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metabolite NAPQI by providing additional glutathione substrate. 7 Baseline blood work and follow-up biochemical panels should be performed to monitor for the presence of metHb, Heinz body anemia, or evidence of hepatotoxicity. Generally, prognosis is fair to excellent with therapy. If clinical signs resolve and liver enzymes are within normal limits after 48 hours of NAC therapy, patients can be discharged with SAMe (for 30 days). Those with severe hepatic failure have a poorer prognosis. ASTHMA INHALERS (e.g., ALBUTEROL) Asthma inhalers are often used in both human and veterinary medicine. Various types of medications may be used, including steroids (e.g., fluticasone) or beta agonists (e.g., albuterol, salbutamol, etc.). When beta-agonist inhalers are accidentally chewed and punctured by dogs, they can result in a severe, life-threatening, acute toxicosis. (Inhaled steroids are not a large toxicity issue). Because inhalers often contain approximately 200 metered, concentrated doses, a massive amount of beta- agonist is released with just one puncture. Clinical signs include cardiac (e.g., tachycardiac, a “racing heart rate” per the owner, injected gums, hypotension, hypertension, severe arrhythmias), electrolyte changes (e.g., severe hypokalemia, hyperglycemia), GI (e.g., vomiting), and CNS (e.g., mydriasis, agitation, weakness, collapse, death). Treatment includes stat electrolyte monitoring, IV fluids, potassium supplementation, blood pressure and ECG monitoring, sedation/anxiolytics (if the patient is agitated, hypertensive, and tachycardiac), anti-arrhythmics such as beta-blockers (e.g., propranolol, esmolol, etc.), and symptomatic supportive care. Treatment for 24-36 hours is typically necessary, until clinical signs resolve. DECONGESTANTS Cold and flu medications (e.g., “Claritin-D”) often carry decongestants such as pseudoephedrine (PSE) and phenylephrine (PE). The exact mechanism of how these drugs work is unknown but thought to stimulate alpha and beta-adrenergic receptors by releasing norepinephrine. Phenylephrine is typically considered to be less toxic than PSE as it is less bioavailable with oral ingestion. Clinical signs seen with decongestant ingestion include cardiac (e.g., tachycardia, hypertension, reflex bradycardia), CNS (e.g., mydriasis, agitation, trembling, seizures), and various miscellaneous signs (e.g., hyperthermia). With PSE, moderate to severe clinical signs can be seen at 5-6 mg/kg, while death has been reported at 10-12 mg/kg. With phenylephrine, similar clinical signs can be seen, although GI signs such as vomiting are the most common sign observed. Treatment includes decontamination (if appropriate), administration of one dose of charcoal with a cathartic, IV fluid therapy (to enhance urinary elimination), blood pressure monitoring, anti-emetics, sedatives/anxiolytics (e.g., acepromazine), muscle relaxants for tremoring (e.g., methocarbamol 22-100 mg/kg, IV PRN), anticonvulsants (e.g., phenobarbital 4-6 mg/kg, IV, PRN), and rarely, anti-hypertensives (e.g., hydralazine).

and toxic dose was ingested. For example, in dogs, ibuprofen results in GI signs at doses as low as 16-50 mg/kg, while severe GI signs may be seen at 50-100 mg/kg. 6 Renal compromise may be seen at doses of 100-250 mg/kg (resulting in potential AKI), and fatalities have been reported at doses > 300 mg/kg. 6 This differs tremendously from naproxen sodium (dogs), where severe clinical signs can be seen at doses as low as 5 mg/kg. 6 Clinical signs of NSAID toxicosis include anorexia, vomiting, hematemesis, diarrhea, melena, abdominal pain, lethargy, malaise, uremic halitosis, dehydration, etc. Treatment includes decontamination, the use of activated charcoal (often multiple doses due to enterohepatic recirculation, if appropriate), GI protectants (e.g., H2 blockers, sucralfate), aggressive IV fluid therapy (to help maintain renal blood flow), anti-emetic therapy, and symptomatic and supportive care. With high doses, anticonvulsants may also be necessary if CNS signs develop. ACETAMINOPHEN Acetaminophen (N-acetyl-p-aminophenol), a cyclooxygenase (COX)-3 inhibitor, is a popular OTC analgesic and antipyretic medication used frequently in humans. It is not considered a true NSAID as it lacks anti-inflammatory properties. Normally, part of this drug is metabolized into non-toxic conjugates via the metabolic pathways (glucuronidation and sulfation); 7 some is metabolized into the toxic metabolite, N-acetyl-para- benzoquinoneimine [NAPQI] via the cytochrome P-450 enzyme pathway. 7 Typically, NAPQI is detoxified by conjugation with glutathione in the liver. 7 Toxicosis occurs when glucuronidation and sulfation pathways are depleted; this results in toxic metabolites building up and secondary oxidative injury occurring. 7 While this drug is very safe for human use, it has a narrow margin of safety in dogs and cats; the severity of toxicosis and development of clinical signs is species dependent. Cats have an altered glucuronidation pathway and a decreased ability to metabolize acetaminophen, making them much more susceptible to toxicosis. In cats, red blood cell (RBC) injury is more likely to occur in the form of methemoglobinemia (metHb), and toxicity can develop at doses as low as 10 mg/kg. 7 In cats, lethargy, swelling of the face or paws, respiratory distress, brown mucous membranes, cyanosis, vomiting, and anorexia may be seen secondary to metHb. In dogs, hepatic injury is more likely to occur; acetaminophen toxicosis can occur at doses > 100 mg/ kg, while metHb can develop at doses of > 200 mg/kg. 7 Dogs may develop clinical signs of keratoconjunctivitis sicca (dry eye), malaise, anorexia, hepatic encephalopathy, vomiting, melena, and icterus secondary to hepatotoxicity. Treatment includes decontamination, administration of activated charcoal (AC), anti-emetic therapy, IV fluid therapy, treatment for hypoxemia (e.g., oxygen, blood transfusion, etc.), antioxidant therapy (e.g., Vitamin C), provision of a glutathione source (S-adenosyl-methionine or SAMe), and the antidote n-acetylcysteine (NAC, ideally IV) to limit formation of the toxic


Top 10 Human Medications Poisonous to Dogs and Cats


toxicosis, secondary stimulation of certain body systems can result in significant clinical signs: GI (e.g., vomiting, diarrhea, hypersalivating), CNS (e.g., agitation, mydriasis, tremors, seizures), cardiovascular (e.g., tachycardia, hypertension), and respiratory (e.g., panting). Both clinical signs and treatment for amphetamine toxicosis are similar to SSRI toxicosis, and include IV fluids, cooling measures, sedation (e.g., with acepromazine or chlorpromazine), muscle relaxants, anticonvulsants, thermoregulation, blood pressure monitoring, and symptomatic/ supportive care. NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS) NSAIDs are competitive inhibitors of prostaglandin synthesis (cyclooxygenase or “COX” inhibitors) and result in decreased prostaglandin, which is important for normal homeostatic function (including maintaining renal blood flow, maintaining mucous production in the stomach, etc.). Common OTC human NSAIDs include active ingredients such as ibuprofen and naproxen sodium. Examples of human NSAIDs include Advil®, Aleve®, certain types of Motrin®, etc. Common prescription veterinary NSAIDs can also result in toxicosis, particularly when available in the chewable, palatable formulation. Examples of veterinary NSAIDs include carprofen, deracoxib, etogesic, previcoxib, etc. With NSAID toxicosis, the GI tract, kidneys, CNS, and platelets can be affected. Cats and certain breeds of dogs (e.g., German shepherds) seem to be more sensitive to NSAIDs and should be treated aggressively. With cats, severe acute kidney injury (AKI) is often more clinically seen with NSAID toxicosis at lower doses (as compared to dogs). With dogs, signs secondary to GI ulceration (e.g., vomiting, diarrhea, melena, hematemesis, etc.) are more commonly seen initially, followed by secondary AKI. With NSAID toxicosis, it is important to keep in mind that each NSAID has a different toxic dose, margin of safety, half-life, and route of excretion, and the ASPCA Animal Poison Control Center should be contacted to identify what specific NSAID

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Sedation or central nervous system (CNS) stimulation

Anorexia Lethargy

Serotonin syndrome

Clinical signs of serotonin syndrome include gastrointestinal (GI) signs (e.g., hypersalivation, vomiting, diarrhea, abdominal pain) and CNS signs (e.g., stimulation, mydriasis, tremors, seizures, hyperthermia secondary to tremoring and seizures). Treatment for antidepressants includes decontamination (ideally done at a veterinarian, due to the rapid onset of clinical signs), sedation (e.g., with acepromazine or chlorpromazine), intravenous (IV) fluid therapy, blood pressure and electrocardiogram (ECG) monitoring, thermoregulation, muscle relaxants (for tremors; methocarbamol 22-55 mg/kg, IV, PRN), anticonvulsants (e.g., phenobarbital 4-16 mg/kg, IV, PRN; diazepam 0.25-0.5 mg/kg, IV, PRN), serotonin antagonists [e.g., cyproheptadine (1.1 mg/ kg for dogs or 2-4 mg total per cat) PO or rectally q. 6-8], and supportive and symptomatic care. In general, the prognosis for antidepressant toxicosis is excellent. AMPHETAMINES Amphetamines are used for a variety of medical and illicit reasons. Legal forms include prescription medications for attention-deficit disorder/attention deficit-hyperactivity disorder (ADD/ADHD), weight loss, and narcolepsy. Examples of amphetamines include dextroamphetamine, amphetamine (Adderall®), d-amphetamine (Dexedrine®), methamphetamine (Desoxyn®) and lisdexamfetamine (Vyvanse®). Illegal forms of amphetamines include street drugs like methamphetamine, crystal meth, and ecstasy. This class of drugs acts as sympathomimetic agents, meaning they stimulate the sympathetic system. Amphetamines also cause stimulation of alpha and beta-adrenergic receptors and stimulate release of serotonin and norepinephrine; this results in increased catecholamine stimulation in the synapse. Amphetamines also increase release of serotonin from the presynaptic membrane, resulting in serotonin syndrome. With amphetamine

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