Greet Hermans1,2, Helena Van Mechelen3, Frans Bruyninckx4, Tine Vanhullebusch3, Beatrix Clerckx5, Philippe Meersseman6, Yves Debaveye3,5, Michael P Casaer3,5, Alexander Wilmer6, Pieter J Wouters3,5, Ilse Vanhorebeek3, Rik Gosselink7, Greet Van den Berghe3,5. 1. Laboratory of Intensive Care Medicine, Division of Cellular and Molecular Medicine, KU Leuven, Herestraat 49, 3000, Leuven, Belgium. Greet.Hermans@uzleuven.be. 2. Medical Intensive Care Unit, Department of General Internal Medicine, University Hospitals, Leuven, Belgium. Greet.Hermans@uzleuven.be. 3. Laboratory of Intensive Care Medicine, Division of Cellular and Molecular Medicine, KU Leuven, Herestraat 49, 3000, Leuven, Belgium. 4. Department of Physical Medicine and Rehabilitation, University Hospitals Leuven, Leuven, Belgium. 5. Department of Intensive Care Medicine, University Hospitals Leuven, Leuven, Belgium. 6. Medical Intensive Care Unit, Department of General Internal Medicine, University Hospitals, Leuven, Belgium. 7. Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium.
Abstract
PURPOSE:Muscle weakness in long-stay ICU patients contributes to 1-year mortality. Whether electrophysiological screening is an alternative diagnostic tool in unconscious/uncooperative patients remains unknown. We aimed to determine the diagnostic properties of abnormal compound muscle action potential (CMAP), sensory nerve action potential (SNAP), and spontaneous electrical activity (SEA) for Medical Research Council (MRC)-defined weakness and their predictive value for 1-year mortality. METHODS: Data were prospectively collected during the EPaNIC trial (ClinicalTrials.gov: NCT00512122). First, sensitivity, specificity, positive (PPV) and negative predictive values (NPV) of abnormal CMAP, SNAP, and SEA for weakness were determined. Subsequently, association between 1-year mortality and abnormal findings on electrophysiological screening was assessed by univariate and multivariate analyses correcting for weakness and other risk factors and the prediction model involved only a development phase. RESULTS: A total of 730 patients were electrophysiologically screened of whom 432 were tested for weakness. On day 8, normal CMAP excluded weakness with a high NPV (80.5 %). By day 15, abnormal SNAP and the presence of SEA had a high PPV (91.7 and 80.0 %, respectively). Only a reduced CMAP on day 8 was associated with higher 1-year mortality [35.6 vs 15.2 % (p < 0.001)]. This association remained significant after correction for weakness and other risk factors [OR 2.463 (95 % CI 1.113-5.452), p = 0.026]. Also among conscious/cooperative patients without weakness, reduced CMAP was independently associated with a higher likelihood of death occurring during 1 year [HR 2.818 (95 % CI 1.074-7.391), p = 0.035]. CONCLUSIONS: The diagnostic properties of electrophysiological screening vary over time. Abnormal CMAP documented early during critical illness carries information about longer-term outcome, which should be further investigated mechanistically.
RCT Entities:
PURPOSE:Muscle weakness in long-stay ICU patients contributes to 1-year mortality. Whether electrophysiological screening is an alternative diagnostic tool in unconscious/uncooperative patients remains unknown. We aimed to determine the diagnostic properties of abnormal compound muscle action potential (CMAP), sensory nerve action potential (SNAP), and spontaneous electrical activity (SEA) for Medical Research Council (MRC)-defined weakness and their predictive value for 1-year mortality. METHODS: Data were prospectively collected during the EPaNIC trial (ClinicalTrials.gov: NCT00512122). First, sensitivity, specificity, positive (PPV) and negative predictive values (NPV) of abnormal CMAP, SNAP, and SEA for weakness were determined. Subsequently, association between 1-year mortality and abnormal findings on electrophysiological screening was assessed by univariate and multivariate analyses correcting for weakness and other risk factors and the prediction model involved only a development phase. RESULTS: A total of 730 patients were electrophysiologically screened of whom 432 were tested for weakness. On day 8, normal CMAP excluded weakness with a high NPV (80.5 %). By day 15, abnormal SNAP and the presence of SEA had a high PPV (91.7 and 80.0 %, respectively). Only a reduced CMAP on day 8 was associated with higher 1-year mortality [35.6 vs 15.2 % (p < 0.001)]. This association remained significant after correction for weakness and other risk factors [OR 2.463 (95 % CI 1.113-5.452), p = 0.026]. Also among conscious/cooperative patients without weakness, reduced CMAP was independently associated with a higher likelihood of death occurring during 1 year [HR 2.818 (95 % CI 1.074-7.391), p = 0.035]. CONCLUSIONS: The diagnostic properties of electrophysiological screening vary over time. Abnormal CMAP documented early during critical illness carries information about longer-term outcome, which should be further investigated mechanistically.
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