Page 470 - Clinical Small Animal Internal Medicine
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438 Section 5 Critical Care Medicine
and urinalysis. The urinalysis is often incorrectly omitted When considering the approach to a patient known
VetBooks.ir in clinical practice. Failure to perform a urinalysis may to have ingested a toxin, many factors must be consid-
ered. If a patient is asymptomatic, the clinician must
prevent the clinician from uncovering evidence of renal
injury (casturia, crystalluria, etc.) prior to the onset of
Although the exact dosage of toxin exposure is not
azotemia. Once azotemia develops, the window of consider the likelihood of toxic symptoms developing.
opportunity for successful therapeutic intervention may always known, treatment should proceed according to
have closed for some patients. More specific diagnostic the maximum possible dose. Let us consider, for exam-
testing may be recommended on a case‐by‐case basis, ple, an 80‐pound Labrador retriever with exposure to a
depending on the specific toxin suspected. For instance, bottle of 200 mg ibuprofen tablets. The bottle initially
blood ethylene glycol testing and determination of anion contained 100 tablets, but it had been opened prior to
gap and measurement of blood osmolality (if possible) this exposure. Twenty tablets were counted following
are recommended if ethylene glycol ingestion is sus- the ingestion but the owner is unsure how many tablets
pected. Coagulation testing, such as prothrombin time are missing. In this scenario, the clinician should
(PT) and activated partial thromboplastin time (aPTT), approach the treatment of the dog as if 80 of the tablets
is recommended for suspected cases of rodenticide were ingested, constituting a toxic exposure dose of
ingestion. 220 mg/kg, even though the actual exposure was likely
The use of urine testing kits for illicit drug intoxica- less than this amount. Ibuprofen dosages above 125 mg/kg
tion in veterinary patients has been described. One study have been reported to cause acute kidney injury in
comparing urine test screen results with the gold standard dogs, so the clinician in this case should warn the client
of urine toxin detection (gas chromatography/mass of this risk and treat accordingly.
spectrometry) found that an on‐site urine toxin screen Every attempt should be made to establish a likely
(QuickScreen Pro Multi‐Drug Screening Test) accurately timeline of exposure. When the development of signifi-
detected the presence of amphetamines, barbiturates, cant symptomatic toxicity is a possibility, decontamina-
benzodiazepines, and opiates in canine urine but did not tion should be considered. Ingestion is the most common
reliably detect THC (the main psychoactive substance in route of toxin exposure so GI decontamination is often
marijuana) or methadone. needed. GI decontamination is no longer recommended
for every case of ingestion of a known toxin, but decon-
tamination should be considered if there is a likelihood
Certain Exposure to a Known Toxin
of toxic symptoms developing (see “GI decontamination”
When a patient is known to have ingested a specific later in this chapter).
substance, the clinician has a unique opportunity to When the specific toxin and dosage are known and
intervene. Contacting an animal poison control service symptoms are expected or present, available antidotes
(such as the Animal Poison Control Center Hotline should be administered as soon as possible. Timely
[888‐426‐4435] or Pet Poison Helpline [855‐764‐7661]) administration of an antidote following toxin exposure
provides access to a database containing all known is of utmost importance. Examples of common toxins for
pharmacokinetics of the toxin, including toxic dose, which antidotes exist include ethylene glycol, anticoagulant
routes of metabolism, and excretion. Expected symp- rodenticides, organophosphates, acetaminophen, and
toms and recommended therapies to offset the toxicity opioids.
are also provided by these hotlines. A one‐time fee is
charged by the providers of these services. Two Common Examples: Timing is Everything
If contacting a poison control center is not an An in‐depth discussion of all known toxins is beyond
option, an internet‐based search utilizing a veterinary‐ the scope of this chapter, but vitamin K antagonist anti-
specific network (such as the Veterinary Information coagulant rodenticides and ethylene glycol are two of
Network [VIN.com]) often provides much of the same the most common toxins encountered in small animal
information. Even a search of free, nonveterinary practice. The importance of establishing a timeline of
websites such as www.pubmed.gov can help locate exposure whenever possible is highlighted by these two
useful information or publications regarding treat- poisons, because a successful outcome following intoxi-
ment of a known toxin. If the toxin is a manufactured cation depends on timely diagnosis and intervention.
product (i.e., not a naturally occurring toxin such as a Vitamin K1 antagonists inhibit activation of the vita-
plant), the manufacturer of the product can be con- min K‐dependent clotting factors II, VII, IX, X, protein C
tacted. The manufacturer will have information and S. These toxins typically take up to 48 hours to cause
regarding the toxic potential of the substance and prolongation in clotting times; clinical symptoms of
may be able to provide treatment recommendations bleeding may take 4–5 days or longer to develop. Factor
based on the type of exposure. VII has a significantly shorter half‐life than factors II, IX,