Chocolate Poisoning-Dog
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Introduction
Toxicity is due to the presence of methylxanthines such as theobromine and caffeine in chocolate.[1]. The concentration of methylxanthines in chocolate differs between products. For example the average methylxanthine content of milk chocolate is 2mg/g, while that of baking chocolate is 16mg/g. [1].
Signalment
Dog that live indoors are more likely to have access to chocolate. Also puppies are at a greater risk of eating food that is not intended for their consumption [1].
Diagnosis
Clinical Signs
Chocolate poisoning results in CNS, gastrointestinal, cardiovascular and urological signs.[1], Cite error: Closing </ref> missing for <ref> tag
- CNS: hyperexcitability, hyperactivity, ataxia initially can evolve into muscle tremors, clonic seizures and hyperthermia.[1], [2]
- Gastrointestinal: diarrhoea, emesis, haematemesis, colic.[1], [2]
- Cardiovascular: arrhythmias,infrequently bradycardia but usually tachycardia.[1], [2]
- 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. The following laboratory tests are possible but not commonly used;
- Detection of methylxanthines in bodily fluids such as plasma, urine and stomach contents [1].
- Blood Glucose: Hypoglycaemia as a consequence of 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
Pathology
The methylxanthines yield their effects through
- Antagonism of Adenosine Receptors:[1] this antagonism results in stimulation of the central nervous system, vasoconstriction and increase in heart rate [1] and also diureses [1]
- Inhibition of Cyclic Nucleotide Phosphodiesterase:[2] 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:Enhanced uptake and decreased sequestration within the cell leads to amplification of intracellular calcium levels in cardiac and skeletal muscle, the net result of which is a positive inotropic effect on these muscles. [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: slow intravenous bolus of 2mg to 6mg per kg of lidocaine. Following this a constant rate infusion of 20ug to 70ug per kg per minute [1]
- Bradycardia: Atropine at a dose of 0.01mg to 0.02mg per kg [1]
- Inital stabilisation of Cardiorespiratory System:
- Once stable treat as outlined below
- Of dogs with a known history of recent chocolate ingestion but who have not yet developed clinical signs
Prognosis
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 BSAVA Manual of Canine and Feline Emergency and Critical CareChapter 19, Second Edition,2007 Cite error: Invalid
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<ref>tag; name "multiple" defined multiple times with different content Cite error: Invalid<ref>tag; name "multiple" defined multiple times with different content Cite error: Invalid<ref>tag; name "multiple" defined multiple times with different content - ↑ 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