Organophosphorus compound poisoning in dogs

[etiology]

Organophosphorus compounds can be poisoned by entering dogs through digestive tract, respiratory tract or skin. For example, if you accidentally eat food spread with organophosphorus pesticides and drink contaminated surface water near the area where organophosphorus pesticides are spread; when preparing or spreading organophosphorus pesticides, the droplets of scattered powder or liquid contaminate kennels or food near or downwind, and are licked by dogs, or dogs are poisoned by inhaling aerosols containing the above agents during training, homework or games. Improper use of drugs, such as the abuse of organophosphorus pesticides to treat external parasites, or excessive administration of trichlorfon to dispel gastrointestinal parasites, and the poisoning of bad molecules are all causes of poisoning.

[main points of diagnosis]

Due to the different toxicity, intake, poisoning pathways and health status of various organophosphorus pesticides, the clinical manifestations and development of poisoning are also varied. However, in most acute cases, sick dogs often develop suddenly within hours of inhalation, ingestion or skin exposure to organophosphorus pesticides. At the beginning of the disease, mental excitement and muscle spasms generally start from the eyelid and facial muscles, and soon extend to the neck, trunk cadres and even the whole body muscles, light tremor, severe convulsions, and limb muscle clonus, the sick dog steps frequently, while lying on his back, he makes swimming movements. The pupils are dilated and linear in severe cases. Sick dogs salivate, loss of appetite or abstinence, abdominal pain, high intestinal sound, continuous, continuous defecation, and even defecation incontinence. In the later stage of severe illness, the intestinal sound weakened or even disappeared. Sweat dripping all over the body, especially in the chest, perineum and around the scrotum. The body temperature rises and it is obviously difficult to breathe. Rapid heartbeat, weak pulse, conjunctival cyanosis, and finally died of asphyxiation.

According to the etiology and clinical symptoms, the diagnosis can be made basically.

[treatment]

Atropine sulfate was injected intravenously. The dosage can be 1 mg / kg body weight, and the drug can be used repeatedly when the symptoms are not alleviated after 1-2 hours. When the dog appears dry mouth, dilated pupils, smooth breathing, rapid heartbeat, that is, the so-called "atropinization", medication can be stopped. Because atropine can not revive the choline ester which has been combined with organophosphorus, it is best to use it in combination with pralidoxime iodide and pralidoxime chloride in severe cases.

Pralidoxime iodide (Pam) and pralidoxime chloride (pralidoxime chloride) are cholinesterase reactivating agents. They have strong phosphophilic effect, which can seize the phosphoryl group bound to cholinesterase and restore the hydrolysis ability of the enzyme. At the same time, it can also make the organophosphate into the body lose its toxicity. Therefore, it is a cure for acute poisoning of organophosphorus compounds. However, the effect on dichlorvos, dimethoate, trichlorfon and malathion poisoning is poor, so it must be used at the same time with atropine. The dosage of pralidoxime iodide is 20 mg / kg body weight for intravenous injection. The dosage of pralidoxime chloride is 20 mg / kg body weight. The recovery effect of double compound phosphorus on cholinesterase activity is better than that of pralidoxime iodide, and it can pass through the blood-brain barrier, which has Atto-like effect. Its dosage is 15-30 mg / kg body weight.