Muscle injury in organophosphorous poisoning and its role in the development of intermediate syndrome.

Muscle injury and its role in the development of Type II paralysis was studied in 25 patients with acute organophosphate poisoning. All patients were assessed for severity of poisoning at admission and through the course of poisoning for the development and duration of intermediate syndrome (IS) (Type II paralysis). Blood levels of acetylcholinesterase, creatine kinase, creatine kinase MM, LDH and LDH5 were estimated through the course of the poisoning. Of the 25 patients, 22 were severely poisoned and 3 had mild to moderate poisoning. Severely poisoned patients had a significantly greater rate of developing intermediate syndrome (17/22) (P = 0.026). Type I paralysis and fasciculations occurred in 76 and 70.5% of patients who developed intermediate syndrome, in comparison to 38 and 50%, respectively, of those who did not develop intermediate syndrome. Weakness developed in the same groups of muscles in both Types I and II paralysis but was of longer duration in patients who developed Type II paralysis. Acetylcholinesterase was inhibited > 90% throughout the course of poisoning with greater inhibition in patients with longer duration intermediate syndrome. Muscle injury was seen in all patients beginning at admission, peaking over the first 5 days and then declining over the next 5 days. Temporal profiles of blood muscle isoenzymes showed significantly greater muscle injury in those patients with greater severity of poisoning at admission, those who developed intermediate syndrome and in patients with longer duration intermediate syndrome. The findings of this study suggest that Types I and II paralysis in organophosphate poisoning are not separate syndromes but a clinical continuum determined by the severity of poisoning. The magnitude of organophosphate exposure and of muscle injury during the cholinergic crises appears to determine the occurrence and severity of intermediate syndrome.