With the establishment of the inadequate efficiency of atropines and oximes in reducing morbidity and mortality of patients poisoned by organophosphates, more attention is given to using other methods such as Fresh Frozen Plasma (FFP) as a bioscavenger to mop up organophosphate toxins. This randomized clinical trial was conducted on 56 organophosphate poisoned patients who were randomly assigned to the FFP and control groups in order of admission. The routine treatment in both groups included atropine and, in moderate to severe cases of poisoning, pralidoxime. The FFP group received four packs of FFP as stat dose at the beginning of treatment. No significant difference was seen between the two groups on the atropine and pralidoxime dosage, hospitalization length and mortality. The present study showed that using four packs of FFP as stat dose at the onset of treatment had no significant effect on the clinical course of organophosphate poisoned patients.
Organophosphorous poisoning causing isolated laryngeal paralysis has only been rarely reported before. We describe a case of difficult extubation in a patient with organophosphorous poisoning, the cause of which was found to be bilateral vocal fold palsy. This is a type of intermediate paralysis that recovers with time. Such a condition should be thought of as a cause of dyspnoea or difficult extubation in patients with organophosphorous poisoning.
In acute severe anticholinesterase poisoning by organophosphate compounds, pralidoxime (P-2-AM, pyridine-2-aldoxime methiodide) used in the recommended doses, intravenously, has not been shown to reactivate the inhibited cholinesterase, as evidenced both clinically and biochemically. In vitro studies using pralidoxime iodide up to ten times the recommended concentrations, produced insignificant reactivation of cholinesterases inhibited by the organophosphate insecticide Bidrin (di-methyl-3-hydroxyl-N, N-dimethyl-crotonamide phosphate). This was even so despite prolonged exposure of the inhibited cholinesterases to the oxime. The value of pralidoxime as a reactivator of phosphorylated cholinesterases is therefore in doubt, and should not be used in preference to large doses of atropine and other supportive treatment in poisoning by organophosphate insecticides.