In this study whole blood cholinesterase activities were determined (tintometric method) of agricultural pesticide users exposed to organophosphorus compounds in Indonesia, Malaysia, Sri Lanka and Thailand. Analysis of the data demonstrated a universal relationship between cholinesterase levels and the time between the last exposure to organophosphorus compounds and the day of blood collection for cholinesterase determination. It is suggested that it takes approximately 5 days before whole blood cholinesterase levels revert to their normal values. No relationship between whole blood cholinesterase levels and the sex of pesticide users was demonstrated except in Sri Lanka where female sprayers had lower values. It is suggested that these lower values are associated with the anaemic status of female agricultural workers. No relationship between whole blood cholinesterase level and age was demonstrated. The measurement of pre-exposure cholinesterase values is essential for comparison of values after pesticide application.
A patient with organophosphate poisoning who survived the acute phase and subsequently developed delayed neuropathy is presented. The features of this form of delayed neuropathy are described and the implications in our local context discussed.
Accidental organophosphate poisoning may occur in persons coming in close contact with animals being treated toitb organophosphate pesticides. The poisoning may manifest itself as a severe systemic disorder, but can be diagnosed by an alert physician and confirmed by specific tests of reduced cholinesterase activity in the blood, plasma and red blood cells. Treatment is with intravenous atropine. Supportive measures may be necessary.
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.
From 1970 to 1984, 100 patients suffering from organophosphate poisoning were treated in the Intensive Care Unit at the University Hospital. These patients developed signs and symptoms of cholinergic over-activity and were treated with continuous intravenous atropine. Many of the patients also developed acute respiratory failure, which necessitated ventilatory support in the form of intermittent positive pressure ventilation. Other measures included the use of inotropes and nutritional support. Daily estimation of serum cholinesterase levels were useful in assessing degree of recovery of the patients from the effects of the organophosphates.