M Eikermann1,2, G Koch3, M Gerwig4, C Ochterbeck3, M Beiderlinden3, S Koeppen4, M Neuhäuser5, J Peters3. 1. Sleep Disorders Research Program, Brigham and Women's Hospital and Harvard Medical School, MA 02115, 75 Francis Street, Boston, USA. meikermann@rics.bwh.harvard.edu. 2. Klinik für Anästhesiologie und Intensivmedizin, Universitätsklinikum Essen, 45122, Essen, Germany. meikermann@rics.bwh.harvard.edu. 3. Klinik für Anästhesiologie und Intensivmedizin, Universitätsklinikum Essen, 45122, Essen, Germany. 4. Klinik und Poliklinik für Neurologie, Universitätsklinikum Essen, 45122, Essen, Germany. 5. Institut für Medizinische Informatik, Biometrie und Epidemiologie, Universitätsklinikum Essen, 45122, Essen, Germany.
Abstract
INTRODUCTION: 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. OBJECTIVES: 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. DESIGN AND SETTING: Prospective study; university intensive care unit and laboratory. PATIENTS: Patients with sepsis and MOF (sequential organ failure assessment (SOFA) score >10) and healthy volunteers. INTERVENTIONS: Fatigue was evoked during 20[Symbol: see text]min of intermittent tetanic ulnar nerve stimulation achieving 50% of maximum AP muscle force. MEASUREMENTS AND RESULTS: 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. CONCLUSION: 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.
INTRODUCTION: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. OBJECTIVES: 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. DESIGN AND SETTING: Prospective study; university intensive care unit and laboratory. PATIENTS: Patients with sepsis and MOF (sequential organ failure assessment (SOFA) score >10) and healthy volunteers. INTERVENTIONS:Fatigue was evoked during 20[Symbol: see text]min of intermittent tetanic ulnar nerve stimulation achieving 50% of maximum AP muscle force. MEASUREMENTS AND RESULTS: 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. CONCLUSION: 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.
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