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Rodenticides—An Oldie but a Goodie Ahna Brutlag, DVM Pet Poison Helpline, Bloomington, MN, USA

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Rodenticides—An Oldie but a Goodie Ahna Brutlag, DVM Pet Poison Helpline, Bloomington, MN, USA 82nd Western Veterinary Conference V315 Rodenticides—An Oldie But a Goodie Ahna Brutlag, DVM Pet Poison Helpline, Bloomington, MN, USA KEY POINTS . Do not assume all rodenticides are anti-coagulants. The active ingredient of a rodenticide cannot be determined by the color or shape of the product. Due to better absorption and less chance of reaction, the oral administration of Vitamin K1 is preferred over injectable unless the animal is coagulopathic. OVERVIEW OF THE ISSUE Rodenticides (chemicals used to kill mice, rats, moles, gophers and other vermin) have been marketed in the US for many decades. They are available in several formulations with blue or green pellets or paraffin blocks being the most common preparations. Powders and liquid products also exist. Grain and other attractants are often added to the solid formulations. While many contain bittering agents to prevent accidental ingestion by children, these agents appear to have limited effectiveness in animals. The color or formation of the rodenticide is unrelated to the active ingredient and cannot be relied upon for ingredient identification. Thus, make no assumptions about the active ingredient based on the appearance of the bait alone. Currently, anticoagulant rodenticides are the most widely used in the US. Other commonly used active ingredients include cholecalciferol, zinc or aluminum phosphides, and bromethalin. The availability of strychnine has become severely restricted and is not often available to the general public. The currently marketed array of rodenticides can lead to a wide variety of toxidromes, thereby making the management of the poisoned patient difficult and costly. Rodenticide toxicity is among the top three most common sources of toxin exposures in dogs. Cats suffer from rodenticide toxicity much less frequently. The reason for this is likely dependent on species sensitivities with cats being more resistant to the effects of many anticoagulant rodenticides as compared to dogs. These notes will review the most commonly marketed rodenticides, the clinical signs associated with poisoning, preferred diagnostic testing, and treatment recommendations for poisoning. ANTI-COAGULANTS . Short acting anticoagulants: Warfarin (rarely used) . Long acting anticoagulants: Bromadiolone, brodifacoum, diphacinone, difenthiolone, chlorphacinone For purposes of this lecture, anticoagulant rodenticides will be discussed as short-acting or long- acting. It is the duration of action that is most important to health care providers because this dictates the duration of treatment needed. Anticoagulant rodenticides are Vitamin K antagonists and thus interfere with the production of Vitamin K dependent clotting factors in the liver (factors 2, 7, 9 and 10 or the prothrombin complex). The coagulation system generally continues to function well until about 24 to 36 hours after ingestion when the natural decay of clotting factors occurs. As a group, anticoagulant rodenticides are well absorbed orally (about 90%) with peak plasma levels occurring within 12 hours after ingestion. Warfarin, the most common short-acting anticoagulant (SAAC) has a half-life of 12–18 hours and treatment with Vitamin K1 for 5–6 days is often sufficient. Due to widespread resistance amongst rats, warfarin is rarely used as a rodenticide in the US. More typical are the long-acting anticoagulants (LAACs) such as bromadiolone and brodifacoum. LAACs have an exceedingly longer half life of days to weeks; treatment is recommended for 3–4 weeks. Range of Toxicity The margin of safety for anticoagulant rodenticides is quite narrow though the LD50 varies dramatically amongst active ingredients, as well as from species to species. Cats are significantly more resistant to the effects of LAACs than dogs and rarely suffer toxicity. For an easy estimation of toxicity based on finished bait products, see Table 1. Refer to Table 4 for a listing of oral LD50s. Table 1. Estimates of toxicity based on 0.005% concentration of LAAC rodenticides. Active ingredient Canine toxic dose Feline toxic dose (grams finished bait/kg) (grams finished bait/kg) Bromadiolone* 23 gm/kg 53 gm/kg Brodifacoum** 0.99 gm/kg 132 gm/kg Diphacinone* 2.0 gm/kg 33 gm/kg * Based on 1/10 of the oral LD50 ** Based on ¼ of the oral canine LD50 and 1/10 of the oral feline LD50 Animals with hepatic or renal compromise and those with GI malabsorption syndromes may be at a higher risk of toxicity. The pediatric and geriatric population, as well as those with very low body weights, also have a higher risk of toxicity and more conservative estimates of toxicity must be used. Additionally, animals taking highly protein-bound drugs (i.e., deracoxib or carprofen) may also be an increased risk of toxicity. Additionally, anticoagulant rodenticides cross the placental barrier and may lead to uterine bleeding or fetal toxicity. To a very limited extent, they are excreted in breast milk. Clinical Signs The most common signs of toxicity in dogs and cats include generalized signs such as lethargy, exercise intolerance, inappetence, pallor, and dyspnea or wheezing. These signs typically begin 3–5 days following exposure. Gingival bleeding, epistaxis, ecchymoses, petechiae, hematuria, hemoptysis, hematemesis and melena may also be present but are often not noted by pet owners. Rarely, animals may present with generalized pain, fever, or lameness and neurologic abnormalities. As opposed to coagulopathies secondary to thrombocytopenia, bleeding is typically intracavital versus serosal. Massive blood loss into the thoracic and abdominal cavities is common and is often the cause of death. Diagnosis A tentative diagnosis is often made by a history of ingestion and clinical signs. This may be supported with a finding of anemia, delayed whole blood clotting times, and an ACT from 2 to 10+ times normal. These results are confirmed by prolonged PT and APPTs with normal to slightly low platelets and normal fibrin degradation products. While mild thrombocytopenia is a typical diagnostic finding, anticoagulant rodenticides do not interfere with platelet production or function. A finding of severe thrombocytopenia is either secondary to blood loss or due to other causes. For acute exposures or asymptomatic animals, a baseline PT as well as a PT performed 36–48 hours post-ingestion may be performed in lieu of empirical antidotal treatment. This allows enough time for the currently present clotting factors to decay but does not (typically) provide enough time for the onset of clinical signs. Should the PT be prolonged on the subsequent test, Vitamin K1 therapy is necessary. Likewise, a PT should be performed 36–48 hours following the final dose of Vitamin K1 to ensure that further treatment is no longer needed. Laboratory assays for specific LAACs may be performed on plasma, stomach contents, and kidney and liver specimens. Treatment Decontamination via emesis followed by one dose of activated charcoal is recommended following recent toxic ingestions. Vitamin K1 (phytonadione) is antidotal and is dosed at 2.5–5 mg/kg per day or divided into two daily doses. Oral Vitamin K1 is preferred over injectable if the exposure was less than 24 hours ago and the animal is asymptomatic. Injectable Vitamin K1 given subcutaneously should be reserved for coagulopathic animals. Oral Vitamin K1 should be administered for a minimum of 21–30 days for LAAC toxicity and 4–6 days for SAAC toxicity. A PT should be obtained 36–48 hours after treatment is discontinued to assure proper duration of treatment. If the PT is prolonged, Vitamin K1 should be re- instituted for another 21 days and rechecked at termination. Vitamin K1 has no direct effect on coagulation and it takes 6–12 hours to make new clotting factors once therapy is instituted. Animals suffering significant blood loss may need a transfusion of fresh whole blood or plasma to provide clotting factors. Animals with severely compromised respiratory systems may need a thoracocentesis. CHOLECALCIFEROL Cholecalciferol or Vitamin D3 is gaining popularity as a rodenticide. Toxicity from cholecalciferol results in life-threatening hypercalcemia and hyperphosphatemia leading to dystrophic mineralization and subsequent renal failure. Death from cardiac failure secondary to hypercalcemia may also occur though is much less likely. Range of Toxicity Estimating toxicity levels can be difficult. While the published range of oral canine LD50 is relatively large (10–85 mg/kg), clinical signs have been documented at 0.1–0.5 mg/kg. Cats are more sensitive to cholecalciferol than dogs. Refer to Table 4 for a listing of common rodenticides and their respective canine and feline oral LD50. For an easy estimation of toxicity based on finished bait products, see Table 2. Table 2. Estimates of toxicity* based on 0.075% concentration of cholecalciferol bait. Active Canine toxic dose Feline toxic dose Ingredient (grams finished bait/kg of body (grams finished bait/kg of body weight) weight) Cholecalciferol 0.66 gm bait/kg 0.53 gm bait/kg * Based on an estimate of 0.5 mg/kg toxicity in dogs and 1/10 of the LD50 in cats. Clinical Signs Signs typically begin 12–24 hours after ingestion and may be non-specific at the onset. While the renal system is often most acutely affected, eventually the cardiac, pulmonary GI and CNS systems may be as well. 0–24 hours: PU/PD, hypercalcemia, hyperphosphatemia . 12–36 hours: Anorexia, vomiting, weakness, lethargy, melena . 2–4 days: Acute renal failure . 3–5 days: Depression, frank bloody diarrhea, hematuria, prominent bradycardia, death Diagnosis A diagnosis is made by a history of ingestion and clinical signs, and is supported by laboratory findings of hypercalcemia and hyperphosphatemia. Additionally, azotemia, calciuria, hypothsenuria, and radiographic evidence of dystrophic mineralization support the diagnosis of cholecalciferol toxicity. A definitive diagnosis based on serum and tissue testing for cholecalciferol and its metabolites may be done but is rarely performed. Suggested laboratory monitoring: . Serum phosphorous (typically rises 12–24 hr post exposure) . Serum calcium (typically rises 24–36 hr post exposure) . Ionized calcium levels (typically rises 24–36 hr post exposure) .
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