Answer: Dead dog.
This is a hard way to start an article to be read by dog lovers, but the reality is this: If you are not prepared to treat poisoning resulting from ingesting a toxic substance, you lose. Not only do you lose, but your dog dies. Acute poisoning requires accurate assessment. The threat is not only related to the potency of the poison, but also to the quantity consumed, the duration of exposure, and to the presence of other active ingredients, such as adjuvant and solvents. The difference between immediate appropriate action and delayed response is the difference between life and death. To this end, the authors advocate that a significant effort be made to be prepared for what might happen, given the environment in which you keep your animals. Being prepared means not only having antidotes and treatment materials on hand, but it means being familiar with the signs and symptoms of poisoning, and knowing what risks are in your dog's environment.
The first step in treating poisoning is prior knowledge. You have to be able to recognize that there has been a poisoning. Symptoms vary significantly from animal to animal, from substance to substance and with the amount ingested. You must be accurate in your differential diagnosis. To treat based on the wrong diagnosis is to increase the probability of death. The second step intreating poisoning is prior knowledge. You have to know the poisons that are in your dog's environment. So many potential poisons are readily available, it is truly amazing more dogs are not poisoned. The third step in treating poisoning is prior knowledge. You must know the immediate actions required, which can include artificial respiration/resuscitation. If you are picking up on a trend here, it is intentional. Because there may be little time in which to reflect on or to research the subject, or to find a veterinarian because of time of day, or distance from a veterinary facility, etc., the owner who is not equipped with the knowledge of the symptoms, the effects of various poisons, and what treatment regimen goes with what poison, stands a very good chance of losing the dog. Remember, also, that not all poisonings are accidental.
One excellent way to think of poisoning in dogs is to relate it to poisoning in human children. Whatever poisons are available for a child to ingest, are also available to poison a dog. Children and dogs tend to be attracted to many of the same things. For example, a dog walking through antifreeze might lick its paws afterwards, much as a child might put its fingers in its mouth after playing with an attractive looking puddle of green stuff on the driveway.
Potential dangers in the child's environment tend to be the same as in the puppy's environment. According to the Agency for Toxic Substances and Disease Registry of U.S. Department of Health and Human Services,the element lead is first on the prioritized list of 275 toxic substances. (1) The poisoning of greatest concern for children is lead poisoning. That poisoning is also one of the great concerns for puppies who may chew surfaces painted with lead based paint. Since 1978 Federal regulations control use of lead in paint and other products; however, there are enough old products in your dog's environment to constitute a very real hazard. Morgan, et al, looked at lead poisoning in 347 companion animals.(2) Ramsey, et al, concluded that succimer (meso- 2,3-dimercaptosuccinic acid) administered orally for 10 days, effectively reduced blood lead concentrations and eliminated clinical signs of lead poisoning.(3) Berny, et al, concluded that paint was the most common source of lead poisoning in dogs (537 cases) in Europe and North America 1985-1989.(4) One of the more common sources of lead is in copper water pipes with lead solder joints. In 1988, Congress banned using pipe with more than 8% lead and the use of solder with more than 0.2% lead. Note that carbon, sand and cartridge water filters do not remove lead. Only areverse osmosis system removes lead. It is commonly believed that significant amounts of lead are present in soil and in various sources of dust that have accumulated from years of vehicle emissions from leaded gasoline.
Over time, as lifestyles change, the types of toxic substances available to companion dogs have increased significantly. Lead is not the only hazard. Household cleaners are notoriously toxic. Just think’Tidy Bowl® does to your dog just what it does to that which you want it to remove from the toilet bowl. Similar effects may be expected with Draino® and other drain cleaners. For most households, the area under the kitchen sink, with its cleaners, polishes and dishwasher soaps, is a chemical warfare zone waiting to happen. Likewise, the garage with its paint removers, carburetor cleaners, antifreeze, bird repellents, insecticides, rodenticides, snail bait, herbicides, fertilizers and concrete driveway cleaners, is a dangerous place, indeed, for the inquisitive puppy. Figure 1. lists easily accessible ingestible poisons and their sources. As if this were not enough, many common household and garden plants are extremely toxic. It is a wonder that more dogs and children are not poisoned. The opportunity is there. The best way to treat poisoning is to prevent access to toxic substances. While this sounds good at first, it is not always possible to do, as will become quickly evident when scanning the Figure 2. list of toxic plants. Even the landscape timbers edging the flower beds tend to be toxic, having been "preserved" to prevent termite infestation and wood rot. The mole holes may be poisoned with strychnine, out of reach of your dog. The mole, however, may die above ground and be scavenged by the dog. Strychnine, whether or not in a mole, is strychnine nonetheless.
The medicine cabinet is another major repository of doggie-killing substances. Over the counter analgesics/NSAIDS are responsible for many poisonings, and are not safe for dogs, except in very narrowly defined amounts. The following are presented to make the point that commonly available over-the-counter drugs often given to dogs by their owners are potentially dangerous at some level of ingestion. The Georgia Animal Poison Information Center over a 19 month period, 1989-1990 documented 240 cases of NSAID toxicosis through administration by owners or accidental consumption of improperly safeguarded drugs.(5) The most common cases were ibuprofen, acetaminophen, aspirin and indomethacin.
Aspirin (salicylic acid)’toxic doses disrupt the acid/base balance and may result in metabolic acidosis (low blood pH) or compensated respiratory alkalosis (high blood pH). Symptoms include restlessness, hyperventilation, deafness, tachycardia (rapid pulse), nausea, vomiting, hyperthermia (high temperature), dehydration, pulmonary edema (abnormally large amounts of fluid in intercellular tissue spaces), acute renal (kidney) failure, hypokalaemia (less alkaline than normal), hypoglycaemia (abnormally low blood glucose levels), hypothrombinaemia (deficiency of thrombin in blood’leads to abnormal bleeding). Stupor and coma are indications of severe poisoning. Pepto- Bismol®, commonly used to combat upset stomach and diarrhea, also contains salicylates (aspirin), and must be evaluated for use with all of its active ingredients in mind.
NSAIDS’are non-steroidal anti-inflammatory drugs with narrow safety ranges. Acute poisoning may produce symptoms of nausea, vomiting, epigastric pain, deafness, dizziness, and oliguria (diminished urine output relative to fluids intake). Apnea (cessation of breathing) and near coma, hepatic (liver) and renal (kidney) failure are possible. Mefenamic acid preparations (Ponstel®) are prescription NSAIDS used to treat moderate pain and dysmenorrhea and may cause convulsions in overdose quantities. Note: acetaminophen is found in many over-the-counter products with antihistamines and decongestants (Co-Tylenol®, Nyquil®, etc.).
With the advent of widespread drug abuse, it is not uncommon to find dogs getting into "the stash" with the result that dogs, too, overdose. Opiates remain the ultimate drug of choice for abusers, however cocaine and barbiturates and steroids are also commonly abused. Respiratory depression is the most important toxic effect of the opiod analgesics, and death is common from respiratory arrest. Symptoms include drowsiness ("on the nod"), coma, shallow respiration or apnea, miosis (excessive contraction of the pupils), hypotension (lowered blood pressure) and hypothermia (low body temperature).
This article contains a number of charts and tables. It is not practical to memorize them; therefore, we suggest that you save this article and keep it handy in your "dog medicine" cabinet for reference in case of poisoning. Probably the easiest way to think of poisons is by category. This organization makes it possible to treat a class of poisons with relative confidence, even when the identity of the exact poison is unknown. Figure 1. Lists the categories we have found helpful. Please note that common classification schemes are ordered by symptom, by treatment, or by mechanism of poisoning. For the dog owner, who rarely treats for poisoning, diagnosis by category of poison is probably the most important information that can be given to the attending veterinarian. We recommend that you keep a copy of Michelle Bamberger, D.V.M.'s book Help1 The Quick Guide to First Aid for Your Dog, Howell Book House, NY, and the revised and expanded Dog Owner's Home Veterinary Handbook, by D.G. Carlson and J.M. Griffin, put out by the same publisher. Books are nice, but if you really need help and you are unsure of the situation, the telephone number for the National Animal Poison Control Center run by the American Society for Prevention of Cruelty to Animals, is the number to call. This non-profit database is maintained by Dr. Louise M. Cote and her husband Dr. W. M. Buck. There is a $30 fee for a consultation. It is worth every penny, as these two veterinarians are the premier consulting toxicology veterinarians, and have thousands of successful interventions under their belts. Their number is 1-800-548-2423/1-900-680- 000 and a direct line to Dr. Cote is (217) 333-2053.
Being prepared also means that you must have certain supplies on hand. The absolute minimum is: Syrup of Ipecac, 3% hydrogen peroxide, activated charcoal and vegetable or mineral oil. Some breeders also keep Valium® on hand to reduce convulsions, or to take themselves, we are not sure which. Author Cargill routinely keeps a blood volume expander and IV kit to treat for shock. If you are comfortable with starting an IV, nothing beats extra blood volume in preventing shock or dehydration. If a dog is on a farm where concentrated agricultural pesticides are mixed, it might be worthwhile to keep atropine and 2-PAM in case of organophosphate poisoning. Crop dusters regularly stock atropine auto-injectors (like those used by military when under chemical threat) and 2-PAM in case of accidents. Organophosphates do not have to be ingested. They work quite nicely on contact. The lethality of modern toxins is such that the niceties of having a veterinarian administer all treatment is overcome by events and a lack of time in which to respond.
When a dog has been poisoned, it will often present with drooling, vomiting, fatigue or weakness and convulsions. While many things will make a dog drool, vomit, be tired or have convulsions, this combination in an otherwise healthy animal, not known to have central nervous system problems from trauma, high fever or distemper, etc., is immediately suggestive of poisoning. Following is a listing of categories of poisons and their associated treatments. The immediate first aid generally breaks out into two protocols:
- Corrosives--do not induce vomiting, give some oil orally.
- Non-corrosives--induce vomiting followed by gastric lavage and/or activated charcoal slurry.
Gastric emptying is not controversial, but Pond, et al, in a prospective randomized controlled trial of 876 humans, aged 13-82, presenting with overdoses occurring within twelve hours prior to presentation, concluded that there was no apparent benefit of gastric emptying in drug overdose patients.(6) They recommend that gastric emptying be omitted in adults with acute oral overdose, to include those presenting shortly after ingestion and exhibiting severe signs and symptoms. On the other hand, Teshima, et al, determined that induced vomiting could recover 42-65% of acetaminophen ingested.(7) The American College of Emergency Physicians (ACEP) recommends keeping Ipecac syrup for inducing vomiting and activated charcoal for gastric lavage.(8) Similarly, Bamberger in Help! The Quick Guide to First Aid for Your Dog, recommends the use of 3% hydrogen peroxide, 1-2 teaspoons by mouth every 15 minutes until vomiting occurs; or syrup of ipecac, 2-3 teaspoons by mouth, given once. For dogs with "cast iron" stomachs that do not respond to hydrogen peroxide, ipecac or soapy water, your vet may try Apomorphine. After vomiting, follow with activated charcoal mixed with water to a slurry consistency (1 teaspoon for dogs <25 lbs., 2 teaspoons for dogs >25 lbs.)(9) A quick survey of medical and veterinary texts yielded generally the same recommendation as Bamberger.
With the above caveat having been made, we will address the various categories of poisons and their related treatment protocols. Common examples are given following the category name. Please note that it is impossible to provide a comprehensive list of products in each category, and some products contain more than one active ingredient. For example, there are many aspirin combinations, and many narcotic combinations.
"Do not induce Vomiting" poisons:
Acids’Do not induce vomiting; rinse mouth and any other areas which came in contact with the acid; give 1-2 tablespoons of cooking or mineral oil. Alkalis (Laundry detergents, ammonia, paint removers)’Do not induce vomiting; rinse mouth and any other areas which came in contact with the acid; give 1-2 tablespoons of cooking or mineral oil.
Petroleum distillates (Gasoline, paint thinner, charcoal lighter,l)’Do not induce vomiting; rinse mouth and any other areas which came in contact with the acid; give 1-2 tablespoons of cooking or mineral oil.
Stinging nettles (Bull nettles, nettle spurge, etc.)’ Do not induce vomiting; rinse mouth and any other areas which came in contact with the acid; give 1-2 tablespoons of cooking or mineral oil. Note: may exhibit slow and irregular pulse.
"Induce Vomiting" poisons:
4-Aminopyridine (Avitrol®, 4-AP)’4-AP is an extremely toxic white powder sometimes used as a bird repellent. The cries and excited behavior of affected birds frighten away other birds. Symptoms include excitability, increased salivation, tremors, uncoordination, convulsions, and cardiac or respiratory arrest. If responsive, induce vomiting; give activated charcoal slurry. Seizures may require anti-convulsant medications.
Anticoagulant rodenticides (Vitamin D3, brodifacoum [d-Con® Mouse Pruff II, Enforcer® Mouse Kill, Havoc® Klerat®,Ratak Plus®, Talon®, Volid®], bromethalin[Bromathone®, Contrac®, Hot Shot® Sudden Death®; Ratimus®, Tamogen®11, warfarine [d-Con®]) Vomiting, abdominal pain, bloody stool, lethargy. If ingestion has occured less thn 12 hours you may induce vomiting; give activated charcoal slurry. Follow-up care: Vitamin K treatment by veterinarian. The new generation of rotenticides can persist in the body for up to six months, as the liver keeps changing them to another form of antioagulant, therefore treatment should continue for at least six months.
Anti-depressants (Amitriptyline [Elavil®], amoxapine [Ascending], despriamine, dexfenfluramine [Redux®],doxepin, fluoxtetine [Prozac®], imipramine, nortriptyline [Aventyl®, Pamelor®], phenelzine [Nardil®], protiptyline [Vivactil®], sertraline [Zololft®], trimipramine, trancypromine[Parnatel®], valproate [Depakote®], venlafaxin [Effexor])’Anti-depressants are now some of the most widely prescribed drugs and Redux®, in particular, is being widely used as an appetite suppressant. Overdose symptoms include drowsiness, agitation, hyperactive reflexes, muscle twitching, rigidity, convulsions, respiratory depression, coma, hypotension (low blood pressure), arrhythmia (irregular pulse). Induce vomiting if responsive; give activated charcoal slurry. Treat seizures with diazepam (Valium®). Arousal using toe pinches can keep them from drifting into coma while on the way to the vet.
Arsenic (Herbicides, insecticides)’Induce vomiting; give activated charcoal slurry; antidotes are available from veterinarians. The follow-on treatment is beyond home care.
Aspirin and salicylates (Alka-Seltzer®, Anacin®, Axotal®, Bufferin®, Excedrine®, Fiorinal®, Norgesic®, Talwin®)’Induce vomiting; give activated charcoal slurry. Follow-on veterinary treatment may include giving sodium bicarbonate to cause alkalinisation of the urine (alkalinuria) to increase excretion of salicylates. Antacids may be required to counteract gastric irritation.
Barbiturates (butabarbital [Butisol Sodium®],hexobarbitone, methobarbital [Mebaral®], pentobarbitone, secobarbitone), pentobarbitol [Nembutal®], thiopental sodium [Pentothal®], phenobarbital [Antrocol, Belladenal®, Donnatel®, Primatene®, Quadrinal™, Tedral®, secobarbitol’Characteristic signs and symptoms include drowsiness, ataxia (failure of muscular coordination), confusion, stupor and coma. Deaths may occur from cardiac and respiratory arrests. Induce vomiting; give activated charcoal slurry. Hypotension may be corrected by various blood volume expanders. Vasoconstrictors, such as dopamine or dobutamine may be required to increase blood pressure. In extreme cases, charcoal hemoperfusion may be required.
Bufo sp. Toads’Some 16 species of bufo toads are found around the world. Bufo alvarius (Colorado River toad) is found in the Southwest, and Bufo marinus is found in Florida and Hawaii. Bufo's are attracted to dogs' watering dishes, and may sit in the rim long enough to leave enough toxin to make a dog ill. Untreated death rate, especially for Bufo marinus may approach 100%. Dogs may mouth bufo toads, thus getting a large dose of the bufo's toxins, secreted from the skin and paratid glands. Symptoms generally include profuse foamy salivation that looks like shaving cream, difficulty breathing, convulsions, paralysis, ventricular fibrillation, vomiting, cyanosis, and hallucination. Author Cargill had experience with an adult Doberman bitch, Kiku, and a Bufo marinus several years ago while in Hawaii. She salivated profusely, had labored breathing, an irregular heart beat, and the wildest-looking eyes ever seen in a Doberman. It took her the better part of a day and a night to recover untreated. Treatment involves dealing with three poisoning mechanisms: cardiac glycoside effects, pressor (tending to increase blood pressure) effects and hallucinogenic effects. Emesis (vomiting) may be indicated if there was a recent substantial ingestion and the dog is sufficiently alert. Repeated oral charcoal doses (every 2-6 hours) may help reduce the duration of poisoning. A saline cathartic or Sorbitol™ may be given with the first charcoal dose. Intravenous insulin, glucose, and sodium bicarbonate may be required to combat life-threatening hyperalalkemia (elevated serum pH levels). Atropine, phenytoin and lidocane may be useful in the management of bradycardia (abnormally slow pulse) and other cardiac irregularities. Cholestryamine may enhance elimination of bufagin (one of the several bufo venon toxins). Bufo toads are not all that uncommon in some parts of the nation, but very serious business, indeed.
Carbamates (Insecticides’Carbaryl®, Sevin®, Propoxur®)’’Induce vomiting; give activated charcoal slurry; atropine administration should be started as soon as possible under the supervision of a veterinarian.
Calcium cyanamide (Cyanamide, nitrolime)’used as a fertilizer, insecticide and herbicide. Note: cyanamide has different toxic properties than cyanide. Symptoms are vertigo, dyspnea (difficult or labored breathing), tachycardia (abnormally quick pulse), hypotension. Induce vomiting, give activated charcoal slurry and Sorbitol™. Note: atropine is not antidotal. Give IV fluids (plasma or blood) if needed and vasopressor drugs if necessary.
Chocolate’Confectionary chocolate and dogs do not mix. While chocolate is not poisonous, theobromine which is found in chocolate is. Theobromine triggers epileptic seizures in susceptible animals, and can cause cardiac irregularity leading to myocardial infarct and death. Additionally, chocolate irritates the gastrointestinal tract, even to the extent that it causes such internal bleeding that it can kill within a couple of days. Induce vomiting; give activated charcoal slurry.
Cyanide (Rodenticide)’Cyanide is one of the most rapidly acting of all poisons with death occuring in just a few minutes. Symptoms usually appear within seconds to minutes after exposure, and include giddiness, palpitations, dyspnea, loss of consciousness, convulsions and death. If responsive, induce vomiting; give activated charcoal slurry. Administer 100% oxygen as soon as possible as oxygen contributes to the reversal of the cyanide-cytochrome complex. Antidotes include dicobalt edetate (Kelocyanor®), amyl nitrate, and a sodium nitrate and sodium thiosulphate solution (Trypac-Cyano®).
Ethylene glycol ( Antifreeze, color film processing solutions (diethylene glycol) , heat-exchange fluids, ice-rink freezing equipment, as well as in windshield deicer, brake, and transmission fluids)
Quick treatment is necessary to prevent the formation of toxic metabolites. Symptoms are s imilar to alcohol intoxication and include staggering (ataxia), excessive thirst, (polydipsia), excessive urination (polyuria), nausea, vomiting. If treatment is provided less than 4 hours after ingestion, absorption can be prevented through emesis (vomiting) and gastric lavage (stomach wash). After that, metabolism of ethylene glycol must be blocked by other means. Until recently, only ethanol has been available to inhibit the formation of toxic metabolites. Ethylene glycol and ethyl alcohol look and act very similarly to each other., and so competitive inhibition occurs. You see alcohol dehydrogenase ( a liver enzyme) is much more reactive with ethanol than with ethylene glycol, so it preferentially breaks down ethanol. This prevents the toxic products from the breakdown of ethylene glycol from forming and allows it to be excreted from the body through urination. However, ethanol therapy has its own toxic side effects. At one time, ethanol therapy was the only option available for alcohol dehydrogenase inhibition. An alternative, 4-methylpyrazole 5%, has since been used successfully as an inhibitor in dogs. Preference has been given to 4-methylpyrazole as it does not suppress the central nervous system like ethanol. Finally, to treat severe metabolic acidosis, sodium bicarbonate (baking soda) is often administered in liquid form as an IV, but must be monitored closely so that electrolyte abnormalities are prevented. Force fluids.
Lead (Paint, insecticides, ceramics, lEheinoleum, golf balls)’Symptoms include seizures, bizarre behavior, inability to coordinate voluntary muscle movements, lethargy, sporadic vomiting. If you live in a house built or painted before 1980, you may realistically suspect that there is lead in the environment. Puppies are at greater risk than are adult dogs. If lead has been ingested (most commonly in the form of paint chips, induce vomiting; give activated charcoal slurry. Administer succimer (meso-2, 3- dimercaptosuccinic acid) at a rate of 10mg/kg of body weight for ten days to reduce blood lead concentrations.
Metaldehyde (Antimilace®, Bug-Geta®, Corry's® Slug and Snail Death, Halizan®, Metason®, Namekil®)’Symptoms include increased salivation, abdominal cramps, vomiting and generalized tremors or seizures. Some cases exhibit ataxia, hyperesthesia, hyperthermia and tachcardia. Induce vomiting; give activated charcoal slurry. Anti- convulsants may be necessary. Intravenous fluids help to protect the liver, assist detoxification and facilitate excretion. Acidosis may occur necessitating correction with sodium bicarbonate.
Non-steroidal anti-inflammatory agents/NSAIDS (acetaminophen [Tylenol®, Daytril®, Panadol®, Anacin®, Excedrin®], ibuprofen [Advil®, Medipren®, Midol®, Motrin®, Nuprin®], indomethecin [Indocin®], mefenamic acid [Ponstel®] and naproxen [Naprosyn®])’Induce vomiting; give activated charcoal slurry. Magnesium- and aluminum hydroxide may be used to control gastric irritation. diazepam (Valium®) may be given to control seizures.
Opiates (Bancap®, Codeine, Co-Gesic®, Damason-P®, Darvocet-N®, Darvon®, Demerol®, Morphine, Percocet®, Perdodan®, Ponstel®, Roxanol®, Roxicodone®, Synalgos®,Talwin®, Tegretol®, Tylenol® with Codeine, Tylox®, Vicodin®, Zydone®)’Poisoning with morphine and other opiods depresses the central nervous system, resulting in drowsiness to deep coma, respiratory depression to include shallow respiration or apnea, miosis, hypotension and hypothermia. Spasticity, muscle twitching and convulsions may be present. Induce vomiting; give activated charcoal slurry. Cathartics (purgatives) such as sodium sulphate, magnesium citrate, magnesium sulphate and Sorbitol™, a narcotic antagonist (an agent that acts to nullify the action of another agent, such as naloxone [Narcan®, Trexan™]) may be administered to counter the effects of the opiate. Note: if improvement does not occur rapidly, the diagnosis may need to be reconsidered.
Organophosphates (Insecticides’Diazinon®,Dichlorvos®, Fenthion®, Malathion®, Parathion®, Ronnel®, Trichlorofon®)’Military nerve gases are organophosphates. They are characteristically very quick acting. Constricted pupils, increased salivation, bradycardia and hypotension, bronchoconstriction, vomiting, diarrhea, urinary incontinence, muscular weakness, restlessness, anxiety, convulsions, coma and respiratory failure are symptoms. If sufficiently alert, induce vomiting; give activated charcoal slurry. If oxygen is available, improve tissue oxygenation as much as possible before administering atropine. Begin atropine administration as soon as possible. It may be necessary to maintain atropinization for several hours to reduce miosis, nausea and bradycardia. Diazepam (Valium®) may be useful to control confusion and convulsions due to the effects of the organophosphates and also for excess atropine. Organophosphates are anti-cholinesterase agents. Administer pralidoxime (Protopam®, 2-PAM), a cholinesterase reactivator, if respiratory depression and muscle weakness or twitching is severe. This is one time when the diagnosis must be right, because pralidoxime can be hazardous in carbamate poisoning. Note: if the dog is unconcious, the stomach still must be emptied. This will require gastric intubation by the veterinarian. If a significant amount of organophosphates have been ingested, atropine may have to be continued for several days, as the toxin may take 5-14 days to eliminate. Respiratory failure may be possible for several days.
Phenols (Lysol®, creosote, fungicides, herbicides, wood preservatives)’treated lumber is often used for decks and landscaping. Puppies chewing preserved lumber and ingesting the pieces can develop a problem. Symptoms are salivation, vomiting, dyspnea, dizziness, loss of pupillary reflexes, hyperthermia, convulsions and coma. Vascular collapse is the usual cause of death, with respiratory depression a contributing factor. Induce vomiting; give activated charcoal slurry. In the case of creosote or Lysol poisoning, if pharyngeal redness or swelling are evident, induced vomiting and gastric lavage may be contraindicated. Diazepam (Valium®) may be required to control tremors or seizures.
Salamanders (California newt Taricha torosa)’Found in California, this is the only poisonous salamander in the United States. Symptoms are weakness and in- coordination, vomiting and diarrhea (more common in puppies) and paralysis. Poisoning episodes are generally self-limiting, but may be reduced in duration by flushing the dog's mouth with copious quantities of water.
Sodium chorate (Atratol®, De-Fol-Ate®, Dervan®, Drexol Defol®, Drop-Leaf®, Klorex®, Kusatol®)’A defoliant and soil sterilant. Onset of symptoms may be delayed as much as twelve hours after ingestion. Symptoms include vomiting, abdominal pain, diarrhea, hypotension. Hyperalkalemia resulting from potassium released from destruction of red cells may further cause cardiac effects. Death results from shock, anoxemia (lack of oxygen in the blood), heart failure or disseminated intravascular coagulation. Induce vomiting; give activated charcoal slurry. Give sodium thiosulfate to decompose remaining chlorate. Sorbitol® may be administered if diarrhea is not present. Oxygen may be necessary if respiration is depressed. IV fluids may be used to sustain chlorate excretion with sodium bicarbonate as necessary, to maintain urine pH in the alkaline range. Blood transfusion may be required.
Strychnine (Rodenticide)’Symptoms include exaggerated reflexes and muscle contractions, especially in the dog's legs. If responsive, and the reflexive symptoms have not yet started, induce vomiting; give activated charcoal slurry. Otherwise, these symptoms can be controled at the vets with IV succinylcholine. Diazepam (Valium®) may be also be useful for controlling convulsions. By keeping the dog very quiet, you may be able to avoid the onset of convulsions.
Sympathomimetic agents (amphetamines, adrenaline, ephedrine, naphazoline, various "cold and flu" decongestants, cough mixtures, appetite suppressants’Symptoms include spathetic overactivity with irritability, agitation, hyperactivity, dilated pupils, tachycardia. Confused mental states may be observed, and in the severe overdose, seizures and cardiac failure. Induce vomiting; give activated charcoal slurry followed by a cathartic. For hypertensive reactions, niphedipine (Adalat®, Procardia®) may be used. Diazepam (Valium®) may be used to reduce hyperactivity and convulsions.
Theophylline and related drugs (Bronkaid®, Primatene®, Quibron®, Sustaire®, Theo-dur®, Theospan®, Theostat®)’these common asthma medications tend to be left out where they can be reached easily, thus giving access to an inquisitive dog. Clinical features of overdose by ingestion include nausea, severe and intractable vomiting, abdominal pain, gastrointestinal hemorrhage with severe toxicity, agitation, restlessness, dilated pupils, convulsion and cardiac effects. Induce vomiting, if vomiting has not already occurred; give activated charcoal slurry if vomiting can be controlled. Control convulsions with diazepam (Valium®). Hydration may be required as a result of extensive vomiting. Most cases can be treated satisfactorily with supportive measures, but charcoal hemoperfusion may be required in extreme overdoses.
Tobacco (chewing or snuff)’It is unlikely that a dog will chew on a tobacco plant, or even ingest a cigarette or do much more than mouth a cigar. It is not unlikely that a puppy, will eat pleasantly palatable chewing tobacco, with untoward effects. Nicotine, an active ingredient in tobacco, is extremely toxic and very little is required to kill a dog. Remember, tobacco has a history of having been used as an insecticide, and has very potent properties, other than causing cancer. Ingest enough of it, and you will not have to wait for cancer. After ingestion, a dog may present with central nervous system derangement, miosis, hypersalivation, vomiting, diarrhea, tachycardia, hypertension, and hyperthermia, followed by total collapse. Induce vomiting if conscious and responsive; give activated charcoal slurry and provide follow-on supportive treatment.
Hops Homulus lupulus -- the spent hops from the home brewing of beer presents a new danger to dogs. Since 1994, the National Animal Poison Control Center has been consulted on five dogs, only one of whom survived. The dogs present with panting, restlessness, and signs of increasing pain. The most significant symptom is a rapid increase in temperature called malignant hyperthermia. Treatment includes gastric lavage, charcoal slurry, coldwater baths and IV sodium bicarbonate to reverse metabolic acidosis. Hops contain a variety of biologically active compounds, the most suspect however is an uncharacterized alkaloid.
Plant Poisons
Poisonous plants are common, and are within easy access for most dogs. It is virtually impossible to eliminate poisonous plants from most dogs' environments. A complete list of poisonous plants is beyond the scope of this article. Treatment generally involves inducing vomiting, giving activated charcoal slurry, with CPR and supportive treatment as necessary.
Plant poisoning mechanisms are extremely varied, but can be broken down into the twelve basic categories listed in Figure 3. As with the previously listed non-plant toxins, treatment varies somewhat by category. Most adult dogs leave toxic plants alone, but this cannot be said of puppies before their brains have caught up with their mobility and ability to mouth, chew and swallow. Example: What puppy can resist mouthing mushrooms? Both authors have caught their puppies playing with mushrooms of various varieties. Fortunately, they never played with Amanita phalloides (death cap), A. verna (fool's mushroom), A. virosa (death angel), or A. bisporiger (smaller death angel). Amanita sp. are abundantly available in the United States, especially in the Mid- Atlantic down to Florida and west to Texas. Expect them between October and December. There are no approved antidotes. However, the human literature does list recoveries after liver transplants! The preceding was to set the stage for other really poisonous plants like oleander and dumb cane and jimson weed and choke cherry.
Note that many of the poisonous plants are ornamentals common in the United States. Next time you trim back the English ivy, English holly, the Oleander bush, the laurel bush, or trim the privet hedge, do not leave the trimmings on the grass to be mulched up next time you mow the lawn with a mulching lawnmower. Your dog may just drop a sticky bone on a mulched pile of trimmings and go off to chew his bone later. It is not just puppies that are at risk from poisoning; adults dogs may not set out to intentionally chew or ingest a poisonous plant, but they can come by the poisons quite innocently (as in the example) or by grooming themselves.
Categories of Poisonous Plants by their Active Ingredients
One of ways the liver helps to rid the body of toxins is to chemically alter them so as to make them more water-soluble; at this point the poison can be excreted by the kidneys and to some extent the skin and lungs. But sometimes, these breakdown products, or metabolites, can actually be more dangerous in their chemically activated forms. Ethelene glycol (a major component of anti-freeze) is a good example of this. The various metabolites formed when the liver breaks down this substance will sequentially attack the central nervous system, lower the pH of the blood to fatal levels and damage the kidneys.
Detoxification by the liver is carried out by three principal enzyme systems. Enzymes are proteins that catalyze chemical reactions; i.e., they increase the rate of these reactions. The first system is called Phase I. At this point in the detox cascade, chemical modification is handled by a series of mixed-function oxidase enzymes. One of the major routes is a two-step pathway involving the enzymes of the liver (cytochromes P450) and an enzyme associated with the high-density lipoprotein (HDL, or good cholesterol particle). The second enzyme is called paraoxonase or PON1. In humans, an amino acid substitution at position 192 of this protein results in the existence of two different forms of this enzyme in the serum, one with the amino acid arginine at this position and a second with the amino acid glutamine at this position. Thus, people and animals are genetically capable of breaking down poisons at different rates. One form is better for some insecticides, while the second is better for other insecticides. In addition to the activity differences observed with the two different genetic types, individuals can have varying levels of the protein in their blood. The combined effect of different levels of enzyme and its form, can cause up to a 100-fold difference in the clearance rates for a given insecticide. Much research is being carried out by Dr. Clement Furlong and coworkers at the University of Washington.14 In addition to examining the molecular basis of differential sensitivity to insecticides, they also are working on developing treatment procedures for organophosphate poisoning in humans and animals. Drs. Furlong, Lucio Costa and graduate student Wan-Fen Li have shown injected PON1 provides protection against organophosphate poisoning either pre- or postexposure. They are working on procedures for producing large quantities of recombinant enzyme. One other comment should be made regarding exposure of young animals (or humans) to organophosphate compounds processed through the P450/PON1 pathway. Newborns have very low levels of PON1 and are correspondingly much more sensitive to these compounds, so extreme caution should be taken to avoid such exposure.
Those metabolites not excreted by the kidneys are processed by the Phase II system enzymes. These are fat-soluble toxins preferentially stored in the fat cells. Phase III enzymes have a similar function. However, if there is a lack of Phase II enzymes, the "activated" metabolites produced by the Phase I enzymes build up in the bloodstream and wreak havoc on the liver and kidneys. If the level of Phase I enzymes is high and the amount of Phase II enzymes is low, there is great danger of a toxic detox reaction, because the intermediate metabolites are processed too slowly. Nutritional support favors the sequential elimination of toxins and can prevent or ameliorate the damage done to the liver and kidneys. What follows are specific recommendations for the canine only. Cats have unique metabolic and dietary needs that cannot be addressed here.
Recovery
The road to recovery after a major poisoning episode may be long and uphill. Nutritional support is considered by many to be effective. First reduce the workload of the liver and the kidney. A bland diet of cooked white rice is recommended for several days. Do not feed any proteins or fats because these are processed by the liver and kidneys. To counteract the effects of the Phase I metabolites, some veterinarians suggest giving antioxidant vitamins and minerals. These include Ester-C or calcium ascorbate, vitamin E, selenium, beta carotene, bioflavonoids, selenium, copper, zinc and manganese, Coenzyme Q10, thiols (from garlic) and superoxide dismutase. Support for the Phase II enzymes: Do not fast the animal. Substances used by Phase II enzymes include sulfhydryl donors (N-acetylcysteine, cysteine, cystine, methionine and glutathione), sulfates (good sources are glutathione and cystine), pantothenic acid (B5), glycine, taurine, glutamine, arginine, ornithine, selenium and riboflavin. (Many of these nutritional supplements are available in Ultra Clear Plus available from Metagenics and similar manufacturers.)16 These substances can be used to speed up Phase II reactions. Glutathione levels are lowered with stress, so stress reduction especially is important when detoxing. After reviewing the symptoms, the treatment and follow-on veterinary and dietary care necessary to recover from poisoning, we think you will agree with our conclusion:
Conclusion
Prevention is better than cure. Potential for serious poisoning is everywhere. Anything you would do to "poison proof" your house, yard, garden, garage, etc., is worth doing for your dogs. Unfortunately, it is not feasible to remove all potential toxins from the environment. Therefore, being prepared includes knowing what toxins are in the environment, where they are located, and what to do in a poisoning situation. We suggest that dog owners conduct a survey of their animal's environment. Write down the potential toxins to include the active ingredients in each product, and keep that survey with a copy of this article and one or both of the books mentioned immediately available for reference.
Acids’Do not induce vomiting; rinse mouth and any other areas which came in contact with the acid; give 1-2 tablespoons of cooking or mineral oil. Alkalis (Laundry detergents, ammonia, paint removers)’Do not induce vomiting; rinse mouth and any other areas which came in contact with the acid; give 1-2 tablespoons of cooking or mineral oil.
Petroleum distillates (Gasoline, paint thinner, charcoal lighter,l)’Do not induce vomiting; rinse mouth and any other areas which came in contact with the acid; give 1-2 tablespoons of cooking or mineral oil.
Stinging nettles (Bull nettles, nettle spurge, etc.)’ Do not induce vomiting; rinse mouth and any other areas which came in contact with the acid; give 1-2 tablespoons of cooking or mineral oil. Note: may exhibit slow and irregular pulse.
"Induce Vomiting" poisons:
4-Aminopyridine (Avitrol®, 4-AP)’4-AP is an extremely toxic white powder sometimes used as a bird repellent. The cries and excited behavior of affected birds frighten away other birds. Symptoms include excitability, increased salivation, tremors, uncoordination, convulsions, and cardiac or respiratory arrest. If responsive, induce vomiting; give activated charcoal slurry. Seizures may require anti-convulsant medications.
Anticoagulant rodenticides (Vitamin D3, brodifacoum [d-Con® Mouse Pruff II, Enforcer® Mouse Kill, Havoc® Klerat®,Ratak Plus®, Talon®, Volid®], bromethalin[Bromathone®, Contrac®, Hot Shot® Sudden Death®; Ratimus®, Tamogen®11, warfarine [d-Con®]) Vomiting, abdominal pain, bloody stool, lethargy. If ingestion has occured less thn 12 hours you may induce vomiting; give activated charcoal slurry. Follow-up care: Vitamin K treatment by veterinarian. The new generation of rotenticides can persist in the body for up to six months, as the liver keeps changing them to another form of antioagulant, therefore treatment should continue for at least six months.
Anti-depressants (Amitriptyline [Elavil®], amoxapine [Ascending], despriamine, dexfenfluramine [Redux®],doxepin, fluoxtetine [Prozac®], imipramine, nortriptyline [Aventyl®, Pamelor®], phenelzine [Nardil®], protiptyline [Vivactil®], sertraline [Zololft®], trimipramine, trancypromine[Parnatel®], valproate [Depakote®], venlafaxin [Effexor])’Anti-depressants are now some of the most widely prescribed drugs and Redux®, in particular, is being widely used as an appetite suppressant. Overdose symptoms include drowsiness, agitation, hyperactive reflexes, muscle twitching, rigidity, convulsions, respiratory depression, coma, hypotension (low blood pressure), arrhythmia (irregular pulse). Induce vomiting if responsive; give activated charcoal slurry. Treat seizures with diazepam (Valium®). Arousal using toe pinches can keep them from drifting into coma while on the way to the vet.
Arsenic (Herbicides, insecticides)’Induce vomiting; give activated charcoal slurry; antidotes are available from veterinarians. The follow-on treatment is beyond home care.
Aspirin and salicylates (Alka-Seltzer®, Anacin®, Axotal®, Bufferin®, Excedrine®, Fiorinal®, Norgesic®, Talwin®)’Induce vomiting; give activated charcoal slurry. Follow-on veterinary treatment may include giving sodium bicarbonate to cause alkalinisation of the urine (alkalinuria) to increase excretion of salicylates. Antacids may be required to counteract gastric irritation.
Barbiturates (butabarbital [Butisol Sodium®],hexobarbitone, methobarbital [Mebaral®], pentobarbitone, secobarbitone), pentobarbitol [Nembutal®], thiopental sodium [Pentothal®], phenobarbital [Antrocol, Belladenal®, Donnatel®, Primatene®, Quadrinal™, Tedral®, secobarbitol’Characteristic signs and symptoms include drowsiness, ataxia (failure of muscular coordination), confusion, stupor and coma. Deaths may occur from cardiac and respiratory arrests. Induce vomiting; give activated charcoal slurry. Hypotension may be corrected by various blood volume expanders. Vasoconstrictors, such as dopamine or dobutamine may be required to increase blood pressure. In extreme cases, charcoal hemoperfusion may be required.
Bufo sp. Toads’Some 16 species of bufo toads are found around the world. Bufo alvarius (Colorado River toad) is found in the Southwest, and Bufo marinus is found in Florida and Hawaii. Bufo's are attracted to dogs' watering dishes, and may sit in the rim long enough to leave enough toxin to make a dog ill. Untreated death rate, especially for Bufo marinus may approach 100%. Dogs may mouth bufo toads, thus getting a large dose of the bufo's toxins, secreted from the skin and paratid glands. Symptoms generally include profuse foamy salivation that looks like shaving cream, difficulty breathing, convulsions, paralysis, ventricular fibrillation, vomiting, cyanosis, and hallucination. Author Cargill had experience with an adult Doberman bitch, Kiku, and a Bufo marinus several years ago while in Hawaii. She salivated profusely, had labored breathing, an irregular heart beat, and the wildest-looking eyes ever seen in a Doberman. It took her the better part of a day and a night to recover untreated. Treatment involves dealing with three poisoning mechanisms: cardiac glycoside effects, pressor (tending to increase blood pressure) effects and hallucinogenic effects. Emesis (vomiting) may be indicated if there was a recent substantial ingestion and the dog is sufficiently alert. Repeated oral charcoal doses (every 2-6 hours) may help reduce the duration of poisoning. A saline cathartic or Sorbitol™ may be given with the first charcoal dose. Intravenous insulin, glucose, and sodium bicarbonate may be required to combat life-threatening hyperalalkemia (elevated serum pH levels). Atropine, phenytoin and lidocane may be useful in the management of bradycardia (abnormally slow pulse) and other cardiac irregularities. Cholestryamine may enhance elimination of bufagin (one of the several bufo venon toxins). Bufo toads are not all that uncommon in some parts of the nation, but very serious business, indeed.
Carbamates (Insecticides’Carbaryl®, Sevin®, Propoxur®)’’Induce vomiting; give activated charcoal slurry; atropine administration should be started as soon as possible under the supervision of a veterinarian.
Calcium cyanamide (Cyanamide, nitrolime)’used as a fertilizer, insecticide and herbicide. Note: cyanamide has different toxic properties than cyanide. Symptoms are vertigo, dyspnea (difficult or labored breathing), tachycardia (abnormally quick pulse), hypotension. Induce vomiting, give activated charcoal slurry and Sorbitol™. Note: atropine is not antidotal. Give IV fluids (plasma or blood) if needed and vasopressor drugs if necessary.
Chocolate’Confectionary chocolate and dogs do not mix. While chocolate is not poisonous, theobromine which is found in chocolate is. Theobromine triggers epileptic seizures in susceptible animals, and can cause cardiac irregularity leading to myocardial infarct and death. Additionally, chocolate irritates the gastrointestinal tract, even to the extent that it causes such internal bleeding that it can kill within a couple of days. Induce vomiting; give activated charcoal slurry.
Cyanide (Rodenticide)’Cyanide is one of the most rapidly acting of all poisons with death occuring in just a few minutes. Symptoms usually appear within seconds to minutes after exposure, and include giddiness, palpitations, dyspnea, loss of consciousness, convulsions and death. If responsive, induce vomiting; give activated charcoal slurry. Administer 100% oxygen as soon as possible as oxygen contributes to the reversal of the cyanide-cytochrome complex. Antidotes include dicobalt edetate (Kelocyanor®), amyl nitrate, and a sodium nitrate and sodium thiosulphate solution (Trypac-Cyano®).
Ethylene glycol ( Antifreeze, color film processing solutions (diethylene glycol) , heat-exchange fluids, ice-rink freezing equipment, as well as in windshield deicer, brake, and transmission fluids)
Quick treatment is necessary to prevent the formation of toxic metabolites. Symptoms are s imilar to alcohol intoxication and include staggering (ataxia), excessive thirst, (polydipsia), excessive urination (polyuria), nausea, vomiting. If treatment is provided less than 4 hours after ingestion, absorption can be prevented through emesis (vomiting) and gastric lavage (stomach wash). After that, metabolism of ethylene glycol must be blocked by other means. Until recently, only ethanol has been available to inhibit the formation of toxic metabolites. Ethylene glycol and ethyl alcohol look and act very similarly to each other., and so competitive inhibition occurs. You see alcohol dehydrogenase ( a liver enzyme) is much more reactive with ethanol than with ethylene glycol, so it preferentially breaks down ethanol. This prevents the toxic products from the breakdown of ethylene glycol from forming and allows it to be excreted from the body through urination. However, ethanol therapy has its own toxic side effects. At one time, ethanol therapy was the only option available for alcohol dehydrogenase inhibition. An alternative, 4-methylpyrazole 5%, has since been used successfully as an inhibitor in dogs. Preference has been given to 4-methylpyrazole as it does not suppress the central nervous system like ethanol. Finally, to treat severe metabolic acidosis, sodium bicarbonate (baking soda) is often administered in liquid form as an IV, but must be monitored closely so that electrolyte abnormalities are prevented. Force fluids.
Lead (Paint, insecticides, ceramics, lEheinoleum, golf balls)’Symptoms include seizures, bizarre behavior, inability to coordinate voluntary muscle movements, lethargy, sporadic vomiting. If you live in a house built or painted before 1980, you may realistically suspect that there is lead in the environment. Puppies are at greater risk than are adult dogs. If lead has been ingested (most commonly in the form of paint chips, induce vomiting; give activated charcoal slurry. Administer succimer (meso-2, 3- dimercaptosuccinic acid) at a rate of 10mg/kg of body weight for ten days to reduce blood lead concentrations.
Metaldehyde (Antimilace®, Bug-Geta®, Corry's® Slug and Snail Death, Halizan®, Metason®, Namekil®)’Symptoms include increased salivation, abdominal cramps, vomiting and generalized tremors or seizures. Some cases exhibit ataxia, hyperesthesia, hyperthermia and tachcardia. Induce vomiting; give activated charcoal slurry. Anti- convulsants may be necessary. Intravenous fluids help to protect the liver, assist detoxification and facilitate excretion. Acidosis may occur necessitating correction with sodium bicarbonate.
Non-steroidal anti-inflammatory agents/NSAIDS (acetaminophen [Tylenol®, Daytril®, Panadol®, Anacin®, Excedrin®], ibuprofen [Advil®, Medipren®, Midol®, Motrin®, Nuprin®], indomethecin [Indocin®], mefenamic acid [Ponstel®] and naproxen [Naprosyn®])’Induce vomiting; give activated charcoal slurry. Magnesium- and aluminum hydroxide may be used to control gastric irritation. diazepam (Valium®) may be given to control seizures.
Opiates (Bancap®, Codeine, Co-Gesic®, Damason-P®, Darvocet-N®, Darvon®, Demerol®, Morphine, Percocet®, Perdodan®, Ponstel®, Roxanol®, Roxicodone®, Synalgos®,Talwin®, Tegretol®, Tylenol® with Codeine, Tylox®, Vicodin®, Zydone®)’Poisoning with morphine and other opiods depresses the central nervous system, resulting in drowsiness to deep coma, respiratory depression to include shallow respiration or apnea, miosis, hypotension and hypothermia. Spasticity, muscle twitching and convulsions may be present. Induce vomiting; give activated charcoal slurry. Cathartics (purgatives) such as sodium sulphate, magnesium citrate, magnesium sulphate and Sorbitol™, a narcotic antagonist (an agent that acts to nullify the action of another agent, such as naloxone [Narcan®, Trexan™]) may be administered to counter the effects of the opiate. Note: if improvement does not occur rapidly, the diagnosis may need to be reconsidered.
Organophosphates (Insecticides’Diazinon®,Dichlorvos®, Fenthion®, Malathion®, Parathion®, Ronnel®, Trichlorofon®)’Military nerve gases are organophosphates. They are characteristically very quick acting. Constricted pupils, increased salivation, bradycardia and hypotension, bronchoconstriction, vomiting, diarrhea, urinary incontinence, muscular weakness, restlessness, anxiety, convulsions, coma and respiratory failure are symptoms. If sufficiently alert, induce vomiting; give activated charcoal slurry. If oxygen is available, improve tissue oxygenation as much as possible before administering atropine. Begin atropine administration as soon as possible. It may be necessary to maintain atropinization for several hours to reduce miosis, nausea and bradycardia. Diazepam (Valium®) may be useful to control confusion and convulsions due to the effects of the organophosphates and also for excess atropine. Organophosphates are anti-cholinesterase agents. Administer pralidoxime (Protopam®, 2-PAM), a cholinesterase reactivator, if respiratory depression and muscle weakness or twitching is severe. This is one time when the diagnosis must be right, because pralidoxime can be hazardous in carbamate poisoning. Note: if the dog is unconcious, the stomach still must be emptied. This will require gastric intubation by the veterinarian. If a significant amount of organophosphates have been ingested, atropine may have to be continued for several days, as the toxin may take 5-14 days to eliminate. Respiratory failure may be possible for several days.
Phenols (Lysol®, creosote, fungicides, herbicides, wood preservatives)’treated lumber is often used for decks and landscaping. Puppies chewing preserved lumber and ingesting the pieces can develop a problem. Symptoms are salivation, vomiting, dyspnea, dizziness, loss of pupillary reflexes, hyperthermia, convulsions and coma. Vascular collapse is the usual cause of death, with respiratory depression a contributing factor. Induce vomiting; give activated charcoal slurry. In the case of creosote or Lysol poisoning, if pharyngeal redness or swelling are evident, induced vomiting and gastric lavage may be contraindicated. Diazepam (Valium®) may be required to control tremors or seizures.
Salamanders (California newt Taricha torosa)’Found in California, this is the only poisonous salamander in the United States. Symptoms are weakness and in- coordination, vomiting and diarrhea (more common in puppies) and paralysis. Poisoning episodes are generally self-limiting, but may be reduced in duration by flushing the dog's mouth with copious quantities of water.
Sodium chorate (Atratol®, De-Fol-Ate®, Dervan®, Drexol Defol®, Drop-Leaf®, Klorex®, Kusatol®)’A defoliant and soil sterilant. Onset of symptoms may be delayed as much as twelve hours after ingestion. Symptoms include vomiting, abdominal pain, diarrhea, hypotension. Hyperalkalemia resulting from potassium released from destruction of red cells may further cause cardiac effects. Death results from shock, anoxemia (lack of oxygen in the blood), heart failure or disseminated intravascular coagulation. Induce vomiting; give activated charcoal slurry. Give sodium thiosulfate to decompose remaining chlorate. Sorbitol® may be administered if diarrhea is not present. Oxygen may be necessary if respiration is depressed. IV fluids may be used to sustain chlorate excretion with sodium bicarbonate as necessary, to maintain urine pH in the alkaline range. Blood transfusion may be required.
Strychnine (Rodenticide)’Symptoms include exaggerated reflexes and muscle contractions, especially in the dog's legs. If responsive, and the reflexive symptoms have not yet started, induce vomiting; give activated charcoal slurry. Otherwise, these symptoms can be controled at the vets with IV succinylcholine. Diazepam (Valium®) may be also be useful for controlling convulsions. By keeping the dog very quiet, you may be able to avoid the onset of convulsions.
Sympathomimetic agents (amphetamines, adrenaline, ephedrine, naphazoline, various "cold and flu" decongestants, cough mixtures, appetite suppressants’Symptoms include spathetic overactivity with irritability, agitation, hyperactivity, dilated pupils, tachycardia. Confused mental states may be observed, and in the severe overdose, seizures and cardiac failure. Induce vomiting; give activated charcoal slurry followed by a cathartic. For hypertensive reactions, niphedipine (Adalat®, Procardia®) may be used. Diazepam (Valium®) may be used to reduce hyperactivity and convulsions.
Theophylline and related drugs (Bronkaid®, Primatene®, Quibron®, Sustaire®, Theo-dur®, Theospan®, Theostat®)’these common asthma medications tend to be left out where they can be reached easily, thus giving access to an inquisitive dog. Clinical features of overdose by ingestion include nausea, severe and intractable vomiting, abdominal pain, gastrointestinal hemorrhage with severe toxicity, agitation, restlessness, dilated pupils, convulsion and cardiac effects. Induce vomiting, if vomiting has not already occurred; give activated charcoal slurry if vomiting can be controlled. Control convulsions with diazepam (Valium®). Hydration may be required as a result of extensive vomiting. Most cases can be treated satisfactorily with supportive measures, but charcoal hemoperfusion may be required in extreme overdoses.
Tobacco (chewing or snuff)’It is unlikely that a dog will chew on a tobacco plant, or even ingest a cigarette or do much more than mouth a cigar. It is not unlikely that a puppy, will eat pleasantly palatable chewing tobacco, with untoward effects. Nicotine, an active ingredient in tobacco, is extremely toxic and very little is required to kill a dog. Remember, tobacco has a history of having been used as an insecticide, and has very potent properties, other than causing cancer. Ingest enough of it, and you will not have to wait for cancer. After ingestion, a dog may present with central nervous system derangement, miosis, hypersalivation, vomiting, diarrhea, tachycardia, hypertension, and hyperthermia, followed by total collapse. Induce vomiting if conscious and responsive; give activated charcoal slurry and provide follow-on supportive treatment.
Hops Homulus lupulus -- the spent hops from the home brewing of beer presents a new danger to dogs. Since 1994, the National Animal Poison Control Center has been consulted on five dogs, only one of whom survived. The dogs present with panting, restlessness, and signs of increasing pain. The most significant symptom is a rapid increase in temperature called malignant hyperthermia. Treatment includes gastric lavage, charcoal slurry, coldwater baths and IV sodium bicarbonate to reverse metabolic acidosis. Hops contain a variety of biologically active compounds, the most suspect however is an uncharacterized alkaloid.
Plant Poisons
Poisonous plants are common, and are within easy access for most dogs. It is virtually impossible to eliminate poisonous plants from most dogs' environments. A complete list of poisonous plants is beyond the scope of this article. Treatment generally involves inducing vomiting, giving activated charcoal slurry, with CPR and supportive treatment as necessary.
Plant poisoning mechanisms are extremely varied, but can be broken down into the twelve basic categories listed in Figure 3. As with the previously listed non-plant toxins, treatment varies somewhat by category. Most adult dogs leave toxic plants alone, but this cannot be said of puppies before their brains have caught up with their mobility and ability to mouth, chew and swallow. Example: What puppy can resist mouthing mushrooms? Both authors have caught their puppies playing with mushrooms of various varieties. Fortunately, they never played with Amanita phalloides (death cap), A. verna (fool's mushroom), A. virosa (death angel), or A. bisporiger (smaller death angel). Amanita sp. are abundantly available in the United States, especially in the Mid- Atlantic down to Florida and west to Texas. Expect them between October and December. There are no approved antidotes. However, the human literature does list recoveries after liver transplants! The preceding was to set the stage for other really poisonous plants like oleander and dumb cane and jimson weed and choke cherry.
Note that many of the poisonous plants are ornamentals common in the United States. Next time you trim back the English ivy, English holly, the Oleander bush, the laurel bush, or trim the privet hedge, do not leave the trimmings on the grass to be mulched up next time you mow the lawn with a mulching lawnmower. Your dog may just drop a sticky bone on a mulched pile of trimmings and go off to chew his bone later. It is not just puppies that are at risk from poisoning; adults dogs may not set out to intentionally chew or ingest a poisonous plant, but they can come by the poisons quite innocently (as in the example) or by grooming themselves.
Categories of Poisonous Plants by their Active Ingredients
- Oxylates’irritating: mouth gets swollen; tongue pain, sore lips; some swell so quickly that a tracheotomy is required to prevent asphyxiation.
- Histamines
- Alkaloids
- Saponic gylcosides
- Coumarin glycosides
- Toxalbumins
- Solanine glycosides
- Digitalis glycosides
- Cyanogentic glycosides
- Taxine (alkolid)
- Nicotinic stimulants
- Atropinelike agents
One of ways the liver helps to rid the body of toxins is to chemically alter them so as to make them more water-soluble; at this point the poison can be excreted by the kidneys and to some extent the skin and lungs. But sometimes, these breakdown products, or metabolites, can actually be more dangerous in their chemically activated forms. Ethelene glycol (a major component of anti-freeze) is a good example of this. The various metabolites formed when the liver breaks down this substance will sequentially attack the central nervous system, lower the pH of the blood to fatal levels and damage the kidneys.
Detoxification by the liver is carried out by three principal enzyme systems. Enzymes are proteins that catalyze chemical reactions; i.e., they increase the rate of these reactions. The first system is called Phase I. At this point in the detox cascade, chemical modification is handled by a series of mixed-function oxidase enzymes. One of the major routes is a two-step pathway involving the enzymes of the liver (cytochromes P450) and an enzyme associated with the high-density lipoprotein (HDL, or good cholesterol particle). The second enzyme is called paraoxonase or PON1. In humans, an amino acid substitution at position 192 of this protein results in the existence of two different forms of this enzyme in the serum, one with the amino acid arginine at this position and a second with the amino acid glutamine at this position. Thus, people and animals are genetically capable of breaking down poisons at different rates. One form is better for some insecticides, while the second is better for other insecticides. In addition to the activity differences observed with the two different genetic types, individuals can have varying levels of the protein in their blood. The combined effect of different levels of enzyme and its form, can cause up to a 100-fold difference in the clearance rates for a given insecticide. Much research is being carried out by Dr. Clement Furlong and coworkers at the University of Washington.14 In addition to examining the molecular basis of differential sensitivity to insecticides, they also are working on developing treatment procedures for organophosphate poisoning in humans and animals. Drs. Furlong, Lucio Costa and graduate student Wan-Fen Li have shown injected PON1 provides protection against organophosphate poisoning either pre- or postexposure. They are working on procedures for producing large quantities of recombinant enzyme. One other comment should be made regarding exposure of young animals (or humans) to organophosphate compounds processed through the P450/PON1 pathway. Newborns have very low levels of PON1 and are correspondingly much more sensitive to these compounds, so extreme caution should be taken to avoid such exposure.
Those metabolites not excreted by the kidneys are processed by the Phase II system enzymes. These are fat-soluble toxins preferentially stored in the fat cells. Phase III enzymes have a similar function. However, if there is a lack of Phase II enzymes, the "activated" metabolites produced by the Phase I enzymes build up in the bloodstream and wreak havoc on the liver and kidneys. If the level of Phase I enzymes is high and the amount of Phase II enzymes is low, there is great danger of a toxic detox reaction, because the intermediate metabolites are processed too slowly. Nutritional support favors the sequential elimination of toxins and can prevent or ameliorate the damage done to the liver and kidneys. What follows are specific recommendations for the canine only. Cats have unique metabolic and dietary needs that cannot be addressed here.
Recovery
The road to recovery after a major poisoning episode may be long and uphill. Nutritional support is considered by many to be effective. First reduce the workload of the liver and the kidney. A bland diet of cooked white rice is recommended for several days. Do not feed any proteins or fats because these are processed by the liver and kidneys. To counteract the effects of the Phase I metabolites, some veterinarians suggest giving antioxidant vitamins and minerals. These include Ester-C or calcium ascorbate, vitamin E, selenium, beta carotene, bioflavonoids, selenium, copper, zinc and manganese, Coenzyme Q10, thiols (from garlic) and superoxide dismutase. Support for the Phase II enzymes: Do not fast the animal. Substances used by Phase II enzymes include sulfhydryl donors (N-acetylcysteine, cysteine, cystine, methionine and glutathione), sulfates (good sources are glutathione and cystine), pantothenic acid (B5), glycine, taurine, glutamine, arginine, ornithine, selenium and riboflavin. (Many of these nutritional supplements are available in Ultra Clear Plus available from Metagenics and similar manufacturers.)16 These substances can be used to speed up Phase II reactions. Glutathione levels are lowered with stress, so stress reduction especially is important when detoxing. After reviewing the symptoms, the treatment and follow-on veterinary and dietary care necessary to recover from poisoning, we think you will agree with our conclusion:
Conclusion
Prevention is better than cure. Potential for serious poisoning is everywhere. Anything you would do to "poison proof" your house, yard, garden, garage, etc., is worth doing for your dogs. Unfortunately, it is not feasible to remove all potential toxins from the environment. Therefore, being prepared includes knowing what toxins are in the environment, where they are located, and what to do in a poisoning situation. We suggest that dog owners conduct a survey of their animal's environment. Write down the potential toxins to include the active ingredients in each product, and keep that survey with a copy of this article and one or both of the books mentioned immediately available for reference.
