INFORMATION FOR HEALTH PROFESSIONALS
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have access to this product information in the interim.
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Pralidoxime Iodide Injection (P.A.M.) is available as 0.5g pralidoxime iodide in 20mL.
The principle action of Pralidoxime Iodide Injection (P.A.M.) is to reactivate cholinesterase (mainly outside of the central nervous system) which has been inactivated by phosphorylation due to an organophosphate pesticide or related compound. The reactivation of cholinesterase allows the normal metabolism of acetylcholine to occur, thus allowing the neuromuscular junction and other sites of action to function normally. This includes muscarinic signs to a certain extent. Pralidoxime Iodide Injection (P.A.M.) also slows the process of "aging" of phosphorylated cholinesterase to a non-reactivatable form, and detoxifies certain organophosphates by direct chemical reaction. The drug has its most critical effect in relieving paralysis of the muscle of respiration. Pralidoxime Iodide Injection (P.A.M.) relieves muscarinic symptoms, i.e. salivation, bronchospasm, etc., but this action is relatively unimportant since atropine is adequate for this purpose.
Pralidoxime Iodide Injection (P.A.M.) antagonizes the effects on the neuromuscular junction of the carbamate anticholinesterases, neostigmine, pyridostigmine and ambenonium, used in the treatment of myasthenia gravis. However, it is not nearly as effective as an antidote to these drugs as it is to the organophosphates.
Pralidoxime Iodide Injection (P.A.M.) is distributed throughout the extracellular water; it is not bound to plasma protein. The drug is rapidly excreted in the urine partly unchanged, and partly as a metabolite produced by the liver. The elimination half life is approximately one to two hours. Consequently, Pralidoxime Iodide Injection (P.A.M.) is relatively short acting. In some cases repeated doses or a continuous infusion may be needed, especially where there is evidence of continuing absorption of the poison.
LD50 in mice (mg/kg): 140-178 intravenously, 136-260 intraperitoneally, 290-340 subcutaneously, 1500-4000 orally.
Pralidoxime Iodide Injection (P.A.M.) is indicated as an antidote:
Pralidoxime Iodide Injection is extremely well tolerated in healthy volunteers. Single oral doses up to 7 grams have produced minimal side effects. Intravenous doses are even better tolerated with doses as large as 40.5 grams over a seven day period having no reported side effects.
Treatment of organophosphate poisoning consists of
Pralidoxime Iodide Injection (P.A.M.) administration should be started at the same time as atropine.
Pralidoxime Iodide Injection is initially administered as a slow intravenous dose of 1 to 2 grams. Signs of recovery (increasing consciousness, decreasing fasciculations and weakness) should occur rapidly. If the symptoms reappear, then an infusion of 2.5 percent pralidoxime iodide is infused at a rate of 0.5 grams per hour. A continuous infusion maintains adequate blood levels of pralidoxime iodide better than intermittent injections.
Intramuscular and oral administration are also effective but intravenous is preferred because of rapidity of action.
Atropine is administered intravenously until signs of mild atropinization occur and the muscarinic symptoms relieved. Assessing cardiac effects by monitoring heart rate, watching for signs of mydriasis, dry mouth and decreased respiratory symptoms will give a good clinical assessment of atropinization.
The dose should be 20 to 50 mg per kg as intermittent doses required to alleviate symptoms. An infusion can be used after an initial dose has been given. One gram of Pralidoxime Iodide Injection in 250mL of 5 percent dextrose and 0.2 percent saline has been recommended. (Mayer B, American Family Physician, May 1975 p.123).
Treatment will be most effective if given within a few hours after poisoning has occurred. Usually, little will be accomplished if the drug is first administered more than 48 hours after exposure, but in severe poisoning, it is, nevertheless, indicated since occasionally patients have responded after such an interval.
In severe cases, especially after ingestion of the poison, it may be desirable to monitor the effect of therapy electrocardiographically because of the possibility of heart block due to the anticholinesterase. Where the poison has been ingested, it is particularly important to take into account the likelihood of continuing absorption from the lower bowel since this constitutes new exposure. In such cases, additional doses of Pralidoxime Iodide Injection (P.A.M) may be needed every three to eight hours. In effect, the patient should be "titrated" with Pralidoxime Iodide Injection (P.A.M.) as long as sings of poisoning recur.
In the absence of severe gastrointestinal symptoms, resulting from the anticholinesterase intoxication, Pralidoxime Iodide Injection (P.A.M.) may be administered orally in doses of 1 to 3 g (2 to 6 ampoules) every five hours. As in all cases of organiphosphate poisoning, care should be taken to keep the patient under observation for at least 24 hours.
If convulsions interfere with respiration, sodium thiopentone (2.5 percent solution) may be given intravenously with care.
As an antagonist to such anticholinesterases as neostigmine, pyridostigmine, and ambenonium, which are used in the treatment of myasthenia gravis, Pralidoxime Iodide Injection (P.A.M.) may be given in a dosage of 1 to 2 g intravenously followed by increments of 250 mg every five minutes.
Pralidoxime Iodide Injection (P.A.M.) is contraindicated in patients who may be hypersensitive to it.
Pralidoxime Iodide Injection (P.A.M.) is not effective in the treatment of poisoning due to phosphorus, inorganic phosphates or organophosphates not having anticholinesterase activity.
As the use of Pralidoxime Iodide Injection for the treatment of poisoning of the carbamate class is relatively ineffective, and the fact that its use with carbamyl poisoning may lead to increased toxicity, Pralidoxime Iodide Injection is not recommended for use in this class of poison.
This product contains Iodine and the use of this product in patients who are allergic to Iodine must remain the decision of the treating physician based on clinical factors. No data is currently available.
Intravenous administration of Pralidoxime Iodide Injection (P.A.M.) should be carried out slowly and, preferably, but infusion, since certain side effects, such as tachycardia, laryngospasm, and muscle rigidity, have been attributed in a few cases to a too rapid rate of injection. (See Dosage and Administration). Because Pralidoxime Iodide Injection is excreted in the urine, a decrease in renal function will result in increased blood levels of the drug. Thus, the dosage of Pralidoxime Iodide Injection (P.A.M.) should be reduced in the presence of renal insufficiency.
Pralidoxime Iodide Injection should be used with great caution in treating organiphosphate overdosage in cases of myasthenia gravis since it may precipitate a myasthenic crisis.
The following precautions should be noted in the treatment of anticholinesterase poisoning, although they do not bear directly on the use of Pralidoxime Iodide Injection (P.A.M.): barbiturates should be used cautiously in the treatment of conclusions since they are potentiated by anticholinesterases; morphine, theophylline, aminophylline, succinylcholine, reserpine, and phenothiazine-type tranquilizers should be avoided in patients with organophosphate poisoning.
There is no information available in the safety of this product during Pregnancy and Lactation.
Refer to Warnings and Precautions.
Dizziness, blurred vision, diplopia and impaired accommodation, headache, drowsiness, nausea, tachycardia, hyperventilation, and muscular weakness have been reported after the use of Pralidozime Iodide Injection (P.A.M.), but it is very difficult to differentiate the toxic effects produced by atropine or the organiphosphate compounds from those of the medicine. When atropine and Pralidoxime Iodide Injection (P.A.M.) are used together, the signs of atropinization may occur earlier than might be expected when atropine is used alone. This is especially true if the total dose of atropine has been large and the administration of Pralidoxime Iodide Injection (P.A.M.) has been delayed. Excitement and manic behaviour immediately following recovery of consciousness have been reported in several cases. However, similar behaviour has occurred in cases of organophosphate poisoning that were not treated with Pralidoxime Iodide Injection (P.A.M.).
Artificial respiration and other supportive therapy should be administered as needed.
Store below 25°C.
Prescription Medicine
Pralidoxime Iodide Injection (PAM) is packaged as 5 x 20mL clear glass ampoules.
AFT Pharmaceuticals Ltd.
Box 33-203
Takapuna
Auckland
Ph: (09) 4880232
Ph: (09) 4880234
22 November 2004