De Bleecker J, Van den Neucker K, Colardyn F
Department of Neurology, University Hospital, Ghent, Belgium.
Crit Care Med. 1993 Nov;21(11):1706-11. doi: 10.1097/00003246-199311000-00020.
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.
A 3-yr prospective study.
University teaching hospital intensive care unit.
Consecutive patients with acute organophosphorus poisoning (n = 19).
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.
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.
评估有机磷中毒患者中间综合征的发生率，并探讨其与胆碱酯酶抑制及肌电图表现的关系。部分患者可进行肌肉活检。
一项为期3年的前瞻性研究。
大学教学医院重症监护病房。
连续收治的急性有机磷中毒患者（n = 19）。
我们测定了各类有机磷中毒患者中间综合征的发生率、（乙酰）胆碱酯酶抑制及代谢产物排泄的持续时间、重复神经刺激时变化的演变过程、肌肉病变的类型和发生率。19例患者中共有8例发生中间综合征。部分患者在中间综合征基础上出现毒蕈碱样症状的短暂复发。甲基对硫磷、倍硫磷和乐果等制剂导致中间综合征的风险较高，但我们也注意到1例对硫磷中毒患者出现了迁延性中间综合征。所有患者在中间综合征期间均出现了持续且严重的胆碱酯酶抑制，代谢产物排泄时间延长。随着中间综合征的进展，重复神经刺激最初表现为波幅递减，随后递增，最终恢复正常。肌肉活检发现有坏死纤维，但这些纤维数量过少，无法解释严重的肌无力，且有无中间综合征的患者表现相似。无一例患者发生迟发性神经病。
中间综合征并不罕见。虽然某些有机磷制剂更易引发该综合征，但并非仅限于少数特定化合物。该综合征与胆碱酯酶的持续抑制相关，并非由肌纤维坏死所致。综合来看，临床和肌电图特征最好用神经肌肉传递的突触前和突触后联合功能障碍来解释。中间综合征与迟发性神经病初期无关。
