Chocolate Toxicity (Canine)

Key Points

Clinical signs often occur within 2–4 hours of ingestion but can sometimes occur after 6–12 hours
Chocolate may also contain other toxic substances – raisins, nuts or xylitol
Initial signs include vomiting, diarrhoea, restlessness, PUPD but may progress to tremors, seizures, tachycardia and arrhythmia
Indications for treatment depends on amounts and type of chocolate ingested
White chocolate: No treatment required
Milk chocolate: Treat for ≥ 14 g/kg
Dark chocolate: Treat for ≥ 3.5 g/kg
Cocoa powder: Treat for ≥ 0.5 g/kg
Drinking chocolate: Treat for ≥ 40 g/kg
Treatment involves i/v fluids, emesis, charcoal, tremor control, seizure control and treatment of arrhythmia
Prognosis is excellent with supportive care but more guarded in dogs with seizures or arrhythmia

Definition

Chocolate poisoning refers to an overdosage of methylxanthines (primarily theobromine) from ingestion of chocolate

Chocolate poisoning refers to an overdosage of methylxanthines (primarily theobromine) from ingestion of chocolate

Prevalence

Common intoxication
In the VPIS top 10 poison enquiries 2019 and 10% of APCC’s cases
[30][31][34]

Common intoxication in dogs³⁴
In the VPIS top 10 most common poison enquiries 2019³⁰
10% of APCC cases 2018³¹

Causes

Effects are due to the methylxanthine content (theobromine and caffeine)
Methylxanthine intoxication leads to CNS, cardiac and respiratory stimulation
Average theobromine content depends on the product
Milk chocolate – 1.4 mg/g
Dark chocolate – 5.3 mg/g
Cocoa powder – 26 mg/g
or can be calculated based on % cocoa
e.g. 16 × % cocoa = theobromine in mg/g
e.g. 80% cocoa is 16 × 0.8 = 12.8 mg/g
Toxic doses
20 mg/kg theobromine (mild) vomiting / diarrhoea / polydipsia
40–50 mg/kg theobromine (severe) cardiotoxic effects
60 mg/kg theobromine (seizures)
CAUTION Chocolate may also contain other toxic substances such as raisins, nuts or xylitol
[4][5][6][7][8][9][15][18][21][24][28][46]

Effects

Effects are due to the methylxanthine content (theobromine and caffeine)^15,18,46
In most chocolate products, theobromine is the predominant toxic with caffeine found in much smaller amounts¹⁰
Theobromine is absorbed in the GI tract, metabolised by the liver, undergoes enterohepatic recirculation, then is excreted in the urine^21,24,46

Actions of methylxanthines

Competitive inhibition of adenosine receptors leads to CNS stimulation, tachycardia and diuresis^6,10,46
Increased cellular calcium entry and inhibits calcium reuptake which causes increased contractility of skeletal and cardiac muscle^{6,10,18,21,24,46}
Inhibition of phosphodiesterase causing an increase in cAMP^6,10,⁴⁶
Methylxanthines may also exert their effects by competing for benzodiazepine receptors within the CNS and by increasing circulating levels of catecholamines^24,46

Methylxanthine intoxication leads to CNS, cardiac and respiratory stimulation⁶

Toxic doses ^4,5,6,15

20 mg/kg theobromine – mild (vomiting / diarrhoea / polydipsia)
40–50 mg/kg theobromine – severe (cardiotoxic effects)
60 mg/kg theobromine (seizures)
Theobromine is the most abundant methylxanthine in chocolate⁴
Theobromine LD₅₀has a reported range of 100–500 mg/kg (dogs)^15,24
Fatal cases have occurred after ingestion of 80 – 300 mg/kg²⁸
t _1/2 Theobromine is 17.5 hours in dogs so clinical signs may persist for 72 hrs in severely affected cases^6,7,8,21,24
CAUTION Chocolate may also contain other toxic substances such as raisins, nuts or xylitol⁶
Methylxanthines can cross the placenta and pass into milk¹⁵

Type of chocolate	Methylxanthine content/g^9,24	Theobromine content/g⁴	Amount of product equivalent to 20mg theobromine⁴	Treatment dose⁵
Milk chocolate	2.3 mg/g	median 1.4 mg/g	14.3 g	> 14 g/kg
Dark chocolate	5.7 mg/g	median 5.3 mg/g	3.8 g	> 3.5 g/kg
Cocoa powder	28.5 mg/g	median 26 mg/g	0.78g	> 0.5 g/kg
White chocolate	Insignificant amount	Insignificant amount	N/A	NO treatment

Calculation based on labelled % cocoa
16 x % cocoa = Theobromine in mg/g
e.g. 80% cocoa
16 x 0.8 = 12.8 mg/g⁹

Risk Factors

Small dogs
Indiscriminate eating habits
Easter and Christmas
Potential risk in young dogs < 4 years
CAUTION May be a genetic component in some breeds due to a reduced metabolism
[4][17][20][24][29][33][46]

Small dogs^17,20,24
Indiscriminate eating habits²⁴
Christmas and Easter^33,46
Potential risk in young dogs < 4 years³³
CAUTION There may be a genetic component to individual susceptibility to chocolate toxicity^4,6
Breeds with CYP1A2 1117C> T polymorphism may be more at risk of toxicity due to a reduced metabolism⁴
This polymorphism has been reported in Beagle, Australian Shepherd, Bearded Collie, Berger Blanc Suisse, Border Collie, Collie, Dalmatian, Deerhound, German Shepherd, Greyhound, Irish Wolfhound, Jack Russell Terrier, Shetland Sheepdog and Whippet²⁹

Clinical Features

Clinical signs often occur within 2–4 hours of ingestion but can sometimes occur after 6–12 hours
Clinical signs depend on dose ingested
Initial signs include vomiting, diarrhoea, restlessness, PUPD
Progression to tremors, seizures, tachycardia, arrhythmia, hyperthermia, acute kidney injury and coma
Death usually occurs due to hyperthermia, respiratory failure cardiac arrhythmia
In susceptible animals, the high fat content of some chocolates may trigger pancreatitis
[1][6][9][10][15][17][18][19][20][21][22][23][24][25][26][46]

Clinical signs often occur within 2–4 hours of ingestion but can sometimes occur after 6–12 hours^6,15,18
If chocolates are wrapped, the effects of the toxin may be delayed by several hours to days
Initial signs
Vomiting, diarrhoea, abdominal discomfort, restlessness, polyuria, polydipsia^{1,6,15,17,19,20,21,24,26,33,46}
Progression to
Tremors, hyperactivity, agitation, rigidity, seizures, tachycardia, arrhythmias, tachypnoea, hypertension, hyperthermia, acute kidney injury and coma^{15,17,19,21,24,25,26,33,46}
Less common signs are bradycardia and hypotension^1,6,15
Death can occur^22,23
Usually due to hyperthermia, respiratory failure, cardiac arrhythmias^{9,10,15,21,24}
Has been reported to occur as quickly as 1 hour, or > 12 hours after ingestion^6,22,25,32
Pancreatitis
In susceptible animals, the high fat content of some chocolates may trigger pancreatitis^6,10,15

Investigations

1st line diagnostics	Haematology Biochemistry Urinalysis ECG Blood pressure
Haematology	PCV/TP May see evidence of dehydration [17]
Biochemistry	Hyperglycaemia or hypoglycaemia Hypokalaemia may be found late in the course of the toxicosis Monitor for hypernatraemia if using charcoal Canine specific pancreatic lipase to rule out concurrent pancreatitis Hyperlactataemia Raised ALT/AST [1][6][9][10][15][35][36][39][40][46]
Urinalysis	Low SG due to diuretic effects of methylxanthines
ECG	Sinus tachycardia, sinus bradycardia or arrhythmia Typically VPCs [6][10][19][20][46]
Blood pressure	Hypertension or (less commonly) hypotension [10]

Haematology	PCV/TP May see evidence of dehydration¹⁷
Biochemistry	Glucose Findings include hyperglycaemia⁴⁶ or hypoglycaemia¹ Electrolytes Hypokalaemia may be found late in the course of the toxicosis^1,9,10,15,46 This is thought to be due to GI loss, respiratory alkalosis from panting and epinephrine-related translocation of potassium into the cells⁴⁶ Monitor for hypernatraemia if using activated charcoal, avoid sorbitol-containing products^36,39,40 Canine specific pancreatic lipase to rule out concurrent pancreatitis^6,10,15 Hyperlactateamia⁴⁶ Raised ALT/AST which is thought to be caused by muscle tremors and spasms or liver hypoperfusion due to severe arrhythmias⁴⁶
Urinalysis	Low SG due to diuretic effects of methylxanthines
ECG	Sinus tachycardia, sinus bradycardia or arrhythmia (classically, premature ventricular contractions)^{6,10,19,20,46}
Blood pressure	Hypertension or (less commonly) hypotension¹⁰

Diagnosis

History of exposure and clinical signs

History of exposure and clinical signs

Differential Diagnosis

Differentials for tremors, twitching and seizures

Drugs / other toxins, e.g. blue / green algae, bromethalin, illicit drugs, nicotine, caffeine
Metabolic, e.g. hepatic / uraemic encephalopathy, hypoadrenocorticism, hypoglycaemia,
Neurological, e.g. inflammatory CNS disease, epilepsy, tremor syndrome, neoplasm, trauma, intervertebral disc disease
Physiological eg. cold, fear, weakness
[42][44][45]

Differentials for tremors, twitching and seizures^42,44,45

Drugs / other toxins, e.g. blue / green algae, bromethalin, mycotoxins, chlorinated hydrocarbons, zinc phosphide, strychnine, nicotine, caffeine, macadamia nuts, lead, insecticides, e.g. organophosphates / pyrethroid, and illicit drugs such as amphetamines
Metabolic, e.g. hepatic or uraemic encephalopathy, hypoadrenocorticism, hypoglycaemia, hypocalcaemia, hypercalcaemia, ischaemia
Neurological, e.g. inflammatory CNS disease, epilepsy, generalised tremor syndrome (‘white-dog shaker disease’), cerebellar disease, myelin abnormalities, neoplasia, vascular, trauma, intervertebral disc disease
Physiological, e.g. cold, fear, weakness

Treatment

When to treat	White chocolate: no treatment required Milk chocolate: treat for ≥ 14 g/kg Dark chocolate: treat for ≥ 3.5 g/kg Cocoa powder: treat for ≥ 0.5 g/kg Drinking chocolate: treat for ≥ 40 g/kg [5]
Fluid therapy	i/v fluids will both enhance urinary excretion and support the cardiovascular system 4–8 ml/kg but tailor to the individual depending on the degree of dehydration and the presence of comorbidities such as heart disease [6][10][19]
Emesis / gastric lavage	Emesis can be induced up to 6h following exposure Apomorphine CAUTION Common mistake is to induce emesis despite non-toxic dose of theobromine documented CAUTION NOT if hyperactivity / seizure activity, drowsy / unconscious, reduced cough reflex or risk of aspiration pneumonia, e.g. laryngeal paralysis or megaoesophagus If sedated after treatment for seizures consider gastric lavage [4][6][10][12][14][16][21][24][37][38]
Tremor control	Diazepam Methocarbamol [1][3][6][19]
Seizure control	First line Diazepam or midazolam Second line One or more of phenobarbital / levetiracetam Propofol for refractory seizures [1][3][6][13][19][24][41][43]
Activated charcoal	Activated charcoal q4–6h for 24h CAUTION NOT if dehydration or hypovolaemia May need maropitant to control emesis and allow timely administration of charcoal CAUTION Dehydration and osmotic effects of sugar from chocolate and charcoal can predispose to hypernatraemia Reserve for cases ingesting high doses or where response to emesis has been poor [1][3][13][21][24][36][39][40]
Frequent urination or urinary catheterisation	Frequent urination or urinary catheterisation may help prevent further absorption of theobromine across the bladder wall [1][7][8][10][21]
Treatment of arrhythmias	Lidocaine Metoprolol (First choice if available) or propranolol Atropine [1][3][7][10][15][21][24]
Hyperthermia	Generally resolves once the CNS signs are controlled although ancillary cooling may be required CAUTION Do not overcool [15]

When to treat	Revised treatment doses for chocolate 2014⁵ White chocolate: no treatment required Milk chocolate: treat for ≥ 14 g/kg Dark chocolate: treat for ≥ 3.5 g/kg Cocoa powder: treat for ≥ 0.5 g/kg Drinking chocolate: treat for ≥ 40 g/kg
Fluid therapy	i/v crystalloids will both enhance urinary excretion and support the cardiovascular system^6,10,19 Range 4–8 ml/kg but the rate should be tailored to the patient depending on the degree of dehydration and the presence of comorbidities such as heart disease Fluid resuscitation plan
Emesis / gastric lavage	Apomorphine (1 mg/ml)^21,24,37,38 0.1 mg/kg (0.1 ml/kg) s/c¹² Emesis can be induced up to 6h following exposure¹ CAUTION Common mistake is to induce emesis despite a non-toxic dose of theobromine documented¹⁰ CAUTION NOT if hyperactivity / seizure activity, drowsy / unconscious, reduced cough reflex or risk of aspiration pneumonia, e.g. laryngeal paralysis or megaoesophagus^4,6 If sedated after treatment for seizures, consider gastric lavage^14,24 Induction of emesis Gastric lavage for toxin decontamination
Tremor control	Diazepam¹⁹ 2–10 mg/dog p/o q8–12h^1,3,6or Methocarbamol¹⁹ 20–45 mg/kg p/o q8h Maximum dose 330 mg/kg/day^1,3,6
Seizure control	Diazepam^19,24 0.5–1 mg/kg i/v or intrarectally q10min up to three times^1,3,6 CRI 0.5–2 mg/kg/h (avoid overdosing, monitor liver enzymes³) or Midazolam 0.2–0.3 mg/kg i/v, i/m or intranasally q10min up to three times³ Rectal administration is likely of limited efficacy for treating seizures in dogs⁴¹ CRI 0.3 mg/kg/h Then, if seizures persist Phenobarbital 4 mg/kg i/v q4h × four doses to load¹³ Not to exceed 16–20 mg/kg/day, and/or Levetiracetam⁴³ 60 mg/kg i/v, q8h^3,43 Propofol for refractory seizures 1–6 mg/kg slow i/v to effect, followed by CRI at 0.1–0.6 mg/kg/min¹³ Status epilepticus
Activated charcoal	Activated charcoal²¹ 0.5–4 g/kg p/o³ Followed by 1–2 g/kg q4–6h for 24 hours as theobromine undergoes enterohepatic recirculation^1,3,21,24 CAUTION NOT if dehydration or hypovolaemia¹³ CAUTION Dehydration and osmotic effects of sugar from chocolate and charcoal can predispose to hypernatraemia, suggested to reserve for high dose cases where emesis has been poor^36,39,40 Maropitant may be indicated to control vomiting to allow timely administration of charcoal and prevent aspiration¹³ Activated charcoal
Frequent urination or urinary catheterisation	Frequent urination or urinary catheterisation may help prevent further absorption of theobromine across the bladder wall^1,7,8,10,21
Treatment of arrhythmia	Frequent VPCs or clinically significant ventricular tachycardia Lidocaine^21,24 2–8 mg/kg i/v in 2 mg boluses followed by a CRI 0.025–0.1 mg/kg/minute^1,3,7 Severe or prolonged sinus tachycardia causing cardiovascular compromise or supraventricular tachycardia Propranolol^21,24 0.02–0.08 mg/kg i/v slowly over 5 minutes q8h or 0.1–1.5 mg/kg p/o q8h³ or Metoprolol^10,15,21,24 0.2–0.4 mg/kg p/o q12h CAUTION Propranolol has been reported to reduce the renal excretion of methylxanthines so, if available, metoprolol should be used in preference Bradyarrhythmias Atropine²¹ 0.01–0.03 mg/kg i/v Low doses may exacerbate bradycardia^3,10
Hyperthermia	Hyperthermia secondary to excessive muscle activity generally resolves once the CNS signs are controlled although ancillary cooling may be required¹⁵ CAUTION Aggressive attempts to treat hyperthermia (e.g. cold-water enemas or baths) may lead to hypothermia¹⁵

Complications

Aspiration pneumonia
Cardiovascular collapse
Hyperthermia
Case report of secondary non-cardiogenic pulmonary oedema in a puppy
Death
[1][6][20][32][46]

Aspiration pneumonia¹
Cardiovascular collapse⁶
Hyperthermia⁶
Case report of secondary non-cardiogenic pulmonary oedema in a puppy²⁰
Death^32,46

Prognosis

Most patients with appropriate and aggressive treatment will make a full recovery
Mortality rate reported to be < 3% with appropriate decontamination and supportive therapy
Fatal cases have reportedly occurred in dogs after ingestion of 64–300 mg/kg
Prognosis is more guarded in dogs with seizures or arrhythmia
Median hospitalisation stay is 2 days (range 1-4 days)
Can take 3 days to 1 week for full recovery
[1][10][18][20][26][27][33][46]

Reported prognosis

Excellent with supportive care^1,33
Mortality rate reported to be < 3% with appropriate decontamination and supportive therapy⁴⁶
Most patients with appropriate and aggressive treatment will make a full recovery¹⁰
Rarely fatal (VPIS stats) 5/1000
Fatal cases have been reported in dogs after ingestion of 80–300 mg/kg (European Food Safety Authority 2008) and one dog is also reported to have died despite therapy after presenting 12 hrs after ingestion of 64 mg/kg theobromine⁴⁶
Prognosis is more guarded in dogs with seizures or arrhythmias⁶
Median hospitalisation stay is 2 days (range 1-4 days)⁴⁶
Can take 3 days to 1 week for full recovery^18,20,26,27

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Abstract

How this topic was developed

Primary search terms

title:(chocolate) OR title:(theobromine) AND title:((dog or dogs or canine or canines)OR (cat or cats or feline or feline)) AND yr:[1989 TO 2020]

Contributors

Writers

Zoë Coker BSc (Hons) CertGP (EM&S) BVM&S MRCVS

Specialist reviewers

Sophie Adamantos BVSc CertVA DACVECC DipECVECC MRCVS FHEA
Yvonne McGrotty BVMS CertSAM DipECVIM-CA MRCVS

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