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Also known as: '''''warfarin toxicity/poisoning — anticoagulant rodenticide poisoning — vitamin K antagonist toxicity/poisoning

 

Also known as: warfarin toxicity/poisoning, anticoagulant rodenticide poisoning, vitamin K antagonist toxicity/poisoning.

 

Anticoagulant rodenticides were first discovered during investigations into mouldy sweet clover poisoning in cattle¹. In this condition, naturally occuring coumarin in clover is converted by fungi to a toxic agent, dicumarol, which causes a haemorrhagic syndrome when ingested. Initially, warfarin was synthesised and used in this way for rodent control, but as rodents have developed a resistance to the substance new, second generation anticoagulant rodenticides have been developed. These include coumarin (bromadiolone and brodifacoum) and indandione (pindone and diaphacinone) rodenticides, which along with warfarin may cause toxicity following accidental ingestion or malicious administration in animals.  

Anticoagulant rodenticides were first discovered during investigations into mouldy sweet clover poisoning in cattle¹. In this condition, naturally occuring coumarin in clover is converted by fungi to a toxic agent, dicumarol, which causes a haemorrhagic syndrome when ingested. Initially, warfarin was synthesised and used in this way for rodent control, but as rodents have developed a resistance to the substance new, second generation anticoagulant rodenticides have been developed. These include coumarin (bromadiolone and brodifacoum) and indandione (pindone and diaphacinone) rodenticides, which along with warfarin may cause toxicity following accidental ingestion or malicious administration in animals.  

===Similar Conditions===

===Similar Conditions===

Malabsorption syndromes and sterilisation of the gastrointestinal tract by prolonged antibiotic usage will also result in the depletion of vitamin K-dependent clotting factors⁷. 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.

Malabsorption syndromes and sterilisation of the gastrointestinal tract by prolonged antibiotic usage will also result in the depletion of vitamin K-dependent clotting factors⁷. 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.

==Signalment==

==Signalment==

Anticoagulant rodenticide toxcity is most often seen in dogs, due to their scavenging behaviour and the fact they appear to find rodent bait especially palatable. Farm dogs are particularly at risk since rodenticides are frequently used in this environment and many dogs are allowed to roam freely outdoors. In the cat, toxicity usually occurs via the consumption of poisoned rodents. Anticoagulant rodenticide toxicity has been reported in the pig, and also in barn owls who have consumed rodents poisoned with second generation anticoagulant rodenticides⁶.

Anticoagulant rodenticide toxcity is most often seen in dogs, due to their scavenging behaviour and the fact they appear to find rodent bait especially palatable. Farm dogs are particularly at risk since rodenticides are frequently used in this environment and many dogs are allowed to roam freely outdoors. In the cat, toxicity usually occurs via the consumption of poisoned rodents. Anticoagulant rodenticide toxicity has been reported in the pig, and also in barn owls who have consumed rodents poisoned with second generation anticoagulant rodenticides⁶.

==Diagnosis==

==Diagnosis==

Ideally, a diagnosis of anticoagulant rodenticide toxicosis should be made based on a history of ingestion of the substance. Failing this, clinical signs, certain laboratory parameters and response to treatment will be suggestive of the condition.

Ideally, a diagnosis of anticoagulant rodenticide toxicosis should be made based on a history of ingestion of the substance. Failing this, clinical signs, certain laboratory parameters and response to treatment will be suggestive of the condition.

===Clinical Signs===

===Clinical Signs===

As described above, the onset of clinical signs in anticoagulant rodenticide toxicosis is delayed for up to five days while vitamin K dependent factors become depleted, due to the gradual degradation of functional factors already in the circulation. When signs occur, they are related to defective haemostasis and unchecked haemorrhage although depression and anorexia may be seen before bleeding begins. Visible signs can include external haematomas, bruising, epistaxis, hyphaema, haematemesis, haemtotochezia, melaena, haematuria or excessive bleeding from sites of venupuncture or injury^1-8. Lameness may also occur if there are haemorrhages into joints. Non-specific symptoms are also possible, related to internal bleeding. Such examples are weakness, ataxia, dyspnoea, abdominal swelling and pallor.  

As described above, the onset of clinical signs in anticoagulant rodenticide toxicosis is delayed for up to five days while vitamin K dependent factors become depleted, due to the gradual degradation of functional factors already in the circulation. When signs occur, they are related to defective haemostasis and unchecked haemorrhage although depression and anorexia may be seen before bleeding begins. Visible signs can include external haematomas, bruising, epistaxis, hyphaema, haematemesis, haemtotochezia, melaena, haematuria or excessive bleeding from sites of venupuncture or injury^1-8. Lameness may also occur if there are haemorrhages into joints. Non-specific symptoms are also possible, related to internal bleeding. Such examples are weakness, ataxia, dyspnoea, abdominal swelling and pallor.  

===Laboratory Tests===

===Laboratory Tests===

Routine haematology reveals an anaemia due to loss of whole blood. Because time is required for regeneration to begin, the anaemia may initially appear non-regenerative. Haemorrhage is also likely to give a reduction in total protein and/or indications of dehydration (e.g. increased urea and creatinine) on biochemistry. Secondary complications such as pre-renal azotaemia are possible.

Routine haematology reveals an anaemia due to loss of whole blood. Because time is required for regeneration to begin, the anaemia may initially appear non-regenerative. Haemorrhage is also likely to give a reduction in total protein and/or indications of dehydration (e.g. increased urea and creatinine) on biochemistry. Secondary complications such as pre-renal azotaemia are possible.

===Pathology===

===Pathology===

 

Pathologic findings commonly include free blood in the thorax, lungs and abdominal cavity⁷. Haemorrhage into the gastrointestinal tract, cranial vault and urinary tract may also be seen, as well as intramuscular and subcutaneous bleeding.

Pathologic findings commonly include free blood in thte thorax, lungs and abdominal cavity⁷. Haemorrhage into the gastrointestinal tract, cranial vault and urinary tract may also be seen, as well as intramuscular and subcutaneous bleeding.

==Treatment==

==Treatment==

If ingestion of rodenticide occured in the past three hours, vomiting should be induced in an attempt to reduce absorption. If animals fail to vomit, stomach lavage may be indicated.  

If ingestion of rodenticide occured in the past three hours, vomiting should be induced in an attempt to reduce absorption. If animals fail to vomit, stomach lavage may be indicated.  

The treatment of anticoagulant rodenticide poisoning aims to correct the hypovolaemia and coagulopathy. A whole blood or plasma tranfusion provides immediate access to vitamin K dependent clotting factors, helps to restore blood volume and, in the case of whole blood, supplements red blood cells and platelets^1-9. This may need to be followed with larger volumes of crystalloids to compensate for large volumes of fluid loss. The specific treatment of anticoagulant rodenticide toxicosis is administration of vitamin K₁. This is given as a subcutaneous loading dose at 5mg/kg, and is followed by oral or subcutaneous administration at 2.5-5mg/kg once daily, for 1-6 weeks. If given ''per os'', giving a small amount of fat such as canned dog food aids absorption^{7, 8}. Intravenous administration of vitamin K₁ is contraindicated as anaphylactic reactions may occur. Treatment with the less expensive vitamin K₃ is also contraindicated as it is not efficacious in the face of anticoagulant rodenticide toxicity. The duration of treatment depends on the anticoagulant as well as patient factors, and coagulation parameters should be monitored to detmine the progress being made.

The treatment of anticoagulant rodenticide poisoning aims to correct the hypovolaemia and coagulopathy present. A whole blood or plasma tranfusion immediately provides vitamin K dependent clotting factors, helps to restore blood volume and, in the case of whole blood, supplements red blood cells^1-9. This may need to be followed with larger volumes of crystalloids to compensate for large volumes of fluid loss. The specific treatment of anticoagulant rodenticide toxicosis is administration of vitamin K₁. This is given as a subcutaneous loading dose at 5mg/kg, and is followed by oral or subcutaneous administration at 2.5-5mg/kg once daily, for 1-6 weeks. If given ''per os'', providing a small amount of fat such as canned dog food aids absorption^{7, 8}. Intravenous administration of vitamin K₁ is contraindicated as anaphylactic reactions may occur. Treatment with the less expensive vitamin K₃ is also contraindicated as it is not efficacious in the face of anticoagulant rodenticide toxicity. The duration of treatment depends on the anticoagulant as well as patient factors, and coagulation parameters should be monitored to detmine the progress being made.

Hypocoagulable patients are at risk of internal haemorrhage, so physical activity should be kept to minimum. Unnecessary surgical procedures and venupuncture should be avoided, although thoracocentesis may be required in the event of haemothorax⁷.

Hypocoagulable patients are at risk of internal haemorrhage, so physical activity should be kept to minimum. Unnecessary surgical procedures and venupuncture should be avoided, although thoracocentesis may be required in the event of haemothorax⁷.

==Prognosis==

==Prognosis==

The prognosis for anticoagulant rodenticide toxicity is guarde, but improves if the patient survives the first 48 hours of acute coagulopathy⁷.

|Vetstream = [https://www.vetstream.com/canis/Content/Disease/dis02574.asp, Anticoagulant rodenticide toxicity]

|literature search = [http://www.cabdirect.org/search.html?q=title:(Anticoagulant+)+AND+title:(Rodenticide)+AND+title:(Toxicity) Anticoagulant rodenticide toxicity publications]

==Links==

==Links==

*[http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/213000.htm The Merck Veterinary Manual - Rodenticide Poisoning]

*[http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/213000.htm The Merck Veterinary Manual - Rodenticide Poisoning]

*[http://www.vetstreamfelis.com/ACI/October/VMD2/dis02574.asp VetStream Felis - Anticoagulant rodenticide poisoning]

*[http://www.vetstreamfelis.com/ACI/October/VMD2/dis02574.asp VetStream Felis - Anticoagulant rodenticide poisoning]

==References==

==References==

#Murphy, M J and Talcott, P A (2005) Anticoagulant Rodenticides. In '''Small Animal Toxicology (Second Edition)''', ''Saunders''.

#Murphy, M J and Talcott, P A (2005) Anticoagulant Rodenticides. In '''Small Animal Toxicology (Second Edition)''', ''Saunders''.

#Campbell, A (1999) Common causes of poisoning in small animals. ''In Practice'', '''21(5)''', 244-249.

#Campbell, A (1999) Common causes of poisoning in small animals. ''In Practice'', '''21(5)''', 244-249.

[[Category:Stomach_and_Abomasum_-_Pathology]] [[Category:WikiClinical Canine]] [[Category:WikiClinical Feline]]

[[Category:Stomach_and_Abomasum_-_Pathology]] [[Category:Gastric Diseases - Dog]] [[Category:Gastric Diseases - Cat]][[Category:Coagulation Defects|Z]]

[[Category:To_Do_-_Lizzie]]

[[Category:Lymphoreticular and Haematopoietic Diseases - Dog]][[Category:Lymphoreticular and Haematopoietic Diseases - Cat]]

[[Category:Cardiology Section]]