Abstract
IntroductionSepsis-induced myopathy and critical illness myopathy (CIM) are possible causes of muscle weakness in intensive care patients. They have been attributed to muscle membrane dysfunction. The aim of this study was to investigate membrane properties in the early stage of experimental sepsis by evaluating muscle excitability.MethodsIn total, 20 anaesthetized and mechanically ventilated pigs were randomized to either faecal peritonitis (n = 10) or to non-septic controls (n = 10). Resuscitation with fluids and vasoactive drugs was started 3 hours after peritonitis induction. Muscle membrane properties were investigated by measuring muscle velocity recovery cycles before induction of peritonitis as well as 6, 18 and 27 hours thereafter. Muscle relative refractory period (MRRP) and early supernormality (ESN) were assessed.ResultsPeritonitis lasting 27 hours was associated with an increase of MRRP by 28% from 2.38 ± 0.18 ms (mean ± SD) to 3.47 ± 1.79 ms (P <0.01) and a decrease of ESN by 31% from 9.64 ± 2.82% to 6.50 ± 2.64% (P <0.01). ESN reduction was already apparent 6 hours after induction of peritonitis. Values in controls did not show any significant alterations.ConclusionsMuscle membrane abnormalities consistent with membrane depolarization and/or sodium channel inactivation occurred within 6 hours of peritonitis induction. This indicates that changes that have been described in established sepsis-induced myopathy and/or CIM start early in the course of sepsis. Muscle excitability testing facilitates evaluation of the time course of these changes.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-014-0484-2) contains supplementary material, which is available to authorized users.
Highlights
Sepsis-induced myopathy and critical illness myopathy (CIM) are possible causes of muscle weakness in intensive care patients
The entities that variably contribute to Intensive care unit (ICU)-acquired weakness are critical illness polyneuropathy (CIP) and myopathy (CIM) and/or sepsis-induced myopathy [1,2,3]
There was a progressive increase of heart rate and decrease of stroke volume, whereas these parameters remained unchanged in controls over time (Figure 2)
Summary
Sepsis-induced myopathy and critical illness myopathy (CIM) are possible causes of muscle weakness in intensive care patients. They have been attributed to muscle membrane dysfunction. The aim of this study was to investigate membrane properties in the early stage of experimental sepsis by evaluating muscle excitability. Intensive care unit (ICU)-acquired weakness is a frequent and severe complication in ICU patients. These patients develop diffuse muscle weakness and failure to wean from mechanical ventilation. The entities that variably contribute to ICU-acquired weakness are critical illness polyneuropathy (CIP) and myopathy (CIM) and/or sepsis-induced myopathy [1,2,3].
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