Submitted by friends of NetPets.Org
Please, contact your veterinarian in case of any emergency!
There are many ways that our feline companions get poisoned. Sometimes by accident, and other times by well-meaning adults. Irreguardless, the most important things to know are what are the signs and what to do if that situation arises.
Over the Counter Drugs:
The use and variety of analgesic drugs has greatly increased in both human and veterinary medicine. This has resulted in an increase in acute toxicoses in pets. Generally, overdoses of over the counter drugs happen either accidentally or may be due to excessive administration by a well-meaning owner.
Aspirin is the world's most extensively used over-the-counter drug, commonly used as an antiinflammatory drug in companion animals. It comes in 80, 325, and 500 mg per tablet strengths. Cats are especially sensitive to the toxicities of aspirin because thay are deficient in certain types of glucuronosyltransferase, including the one that is required for aspirin metabolism. The dose recommended in cats for relief of pain and fever is 10 mg/kg every 48 hours. The toxic dose is 80 to 120 mg/kg for 10 to 12 days.
Clinical signs of aspirin toxicoses in cats are dose-dependant and may include CNS depression, anorexia, vomiting, gastric hemorrhage, toxic hepatitis, anemia, bone marrow hypoplasia, hyerpnea and hyperpyrexia, hyperthermia, hyperglycemia, and glycosuria. Early in the syndrome, respiratory alkalosis may develop secondarily to the salicylate-induced metabolic acidosis. This would cause hyperventilation, which inturn, stimulates renal secretion of bicarbonate.
Thrombocytopenia, anemia, and Heinz bodies are evident in cats with chronic exposure. Elevated sodium and reduced potassium concentrations are characteristic but not diagnostic of aspirin toxicosis. Inco-ordination, loss of balance and falling, hypersensitivity and loss of appetite are also some clinical signs. Vomiting occurs, sometimes it may be bloodstained.
If discovered at home, and is only one tablet, induce vomiting and give water or milk, then take to the veterinarians. The primary treatment for aspirin over dose is gastrointestinal decontamination (within four hours of over dose) using emetics, activated charcoal, and osmotic cathartics. Acid-base imbalance should also be corrected witha slow infusion of sodium bicarbonate, but must be carefully monitored and adjusted if pulmonary edema develops. The resulting hyperthermia should be controlled by external cooling; the use of antipyretic drugs should be avoided. If this is still not enough, or as in a severe acute case of poisoning, peritoneal dialysis with an osmotic alkaline fluid may be needed. Treatment for the gastrointestinal mucosa would include histamine receptor antagonists to control the inflammation.
Acetaminophen is another common household analgesic and antipyretic. It comes in 325 to 500 mg strength tablets and is most commonly purchased under the brand name "Tylenol". It is important to note that acetaminophen is not an antiinflammatory agent in cats or dogs. Cats are extremely sensitive to acetaminophen toxicity. The feline toxic dose is 50 to 100 mg/kg. One regular strength tablet may be toxic to a cat, and a second one ingested 24 hours later may be lethal.
Cats gums are a dirty brown color, difficulty breathing, blood in urine, jauntice and facial swelling would be noticable signs at home. Clinical signs are cyanosis, dyspnea, facial and paw edema, hypothermia, and vomiting. Less common signs include coma, generalized weakness, and death. Normally, methemoglobin is reduced to hemoglobin by glutathione, but in the presences of a toxic amount of acetaminophen, glutathione synthesis is reduced, and insufficient free glutathione is available to reduce methemoglobin and bind the reactive metabolite, consequently, the tissues are starved for oxygen.
1.If ingestion is recent (less than 2 hours), emesis should be induced and activated charcoal administered at 2g/kg along with a saline or osmotic cathartic.
2. If severe cyanosis is present, oxygen therapy should administered, and the animal should be subject to as little stress as possible.
3. IV administration of acetylcysteine, 140mg/kg/hr for 7 hours. Acetylcysteine is a precursor of glutathione, thereby facilitating the detoxification of the reactive intermediate.
4. Ascorbic acid, 30 mg/kg orally to reduce methemoglobinemia to Hb +2 5. Supply supportive care including fluid therapy for possible metabolic acidosis.
Ibuprofen is a common antinflammatory drug for humans. Its action is to block prostaglandin synthetase. Prostaglandins are active in the gastrointestinal tract by decreasing acid production, and stimulating mucus and bicarbonate secretion by epithelial cells. The toxic effect is depends on the dose, number of doses ingested, age of the cat, and many other factors. Currently, it is known that an acute ingestion of 50mg/kg will produce toxic effect.
Cats are extremely sensitive to the toxic effects of NSAIDS due to their higher gastrointestinal absorption rates, longer plasma half-lives, and higher plasma drug concentrations. At home you may see vomiting, depression, anorexia, and diarrhea. The clinical signs are gastrointestinal irritiation, hemmorhage, and ataxia.
Gastric emptying if within two hour of ingestion, followed by administration of activated charcoal and saline. Careful monitoring for development of gastric ulcers or hemorrhaging, and mange as necessary. If gastrointestinal irritation occurs, it can be treated with histamine receptor antagonists such as, cimetidine, rantidine, or omeprazole. Also sucralfate, an ulcer coating agent, metoclopramide, an antiemetic, and misoprostol, a prostaglandin analogue, could also be used if thesymptoms indicated need.
Includes caffeine, theobromine, and theophylline. These are found in coffee, tea, stimulants, medications, and chocolate. Some people do not know the dangers of feeding their cats chocolate, or the cat may get into it if it is left out where they can get to it. A lethal dose varies from 100-300 mg/kg.
Clinical signs develop within one to fours hours after ingestion and include vomiting, diarrhea, polyuria,weakness, hyperexcitability, tremors, seizures, and coma. Secondary pancreatitis amy develop in some animals. Death results from seizures or cardiac arrhythmias.
Treatment includes the administration of emetic agents followed by activated charcoal and a cathartic ifexposure was within the last two hours. Since methylxanthines may undergo enterohepatic recycling,activated charcoal should be administered every 3-6 hour until cat is asymptomatic. Diazepam or phonobarbitol may be used to control seizures. Fluid therapy may be indicated, but steroids should be avoided because they reduce urinary excretion of methylxanthines. The prognosis for a full recovery is generally good with appropriate therapy.
Remains one of the most common causes of poisoning in small animals. Cats like the smell and taste of it, and it only takes 1.5ml/kg for a lethal dose in cats.
Triphasic clinical syndrome. Phase 1 signs include ataxia and a drunken appearance within 1 hour of exposure. Phase 2 is characterized by cardiopulmonary involvment (eg. cardiac failure) and develops 12-24 hours after ingestion. Phase 3 exhibits renal failure, vomiting, depression, renal pain, enlarged kidneys, crystaluria, anorexia, hypothermia, coma, and death.
If discovered within two hours of ingestion, induce vomiting, followed with activated charcoal and cathartics. The use of ethanol and bicarbonate is widely accepted. Ethanol blocks alcohol dehydrogenase activity. This stops the first rate-limiting step of ethylene glycols metabolism to glycoaldehyde by alcohol dehydrogenase. Glycoaldehyde is metabolized to glycolic acid, the primary metabolite for metabolic acidosis, and glyoxylic acid. Glyoxylic acid is further metabolized to oxalic acid, glycine, and formic acid. Fluid diuresis, with furosemide, mannitol, and dopamine, may be required to correct for partial renal failure and/or pulmonary edema. Peritoneal dialysis may be used if acute renal failure occurs. A recent treatment of 4-methylpyrazole is being widely used, however, it does not work on cats. Animals exhibiting clinical signs have a poor prognosis because of renal involvement. Renal tubular regeneration is possible, since tubular basement membranes tend to be spared.
Lead is not a common toxilogical problem but may occur from ingestion of lead-containing dust or paint when they groom their contaminated coat.
Clinical signs of chronic low level poisoning produce gastrintestinal signs, such as vomiting, abdominal pain, anorexia, diarrhea, and megaesophagus. Acute poisoning result in CNS signs, such as convulsions, hysteria, ataxia, tremors, and blindness.
Treatment should include eliminating the lead source, and limiting further gastrointestinal absorption. Magnesium or sodium sulfate can be used to precipitate lead in the intestine and pass through, or chelation therapy may be used with calcium disodium EDTA. Oral D-penicillamine is also a chelating agent often used after calcium disodium EDTA. Both to be used only for 1-2 weeks.
Zinc toxicosis is becoming a larger problem, and can result from the ingestion of zinc nuts (transportation crates), or from ingesting pennies minted after 1983.
Zinc poisoning from elemental zinc results in hemolysis, regenerative anemia, or renal failure. Hypocupremia amy be present, due to the zinc-copper antagonism of absorption in the gastrointestinal tract. Zinc oxide poisoning can occur from the ingestion of houshold products containing zinc oxide such as diaper rash products, rubber products, cosmetics, batteries, soaps, and printing inks. Acute zinc oxide toxicity results in severe vomiting, CNS depression, and lethargy.
Treatment involves removing the source through emensis or surgery, suportive therapy, and chelation therapy with calcium disodium EDTA.
Ingestion of button batteries can cause esophageal erosions due to the release of sodium hydroxide or potassium hydroxide, occurring within 12 hours of ingestion. Also, the batteries may contain mercuric oxide, lithium, cadmium, and zinc.
Clinical signs of mercuric toxicity are CNS stimulation, weight loss, anorexia, and ataxia.
Batteries lodged in the esophagus should be removed endoscopically, and should be followed by chelation therapy with DMSA.
Pesticides are divided into four groups, rodenticides, molluscacides, insecticides, and herbicides. Rodenticides are further divided by their mode of action. The first class is anticoagulants, such as Warfarin, Coumateryl, and brodifacoum. This class of rodenticides acts by interfering with vitamin K epoxide reductase, which is responsible for converting "inactive" vitamin K to its "active" state. An single ingestion of 5-50mg/kg or a daily ingestion of 1mg/kg will result in severe toxicoses. Cats probably not poisoned directly, but may eat rats or mice slowed down by their last meal of the bait.
The clinical signs appear one to four days after ingestion. Clincal signs are depression, weakness, staggering, pallor, dyspnea, coughing, and subcutaneous hematomas, making diagnosis difficult.. Hematemesis, epistaxis, melena, ataxia, paresis, seizures, and sudden death have also been observed.
If the exposure has occurred within the last 24 hours, emetics, activated charcoal, and cathartics are warranted. Once the clotting factors are depleted, aggressive treatment is necessary, since synthesis of clotting factors takes at least 12 hours. The cat is given IV transfusions of blood or plasma and vitamin K. Administering a small amount of fatty food will aid in the absorption of vitamin K. The therapy may continue for up to 28 days depending on the amount of rodenticide ingested.
Another rodenticide is cholecalciferol. In dogs, a lethal dose can be as little as 5mg/kg, indicating an even lower dose for cats. Cholecalciferol has three mechanisms of action, they are;
1)increase absorption of calcium and phosphorus from the intestinal tract.
2) increase osteoclastic reabsorption of bone.
3) increase renal distal tubular reabsorption of calcium, all resulting in persistant hypercalcemia and hyperphosphatemeia.
Clinical signs appear within 12- 36 hours after ingestion, and they are initially anorexia, depression, vomiting, muscle weakness, and constipation. As the disease progresses, hypertension, polyuria, and polydipsia. Mineralization of cardiac and renal tissues eventually lead to cardiac or renal failure.
Treatment, if caught right away is emensis, activated charcoal and cathartis. Howeve, this is not ususally the case. Clinically, furosemide is given to assist in renal calcium excretion, prednisone aids in decreasing both osteoclastic activity and gastrointestinal calcium absorption. Calcitonin is injected subcutaneously every two to three hour to help lower plasma calcium levels, and aluminum hydroxide will help lower plasma phosphorus levels by preventing gastrintestinal absorption. Long term treatment may include a low calcium diet until calcium and phosphorus levels have stabilized.
Another rodenticide is soduim fluoroacetate, "1080." This rodenticide should never be used around any animals, since there is no specific therapy for this toxicosis.
Signs start within 4- 10 hours after ingestion, and they are aimless wandering, confusion, disorientation, unusual vocalization,, vomiting, urination, and repeated bowel movement, progressing to frothing at the mouth, labored breathing, and convulsions. Death from respiratory failure ensues within 2 to 12 hours after onset of signs.
Strychnine can be used as a rodenticide or insecticide, but it is most commonly used maliciously. First signs are apprehension, irritability, tenseness, and stiffness. This progresses to violent convulsions stimulated by loud noises or by touching the cat. Death usually occurs from exhaustion or anoxia during a tetatanic seizure. The entire syndrome, if untreated last less than 2 hours. The cat is only marginally savable if it has not reached the convulsion stage. If not convulsing, induce vomiting immediately, then transport to your vet for further treatment.
Insecticides are further reduced to several groups such as; amitraz, borates, carbamates, citrus oils, insect repellents, organochlorine, organophosphates, pyrethrins and pyrethroids, and rotenines. There are many insecticides, and I will discuss the most common ones.
Amitraz poisoning occurs from ingestion of a tick collar. A toxic dose falls in the range of 10-20mg/kg, and occurs within onehour of ingestion.
Clinical signs occur within one hour of ingestion.
Treatment involves emensis, activated charcoal, and cathartics, or physical retrieval of the collar through endoscopy, and repeated injections of yohimbine to reverse amitraz's adrenergic agonist effects.
Pyrethrins and pyrethyoids are used to treat ectoparasites of cats, dogs and birds. However, if used improperly they will cause severe illness. The primary action is to keep the sodium channel open in excitable cells. The onset of toxicosis occurs within 1 to 4 hours after dermal and subsequent oral exposure.
The clinical signs are depression, hypersalivation, muscle tremors, vomiting, ataxia, dypsnea, and anorexia.
Treatment includes bathing, and a combination of emensis, and activated charcoal. Diazepam or methocarbamol after the cat starts to relax to control muscle tremors and seizures, anf atropine to control hypersalivation. Most animal recover within 24 to 72 hours after exposure. Insect repellent poisoning (deet) has similar signs and similar treatments.
Organophosphates and carbamates insecticides are found in flea collars and snail and slug killers, and are potent inhibitorsof cholinesterase activity.
These insecticides produce three effects: 1)muscarinic (salivation, lacrimation, excessive bronchial secretions, vomiting and diarrhea), 2) nicotinic(muscle tremors, and respiratory paralysis), and 3) CNS(depression, seizures, miosis, and hyperactivity). The recovery depends on the resynthesis of the cholinesterase enzyme.
Treatment of organophosphorus or carbamate poisoning begin with life-saving symptomatic therapy. Atropine sulfate to alleviate respiratory distress, enzyme reactivators that act on organophosphorus cholinesterase complexes to free the enzyme and restore function, but only within first 24 hours of intial binding. Pralidoxime chloride is the widest used reactivator and is given intramuscularly to relieve tremors and other nicotinic signs. However, overdoses or rapid IV administration can cause tachycardia, and cardiac arrhythmias as well as depression.
Borate, or boric acid is used as a homemade insecticide. It has a low oral toxicity.
Vomiting, diarrhea, anorexia, CNS depression, muscle weakness, ataxia, and possible seizures.
The problem with this poisoning is that activated charcoal does not absorb it, the only way to get it out of the system is through dialysis.
Herbicides are not a serious problem for cats because they would have to be outside and eat treated grass. If the weedkiller was of chlorophenoxy type(2,4-D,MCPA) the prognosis is good.
Signs: Gastrointestinal and neuromuscular signs within 12 hours of exposure. Transient anorexia, vomiting, and diarrhea, and with more severe toxicosis, myotonia (disinclination to move).
Treatment is nonspecific and includes decontamination (emensis, activated charcoal, and cathartics), and maintaining normal fluid and electrlyte balance. Prognosis is excellent, with clinical signs abating within 72 hours.
However, if the weedkiller was dipyridyl type(paraquat, diquat), then the prognosis is not very good.
Gut clinical signs appear first, vomiting, abdominal pain, and depression, then 3-4 weeks later respiratory distress signs occur, such as difficulty breathing, rapid respiratory rate, resulting in irreverisible lung consolidation.
Early veterinary treatment is essential. Mineral absorbants such as kaolin or Fuller's Earth can be used to absorb paraquat from the stomach.
Molluscacides(metaldehyde,"defender"), used in gardens, are dangerous for cats, since they find them attractive. A lethal dose is 100-360mg/kg.
Clinical signs develop within three hours of ingestion and include tachycardia, salivation, tremors, and seizures, hyperthermia, diarrhea, and depression. Death may occur within 4-24 hours from rspiratory failure. Death due to liver failure may occur in three ot four days after ingestion.
First treatment is to induce vomiting, then take the cat immediately to the veterinarians.
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