Rat Poison Intoxication Rodenticide
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Rat Poison Intoxication (Rodenticide) Rat poison ingestion is a common occurrence in the household pet. There are several different active ingredients and preparation of rat poison. The three most common method of action include the inhibition of vitamin k, calcifying substances and uncoupling of oxidative phosphorylation. V itamin K is e ssential to the function of several coagulation factors. When vitamin K can not be made or utilized in the body it inhibits blood clot formation. Since the blood clot is the foundation of stopping bleeding, antogonization of this process lead to bleeding into multiple body spaces and dead if left untreated. There is a 2-7 day lag period between ingestion and the onset of bleeding, varying between compounds (warfarin, diphacinone, brodifacoum and bromadiolone). But immediate veter inary attention should al ways be sought as soon as possible, even if ingestion is only partially sus pected. If caught early enough, vomiting can be induced and prevent systemi c absorption. T reatment before clinical signs of bleeding is much more effective and less costly than treatment after bleeding begins. T ypically vomitus from dogs that have ingested one of these compounds is bright blue-green in color. The most common clinical signs, once bleeding be gins, are weakness, lethargy , collapse, pale mucous membranes, panting, an increased respiratory effort, possibly perceivable abdominal distention and/or pain to the touch of the chest or abdomen. Emergency veterinary care must be s ought immediately when bleeding is suspected. A presumptive diagnosis by the veterinarian is usually made by history , possible exposure and documentation of prolongation of the PT coagulation t est. Initial therapy generally involves oxygen supplementation, aggressive fluid therapy, plasma and/or whole blood transfusions, injectable V itamin K administration and other gener al supportive/sympt omatic therapies. Intensive monitoring is generally necessary over the first 24-48 hou rs. Once no signs of further bleeding or systemic compromise are present and the coagulation times are normal, the patient can usually be sent home on oral Vitamin K. The length of time that oral V itamin K needs to b e administered varies between products. Generally , at least 2 to 3 weeks of therapy i s required. After a that time the V itamin K is discontinued and a coagulation screen in re-checked in two to three da ys after the last supplementation dose. If the screen is normal, no further treatment is indicated. If there is still significant prolongation, Vitamin K therapy is re-instituted for another two weeks, then the PT repeated. The next most common category of rodenticides to cause small animal intoxication is the calcifying substances. Cholecalciferol or Vitamin D3 pr oducts increase blood calcium concentrations muc h higher than normal. The calcium then deposits in various tissues, disr upting normal function. The major organs damaged are the kidneys, intestines and li ver . Signs of renal and liv er failure and
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Transcript of Rat Poison Intoxication Rodenticide
8/10/2019 Rat Poison Intoxication Rodenticide
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Rat Poison Intoxication (Rodenticide)
Rat poison ingestion is a common occurrence in the household pet. Thereare several different active ingredients and preparation of rat poison. The three mostcommon method of action include the inhibition of vitamin k, calcifyingsubstances and uncoupling of oxidative phosphorylation. Vitamin K is essential tothe function of several coagulation factors. When vitamin K can not be made orutilized in the body it inhibits blood clot formation. Since the blood clot is thefoundation of stopping bleeding, antogonization of this process lead to bleedinginto multiple body spaces and dead if left untreated.
There is a 2-7 day lag period between ingestion and the onset of bleeding,varying between compounds (warfarin, diphacinone, brodifacoum andbromadiolone). But immediate veterinary attention should always be sought assoon as possible, even if ingestion is only partially suspected. If caught early
enough, vomiting can be induced and prevent systemic absorption. Treatmentbefore clinical signs of bleeding is much more effective and less costly thantreatment after bleeding begins. Typically vomitus from dogs that have ingestedone of these compounds is bright blue-green in color.
The most common clinical signs, once bleeding begins, are weakness,lethargy, collapse, pale mucous membranes, panting, an increased respiratoryeffort, possibly perceivable abdominal distention and/or pain to the touch of thechest or abdomen. Emergency veterinary care must be sought immediately whenbleeding is suspected. A presumptive diagnosis by the veterinarian is usually madeby history, possible exposure and documentation of prolongation of the PT
coagulation test. Initial therapy generally involves oxygen supplementation,aggressive fluid therapy, plasma and/or whole blood transfusions, injectable VitaminK administration and other general supportive/symptomatic therapies. Intensivemonitoring is generally necessary over the first 24-48 hours.
Once no signs of further bleeding or systemic compromise are present andthe coagulation times are normal, the patient can usually be sent home on oralVitamin K. The length of time that oral Vitamin K needs to be administered variesbetween products. Generally, at least 2 to 3 weeks of therapy is required. After athat time the Vitamin K is discontinued and a coagulation screen in re-checked intwo to three days after the last supplementation dose. If the screen is normal, no
further treatment is indicated. If there is still significant prolongation, Vitamin Ktherapy is re-instituted for another two weeks, then the PT repeated.
The next most common category of rodenticides to cause small animalintoxication is the calcifying substances. Cholecalciferol or Vitamin D3 productsincrease blood calcium concentrations much higher than normal. The calciumthen deposits in various tissues, disrupting normal function. The major organsdamaged are the kidneys, intestines and liver. Signs of renal and liver failure and
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GI signs begin to be seen 24-48 hours after ingestion. If caught early,treatment to chelate/bind the calcium and potentiate its excretion can be instituted.Even in this situation, the prognosis is fair. If not recognized until the later stages,calcification of the tissues can not be reversed and the prognosis is very poor.
The uncouplers of oxidative phosphorylation (active ingredient Bromethalin)inhibit cellular respiration. At higher doses, the body system usually affected first isthe central nervous system. Thus, the first clinical signs seen include: severeexcitation, tremoring and/or seizing. At lower doses, lethargy, depression,gastrointestinal signs and anorexia predominate. Death occurs with low doses aswell as high, especially if low dose exposure occurs repeatedly. Cats are reportedlymore sensitive than dogs. Either species however must be treated as an emergency.Death ensues from respiratory muscle failure. There are no known antidotes forBromethalin. Treatment is primarily supportive- control of swelling in the brain,oxygen supplementation or ventilation if complete respiratory failure and control ofseizures. The overall prognosis is poor with out prolonged intensive care.
Overall, it is imperative to seek immediate emergency attention if a pet hasingested or is even suspected to have ingested a rodenticide. There are certainlyother types that exist and that a pet may be exposed to. The three mentioned aboveare the most common. Prognosis varies among products, but may be improved byearly veterinary care. If the owner/veterinarian can induce vomiting with in 1 hourof ingestion, absorption may be decreased/prevented and is the best possiblesituation. Additional procedures by the veterinarian to decrease absorption, suchas activated charcoal and cathartic administration, can also improve the prognosis.
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