Explore the vast range of titles available.

Purpose Lung volumes, especially functional residual capacity (FRC), are decreased in acute respiratory distress syndrome (ARDS). Positive end-expiratory pressure (PEEP) contributes to increased end-expiratory lung volume (EELV) and to improved oxygenation, but differentiating recruitment of previously nonaerated lung units from distension of previously open lung units remains difficult. This study evaluated simple methods derived from bedside EELV measurements to assess PEEP-induced lung recruitment while monitoring strain. Methods Prospective multicenter study in 30 mechanically ventilated patients with ARDS in five university hospital ICUs. Two PEEP levels were studied, each for 45 min, and EELV (nitrogen washout/washin technique) was measured at both levels, with the difference (Δ) reflecting PEEP-induced lung volume changes. Alveolar recruitment was measured using pressure-volume (PV) curves. High and low recruiters were separated based on median recruitment at high PEEP. Minimum predicted increase in lung volume computed as the product of ΔPEEP by static compliance was subtracted from ΔEELV as an independent estimate of recruitment. Estimated and measured recruitments were compared. Strain induced by PEEP was also calculated from the same measurements. Results FRC was 31 ± 11% of predicted. Median [25th–75th percentiles] PEEP-induced recruitment was 272 [187–355] mL. Estimated recruitment correlated with recruited volume measured on PV curves (ρ = 0.68), with a slope close to identity. The ΔEELV/FRC ratio differentiated high from low recruiters (110 [76–135] vs. 55 [23–70]%, p  = 0.001). Strain increase due to PEEP was larger in high recruiters ( p  = 0.002). Conclusion PEEP-induced recruitment and strain can be assessed at the bedside using EELV measurement. We describe two bedside methods for predicting low or high alveolar recruitment during ARDS.

Rationale Lung volume available for ventilation is markedly decreased during acute respiratory distress syndrome. Body positioning may contribute to increase lung volume and partial verticalization is simple to perform. This study evaluated whether verticalization had parallel effects on oxygenation and end expiratory lung volume (EELV). Methods Prospective multicenter study in 40 mechanically ventilated patients with ALI/ARDS in five university hospital MICUs. We evaluated four 45-min successive trunk position epochs (supine slightly elevated at 15°; semi recumbent with trunk elevated at 45°; seated with trunk elevated at 60° and legs down at 45°; back to supine). Arterial blood gases, EELV measured using the nitrogen washin/washout, and static compliance were measured. Responders were defined by a PaO 2 /FiO 2 increase >20 % between supine and seated position. Results are median [25th–75th percentiles]. Results With median PEEP = 10 cmH 2 O, verticalization increased lung volume but only responders (13 patients, 32 %) had a significant increase in EELV/PBW (predicted body weight) compared to baseline. This increase persisted at least partially when patients were positioned back to supine. Responders had a lower EELV/PBW supine [14 mL/kg (13–15) vs. 18 mL/kg (15–27) ( p  = 0.005)] and a lower compliance [30 mL/cmH 2 O (22–38) vs. 42 (30–46) ( p  = 0.01)] than non-responders. Strain decreased with verticalization for responders. EELV/PBW increase and PaO 2 /FiO 2 increase were not correlated. Discussion Verticalization is easily achieved and improves oxygenation in approximately 32 % of the patients together with an increase in EELV. Nonetheless, effect of verticalization on EELV/PBW is not predictable by PaO 2 /FiO 2 increase, its monitoring may be helpful for strain optimization.

Acute respiratory distress syndrome (ARDS) in humans is characterized by the infiltration of polymorphonuclears in the alveolar spaces. However, the role of T-cells in ARDS is unknown. Our aim was to characterize the T-cell phenotype in bronchoalveolar lavage (BAL) during the early phase of acute lung infection(ALI)/ARDS-infected patients in comparison to a control group (CG). BAL lymphocyte phenotypes of two ALI, 16 ARDS, and eight CG were examined by flow cytometry. ALI/ARDS showed a significant increase in CD4 and CD8 T-cell activation as compared to CG. Moreover, a significant level of proliferation was observed using the Ki67 marker in ARDS patients as compared to controls (median): 37 versus 6 % for CD4 T-cells ( p  = 0.022) and 34 versus 2 % for CD8 T-cells ( p  = 0.009). In contrast, the percentage of T-regulatory cells and apoptotic T-cells were similar in both groups. Among costimulatory molecules, we observed an overexpression of CTLA-4/CD152 on CD4 T-cells in ALI/ARDS as compared to CG: 30 versus 7 %, respectively ( p  = 0.063). In further characterizing T-cell subsets expressing high levels of CD152, we found the presence of IL-17 secreting CD4 T-cells in ALI/ARDS. In humans, ALI/ARDS due to infection is associated with a high level of T-cell activation and proliferation, along with the presence of Th17 cells, which are known to attract polymorphonuclears.

T-cell apoptosis during septic shock (SS) has been associated with deleterious outcome, but the mechanisms of apoptosis are not well understood. As T-cells are not infected in bacterial infection, our hypothesis was that deleterious interactions between lymphocytes and monocytes could be involved. This is a cross-sectional study of 27 patients presenting with community-acquired SS, 23 infected patients without SS and 18 controls. Cytofluorometric techniques were used to study apoptosis, the costimulatory pathway and cytokine synthesis. Apoptosis was increased in SS compared to infected patients without SS and controls: the median values were 18, 2 and 3%, respectively, for CD4⁺ T-cells (P < 0.001), and 12, 5 and 2%, respectively, for CD8⁺ T-cells (P < 0.001). Patients with SS exhibited significant CD152 over-expression on T-cells, while CD86 expression was decreased on monocytes (P = 0.004). The synthesis of interleukin-2 was decreased in patients with SS compared to the other groups, while secretions of interferon-gamma and TNF-alpha were not altered. Ten surviving patients with SS showed a trend towards the normalisation of these parameters on day 7. In SS, T-cell apoptosis is related, at least in part, to the alteration of the costimulatory pathway, which, in turn, leads to significant modification of the cytokine network.

a) To investigate the functional consequences of sepsis on the beta-adrenergic signal transduction in human circulating lymphocytes; b) to appreciate sepsis-associated catecholamine and cytokine release. Experimental, comparative study. Research laboratory in a university hospital. Healthy controls (n = 10); critically ill patients who were not septic (n = 7); septic patients with severe sepsis or septic shock (n = 11). Experiments were carried out using freshly isolated peripheral blood mononuclear cells (PBMC). We measured beta-adrenergic receptor (betaAR) number and affinity, and intracellular cAMP content at baseline and after the pharmacological stimulation of each component of the beta-adrenergic complex: betaAR with isoproterenol, Gs-protein with sodium fluoride (NaF), adenylate cyclase with forskolin. Catecholamine (adrenaline, noradrenaline) and cytokine (TNFalpha, IL-1alpha, IL-1beta, IL-6) serum levels were measured. In both septic and non-septic patients we observed a similar 40 % down-regulation of betaARs compared to controls, and a reduced basal and isoproterenol-stimulated cAMP accumulation (p < 0.05). The cAMP production elicited by NaF or forskolin was lower in septic patients than in the controls (p < 0.01). Forskolin-stimulated cAMP accumulation was significantly lower in septic patients than it was in non-septic ones (p < 0.001). Catecholamine serum concentrations were increased in the two patient groups without any significant difference. Elevated cytokine serum levels were detected in 45% of the septic patients (versus 14% of non-septic patients p < 0.05). Patients presenting with severe sepsis or septic shock have extended postreceptor defects of the beta-adrenergic signal transduction. This finding suggests a heterologous desensitization of adenylate cyclase stimulation.

BackgroundSystemic rheumatic diseases (SRD) are a rare and heterogeneous group of diseases, associated with a high mortality rate due to the natural evolution of the disease and/or consequences of their specific treatments (infections, toxicity).ObjectivesTo describe the clinical features, outcomes and prognostic factors for patients with SRD admitted to the intensive care unit (ICU).MethodsSingle-center retrospective observational cohort study of 98 patients with SRD over an 11-year period in an ICU of a French teaching hospital.ResultsNinety-eight patients (57% women; median age, 57 years [19–81years]) accounted for 108 admissions. Connective tissue disease (primarily systemic lupus erythematosus) and systemic vasculitides (mainly ANCA-associated vasculitides) represented respectively 55% and 30% of SRD. For nineteen patients, diagnosis of SRD was made at admission. Reasons for admission were: SRD exacerbations (43%), isolated infections (34%), SRD exacerbations associated with infections (12%) or other (11%). Respiratory failure was the most common organ dysfunction. Mechanical ventilation was necessary for 43 patients (44%), vasoactive drugs for 47 (48%) and extra-renal replacement therapy for 38 (39%). The ICU mortality rate was 30% and 37% one year after admission. Infection was the main cause of death (69%). The factors significantly associated with mortality in the ICU were (multivariate analysis): diabetes, cardiovascular diseases and immunosuppressive treatments on admission. At 1 year of follow-up, additional risk factors were: number of organ dysfunction at ICU admission and mechanical ventilation. It is to be noted that at 1 year of follow-up, diabetes was not anymore a prognostic factor.ConclusionsPatients with SRD admitted to the ICU have a severe prognosis. Causes of mortality are mainly infections. Our study points out the importance of vaccination and developing new therapeutic strategies. Diagnosis of SRD in the ICU is not rare and should be systematically considered on admission. Prognostic factors of mortality in the ICU were patient comorbidities and immunosuppressive therapy at admission. In addition, mechanical ventilation and multiple organ failure were risk factors for mortality at 1 year.Disclosure of InterestNone declared

Cutaneous manifestations of miliary tuberculosis are extremely rare. We describe a 62-year-old woman with leukopenia who developed infiltrated dermal-hypodermal and ulcerative cutaneous lesions during the course of miliary tuberculosis. Miliary tuberculosis was diagnosed when Mycobacterium tuberculosis bacilli were isolated by cultures of the bronchoalveolar lavage fluid and blood and when acid-fast bacilli were detected on histopathologic examination of hepatic, pulmonary, and cutaneous biopsy specimens. With the increasing incidence of immunocompromised patients, unusual presentations of tuberculosis may be observed more often. Acute miliary tuberculosis of the skin is an exceptional manifestation that is due to acute hematogenous dissemination of M. tuberculosis to the skin. We describe a patient who had unusual cutaneous manifestations of miliary tuberculosis.

To evaluate the influence of changes in alveolar ventilation on the following tonometry-derived variables: gastric intramucosal CO2 tension (PtCO2), gastric arterial CO2 tension difference (PgapCO2), gastric intramucosal pH (pHi) and arterial pH-pHi difference (pHgap). Clinical prospective study. A medical intensive care unit in a university hospital. Ten critically ill, mechanically ventilated patients requiring hemodynamic monitoring with pulmonary artery catheter. Gastric tonometer placement. A progressive increase in tidal volume (V(T)) from 7 to 10 ml/ kg followed by an abrupt return to baseline V(T) level. Tonometer saline PtCO2 and hemodynamic data were collected hourly at various V(T) levels: H0 and H0' (baseline V(T) = 7 ml/kg), H1 (V(T) = 8 ml/kg), H2 (V(T) = 9 ml/kg), H3 (V(T) = 10 ml/kg), H4 (baseline V(T)). During the \"hyperventilation phase\" (H0-H3), pHi (p<0.01) and pHgap (p<0.05) increased but PgapCO2 remained unchanged. Cardiac output (CO) was not affected by ventilatory change. During the \"hypoventilation phase\" (H3-H4), pHi fell from 7.27+/-0.11 to 7.23+/-0.09 (p<0.01) and PgapCO2 decreased from 16+/-5 mm Hg to 13+/-4 mm Hg (p<0.05). V(T) reduction was associated with a significant cardiac output elevation (p<0.05). PaCO2 and PtCO2 are similarly influenced by the changes in alveolar ventilation. Unlike pHi, the PgapCO2 is not affected by ventilation variations unless CO changes are associated.