Presenting problem: Anticoagulant Rodenticide Toxicosis in Free-Living Birds of Prey

Understanding anticoagulant rodenticide toxicosis in birds of prey

Mechanism of action

Anticoagulant rodenticides (ARs) interfere with blood clotting by inhibiting the enzyme vitamin K epoxide reductase, which functions to activate vitamin K. This inhibition results in the accumulation of an inactive form of vitamin K, which in turn is unable to activate the vitamin-K dependent clotting factors (II, VII, IX, and X). The depletion of these activated clotting factors causes coagulopathy and hemorrhage.


Avian coagulation

The process of coagulation is largely similar among avian and mammalian species. Although birds lack factors XI and XII, both the tissue factor pathway (formerly referred to as the extrinsic pathway) and the amplification or contact pathway (formerly referred to as the intrinsic pathway) function in avian coagulation. It was previously thought that birds also lacked factors VII and X; however, these conclusions were drawn from studies that used non-avian tissue thromboplastin in their laboratory assays, which is now recognized to produce inaccurate results. A study in poultry has shown that birds do in fact have factors VII and X and confirmed the importance of the tissue factor pathway as playing a primary role in avian coagulation (Thomson 2002).


Anticoagulant rodenticide exposure in birds of prey

Anticoagulant rodenticides have been commonly used over the past decades for control of commensal rodent populations. Anticoagulant rodenticides cause toxicosis in birds of prey via a secondary route—that is, consumption of poisoned prey results in toxicosis in the predator. ARs are divided into two categories: first generation ARs (FGARs) like warfarin and second generation ARs (SGARs), such as brodifacoum. Second generation ARs are more toxic than FGARs and also have a longer tissue persistence time.

Anticoagulant rodenticide exposure in birds of prey has been documented in the United States, Canada, and Europe (Murray 2011, Stone 2003, Albert 2010, Walker 2008, Berny 2008). Studies on AR exposure among birds of prey in Massachusetts and in New York State, USA, found that high percentages of birds had residues of ARs, particularly SGARs, in liver tissue (Murray 2011, Stone 2003). In Massachusetts, 86% of 161 birds were positive for SGARs, predominantly brodifacoum. All four species tested: red-tailed hawks (Buteo jamaicensis), barred owls (Strix varia), eastern screech-owls (Megascops asio), and great horned owls (Bubo virginianus) were highly exposed (Murray 2011). Studies in the United States and Canada have found comparatively high exposure in great horned owls (Murray 2011, Thomas 2011, Stone 2003). In Europe, the red kite (Milvus milvus) has been noted to be vulnerable to AR toxicosis (Hughes 2013, Berny 2008).

Second generation ARs are the subject of new US Environmental Protection Agency (EPA) regulations that aim to prohibit their sale to the general consumer. Unfortunately as of July 2013, not all rodenticide manufacturers were in compliance with these regulations; therefore SGARs may still be available in some general consumer markets. Most manufacturers have complied with the EPA and have brought replacement products containing FGARs (chlorophacinone or diphacinone) and/or the neurotoxin bromethalin to the market.

Under new EPA regulations, SGARs use is still permissible by licensed pest professionals and in agricultural settings. Therefore toxicosis from either SGARs or FGARs may be encountered when treating free-living birds of prey in the US.


Key points of urgent care


Free-living birds of prey suffering from AR toxicosis are often presented with a history of “not flying” and, if found by a road, are commonly presumed by the finder to have been hit by a car. Maintaining an index of suspicion for AR toxicosis when examining a wild raptor will ensure that this diagnosis is made promptly.

All species of raptors should be considered susceptible to AR toxicosis, including birds that do not primarily feed on mammals. Anticoagulant rodenticide exposure has been documented in accipiters and falcons, which mainly prey on other birds (Hughes 2012, Thomas 2011, Stone 2003). The most frequently affected species seen at the Tufts Cummings School of Veterinary Medicine Wildlife Clinic is the red-tailed hawk.


Physical examination

On physical examination, poisoned birds will exhibit dull mentation, profound pallor of the mucous membranes, and collapse of the cutaneous ulnar vein due to hypovolemic shock. Bleeding may or may not be obvious. In many cases extensive subcutaneous hemorrhage and intramuscular bruising will be present but can only be appreciated if the feathers are parted with isopropyl alcohol (Fig 1).

IM and SC hemorrhage

Figure 1. Ventral aspect of the left wing and axillary area of a great horned owl (Bubo virginianus) with anticoagulant rodenticide toxicosis. Note the severe intramuscular and subcutaneous hemorrhage, which would not be evident unless the feathers are parted with alcohol. Photo provided by Dr. Maureen Murray. Click image to enlarge.

In other instances, a traumatically induced injury may be present but the extent of hemorrhage will be disproportionate to the injury. For example, severe external hemorrhage can develop from a minor laceration or excessively large hematoma may form at a point of possible traumatic impact (Fig 2). In some cases, hemorrhage will be internal. An increased respiratory rate and/or effort can indicate hemorrhage involving the respiratory system.

Red-tailed hawk with anticoagulant rodenticide toxicosis

Figure 2. Red-tailed hawk (Buteo jamaicensis) with anticoagulant rodenticide toxicosis showing severe swelling around the left eye, which was likely a point of traumatic impact. The degree of periocular hemorrhage is in excess of what is seen with uncomplicated trauma. Photo by Maureen Murray. Click image to enlarge.


Obtaining a small amount of blood can help confirm the diagnosis of AR toxicosis and differentiate this condition from straightforward trauma. Profound anemia and hypoproteinemia will be present in poisoned birds. There are no commercially available laboratory tests for avian coagulation, and tests run with mammalian thromboplastin will provide inaccurate results. Nevertheless the lack of clotting in these birds is usually quite evident if 0.1-0.2 ml of blood are placed in a serum collection tube and simply observed. In normal birds, signs of clot formation in the tube should be obvious within 5 minutes. In most AR poisoned birds, no signs of clotting are seen after several hours.

Many diagnostic laboratories can identify rodenticides from a plasma sample. False negatives are possible however, as the half-life of ARs in blood is short. Also, the need to pursue AR identification should be weighed against the drawbacks of taking additional blood for testing from an anemic and shocky bird.


Case management


The antidote for AR toxicosis is administration of vitamin K1, which should be administered at a dose of 2.5 mg/kg subcutaneously (SC) immediately and repeated every 8-12 hours until signs of hemorrhage resolve. Once the bird’s condition has stabilized, vitamin K1 can be given at 2.5 mg/kg once daily orally with food, which enhances absorption. Duration of therapy is dependent on the type of rodenticide, with SGARs requiring longer treatment than FGARs due to their longer half-lives. With free-living birds, the type of rodenticide is often unknown. Therefore, assuming that toxicosis is due to an SGAR is the safest course of action. Four weeks of vitamin K1 therapy in raptors with SGAR toxicosis has been successful.

Although the ideal treatment of AR toxicosis would be administration of whole blood to supply both clotting factors and red blood cells and to restore blood volume, this option is usually not available to wildlife clinicians due to lack of appropriate donors and blood products. Fortunately birds are more tolerant of acute blood loss than mammals and erythropoiesis occurs very rapidly. A study of acute blood loss in pigeons comparing the efficacy of crystalloid fluid therapy versus homologous and heterologous blood transfusions found no benefit in treatment with homologous whole blood over treatment with crystalloids alone (Bos 1990). If a blood transfusion is attempted, homologous transfusion is recommended as heterologous red blood cells have been shown to have short survival times (Degernes 1999a, Degernes 1999b, Finnegan 1997) In my experience, raptors with AR toxicosis can respond very well to vitamin K1 administration, crystalloid fluid replacement (SC or intraosseous), supplemental oxygen therapy, and basic supportive care.



Successful treatment, rehabilitation, and release of even severely anemic raptors with AR toxicosis is possible. Based on those birds treated at Tufts Wildlife Clinic, prognosis appears to largely depend on the location of hemorrhage. Birds with external, intramuscular, or subcutaneous hemorrhage have a better prognosis for survival than birds that bleed internally, such as into the respiratory tract, pericardial sac, or central nervous system.



Suspected cases of anticoagulant rodenticide toxicosis in wildlife species can be reported to the EPA via the National Pesticide Information Center, which is coordinated by Oregon State University. The Ecological Pesticide Incident Reporting Portal can be accessed at




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