Rat Poison (Rodenticide Toxicosis) in Cats and Dogs

Dr Michelle Safranek BVSc, PG Dip (Vet Clin Sci)

There are three main types of rodenticides used to eliminate unwanted pests in our homes. These include anticoagulants, cholecalciferol and neurotoxins. The former two are commonly used in South African households. Clinical signs vary according to the type of rodenticide. Treatment regimes differ depending on the active ingredient. Anticoagulants have a readily available antidote, namely Vitamin K. The other rodenticides are more toxic and have no antidote.

ANTICOAGULANTS

The clotting of blood requires important clotting factors to make fibrin which helps platelets properly clump together into a permanent platelet plug on a wound to stop the bleeding. Clotting factors already present in the blood degrade naturally and are used up slowly over time. Clotting factors, like prothrombin, require Vitamin K for the liver to manufacture (synthesize) them. In basic terms, anticoagulants cause bleeding because they stop Vitamin K from being recycled and block Vitamin K-dependant synthesis of clotting factors.

Clinical signs of anticoagulant rodenticide toxicity are not evident immediately, but require at least 3 to 7 days to show up, but may take up to three weeks. This is because it takes several days for the liver’s stores of Vitamin K to be depleted, but after it is used up and there is no more Vitamin K available, the bleeding cannot be stopped, and even the slightest bump or minor trauma can lead to life-threatening bleeding.

The clinical signs may include:

• Weakness, lethargy
• Pale gums (palor), bleeding gums (petechiae), bruises (ecchymoses)
• Coughing up blood (haemoptysis), nosebleeds (epistaxis)
• Difficulty breathing (dyspnoea) due to internal bleeding into the chest cavity (haemothorax)
• Swollen abdomen due to internal bleeding into the abdomen (haemabdomen), and even death

Common anticoagulant active ingredients are: difethialone (first generation), brodifacoum and bromadiolone (second generation), amongst others. Most of these products include green or blue dyes, sometimes red, and may be present in your pet’s vomit or faeces. Second generation anticoagulants are more toxic and longer lasting than first generation anticoagulants, requiring longer treatment.

Treatment starts with emesis (vomiting). Usually, vomiting can be induced within the first 2 hours of ingestion, before food passes out of the stomach. Further treatment includes administering activated charcoal with a laxative to help bind and excrete the toxin which has already been absorbed by the stomach and that undergoes enterohepatic recirculation (recycling via the gut-liver-cycle).

Not all cases of suspected ingestion of anticoagulants require the antidote. Your vet will assess each case on its merits. In obvious cases of bleeding with a known history of anticoagulant rodenticide, Vitamin K, may be administered. Vitamin K is a fat soluble Vitamin, so it should be administered to your pet with a fatty meal to improve absorption, and should not be dosed with the activated charcoal, but about 2 hours before.

In unclear cases, your vet may need to do further tests to rule out any other causes of bleeding problems (haemorrhagic diatheses) or anaemia. For suspected anticoagulant rodenticide cases, the pet’s clotting factors can be tested and if the prothrombin time (PT) is abnormal, Vitamin K may be administered. Vitamin K therapy is lengthy and expensive, often requiring 2 to 4 weeks of treatment, or longer, based on monitoring your pet’s PT test, and only once the PT test is normal will the poisoning be resolved. During monitoring, the PT test is done 48-72 hours after completing the Vitamin K course of treatment. Therefore, it is important to keep follow-up appointments with your vet. Continue to closely monitor your pet if they are on home therapy, and take them back to the vet if any clinical signs recur (e.g. palor, lethargy, bleeding).

In more serious cases of blood loss, your pet may additionally require a blood transfusion (to replace the red blood cells), and/or a plasma transfusion (to replace the clotting factors) in hospital. Although these transfusion may be life saving in such cases, they are temporary, costly and there is risk of complications, like anaphylaxis, especially if more than one transfusion is necessary. It is important to disclose to your vet any chronic medication that your pet may be on (such as anti-inflammatories or pentosan polysulphate), as these may complicate your pet’s therapy and interfere with normal blood clotting.

CHOLECALCIFEROL

Cholecalciferol, also known as Vitamin D3, is metabilised by the body into its active form, calcitriol. Vitamin D3 and its metabolites increase the absorption of calcium and phosphorus from the gut, increase reabsorption of calcium from the kidneys, and increase calcium resorption from the bones. The resulting high levels of calcium (hypercalcaemia) causes dystrophic calcification (pathological mineralisation) in the kidneys, gastrointestinal tract, and other organs. This manifests as acute kidney injury (AKI),  gastrointestinal ulceration, and even death.

Clinical signs of cholecalciferol toxicity usually present within the first 8-12 to 72 hours after ingestion, but can take longer, and may include:

• Lethargy, weakness, anorexia
• Increased thirst (polydipsia), increased urination (polyuria), dehydration
• Vomiting, abdominal pain, vomiting up blood (haematemesis), passing digested blood in the stool (malaena)
• Infrequently, muscle twitching, seizures, pulmonary haemorrhage, and rarely bradycardia

Other causes of hypercalcaemia in dogs, may include chronic kidney disease, lymphoma or endocrine diseases, and less likely accidental ingestion of human Vitamin D supplements.

Cholecalciferol has a narrow margin of safety in dogs, which means that even a low dose may cause clinical signs or even death, and therefore treatment should be proactive. Treatment in cholecalciferol toxicosis also starts with inducing vomition within the first 2 hours. Your vet will advise baseline bloods for calcium (Ca) and phosphorus (Phos), and if they are high (or the Ca x Phos product is above a certain threshold), aggressive treatment is needed. Activated charcoal is administered for enterohepatic circulation with lactulose every 4 to 6 hours over 24 to 48 hours. Further treatment may include the following:

• Bile acid binding resins have proved useful because cholecalciferol is excreted mainly in the bile and faeces.
• Intravenous saline diuresis competes with, and prevents reabsorption of Calcium.
• Intralipid emulsion may be used early in the course of the disease because cholecalciferol and its metabolites are fat soluble.
• Furosemide inhibits Calcium re-uptake in the kidneys.
• Glucocorticoids may be considered because they increase renal Calcium excretion, and decrease intestinal Calcium uptake.
• If Calcium levels are not responding to initial measures, biphosphonates may be used.
• Phosphate binders may be used to decrease high Phosphorous/phosphate levels, and renal diets are fed which are low in Calcium and Phosphorous/phosphate.

Renal parameters, electrolytes, urine specific gravity, Calcium and Phosphorous/phosphate values are monitored over time e.g. 0, 12, 24, 48, 72, 96 hours, then weekly. Therapy is intensive, costly, and not without complication. Feeding tubes are placed in anorexic patients with the addition of antinausea medication and gastroprotectants. Hospitalisation may be as little as four days for cases with good outcomes (prognosis), but several weeks for severe or advanced cases. Prognosis is poorer in cases of prolonged hypercalcaemia, renal failure or soft tissue calcification.

NEUROTOXIN

Bromethalin, a neurotoxic rodenticide, causes sodium accumulation in the cells by disrupting oxidative phosphorylation in the brain and liver, and can result in swelling of the central nervous system (CNS) and brain (brain oedema) because it increases cerebrospinal fluid pressure. Clinical signs are dose-dependent, and the onset depends on the amount ingested, and may show within 2 to 24 hours.

Clinical signs may include:

• Depression or CNS stimulation (hyperexcitability)
• Unsteady gait (ataxia)
• Abnormal behaviour, increased sensitivity to sensory stimuli (hyperaesthesia)
• Tremors, paralysis, seizures, and coma

Treatment may be intensive and includes early decontamination (e.g. emesis induction, administering activated charcoal); preventing brain oedema (e.g. administering mannitol), and supportive care (e.g. intravenous fluid therapy, oxygen support). The prognosis is fair to good with appropriate treatment before the development of clinical signs, but a poorer prognosis for persistent seizures or paralytic syndrome.

What to do?

If you suspect that your pet ingested rat poison, take them to your vet immediately and bring the poison bait product packaging information as well to identify the specific active ingredient to help best treat your pet. It is important to know what poison was ingested.

Your vet will discuss options with you and most likely advise to induce vomiting in your pet – the first step of decontamination to try reduce the risk of toxicity. Further treatment and hospitalisation depends mainly on the active ingredient, the amount ingested, the time since ingestion, and the severity of clinical signs.

The amount of active ingredient ingested relative to the weight of your pet, and the time frame since ingestion, are all factors in determining the relative risk of toxicosis and the development of complications. Some rodenticides may contain more than one type of active ingredient, for example, coumatetralyl (an anticoagulant) and cholecalciferol. Therapy in such cases is likely to be more complicated and intensive.

Sometimes, a diagnosis may be difficult to ascertain at initial presentation, especially when clinical signs are vague (i.e. lethargy) or there is no history of exposure to rat poison. Therefore, your vet may need to do further tests to exclude other causes of anaemia or bleeding or hypercalcaemia.

General considerations

Rodenticides are designed to kill mammals, and may be lethal to your pets, and even humans (children), so beware of false claims that rat poison is pet friendly or “eco” or safe for pets. No rat poison with these active ingredients is safe for pets, even if placed in tamper-proof bait boxes because the rodent may pick up a piece of bait and carry it out of the box and drop it along their path for a pet to accidentally ingest. Please find out or enquire what poison is being used in the bait stations in case of accidental ingestion.

If you are moving into a new home or spring cleaning your own home, take care to keep pets safely away in the interim, as rat poison bait may be discovered that was hidden by previous owners or forgotten. Dogs are especially quick to grab and ingest non-food or toxic items. Keeping them safely away, may prevent accidental ingestion. Find out what type of rodenticide (active ingredient) the poison company, the neighbourhood or body corporate use. This key information is vital for your vet to treat your pet if affected.

Rodenticides should be used only as a last resort, and if used, homeowners need to practice extreme caution when choosing to control rodents in this way. When dealing with a rodent problem it is best to consider all alternative, non-toxic approaches in rodent control to prevent unintentionally poisoning pets. These include the use of natural predators (e.g. cats and owls), and maintaining a tidy household. Rodents are attracted to places with overgrown vegetation, easy access to refuse or pet food or bird seed, they nest in storage areas, and hide in places like cluttered garages, inside roofs and cellars.

Dogs are more likely than cats to eat rat baits accidentally. Puppies are more susceptible to cholecalciferol toxicity, whereas cats are more resistant. Cats are more sensitive than dogs to bromethalin. Both dogs and cats may be affected by secondary poisoning if they eat rodent prey that have ingested rodenticides, but it is rare, and more likely in a hunter that relies heavily on rats for food (e.g. a barn cat). Although, some of these bait products may contain a bitter substance to prevent accidental ingestion by humans or pets, our practice still sees cases amongst puppies and dogs.

Useful contact

Please call your vet at Bryanston Veterinary Hospital (011) 706 6023.  

BVH does not advocate (or advise) use of rat poisons

References

Bates, N. 2017. Vitamin D toxicosis. Companion Animal. 22 (12): 700-6.

Cote, E. 2015. Clinical Veterinary Advisor Dogs and Cats. 3rd ed. Elsevier. Missouri.

Ettinger, S.J. et al. 2017. Textbook of Veterinary Internal Medicine. 8th ed. Elsevier. Missouri.

Morrow, C. 2001. Cholecalciferol Poisoning. Vet Med. 30 (12): 905-11.