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Additional file 1. Flow chart. Additional file 2. Number of patients with AC included in each center. Additional file 3. Variables associated with EBSL infection. Additional file 4. AC-associated mortality in participating centers. Crude mortality rate by center (left) and distribution of center effects on mortality rate (right) adjusted on individual confounders. Centers are sorted by study size. Black squares represent adjusted center effects on the mean mortality risk as odds ratio (OR) (comparison of each center to a theoretical average reference center with OR = 1).

Metabolic acidosis is commonly observed in critically ill patients. Experimental studies suggested that acidosis by itself could impair vascular function, but this has been poorly investigated in human.Prospective observational study.Medical ICU in a tertiary teaching hospital.To assess the relationship between metabolic acidosis severity and microvascular reactivity, we included adult diabetic patients admitted in ICU for ketoacidosis. Microvascular response to acetylcholine iontophoresis was measured at admission (baseline) and after correction of metabolic acidosis (24 hr).None.Thirty-nine patients with diabetic ketoacidosis were included (68% male), with a median age of 43 (31-57) years. At admission, microvascular reactivity negatively correlated with acidosis severity (R = -0.53; p0.001). Microvascular response was strongly depressed at pH less than 7.20 (area under the curve, 1,779 [740-3,079] vs 12,944 [4,874-21,596] at pH7.20; p0.0001). In addition, acidosis severity was significantly correlated with capillary refill time (R = 0.50; p = 0.02). At H24, after rehydration and insulin infusion, clinical and biological disorders were fully corrected. After acidosis correction, microvascular reactivity increased more in patients with severe baseline acidosis (pH7.20) than in those with mild baseline acidosis (area under the curve, +453% [213%-1,470%] vs +121% [79%-312%]; p0.01).We identified an alteration of microvascular reactivity during metabolic acidosis in critically ill patients with diabetic ketoacidosis. Microvascular hyporeactivity recovered after acidosis correction.

International audience; We aimed to assess the relationship between alterations of tissue perfusion parameters at admission (highly predictive of mortality in septic shock) and outcome in patients admitted to the intensive care unit (ICU) for acute pulmonary embolism (PE). We conducted a retrospective study to analyze the association between arterial lactate level, skin mottling and urinary output, and 28-day mortality.Over a 22-year period, 317 patients with PE were identified but we finally analyzed 108 patients whose main diagnosis for ICU admission was acute PE. At admission, the sequential organ failure assessment score was 2 (0-6) and the simplified acute physiology score II was 29 (16-43). Thirty patients (28%) received vasopressors and 37 patients (34%) received thrombolytic therapy. Day 28 mortality rate was 25% (n = 27). When compared to 28-day survivors, nonsurvivor patients had higher lactate level (4.5 [2.3-10.3] mmol/L vs 1.4 [1-2.9] mmol/L, P < .0001), more frequent mottling around the knee area (56% vs 25%, P = .003) and a lower urinary output (during the first 6 hours) (0.35 [0-1] mL/kg/h vs. 0.88 [0.62-1.677] mL/kg/h, P = .0002). Mortality increased with the number of tissue perfusion alterations present upon admission, 8% for none, 21% for 1, 28% for 2, and finally reached 85% for 3 tissue perfusion alterations (P < .0001). In a multivariate analysis, the relationship between the number of tissue perfusion alterations and 28-day mortality was maintained after adjustment on the presence of shock and right ventricular dilation at admission.In ICU patients admitted for acute PE, tissue perfusion alterations correlated with 28-day mortality independently of blood pressure and right ventricular dilation.

BACKGROUND: Current clinical practice guidelines promote a goal-directed approach for oxygen delivery with respect to SpO 2 objectives. We evaluated the efficiency of a strategy based on goal-directed O 2 delivery in the ICU. METHODS: A group of 30 patients (Group 1) with a proven history of chronic obstructive pulmonary disease suffering from acute hypercarbic exacerbation was compared to 2 other groups of patients admitted for acute respiratory failure with no history of pulmonary disease: 30 patients requiring oxygen supply and/or non-invasive ventilation (Group 2) and 30 requiring invasive ventilation (Group 3). The delivery of oxygen was based on SpO 2 measurement: 88−94% for Group 1 and 90−96% for others. The time spent with an SpO 2 below, within and above the prescribed limits was collected. RESULTS: The mean time spent within the prescribed range was for Groups 1, 2 and 3, respectively as follows: 61.9% [60.5−63.2], 63.7% [62.3−65] and 56.4% [55.3−57.6] ( P < 0.001 for each group). A history of chronic obstructive pulmonary disease was not correlated with better results ( P = 0.11), while invasive ventilation was related to the time spent out of the prescribed range ( P < 0.001; OR 1.3 [1.22−1.28]) especially in hyperoxaemia (40.7% [39.6−41.8] P < 0.001). Efficiency seems unrelated to nursing workload or night team exhaustion (r = −0.09, P = 0.77). CONCLUSIONS: Goal-directed oxygen delivery based on SpO 2 objectives in ICU patients ensures that in only approximately 64% of the time, SpO 2 stays within the prescribed range.