pralidoxime has been researched along with Nausea* in 2 studies
1 review(s) available for pralidoxime and Nausea
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Management of acute childhood poisonings caused by selected insecticides and herbicides.
Most childhood exposures to insecticides and herbicides do not result in poisonings. Decontamination and observation are usually adequate treatments. The most frequent exposures involve carbamate and organophosphate insecticides. These compounds inhibit acetylcholinesterase, resulting in cholinergic signs that are reversible with atropine administration. Recent reports from poison control centers indicate that organophosphates have been associated with most of the serious childhood poisonings. Pralidoxime, a cholinesterase reactivator, must be administered along with atropine to patients with serious organophosphate poisoning, to reverse nicotinic receptor effects--in particular, respiratory paralysis. Although carbamates and organophosphates may cause clinically indistinguishable physical signs, pralidoxime therapy may be contraindicated for carbamate intoxications. In the event of a serious poisoning caused by a combination of organophosphate and carbamate insecticides, or by an unknown cholinergic agent, pralidoxime should not be withheld. Many organochlorine insecticides are restricted or are no longer available in the United States. CNS excitation and seizures, manifestations of organochlorine intoxication, can occur following ingestion or inappropriate application of the 1 per cent topical formulation of lindane used to treat scabies and lice. Treatment of such intoxication consists of decontamination measures and anticonvulsant administration. Pyrethrins are generally nontoxic in doses commonly ingested. Individuals with an allergic history may be at greatest risk for the most common adverse effects, contact dermatitis and hypersensitivity reactions. Of all insecticides or herbicides, paraquat is the most toxic. Any exposure to paraquat must be evaluated, even if several days have passed since the herbicide was ingested. Signs of pulmonary status deterioration usually portend a grave prognosis in paraquat poisoning. Despite in vitro toxicity similar to paraquat, diquat does not cause lung effects in human poisonings, and reported deaths have been from other causes. Poisoned patients who receive appropriate and timely treatment are virtually assured of complete recovery from most insecticide and herbicide poisonings. Deaths and long-term sequelae most often result from respiratory complications, which may occur as complications of the intoxication or from other constituents in the insecticide or herbicide formulation. Good supportive care with metic Topics: Absorption; Adolescent; Animals; Anticonvulsants; Atropine; Carbamates; Central Nervous System; Child; Child, Preschool; Cholinesterase Inhibitors; Dose-Response Relationship, Drug; Gastric Lavage; Herbicides; Humans; Insecticides; Nausea; Organophosphorus Compounds; Paraquat; Pralidoxime Compounds; Seizures; Vomiting | 1986 |
1 other study(ies) available for pralidoxime and Nausea
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Adverse behavioral effects of the anticholinesterase poisoning protector pralidoxime methanesulfonate.
Pralidoxime methanesulfonate (P2S) has anticholinesterase protective properties, but it also has an array of gastrointestinal (GI) symptoms. Because such a symptom would be disadvantageous to occupational workers who handled and used organophosphorus anticholinesterase continuously, and to soldiers who have had oral pretreatment in a situation where anticholinesterase agent poisoning is a possibility, this question was investigated in rats using three behavioral paradigms to evaluate the feasibility of the oral prophylactic regimen. These are: (1) conditioned taste aversion (CTA), (2) operant behavior and (3) spontaneous locomotor activity (SMA); these three behavioral parameters are analogous to toxicant-induced gastrointestinal (GI) disturbances, performance of learned tasks and behavioral arousal, respectively. Dose-response studies of P2S in dose levels of 0.2, 0.4, 0.8 and 1.6 gm/kg (P.O.) were evaluated. The results consistently demonstrated that only the highest dose significantly produced marked decreases in consumption of flavored solution associated with its ingestion, suppressed keypress response maintained under a 20-response fixed-ratio schedule of water presentation, and inhibited SMA. By inference, if CTA, operant behavior and SMA are appropriate paradigms, P2S, on an acute single oral high dose level, would cause GI disturbances, impair task performance and induce sedation in man. Topics: Animals; Avoidance Learning; Cholinesterase Inhibitors; Drinking Behavior; Exploratory Behavior; Gastrointestinal Diseases; Male; Nausea; Pralidoxime Compounds; Rats; Rats, Inbred Strains; Taste | 1984 |