Eikermann M, Koch G, Gerwig M, Ochterbeck C, Beiderlinden M, Koeppen S, Neuhäuser M, Peters J
Sleep Disorders Research Program, Brigham and Women's Hospital and Harvard Medical School, MA 02115, 75 Francis Street, Boston, USA.
Klinik für Anästhesiologie und Intensivmedizin, Universitätsklinikum Essen, 45122, Essen, Germany.
Intensive Care Med. 2006 Feb;32(2):251-259. doi: 10.1007/s00134-005-0029-x. Epub 2006 Jan 27.
Neuromuscular abnormalities are found frequently in sepsis and multiorgan failure (MOF). Surprisingly, however, there are no data on maximum skeletal muscle force and fatigue in these patients.
To test the research hypotheses that adductor pollicis (AP) force would be lower in patients with sepsis, whereas fatigue would not differ between patients and immobilized but not infected volunteers.
Prospective study; university intensive care unit and laboratory.
Patients with sepsis and MOF (sequential organ failure assessment (SOFA) score >10) and healthy volunteers.
Fatigue was evoked during 20[Symbol: see text]min of intermittent tetanic ulnar nerve stimulation achieving 50% of maximum AP muscle force.
We measured evoked AP muscle force and fatigue, and compound muscle action potential (CMAP), and performed standard electrophysiological tests in 13 patients, and in 7 volunteers before and after immobilization. Maximum force (20+/-16 vs 65+/-19N; p<0.01) and CMAP (3.6+/-2.5 vs 10+/-2.5 mV; p<0.05) were markedly decreased in patients; however, fatigue and ulnar nerve conduction velocity did not differ from volunteers, and a decrement of CMAP was not observed with nerve stimulation frequencies up to 40 Hz. All patients with critical illness polyneuropathy, and an additional 50% of those without, had significant muscle weakness.
Peripheral muscle force is markedly decreased in sepsis, without evidence for an increased fatigability. Muscle weakness was most likely due to a sepsis-induced myopathy and/or axonal neuropathy, and was not the result of an immobilization atrophy.
脓毒症和多器官功能衰竭(MOF)患者常出现神经肌肉异常。然而,令人惊讶的是,尚无关于这些患者最大骨骼肌力量和疲劳情况的数据。
检验研究假设,即脓毒症患者的拇收肌(AP)力量会降低,而患者与固定不动但未感染的志愿者之间的疲劳程度无差异。
前瞻性研究;大学重症监护病房和实验室。
脓毒症和MOF患者(序贯器官衰竭评估(SOFA)评分>10)及健康志愿者。
在20分钟的间歇性强直尺神经刺激过程中诱发疲劳,刺激强度达到最大AP肌肉力量的50%。
我们测量了诱发的AP肌肉力量和疲劳程度,以及复合肌肉动作电位(CMAP),并对13例患者以及7名志愿者在固定前后进行了标准电生理测试。患者的最大力量(20±16 vs 65±19N;p<0.01)和CMAP(3.6±2.5 vs 10±2.5 mV;p<0.05)显著降低;然而,患者的疲劳程度和尺神经传导速度与志愿者无差异,且在高达40Hz的神经刺激频率下未观察到CMAP递减。所有患有重症疾病多发性神经病的患者,以及另外50%未患该病的患者,均有明显的肌肉无力。
脓毒症患者外周肌肉力量显著降低,无疲劳性增加的证据。肌肉无力很可能是由脓毒症诱发的肌病和/或轴索性神经病所致,而非固定性萎缩的结果。