Difference between revisions of "Chocolate Poisoning-Dog"
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==Introduction== | ==Introduction== | ||
− | Toxicity is due to the presence of methylxanthines such as theobromine and caffeine in chocolate | + | Toxicity is due to the presence of methylxanthines such as theobromine and caffeine in chocolate.<ref name="multiple"> '''BSAVA Manual of Canine and Feline Emergency and Critical Care'''Second Edition,2007 </ref> |
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==Signalment== | ==Signalment== | ||
− | Dog that live indoors are more likely to have access to chocolate. | + | Dog that live indoors are more likely to have access to chocolate.<ref name="multiples">Tilley Smith'''The 5-Minute Veterinary Consult Canine and Feline''' (Second Edition), ''Lippincott, Williams and Wilkins''</ref> |
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==Diagnosis== | ==Diagnosis== | ||
===Clinical Signs=== | ===Clinical Signs=== | ||
− | Chocolate poisoning results in CNS, gastrointestinal, cardiovascular | + | Chocolate poisoning results in CNS, gastrointestinal, cardiovascular and urological signs.<ref name="multiples">Tilley Smith'''The 5-Minute Veterinary Consult Canine and Feline''' (Second Edition), ''Lippincott, Williams and Wilkins''</ref>, <ref name="multiple"> '''http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/211104.htm'''. These signs are observed quite quickly after ingestion of toxic amount of chocolate.<ref name="multiple"> '''BSAVA Manual of Canine and Feline Emergency and Critical Care'''Second Edition,2007 </ref> |
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+ | *'''CNS:''' hyperexcitability, hyperactivity, ataxia initially can evolve into muscle tremors, clonic seizures and hyperthermia.<ref name="multiples">Tilley Smith'''The 5-Minute Veterinary Consult Canine and Feline''' (Second Edition), ''Lippincott, Williams and Wilkins''</ref>, <ref name="multiple">'''BSAVA Congress 2007 Scientific Proceedings''', p253-254</ref> | ||
+ | *'''Gastrointestinal:''' diarrhoea, emesis, haematemesis, colic.<ref name="multiples">Tilley Smith'''The 5-Minute Veterinary Consult Canine and Feline''' (Third Edition), ''Lippincott, Williams and Wilkins''</ref>, <ref name="multiple">BSAVA Congress 2007 Scientific Proceedings p253-254</ref> | ||
+ | *'''Cardiovascular:''' arrhythmias,infrequently bradycardia but usually tachycardia.<ref name="multiples">Tilley Smith'''The 5-Minute Veterinary Consult Canine and Feline''' (Second Edition), ''Lippincott, Williams and Wilkins''</ref>, <ref name="multiple">'''BSAVA Congress 2007 Scientific Proceedings''', p253-254</ref> | ||
+ | *'''Urological:''' polydypsia and polyuria may also be present <ref name="multiples"> '''http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/211104.htm''', accessed on 02.10.2010 </ref> | ||
===Laboratory Tests=== | ===Laboratory Tests=== | ||
− | Diagnosis is usually on the basis of clinical signs and a known history of chocolate ingestion | + | 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 <ref name="multiples">Tilley Smith'''The 5-Minute Veterinary Consult Canine and Feline''' (Third Edition), ''Lippincott, Williams and Wilkins''</ref>. | |
− | * | + | * Blood Glucose: Hypoglycaemia as a consequence of hyperactivity. not seen consistently with chocolate poisoning <ref name="multiples">Tilley Smith'''The 5-Minute Veterinary Consult Canine and Feline''' (Third Edition), ''Lippincott, Williams and Wilkins''</ref>. |
− | * Blood Glucose: Hypoglycaemia as a | + | * Urinalysis: Proteinuria, low specific gravity; not seen consistently with chocolate poisoning <ref name="multiples">Tilley Smith'''The 5-Minute Veterinary Consult Canine and Feline''' (Third Edition), ''Lippincott, Williams and Wilkins'' </ref>. |
− | * Urinalysis: Proteinuria, low specific gravity; not seen consistently with chocolate poisoning | ||
===Other=== | ===Other=== | ||
− | *ECG: rate and rhythm abnormalities | + | *ECG: rate and rhythm abnormalities |
===Pathology=== | ===Pathology=== | ||
− | + | The methylxanthines yield their effects through | |
− | + | *'''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, vasoconstriction and 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 its effects <ref name="multiples">Tilley Smith'''The 5-Minute Veterinary Consult Canine and Feline''' (Third Edition), ''Lippincott, Williams and Wilkins'' </ref>. | |
− | *'''Antagonism of Adenosine Receptors:'''<ref name=" | + | *'''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. <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"> | + | Ventricular fibrillation, and other cardiac dysrhythmias are most frequently the ultimate cause of death.<ref> Carson TL (2006) Methylxanthines. In: ''Small Animal Toxicology'', ed. MEPeterson, PA Talcott, pp.845-852. Elsevier Saunders, St. Louis in '''BSAVA Manual of Canine and Feline Emergency Care''' 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> |
− | *'''Modulation of Intracellular Calcium Concentrations:''' <ref name= | ||
− | Ventricular fibrillation, and other cardiac dysrhythmias are most frequently the ultimate cause of death.<ref> Carson TL (2006) Methylxanthines. In: ''Small Animal Toxicology'', ed. | ||
==Treatment== | ==Treatment== | ||
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==Prognosis== | ==Prognosis== | ||
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==References== | ==References== | ||
<references/> | <references/> | ||
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Revision as of 09:48, 7 November 2010
This article is still under construction. |
Introduction
Toxicity is due to the presence of methylxanthines such as theobromine and caffeine in chocolate.[1]
Signalment
Dog that live indoors are more likely to have access to chocolate.[2]
Diagnosis
Clinical Signs
Chocolate poisoning results in CNS, gastrointestinal, cardiovascular and urological signs.[2], Cite error: Closing </ref>
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- CNS: hyperexcitability, hyperactivity, ataxia initially can evolve into muscle tremors, clonic seizures and hyperthermia.[2], [1]
- Gastrointestinal: diarrhoea, emesis, haematemesis, colic.[2], [1]
- Cardiovascular: arrhythmias,infrequently bradycardia but usually tachycardia.[2], [1]
- Urological: polydypsia and polyuria may also be present [2]
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 [2].
- Blood Glucose: Hypoglycaemia as a consequence of hyperactivity. not seen consistently with chocolate poisoning [2].
- Urinalysis: Proteinuria, low specific gravity; not seen consistently with chocolate poisoning [2].
Other
- ECG: rate and rhythm abnormalities
Pathology
The methylxanthines yield their effects through
- Antagonism of Adenosine Receptors:[2] this antagonism results in stimulation of the central nervous system, vasoconstriction and increase in heart rate [2] and also diureses [2]
- Inhibition of Cyclic Nucleotide Phosphodiesterase:[1] consequently there is an increase in cyclic AMP, which in turn leads to greater catecholamine release and its effects [2].
- 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. [2].
Ventricular fibrillation, and other cardiac dysrhythmias are most frequently the ultimate cause of death.[3], [4]
Treatment
Prognosis
References
- ↑ 1.0 1.1 1.2 1.3 1.4 BSAVA Manual of Canine and Feline Emergency and Critical CareSecond Edition,2007 Cite error: Invalid
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tag; name "multiple" defined multiple times with different content - ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 Tilley SmithThe 5-Minute Veterinary Consult Canine and Feline (Second Edition), Lippincott, Williams and Wilkins Cite error: Invalid
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tag; name "multiples" defined multiple times with different content - ↑ Carson TL (2006) Methylxanthines. In: Small Animal Toxicology, ed. MEPeterson, PA Talcott, pp.845-852. Elsevier Saunders, St. Louis in BSAVA Manual of Canine and Feline Emergency Care 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