Anticoagulant rodenticide poisoning (Brodifacoum Bromadiolone Chlorofacinone Coumafen Coumatetralyl Ifenacoum Diphacinone Warfarin)

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• Anticoagulant rodenticides available commercially in cereal-based baits at a concentration of 0.02% to 1.0%.
• Cats are rarely poisoned.
• Cause:ingestion of rodenticide blocks action of Vitamin K1.
• Signs: delayed from 1-5 days post exposure: internal and external hemorrhage and bruising.
• Treatment: vitamin K1 (phytomenadione) , whole blood transfusion if required.
   Do not use vitamin K3 as it is less effective.
• Prognosis: good with appropriate therapy.

• Weakness.
• Lethargy.
• Dyspnea.
• Pallor.
• Epistaxis and/or melena and/or hemoptysis and/or hematomas and/or lameness.
• Seizures, paresis or paralysis may occur if bleeding occurs within the CNS.

• Hemorrhage into a major body cavity may cause acute collapse.

• Single doses of short acting anticoagulants may produce minimal symptoms.

 Petechiae on mucous membranes indicate defect primary hemostasis, eg thrombocytopenia, NOT a feature of anticoagulant rodenticide toxicity.

• Hypovolemic shock following massive internal bleeding.
• May be accompanied by dyspnea in hemo-thorax or abdominal distension in hemo-peritoneum.

• Outdoor cats with access to poison or poisoned prey.

• Cats are less often poisoned by dogs, but poisoning may follow ingestion of poisoned rodents.
• Reported acute oral LD 50s for the cat:
  • Warfarin 5-30 mg/kg
  • Diphacinone 15 mg/kg
  • Brodifacoum >25 mg/kg.
  • Bromadiolone > 25 mg/kg.

• Anticoagulant rodenticides inhibit Vitamin K epoxide reductase, the enzyme involved in production of active vitamin K.
• Clotting factors II (prothrombin), VII, IX and X all require active vitamin K to function effectively.
• Factor VII has shortest half-life and is therefore first to be affected by anti-coagulant poisoning.
• Depletion of clotting factors results in coagulopathy and profuse bleeding following trauma.

• Short acting rodenticides (eg warfarin, coumafuryl and pindone) generally require multiple exposures before coagulopathy occurs and toxic effects may resolve after 7 to 10 days.
• Second generation (longer acting) rodenticides (eg diphacinone, brodifacoum and bromadiolone) may produce a coagulopathy after a single dose and toxic effects may persist for more than 3 weeks.
• Signs do not develop until body reserves of vitamin K have been depleted, ie >24 hours after ingestion of rodenticide.
• Toxicity may be potentiated by phenylbutazone, diphenylhydantoin, adrenocorticosteroids, and sulfonamides.

• Clinical signs of poisoning usually appear 3-5 days following ingestion.
• Morbidity/recovery related to site of hemorrhage.
• Death, if it occurs, is usually within 1-6 days.

• Coagulopathy.

• Dyspnea.
• Visible hemorrhage.
• Depression.
• Local use of poison.

• Anorexia.

• Signs related to site of hemorrhage.
• Coughing.
• Dyspnea very common (intrathoracic or pulmonary).
• Bruising.
• Partial paralysis (CNS or intramuscular).
• Hemorrhagic gastroenteritis (intestinal).
• Hematuria (genitourinary).
• Cardiac tamponade ie right-sided failure (hemopericardium).
• Seizures or depression (meningeal or cerebral).

• Pallor due to anemia and hypovolemia (especially apparent in final stages).

• Hypothermia .

• Routine hematology to assess severity of blood loss (see anemia due to hemorrhage .
   PCV may not be reduced in acute bleeding.
• Platelet count usually normal.

Other

• Activated coagulation time at least doubled.
• Activated prothrombin time at least doubled.
• Activated partial thromboplastin time at least doubled.
• Activated prothrombin time is the first to increase.

• Thoracic and abdominal films to show site and extent of internal bleeding.

• Thoracocentesis or abdominocentesis are usually not required and may be risky.
• Thoracocentesis may be indicated in severely dyspneic patient.

• Signs

• History of access to bait/baited rodents.
• Coagulation times increased.
• Demonstration of poison in samples of liver, kidney.
• Response to vitamin K.
• Measurement of PIVKA (proteins induced by vitamin K absence) ie accumulated non-functional forms of vitamin K dependent clotting factors .

• Gross findings may include:
• Extensive hemorrhages in subcutaneous tissues, thymus.
• Hemothorax.
• Hemoperitoneum.
• Hemorrhage to peritoneal aspect of bladder.
• Mild to moderate hepatic degeneration.

• Other coagulopathies: primary (inherited) , other secondary (acquired ).
• DIC .
• Vit K1 responsive coagulopathies.

• Cirrhosis .
• Malabsorption syndromes .

• Chronic cholestasis .

• Emesis or activated charcoal if presented immediately following ingestion.
   Signs will not develop for 1-2 days by which time there will be no poison in gastrointestinal tract.
• In acute life-threatening anemia and hypovolemia, whole blood transfusion or fresh/frozen plasma if PCV <15%.
• Gentle handling essential to minimize risk of further hemorrhage.

• Oxygen therapy may be required.
• Antibiotic cover until hematoma resorbed.

• Thoracocentesis may be required in severe dyspnea but further hemorrhage may make problem worse.

• Initial dose 2-5mg/kg orally or subcutaneously.
• IM injection may cause further hemorrhage.
• IV administration carries risk of anaphylaxis. 
• Significant synthesis of clotting factors takes 6 to 12 hours.
• Vitamin K3 is much less effective than vitamin K1.
• Maintenance dose up to to 5mg/kg orally in single.
• Absorption of oral vitamin K enhanced if given with fatty meal.
• Treat for at least 10-14 days.

• Check coagulation times 36-48 hours after cessation of therapy.
• If coagulation times at 36-48 hours are normal, check again after another 36-48 hours.
• Resume Vitamin K1 therapy if coagulation times increase.
• Poisoning with second-generation rodenticides frequently requires antidotal therapy for 21-30 days, or even longer in the case of difethialone.

• Limit access to both anticoagulant rodenticides and to rodents poisoned with anticoagulant rodenticides.

• Coagulation times should be regularly monitored for the first week after possible exposure to anticoagulant rodenticides.

• Good: if treatment started soon after exposure and clotting time carefully monitored.
• Guarded: if severe case. Depends on site of hemorrhage.

• Normal coagulation times.
• Color returns to mucous membranes.
• Patient becomes more alert/responsive.
• Resorption hematomata/hemorrhages.
• Increase in erythrocyte count and PCV in longer term.

• Non-detection of hemorrhage (eg internal).
• Delay in treatment.
• Inadequate doses vitamin K1 given, or given by inappropriate route.
• Inadequate supportive therapy (plasma or blood) in period during which new clotting factors are being synthesized following Vitamin K1 administration.
• Insufficient duration of treatment.

• Recent references from PubMed.
• Kohn B, Weingart C & Giger U (2003) Haemorrhage in seven cats with suspected anticoagulant rodenticide intoxication. J Feline Med Surg 5 (5), 295-304 PubMed.

• Murphy M J & Talcott P A (2001) Anticoagulant Rodenticides. In Small Animal Toxicology. Eds: M E Peterson and P A Talcott. Philadelphia: W B Saunders. ISBN: 0 7216 7826 2.
• Osweiler G D (1995) Toxicology. Philadelphia: Williams and Wilkins. ISBN: 0 6830 6664 1.

• Rosalind Dalefield BVSc PhD DABVT DABT, 37479 Branchriver Road, Purcellville, Virginia 20132, USA.

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