Difference between revisions of "Chocolate Poisoning-Dog"
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===Pathology=== | ===Pathology=== | ||
− | Following absorption from the gastrointestinal tract caffeine and theobromine are metabolised in the liver <ref name="multiples"> '''http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/211104.htm''', accessed on 04.10.2010 </ref>. Caffeine has a half life of 4.5 hours in dogs while theobromine has a half life of 17.5 hours <ref name="multiples"> '''http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/211104.htm''', accessed on 04.10.2010 </ref>. 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 | + | Following absorption from the gastrointestinal tract caffeine and theobromine are metabolised in the liver <ref name="multiples"> '''http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/211104.htm''', accessed on 04.10.2010 </ref>. Caffeine has a half life of 4.5 hours in dogs while theobromine has a half life of 17.5 hours <ref name="multiples"> '''http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/211104.htm''', accessed on 04.10.2010 </ref>. 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:'''<ref name="multiples"> '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' Second Edition, 2007</ref> this antagonism results in stimulation of the central nervous system | + | *'''Antagonism of Adenosine Receptors:'''<ref name="multiples"> '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' Second Edition, 2007</ref> this antagonism results in stimulation of the central nervous system and an increase in heart rate <ref name="multiples">Tilley Smith'''The 5-Minute Veterinary Consult Canine and Feline''' (Third Edition), ''Lippincott, Williams and Wilkins'' </ref> and also diureses <ref name="multiples"> '''http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/211104.htm''', accessed on 04.10.2010 </ref> |
*'''Inhibition of Cyclic Nucleotide Phosphodiesterase:'''<ref name="multiple"> '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' Second Edition,2007</ref> consequently there is an increase in cyclic AMP, which in turn leads to greater catecholamine release and their effects <ref name="multiples">Tilley Smith'''The 5-Minute Veterinary Consult Canine and Feline''' (Third Edition), ''Lippincott, Williams and Wilkins'' </ref>. | *'''Inhibition of Cyclic Nucleotide Phosphodiesterase:'''<ref name="multiple"> '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' Second Edition,2007</ref> consequently there is an increase in cyclic AMP, which in turn leads to greater catecholamine release and their effects <ref name="multiples">Tilley Smith'''The 5-Minute Veterinary Consult Canine and Feline''' (Third Edition), ''Lippincott, Williams and Wilkins'' </ref>. | ||
− | *'''Modulation of Intracellular Calcium Concentrations:''' | + | *'''Modulation of Intracellular Calcium Concentrations:''' <ref name=multiples> '''http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/211104.htm''', accessed on 04.10.2010 </ref>. |
Ventricular fibrillation, and other cardiac dysrhythmias are most frequently the ultimate cause of death.<ref> 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 </ref>, <ref> 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 </ref> | Ventricular fibrillation, and other cardiac dysrhythmias are most frequently the ultimate cause of death.<ref> 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 </ref>, <ref> 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 </ref> | ||
Revision as of 23:19, 9 January 2011
This article is still under construction. |
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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], [2] 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], [2], [1]
- Gastrointestinal: diarrhoea, emesis, haematemesis [1], [2]
- Cardiovascular: arrhythmias,tachycardia, bradycardia sometimes, hypotension [1], [2]
- 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 [3]. 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:[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: [1].
Ventricular fibrillation, and other cardiac dysrhythmias are most frequently the ultimate cause of death.[4], [5]
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
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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