 2006) since not
all dogs that ingest more than 0.5 g/kg develop liver failure (Piscitelli
et al, 2010).
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Dogs have survived xylitol doses of up to 45  g/kg with
treatment (Dunayer 2004; Dunayer and Gwaltney-Brant, 2006;
Todd and Powell, 2007; Fawcett et al, 2010; Schmid and Hovda,
2016, Veterinary Poisons Information Service case data; see Case
Reports, Boxes 4 and 5).
The xylitol content of many products is not provided on the
packaging; for medicines this is because it is an excipient and not an
active ingredient. Xylitol is present in some veterinary medicines
but xylitol poisoning from these sources does not appear to have
been reported. A poisons information centre may be able to help
or give guidance on the possible maximum concentration in the
type of products involved, as poisons information centres actively
seek this information from manufacturers. The amount of xylitol
in sugar-free gums varies enormously (1–90%).
In many cases, however, it may not be possible to determine
how much product has been ingested: for example the dog may
have eaten or chewed the packaging, or the owner may not recall
how much product was left in the container or packet.
Clinical effects
Onset
Xylitol-induced hypoglycaemia can occur rapidly, sometimes
within an hour (Dunayer, 2006) but it may be several hours after
ingestion of chewing gum (up to 12 hours in some cases). This
delay in hypoglycaemia with xylitol-containing chewing gums is
likely due to the formulation and because dogs generally do not
chew the gum but tend to swallow it whole (Murphy and Coleman,
2012). In some cases, particularly those with subsequent liver
damage, hypoglycaemia can even be delayed 24–48 hours (Dunayer
and Gwaltney-Brant, 2006), making diagnosis in the absence of
observed ingestion difficult. Liver failure can occur in the absence
of hypoglycaemia and signs occur 2–72 hours after ingestion
(Dunayer and Gwaltney-Brant, 2006; Murphy and Coleman, 2012;
Schmid and Hovda, 2016), but liver enzymes generally start to rise
within 4–24 hours (Xia et al, 2009; Murphy and Coleman, 2012).
Hypoglycaemia
The fall in blood glucose concentration in dogs after ingestion
of xylitol is due to the release of insulin. Clinical features of
hypoglycaemia include tachycardia, ataxia, lethargy, weakness,
coma, convulsions, hemiparesis, hypokalaemia, hypomagnesaemia
and hypophosphataemia. Vomiting is common after ingestion of
xylitol (Dunayer, 2006).
In animals with severe hypoglycaemia there may be metabolic
acidosis, status epilepticus, cerebral oedema, hypotension,
ventricular tachycardia and cardiovascular collapse. Permanent
neurological sequelae may occur, usually as a result of delayed
recognition leading to prolonged hypoglycaemia.
Hyperglycaemia may sometimes occur with xylitol ingestion and
is a result of the Somogyi phenomenon (rebound hyperglycaemia
or post-hypoglycaemic hyperglycaemia) that can occur
with insulin overdose.
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Liver failure
There are numerous reports of xylitol-induced liver failure in
dogs (Foss, 2004; Dunayer and Gwaltney-Brant, 2006; Todd and
Powell, 2007; Schmid and Hovda, 2016). There is raised alanine
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TOXICOLOGY
aminotransferase (ALT) and aspartate aminotransferase (AST), with a
less marked rise in alkaline phosphatase (ALP), and elevated bilirubin.
More rarely there is prolonged clotting time, thrombocytopenia and
hyperphosphataemia (secondary to liver failure).
Diagnosis
There is no simple test to confirm xylitol poisoning. Diagnosis is
based on a history of exposure, clinical signs and ruling out other
potential causes of hypoglycaemia (see Box 3).
Treatment
Aggressive treatment is recommended in dogs after ingestion of
xylitol. The aims of treatment are to monitor blood glucose and
correct hypoglycaemia, and to support liver function.
Box 1. Sources of xylitol
zzChewing gum — this is the most common source in dogs (DuHadway et
al, 2016).
zzMedicines including prescription and over-the-counter medicines — be
suspicious of any chewable formulations
zzDrinking water additives for oral hygiene
zzDiet bars and drink powders
zzToothpaste
zzPeanut butter
zzIce cream
zzSugar substitute for baking, therefore homemade cakes, biscuits,
muffins, etc.
Box 2. Toxic dose of xylitol in dogs
zz50–100 mg/kg — mild hypoglycaemia (Murphy and Coleman, 2012).
zz100–500 mg/kg — hypoglycaemia (Dunayer, 2006).
zz>500 mg/kg — hypoglycaemia and liver failure (Dunayer, 2006).
Box 3. Differential diagnoses for hypoglycaemia
zzInsulin overdose
zzIngestion of oral hypoglycaemia drugs
zzJuvenile hypoglycaemia (toy and miniature breeds)
zzOther drug and toxin-associated causes (e.g. beta-blockers, ACE inhibitor
drugs, ethylene glycol toxicity)
zzExtrapancreatic neoplasia
zzIslet cell hyperplasia
zzHypopituitarism
zzPancreatic beta-cell tumour (insulinoma)
zzGlycogen storage disease
zzSepsis
zzHypothyroidism
zzHypoadrenocorticism
zzExtreme exertion
zzGrowth hormone deficiency
zzHepatic failure
zzHunting dog hypoglycaemia (a poorly described disease entity)
(Thrall et al, 2004; Thomas and Boag, 2008)
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TOXICOLOGY
Gut decontamination
If the dog has not vomited already, ingestion occurred within
1  hour and the dog is asymptomatic, emesis can be induced.
Emesis is generally not recommended in dogs with clinical signs
of hypoglycaemia, due to the risk of aspiration if the dog has
hypoglycaemic-induced central nervous system (CNS) depression.
Xylitol is also rapidly absorbed, so delayed emesis is unlikely to
be useful. The binding of xylitol to activated charcoal is low, but
activated charcoal may still be beneficial if given within 1  hour
of ingestion, particularly if a large dose has been ingested (Cope,
2004). It should not be given if the dog has CNS depression, due to
the risk of aspiration.
Monitoring
Dogs that have ingested a potentially toxic dose of xylitol (Box 2)
should be admitted for monitoring. The following parameters
should be obtained as baseline and monitored: blood glucose
every 1–2 hours for at least 12 hours (Dunayer, 2006), potassium
and phosphorus concentrations every 4–6  hours and corrected
if necessary (Piscitelli et al, 2010), total bilirubin, liver enzymes,
Box 4. Case 1
A 11.4 kg Cocker Spaniel raided the bin and ate an entire cake containing
450 g of xylitol, which the owner had found too sweet and thrown away.
The dose of xylitol ingested was 39.5 g/kg. Within 1 hour the dog began
vomiting and then collapsed. On admission he had severe hypoglycaemia.
He was unstable for the first 12 hours and the glucose had to be monitored
every 5–10 minutes using a continuous monitor. He was treated with glucose
boluses intravenously but then required a continuous rate infusion with the
occasional bolus. The liver enzymes were elevated when tested at 4 hours
and he was started on S-adenosyl-L-methionine (SAMe). He was discharged
at 72 hours. When retested on day 3, the liver enzyme levels were improving
and had halved from their initial elevated values (VPIS case report 230385).
Box 5. Case 2
An 18-month-old, 15.8 kg Staffordshire Bull Terrier cross presented with
a 48-hour history of vomiting after she had eaten homemade muffins
containing xylitol. The estimated dose ingested was 10.5 g/kg. She
had vomited 3 hours after ingestion and the owners had noticed she
was very thirsty. On examination she was quiet, with marked jaundice.
She had increased urea, haematocrit, alkaline phosphatase (ALP) and
hypoglycaemia. The alanine aminotransferase (ALT) was too high to
measure in-house, despite serial dilution of samples. She received
intravenous (IV) glucose, IV fluids and maropitant. Financial constraints
meant she could not be transferred to a critical care facility. The next
day she had marked depression, with haematomas and bruising around
venepuncture site. She was normoglycemic with an alanine transferase
of 26 050 IU/L and was started on acetylcysteine, S-adenosyl-L-methionine
(SAMe), vitamin E, vitamin K, ascorbic acid, omeprazole and ampicillin.
She was brighter by day 3 but still jaundiced, with thrombocytopenia. She
continued to improve, hepatic enzyme activities began to decline from day
5, and she was discharged. On examination 5 days later she was well, with
normal liver enzymes (Fawcett et al, 2010).
186
platelets, erythrocyte count and clotting parameters every 24 hours
for at least 72 hours (Dunayer, 2006). As regular sampling is required
in these patients, it may be beneficial to use a sampling line.
It is also important to monitor mentation and cardiovascular
status, as these can change in animals with low blood glucose
concentrations.
Initial management
In dogs without clinical features of hypoglycaemia, frequent small
meals or oral sugar may be given for 8–12 hours (Dunayer, 2004).
An antiemetic may be required to control vomiting.
Dogs that have ingested more than >0.5 g/kg (500 mg/kg)
should be started on IV dextrose therapy, with monitoring of the
blood glucose ever 2-4 hours (Dunayer, 2006). Dextrose therapy
can be stopped after 24 hours if the blood glucose remains normal
(Piscitelli et al, 2010).
Dogs that have ingested a potentially hepatotoxic dose
should also be given liver protectants, although their efficacy in
xylitol-induced liver damage has not been evaluated. S-adenosyl-
L-methionine (SAMe, 20 mg/kg orally), silymarin (50 mg/kg
orally) or acetylcysteine can be considered (Piscitelli et al, 2010).
For acetylcysteine the paracetamol treatment regimen can be
used (140 mg/kg oral or IV, then 70 mg/kg orally every 6 hours for
36 hours or more).
Supportive fluid therapy may be required, particularly if the dog
is not eating or drinking or requires rehydration following vomiting.
Electrolyte supplementation may be required, and this can be given
orally or IV, depending on the clinical condition of the dog and
severity of biochemical changes.
Management of hypoglycaemia
If feeding is ineffective or the dog is symptomatic, then
hypoglycaemia should be corrected with an IV bolus dose of 1 ml/
kg of 50% dextrose (0.5 g/kg) diluted 1:2 in crystalloid solution
(Piscitelli et al, 2010). A 2.5% or 5% dextrose constant rate infusion
may be required in severe cases to maintain blood glucose.
If possible, the electrocardiogram should be monitored,
because hypokalaemia can cause arrhythmias.
Management of liver damage
The management of dogs in liver failure is supportive. Plasma
transfusions and vitamin K1 may be required in animals with
coagulopathy.
Prognosis
The prognosis for uncomplicated xylitol-induced hypoglycaemia
that is managed promptly is good. Mild increases in liver enzymes
usually resolve within a few days if supportive care is provided. The
prognosis in dogs with repeated episodes of severe hypoglycaemia
or severe elevation of liver enzymes with clotting abnormalities is
guarded to poor. Hyperphosphataemia, which occurs secondary to
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liver failure, is also an indicator of poor prognosis (Dunayer, 2006;
Murphy and Coleman, 2012). In one review of cases, four of the
five dogs that died or were euthanised had hyperphosphataemia;
a phosphate concentration was not available for the fifth dog
(Dunayer, 2006).
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Severe poisoning can be survived with aggressive treatment (see
case reports).
Conclusions
Xylitol can cause hypoglycaemia in dogs, followed by liver failure
in some cases, although the hepatotoxic effect is not dose-related
and the mechanism is unknown. Management includes gut
decontamination (depending on the time since ingestion),
followed by monitoring of blood sugar and liver parameters. The
blood glucose should be corrected with dextrose, if required, and
liver protectants should be considered in dogs that have ingested
>0.5 g/kg. Prognosis is good in dogs with corrected hypoglycaemia
and no complications of liver failure.
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TOXICOLOGY
KEY POINTS
zzXylitol may be found in a variety of foods and medicines.
Check the ingredients of any medicine labelled ‘chewable’
or ‘sugar-free’.
zzXylitol can cause hypoglycaemia and liver failure.
zzDepending on the xylitol-containing product involved,
hypoglycaemia may be rapid in onset or occur several
hours after ingestion.
zzThe risk of liver failure is not dose-related.
zzXylitol does not cause hypoglycaemia or liver failure in
cats, rabbits or rodents but poisoning has been reported
in birds.
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Murphy LA, Coleman AE. Xylitol toxicosis in dogs. Vet Clin North Am Small Anim
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Nayak PA, Nayak UA, Khandelwal V. The effect of xylitol on dental caries and oral
flora. Clin Cosmet Investig Dent. 2014;6:89–94. doi:10.2147/CCIDE.S55761
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