Free
Critical Care Medicine  |   May 2014
Sepsis Is Associated with a Preferential Diaphragmatic Atrophy: A Critically Ill Patient Study Using Tridimensional Computed Tomography
Author Affiliations & Notes
  • Boris Jung, M.D., Ph.D.
    From the Department of Critical Care Medicine and Anesthesiology, Saint Eloi Teaching Hospital, Montpellier, France, and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France (B.J., M.C., Y.C., G.C., S.J.); Department of Abdominal Imaging, Saint Eloi Teaching Hospital, Montpellier, France (S.N.); Department of Anesthesiology and Critical Care, Clermont-Ferrand University Hospital, Clermont-Ferrand, France (E.F.); Department of Medical Statistics, Arnaud de Villeneuve Saint Eloi Teaching Hospital; Montpellier, France (N.M.); Department of Physiology, Arnaud de Villeneuve Teaching Hospital and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France (S.M.); and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier 1, University Montpellier 2, Montpellier, France (A.L.).
  • Stephanie Nougaret, M.D., M.Sc.
    From the Department of Critical Care Medicine and Anesthesiology, Saint Eloi Teaching Hospital, Montpellier, France, and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France (B.J., M.C., Y.C., G.C., S.J.); Department of Abdominal Imaging, Saint Eloi Teaching Hospital, Montpellier, France (S.N.); Department of Anesthesiology and Critical Care, Clermont-Ferrand University Hospital, Clermont-Ferrand, France (E.F.); Department of Medical Statistics, Arnaud de Villeneuve Saint Eloi Teaching Hospital; Montpellier, France (N.M.); Department of Physiology, Arnaud de Villeneuve Teaching Hospital and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France (S.M.); and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier 1, University Montpellier 2, Montpellier, France (A.L.).
  • Matthieu Conseil, M.D., M.Sc.
    From the Department of Critical Care Medicine and Anesthesiology, Saint Eloi Teaching Hospital, Montpellier, France, and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France (B.J., M.C., Y.C., G.C., S.J.); Department of Abdominal Imaging, Saint Eloi Teaching Hospital, Montpellier, France (S.N.); Department of Anesthesiology and Critical Care, Clermont-Ferrand University Hospital, Clermont-Ferrand, France (E.F.); Department of Medical Statistics, Arnaud de Villeneuve Saint Eloi Teaching Hospital; Montpellier, France (N.M.); Department of Physiology, Arnaud de Villeneuve Teaching Hospital and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France (S.M.); and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier 1, University Montpellier 2, Montpellier, France (A.L.).
  • Yannaël Coisel, M.D., M.Sc.
    From the Department of Critical Care Medicine and Anesthesiology, Saint Eloi Teaching Hospital, Montpellier, France, and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France (B.J., M.C., Y.C., G.C., S.J.); Department of Abdominal Imaging, Saint Eloi Teaching Hospital, Montpellier, France (S.N.); Department of Anesthesiology and Critical Care, Clermont-Ferrand University Hospital, Clermont-Ferrand, France (E.F.); Department of Medical Statistics, Arnaud de Villeneuve Saint Eloi Teaching Hospital; Montpellier, France (N.M.); Department of Physiology, Arnaud de Villeneuve Teaching Hospital and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France (S.M.); and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier 1, University Montpellier 2, Montpellier, France (A.L.).
  • Emmanuel Futier, M.D., Ph.D.
    From the Department of Critical Care Medicine and Anesthesiology, Saint Eloi Teaching Hospital, Montpellier, France, and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France (B.J., M.C., Y.C., G.C., S.J.); Department of Abdominal Imaging, Saint Eloi Teaching Hospital, Montpellier, France (S.N.); Department of Anesthesiology and Critical Care, Clermont-Ferrand University Hospital, Clermont-Ferrand, France (E.F.); Department of Medical Statistics, Arnaud de Villeneuve Saint Eloi Teaching Hospital; Montpellier, France (N.M.); Department of Physiology, Arnaud de Villeneuve Teaching Hospital and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France (S.M.); and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier 1, University Montpellier 2, Montpellier, France (A.L.).
  • Gerald Chanques, M.D., Ph.D.
    From the Department of Critical Care Medicine and Anesthesiology, Saint Eloi Teaching Hospital, Montpellier, France, and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France (B.J., M.C., Y.C., G.C., S.J.); Department of Abdominal Imaging, Saint Eloi Teaching Hospital, Montpellier, France (S.N.); Department of Anesthesiology and Critical Care, Clermont-Ferrand University Hospital, Clermont-Ferrand, France (E.F.); Department of Medical Statistics, Arnaud de Villeneuve Saint Eloi Teaching Hospital; Montpellier, France (N.M.); Department of Physiology, Arnaud de Villeneuve Teaching Hospital and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France (S.M.); and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier 1, University Montpellier 2, Montpellier, France (A.L.).
  • Nicolas Molinari, Ph.D.
    From the Department of Critical Care Medicine and Anesthesiology, Saint Eloi Teaching Hospital, Montpellier, France, and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France (B.J., M.C., Y.C., G.C., S.J.); Department of Abdominal Imaging, Saint Eloi Teaching Hospital, Montpellier, France (S.N.); Department of Anesthesiology and Critical Care, Clermont-Ferrand University Hospital, Clermont-Ferrand, France (E.F.); Department of Medical Statistics, Arnaud de Villeneuve Saint Eloi Teaching Hospital; Montpellier, France (N.M.); Department of Physiology, Arnaud de Villeneuve Teaching Hospital and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France (S.M.); and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier 1, University Montpellier 2, Montpellier, France (A.L.).
  • Alain Lacampagne, Ph.D.
    From the Department of Critical Care Medicine and Anesthesiology, Saint Eloi Teaching Hospital, Montpellier, France, and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France (B.J., M.C., Y.C., G.C., S.J.); Department of Abdominal Imaging, Saint Eloi Teaching Hospital, Montpellier, France (S.N.); Department of Anesthesiology and Critical Care, Clermont-Ferrand University Hospital, Clermont-Ferrand, France (E.F.); Department of Medical Statistics, Arnaud de Villeneuve Saint Eloi Teaching Hospital; Montpellier, France (N.M.); Department of Physiology, Arnaud de Villeneuve Teaching Hospital and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France (S.M.); and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier 1, University Montpellier 2, Montpellier, France (A.L.).
  • Stefan Matecki, M.D., Ph.D.
    From the Department of Critical Care Medicine and Anesthesiology, Saint Eloi Teaching Hospital, Montpellier, France, and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France (B.J., M.C., Y.C., G.C., S.J.); Department of Abdominal Imaging, Saint Eloi Teaching Hospital, Montpellier, France (S.N.); Department of Anesthesiology and Critical Care, Clermont-Ferrand University Hospital, Clermont-Ferrand, France (E.F.); Department of Medical Statistics, Arnaud de Villeneuve Saint Eloi Teaching Hospital; Montpellier, France (N.M.); Department of Physiology, Arnaud de Villeneuve Teaching Hospital and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France (S.M.); and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier 1, University Montpellier 2, Montpellier, France (A.L.).
  • Samir Jaber, M.D., Ph.D.
    From the Department of Critical Care Medicine and Anesthesiology, Saint Eloi Teaching Hospital, Montpellier, France, and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France (B.J., M.C., Y.C., G.C., S.J.); Department of Abdominal Imaging, Saint Eloi Teaching Hospital, Montpellier, France (S.N.); Department of Anesthesiology and Critical Care, Clermont-Ferrand University Hospital, Clermont-Ferrand, France (E.F.); Department of Medical Statistics, Arnaud de Villeneuve Saint Eloi Teaching Hospital; Montpellier, France (N.M.); Department of Physiology, Arnaud de Villeneuve Teaching Hospital and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France (S.M.); and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier 1, University Montpellier 2, Montpellier, France (A.L.).
  • Presented in part at the 2013 Annual Meeting of the American Society of Anesthesiologists (San Francisco, California, October 12–16, 2013). The first two authors contributed equally to this work (B.J. and S.N.).
    Presented in part at the 2013 Annual Meeting of the American Society of Anesthesiologists (San Francisco, California, October 12–16, 2013). The first two authors contributed equally to this work (B.J. and S.N.).×
  • Submitted for publication August 5, 2013. Accepted for publication January 24, 2014.
    Submitted for publication August 5, 2013. Accepted for publication January 24, 2014.×
  • Correspondence: Address correspondence to Dr. Jaber: Department of Critical Care Medicine and Anesthesiology, Saint Eloi Teaching Hospital, 80 Avenue Augustin Fliche, F-34295 Montpellier, Cedex 5, France, and Institut National de la Santé et de la Recherche Médicale (INSERM U-1046), University Montpellier I, Montpellier II, Montpellier, France. s-jaber@chu-montpellier.fr. Information on purchasing reprints may be found at www.anesthesiology.org or on the masthead page at the beginning of this issue. Anesthesiology’s articles are made freely accessible to all readers, for personal use only, 6 months from the cover date of the issue.
Article Information
Critical Care Medicine / Clinical Science / Critical Care / Infectious Disease / Radiological and Other Imaging / Respiratory System
Critical Care Medicine   |   May 2014
Sepsis Is Associated with a Preferential Diaphragmatic Atrophy: A Critically Ill Patient Study Using Tridimensional Computed Tomography
Anesthesiology 05 2014, Vol.120, 1182-1191. doi:10.1097/ALN.0000000000000201
Anesthesiology 05 2014, Vol.120, 1182-1191. doi:10.1097/ALN.0000000000000201
Abstract

Background:: Diaphragm and psoas are affected during sepsis in animal models. Whether diaphragm or limb muscle is preferentially affected during sepsis in the critically ill remains unclear.

Methods:: Retrospective secondary analysis study including 40 patients, comparing control (n = 17) and critically ill patients, with (n = 14) or without sepsis (n = 9). Diaphragm volume, psoas volume, and cross-sectional area of the skeletal muscles at the third lumbar vertebra were measured during intensive care unit (ICU) stay using tridimensional computed tomography scan volumetry. Diaphragm strength was evaluated using magnetic phrenic nerve stimulation. The primary endpoint was the comparison between diaphragm and peripheral muscle volume kinetics during the ICU stay among critically ill patients, with or without sepsis.

Results:: Upon ICU admission, neither diaphragm nor psoas muscle volumes were significantly different between critically ill and control patients (163 ± 53 cm3 vs. 197 ± 82 cm3 for the diaphragm, P = 0.36, and 272 ± 116 cm3 vs. to 329 ± 166 cm3 for the psoas, P = 0.31). Twenty-five (15 to 36) days after admission, diaphragm volume decreased by 11 ± 13% in nonseptic and by 27 ± 12% in septic patients, P = 0.01. Psoas volume decreased by 11 ± 10% in nonseptic and by 19 ± 13% in septic patients, P = 0.09. Upon ICU admission, diaphragm strength was correlated with diaphragm volume and was lower in septic (6.2 cm H2O [5.6 to 9.3]) than that in nonseptic patients (13.2 cm H2O [12.3 to 15.6]), P = 0.01.

Conclusions:: During the ICU stay, both diaphragm and psoas volumes decreased. In septic patients, the authors report for the first time in humans preferential diaphragm atrophy compared with peripheral muscles.

Comparisons between 14 people with sepsis to 9 similar patients without sepsis documented a significant loss of diaphragm muscle volume compared with the psoas muscle volume in the septic patients. The loss of diaphragm muscle was associated with loss of strength

What We Already Know about This Topic
  • Septic patients lose significant muscle mass

What This Article Tells Us That Is New
  • Comparisons between 14 people with sepsis and 9 similar patients without sepsis documented a significant loss of diaphragm muscle volume compared with the psoas muscle volume in the septic patients

  • The loss of diaphragm muscle was associated with loss of strength

THE diaphragm is the main respiratory muscle, its dysfunction is one of the main causes of difficulties to wean from the ventilator in the intensive care unit (ICU) and sepsis affects its contractility in the critically ill.1–5  Along with others, we have recently confirmed in humans that mechanical ventilation (MV) per se is associated with diaphragm dysfunction, a condition named ventilator-induced diaphragmatic dysfunction.4,6–8  Although ventilator-induced diaphragmatic dysfunction has recently emerged as a potentially important clinical condition, sepsis has been reported to be associated with diaphragm dysfunction in relation with both myopathy and neuropathy9  and is the consequence of both functional (specific force generation) and morphological (atrophy) damages.10  However, whether limb muscles or diaphragm is similarly or differentially affected during sepsis remains controversial2,11–13  and determining the main victim may be helpful for clinicians confronted with patients recovering from severe sepsis. Indeed, the Extended Prevalence of Infection in Intensive Care study II reported an incidence of 46 to 60% of ICU beds occupied by a “sepsis case” around the world,14  and although as many as 33% of the patients eventually died during their hospital stay, more and more patients do survive after sepsis. However, these survivors increasingly present profound skeletal muscle weakness and there is a need to better identify and treat sepsis-induced myopathy in the critically ill patients.1  Our team developed a three-dimensional volumetry tool using computed tomography (CT)15–18  which may be of interest to compare diaphragm and peripheral muscle volume kinetics in the critically ill.
The aims of our study were therefore to compare diaphragm and psoas volumes between septic and nonseptic critically ill patients during the ICU stay and to describe the relation between diaphragm volume and diaphragm contractility in critically ill patients. We hypothesized that sepsis is associated with a preferential diaphragmatic atrophy, which is negatively correlated with diaphragm contractility.
Materials and Methods
Study Design
This study was conducted from July 2008 to August 2009 in a 16-bed medical–surgical ICU (Saint Eloi Teaching Hospital ICU, Montpellier, France) and is a retrospective secondary analysis of a trial performed with some of the patients (critically ill patients).2  Given that this post hoc analysis did not modify current diagnostic or therapeutic strategies, the need for written consent was waived according to the French Law (Law 88–1138 relative to Biomedical Research of December 20, 1988, modified on August 9, 2004). The study design is represented in figure 1.
Fig. 1.
Design of the study. Diaphragm force evaluation and the first computed tomography (CT) volume measurement were performed upon intensive care unit (ICU) admission. Second CT volume measurement was done during the ICU stay when a CT was indicated for diagnostic purposes.
Image Not Available
Fig. 1.
Design of the study. Diaphragm force evaluation and the first computed tomography (CT) volume measurement were performed upon intensive care unit (ICU) admission. Second CT volume measurement was done during the ICU stay when a CT was indicated for diagnostic purposes.
×
Study Population
A flow chart of the study is represented in figure 2. Critically ill patients were included in the post hoc analysis if they were admitted to the ICU and had had (1) an abdominal CT scan before the ICU admission, (2) a second abdominal CT scan during the ICU stay, and (3) at least one measure of diaphragmatic contractility by measuring the change in endotracheal tube pressure induced by application of bilateral magnetic twitch stimulation of the phrenic nerves during airway occlusion (TwPtr) while being intubated.2,4  Patients were excluded if the CT scan did not allow measurement of the diaphragm and the psoas muscle volumes (cut diaphragm and/or psoas and artifacts) or in the case of a previously identified chronic neuromuscular disease associated with muscle atrophy. Patients in the ICU group were separated into septic and nonseptic groups according to Bone’s criteria.19  Seventeen consecutive outpatients, explored with a virtual colonoscopy at our institution and who had a normal abdominal CT scan, served as controls (control group).
Fig. 2.
Flow chart of the study. CT = computed tomography.
Image Not Available
Fig. 2.
Flow chart of the study. CT = computed tomography.
×
Measurements
We collected data for sex, age, height, weight, body mass index, Simplified Acute Physiology Score II,20  Sequential Organ Failure Assessment score,14  presence of a sepsis, length of ICU stay, and ICU mortality for all patients in the ICU (table 1).
Table 1.
Characteristics of the 40 Studied Patients
Characteristics of the 40 Studied Patients×
Image Not Available
Table 1.
Characteristics of the 40 Studied Patients
Characteristics of the 40 Studied Patients×
×
Semiautomatic measurements of the diaphragm and the limb muscle volumes by CT scan were performed using the same technique as previously described15,17,18  and are illustrated in figure 3. In brief, examination of the diaphragm and the psoas was performed with 64-section spiral CT (Aquilon 64; Toshiba Medical Systems, Nasu, Japan). One radiologist (S.N.), blinded of the patient’s condition and of the TwPtr value, traced the diaphragm contour semiautomatically every 1 mm section after transfer to a dedicated workstation (Advantage Window 4.5 with Volume Viewer; General Electric, Milwaukee, WI). The radiologist manually traced the diaphragm borders, and then the volumetry software calculated the whole diaphragm volume using an algorithm summing up each of the cross-sectional volumes (multiply cross-sectional area by section thickness). The psoas volumes were measured with the same technique. In the critically ill, abdominal wall and paraspinal muscle cross-sectional area were measured at the level of the third lumbar vertebra as described elsewhere.21  Skeletal muscles were distinguished from the organs and edema by the Houns field unit thresholds (−29 to +150)22  and cross-sectional areas of all those muscles were summed and expressed as normalized to body surface.21  We assessed whether diaphragm and psoas volumes were correlated with weight, height, and body mass index.
Fig. 3.
Psoas and diaphragm volume measurements with three-dimensional computed tomography reconstruction and dedicated software for volumetry measurement (Advantage Window 4.5 with Volume Viewer; General Electric, Milwaukee, WI). After circling, the diaphragm and the psoas shapes on millimetric slide (A), the software automatically isolated the diaphragm from the abdomen and the chest wall (B, C), and calculated the diaphragm volume (average volume 163 ± 53 cm3). Psoas volumes were measured using the same technique (average volume 272 ± 116 cm3) (D). Cross-sectional area of the paraspinal and abdominal wall muscles was measured at the level of the third lumbar vertebra (average cross sectional area 17.1 ± 5.4 cm2/m2 (E).
Image Not Available
Fig. 3.
Psoas and diaphragm volume measurements with three-dimensional computed tomography reconstruction and dedicated software for volumetry measurement (Advantage Window 4.5 with Volume Viewer; General Electric, Milwaukee, WI). After circling, the diaphragm and the psoas shapes on millimetric slide (A), the software automatically isolated the diaphragm from the abdomen and the chest wall (B, C), and calculated the diaphragm volume (average volume 163 ± 53 cm3). Psoas volumes were measured using the same technique (average volume 272 ± 116 cm3) (D). Cross-sectional area of the paraspinal and abdominal wall muscles was measured at the level of the third lumbar vertebra (average cross sectional area 17.1 ± 5.4 cm2/m2 (E).
×
Diaphragmatic contractile function was evaluated as previously described.2,4  In brief, we measured the change in endotracheal tube pressure provoked by application of bilateral magnetic twitch stimulation of the phrenic nerves during airway occlusion. TwPtr was obtained upon ICU admission but not afterwards as detailed in a previous study from our group.2  In the control group, no diaphragmatic contractile measure was performed.
Study Endpoints
The primary endpoint was to compare diaphragm and psoas volume changes between septic and nonseptic critically ill patients. The secondary endpoint was to describe the relation between diaphragm volume and diaphragm contractility.
Statistical Analysis
The results are expressed as mean ± SD, median (25th to 75th percentiles), and number and percentage. Demographic characteristics, muscle volumes, and muscle surfaces were compared between controls, nonseptic, and septic patient groups using the Kruskall–Wallis, repeated-measure ANOVA, or chi-square tests according to the distribution of the variables. To compare volume kinetic in the critically ill according to the presence or the absence of sepsis, the Wilcoxon rank sum test for paired data was used. The Pearson correlation coefficient was used to assess the correlation between the muscle volume and weight, height, body mass index, and contractility. After preliminary measures conducted for the current study, we assumed a mean diaphragm volume of approximately 210 cm3 with an SD of 60 cm3 in the control patients. We then hypothesized a 30% decrease in diaphragmatic volume in critically ill during the ICU stay. Because we did not expect the possibility of muscle hypertrophy during the ICU stay, we calculated that 12 patients per group would be necessary to test our hypothesis with 80% statistical power and a one-sided α value of 0.05. Statistical analysis was performed by the Medical Statistical Department of the Montpellier University Hospital (N.M.), with R software (v2.15.2; Vienna, Austria). A P value of less than 0.05 was considered statistically significant.
Results
A total of 40 patients were included. Seventeen constituted the control group and 23 in the ICU group; of the ICU group, 14 of them were septic and 9 were not septic (fig. 2). Table 1 shows their main characteristics. No differences were observed among septic and nonseptic patients. Sepsis started 2 days (3 to 5) before ICU admission. Nine of the 14 septic patients presented with an intraabdominal infection, 4 presented with a pneumonia, and 1 presented with an endocarditis. Among the nine patients without sepsis, three were admitted for multiple trauma, three for scheduled esophageal surgery, one for acute on chronic respiratory failure, and two for acute liver failure.
Diaphragm and psoas volumes were both correlated with weight, height, and body mass index (fig. 4).
Fig. 4.
Scatterplot showing the results of regression analysis of diaphragm volume and patient weight (A), (B) height, and (C) body mass index. Correlation was calculated for the entire sample (critically ill and controls). There was a linear correlation between total diaphragm volume and weight, height, and body mass index. Scatterplot showing the result of regression analysis of psoas volume and intensive care unit patient weight (D), height (E), and body mass index (F). There was a linear correlation between total psoas volume and weight, height, and body surface area.
Image Not Available
Fig. 4.
Scatterplot showing the results of regression analysis of diaphragm volume and patient weight (A), (B) height, and (C) body mass index. Correlation was calculated for the entire sample (critically ill and controls). There was a linear correlation between total diaphragm volume and weight, height, and body mass index. Scatterplot showing the result of regression analysis of psoas volume and intensive care unit patient weight (D), height (E), and body mass index (F). There was a linear correlation between total psoas volume and weight, height, and body surface area.
×
In the ICU group, the first diaphragm volume measurement, performed the day of admission (−3 to 0) (with extremes ranged from 33 days before admission to 1-day postadmission), was 163 ± 53 cm3 compared with 197 ± 82 cm3 in the control group (P = 0.36). The first psoas volume measurement was 272 ± 116 cm3 in the ICU group compared with 329 ± 166 cm3 in the control group (P = 0.31).
The second volume measurement was performed 25 (15 to 36) days after the first measurement. In the critically ill, diaphragm volume decreased from 163 ± 53 cm3 to 130 ± 52 cm3 (P < 0.01) during the ICU stay. Psoas volume decreased from 272 ± 116 cm3 to 233 ± 108 cm3 (P < 0.01) during the ICU stay. No correlation was found between diaphragm or psoas volume loss and time between the two CTs. Cross-sectional areas of skeletal muscles at the level of the third lumbar vertebra did not significantly decrease during the ICU stay (first measurement: 17.1 ± 5.4 cm2/m2 and second measurement: 16.1 ± 5.2 cm2/m2). When the volume drop between the two measures was considered, septic patients experienced a larger decrease of diaphragmatic volume compared with that by the nonseptic patients (fig. 5A). On the contrary, comparing changes in psoas volume and muscle surface on the level of the third lumbar vertebra between septic and nonseptic patients revealed no differences (fig. 5, B and C).
Fig. 5.
(A) Diaphragm volume kinetic between the two volume measurements in nonseptic patients and septic patients. Compared with the first measurement, volume drop was larger in septic (162 ± 55 cm3 to 120 ± 52 cm3) than that in nonseptic patients (164 ± 53 cm3 to 145 ± 51 cm3) (P = 0.01). (B) Psoas volume kinetic between the two volumes measurements in nonseptic patients and septic patients. Volume drop did not differ between the two groups. (C) Skeletal total muscle surface measured at the level of the third lumbar vertebra in nonseptic patients and septic patients. Surface drop did not differ between the two groups.
Image Not Available
Fig. 5.
(A) Diaphragm volume kinetic between the two volume measurements in nonseptic patients and septic patients. Compared with the first measurement, volume drop was larger in septic (162 ± 55 cm3 to 120 ± 52 cm3) than that in nonseptic patients (164 ± 53 cm3 to 145 ± 51 cm3) (P = 0.01). (B) Psoas volume kinetic between the two volumes measurements in nonseptic patients and septic patients. Volume drop did not differ between the two groups. (C) Skeletal total muscle surface measured at the level of the third lumbar vertebra in nonseptic patients and septic patients. Surface drop did not differ between the two groups.
×
Contractile function of the diaphragm upon ICU admission was evaluated after magnetic stimulation of the phrenic nerves. Tracheal pressure was 9.8 cm H2O (6.0 to 13.1). Upon ICU admission, tracheal pressure was lower in the septic patients (6.2 cm H2O [5.6 to 9.3]) compared with the nonseptic patients (13.2 cm H2O [12.3 to 15.6]), P = 0.01. Diaphragm volume was correlated with tracheal pressure obtained upon ICU admission (r = 0.43 [0.02 to 0.72], P = 0.04) (fig. 6). One representative patient is presented on figure 7.
Fig. 6.
Correlation between tracheal pressure measured upon intensive care unit admission and the first diaphragm volume measured upon admission (0 day [−3 to 0] before admission) in septic and nonseptic patients. There was a correlation between tracheal pressure (Ptrach) and diaphragm volume (r = 0.43 [0.02–0.72], P = 0.04). Regardless of the diaphragm volume, all but two septic patients had a Ptrach below 11 cm H2O, which is the threshold of diaphragm dysfunction.2 
Image Not Available
Fig. 6.
Correlation between tracheal pressure measured upon intensive care unit admission and the first diaphragm volume measured upon admission (0 day [−3 to 0] before admission) in septic and nonseptic patients. There was a correlation between tracheal pressure (Ptrach) and diaphragm volume (r = 0.43 [0.02–0.72], P = 0.04). Regardless of the diaphragm volume, all but two septic patients had a Ptrach below 11 cm H2O, which is the threshold of diaphragm dysfunction.2 
×
Fig. 7.
Illustrative case. Mean and SD volume variation is labeled for the critically ill groups. (A) Mean diaphragm volume drop comparison between septic and nonseptic patients. Volume drop was significantly greater in the septic patients compared with that in the nonseptic patients, P = 0.01. (B) Mean psoas volume drop comparison between septic and nonseptic patients. Volume drop was not affected by the presence of sepsis, P = 0.09.
Image Not Available
Fig. 7.
Illustrative case. Mean and SD volume variation is labeled for the critically ill groups. (A) Mean diaphragm volume drop comparison between septic and nonseptic patients. Volume drop was significantly greater in the septic patients compared with that in the nonseptic patients, P = 0.01. (B) Mean psoas volume drop comparison between septic and nonseptic patients. Volume drop was not affected by the presence of sepsis, P = 0.09.
×
Discussion
This study, through combined functional and morphological data, shows for the first time in humans that sepsis is associated with preferential loss of diaphragm volume compared with the psoas. This loss of volume was associated with a lower diaphragm contractile force, evaluated by magnetic stimulation of the phrenic nerves.
Our study has some limitations. It is a single-center study with limited patients. It highlights the atrophy that occurred during the ICU stay and provides additional data about diaphragmatic susceptibility to atrophy in the case of sepsis, but lacks mechanistic explanations, as well as data about psoas contractile force because of the study’s design. However, obtaining diaphragm biopsies in humans who do not need surgery is not acceptable regarding the risk of such biopsies. Diaphragm volume was measured without data about inspiration–expiration cycling. Although knowing lung volume is of interest when diaphragm volume is evaluated, diaphragm volume measurement was performed using the same technique for all critically ill patients, thereby diluting the impact of lung volume on diaphragm volume in the current study. Finally, we provided only two measurements of muscle volume, but repeating high-resolution CT scans would have been outside the standard of care.
In the current study, we used the same technique as we did in other situations with the aid of an experienced radiologist (S.N.)15–18  and a licensed software (Advantage Window 4.5 with Volume Viewer; General Electric) that allows tridimensional reconstruction of the diaphragm. We report that diaphragm and psoas volumes are correlated with height, weight, and body mass index (fig. 4). To our knowledge, no study has evaluated the relation between diaphragm volume and body measurements and there is no definitive standard for diaphragm volume measurement.23  At the bedside, ultrasound is an interesting noninvasive technique to evaluate diaphragm contractile properties.24–27  Ultrasound can also be used to measure diaphragm thickness in mechanically ventilated patients.28  However, when diaphragm trophicity is questioned, ultrasound might be limited as it usually measures the right hemidiaphragm thickness at a single point on the midaxillary line.28  Moreover, up to 10% of the patients cannot be evaluated by ultrasound because of a poor acoustic window.26 
In the current study, we report the absence of diaphragm and psoas volume differences between the 17 controls and the 23 critically ill patients upon ICU admission. The absence of previous diseases that are known to be associated with diaphragmatic atrophy (e.g., chronic obstructive pulmonary disease29  or cancer)30  in 17 among 23 critically ill patients (75%) may have explained the absence of difference of diaphragm and psoas volumes between controls and critically ill.
In the 23 critically ill patients, we report that both psoas and diaphragm volumes decreased during the ICU stay. Prolonged stay in the ICU has been associated with skeletal muscle atrophy and neuromuscular impairment9  and is the consequence of several mechanisms such as inadequate energy supply, increased catabolism, proteolysis, and protein synthesis impairment which are the consequences of systemic aggression.1 
In the 14 critically ill patients with sepsis, we report that diaphragm volume loss is predominant compared with psoas, and that diaphragm volume is correlated with diaphragm force (fig. 6). Sepsis is recognized to be one of the main risk factors for development of critical illness myopathy,9  and as early as 1892, William Osler31  reported the “rapid loss of flesh” that occurs with severe sepsis. Using animal models of sepsis, it has been suggested that both limb and diaphragm muscles are affected, but to a different extent.10–13,32  In Human studies, our group recently demonstrated early diaphragmatic force impairment in sepsis.2 
Others have shown, using invasive techniques with percutaneous stimulation and diaphragm needle electrodes, that both diaphragmatic and limb muscles were affected during the early phase of sepsis.33  Although the current study was not designed to explore the mechanisms leading to a preferential diaphragm volume loss in sepsis, some hypotheses can be made. Early host response to pathogen and pathogen toxins induces proinflammatory cytokines release, reactive oxygen species production, sarcoplasmic reticulum calcium release channel, ryanodine receptor dysfunction,10  and sarcolemmal injuries.34  In more prolonged models of sepsis, muscle wasting results from exaggerated proteolysis and decreased protein synthesis.32,35,36  One explanation that might explain a preferential diaphragmatic loss of volume during sepsis is its ability to overproduce proinflammatory cytokines consecutively to a lipopolysaccharide challenge.32 
In septic patients, MV may have exacerbated the amplitude of diaphragmatic weakness caused by sepsis or might have slowed the subsequent recovery of diaphragmatic function once sepsis has resolved. Indeed, it is accepted that MV per se induces diaphragm dysfunction.4,6,8,37,38  Although one animal study reported that the diaphragm was protected by MV in the early stages of sepsis,39  the interaction between sepsis and MV can also be deleterious.40  Indeed, it has been reported that both MV41  and sepsis share activation of toll-like receptor 4 pathway.35 
In the current study, we combined functional and morphological analyses and reported that as soon as the patient is admitted to the ICU, diaphragm contractile force is decreased in septic compared with nonseptic patients. We also determined a statistically significant correlation coefficient between diaphragm volume and force (fig. 6).
In conclusion, in septic patients, the current study reports a preferential loss of diaphragm volume compared with psoas. Upon ICU admission, diaphragm volume was correlated with diaphragm force, evaluated using magnetic stimulation of the phrenic nerves. Muscle volume measurement using dedicated tridimensional CT scan software may be considered for global evaluation of diaphragm atrophy in the critically ill. The association between muscle volume and function remains to be explored.
Acknowledgments
The authors thank Albert Prades, M.Sc., Department of Critical Care Medicine and Anesthesiology, Saint Eloi Teaching Hospital, Montpellier, France, for his help conducting research in this topic, and Patrick McSweeny, Fisher Paykel, Paris, France, for his English editing.
This study was funded by the French Society of Radiology, Paris, France (research grant 10,000 €).
Competing Interests
Dr. Jung reports personal fees from Merck (Whitehouse Station, New Jersey) and Astellas (Tokyo, Japan) without relations with the current study; Dr. Futier reports consulting fees from General Electric Medical System (Milwaukee, Wisconsin), and lecture fees from Fresenius Kabi (Bad Homburg, Germany) without relations with the current study; Dr. Jaber reports personal fees from Maquet (Getinge, Sweden), Draeger (Lübeck, Germany), Hamilton Medical (Bonaduz, Switzerland), Fisher Paykel (Auckland, New Zealand), and Abbott (Abbott Park, Illinois) without relations with the current study. All other authors have no competing interests.
References
Doorduin, J, van Hees, HW, van der Hoeven, JG, Heunks, LM Monitoring of the respiratory muscles in the critically ill.. Am J Respir Crit Care Med. (2013). 187 20–7 [Article] [PubMed]
Demoule, A, Jung, B, Prodanovic, H, Molinari, N, Chanques, G, Coirault, C, Matecki, S, Duguet, A, Similowski, T, Jaber, S Diaphragm dysfunction on admission to the intensive care unit. Prevalence, risk factors, and prognostic impact—A prospective study.. Am J Respir Crit Care Med. (2013). 188 213–9 [Article] [PubMed]
Jaber, S, Jung, B, Matecki, S, Petrof, BJ Clinical review: Ventilator-induced diaphragmatic dysfunction—Human studies confirm animal model findings!. Crit Care. (2011). 15 206 [Article] [PubMed]
Jaber, S, Petrof, BJ, Jung, B, Chanques, G, Berthet, JP, Rabuel, C, Bouyabrine, H, Courouble, P, Koechlin-Ramonatxo, C, Sebbane, M, Similowski, T, Scheuermann, V, Mebazaa, A, Capdevila, X, Mornet, D, Mercier, J, Lacampagne, A, Philips, A, Matecki, S Rapidly progressive diaphragmatic weakness and injury during mechanical ventilation in humans.. Am J Respir Crit Care Med. (2011). 183 364–71 [Article] [PubMed]
McCool, FD, Tzelepis, GE Dysfunction of the diaphragm.. N Engl J Med. (2012). 366 932–42 [Article] [PubMed]
Levine, S, Nguyen, T, Taylor, N, Friscia, ME, Budak, MT, Rothenberg, P, Zhu, J, Sachdeva, R, Sonnad, S, Kaiser, LR, Rubinstein, NA, Powers, SK, Shrager, JB Rapid disuse atrophy of diaphragm fibers in mechanically ventilated humans.. N Engl J Med. (2008). 358 1327–35 [Article] [PubMed]
Petrof, BJ, Jaber, S, Matecki, S Ventilator-induced diaphragmatic dysfunction.. Curr Opin Crit Care. (2010). 16 19–25 [Article] [PubMed]
Hussain, SN, Mofarrahi, M, Sigala, I, Kim, HC, Vassilakopoulos, T, Maltais, F, Bellenis, I, Chaturvedi, R, Gottfried, SB, Metrakos, P, Danialou, G, Matecki, S, Jaber, S, Petrof, BJ, Goldberg, P Mechanical ventilation-induced diaphragm disuse in humans triggers autophagy.. Am J Respir Crit Care Med. (2010). 182 1377–86 [Article] [PubMed]
de Jonghe, B, Lacherade, JC, Sharshar, T, Outin, H Intensive care unit-acquired weakness: Risk factors and prevention.. Crit Care Med. (2009). 37 309–15 [Article]
Callahan, LA, Supinski, GS Sepsis-induced myopathy.. Crit Care Med. (2009). 3710 suppl S354–67 [Article] [PubMed]
Divangahi, M, Matecki, S, Dudley, RW, Tuck, SA, Bao, W, Radzioch, D, Comtois, AS, Petrof, BJ Preferential diaphragmatic weakness during sustained Pseudomonas aeruginosa lung infection.. Am J Respir Crit Care Med. (2004). 169 679–86 [Article] [PubMed]
Mofarrahi, M, Sigala, I, Guo, Y, Godin, R, Davis, EC, Petrof, B, Sandri, M, Burelle, Y, Hussain, SN Autophagy and skeletal muscles in sepsis.. PLoS One. (2012). 7 e47265 [Article] [PubMed]
Prentice, CE, Paratz, JD, Bersten, AD Differences in the degree of respiratory and peripheral muscle impairment are evident on clinical, electrophysiological and biopsy testing in critically ill adults: A qualitative systematic review.. Crit Care Resusc. (2010). 12 111–20 [PubMed]
Vincent, JL, de Mendonça, A, Cantraine, F, Moreno, R, Takala, J, Suter, PM, Sprung, CL, Colardyn, F, Blecher, S Use of the SOFA score to assess the incidence of organ dysfunction/failure in intensive care units: Results of a multicenter, prospective study. Working group on “sepsis-related problems” of the European Society of Intensive Care Medicine.. Crit Care Med. (1998). 26 1793–800 [Article] [PubMed]
Constantin, JM, Grasso, S, Chanques, G, Aufort, S, Futier, E, Sebbane, M, Jung, B, Gallix, B, Bazin, JE, Rouby, JJ, Jaber, S Lung morphology predicts response to recruitment maneuver in patients with acute respiratory distress syndrome.. Crit Care Med. (2010). 38 1108–17 [Article] [PubMed]
Jung, B, Nougaret, S, Chanques, G, Mercier, G, Cisse, M, Aufort, S, Gallix, B, Annane, D, Jaber, S The absence of adrenal gland enlargement during septic shock predicts mortality: A computed tomography study of 239 patients.. Anesthesiology. (2011). 115 334–43 [Article] [PubMed]
Nougaret, S, Jung, B, Aufort, S, Chanques, G, Jaber, S, Gallix, B Adrenal gland volume measurement in septic shock and control patients: A pilot study.. Eur Radiol. (2010). 20 2348–57 [Article] [PubMed]
Nougaret, S, Rouanet, P, Molinari, N, Pierredon, MA, Bibeau, F, Azria, D, Lemanski, C, Assenat, E, Duffour, J, Ychou, M, Reinhold, C, Gallix, B MR volumetric measurement of low rectal cancer helps predict tumor response and outcome after combined chemotherapy and radiation therapy.. Radiology. (2012). 263 409–18 [Article] [PubMed]
Bone, RC, Balk, RA, Cerra, FB, Dellinger, RP, Fein, AM, Knaus, WA, Schein, RM, Sibbald, WJ Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine.. Chest. (1992). 101 1644–55 [Article] [PubMed]
Le Gall, JR, Lemeshow, S, Saulnier, F A new Simplified Acute Physiology Score (SAPS II) based on a European/North American multicenter study.. JAMA. (1993). 270 2957–63 [Article] [PubMed]
Prado, CM, Lieffers, JR, McCargar, LJ, Reiman, T, Sawyer, MB, Martin, L, Baracos, VE Prevalence and clinical implications of sarcopenic obesity in patients with solid tumours of the respiratory and gastrointestinal tracts: A population-based study.. Lancet Oncol. (2008). 9 629–35 [Article] [PubMed]
Mitsiopoulos, N, Baumgartner, RN, Heymsfield, SB, Lyons, W, Gallagher, D, Ross, R Cadaver validation of skeletal muscle measurement by magnetic resonance imaging and computerized tomography.. J Appl Physiol (1985). (1998). 85 115–22 [PubMed]
Nason, LK, Walker, CM, McNeeley, MF, Burivong, W, Fligner, CL, Godwin, JD Imaging of the diaphragm: Anatomy and function.. Radiographics. (2012). 32 E51–70 [Article] [PubMed]
Lerolle, N, Guérot, E, Dimassi, S, Zegdi, R, Faisy, C, Fagon, JY, Diehl, JL Ultrasonographic diagnostic criterion for severe diaphragmatic dysfunction after cardiac surgery.. Chest. (2009). 135 401–7 [Article] [PubMed]
Kim, WY, Suh, HJ, Hong, SB, Koh, Y, Lim, CM Diaphragm dysfunction assessed by ultrasonography: Influence on weaning from mechanical ventilation.. Crit Care Med. (2011). 39 2627–30 [Article] [PubMed]
Matamis, D, Soilemezi, E, Tsagourias, M, Akoumianaki, E, Dimassi, S, Boroli, F, Richard, JC, Brochard, L Sonographic evaluation of the diaphragm in critically ill patients. Technique and clinical applications.. Intensive Care Med. (2013). 39 801–10 [Article] [PubMed]
Vivier, E, Mekontso Dessap, A, Dimassi, S, Vargas, F, Lyazidi, A, Thille, AW, Brochard, L Diaphragm ultrasonography to estimate the work of breathing during non-invasive ventilation.. Intensive Care Med. (2012). 38 796–803 [Article] [PubMed]
Grosu, HB, Lee, YI, Lee, J, Eden, E, Eikermann, M, Rose, KM Diaphragm muscle thinning in patients who are mechanically ventilated.. Chest. (2012). 142 1455–60 [Article] [PubMed]
Jagoe, RT, Engelen, MP Muscle wasting and changes in muscle protein metabolism in chronic obstructive pulmonary disease.. Eur Respir J Suppl. (2003). 46 52s–63 [Article] [PubMed]
Fearon, K, Arends, J, Baracos, V Understanding the mechanisms and treatment options in cancer cachexia.. Nat Rev Clin Oncol. (2013). 10 90–9 [Article] [PubMed]
Osler, W The Principles and Practice of Medicine: Designed for the Use of Practitioners and Students of Medicine. (1910). New York D. Appleton
Demoule, A, Divangahi, M, Yahiaoui, L, Danialou, G, Gvozdic, D, Petrof, BJ Chemokine receptor and ligand upregulation in the diaphragm during endotoxemia and Pseudomonas lung infection.. Mediators Inflamm. (2009). 2009 860565 [Article] [PubMed]
Santos, PD, Teixeira, C, Savi, A, Maccari, JG, Neres, FS, Machado, AS, de Oliveira, RP, Ribeiro, M, Rotta, FT The critical illness polyneuropathy in septic patients with prolonged weaning from mechanical ventilation: Is the diaphragm also affected? A pilot study.. Respir Care. (2012). 57 1594–601 [Article] [PubMed]
Lin, MC, Ebihara, S, El Dwairi, Q, Hussain, SN, Yang, L, Gottfried, SB, Comtois, A, Petrof, BJ Diaphragm sarcolemmal injury is induced by sepsis and alleviated by nitric oxide synthase inhibition.. Am J Respir Crit Care Med. (1998). 1585 Pt 1 1656–63 [Article] [PubMed]
Lanone, S, Taillé, C, Boczkowski, J, Aubier, M Diaphragmatic fatigue during sepsis and septic shock.. Intensive Care Med. (2005). 31 1611–7 [Article] [PubMed]
Demoule, A, Divangahi, M, Yahiaoui, L, Danialou, G, Gvozdic, D, Labbe, K, Bao, W, Petrof, BJ Endotoxin triggers nuclear factor-kappaB-dependent up-regulation of multiple proinflammatory genes in the diaphragm.. Am J Respir Crit Care Med. (2006). 174 646–53 [Article] [PubMed]
Mrozek, S, Jung, B, Petrof, BJ, Pauly, M, Roberge, S, Lacampagne, A, Cassan, C, Thireau, J, Molinari, N, Futier, E, Scheuermann, V, Constantin, JM, Matecki, S, Jaber, S Rapid onset of specific diaphragm weakness in a healthy murine model of ventilator-induced diaphragmatic dysfunction.. Anesthesiology. (2012). 117 560–7 [Article] [PubMed]
Picard, M, Jung, B, Liang, F, Azuelos, I, Hussain, S, Goldberg, P, Godin, R, Danialou, G, Chaturvedi, R, Rygiel, K, Matecki, S, Jaber, S, Des Rosiers, C, Karpati, G, Ferri, L, Burelle, Y, Turnbull, DM, Taivassalo, T, Petrof, BJ Mitochondrial dysfunction and lipid accumulation in the human diaphragm during mechanical ventilation.. Am J Respir Crit Care Med. (2012). 186 1140–9 [Article] [PubMed]
Ebihara, S, Hussain, SN, Danialou, G, Cho, WK, Gottfried, SB, Petrof, BJ Mechanical ventilation protects against diaphragm injury in sepsis: Interaction of oxidative and mechanical stresses.. Am J Respir Crit Care Med. (2002). 165 221–8 [Article] [PubMed]
Petrof, BJ Diaphragmatic dysfunction in the intensive care unit: Caught in the cross-fire between sepsis and mechanical ventilation.. Crit Care. (2013). 17 R181 [Article] [PubMed]
Schellekens, WJ, van Hees, HW, Vaneker, M, Linkels, M, Dekhuijzen, PN, Scheffer, GJ, van der Hoeven, JG, Heunks, LM Toll-like receptor 4 signaling in ventilator-induced diaphragm atrophy.. Anesthesiology. (2012). 117 329–38 [Article] [PubMed]
Fig. 1.
Design of the study. Diaphragm force evaluation and the first computed tomography (CT) volume measurement were performed upon intensive care unit (ICU) admission. Second CT volume measurement was done during the ICU stay when a CT was indicated for diagnostic purposes.
Image Not Available
Fig. 1.
Design of the study. Diaphragm force evaluation and the first computed tomography (CT) volume measurement were performed upon intensive care unit (ICU) admission. Second CT volume measurement was done during the ICU stay when a CT was indicated for diagnostic purposes.
×
Fig. 2.
Flow chart of the study. CT = computed tomography.
Image Not Available
Fig. 2.
Flow chart of the study. CT = computed tomography.
×
Fig. 3.
Psoas and diaphragm volume measurements with three-dimensional computed tomography reconstruction and dedicated software for volumetry measurement (Advantage Window 4.5 with Volume Viewer; General Electric, Milwaukee, WI). After circling, the diaphragm and the psoas shapes on millimetric slide (A), the software automatically isolated the diaphragm from the abdomen and the chest wall (B, C), and calculated the diaphragm volume (average volume 163 ± 53 cm3). Psoas volumes were measured using the same technique (average volume 272 ± 116 cm3) (D). Cross-sectional area of the paraspinal and abdominal wall muscles was measured at the level of the third lumbar vertebra (average cross sectional area 17.1 ± 5.4 cm2/m2 (E).
Image Not Available
Fig. 3.
Psoas and diaphragm volume measurements with three-dimensional computed tomography reconstruction and dedicated software for volumetry measurement (Advantage Window 4.5 with Volume Viewer; General Electric, Milwaukee, WI). After circling, the diaphragm and the psoas shapes on millimetric slide (A), the software automatically isolated the diaphragm from the abdomen and the chest wall (B, C), and calculated the diaphragm volume (average volume 163 ± 53 cm3). Psoas volumes were measured using the same technique (average volume 272 ± 116 cm3) (D). Cross-sectional area of the paraspinal and abdominal wall muscles was measured at the level of the third lumbar vertebra (average cross sectional area 17.1 ± 5.4 cm2/m2 (E).
×
Fig. 4.
Scatterplot showing the results of regression analysis of diaphragm volume and patient weight (A), (B) height, and (C) body mass index. Correlation was calculated for the entire sample (critically ill and controls). There was a linear correlation between total diaphragm volume and weight, height, and body mass index. Scatterplot showing the result of regression analysis of psoas volume and intensive care unit patient weight (D), height (E), and body mass index (F). There was a linear correlation between total psoas volume and weight, height, and body surface area.
Image Not Available
Fig. 4.
Scatterplot showing the results of regression analysis of diaphragm volume and patient weight (A), (B) height, and (C) body mass index. Correlation was calculated for the entire sample (critically ill and controls). There was a linear correlation between total diaphragm volume and weight, height, and body mass index. Scatterplot showing the result of regression analysis of psoas volume and intensive care unit patient weight (D), height (E), and body mass index (F). There was a linear correlation between total psoas volume and weight, height, and body surface area.
×
Fig. 5.
(A) Diaphragm volume kinetic between the two volume measurements in nonseptic patients and septic patients. Compared with the first measurement, volume drop was larger in septic (162 ± 55 cm3 to 120 ± 52 cm3) than that in nonseptic patients (164 ± 53 cm3 to 145 ± 51 cm3) (P = 0.01). (B) Psoas volume kinetic between the two volumes measurements in nonseptic patients and septic patients. Volume drop did not differ between the two groups. (C) Skeletal total muscle surface measured at the level of the third lumbar vertebra in nonseptic patients and septic patients. Surface drop did not differ between the two groups.
Image Not Available
Fig. 5.
(A) Diaphragm volume kinetic between the two volume measurements in nonseptic patients and septic patients. Compared with the first measurement, volume drop was larger in septic (162 ± 55 cm3 to 120 ± 52 cm3) than that in nonseptic patients (164 ± 53 cm3 to 145 ± 51 cm3) (P = 0.01). (B) Psoas volume kinetic between the two volumes measurements in nonseptic patients and septic patients. Volume drop did not differ between the two groups. (C) Skeletal total muscle surface measured at the level of the third lumbar vertebra in nonseptic patients and septic patients. Surface drop did not differ between the two groups.
×
Fig. 6.
Correlation between tracheal pressure measured upon intensive care unit admission and the first diaphragm volume measured upon admission (0 day [−3 to 0] before admission) in septic and nonseptic patients. There was a correlation between tracheal pressure (Ptrach) and diaphragm volume (r = 0.43 [0.02–0.72], P = 0.04). Regardless of the diaphragm volume, all but two septic patients had a Ptrach below 11 cm H2O, which is the threshold of diaphragm dysfunction.2 
Image Not Available
Fig. 6.
Correlation between tracheal pressure measured upon intensive care unit admission and the first diaphragm volume measured upon admission (0 day [−3 to 0] before admission) in septic and nonseptic patients. There was a correlation between tracheal pressure (Ptrach) and diaphragm volume (r = 0.43 [0.02–0.72], P = 0.04). Regardless of the diaphragm volume, all but two septic patients had a Ptrach below 11 cm H2O, which is the threshold of diaphragm dysfunction.2 
×
Fig. 7.
Illustrative case. Mean and SD volume variation is labeled for the critically ill groups. (A) Mean diaphragm volume drop comparison between septic and nonseptic patients. Volume drop was significantly greater in the septic patients compared with that in the nonseptic patients, P = 0.01. (B) Mean psoas volume drop comparison between septic and nonseptic patients. Volume drop was not affected by the presence of sepsis, P = 0.09.
Image Not Available
Fig. 7.
Illustrative case. Mean and SD volume variation is labeled for the critically ill groups. (A) Mean diaphragm volume drop comparison between septic and nonseptic patients. Volume drop was significantly greater in the septic patients compared with that in the nonseptic patients, P = 0.01. (B) Mean psoas volume drop comparison between septic and nonseptic patients. Volume drop was not affected by the presence of sepsis, P = 0.09.
×
Table 1.
Characteristics of the 40 Studied Patients
Characteristics of the 40 Studied Patients×
Image Not Available
Table 1.
Characteristics of the 40 Studied Patients
Characteristics of the 40 Studied Patients×
×