IntroductionCritically ill patients are characterized by increased loss of muscle mass, partially attributed to sepsis and multiple organ failure, as well as immobilization. Recent studies have shown that electrical muscle stimulation (EMS) may be an alternative to active exercise in chronic obstructive pulmonary disease (COPD) and chronic heart failure (CHF) patients with myopathy. The aim of our study was to investigate the EMS effects on muscle mass preservation of critically ill patients with the use of ultrasonography (US).MethodsForty-nine critically ill patients (age: 59 ± 21 years) with an APACHE II admission score ≥13 were randomly assigned after stratification upon admission to receive daily EMS sessions of both lower extremities (EMS-group) or to the control group (control group). Muscle mass was evaluated with US, by measuring the cross sectional diameter (CSD) of the vastus intermedius and the rectus femoris of the quadriceps muscle.ResultsTwenty-six patients were finally evaluated. Right rectus femoris and right vastus intermedius CSD decreased in both groups (EMS group: from 1.42 ± 0.48 to 1.31 ± 0.45 cm, P = 0.001 control group: from 1.59 ± 0.53 to 1.37 ± 0.5 cm, P = 0.002; EMS group: from 0.91 ± 0.39 to 0.81 ± 0.38 cm, P = 0.001 control group: from 1.40 ± 0.64 to 1.11 ± 0.56 cm, P = 0.004, respectively). However, the CSD of the right rectus femoris decreased significantly less in the EMS group (-0.11 ± 0.06 cm, -8 ± 3.9%) as compared to the control group (-0.21 ± 0.10 cm, -13.9 ± 6.4%; P < 0.05) and the CSD of the right vastus intermedius decreased significantly less in the EMS group (-0.10 ± 0.05 cm, -12.5 ± 7.4%) as compared to the control group (-0.29 ± 0.28 cm, -21.5 ± 15.3%; P < 0.05).ConclusionsEMS is well tolerated and seems to preserve the muscle mass of critically ill patients. The potential use of EMS as a preventive and rehabilitation tool in ICU patients with polyneuromyopathy needs to be further investigated.Trial Registrationclinicaltrials.gov: NCT00882830

The relationship between the electromyographic (EMG) power spectrum and muscle conduction velocity was investigated during both fatiguing and nonfatiguing contractions of the adductor pollicis muscle. Changes in the EMG power spectrum were measured by Fourier transform analysis and by comparing the power in the high (130-238 Hz) and low (20--40 Hz) frequency bands. Changes in conduction velocity were measured during voluntary activity from changes in the muscle mass action potential evoked by periodic maximal shocks to the nerve. This was varied independently either by maintaining a 60-s fatiguing maximal voluntary contraction involving 30--50% loss of force or by changing muscle temperature in the absence of fatigue. Both procedures resulted in similar changes in the power spectrum. However, the change in conduction velocity required to generate equal changes in the EMG was about 10 times greater in the absence of fatigue than those observed during a 60-s maximum contraction initiated at any initial muscle temperature. This suggests that during fatigue of maximal voluntary contractions, factors other than changes in the wave form of individual muscle fiber action potentials must contribute to the observed shift in the total surface EMG frequency components.

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First, patients' serum Ang-2 levels are increased during severe sepsis and associated with disease severity. The strong relationship of serum Ang-2 with serum tumor necrosis factor-alpha suggests that the latter may participate in the regulation of Ang-2 production in sepsis. Second, inflammatory mediators reduce Ang-2 release from human lung microvascular endothelial cells, implying that this vascular bed may not be the source of increased Ang-2 in human sepsis.

CIPM has a high incidence in the ICU setting. Our study revealed the association of aminoglycosides, hyperglycemia and illness severity with CIPM development, as well as the association between Gram (-) bacteremia and development of CIPM in less severely ill patient population.

Coagulation system and platelets are strongly activated in sepsis. In this stage, only factor XII is decreased. In contrast, in severe sepsis and mainly in septic shock, most of the coagulation factors are depleted, PTL is decreased, and global coagulation tests are prolonged, indicating exhaustion of hemostasis. Finally, Gram-positive, Gram-negative, and other microorganisms produce identical impairment of coagulation.

Background: Skeletal muscle wasting commonly occurs in patients with chronic obstructive pulmonary disease (COPD) and has been associated with the presence of systemic inflammation. This study investigated whether rehabilitative exercise training decreases the levels of systemic or local muscle inflammation or reverses the abnormalities associated with muscle deconditioning. Methods: Fifteen patients with COPD (mean (SE) forced expiratory volume in 1 s 36 (4)% predicted) undertook high-intensity exercise training 3 days/week for 10 weeks. Before and after the training programme the concentration of tumour necrosis factor a (TNFa), interleukin-6 (IL-6) and C-reactive protein (CRP) in plasma was determined by ELISA, and vastus lateralis mRNA expression of TNFa, IL-6, total insulinlike growth factor-I (IGF-I) and its isoform mechanogrowth factor (MGF) and myogenic differentiation factor D (MyoD) were assessed by real-time PCR. Protein levels of TNFa, IGF-I and MyoD were measured by Western blotting. Results: Rehabilitation improved peak exercise work rate by 10 (2%) (p = 0.004) and mean fibre crosssectional area from 4061 (254) mm 2 to 4581 (241) mm 2 (p = 0.001). Plasma inflammatory mediators and vastus lateralis expression of TNFa and IL-6 were not significantly modified by training. In contrast, there was a significant increase in mRNA expression of IGF-I (by 67 (22)%; p = 0.044), MGF (by 67 (15)%; p = 0.002) and MyoD (by 116 (30)%; p = 0.001). The increase observed at the mRNA level was also seen at the protein level for IGF-I (by 72 (36)%; p = 0.046) and MyoD (by 67 (21)%; p = 0.012). Conclusions: Pulmonary rehabilitation can induce peripheral muscle adaptations and modifications in factors regulating skeletal muscle hypertrophy and regeneration without decreasing the levels of systemic or local muscle inflammation.