Organophosphate (OP) poisoning are the most frequently reported of all toxins affecting cats, due primarily to the abundance of OP-based flea collars, flea rinse and other insecticidal preparations used by households on pets. Farm cats have also been reported with OP poisoning in areas where OPs are used to spray farmland.
Proprietary formulations include Malathion, parathion, Diazinon, carbaryl (Sevin), bendiocarb (Ficam), propoxur (Baygon, Sendran), chlorpyrifos (Dursban), methylcarbamate, chlorfenvinphos (Dermaton Dip), cythioate (Proban), dichlorvos (Vapona), dioxathion, fenthion (ProSpot), runnel, phosmet, disulfoton (Di-Syston), Golden Malrin (fly bait).
Acetylcholine is utilized as a neuro- transmitter in many nerve junctions. in the normal animal, acetylcholine is quickly inactivated by acetylcholineste rase and pseudocholinesterase. Organ oph osphate s and organocarbamates competitively inhibit acetylcholinesterase and pseudocholinesterase allowing the continued presence of acetylcholine to maintain a constant state of nerve stimulation. Acetylcholinesterase inhibition by organophosphates tends tobe irreversible; inhibition by organocarbarnates tends to be reversible. Organophosphates and carbarnates are readily absorbed from the skin and the G1 tract and by inhalation.
Signs may be muscarinic, nicotinic, or generalized CNS signs; usually a combination of signs are seen, Muscarinic signs include dyspnea (caused by bronchorrhea and bronchoconstriction), excessive lacrimation, salivation, miosis, micturition (urination), and defecation. Bradycardia is often seen, but tachycardia resulting from catecholarnine release may be seen. Nicotinic signs include twitching of facial muscles, tremors, generalized muscle fasciculations, and then weakness and eventually paralysis. Signs referrable to the CNS include convulsions, seizures, ataxia, and anxiety; centrally mediated respiratory depression may lead to respiratory failure and death. Depression or aggression may be seen.
History, exposure to toxin, and blood cholinesterase depression are useful in the diagnosis of organophosphate or organocarbamate poisoning. Blood (not plasma) cholinesterase depression of 50% of normal (or more) indicates exposure. Depression of cholinesterase activity to less than 25% of normal are often seen in toxicitics. Levels may remain depressed for several days to several weeks; some depression is normal after exposure to routine application of insecticides. Although not a definitive test, an atropine trial may be useful Administer atropine IV at 0.02 to 0.04 mg/kg. If signs of atropinization occur (tachycardia, dry mouth, mydriasis), there is little likelihood that the pet has been poisoned by a cholinesterase inhibitor.
Atropine is antidotal for carbamates and organophosphates and relieves muscarinic signs. Nicotinic signs can be controlled with diphenhydramine hydrochloride and sedatives such as diazepam.
Pralidoxime (2-PAM) will reactivate cholinesterase by freeing the active part of the alkylphosphorylated enzyme complex. 2-PAM has been reported to be of no benefit in treating carbamate toxicosis and may actually further inhibit cholinesterase; however, this drug is recommended for chronic OP posoning at 20mg SQ OID for three days.
Most recent literature indicates that, if it is uncertain what the toxin is but signs suggest a cholinesterase inhibitor, the use of 2 -PAM is indicated. If no response is seen within 3 or 4 doses, the value of the drug is minimal and it is discontinued. 2-PAM should be given early (within 24 hours) in the course of treatment to prevent "aging" of the enzyme complex. Acidosis is treated with fluid therapy and bicarbonate as needed. Emesis and gastric lavage are indicated if oral ingestion occurred (drinking the toxin or licking the toxin from the coat).
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