Progression of Type I to Type II paralysis in acute organophosphorous poisoning: Is oxidative stress significant?

Abstract

Organophosphorous poisoning is a common method of deliberate self-harm in countries where the pesticides are readily available and can result in type I, II and/or III paralysis. The in-hospital morbidity and mortality of the poisoning are mostly associated with type II paralysis (intermediate syndrome). The aim of this study was to determine the role of oxidative stress in relation to the severity of poisoning and development of type II paralysis in patients suffering from acute organophosphate poisoning. This prospective study was carried out at the Christian Medical College Hospital. Thirty-two patients with acute organophosphorous poisoning, admitted in one medical unit over 17 months, were included in the study. They were clinically assessed for severity of poisoning and paralysis during the first 10 days of their hospitalisation. Temporal profiles of butyrylcholinesterase (BuChE) and oxidative stress parameters, for 4, 7 and 10 days of hospitalisation, were established in 25 of these patients. Type I and II paralysis were associated with severe poisoning. The majority of patients with type II paralysis had prior evidence of type I paralysis. The pattern of muscles that were paralysed in type I paralysis occurring alone and in type I paralysis proceeding to type II paralysis were similar. BuChE was significantly inhibited in all patients. Oxidative stress occurred in acute organophosphate poisoned patients and was greater in severe poisoning. The results suggest that type I paralysis may progress to type II paralysis in severely poisoned patients. They demonstrate early occurrence of oxidative stress in severe acute organophosphate poisoning. However, the development of type II paralysis is not associated with the level of oxidative stress. They suggest that mechanisms other than acetylcholine induced oxidative stress may be involved in the progression of type I to type II paralysis.