Citation

De Bleecker J, Van den Neucker K, Colardyn F. Crit. Care Med. 1993; 21(11): 1706-1711.

Affiliation

Department of Neurology, University Hospital, Ghent, Belgium.

Copyright

(Copyright © 1993, Society of Critical Care Medicine, Publisher Lippincott Williams and Wilkins)

DOI

unavailable

PMID

8222687

Abstract

OBJECTIVES: To estimate the frequency of the intermediate syndrome in organophosphorus-poisoned patients, and examine its relationship to cholinesterase inhibition and electromyographic findings. Muscle biopsies were available in some patients. DESIGN: A 3-yr prospective study. SETTING: University teaching hospital intensive care unit. PATIENTS: Consecutive patients with acute organophosphorus poisoning (n = 19). MEASUREMENTS AND MAIN RESULTS: We determined the frequency of the intermediate syndrome in poisonings with various organophosphates, duration of (acetyl) cholinesterase inhibition and metabolite excretion, evolution of alterations on repetitive nerve stimulation, type and frequency of muscle lesions. A total of eight of 19 patients developed an intermediate syndrome. In some patients, short relapses of muscarinic symptoms superimposed on the intermediate syndrome. Agents such as methylparathion, fenthion, and dimethoate carry a high risk, but we also noted a prolonged intermediate syndrome in an ethyl-parathion-poisoned patient. Prolonged and severe cholinesterase inhibition occurred during the intermediate syndrome in all patients, and metabolite excretion was prolonged. As the intermediate syndrome evolved, repetitive nerve stimulation initially demonstrated decrement, then increment, and finally, normal responses. Necrotic fibers were noted in muscle biopsies, but these fibers were too sparse to explain severe muscle weakness and were similar in patients with and without the intermediate syndrome. No patients developed delayed neuropathy. CONCLUSIONS: The intermediate syndrome is not rare. Although it is more likely to occur with some organophosphates, it is not confined to a few distinct compounds. This syndrome coincides with prolonged cholinesterase inhibition, and is not due to muscle fiber necrosis. When viewed together, the clinical and electromyographic features are best explained by combined pre- and postsynaptic dysfunction of neuromuscular transmission. The intermediate syndrome is not related to an incipient delayed neuropathy.

Language: en