Recently diagnosed immunodeficiency is associated with a much better prognosis in ECMO-treated severe ARDS. However, low 6-month survival of our large cohort of immunocompromised patients supports restricting ECMO to patients with realistic oncological/therapeutic prognoses, acceptable functional status and few pre-ECMO mortality-risk factors.

Acute mesenteric ischemia in ICU patients was associated with a 58 % ICU death rate. Age and SOFA severity score at diagnosis were risk factors for mortality. Plasma lactate concentration over 2.7 mmol/l was also an independent risk factor, but values in the normal range did not exclude the diagnosis of AMI.

BackgroundNon-occlusive mesenteric ischemia (NOMI) is a common complication and accounts for a major cause of death in critically ill patients. The diagnosis of NOMI with respect to the eventual indications for surgical treatment is challenging. We addressed the performance of the diagnostic strategy of NOMI in the intensive care unit, with emphasis on contrast-enhanced abdominal CT-scan.MethodsThis was a retrospective monocenter study. Patients with clinically suspected acute mesenteric ischemia were included if a comprehensive diagnostic workup was carried out including surgical and/or endoscopic digestive explorations. Patients with evidence of occlusive mesenteric ischemia were excluded. A definite diagnosis of NOMI only relied on surgical or endoscopic findings. Abdominal CT-scans were reviewed by two radiologists blinded from the final diagnosis.ResultsA diagnosis of NOMI could be definitely confirmed or ruled out through surgical or endoscopic explorations of the digestive tract in 147 patients. With respect to their clinical characteristics, only a history of atrial fibrillation was an independent predictor of NOMI (odds ratio 8.3, 95% confidence interval 2.0–35.2, p = 0.004). Among them, 114 patients (75 with and 39 without NOMI) had previously been subjected to contrast-enhanced abdominal CT-scan. Portal venous gas, pneumatosis intestinalis and, to a lesser extent, abnormal contrast-induced bowel wall enhancement were poorly sensitive, but exhibited good specificities of 95, 85 and 71%, respectively. Nineteen out of 75 patients (25.3%) without any suggestive radiological signs finally exhibited mesenteric ischemia, including ten with intestinal necrosis.ConclusionsThe performance of abdominal CT-scan for the diagnosis of NOMI is limited. Radiological signs of advanced-stage ischemia are good predictors of definite mesenteric ischemia, while their absence should not be considered sufficient to rule out the diagnosis.Electronic supplementary materialThe online version of this article (doi:10.1186/s13613-016-0213-x) contains supplementary material, which is available to authorized users.

ClinicalTrials.gov identifier: NCT01818895.

Objective-Abdominal aortic aneurysm is an inflammatory disease leading to destructive vascular remodeling and ultimately to lethal aortic rupture. Despite its frequent association with atherosclerosis, compelling studies have shown striking differences and potentially opposite roles of T-cell helper responses in aneurysm as compared with atherosclerosis, casting doubt on the relevance and suitability of T-cell-targeted therapies in this context. Approach and Results-Here, we show that selective depletion of T regulatory (Treg) cells using a CD25-specific monoclonal antibody significantly enhances the susceptibility of C57Bl/6 mice to angiotensin II-induced abdominal aortic aneurysm and promotes aortic rupture (n=25-44 mice/group). Similar results are observed in angiotensin II-treated Cd80or Cd28 −/− mice with impaired Treg cell homeostasis (n=18-23 mice/group). Treg cell depletion is associated with increased immune cell activation and a blunted interleukin (IL)-10 anti-inflammatory response, suggesting an immunoinflammatory imbalance. Interestingly, Il-10 −/− mice (n=20 mice/group) show increased susceptibility to angiotensin II-induced abdominal aortic aneurysm and aortic rupture and are insensitive to Treg cell depletion. Finally, reconstitution of Cd28Treg-deficient mice with Treg cells (n=22 mice/group) restores a balance in the immunoinflammatory response, rescues the animals from increased susceptibility to aneurysm, and prevents aortic dissection. Conclusions-These results identify a critical role for Materials and MethodsMaterials and Methods are available in the online-only supplement. Figure 1A) led to important T-cell activation ( Figure 1B), significantly increased the incidence and severity of aneurysm, and predisposed to fatal aortic rupture ( Figure 1C and 1D). Enhanced susceptibility to AAA in Treg-depleted mice was associated with increased vascular accumulation of T cells ( Figure 1E) and marked elastin degradation ( Figure 1F). −/− mice (n=18) already at day 7 after angiotensin II (AngII) infusion compared with controls (n=18). This is associated with a significant increase of T-cell infiltration within the aortic wall of CD28 −/− mice infused with AngII (B), mostly in the adventitia (n=8/group). C, A shift of the immune response toward reduced ratio of Having established that genetic or antibody-induced Treg deficiency promotes AAA formation and rupture, we wanted to address the underlying mechanisms. We found that Treg-deficient Cd28 −/− mice displayed increased AAA development already at day 7 after AngII infusion ( Figure 3A), indicating an early acceleration of the disease in the absence of Treg cells. Enhanced susceptibility to AAA in Cd28 −/− mice was associated with increased vascular accumulation of leukocytes ( Figure I in the onlineonly Data Supplement), particularly T cells ( Figure 3B), and an imbalance of the systemic (spleen, Figure 3C) and local (aortic, Figure 3D) immunoinflammatory response as reflected by low interleukin (IL)-10 but high expression of IL-12 and inter...

After initial septic shock resuscitation, StO(2) measured around the knee is a strong predictive factor of 14-day mortality.

Background: Prone positioning (PP) during veno-venous ECMO is feasible, but its physiological effects have never been thoroughly evaluated. Our objectives were to describe, through electrical impedance tomography (EIT), the impact of PP on global and regional ventilation, and optimal PEEP level. Methods:A monocentric study conducted on ECMO-supported severe ARDS patients, ventilated in pressurecontrolled mode, with 14-cmH 2 O driving pressure and EIT-based "optimal PEEP". Before, during and after a 16-h PP session, EIT-based distribution and variation of tidal impedance, VT dorsal /VT global ratio, end-expiratory lung impedance (EELI) and static compliance were collected. Subgroup analyses were performed in patients who increased their static compliance by ≥ 3 mL/cmH 2 O after 16 h of PP.Results: For all patients (n = 21), tidal volume and EELI were redistributed from ventral to dorsal regions during PP. EIT-based optimal PEEP was significantly lower in PP than in supine position. Median (IQR) optimal PEEP decreased from 14 (12-16) to 10 (8-14) cmH 2 O. Thirteen (62%) patients increased their static compliance by ≥ 3 mL/cmH 2 O after PP on ECMO. This subgroup had higher body mass index, more frequent viral pneumonia, shorter ECMO duration, and lower baseline VT dorsal /VT global ratio than patients with compliance ≤ 3 mL/cmH 2 O (P < 0.01). Conclusion:Although baseline tidal volume distribution on EIT may predict static compliance improvement after PP on ECMO, our results support physiological benefits of PP in all ECMO patients, by modifying lung mechanics and potentially reducing VILI. Further studies, including a randomized-controlled trial, are now warranted to confirm potential PP benefits during ECMO.

EGFR blockade induced T cell anergy in vitro and in vivo and reduced atherosclerosis development. Targeting EGFR may be a novel strategy to combat atherosclerosis.