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Purpose To evaluate the efficiency, safety and outcome of high flow nasal cannula oxygen (HFNC) in ICU patients with acute respiratory failure. Methods Pilot prospective monocentric study. Thirty-eight patients were included. Baseline demographic and clinical data, as well as respiratory variables at baseline and various times after HFNC initiation during 48 h, were recorded. Arterial blood gases were measured before and after the use of HFNC. Noise and discomfort were monitored along with outcome and need for invasive mechanical ventilation. Results HFNC significantly reduced the respiratory rate, heart rate, dyspnea score, supraclavicular retraction and thoracoabdominal asynchrony, and increased pulse oxymetry. These improvements were observed as early as 15 min after the beginning of HFNC for respiratory rate and pulse oxymetry. PaO 2 and PaO 2 /FiO 2 increased significantly after 1 h HFNC in comparison with baseline (141 ± 106 vs. 95 ± 40 mmHg, p  = 0.009 and 169 ± 108 vs. 102 ± 23, p  = 0.036; respectively). These improvements lasted throughout the study period. HFNC was used for a mean duration of 2.8 days and a maximum of 7 days. It was never interrupted for intolerance. No nosocomial pneumonia occurred during HFNC. Nine patients required secondary invasive mechanical ventilation. Absence of a significant decrease in the respiratory rate, lower oxygenation and persistence of thoracoabdominal asynchrony after HFNC initiation were early indicators of HFNC failure. Conclusions HFNC has a beneficial effect on clinical signs and oxygenation in ICU patients with acute respiratory failure. These favorable results constitute a prerequisite to launching a randomized controlled study to investigate whether HFNC reduces intubation in these patients.

Two studies recently suggested the potential benefit of renin-angiotensin system (RAS) blockers (angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs)) after AKI [3, 4]. Table 1 Patient characteristics ACEi/ARB + (N = 45) ACEi/ARB - (N = 303) p Characteristic at ICU admission Age—years 64.4 ± 15.1 63.1 ± 14.7 0.6 Male sex—no. (%) 32 (71) 193 (63) 0.3 Weight—kg 85.8 ± 23.7 82.4 ± 20.5 0.3 Main reason for ICU admission—no. (%) Medical 37 (82) 263 (87) Surgical, emergency 5 (11) 66 (22) Surgical, scheduled 3 (7) 19 (6) Serum creatinine before ICU admission 92.0 ± 24.7 83.4 ± 24.0 0.03 Coexisting condition—no. (%) Chronic renal failure 6 (13) 26 (9) 0.3 Hypertension 28 (62) 152 (50) 0.1 Diabetes mellitus 3 (7) 31 (10) 0.67 Congestive heart failure 6 (13) 17 (6) 0.05 Ischemic heart disease 8 (18) 26 (9) 0.05 SAPS III at ICU admission 63.0 ± 14.0 68.3 ± 14.3 0.02 Septic shock—no. (%) 26 (58) 128 (42) 0.05 Biological characteristics Serum creatinine—µmol/L 203.9 (133.1) 219.6 (136.9) 0.47 Blood urea nitrogen—mmol/L 13.0 (8.4) 14.4 (9.3) 0.34 Serum potassium—mmol/L 4.1 (0.8) 4.3 (0.9) 0.37 Serum bicarbonate—mmol/L 19.9 (5.0) 18.7 (5.7) 0.17 Characteristic of ICU stay Physiological support during ICU stay—no. (%) Invasive mechanical ventilation 41 (91) 260 (86) 0.33 Vasopressor support (epinephrine or norepinephrine) 31 (69) 257 (85) 0.008 Number of patients who received RRT—no. (%) 28 (62) 211 (70) 0.32 Ventilator duration—median (IQR) 5 (5–13) 5 (4–10) 0.40 Vasopressor-free days—median (IQR) 3 (2–5) 4 (2–7) 0.11 Length of ICU stay—median (IQR) 18 (11–20) 15 (8–22) 0.35 RRT dependence—no. (%) At day 28 4 (9) 27 (9) 0.99 At day 60 1 (2) 9 (3) 0.77 Mortality—no. (%[95% CI]) At day 60 6 (13) 39 (12) 0.73 Creatinine at ICU discharge 183.6 ± 136.4 177.9 ± 150.1 0.81 ACEi angiotensin-converting enzyme inhibitors, ARB angiotensin receptor blockers, ICU intensive care unit, IQR interquartile range, RRT renal replacement therapy, CI confidence interval Table 2 Multivariate analysis Variable OR 95%CI p Age 1.02 [1.00–1.05] 0.04 MacCabe 3.10 [1.64–5.87] < 0.001 SAPS3 1.04 [1.02–1.07] < 0.01 CKD 1.99 [0.77–4.89] 0.14 Congestive heart failure 2.12 [0.66–6.43] 0.19 History of acute stroke 1.91 [0.80–4.38] 0.13 ACEi/ARB at ICU discharge 1.71 [0.71–3.90] 0.21 CKD chronic kidney disease We acknowledge that our study did not assess introduction nor interruption of ACEi/ARB after ICU discharge. According to French law, because the treatments and strategies used in the study were classified as standard care, there was no requirement for signed consent, but the patients or next of kin were informed about the study before enrolment and confirmed this fact in writing.

The purpose of this study is to investigate whether exposure to nonsteroidal antiinflammatory drugs (NSAIDs) at the early stage of severe pneumococcal community-acquired pneumonia (CAP) requiring intensive care unit (ICU) admission may affect its presentation and outcome. Medical records of ICU adult patients (12-year period) with a pneumococcal CAP diagnosis were retrospectively analyzed according to previous NSAID exposure. One hundred six confirmed pneumococcal CAP were identified, 20 received NSAIDs within 4 (2-6) days before admission. Nonsteroidal antiinflammatory drug–exposed patients were younger (43.3 vs 62.2 years; P < .0001), had less frequently at least one chronic comorbid condition (40% vs 75%; P = .003), had more often complicated pleural effusions (20% vs 2.3%; P = .01), and more frequent pleuropulmonary complications (odds ratio: 5.75 [1.97-16.76]). Nonsteroidal antiinflammatory drug patients required more often noninvasive ventilatory support (25% vs 4.6%; P = .003). Intensive care unit length of stay and mortality were similar. We report as severe pneumococcal pneumonia in young and healthy patients exposed to NSAIDs as in older, more comorbid, and nonexposed ones. Nonsteroidal antiinflammatory drug use may mask initial symptoms and delay antimicrobial therapy, thus predisposing to worse outcomes.

See related research by Zou et al. https://ccforum.biomedcentral.com/articles/10.1186/s13054-017-1707-0 This comment refers to the article available at: https://doi.org/10.1186/s13054-017-1707-0.

Background. Evidence from a recent randomized controlled trial suggests that dexamethasone as adjunct therapy in adult pneumococcal meningitis reduces mortality and neurological sequelae. However, adding dexamethasone has the potential to reduce penetration of vancomycin into the cerebrospinal fluid (CSF). We sought to determine concentrations of vancomycin in serum and CSF of patients with suspected or proven pneumococcal meningitis receiving dexamethasone to assess the penetration of vancomycin into the CSF during steroid therapy. Methods. In an observational open multicenter study, adult patients admitted to the intensive care unit because of suspected pneumococcal meningitis received recommended treatment for pneumococcal meningitis, comprising intravenous cefotaxime (200 mg per kg of body weight per day), vancomycin (administered as continuous infusion of 60 mg per kg of body weight per day after a loading dose of 15 mg per kg of body weight), and adjunctive therapy with dexamethasone (10 mg every 6 h). Vancomycin levels in CSF were measured on day 2 or day 3 of therapy and were correlated with protein levels in CSF and vancomycin levels in serum (determined at the same time as levels in CSF). Results. Fourteen patients were included. Thirteen had proven pneumococcal meningitis; 1 patient, initially suspected of having pneumococcal meningitis, was finally determined to have meningitis due to Neisseria meningitidis. Mean levels of vancomycin in serum and CSF were 25.2 and 7.2 mg/L, respectively, and were positively correlated (r = 0.6; P = .025). A positive correlation was also found between the ratio of vancomycin in CSF to vancomycin in serum and the level of protein in CSF (r = 0.66; P = .01). Conclusions. Appropriate concentrations of vancomycin in CSF may be obtained even when concomitant steroids are used. Dexamethasone can, therefore, be used without fear of impeding vancomycin penetration into the CSF of patients with pneumococcal meningitis, provided that vancomycin dosage is adequate. This study is registered at http://www.ClinicalTrials.gov/ (registration number NCT00162578).

Renal replacement therapy (RRT) is a major supportive treatment of acute kidney injury (AKI) in intensive care unit (ICU), but the timing of its initiation remains open to debate. We retrospectively analyzed ICU patients who had AKI associated with at least one usual RRT criteria: serum creatinine concentration greater than 300 μmol/L, serum urea concentration greater than 25 mmol/L, serum potassium concentration greater than 6.5 mmol/L, severe metabolic acidosis (arterial blood pH <7.2), oliguria (urine output <135 mL/8 hours or <400 mL/24 hours), overload pulmonary edema. To estimate the risk of death associated with RRT adjusted for risk factors, we performed a marginal structural Cox model with inverse-probability-of-treatment-weighted estimator. Among 4173 patients admitted to the ICU, 203 patients fulfilled potential RRT criteria. Ninety-one patients (44.8%) received RRT and 112 (55.2%) did not. Non-RRT and RRT patients differed in terms of severity of illness: Simplified Acute Physiology Score II (55 ± 17 vs 60 ± 19, respectively; P < .05) and Sequential Organ Failure Assessment score (8 [5-10] vs 9 [7-11], respectively; P = .01). Crude analysis indicated a lower ICU mortality for non-RRT compared with RRT patients (18% vs 45%; P < .001). In the marginal structural Cox model, RRT was associated with increased mortality (P < .01). A conservative approach of AKI was not associated with increased mortality.