Oleander Is Poisonous To Pets
Nerium oleander, commonly known as oleander, is a widely used decorative evergreen shrub or tree in the dogbane family. The plant is so widely cultivated that no precise region of origin can be identified.
Oleander is noted to have erect stems or branches that splay outward as they mature. The dark-green leaves are paired, or in whorls of three, thick and leathery, size varies between 2 to 8 inches in length and .25 to 1.5 inches in width. At the end of each branch, white, pink or red flowers grow in small cluster. They often, but not always have a sweet scent. Oleander can be either a small bush (under 6 feet tall) or a medium sized tree (around 20 feet) depending upon whether or not it is maintained or allowed to grow wild. In California oleander can be found decorating the center median of hundreds if not thousands of miles of highway; as a result it is often referred to as the ‘favorite roadside decorum’ of the California Department of Transportation.
All parts of the plant are toxic and contain cardiac glycosides oleandrin and nerioside which have a cardiotoxic as well as neurotoxic affect on the body. Many consider it to be one of the most poisonous commonly grown garden plants. Oleander is so toxic that deaths of large livestock have occurred from ingesting as little as few leaves. Controlled experiments have shown that 0.005% of body weight or roughly 10-20 leaves can be lethal for a 1500 lb cow. Human deaths have occurred from using oleander twigs as meat skewers while camping, and dogs have reportedly died from chewing on oleander twigs or sticks and become severely sickened when oleander sticks where used as a fetch toy.
The toxins are not destroyed by drying or heating, as a result both fresh and dry plant material as well as the smoke from burning plant material should be avoided. Cattle and horses are the most commonly poisoned animals, most often due to an owner unknowingly allowing the animals access to a field or pasture with oleander or unwittingly placing plant clippings in an area that animals can access. As is the case with some other poisonous plants, oleander is on occasion unknowingly cut down with a field and subsequently dried and bailed with hay or chopped into silage for cattle feed. If possible always inspect hay for signs of unknown plant material and/or purchase hay from a reliable and reputable source.
The signs of intoxication will vary depending upon what species is involved and how much plant material was ingested. The most consistent early symptom across all species is diarrhea with or without blood. Other commonly shared symptoms include anorexia, depression, and excessive salivation (drooling). Dogs and cats will often times have extensive vomiting in conjunction with one or all of the above symptoms. In horses, colic is a common symptom. In more severe cases, it can be expected that than an animal would have any combination or all of the above and cardiac arrhythmias. As the intoxication progresses from bad to worse, animals may display a weak pulse, decreased GI motility, congested mucus membranes, and slow capillary response times (indicative of shock); various arrhythmias, including AV block, ectopic beats, and gallop rhythm with dropped beats; cold extremities, tremors, mydriasis, progressive paralysis, coma, and eventually death. There is no specific treatment once a toxic dose of the plant has been eaten. Symptomatic treatments are often attempted but are usually unsuccessful.
Developed by the California Animal Health and Food Safety Laboratory, there is a test that can detect oleandrin, one of the toxic elements in oleander, in the rumen or cecal contents as well as feces and milk of animals. Although very helpful in determining whether or not a poisoning is the result of oleander when the actual leaves cannot be found, this test is most often performed post mortem. While this may not aid the actual victim at hand, it can provide owners with the knowledge that oleander is or was present as a food source and allow them the opportunity to safeguard any other livestock they may have.
The prognosis for animals that have ingested oleander is going to depend on the amount that was ingested, and the time that has elapsed since the ingestion. In general, for animals that have ingested a large amount (if not detected very early) the prognosis is poor to grave. For animals that may have ingested a small to moderate amount, or in cases where the ingestion was detected early and treatment administered, the prognosis can range from good to guarded. There is no specific treatment available for counteracting the effects of the cardiac glycosides present in oleander. As a result, in many cases even with prompt veterinary treatment the animal will still die. Treatment is going to be symptomatic and supportive. For dogs and cats, vomiting should be induced as soon as possible. This can be accomplished using an emetic such as 3% hydrogen peroxide at dosage of 1 teaspoon per 10 lbs of body weight. Although not practical in the home or a field setting, gastric lavage commonly called stomach pumping or gastric irrigation should also be given consideration as a treatment option. Activated medical charcoal (2-5 g/kg body weight) may also aid in preventing further absorption of the toxins by the body. The use of activated charcoal, given as a single dose or as multiple doses has provided conflicting results in studies conducted on animals that were experimentally poisoned. As a result no recommendation can be made for or against the use of multiple doses of activated charcoal. For cattle, sheep and goats a rumenotomy to remove all traces of the plant from the rumen may be lifesaving.
If the poisoning is severe continuous ECG monitoring for at least 24 hours will be necessary to detect arrhythmias. Cardiac irregularities may be treated using antiarrhythmic drugs such as potassium chloride, procainamide, lidocaine, dipotassium EDTA, or atropine sulfate. Atropine is the most widely used agent in treating bradycardia. However there is no evidence that atropine is beneficial in treating oleander induced bradycardia. Accelerating the heart rate with atropine or other beta-adrenergic agents theoretically increases the risk of tachyarrhythmias; which have a poorer prognosis and are more difficult to treat. Some have claimed that atropine increases tachyarrhythmic deaths, although further studies are required to confirm this. Lidocaine is often the preferred antiarrhythmic; the role of intravenous magnesium is uncertain.
The use of fructose-1,6-diphosphate (FDP), also known as Harden-young ester has effectively prevented hyperkalemia, reversed dysrhythmias and improved hemodynamics and restored sarcolemmal Na(+)-K+ ATPase activity in dogs experimentally poisoned with oleander at the University of Mississippi. Due to the fact that hyperkalemia is a common by product of oleander poisoning, the use of potassium in intravenous fluids should be avoided and serum potassium levels should be monitored closely.
Correction of dehydration with intravenous saline is often necessary, and antiemetics may be used to control severe vomiting. However, fluids containing calcium should not be given as calcium augments the effects of cardiac glycosides. Poisoned animals should be kept as quiet as possible to avoid further stress on the heart.
The use of digoxin-specific antibodies such as Digoxin Immune Fab (Ovine); a digitalis antidote made from the immunoglobulin fragments of sheep immunized with a digoxin derivative, has shown positive results in cases of human oleander poisoning, but has not found application in animal poisonings as of yet. It works by binding to the digoxin, rendering it unable to bind to action sites on target cells. These bound complexes accumulate in the blood, are filtered by the kidneys and finally expelled by the bladder.
In many cases the most telling sign that an animal may have ingested oleander is finding the animal dead in or around an area in which they had access to the plant. The onset of clinical signs is usually rapid and most animals will be in obvious distress within an hour to a few hours of eating the plant. From the onset of clinical signs death may occur very rapidly (minutes to hours) or be delayed a few days. Most often, a fatally poisoned animal will become progressively paralyzed, enter a coma and die. In most cases death occurs in less than 24 hours. Treatment is routinely not successfully. Prevent further ingestion of the plant and seek veterinary care.
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