QUARTERLY BEAT / APRIL 2025
the breakdown of acetylcholine (AcH), resulting in too much AcH and stimulation of sympathetic, parasympathetic, and peripheral nervous systems. This results in AcH accumulation at nerve junctions, resulting in severe clinical “SLUDGE” signs (e.g., salivation, lacrimation, urination, defecation, gastrointestinal). Some carbamates and OPs have various levels of toxicosis (e.g., ranging from low to very high), depending on the active ingredient. Clinical signs can be seen as early as 30-60 minutes, and typically are seen within 6 hours (but rarely seen > 12 hours). By the time patients present to the veterinary clinic, it is typically too late to decontaminate safely. Clinical signs include severe GI signs (e.g., hypersalivation, vomiting, diarrhea), cardiovascular signs (e.g., tachycardia, bradycardia, pallor, shock), CNS signs (e.g., agitation, sedation, mydriasis or miosis, tremors, seizures, coma), and respiratory signs (e.g., tachypnea, dyspnea, hypoxemia). Death may occur due to fluid accumulation with the bronchi, or secondary to disseminated intravascular coagulation (DIC) secondary to hyperthermia from tremors and seizure activity. Very rarely, intermediate syndrome can be seen with OP toxicosis, where clinical signs are seen > 24-72 hours after onset of acute signs; these signs can last up to 7-14 days and include signs of neuromuscular weakness, ventroflexion of the neck, cranial nerve deficits, and even death from respiratory depression and hypoventilation. 10-11 Treatment includes aggressive decontamination (e.g., gastric lavage with an inflated endotracheal tube, administration of activated charcoal with a cathartic), fluid therapy, anti-emetics (e.g., maropitant), muscle relaxants (e.g., methocarbamol), anticonvulsants (e.g., phenobarbital, diazepam, levetiracetam, etc.), thermoregulation, electrocardiogram, blood pressure monitoring, and symptomatic supportive care. Most importantly, aggressive use of the antidote atropine or 2-PAM (which is rarely available from human medical facilities) is warranted. Atropine, an anticholinergic, blocks the neurotransmitter acetylcholine in the central and peripheral nervous systems. Atropine competes with AcH at the post-ganglionic parasympathetic sites (and hence is called an antiparasympathetic or parasympatholytic drug). 10-11 It is also called an antimuscarinic as it antagonizes the muscarine-like actions of AcH. 10-11 It is used for the treatment of SLUDGE signs from organophosphate or carbamate toxicity. With OP toxicosis, atropine should be given despite the tachycardiac; higher doses are often necessary. Doses for atropine are higher than anesthetic doses for bradycardia and range from 0.1-0.5 mg/kg IV or IM as needed. BIFENTHRIN: Bifenthrin is a synthetic derivative of pyrethroids and is commonly found in household insect sprays and insecticides (e.g., permethrin, cypermethrin, cyphenothrin, etc.). Bifenthrin in dogs causes the same clinical signs as permethrin in cats and can be quite profound as compared to other pyrethrins/pyrethroids; rarely, it can result in fatality. 12 Due to a cat’s altered liver glucuronidation metabolism, cats are significantly more sensitive to pyrethrins than dogs. While a precise toxic dose for cats is not well established, products containing greater than a 5-10% concentration of pyrethrins may lead to systemic toxicosis. The diluted amount found in household insect sprays and topical flea sprays and shampoos is typically < 1%. Toxicosis from exposure to these products is highly unlikely. The application of canine spot-on pyrethrin/pyrethroid based insecticides (typically ~40-50% concentration) to cats is the primary cause of feline pyrethrin toxicosis. Cats that groom dogs following recent spot-on applications are also at high risk for toxicosis; ideally, pets should be
separated until the spot-on product has completely dried on the dog to prevent cat exposure. Signs of systemic toxicosis of pyrethroid toxicosis in cats include GI signs (e.g., hypersalivation, vomiting, nausea), CNS signs (e.g., disorientation, weakness, hyperexcitability, tremors, seizures) and respiratory signs (e.g., tachypnea, dyspnea). Tremors are extremely responsive to methocarbamol (22-220 mg/kg IV PRN to effect), a centrally acting muscle relaxant, although oral absorption of methocarbamol is often slower in onset of action. In general, tremors are less responsive to benzodiazepines (e.g., diazepam). Seizures may be controlled with anticonvulsants (phenobarbital, 4-16 mg/ kg IV PRN to effect) or general gas anesthesia. Dermal decontamination is crucial but should be performed after stabilization. This should be performed with a liquid dish detergent (e.g., Dawn, Palmolive) or follicular flushing shampoo. Supportive care including the monitoring and maintenance of hydration, body temperature and blood glucose levels are necessary. Signs may persist for 1-4 days, depending on the animal. The prognosis is excellent with aggressive dermal decontamination and treatment. CONCLUSION: Pet owners should be appropriately educated on how to pet-proof the house and be trained on what common human medications can be toxic to pets. Pet owners should also be appropriately educated on crate training to help minimize toxin exposure. When in doubt, the ASPCA Animal Poison Control Center should be consulted for toxic ingestions that veterinarians are unaware of.
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