Mechanisms of toxicity, clinical features, and management of acute chlorophenoxy herbicide poisoning: A review

Introduction: Chlorophenoxy herbicides are used widely for the control of b road-leaved weeds. They exhibit a variety of mechanisms of toxicity includi ng dose-dependent cell membrane damage, uncoupling of oxidative phosphoryla tion, and disruption of acetylcoenzyme A metabolism. Between January 1962 a nd January 1999, 66 cases of chlorophenoxy herbicide poisoning following in gestion were reported in the literature. Features following ingestion: Adju vants in the formulations may have contributed to some of the features obse rved. Vomiting, abdominal pain, diarrhea, and, occasionally, gastrointestin al hemorrhage were early effects. When present, hypotension was predominant ly due to intravascular volume loss, although vasodilation and direct myoca rdial toxicity may have contributed in some cases. Neurotoxic features incl uded coma, hypertonia, hyperreflexia, ataxia, nystagmus, miosis, hallucinat ions, convulsions, fasciculation, and paralysis. Hypoventilation occurred n ot infrequently, usually in association with central nervous system depress ion, but respiratory muscle weakness was a factor in the development of res piratory failure in some patients. Myopathic symptoms including limb muscle weakness, loss of tendon reflexes, and myotonia were observed and increase d creatine kinase activity was noted in some cases. Other clinical features reported included metabolic acidosis, rhabdomyolysis, renal failure, incre ased aminotransferase activities, pyrexia, and hyperventilation. Twenty-two of 66 patients died.