What to Do If a Dog Is Poisoned by Organophosphorus Compounds
[Cause]
Organophosphorus compounds can enter a dog's body through the digestive tract, respiratory tract or skin and cause poisoning. For example, eating food sprinkled with organophosphorus pesticides by mistake, or drinking contaminated surface water near an area where the pesticide was applied by mistake; when preparing or spreading organophosphorus pesticides, the scattered powder or droplets of the liquid contaminate nearby or downwind kennels and food, which the dog licks up, or the dog inhales an aerosol containing the above agents while training, working or playing in the downwind direction and becomes poisoned; improper medication, such as abusing organophosphorus pesticides to treat external parasites, or overdosing by drenching with trichlorfon to expel gastrointestinal parasites; poisoning by saboteurs, etc., are all causes of poisoning.
[Key Points of Diagnosis]
Because the toxicity of various organophosphorus pesticides, the amount ingested, the route of poisoning and the health status of the body differ, the clinical manifestations and course of development of poisoning are also varied. However, most cases take an acute course, and the sick dog often suddenly falls ill within a few hours after inhaling, eating or getting organophosphorus pesticides on its skin. At the beginning of the illness, the dog is mentally excited and restless, with muscle spasms, generally starting from the muscles of the eyelids and face, quickly spreading to the neck, trunk and even the whole body; in mild cases there is tremors, in severe cases convulsions; when the muscles of the limbs twitch, the sick dog frequently steps in place, and when lying on its side makes swimming-like movements. The pupils constrict, and in severe cases become linear. The sick dog salivates, its appetite is greatly reduced or completely lost, it has abdominal pain, loud and continuous bowel sounds, constantly passes watery stools, and even has fecal incontinence. In the late stage of severe cases, the bowel sounds weaken or even disappear. The whole body is drenched in sweat, especially severe on the chest, perineum and around the scrotum. Body temperature rises, and breathing is obviously difficult. The heartbeat is rapid, the pulse is weak and thready, the conjunctiva is cyanotic, and finally the dog dies of suffocation.
Based on the cause and clinical symptoms, a diagnosis can basically be made.
[Treatment]
Apply atropine sulfate by intravenous injection. The dosage can be 1 mg/kg body weight; if the symptoms have not eased after 1-2 hours, the medication can be repeated. When the dog develops dry mouth, dilated pupils, steady breathing and accelerated heartbeat, the so-called "atropinization", the medication can be stopped. Because atropine cannot revive the cholinesterase already bound to organophosphorus, for severe cases it is best to use it in combination with pralidoxime iodide and pralidoxime chloride.
Pralidoxime iodide (PAM) and pralidoxime chloride (pyraloxime chloride) are cholinesterase reactivators; they have a strong phosphoryl-affinity effect, can seize the phosphoryl group bound to cholinesterase, restore the enzyme's hydrolytic capacity, and at the same time can make the organophosphate esters that have entered the body lose their toxicity. Therefore, they are the rescue drugs for acute poisoning by organophosphorus compounds. However, their efficacy is relatively poor for poisoning by dichlorvos, dimethoate, trichlorfon, malathion, etc., and they must be used at the same time as atropine. The dosage of pralidoxime iodide is 20 mg/kg body weight per dose, for intravenous injection. The dosage of pralidoxime chloride is 20 mg/kg body weight per dose. Obidoxime has a better reactivating effect on cholinesterase activity than pralidoxime iodide, and can pass through the blood-brain barrier, with an atropine-like effect. Its dosage is 15-30 mg/kg body weight per dose.