INTERMEDIATE SYNDROME IN ORGANOPHOSPHORUS POISONING - A PROSPECTIVE-STUDY

Citation
J. Debleecker et al., INTERMEDIATE SYNDROME IN ORGANOPHOSPHORUS POISONING - A PROSPECTIVE-STUDY, Critical care medicine, 21(11), 1993, pp. 1706-1711
Citations number
32
Categorie Soggetti
Emergency Medicine & Critical Care
Journal title
ISSN journal
00903493
Volume
21
Issue
11
Year of publication
1993
Pages
1706 - 1711
Database
ISI
SICI code
0090-3493(1993)21:11<1706:ISIOP->2.0.ZU;2-K
Abstract
Objectives: To estimate the frequency of the intermediate syndrome in organophosphorus-poisoned patients, and examine its relationship to ch olinesterase inhibition and electromyographic findings. Muscle biopsie s were available in some patients. Design: A 3-yr prospective study. S etting: University teaching hospital intensive care unit. Patients: Co nsecutive patients with acute organophosphorus poisoning (n = 19).Meas urements and Main Results: We determined the frequency of the intermed iate syndrome in poisonings with various organophosphates, duration of (acetyl) cholinesterase inhibition and metabolite excretion, evolutio n of alterations on repetitive nerve stimulation, type and frequency o f muscle lesions. A total of eight of 19 patients developed an interme diate syndrome. In some patients, short relapses of muscarinic symptom s superimposed on the intermediate syndrome. Agents such as methyl-par athion, fenthion, and dimethoate carry a high risk, but we also noted a prolonged intermediate syndrome in an ethyl-parathion-poisoned patie nt. Prolonged and severe cholinesterase inhibition occurred during the intermediate syndrome in all patients, and metabolite excretion was p rolonged. As the intermediate syndrome evolved, repetitive nerve stimu lation initially demonstrated decrement, then increment, and finally, normal responses. Necrotic fibers were noted in muscle biopsies, but t hese fibers were too sparse to explain severe muscle weakness and were similar in patients with and without the intermediate syndrome. No pa tients developed delayed neuropathy. Conclusions: The intermediate syn drome is not rare. Although it is more likely to occur with some organ ophosphates, it is not confined to a few distinct compounds. This synd rome coincides with prolonged cholinesterase inhibition, and is not du e to muscle fiber necrosis. When viewed together, the clinical and ele ctromyographic features are best explained by combined pre- and postsy naptic dysfunction of neuromuscular transmission. The intermediate syn drome is not related to an incipient delayed neuropathy.