Download 10 Emerging Poisonings - Buffalo Academy of Veterinary Medicine

10 Emerging Poisonings
Kevin T. Fitzgerald, Ph.D., D.V.M., D.A.B.V.P.
Staff Veterinarian
VCA Alameda East Veterinary Hospital
Denver, Colorado
INTRODUCTION
Companion animals can frequently encounter a variety of intoxicants in or around
the domestic household. The bedroom, the bathroom, the kitchen, basements
and garages, and the yard all may house over-the-counter medications,
prescriptions drugs, pesticides, and a myriad of other molecules capable of
proving toxic. As a consequence of this proximity, veterinary emergency
clinicians treat a large number of poisonings. Successful management of
poisoned animals includes initial telephone triage, obtaining a thorough history
from the client, initial stabilization, decontamination (if appropriate), diagnostic
testing, and careful selection of effective treatment.
Veterinarians must comprehend the mechanism of action of a poison, its
pharmacokinetics (absorption, distribution, metabolism, and excretion), and
whether a toxic dose has been ingested. A number of resources (animal poison
helpline, veterinary colleges, and local toxicologists) are available to clinicians
particularly if the toxic molecule is not well known, if the toxic molecule has a
narrow margin of safety, or if the toxic molecule is a human medication not
familiar to veterinarians.
Each year thousands of new, potentially toxic, molecules receive patents and are
made available to the public. In this discussion, we will look at the toxic potential
for a number of toxins being seen more frequently. Veterinarians must make
every effort to stay current with regard to substances potentially toxic to
companion animals.
1) MARIJUANA
Although for most states, possession of any marijuana is illegal and
federal law bans the drug, some states allow medicinal use of marijuana
under certain circumstances with more states expected to follow suit.
Furthermore, a few states here decriminalized possession of marijuana for
personal use. Similar legislation in other states is anticipated. As a result
of the changes with regard to the legal status of marijuana making it more
accessible, an increase in the number of accidental intoxications in pets
(especially dogs) can be expected. Nowhere is this more probable than in
the ingestion of edible marijuana products by companion animals.



Marijuana: the major psychoactive constituent is delta-9tetrahydrocannabinol (THC).
Mechanism of action: The precise action that THC has upon the
nervous system is as yet unknown. Nevertheless, action at the
cannabinoid receptor is thought to cause all clinical effects of THC.
Toxic dose: THC has a wide margin of safety with the minimum
lethal oral dose greater than 3g/kg. This dose is 1,000 times the
amount needed to see behavioral effects.



Clinical signs: In dogs, clinical signs include ataxia and
incoordination, hypersalivation, disorientation, hypothermia,
mydriasis, bradycardia, vomiting, depression, and tremors. Nearly
half of dogs display urinary incontinence. Signs may vary with
dosage, size and age of the dog, and underlying medical
conditions. In dogs, onset of clinical signs is generally within one
hour of ingest.
Treatment: There is no specific antidote for cannabis.
Prognosis: The majority of dogs ingesting THC recover completely
with no long-term adverse effects.
2) ADDERALL TOXICITY (Amphetamine – Dextroamphetamine)
Attention deficit hyperactivity disorder (ADHD) is the most commonly
diagnosed neurobehavioral disorder affecting 3% to 7% of school-aged
children in the US. Adderall (amphetamine-dexamphetamine salts) is a
drug used in treating ADHA and neurolepsy. Recently, we have seen an
increase in companion animals poisoned with this drug.
 Mechanism of Action: The primary action is the release of
catecholamines (particularly dopamine and norepinephrine) for
presynaptic terminals. These increases in neurotransmitters cause
sympathetic nervous stimulation.
 Toxic dose (dogs): 9 - 11 mg/kg methamphetamine hydrochloride
20 – 27mg/kg amphetamine sulfate
 Clinical signs: hyperactivity, hypersalivation, hyperthermia,
mydriasis, tachycardia, increased blood pressure, ataxia, seizures,
repetitive stereotypical behaviors.
 Treatment: The mainstays of treatment of amphetamine poisoned
animals are supportive care, control of behavior, management of
arrhythmias, stopping seizures, and temperature reduction.
 Prognosis: Although the clinical signs of this toxicity are dramatic,
most animals show no long-term clinical consequences of Adderall
toxicity.
3) XYLITOL
Xylitol is a sugar alcohol and sucrose substitute used in dietetic candies,
gums, and snacks for diabetics.



Mechanism of Action: For dogs, xylitol produces a rapid, dosedependent insulin release followed by a dramatic, significant
hypoglycemia.
Clinical Signs: Vomiting, weakness, ataxia, hypokalemia, seizures,
and coma. Severe cases can lead to liver failure.
Toxic Dose: This can be 0.5 – 1.0 g/kg. Each stick of gum can
contain 1.0 grams.


Treatment: Therapy includes dextrose containing fluids, liver
protectants and antioxidants. Activated charcoal is of no use. Liver
enzymes and coagulation status should be monitored closely.
Prognosis: This depends upon the size of the dog, the amount
ingested, and how long it has been since ingestion.
4) GRAPES AND RAISINS
Some dogs appear particularly sensitive to raisin and grape ingestion.
Other dogs never show clinical signs after ingestion. The smallest amount
of grape/raisin ingestion leading to renal failure has been 0.7oz/kg (for
grapes) and 0.11oz/kg (for raisins). This can be as little as 3 to 7 raisins.




Mechanism of Action: At present, the toxic principle in grapes and
raisins is unknown. Analysis of involved grapes and raisins has
been negative for alcohol, fungi, heavy metals, and pesticides.
Clinical Signs: Signs include anorexia, vomiting, depression, and
dehydration. Signs develop in 6 to 12 hours after ingestion.
Treatment: Therapy includes aggressive intravenous fluid diuresis
for 48 hours at 1 1/2 to 2x maintenance. Renal values and urine
output should be closely monitored. Symptomatic treatment of
vomiting and renal failure may be required.
Prognosis: The outlook is good for dogs with normal values at 48
to 72 hours post-ingestion. Prognosis is guarded for animals
presenting already in renal failure.
5) MACADAMIA NUTS
Macadamia nuts are a popular snack from trees grown primarily in Hawaii.
Recently, macadamia nuts have been reported to cause toxicosis, so far
only documented in dogs.




Mechanism of Toxicity: Currently, the toxic agent responsible for
macadamia nut toxicosis is unknown.
Toxic Dosage: One roasted macadamia nut weighs between 2.1
and 3 grams. The minimum toxic dosage has been reported to be 1
nut/kg. As little as 5 to 40 nuts have been shown to be toxic in a 20
kg dog. Dogs experimentally given 20 g/kg all developed clinical
signs within 6 hours.
Clinical Signs: Weakness, inability to rise, ataxia, tremors, and
occasionally vomiting.
Treatment: Therapy is supportive and symptomatic. Most dogs can
be successfully managed with intravenous fluids and antibiotics.
Many dogs can be treated symptomatically at home.

Prognosis: The prognosis for dogs after macadamia nut ingestion
is excellent. Resolution in the vast majority of cases occurs within
24 to 48 hours. No long term sequellae have been noted.
6) PAINT BALLS
Paint balls contain different colored paints inside gelatin and glycerol
capsules. Recently, dogs ingesting paint balls have been shown to display
clinical signs.




Mechanism of Action: Ingredients in paint balls; glycerol, sorbitol,
and polyethylene glycol are tremendously osmotically active
agents. They cause fluid shifts from body tissue into the bowel
lumen (osmotic diarrhea), and cause dehydration, increased
plasma osmolality, and hypernatremia. These electrolyte disorders
cause acid base imbalances that lead to weakness, ataxia, and
seizures (neurological signs). Occasionally, dogs die.
Clinical Signs: Vomiting, diarrhea, ataxia, weakness, tremors, and
seizures.
Treatment: Therapy includes emesis, if the patient is brought in
early enough, and intravenous fluids with dextrose and halfstrength (0.45%) NaCl. Activated charcoal is of no value. Fluid
rates may need to be high to counter the diarrhea. Warm water
enemas may help stimulate paint ball movement through and out of
the G.I. tract. Electrolytes should be frequently monitored.
Prognosis: Prognosis for paint ball ingestion is good if animals are
made to vomit the paint balls early and if they are put on
intravenous fluids not long after the ingestion incident.
7) CYCAD (SAGO) PALM
Decorative, tropical plants brought into the house as ornamentation. They
are palm-like in appearance.


Mechanism of Action: The major toxicant (Cycasin) is a
gastrointestinal irritant that causes hepatic necrosis. This toxic
glycoside is mutagenic, carcinogenic and teratogenic. The second
toxicant (BMAA) is a neurotoxic amino acid that causes cerebellar
necrosis. A third, as yet unidentified, toxin is also present. All parts
of the plant are toxic, but the highest concentration of toxicants
occurs in the seeds. Only female plants produce seeds. As few as
two seeds can cause symptoms.
Clinical Signs: Signs of sugar palm toxicosis include vomiting,
diarrhea, anorexia, ataxia, liver signs, and seizures. Signs occur


within 12 to 24 hours of ingestion. Lesions produce first G.I.
hemorrhage, then liver cirrhosis and necrosis.
Treatment: Therapy includes emesis if patient presents early
enough, gastrointestinal protectants, intravenous support, and
close electrolyte monitoring. Gastric hemorrhage can be severe
with animals needing a transfusion.
Prognosis: The outcome is good if treatment starts before clinical
signs arise. If severe signs are already in place, the prognosis
becomes guarded.
8) NICOTINE
Animals can be exposed to various forms of nicotine in tobacco products
and smoking cessation aids. Cigarettes, cigars, chewing tobacco, and
snuff contain nicotine ranging from 9 – 15 mg per cigarette to 5 times that
in a cigar. Chewing tobacco often has flavoring agents that make it
attractive to dogs. Nicotine gum has about 4mg per stick and patches
contain up to 114mg of nicotine.




Mechanism of Action: Nicotine stimulates post-synaptic receptors
of the CNS, sympathetic, and parasympathetic nervous systems.
Initial stimulatory effects are followed by blockage of receptors due
to persistent depolarization. Clinical signs develop within one hour
of exposure. The median lethal dose (LD50) is 9.2mg/kg for dogs.
Clinical Signs: Signs of intoxication with nicotine include salivation,
vomiting, diarrhea, increased heart rate, excitement, tremors, and
possibly convulsions. Eventually, depression with paralysis occurs.
Death is caused by paralysis of the diaphragm and chest muscles
leading to cessation of breathing.
Treatment: Therapy begins with emesis, if the patient is seen soon
enough, and activated charcoal. The heart rate should be
monitored and abnormalities treated. Antacids should not be given
as they can increase G.I. absorption of nicotine. Oxygen may be
necessary if respiratory paralysis is a possibility. Seizures can be
controlled with anticonvulsants.
Prognosis: Patients stabilized within 4 hours of ingestion have a
much better chance for survival. Exposures to very high dosages of
nicotine have a poor prognosis.
9) TACROLIMUS
The drug Tacrolimus (Protopic, Prograf) is a human immunosuppressant
used in dogs to treat perianal fistulas. Dermal use on anal ulcers causes
no toxicological signs but ingestion of a tube of the substance can cause
adverse effects.




Mechanism of Action: It is unknown at this time.
Clinical Signs: In both experimental and clinical studies,
Tacrolimus has been shown to cause vomiting and
intussusceptions in dogs. Intussusceptions occur in 2 to 6 days
following ingestion.
Treatment: Therapy for Tacrolimus ingestion involves emesis if
early enough, followed by intravenous fluids, activated charcoal and
vigilance. There is no known antidote.
Prognosis: The prognosis is good if emesis is carried out early and
no signs of intussusceptions have developed. Surgery may be
necessary to repair this intestinal condition.
10) NAPHTHALENE (MOTHBALLS)
Naphthalene is most commonly associated with mothballs. Currently,
paradichlorobenzene has replaced naphthalene in mothballs. Naphthalene
is twice as toxic as “new” mothballs. It is dry appearing, white, and crystal.
It has a characteristic odor.




Mechanism of Action: G.I., dermal, and ocular effects are caused
by the very irritating nature of naphthalene. It causes naphthalene
induced hemolytic anemia, with Heinz body formation, and red cell
lysis. It may lead to cataract formation. Each mothball has about
2.7g of naphthalene. Anemia has been reported at 411 mg/kg.
Clinical Signs: Clinical signs reported include: vomiting, diarrhea,
anorexia, and G.I. bleeding. Gastrointestinal signs are followed by
signs of hemolytic anemia. Pale mucus membranes, dyspnea,
ataxia, and collapse due to the anemia are the final signs.
Treatment: Therapy includes emesis if discovered early enough,
followed by activated charcoal and G.I. protectants. Blood
transfusion and oxygen may be necessary.
Prognosis: Clinical outcome is favorable is therapy is aggressive
and started early.
11) POLYURETHANE ADHESIVES
Polyurethane adhesive expanding wood glues (Gorilla Glue, Elmer’s
Probond Polyurethane Adhesive, etc.) have been associated with gastric
foreign bodies in dogs.

Mechanism of Action: When even a small bottle (2oz of adhesive)
is ingested, the adhesive polymerizes into a large friable ball that
lines the gastric lumen. The adhesive absorbs water, expands, and
continues to expand due to the heat of the stomach environment.



Clinical Signs: Signs resulting from polyurethane adhesive
ingestion are those of a G.I. foreign body. Anorexia, vomiting, and
depression are common.
Treatment: Therapy involves radiographs to visualize the presence
of the foreign body in the stomach and no emesis due to the risk of
the glue expanding into the esophagus. Evidence of a foreign body
may be visible on stomach films at 4 hours but may take 24 hours
to maximally show up. The only therapy for this condition is surgical
removal of the glue ball.
Prognosis: Prognosis depends upon how much glue has been
ingested, the size of the animal, and how long the condition has
gone on. Surgical excision of the foreign body should be curative.
CONCLUSION
Each year 3,400 new molecules are licensed for use in American homes.
Detergents, glues, and cleansers, and this does not begin to list the new plant
species, new drugs, etc. that become available. People (and animals) are
constantly bombarded by new substances and the potential for these new
substances to be toxic. We must be ever vigilant and strive to provide a safe
environment both for ourselves and our companion animals.