Chocolate Poisoning-Dog
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Introduction
Toxicity is due to the presence of methylxanthines such as theobromine and caffeine in chocolate [1]. Concentrations ranging from of 100-250mg/kg of theobromine and 110-200mg/kg of caffeine have been reported to cause fatalities [1]. The consumption of more than 20mg/kg of total methylxanthines, the dose at which mild signs such as vomiting, diarrhoea and polyuria are induced [1], is considered the cut-off point in deciding whether or not to treat [1]. The concentration of methylxanthines differs between products [1] and therefore the number of grammes required to reach this threshold vary according to the product; in a 10kg dog 5000g of white chocolate provides the equivalent 20mg/kg dose of methylxanthines that 12-40g of plain chocolate, 83-117g of milk chocolate or 7-25g of cocoa powder does [1] Methylxanthines are also present in beverages and foods other than chocolates [1].
Signalment
Dog that live indoors are more likely to have access to chocolate. Also puppies and dogs that scavenge are at a greater risk of eating food that is not intended for their consumption. Small breeds of dogs may reach the toxic level of methylxanthine concentration per body weight more easily [1].
Diagnosis
Clinical Signs
Chocolate poisoning results in CNS, gastrointestinal, cardiovascular, respiratory and urological signs.[1], [1] which are evident soon after ingestion of a toxic amount of chocolate [1].
- CNS: hyperactivity, behavioural changes, ataxia, muscle tremors, clonic seizures and hyperthermia [1], [1], [1].
- Gastrointestinal: diarrhoea, emesis, haematemesis [1], [2]
- Cardiovascular: arrhythmias,tachycardia, bradycardia sometimes, hypotension [1], [1].
- Respiratory: tachypnoea [1].
- Urological: polydypsia and polyuria may also be present [1].
Laboratory Tests
Diagnosis is usually on the basis of clinical signs and a known history of chocolate ingestion [1]. The following laboratory tests are possible but not commonly used;
- Assays for detection of methylxanthines in bodily fluids such as plasma, urine and stomach contents [1].
- Blood Glucose: Hypoglycaemia as a sequela to hyperactivity. not seen consistently with chocolate poisoning [1].
- Urinalysis: Proteinuria, low specific gravity; not seen consistently with chocolate poisoning [1].
Other
- ECG: rate and rhythm abnormalities [1].
Pathology
Following absorption from the gastrointestinal tract caffeine and theobromine are metabolised in the liver [1]. Caffeine has a half life of 4.5 hours in dogs while theobromine has a half life of 17.5 hours [1]. In humans the half life of theobromine ranges from 6 to 10 hours, significantly shorter than that in dogs which may explain the susceptibility of dogs to chocolate poisoning REF. Methylxanthines have the following modes of action.
- Antagonism of Adenosine Receptors:[1] this antagonism results in stimulation of the central nervous system and an increase in heart rate [1] and also diureses [1]
- Inhibition of Cyclic Nucleotide Phosphodiesterase:[1] consequently there is an increase in cyclic AMP, which in turn leads to greater catecholamine release and their effects [1].
- Modulation of Intracellular Calcium Concentrations: [1].
Ventricular fibrillation, and other cardiac dysrhythmias are most frequently the ultimate cause of death.[3], [4].
Treatment
Of dogs presenting with clinical signs
- Inital stabilisation of Cardiorespiratory System:
- Tachycardia: beta-blockers, eg orally administered metoprolol at a dose of 0.5mg to 1mg per kg every 8 hours [1].
- Premature Ventricluar Contractions: lidocaine; iv bolus of 2mg to 6mg per kg administered slowly, after which a constant rate infusion of 20ug to 70ug per kg per minute should be given [1].
- Bradycardia: Atropine at a dose of 0.01mg to 0.02mg per kg [1].
- Treatment of seizures and hyperactivity
- Correction of acid/base and electrolyte inbalances [1],
- Insertion of urinary catheter
- Helps prevent further absorption of theobromine and caffeine across bladder wall [1].
Of dogs with a known history of recent chocolate ingestion but who have not yet developed clinical signs
- Administration of apomorphine (0.03mg/kg IV) or hydrogen peroxide (1-5 ml/kg PO) ref 5 min vet consult in order to induce emesis and/or of activated charcoal in order to minimise further absorption of methylxanthines re 5 min vet consult
Prognosis
If treated correctly and early enough ref 5min consult the prognosis is good and a complete recovery can be expected [1]. For animals presenting with seizures and arrhythmias the prognosis is more cautious.
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 1.21 1.22 1.23 1.24 1.25 1.26 1.27 1.28 1.29 1.30 1.31 1.32 1.33 1.34 1.35 1.36 1.37 1.38 1.39 1.40 King, LG, Boag, A (2007) BSAVA Manual of Canine and Feline Emergency and Critical Care(2nd Edition) BSAVA Cite error: Invalid
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- ↑ Carson TL (2006) Methylxanthines. In: Small Animal Toxicology, ed. ME Peterson, PA Talcott, pp.845-852. Elsevier Saunders, St. Louis in BSAVA Manual of Canine and Feline Emergency Care Chapter 19, Second Edition,2007
- ↑ Holmgren P, Norden-Petterson L and Ahlner J (2004)Caffeine fatalaties: four case reports. Forensic Science International 139, 71-73 BSAVA Manual of Canine and Feline Emergency Care Second Edition,2007