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| | ==Introduction== | | ==Introduction== |
| | The absolute or relative deficiency of vitamin K can give rise to defective coagulation. | | The absolute or relative deficiency of vitamin K can give rise to defective coagulation. |
| − | [[Anticoagulant Rodenticide Toxicity|Anticoagulant rodenticide toxiticy]] is one of the most common causes of acquired coagulopathy in small animals. Warfarin itself has a short half-life and a fairly low toxicity in non-rodent species, so unless large or repeated doses are consumed clinical bleeding is rare. However, the second generation anticoagulant rodenticides are far more potent, and it is possible for a domestic animal to acquire secondary poisoning by ingesting a poisoned rodent<sup>1</sup>. Dogs are most commonly effected, but predator species such as cats and owls do occasionally suffer from secondary poisonings.
| + | Anticoagulant rodenticide toxiticy is one of the most common causes of acquired coagulopathy in small animals. Warfarin itself has a short half-life and a fairly low toxicity in non-rodent species, so unless large or repeated doses are consumed clinical bleeding is rare. However, the second generation anticoagulant rodenticides are far more potent, and it is possible for a domestic animal to acquire secondary poisoning by ingesting a killed rodent<sup>1</sup>. |
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| − | The [[Normal_Mechanisms_of_Haemostatic_Control#Coagulation_physiology|clotting factors]] - factor VII, factor XI and factors II and X in the extrinsic, intrinsic and common pathways respectively are dependent on Vitamin K when activated by the coagulation cascade.
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| − | ==Other Causes of Vitamin K deficiencies==
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| − | Malabsorption syndromes and sterilisation of the gastrointestinal tract by prolonged antibiotic usage will also result in the depletion of vitamin K-dependent clotting factors<sup>2</sup>. In herbivores, fungi growing on poorly prepared hay or silage containing sweet vernal grass or sweet clover may break down natural coumarins in the plants to form dicoumarol and cause poisoning.
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| − | ==Replacement of Vitamin K==
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| − | [[Anticoagulant_Rodenticide_Toxicity#Treatment|Vitamin K<sub>1</sub>]] is available as a subcutaneous treatment for cases of [[Anticoagulant Rodenticide Toxicity|rodenticide poisoning]]. Alternatively, whole blood or plasma transfusion provides vitamin K dependent clotting factors, which can control symptoms in severe acute cases.
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| | ==References== | | ==References== |
| − | #Campbell, A (1999) Common causes of poisoning in small animals. ''In Practice'', '''21(5)''', 244-249.
| + | Also see [[Anticoagulant Rodenticide Toxicity]] |
| − | #Tilley, L P and Smith, W K (2007) '''Blackwell's Five Minute Veterinary Consult: Canine and Feline (Fourth Edition)''', ''Blackwell''.
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| − | [[Category:Coagulation Defects]][[Category:Lymphoreticular and Haematopoietic Diseases - Dog]] | + | [[Category:Coagulation Defects]] |
| − | [[Category:Cardiology Section]] | + | [[Category:To Do - Blood]][[Category:To Do - Clinical]] |
Introduction
The absolute or relative deficiency of vitamin K can give rise to defective coagulation.
Anticoagulant rodenticide toxiticy is one of the most common causes of acquired coagulopathy in small animals. Warfarin itself has a short half-life and a fairly low toxicity in non-rodent species, so unless large or repeated doses are consumed clinical bleeding is rare. However, the second generation anticoagulant rodenticides are far more potent, and it is possible for a domestic animal to acquire secondary poisoning by ingesting a killed rodent1.
References
Also see Anticoagulant Rodenticide Toxicity