ESICM LIVES 2016: part one Milan, Italy. 1-5 October 2016
PMCID: PMC5042924
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Results: Among the 2813 patients presenting ARDS in the first 48 h, 266 patients (9.4 %) had no ARDS risk factor identified at admission. Table 2 shows the final ARDS risk factor identified in patients with or without initial risk factor identified.
The patients with no risk factor were older, had more frequent previously known chronic diseases and presented with less severe SOFA (8.7 ± 3.9 vs 9.5 ± 4.1, p < 0.001) and non-pulmonary (5.4 ± 3.9 vs 6.3 ± 4.1, p < 0.001) SOFA scores. ICU mortality was lower in ARDS patients with no risk factor than in others (28.6 % vs 34.9 %, p = 0.047), but in-hospital mortality was not (35.7 % vs 39.8 %, p = 0.20). The lack of ARDS risk factor was not associated with hospital mortality (adjusted OR = 0.86 [0.65-1.13], p = 0.29). In the subgroup of patients with no ARDS risk factor, age, SOFA, concomitant heart failure, and administration of steroids within 72 hours of ARDS onset were associated with hospital mortality (Table 3).
Results: The analysis included 456 patients with moderate or severe ARDS who stayed in the ICU > 24 hours. The relation between PaO2/FiO2 and SpO2/FiO2 was good (R2 = 0.62). Using the predefined cutoffs for SpO2/FiO2 and PEEP, prognostication improved with re-classification after 24 hours (Tables 6 and 7).
Results: Sample preparation or processing issues resulted in exclusion of 14 patients, leaving 467/481 (97 %) for final analysis. Of these, 359 (77 %) subjects received antibiotics upon ICU admission, whereas therapy was initiated on a later date in an additional 14 (3 %) patients. Test results correlated with the probability of infection (p < 0.001) (Fig. 1). Among the 415 patients in whom the test classified sepsis as 'likely´, the false positive rate decreased from 17/39 (44 %) to 36/195 (18 %) with higher probability bands. In the 52 patients in whom the test suggested infection to be unlikely we observed 8 cases of confirmed infection (false negative rate 15 %). As 135 patients could not be categorized with certainty (“undetermined”) formal calculation of sensitivity and specificity was precluded. SeptiCyte test results were not affected by age, prior ICU stay, or immune deficiency. Higher scores of the test were indicative of increased severity of disease and mortality (Fig. 2).
Results: Total 942 patients were identified during study periods. Among them, 14 patients were excluded because of missing values. Demographic characteristics were described in Table 8.
Patients with qSOFA less than 2 accounted for over half of enrolled patients (493/928, 53.1 %) and over one third of mortality cases (88/231, 38.1 %) (Table 9).
AUROC of SIRS, qSOFA, and SOFA to predict 28-day mortality were 0.540 (0.500-0.580), 0.627 (0.587-0.667), and 0.687 (0.646-0.727), respectively. (SIRS vs qSOFA [p < 0.001], qSOFA vs SOFA [p = 0.009]) (Fig. 3).
Results: We evaluated 6,874 patients with CAP, mean age 66 (±19) and in-hospital mortality of 442 patients (6.4 %). Discrimination evaluated through the area under the curve (AUC) is in Table 10. SIRS criteria had the worse discrimination performance compared with qSOFA, CRB and SOFA. Calibration plots were comparable among the scores, although overestimation was more pronounced for qSOFA and SOFA scores. When adding the scores to the baseline risk model, the discrimination of Model + SIRS has no change, although improved with qSOFA, CRB and SOFA. Baseline model calibration improved similarly by adding each score in it. Using the cut-off of two points, the sensitivity/specificity for SIRS was 88/22 %, qSOFA 50/82 %, CRB 39/87 % and SOFA 97/23 %. Similar patterns were observed for secondary outcomes and for other measures of performance (Brier Score, IDI).
Results: 196 patients with severe sepsis or septic shock were included. Applying sepsis-3 criteria resulted in 3 subgroups: sepsis, septic shock and patients with neither SOFA increase nor shock. Results are presented in Fig. 5.
Results: 1651 patients were admitted. 532 (32,2 %) met some CP criteria. In 136 (8,2 %) were detected one or more MRB, 87 of these (64 %) presented CP criteria according to the checklist. 37 met 1 criteria, 31 met 2 criteria and 19 met 3 or more criteria with accumulation of risk (p < 0,001). In 49 (36 %) MRB carriers it was not identified any of the RF from the checklist. Tables 13 and 14 show risk factors and comorbidities that were significant as added risk for MRB.
Results: Main parameters describing pathophysiological characteristics of each group after 8 hours are reported in Tables 15 and 16. Lung lavage and high Vt ventilation following regional embolization led to more severe impairment of oxygenation (p < 0.001), especially in the left embolization group. Lung mechanics at the end of the experiment showed similar trend: plateau pressure was higher and respiratory system compliance lower (p < 0.05) in the embolization + lavage + high Vt groups. Finally, CT-scan revealed higher lung weight in groups 1 and 2 (p < 0.05). Interestingly, in the same groups, the non-embolized lungs were heavier, as if embolization triggered more severe ventilation-induced lung oedema that could develop mainly where perfusion was preserved.
Results: We found no significant associations between SNPs rs8094315 (OR 1.10, p 0.4827), rs12457893 (OR 1.02, p 0.8736), rs2093266 (OR 0.77, p 0.1525), rs1955656 (OR 0.77, p 0.1525) and rs625145 (OR 0.89, p 0.3967) and AKI comparing 354 AKI patients and 299 non-AKI patients (Table 17). AKI patients were significantly older, had higher BMI, more often diabetes and COPD, had received more often colloids before admission to ICU, and had lower platelet count. Multivariate logistic regression analysis with adjustment for sex and these baseline differences did not change our findings.
Results: We included 99 patients, mean age 65, mean APACHE III score 73. 49 patients (49 %) developed AKI within the first week (mean 2.2 days after inclusion). Patients who developed AKI had a significantly higher RRI on inclusion than those who did not: 0.708 (0.687-0.730) vs 0.654 (0.631-0.677), p = 0.001. Compared to patients without AKI, RRI was significantly higher in patients with AKI stage 2 and 3, but not in patients with AKI stage 1 (Fig. 12).
We therefore chose AKI stage 2 and 3 as endpoint in further analysis. On univariate analysis, RRI was a significant predictor of AKI (OR 1.012, 95 % CI 1.006-1.019), along with other parameters including: APACHE III, fluid balance and BIA derived reactance, but not sublingual microcirculation. On multivariate analysis, RRI, APACHE III and fluid balance remained significant. The AUC of RRI for AKI stage 2 and 3 was 0.721 (95 % CI 0.612-0.831). The composite AUC of the multivariate predictors was 0.825 (Fig. 13).
Results: SDF findings (Fig. 14) of S8-T6h showed broadly distributed microcirculation dysfunction. The outlining of tubules became blurred by their enlargement leading to the compression of tubular lumen and of the peritubular microvessels, suggesting an ongoing obstructive phenomenon in a progressive manner by tubular wall edema. The heterogeneous dysfunction pattern was disseminated in entire screen. S9-T6h showed similar findings, however more intensely. The histology (Fig. 15) confirmed the ongoing obstructive phenomena at S8-T6h, and also showed generalized peritubular microvessels congestion, multiple glomerulus without mesangial area, inflammatory infiltrate in the connective tissue and hyaline degeneration suggestive of ongoing cellular dysfunction/death. The histological results of S9-T6h showed similar pattern with the enlargement of the epithelial cells of convoluted tubules with reduced lumen, and with compressed or dilated peritubular microvessels. In addition, numerous tubular epithelial cells showed membrane injury, nuclear pycnosis and necrosis. At S8-T30d, although the general findings were better, as compared to the early phase sepsis (T6h), the histological findings demonstrated a persistence of significant peritubular and glomerular congestions with intense inflammatory infiltrate in the connective tissues, nucleus contractions suggestive of cell death, and collecting ducts injuries. PAS staining demonstrated widespread hyaline degeneration. The more severe sepsis, S9-T30d group, showed a widespread congestion around the collecting tubules and peritubular congestion of the small and large vessels. Also was observed glomerulus without mesangial areas, intense congestion and hyaline degeneration of the collecting tubules and of the cortex tubules region. The general findings were of the ischemic renal injury pattern. These findings showed that renal dysfunction persists at 30 days after sepsis, and that the presence of any pathological stimuli, may decay the renal physiological capacity quickly, justifying the fragility of renal physiology in patients who survived sepsis.
Results: PMBCs incubated with post-operative serum demonstrated a significant reduction in mHLA-DR membrane density (Fig. 19, p = 0.001). The reduction in mHLA-DR density was prevented when co-incubated with GM-CSF and IFNγ (Fig. 19). Incubation with IFNγ but not GM-CSF increased expression of HLA-DRα chain (p = 0.01), Cathepsin S (CTSS) (p = 0.001), suppressor of cytokine signalling 3 (SOCS3) (p = 0.01) and March 1 (p = 0.002) (Fig. 20).
Methods: A prospective multicenter before-after study was conducted in six ICUs in the Netherlands between March 2012 and April 2015. The intervention consisted of a two-phase multifaceted tailored implementation of the PAD guidelines. Multiple implementation strategies were applied to change clinical practice (Table 18). Data of all adult ICU patients were collected during three four-month periods:
Results: A total of 4727 patients were enrolled in the study with a total of 23958 ICU days. Adherence to most PAD guideline recommendations improved significantly whereas early mobilization and reduced benzodiazepine sedation improved only in the last period (Table 19). The incidence of delirium increased from 22 % before to 30 % after implementation (aOR = 1.5, p < 0.01) whereas delirium duration decreased from 6.3 before to 3.6 days after implementation (aBeta = -2.6, p < 0.01). There were no statistically significant differences in ICU length of stay (aBeta = 0.001, p = 0.99); ICU mortality (aOR = 1.2, p = 0.17); and hospital mortality (aOR = 1.2, p = 0.21) after vs. before the implementation. Only length of mechanical ventilation increased with half a day (aBeta = 0.55, p = 0.01).
Methods: Skeletal muscle cells were isolated from biopsies obtained from patients (n = 16) undergoing hip replacement surgery and subsequently exposed to a range of propofol resembling clinical concentrations in human plasma during propofol infusion (0, 1, 2.5, 5 a 10 μg/ml) and to lipid vehicle (Intralipid® – IL). After 96 hours of exposure, mitochondrial metabolism was assessed by extracellular flux analysis (Seahorse Biosciences). Oxygen consumption rate (OCR) was measured at baseline and after addition of ATPase inhibitor, mitochondrial uncoupler and complex III inhibitor. Injection of these agents enables to calculate baseline OCR, ATP turnover rate, proton leak through inner mitochondrial membrane and respiratory chain capacity (uncoupled respiration). The capacity of fatty acid oxidation was measured as etomoxir-inhibitable OCR after adding of uncoupler and palmitate. Values presented in Table 20 are expressed as % of baseline OCR.
Results: In human skeletal muscle cells exposed to propofol, respiratory chain capacity was decreased and uncoupling of inner mitochondrial membrane was increased. The most significant result was propofol-induced inhibition of fatty acid oxidation to 15 %, respectively 11 % of baseline values (see Table 20). Data are presented as median (interquartile range). Statistically significant results are signed as * if p-value < 0.05, ** p-value < 0.001.
Results: Five trials consisting of 613 patients were included for meta-analysis.2,3,4,5,6 Four trials were set in surgical ICUs and one in a mixed ICU. Only one trial was rated at low risk of bias in all domains. There was variation in dosage regimes, from 3x/weekly administration of intravenous iron to daily oral iron for up to 30 days post discharge. Results are shown in Table 21. No trials reported on QoL.
Results: The basic narrative of recovery was “toward a trajectory of new orientation”. The narrative at 3 months described mortal illness in ICU (Being at Death's door), the narrative at 5 months described ongoing fear of relapse (Still not out of the Woods), and the narrative at 10 months had three potential outcomes: downhill (detour on the road), steady-state (end of the road), or progress (The Road to Recovery). New orientation was obtained in steady-state or progressive recovery, Fig. 21.
Results: 61 patients were admitted as unplanned admissions during the first audit period. Patients were elderly, had a high predicted mortality and a significant proportion were clinically frail (CFS ≥ 5). Mean length of stay (LOS) was prolonged and level of organ support was high. These results are summarised in Table 25.
Results: Over the 12 month data collection period 296 tracheostomy patient admissions were tracked across the four sites with similar demographics to previously reported national data.[1] A total of 124 adverse events were identified affecting 29.8 % patients. Analysis of reported incidents over the duration of the project showed a significant reduction in the severity of harm by month (Chi Square p < 0.01, Fig. 22). There was also a significant trend towards lower harm categories for incidents over the duration of the project (Chi Square test for linear trend, r = -0.21, p < 0.01). Monthly analysis of the dataset for percutaneous tracheostomies showed non-significant trend toward earlier speaking valve use and vocalisation (median slope = -0.17, -0.83 to 0.4) associated with improvements in reported patient satisfaction scores.
Results: Fourteen patients were included: 5 patients received 1 g vitamin C and 5 patients 5 g vitamin C iv twice daily for two days. Two patients received 2 g/day vitamin C and 2 patients received 10 g/day by continuous infusion for two days (Table 26). Four patients (28 %) were vitamin C deficient on admission (<20 μmol/L). A two-compartment pharmacokinetic model best described the data (Fig. 23, model parameters not shown). The urinary excretion of vitamin C and oxalate is shown in Table 27.
Results: 231 patients were included in Before and 225 in After group, respectively. The groups are comparable regarding demographics, case-mix and severity of illness. Instalment of feeding protocol resulted in significantly higher cumulative amount of enterally provided calories by day 7 [3165 (1165-5215) kcal in After vs 2360 (450-5075) kcal in Before group, median (IQR), p = 0.043], while less calories were given parenterally [2600 (712-4287) vs 3900 (1725-6645) kcal, p < 0.001]. Cumulative proportion of patients who did not receive any enteral feed was significantly smaller in After group (Fig. 24).
Percentage of enterally received calories from caloric needs was significantly higher in After group (Fig. 25).
Results: At 6 h post-sepsis no differences were seen in renal and hepatic phosphorylation of AMPK, ACC, PDH and HSL between sham and septic animals. While cardiac ACC phosphorylation was strongly increased in septic rats, AMPK phosphorylation did not differ, suggesting that ACC phosphorylation was mediated not by AMPK but rather via the glucagon-PKA pathway. The biggest changes were observed in skeletal muscle. AMPK phosphorylation was increased in gastrocnemius and even more so in soleus in septic rats but this was not accompanied by a corresponding increase in ACC phosphorylation. In both muscles PDH phosphorylation markedly increased while PDH fell, suggesting a fall in pyruvate oxidative decarboxylation and glucose usage as a fuel. HSL phosphorylation was strongly increased in soleus in non-survivors. UCP2 and UCP3 levels were not altered in any organ. Table 31.
Results: We found a progressive and significant reduction in both circulating EMPs (median 207, IQR 95-404 è median 64, IQR 45-90 MPs/mL, p = 0.013) and LMPs (median 432, IQR 93-479 èmedian 39, IQR 35-282 MPs/mL, p = 0.044) between the start of ECMO support (T0) and soon after the decannulation (T2), as shown in Fig. 31. Survivors showed higer levels of LMPs (p = 0.034) compared to non survivors and almost significantly higher levels of EMPs (p = 0.062). Standard laboratory tests (i.e. CRP, PCT, and WBC) did not show any significant difference between the same time points, and between different outcomes. There was no correlation between level of any kind of MPs and heparin dose, bleeding episodes, and mortality.
The evolution of parameters was in the Table 32.
Results: We enrolled 15 severe ARDS patients requiring VV-ECMO. ECMO median duration was 9 (interquartile range 8-14.5) days. Mortality was 53.3 %. We found a strong correlation between maximum clot firmness (MCF) and amplitude of the curve at 10 minutes (A10) in all ROTEM tests (Rho > 0.96, p < 0.001). 67 % of patients had at least one episode of bleeding. 30.5 % of the hemorrhages were severe. PLT was lower in bleeding compared to non-bleeding group (p = 0.02). Among the ROTEM tests, heparinase modified thromboelastometry clotting time and clot formation time (HEPTEM CT and CFT) were significantly higher in bleeding group (p < 0.05) (Fig. 33). The POC tests evaluating the intrinsic and extrinsic coagulation pathways, as well as the thrombin receptor activating peptide-6 test (TRAP-AUC) assessing platelet aggregometry, were different between groups, even though not statistically significant (Fig. 34). There was no difference in PT, aPTT, anti-Xa activity, fibrinogen and ACT between groups.
Results: 1129 patients received RRT for AKI of whom 42 % died in hospital. There was a significant difference in cumulative fluid balance at initiation of RRT between hospital survivors and non-survivors. (Fig. 35)
108 patients (9.6 %) had FO >10 %. They had a significantly higher hospital mortality (X2 = 5,89; p = 0,015) and longer stay in ICU (19.6 days versus 12.8; p < 0,001) but also higher SOFA score compared to patients with FO ≤10 %. (Table 36)
Results: We screened 4087 patients and identified 864 with AKI (Fig. 37) of whom 461 and 255 developed fluid overload above respectively 5 % and 10 % of bodywieght (BW) during their first 5 days in ICU (Fig. 38). At day 28, 514 of the AKI patients had renal recovery and 282 had died (Table 37).
Results and conclusions: SDF at T6h showed broadly distributed microcirculation and tissue dysfunction at both groups (Fig. 39). The outlining of tubules became blurred by their enlargement, with compression of tubular lumen and of the peritubular microvessels, suggesting an obstructive phenomenon by cellular edema. Histology. After 6 hours of sepsis, animals treated with aggressive fluid infusionshowed less peritubular congestion, preserved mesangial space and lower areas with hyaline degenerations and better preservation of the tubular lumen compared to sepsis without aggressive overhydrating. PAS staining showed a very slight hyaline degeneration, better preservation of tissue architecture, lower occurrence of cellular death, suggesting that the aggressive fluid therapy in the early stage of sepsis minimizes the severity of vascular and tissue injury in the kidney. The live animals treated with the aggressive fluid showed less peritubularmicrovesselscongestion compared to S8, better preservation of the mesangial space, minor hyaline degeneration, and less cell death in deeper regions of the cortexafter a month of recovery. However, the general appearance showing a kidney limitation for venous blood drainage. Clearly, the aggressive-fluid therapy attenuates renal damage compared to S8. The results suggest that animals treated with aggressive fluid therapy, at the early stage of sepsis, have better conditions to respond against new harmful challenges to the kidney. Besides, the recover process after sepsis seems to be partial, justifying the occurrence of the post-sepsis syndrome.
Results: Age 41.13 (3.2) years, 50 % men and base CrCl 163 (19.51) mL/min. Median percentage of change between base and maximum CrCl was 123.5 % (78.2-143.2) and because a pick was detected between 3 and four hours after protein load we analysed these two hours together, finding a median change of 80.7 % (69.95-144). Changes between the first and third hours were significant either for absolute values (p 0.023) or % (p 0.031). Hourly changes in CrCl are presented in Fig. 40
Results Forty patients with shock and 52 without shock were included. Patients with eGFR < 30 mL/min were excluded. Mean age was 69 (60-76) vs. 67 (59-76) yrs. and APACHE III score was 81 (63-107) vs. 57 (45-70) (p < 0.001). Shock patients had a higher RRI than patients without shock (median, 0.751 (0.692-0.788) vs. 0.654 (0.610-0.686); p < 0.001), (Fig. 41). On univariate analysis, high age, APACHE III score, vasopressor support, pulse pressure index (PPI: (systolic-diastolic)/systolic blood pressure), central venous pressure and positive fluid balance, and low mean arterial pressure (MAP), reactance/m and creatinine clearance were the markers most significantly associated with high RRI (p < 0.01). Markers of the microcirculation were not. On multivariate analysis, vasopressor support, higher PPI, lower MAP and lower Xc/m remained as independent determinants of RRI (n = 89, Adj. R2 = 0.472).
Most of the staff were not aware of the time since the most recent infections, as can be seen in Table 42.
Results In total 50 patients were prescribed thiopentone. Eight received a bolus and three had other indications. A further 3 patients had a duration under 6 hours and were excluded. Thirty-six patients were reviewed with 1 patient dying during infusion. Patient characteristics are shown in Table 44.
Hypokalaemia (potassium < 3.5) developed in 25 patients (69.4 %) during infusion with the mean lowest at 12 hours (Fig. 49). Subsequently 11 (31.4 %) patients developed hyperkalaemia (potassium > 5.5), mean peak 12 hours after.
Insulin use, duration of infusion, weight, potassium replacement or presence of hypokalaemia had no statistical significance relating to loss of regulation (Tables 45 and 46).
Results In both groups assessed results are presented in Table 48. Starting ventilator patients in both groups were required at different times substantially on average, and the eighth day in both groups were diagnosed with pneumonia.The frequency of hemodynamic disturbances and duration of inotropic support were comparable in both groups. The mortality rate in group 1 was significantly lower than in group 2, which explains the increase in the period of mechanical ventilation and stay of patients in the ICU and in the hospital. Analysis on GOS the surviving patients showed no significant differences.
Results Preliminary data are based on 170 patients (58 % male and 42 % female, 67 (56-73) years old, GCS at admission 7 (6-9)) admitted for intracranial hemorrhage (29 %), subarachnoid hemorrhage (22 %), trauma (21 %), stroke (12 %). Tracheostomy was performed at 10 (7-13) days from admission for compromised neurological status (89 %, GCS at tracheostomy 7 (6-8)). Direct laryngoscopy Fantoni´s translaryngeal technique (TLT), Percutwist, surgical, standard TLT and Dolphin were used in 63 %, 18 %, 11 %, 6 % and 2 % of the cases. ENT specialists and intenstivists performed 46 % and 54 % of the tracheostomy, respectively. No deleterious effect on recorded parameters was detected (see Table 48). Four lesions of the tracheal rings were documented.
Results EA-230 was well tolerated and showed an excellent safety profile. Treatment with the highest dose of EA-230, but not with lower doses, resulted in a significant attenuation of the endotoxin-induced increase in plasma levels of IL-6, IL-8, IL-1RA, MCP-1, MIP-1α, and MIP-1β (IL-6, IL-8, and MCP-1 shown in Fig. 50a, b, and c), and the adhesion molecule VCAM-1 (Fig. 50d). Furthermore, the highest dose of EA-230 reduced fever and flu-like symptoms (Fig. 51). Endotoxemia resulted in a marked increase in GFR, but no differences between groups were observed.
Results LPS administration resulted in a typical increase in plasma levels of cytokines, which was absent in the placebo group (Fig. 52). Following Fluenz challenge, viral shedding for at least one of the four influenza strains present in the vaccine was 12/15 (80 %) in the LPS-Fluenz group compared with 13/15 (87 %) in the placebo-Fluenz group. The increase in viral shedding of the influenza A and B strains was similar between groups (Fig. 53, upper panels). Likewise, the Fluenz-induced increase in levels of the chemokine IP-10 in nasal wash, as well as local symptoms, were not different between the LPS-Fluenz and placebo-Fluenz group (Fig. 53, lower panels).
Results Results show a decrease in circulating lymphocytes, Treg lymphocytes and lung weight in groups treated with MTX compared to the septic group (Fig. 54a-c). The cellular content in alveolus in the CLP MTX group shows a decrease in cell infiltration of polimorfonuclear cells and lymphocytes compared to CLP group, while the number of alveolar macrophages is not altered in the different groups (Fig. 54d-f).
Expression of the inflammatory cells recruitment, matrix remodelling and proinflmatory markers show an increase in septic rats, while with MTX treatment exhibit a reduction. Finally, MTX cause an increase of the expression of the anti-inflammatory cytokine IL4 (Fig. 55).
Methods Live naïve kidney slices (200 μm thick) were exposed to serum from 24 hour sham operated or septic rats for 90 minutes and imaged with a confocal microscope using fluorescent dyes to detect dynamic changes in mitochondrial function (Fig. 60).
Results Septic serum caused a decrease in MMP, an increase in ROS, but no change in NADH at 90 minutes exposure compared to baseline (Fig. 61). Sham serum did not cause any change from baseline and was comparable to slices exposed only to a physiological saline solution.
Results Ten polytrauma patients with a median Injury Severity Score (ISS) of 38 (IQR 29-50) were recruited. This cohort was 80 % male with a median age of 27 (IQR 23-50). There was a decrease in antigen density of mHLA-DR on healthy donor PBMCs when incubated with admission (P < 0.01) or 24HR (P < 0.05) polytrauma serum, compared to incubation with serum from age and sex matched controls (Fig. 62a). Culturing in the presence of IFN-γ (P < 0.01) or GM-CSF (P < 0.05) prevented this decrease in antigen density (Fig. 62b). Pre-incubation with an IL-10 neutralising antibody partially reversed the detrimental effects of the incubation with polytrauma trauma serum (P < 0.001; Fig. 62c).
Results 4033 patients were included (before- and after-period: 1385 and 2632 patients, 15 patients had missing data on covariables). Delirium was independently associated with hospital mortality in crude analysis (OR 1.95, p < 0.001, Table
55). There was significant interaction between APACHE II and delirium (p < 0.001). After adjustment the OR for delirium was 8.61, but the effect was much stronger in the patients with a higher APACHE II score above the median value (≤15; OR 1.68, p = 0.07 versus >15; OR 19.0, p < 0.001). Mortality risk of delirium in the after-period compared with the before-period and with CAM-ICU versus ICDSC (after-period) did not differ (before versus after-period, OR 0.82, p = 0.079 and ICDSC versus CAM-ICU, OR 1.03, p = 0.831).
Results Under propofol sedation, sensitivity and specificity of ANI (AUC = 0.97 and 0.99), SPI (AUC = 0.86 and 0.90) and PRD (AUC = 1.00 and 0.96) for detecting both painful stimuli were high compared to HR, MAP and BIS (AUC = 0.75 and 0.74, 0.74 and 0.76 and 0.53 and 0.58, resp., Fig. 67a + b). Likewise, with propofol sedation and remifentanil 0.2 mcg/kg/min, sensitivity and specificity of ANI (AUC = 0.82 and 0.80.), SPI (AUC = 0.73 and 0.84) and PRD (AUC = 0.63 and 0.68) for detecting both painful stimuli were higher compared to HR, MAP and BIS (AUC = 0.52 and 0.51, 0.48 and 0.48 and 0.52 and 0.60, resp., Fig. 67c-f).
In non responders, PPV and dicrotic pressure did not change significantly during the FC while CCE was significantly reduced from baseline to minute 10 (p < 0.05) (Figs. 69, 70, 71).
Results In a meta-analysis of the 7 included randomised trials (n = 1390), we found a non-significant reduction in mortality with a conservative or deresuscitative fluid strategy (pooled odds ratio 0.86, 95 % confidence interval (CI) 0.68-1.09) compared to a liberal strategy or usual care (Fig. 72). We found a non-significant reduction in RRT use with a conservative or deresuscitative fluid strategy (2 studies, pooled odds ratio 0.73, 95 % CI 0.51-1.05). Four trials reported shorter length of ICU stay or increased number of ICU-free days, and 2 studies reported shorter duration of mechanical ventilation or increased ventilator-free days with a conservative or deresuscitative fluid strategy compared to a liberal strategy or usual care. Marked clinical heterogeneity was present.
There was no significant correlation between 3-day cumulative fluid balance with either LUS, Ee´ ratio, or TFC (Table 56).
There was a significant correlation between TFC & LUS on day 1 & day 3 (r = 0.610, p < 0.01), (r = 0.4, p = 0.05) respectively. There was no relationship between Ee´ ratio & both TFC & LUS on day 1, it became significant on day 3 (Table 57).
TFC correlated significantly with LUS in patients with negative fluid balance but not in those with positive fluid balance. By the same token, LUS was correlated significantly with Ee´ in patients with negative balance only. However, no correlation was found between TFC & Ee´ in patients with either negative or positive fluid balance (Table 58).
Results / conclusions There were 25,419 total hypotensive events. Group 1 contained 1,200 events, 2 had 2,066, 3 had 7,290, and 4 had 5,283. 9,560 events were not used in analysis due to data outliers or meeting more than 1 group criteria. Overall, each group's 5 minute % change profile was different at 5 and 10 minutes (Fig. 75). % change in CO, SVV, and SV were significantly different when comparing Group 1 to 2, 3, and 4 at 10 minutes. % change in Ea dyn and SVR were significantly different when comparing Group 2 to 1, 3, and 4 at 10 minutes prior to event. % change in dP/dt were all significantly different when comparing Group 3 to 1, 2, and 4 at 10 and 5 minutes prior to event. In conclusion, the underlying cause of a hypotensive event can potentially be classified into 1 of 4 prescriptive groups up to 10 minutes prior to the start of an event.
Results During shock and early resuscitation Group A (n = 10) had a mean PVD of 10.5 (SD ± 2.5) mm/mm2, and Group B (n = 12) 5.5 (SD ± 4.1) mm/mm2. During the later resuscitation phases, Group A maintained a significantly higher PVD than Group B. Group A initially had a higher cardiac output but the difference between the groups narrowed as resuscitation progressed. At the end of resuscitation group A had significantly lower plasma lactate, higher lactate clearance, lower standard base deficit, and smaller mixed venous – arterial CO2 gradient. There was no significant difference in blood pressure between the two groups at any stage. There was a wide spread of PVD for a given blood pressure, especially during the shock and early (hypotensive) resuscitation phases (Fig. 78). The choice of initial resuscitation fluid appeared not to produce differing effects in terms of microcirculatory perfusion (Figs. 79 and 80).
478 ICU patients from multiple clinical sites that were not used in the calibration set were used as a test set for the final validation of HPI™. Patients included septic shock (189), post cardiac surgery (208), cardiogenic shock (32), post liver transplantation (19), and others (30, respiratory failure, post non cardiac surgery, etc.). The patient demographics are listed in Table 58. Radial arterial pressure waveforms were recorded with a FloTrac™ sensor (Edwards Lifesciences, Irvine, CA). The waveforms were passed to the algorithm to calculate the hypotension probability. The receiver operating characteristic (ROC) analysis was used to assess algorithm performance.
Results 16,078 hypotensive events were registered, on average 34 events per patient with a duration of 11 (±89) minutes per event. The algorithm was able to predict hypotension with a sensitivity and specificity of 90 %, 87 % and 86 %, for 5, 10, and 15 minutes prior to the event, respectively. The area under the curve (AUC) is 0.96, 0.94, and 0.93, for 5, 10, and 15 minutes prior to the event, respectively (Fig. 81).
Results Data were collected from 34 healthy volunteers (19 male), mean age 23 years [range 20-49] on 4 non-consecutive days. Two distinct stages of cooling and reheating were seen, with a rapid post-occlusion/reheating slope demonstrated at the end of the VOT in all volunteers [Fig. 82]. The mean rate of reheating in the palm was 0.015 °C.s-1 [SD 0.009 °C.s-1]. This is comparable to the mean gradient found when determining a linear model for the same stage, returning a result of 0.0148 °C.s-1 [SD 0.008 °C.s-1].
Results We studied 2313 patients in UHVV group with a mean age of 61.8 ± 12.2 years old (61.3 ± 12.3 vs. 61.9 ± 12.5 vs. 62.2 ± 11.69, p= > 0.05) and 23 % were female (23 % vs. 22 % vs. 22 %; p= > 0.05). In Andalusia group (n = 23167) mean age was 62.3 ± 11.7 years old (62.5 ± 11.7 vs. 62.1 ± 11.8 vs. 61.9 ± 11.9; p= > 0.05) and 23 % were female (24 % vs. 23 % vs. 22 %; p= > 0.05). No significant differences between three periods in both groups The results we can see in the Table 64.
(p 0.013) and ICU LOS (p 0.0009), with a trend towards a reduction in length of renal replacement therapy (p 0.06) (Table 64). Similar benefits were not demonstrated if levosimendan was introduced as a first or second vasoactive agent compared to a third or fourth agent. However survival to discharge was improved (41.5 % vs 33.3 % respectively).
Results We recruited 80 patients. Etiologies of CS were: 33 acute decompensation of chronic cardiomyopathies, 16 acute myocarditis, 16 acute myocardial infarctions and 15 other causes. Baseline variables are reported in Table 66 (*p < 0,05).
Results We studied 946 patients with a mean age of 61.8 ± 12.2 years (61.3 ± 12.3 vs. 61.9 ± 12.5 vs. 62.2 ± 11.69, p= > 0.05) and 22.7 % were female (22 % vs. 23 % vs. 23 %; p= > 0.05), no significant differences between three periods. The results we can see in the Table 66.
Results Ischaemia/reperfusion reduced cell viability from 94 % to 79 % (Fig. 86). MGC-0109 adminstered at the onset of reperfusion increased cell survival in a dose-dependent manner. At the highest concentration survival was similar to cells that did not undergo I/R. Protective effects were also seen with addition of MGC-0109 to H2O2-treated normoxic cells (data not shown).
Results Insult severity (IA/LV ratio) was normally distributed with a mean ± SEM of 19 ± 10 %. The severe group (IA/LV > 19 %) had significantly lower MAP and higher lactate values than the mild severity group (Fig. 87, top panel). Temporal changes in cardiac contractility and output did not however relate to insult severity (Fig. 87, bottom panel).
(p = 0.13). The reduction in the D2B time was driven by a reduction in time from ECG interpretation to activate CCL (28.3 ± 4.1 in the group 1 and 17.6 ± 2.3 minutes in the group 2) (p = .001) shown in Table 69. Mortality rate in group 1 is 12.5 % compare to 2.2 % in group 2 (p = .07), shown in Table 69.
We have reviewed over 4200 patient-days of data in a rolling audit of the effectiveness of our project. Fig. 88 demonstrates the percentage of patients for whom an IBW was recorded and for whom a target oxygen saturation was prescribed each month.
609 patients were admitted, 440 were discharged alive from the hospital. In the Outpatient Clinic, 126 patients were evaluated, 61 % male, age 44 ± 18.19 years, 48 % were smokers and 8 % COPD. The main causes of admission were postoperative elective surgery (26 %) and trauma with head injury (20 %), mean APACHE II 19.08, ICU length of time 7.23 days, hospital length of time 17.75 days, MV > 24 hours 47.62 %, and mean MV time 86.45 hours. The groups showed significant differences in spirometric data, shown in Table 70. In the SF-36 only the areas vitality and social aspects showed statistical difference (Table 71).
Figure 95 shows the mean values of PaO2 during the different phases of WLL. During bipulmonary ventilation gas exchanges improved in response to FiO2 1 and PEEP. Monopulmonary ventilation, instead, induced a clear reduction of PaO2, which increased in lateral position and during liquid tidal ventilation, with a substantial effect of elevated hydrostatic lavage pressures. The wide SD indicates an uneven response of gas exchanges in the studied population.
We included 690 patients with a 90-day mortality rate of 23 %. During the first 3 days in ICU, 65 % of the patients received respiratory support, 57 % circulatory support and 13 % renal replacement therapy (RRT). Patients receiving 3 days of RRT had the worst outcome (OR 6.5 [95 % CI 1.3 – 32.8]) as compared to patients receiving 1 day. For respiratory- and circulatory support the odds ratios were 2.2 [0.9 – 5.3] and 1.2 [0.5 – 2.6], respectively (Fig. 96).
Carbon dioxide levels raised from (mean (SD)) 5.6 kPa (0.40) to 9.2 kPa (0.47) during hypercapnia. The bias (limits of agreement, LoA) for ELV at normocapnia was 303 (131 to 476) ml, and percentage error (PE) was 31 %. During hypercapnia, bias (LoA) decreased to -75 (-188 to 39) ml, and PE to 20 %. The hemodynamic interventions resulted in significant changes in CO, i.e. a decrease by 41 % (caval occlusion) followed by a 59 % increase (dobutamine inf.). ELV and FRC remained stable throughout these changes (Fig. 97).
Thirty-three ARDS patients were enrolled (5 mild, 10 moderate and 18 severe). As shown in Fig. 98, within a given class of severity, the grams of tissue undergoing the intratidal collapse did not change significantly between PEEP 5 or 15 cmH2O (63 ± 26 vs 39 ± 32, 92 ± 53 vs 78 ± 142 and 123 ± 94 vs 96 ± 84 in mild, moderate and severe ARDS respectively). We observed a clear tendency to decrease from PEEP 5 to 15 cmH2O, though it was not statistically significant (p = 0.23, 0.76 and 0.27 respectively in mild, moderate and severe ARDS – paired t-test).
Data was collected by retrospective casenote review during a 3 week period in August 2015. The project was registered as a service evaluation and therefore ethics requirements were waived. Demographics, details of the PT assessment ,and outcomes following extubation were collected (Table 72). Extubation failure was defined as reintubation up to one week following extubation.
Of 7,784 patients, 693 patients had ARDS of which 164 patients with mild ARDS and on invasive ventilation were included in the analysis. Table 75 shows outcomes per group at the moment mild ARDS was diagnosed, and after 24 hours. Reclassification after 24 hours showed an improved prognostication with regard to hospital mortality, ICU- and 90-day mortality and the number of ventilator-free days and alive at day 28.
The results of the demographic and clinical variables are shown in Table 76.
Regarding the evaluation of HRQL by SGRQ, the mean scores were slightly higher in all domains with regard to the reference values from Spanish population by age and sex, indicating subjective respiratory problems with an impact on daily life. Only 7 of our 31 patients (22.6 %) had scores normal in all domains and in the total scores. 18 patients (58.1 %) had higher scores in all domains. The other 6 patients (19.3 %) had a higher score in some of the domains. Table 77
Twenty-seven ARDS patients were studied at PEEP 5 cmH2O. Age 58 [44-72] years (median [IQ range]), BMI 25 [22-29] kg/m2, PaO2/FiO2 105 [83-168], PaCO2 44 [40-51] mmHg, tidal volume 7 [5-8] ml/Kg IBW. Energy delivered per breath (J) was significantly related to lung strain (Fig. 101, upper panel) and inhomogeneity (Fig. 101, lower panel); the relationship between delivered energy and intratidal collapse-decollapse did not reach statististical significance (r2 = 0.10, p = 0.11).
95 % of patients had a decrease in their L3MCSA during their ICU stay. See Table 80.
Ninety pH tests were done and 21 tests missed, for 12 patients. The overall mean pH was 5.2 and median pH 5.7. Stratification by drug therapy results can be found in Table 81. A cumulative percentile chart of pH with acid inhibitor Method is reported in Fig. 103. All patients received EN. The mean calorie deficit observed was 1513 calories, for all reasons, not the gastric pH test alone. EN was held for 1 h before the test. The lab reported results usually in 30 minutes. Length of the feeding tube to insertion point was recorded for 1 patient.
Baseline characteristics were similar in the HES- and the Ringer's groups. By day 2, 13 (11 %) patients in the HES group had died vs. 11 (10 %) in the Ringer's group (P = 0.91). Plasma concentrations of TNF-α, IL-6 and IL-10 decreased from baseline to day 2 in the HES- and the Ringer's groups, but mean delta cytokine concentrations did not differ between the groups (Table 82). Also, no associations were observed between changes in the cytokine plasma concentrations and 90-day mortality (TNF-α: odds ratio for 1-unit increase, 1.000 (95 % Confidence Interval, 0.998 – 1.003), P = 0.87; IL-6: 1.001 (0.999 – 1.002), P = 0.32; IL-10: 1.000 (0.999 – 1.001), P = 0.89).
In sublingual, there was a significant reduction in vascular density of animals with sepsis only after 3 hours of sepsis compared to the sham group. (Fig. 104). This suggests that reducing the density in sepsis is only noticeable during periods of increased severity of sepsis. The comparison between the periods of sepsis showed that only the first two hours had a higher density compared to other periods of sepsis. These results have shown that in sepsis, the density of the microcirculation decreases with the severity of sepsis, however, AVA-3.0 Method was able to show differences only between extreme stages (almost normal with the stages of extreme severity), indicating a low sensitivity of the Method to differentiate small changes in density. In the gut, no changes were detected between groups and between periods, showing that the jejunum density is not variable in sepsis. These data showed that the dynamic microcirculatory is organ-specific and independent of embryological origin. In short, the evaluation of microcirculatory dysfunction is site-dependent and appears to require assessment Method also organ-specific to the kinetic measurement of microcirculatory dysfunction in sepsis.
All animals died during the 30-hour observation period. Results at each time point are presented in Tables 83 and 84, and all data before and after the development of hypotension are presented in Table 85. († = only 12 animals; * = p < 0.05 vs T1).
Thirteen patients attended prehabilitation, with improvements seen for all outcomes on completion (see Table 86).
Figure 110 shows the variables of the study in the groups defined as presence or absence of renal failure. The behavior of the variables analyzed is similar in both study groups.
Of the 1829 patients admitted to level 3 areas at Harefield Hospital during 2015, 229 (12.5 %), required CRRT during their admission. 134 (58.5 %) of those patients were initiated on CRRT due to refractory metabolic acidosis. The median age of this group was 61 years: 70.1 % were male, 47.8 % hypertensive and 19.4 % diabetic. Most patients (113 patients, 84.3 %) were haemodynamically unstable, defined as the need for one inotropic drug at a high dose or the combination of two or more vasoactive drugs. The reason for admission also differed from the general CRRT group, with a higher frequency of heart transplantations and OOHCA, as shown in Table 87 and Fig. 113. Time from admission to ITU to initiation of CRRT was shorter at 1 day in the refractory metabolic acidosis CRRT group vs. 4 days in the general CRRT group. The ITU mortality in the study group was 42.5 % vs. 36.2 % in the general CRRT group.
70 % Of the 134 enrolled patients was male with a mean age of 68 ± 9,5. LUS identified 62 PPCs (46 %), compared to 29 (22 %) by CXR (P = 0,011). PPCs identified were: positive Postero-Lateral Alveolar and/or Pleural Syndrome (PLAPS) 40 % vs 13 %, pulmonary edema (5 % vs 9 %) and pneumothorax (1 % vs 0 %). Incidence of cr-PPCs was 16 (12 %). Table 88 summarizes the diagnostic accuracy of LUS and CXR for the cr-PPCs identified. LUS can be performed within 15 ± 5 minutes compared to 42 ± 16 minutes for CXR,(p < 0.01). Overall inter-observer agreement for LUS showed a near to perfect agreement (k = 0.907, p ≤ 0.000).
18 patients were included. The mean age and total body surface area of burn (TBSA burn) were 21.0 ± 3.0 years old and 56.2 ± 15.0 %, respectively [Table 93].
The total intravenous fluids in the first week in Group A patients (57,363.1 ml) were much less than in Group B patients (68,437.9 ml), and the daily fluids of Group A patients were significantly less at day 4 and day 5 [Table 94] comparing to Group B patients.
Group A patients also had less body weight gain than Group B patients [Fig. 114].
As the results, Group A patients had significantly less days of mechanical ventilation than Group B patients, while length of ICU stay, length of hospitalization, sepsis insults, and organ dysfunctions were all similar in 2 groups [Table 95].
Results 85 patients were included. In Table 96 we described the characteristics of the study population. The beginning of cardiopulmonary resuscitation (CPR) maneuvers were immediate on ward, according to IHCA protocol. The arrival of IHCA team was less than 5 minutes in all cases. Figure 117 shows the distribution of NEWS in the IHCA analyzed.
In 43.5 % of cases there are not enough information to make a NEWS. In the remaining patients it was able to perform the NEWS although we could only obtain all data in 6.5 % of patients, in the remaining 50 % of IHCA in which was calculated the NEWS some data (vital sings) was missing. Respiratory rate and oxygen saturations were the most frequent missed data. It could be probably underestimating the NEWS performed. Figure 118 shows the relationship between a greater hospital mortality and a higher NEWS.
Methods Ten domestic pigs were anesthetized and mechanically ventilated. A bolus of hypertonic saline (10 mL, 20 %), with a higher conductivity than blood was administered into the ascending aorta while EIT data were recorded. The resulting EIT images were analyzed pixel by pixel to identify the aortic pixel (pA), in which the bolus caused the highest transient impedance peak in time (Fig. 120). After completion of the EIT measurements a thoracic computed tomography scan (CT) was performed for each pig. The CT-images were segmented individually for the relevant anatomical structures. EIT images were reconstructed using the GREIT model, based on the individual´s thoracic contours derived from the segmented CT-images.3The resulting spatial resolution of EIT images was 3 mm / pixel.
Results The location of the aorta could be detected by EIT in all animals, showing a mean offset of 15 ± 7.5 mm when compared to the center of the true anatomical location identified by CT (Fig. 121).
Results During hypercapnia the PaCO2 and PvCO2 levels were raised on average 58 % and 40 % (+/- 17 and 16 %) from within normal limits, respectively. Bias (LoA) att baseline before induction of hypercapnia was 0.5 L/min (-0.5 to 1.5) and percentage error (PE) 28 %. During hypercapnia, bias (LoA) was 1.4 L/min (0.2 to 2.7), PE 26 % following lower respiratory rate, 0.7 L/min (-0.7 to 2.2), PE 30 % when tidal volumes were decreased, and 0.5 L/min (-0.4 to 1.4), PE 19 % when dead space was increased. During hemodynamic changes the PE was slightly increased (see Table 100 for all values) and the concordance rate was 100 % (see Fig. 122).
Results Baseline characteristics included: mean heart rate 79 beats per minute (15.7), age 59.2 years (15.6), male 29 (53.7 %), previus cardiac disease 9 (16.7 %), medical diagnosis at admission in 40 patients (74.1 %, with primary cardiac diagnosis in 8 [14.8 %]); 19 mechanically ventilated patients (35.2 %, mean PEEP 6.8 [2.8]), with vasoactive drugs in 13 patients (24.1 %, mean norepinephrine dose .38 [.29] mcg/Kg/min). Median VTILVOT was 24.3 cm (interquartile range [IQR] 8-36), VTIPu-Ps 24.5 cm (IQR: 6-57) and VTIPu-Ms 18.9 cm (IQR: 7-43). The comparison between VTILVOT and VTIPu-Ms revealed a consistency of .52 (95%CI .29 to .69, p < .001), see Fig. 123; and between VTILVOT and VTIPu-Ps .44 (95%CI .13 to .67, p = .004), see Fig. 124. The ICC observed was .93.
Methods This study has been endorsed by the Spanish Society of Intensive Critical and Emergency Care Medicine (SEMICYUC). Data were obtained in a prospective multicenter study in 33 Spanish Intensive Care Units, with a total of 1009 patients. The criteria used to define CA-AKI was the AKIN criteria: a rise of serum creatinine of ≥0.5 mg/dl or a 50 % relative rise in creatinine at 48-72 hours after contrast exposure. The predictive model has been developed employing a binary logistic regression using the software R. The ROC curve was obtained (Fig. 126) and the model was calibrated using this graph. From the model, we have generated a graphical nomogram (Fig. 127) to facilitate its use in a clinical environment. The nomogram includes the 4 variables shown to have prognostic value.
Results 12 % of the patients developed CA-AKI. Predicting factors were elevated APACHE II test score, hemoglobin and baseline serum creatinine, shock or acute myocardium infarct at admission, vasoactive drugs and diuretics at the moment of the contrast administration, and the following comorbidities: chronic heart failure and chronic kidney failure. Significant risk factors in the univariate analysis were selected for the predictive model (Table 102). A bootstrap method was used to select the best subset of risk factors to avoid overfitting the data. The corresponding ROC curve of the model (Fig. 126) has an area under the curve of AUC = 0.75 (range 0.71-0-79).
Results Despite MAP and CVP being stable during the entire study, we found that while HR (106+/-18 in ANH group vs. 76+/-7 in Ctr group, p = 0.025) and CO (6.7+/-1.1 in ANH group vs. 3.9+/-0.1 in Ctr group, p = 0.002) increased, PAP (17.6+/-2.3 in ANH group vs. 22+/-4.3 in Ctr, p = 0.05) decreased significantly at Hct 10 % compared to the Ctr. Oxygen delivery (DO2) did not change but SVR (704+/-128 in ANH group vs. 1259+/-128 in Ctr group, p = 0.001 at T3) and oxygen consumption (VO2) (798+/-137 in ANH group vs. 1046+/-113 in Ctr group, p = 0.02 at T2; 842+/-218 in ANH group vs. 1142+/-78 in Ctr group, p = 0.05 at T3) were found to be lower than the Control. RBF increased at T3 ( 255+/- 55 ml/min. in ANH group and 218+/-42 ml/min. in the Ctrl group, p = 0.046) and was accompanied with slightly right shifted histograms but no significant change in the mean flux values of kidney was found (Figs. 128, 129). No differences was found in creatinine clearance, tubular sodium reabsorption and fractional sodium excretion of kidney between 10 % Hct of ANH and Ctr group at T3.
Results Between January 2014 and May 2015, 17 patients were included in each group, 43 sessions of CVVH were recorded in the E group and 56 in the C group. 16 sessions were interrupted prematurely for NRCES leaving 34 and 49 episodes (respectively E and C group) for analyzing circuit lifespan. Circuit lifespan was statistically increased in the E group compared to the C group. Median lifespans of CVVH circuit were respectively 48 H [21-72] vs 20 H [6-39] in E and C groups (relative risk of session ending: 2.4, 95 % CI [1.41-3.9], log rank p = 0.0009 (Fig. 130). CVVH blood flow was higher and more stable throughout sessions in the E group (p < 0.001) (Fig. 131). Median heparin dose used for anticoagulation was higher in the C group (p < 0.001) (Fig. 132) but without effect on the activated partial thromboplastin time (aPTT) all over the session.
Results Mean age was 57 (±18) years, APACHE II score 27 (±6); Nutrition was enteral in 6 patients, parenteral in 1; 1 patient did not receive nutrition (shock). Total AA loss (mg/h), AA loss by ultrafiltration (mg/h), and AA loss by adsorption (mg/h) at 1-h, 8-h, 24-h after start of CVVH, are shown in Fig. 133. Patient nr 8, with acute ischemic liver failure, had the greatest loss of amino acids. The total amino acid loss (p = 0.276), loss by ultrafiltration (p = 0.876) and loss by adsorption (p = 0.368) did not change during the course of CVVH. The estimated median amino acid losses (g/day) are shown in Table 103.
Results Patients were 61 ± 10 year-old, five were female and PaO2/FiO2 at enrollment was 171 ± 44 mmHg. At higher flow rates (Table 107): PaO2 improved (p < 0.001) while pH and PaCO2 didn't vary; end-expiratory lung volume (ΔEELV) increased (p < 0.05) and peak expiratory flow (PEF) decreased (<0.05) suggesting positive expiratory pressure effect by increased expiratory resistance and/or improved respiratory system compliance; respiratory rate (RR) decreased (p < 0.001) and tidal volume (Vt) didn't change (p > 0.05), anyway yielding decreased minute ventilation (MV) (p < 0.01) and corrected minute ventilation (MVcorr = MV*PaCO2/40 mmHg) (p < 0.01), indicating enhanced CO2 removal; finally, esophageal pressure swing (ΔPes) and pressure-time product (PTPes) decreased (p < 0.01 for both). AIC for linear correlation with flow rates was lower for PaO2, RR, ΔEELV and PEF, as if improved aeration and its effects on oxygenation constantly increase with flow; while non-linear AIC was lower for MV, MVcorr, ΔPes and PTPes, possibly suggesting that most of the improvement in CO2 wash-out from upper airway dead space and its consequences on patient's effort is already obtained at 30 L/min.
Results Over one year 87 patients were eligible for the study; the measure of PCEF was impossible to achieve because of lack of understanding in 14 patients (16 %). Among the 73 patients included for the analysis, there was a significant correlation between the measures obtained with the Piko-1 and the Servo i (rs = 0.831; p < 0.01) (Fig. 135). The linear regression line obtained predicts a cut-off value of PCEF on the Servo i at 60 l/min, corresponding to the value at 35 l/min previously determined with the Piko-1 [1].
Results 12 patients were enrolled (mean age 31.3 years, mean FEV1/FVC 49.9 %, mean FEV1 28.4 % predicted). TFdi was similar with the two techniques, but HFNC, compared to NIV, resulted in a significant decrease in respiratory rate (-20.2 % (18.0) vs -0.2 % (18.7), p = 0.024) and a lower mean arterial pressure (0.3 % (5.6) vs 5.8 % (4.9), p = 0.017). No significant differences were found in heart rate, SpO2, PtcCO2, VT, MV, comfort and dyspnea (Table 111).
Results Treatment with ASA resulted in a profound augmentation of plasma levels of the pro-inflammatory cytokines TNFα, IL6, and IL8 during endotoxemia (Fig. 140), but did not affect anti-inflammatory cytokines IL-10 and IL-1RA. Although the addition of ticagrelor, but not clopidogrel, attenuated the ASA-induced increase in TNFα, these P2Y12 antagonists did not affect the concentration of other pro-inflammatory cytokines (Fig. 140). There was no difference in cytokine response between ticagrelor- and clopidogrel-treated subjects. Treatment with ASA lowered plasma levels of thromboxane B2. Plasma adenosine increased during endotoxemia, without differences between groups. Platelet reactivity was reduced in ticagrelor and clopidogrel treated subjects, without any correlation with cytokine responses.
Sections
"[{\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab2\"], \"section\": \"Correspondence: T. Pham \\u2013 H\\u00f4pital Tenon, APHP, Medical and Surgical ICU, Paris, France\", \"text\": \"\\nResults: Among the 2813 patients presenting ARDS in the first 48\\u00a0h, 266 patients (9.4\\u00a0%) had no ARDS risk factor identified at admission. Table\\u00a02 shows the final ARDS risk factor identified in patients with or without initial risk factor identified.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab3\"], \"section\": \"Correspondence: T. Pham \\u2013 H\\u00f4pital Tenon, APHP, Medical and Surgical ICU, Paris, France\", \"text\": \"The patients with no risk factor were older, had more frequent previously known chronic diseases and presented with less severe SOFA (8.7\\u2009\\u00b1\\u20093.9 vs 9.5\\u2009\\u00b1\\u20094.1, p\\u2009<\\u20090.001) and non-pulmonary (5.4\\u2009\\u00b1\\u20093.9 vs 6.3\\u2009\\u00b1\\u20094.1, p\\u2009<\\u20090.001) SOFA scores. ICU mortality was lower in ARDS patients with no risk factor than in others (28.6\\u00a0% vs 34.9\\u00a0%, p\\u2009=\\u20090.047), but in-hospital mortality was not (35.7\\u00a0% vs 39.8\\u00a0%, p\\u2009=\\u20090.20). The lack of ARDS risk factor was not associated with hospital mortality (adjusted OR\\u2009=\\u20090.86 [0.65-1.13], p\\u2009=\\u20090.29). In the subgroup of patients with no ARDS risk factor, age, SOFA, concomitant heart failure, and administration of steroids within 72\\u00a0hours of ARDS onset were associated with hospital mortality (Table\\u00a03).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab6\", \"Tab7\"], \"section\": \"Correspondence: L. Pisani \\u2013 Academic Medical Center, University of Amsterdam, Amsterdam, Netherlands\", \"text\": \"\\nResults: The analysis included 456 patients with moderate or severe ARDS who stayed in the ICU\\u2009>\\u200924\\u00a0hours. The relation between PaO2/FiO2 and SpO2/FiO2 was good (R2\\u2009=\\u20090.62). Using the predefined cutoffs for SpO2/FiO2 and PEEP, prognostication improved with re-classification after 24\\u00a0hours (Tables\\u00a06 and 7).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig1\", \"Fig2\"], \"section\": \"Correspondence: M. Koster-Brouwer \\u2013 University Medical Center Utrecht, Intensive Care, Utrecht, Netherlands\", \"text\": \"\\nResults: Sample preparation or processing issues resulted in exclusion of 14 patients, leaving 467/481 (97\\u00a0%) for final analysis. Of these, 359 (77\\u00a0%) subjects received antibiotics upon ICU admission, whereas therapy was initiated on a later date in an additional 14 (3\\u00a0%) patients. Test results correlated with the probability of infection (p\\u2009<\\u20090.001) (Fig.\\u00a01). Among the 415 patients in whom the test classified sepsis as 'likely\\u00b4, the false positive rate decreased from 17/39 (44\\u00a0%) to 36/195 (18\\u00a0%) with higher probability bands. In the 52 patients in whom the test suggested infection to be unlikely we observed 8 cases of confirmed infection (false negative rate 15\\u00a0%). As 135 patients could not be categorized with certainty (\\u201cundetermined\\u201d) formal calculation of sensitivity and specificity was precluded. SeptiCyte test results were not affected by age, prior ICU stay, or immune deficiency. Higher scores of the test were indicative of increased severity of disease and mortality (Fig.\\u00a02).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab8\"], \"section\": \"Correspondence: J.I. Ko \\u2013 Seoul National University Hospital, Seoul, Republic of Korea\", \"text\": \"\\nResults: Total 942 patients were identified during study periods. Among them, 14 patients were excluded because of missing values. Demographic characteristics were described in Table\\u00a08.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab9\"], \"section\": \"Correspondence: J.I. Ko \\u2013 Seoul National University Hospital, Seoul, Republic of Korea\", \"text\": \"Patients with qSOFA less than 2 accounted for over half of enrolled patients (493/928, 53.1\\u00a0%) and over one third of mortality cases (88/231, 38.1\\u00a0%) (Table\\u00a09).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig3\"], \"section\": \"Correspondence: J.I. Ko \\u2013 Seoul National University Hospital, Seoul, Republic of Korea\", \"text\": \"AUROC of SIRS, qSOFA, and SOFA to predict 28-day mortality were 0.540 (0.500-0.580), 0.627 (0.587-0.667), and 0.687 (0.646-0.727), respectively. (SIRS vs qSOFA [p\\u2009<\\u20090.001], qSOFA vs SOFA [p\\u2009=\\u20090.009]) (Fig.\\u00a03).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab10\"], \"section\": \"Correspondence: O.T. Ranzani \\u2013 Department of Pulmonology, Hospital Clinic of Barcelona, University of Barcelona, Institut D'investigacions August Pi I Sunyer (IDIBAPS), Barcelona, Spain\", \"text\": \"\\nResults: We evaluated 6,874 patients with CAP, mean age 66 (\\u00b119) and in-hospital mortality of 442 patients (6.4\\u00a0%). Discrimination evaluated through the area under the curve (AUC) is in Table\\u00a010. SIRS criteria had the worse discrimination performance compared with qSOFA, CRB and SOFA. Calibration plots were comparable among the scores, although overestimation was more pronounced for qSOFA and SOFA scores. When adding the scores to the baseline risk model, the discrimination of Model\\u2009+\\u2009SIRS has no change, although improved with qSOFA, CRB and SOFA. Baseline model calibration improved similarly by adding each score in it. Using the cut-off of two points, the sensitivity/specificity for SIRS was 88/22\\u00a0%, qSOFA 50/82\\u00a0%, CRB 39/87\\u00a0% and SOFA 97/23\\u00a0%. Similar patterns were observed for secondary outcomes and for other measures of performance (Brier Score, IDI).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig5\"], \"section\": \"Correspondence: C. Scheer \\u2013 University of Greifswald, Department of Anesthesiology, Greifswald, Germany\", \"text\": \"\\nResults: 196 patients with severe sepsis or septic shock were included. Applying sepsis-3 criteria resulted in 3 subgroups: sepsis, septic shock and patients with neither SOFA increase nor shock. Results are presented in Fig.\\u00a05.\\n\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab13\", \"Tab14\"], \"section\": \"Correspondence: S. Carvalho Brugger \\u2013 Hospital Universitari Arnau de Vilanova, Lleida, Spain\", \"text\": \"\\nResults: 1651 patients were admitted. 532 (32,2\\u00a0%) met some CP criteria. In 136 (8,2\\u00a0%) were detected one or more MRB, 87 of these (64\\u00a0%) presented CP criteria according to the checklist. 37 met 1 criteria, 31 met 2 criteria and 19 met 3 or more criteria with accumulation of risk (p\\u2009<\\u20090,001). In 49 (36\\u00a0%) MRB carriers it was not identified any of the RF from the checklist. Tables\\u00a013 and 14 show risk factors and comorbidities that were significant as added risk for MRB.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab15\", \"Tab16\"], \"section\": \"Correspondence: B. Cambiaghi \\u2013 University of Milan - Bicocca, Monza, Italy\", \"text\": \"\\nResults: Main parameters describing pathophysiological characteristics of each group after 8\\u00a0hours are reported in Tables\\u00a015 and 16. Lung lavage and high Vt ventilation following regional embolization led to more severe impairment of oxygenation (p\\u2009<\\u20090.001), especially in the left embolization group. Lung mechanics at the end of the experiment showed similar trend: plateau pressure was higher and respiratory system compliance lower (p\\u2009<\\u20090.05) in the embolization\\u2009+\\u2009lavage\\u2009+\\u2009high Vt groups. Finally, CT-scan revealed higher lung weight in groups 1 and 2 (p\\u2009<\\u20090.05). Interestingly, in the same groups, the non-embolized lungs were heavier, as if embolization triggered more severe ventilation-induced lung oedema that could develop mainly where perfusion was preserved.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab17\"], \"section\": \"Correspondence: L.M. Vilander \\u2013 University of Helsinki and Helsinki University Hospital, Intensive Care Medicine, Helsinki; Finland\", \"text\": \"\\nResults: We found no significant associations between SNPs rs8094315 (OR 1.10, p 0.4827), rs12457893 (OR 1.02, p 0.8736), rs2093266 (OR 0.77, p 0.1525), rs1955656 (OR 0.77, p 0.1525) and rs625145 (OR 0.89, p 0.3967) and AKI comparing 354 AKI patients and 299 non-AKI patients (Table\\u00a017). AKI patients were significantly older, had higher BMI, more often diabetes and COPD, had received more often colloids before admission to ICU, and had lower platelet count. Multivariate logistic regression analysis with adjustment for sex and these baseline differences did not change our findings.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig12\"], \"section\": \"Correspondence: J.L.G. Haitsma Mulier \\u2013 VU Medical Centre, Intensive Care Adults, Amsterdam, Netherlands\", \"text\": \"\\nResults: We included 99 patients, mean age 65, mean APACHE III score 73. 49 patients (49\\u00a0%) developed AKI within the first week (mean 2.2\\u00a0days after inclusion). Patients who developed AKI had a significantly higher RRI on inclusion than those who did not: 0.708 (0.687-0.730) vs 0.654 (0.631-0.677), p\\u2009=\\u20090.001. Compared to patients without AKI, RRI was significantly higher in patients with AKI stage 2 and 3, but not in patients with AKI stage 1 (Fig.\\u00a012).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig13\"], \"section\": \"Correspondence: J.L.G. Haitsma Mulier \\u2013 VU Medical Centre, Intensive Care Adults, Amsterdam, Netherlands\", \"text\": \"We therefore chose AKI stage 2 and 3 as endpoint in further analysis. On univariate analysis, RRI was a significant predictor of AKI (OR 1.012, 95\\u00a0% CI 1.006-1.019), along with other parameters including: APACHE III, fluid balance and BIA derived reactance, but not sublingual microcirculation. On multivariate analysis, RRI, APACHE III and fluid balance remained significant. The AUC of RRI for AKI stage 2 and 3 was 0.721 (95\\u00a0% CI 0.612-0.831). The composite AUC of the multivariate predictors was 0.825 (Fig.\\u00a013).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig14\", \"Fig15\"], \"section\": \"Correspondence: A.M.A. Liberatore \\u2013 Federal University of S\\u00e3o Paulo, Surgery, S\\u00e3o Paulo, Brazil\", \"text\": \"\\nResults: SDF findings (Fig.\\u00a014) of S8-T6h showed broadly distributed microcirculation dysfunction. The outlining of tubules became blurred by their enlargement leading to the compression of tubular lumen and of the peritubular microvessels, suggesting an ongoing obstructive phenomenon in a progressive manner by tubular wall edema. The heterogeneous dysfunction pattern was disseminated in entire screen. S9-T6h showed similar findings, however more intensely. The histology (Fig.\\u00a015) confirmed the ongoing obstructive phenomena at S8-T6h, and also showed generalized peritubular microvessels congestion, multiple glomerulus without mesangial area, inflammatory infiltrate in the connective tissue and hyaline degeneration suggestive of ongoing cellular dysfunction/death. The histological results of S9-T6h showed similar pattern with the enlargement of the epithelial cells of convoluted tubules with reduced lumen, and with compressed or dilated peritubular microvessels. In addition, numerous tubular epithelial cells showed membrane injury, nuclear pycnosis and necrosis. At S8-T30d, although the general findings were better, as compared to the early phase sepsis (T6h), the histological findings demonstrated a persistence of significant peritubular and glomerular congestions with intense inflammatory infiltrate in the connective tissues, nucleus contractions suggestive of cell death, and collecting ducts injuries. PAS staining demonstrated widespread hyaline degeneration. The more severe sepsis, S9-T30d group, showed a widespread congestion around the collecting tubules and peritubular congestion of the small and large vessels. Also was observed glomerulus without mesangial areas, intense congestion and hyaline degeneration of the collecting tubules and of the cortex tubules region. The general findings were of the ischemic renal injury pattern. These findings showed that renal dysfunction persists at 30\\u00a0days after sepsis, and that the presence of any pathological stimuli, may decay the renal physiological capacity quickly, justifying the fragility of renal physiology in patients who survived sepsis.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig19\", \"Fig19\", \"Fig20\"], \"section\": \"Correspondence: E.R. Longbottom \\u2013 Queen Mary University of London, WHRI, Translational Medicine and Therapeutics, London, United Kingdom\", \"text\": \"\\nResults: PMBCs incubated with post-operative serum demonstrated a significant reduction in mHLA-DR membrane density (Fig.\\u00a019, p\\u2009=\\u20090.001). The reduction in mHLA-DR density was prevented when co-incubated with GM-CSF and IFN\\u03b3 (Fig.\\u00a019). Incubation with IFN\\u03b3 but not GM-CSF increased expression of HLA-DR\\u03b1 chain (p\\u2009=\\u20090.01), Cathepsin S (CTSS) (p\\u2009=\\u20090.001), suppressor of cytokine signalling 3 (SOCS3) (p\\u2009=\\u20090.01) and March 1 (p\\u2009=\\u20090.002) (Fig.\\u00a020).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab18\"], \"section\": \"Correspondence: Z. Trogrlic \\u2013 Erasmus Medical Center, Department of Intensive Care, Rotterdam, Netherlands\", \"text\": \"\\nMethods: A prospective multicenter before-after study was conducted in six ICUs in the Netherlands between March 2012 and April 2015. The intervention consisted of a two-phase multifaceted tailored implementation of the PAD guidelines. Multiple implementation strategies were applied to change clinical practice (Table\\u00a018). Data of all adult ICU patients were collected during three four-month periods:\\n\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab19\"], \"section\": \"Correspondence: Z. Trogrlic \\u2013 Erasmus Medical Center, Department of Intensive Care, Rotterdam, Netherlands\", \"text\": \"\\nResults: A total of 4727 patients were enrolled in the study with a total of 23958 ICU days. Adherence to most PAD guideline recommendations improved significantly whereas early mobilization and reduced benzodiazepine sedation improved only in the last period (Table\\u00a019). The incidence of delirium increased from 22\\u00a0% before to 30\\u00a0% after implementation (aOR\\u2009=\\u20091.5, p\\u2009<\\u20090.01) whereas delirium duration decreased from 6.3 before to 3.6\\u00a0days after implementation (aBeta\\u2009=\\u2009-2.6, p\\u2009<\\u20090.01). There were no statistically significant differences in ICU length of stay (aBeta\\u2009=\\u20090.001, p\\u2009=\\u20090.99); ICU mortality (aOR\\u2009=\\u20091.2, p\\u2009=\\u20090.17); and hospital mortality (aOR\\u2009=\\u20091.2, p\\u2009=\\u20090.21) after vs. before the implementation. Only length of mechanical ventilation increased with half a day (aBeta\\u2009=\\u20090.55, p\\u2009=\\u20090.01).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab20\"], \"section\": \"Correspondence: A. Kraj\\u010dov\\u00e1 \\u2013 Third Faculty of Medicine, Charles University in Prague, Laboratory for Metabolism and Bioenergetics, Prague, Czech Republic\", \"text\": \"\\nMethods: Skeletal muscle cells were isolated from biopsies obtained from patients (n\\u2009=\\u200916) undergoing hip replacement surgery and subsequently exposed to a range of propofol resembling clinical concentrations in human plasma during propofol infusion (0, 1, 2.5, 5 a 10\\u00a0\\u03bcg/ml) and to lipid vehicle (Intralipid\\u00ae - IL). After 96\\u00a0hours of exposure, mitochondrial metabolism was assessed by extracellular flux analysis (Seahorse Biosciences). Oxygen consumption rate (OCR) was measured at baseline and after addition of ATPase inhibitor, mitochondrial uncoupler and complex III inhibitor. Injection of these agents enables to calculate baseline OCR, ATP turnover rate, proton leak through inner mitochondrial membrane and respiratory chain capacity (uncoupled respiration). The capacity of fatty acid oxidation was measured as etomoxir-inhibitable OCR after adding of uncoupler and palmitate. Values presented in Table\\u00a020 are expressed as % of baseline OCR.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab20\"], \"section\": \"Correspondence: A. Kraj\\u010dov\\u00e1 \\u2013 Third Faculty of Medicine, Charles University in Prague, Laboratory for Metabolism and Bioenergetics, Prague, Czech Republic\", \"text\": \"\\nResults: In human skeletal muscle cells exposed to propofol, respiratory chain capacity was decreased and uncoupling of inner mitochondrial membrane was increased. The most significant result was propofol-induced inhibition of fatty acid oxidation to 15\\u00a0%, respectively 11\\u00a0% of baseline values (see Table\\u00a020). Data are presented as median (interquartile range). Statistically significant results are signed as * if p-value\\u2009<\\u20090.05, ** p-value\\u2009<\\u20090.001.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab21\"], \"section\": \"Correspondence: A. Shah \\u2013 Oxford University Hospitals NHS Foundation Trust, Nuffield Division of Anaesthetics, Oxford, United Kingdom\", \"text\": \"\\nResults: Five trials consisting of 613 patients were included for meta-analysis.2,3,4,5,6 Four trials were set in surgical ICUs and one in a mixed ICU. Only one trial was rated at low risk of bias in all domains. There was variation in dosage regimes, from 3x/weekly administration of intravenous iron to daily oral iron for up to 30\\u00a0days post discharge. Results are shown in Table\\u00a021. No trials reported on QoL.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig21\"], \"section\": \"Correspondence: J.F. Jensen \\u2013 Nordsj\\u00e6llands Hospital, University of Copenhagen, Department of Anesthesiology, Hiller\\u00f8d, Denmark\", \"text\": \"\\nResults: The basic narrative of recovery was \\u201ctoward a trajectory of new orientation\\u201d. The narrative at 3\\u00a0months described mortal illness in ICU (Being at Death's door), the narrative at 5\\u00a0months described ongoing fear of relapse (Still not out of the Woods), and the narrative at 10\\u00a0months had three potential outcomes: downhill (detour on the road), steady-state (end of the road), or progress (The Road to Recovery). New orientation was obtained in steady-state or progressive recovery, Fig.\\u00a021.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab25\"], \"section\": \"Correspondence: J. Aron \\u2013 Royal Free Hospital, Intensive Care Unit, London, United Kingdom\", \"text\": \"\\nResults: 61 patients were admitted as unplanned admissions during the first audit period. Patients were elderly, had a high predicted mortality and a significant proportion were clinically frail (CFS\\u2009\\u2265\\u20095). Mean length of stay (LOS) was prolonged and level of organ support was high. These results are summarised in Table\\u00a025.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig22\"], \"section\": \"Correspondence: B.A. McGrath \\u2013 University Hospital South Manchester, Manchester, United Kingdom\", \"text\": \"\\nResults: Over the 12\\u00a0month data collection period 296 tracheostomy patient admissions were tracked across the four sites with similar demographics to previously reported national data.[1] A total of 124 adverse events were identified affecting 29.8\\u00a0% patients. Analysis of reported incidents over the duration of the project showed a significant reduction in the severity of harm by month (Chi Square p\\u2009<\\u20090.01, Fig.\\u00a022). There was also a significant trend towards lower harm categories for incidents over the duration of the project (Chi Square test for linear trend, r\\u2009=\\u2009-0.21, p\\u2009<\\u20090.01). Monthly analysis of the dataset for percutaneous tracheostomies showed non-significant trend toward earlier speaking valve use and vocalisation (median slope\\u2009=\\u2009-0.17, -0.83 to 0.4) associated with improvements in reported patient satisfaction scores.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab26\", \"Fig23\", \"Tab27\"], \"section\": \"Correspondence: H.-J. de Grooth \\u2013 VU University Medical Center, Department of Intensive Care, Amsterdam, Netherlands\", \"text\": \"\\nResults: Fourteen patients were included: 5 patients received 1\\u00a0g vitamin C and 5 patients 5\\u00a0g vitamin C iv twice daily for two days. Two patients received 2\\u00a0g/day vitamin C and 2 patients received 10\\u00a0g/day by continuous infusion for two days (Table\\u00a026). Four patients (28\\u00a0%) were vitamin C deficient on admission (<20\\u00a0\\u03bcmol/L). A two-compartment pharmacokinetic model best described the data (Fig.\\u00a023, model parameters not shown). The urinary excretion of vitamin C and oxalate is shown in Table\\u00a027.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig24\"], \"section\": \"Correspondence: M. Padar \\u2013 Tartu University Hospital, Department of Anaesthesiology and Intensive Care, Tartu, Estonia\", \"text\": \"\\nResults: 231 patients were included in Before and 225 in After group, respectively. The groups are comparable regarding demographics, case-mix and severity of illness. Instalment of feeding protocol resulted in significantly higher cumulative amount of enterally provided calories by day 7 [3165 (1165-5215) kcal in After vs 2360 (450-5075) kcal in Before group, median (IQR), p\\u2009=\\u20090.043], while less calories were given parenterally [2600 (712-4287) vs 3900 (1725-6645) kcal, p\\u2009<\\u20090.001]. Cumulative proportion of patients who did not receive any enteral feed was significantly smaller in After group (Fig.\\u00a024).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig25\"], \"section\": \"Correspondence: M. Padar \\u2013 Tartu University Hospital, Department of Anaesthesiology and Intensive Care, Tartu, Estonia\", \"text\": \"Percentage of enterally received calories from caloric needs was significantly higher in After group (Fig.\\u00a025).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab31\"], \"section\": \"Correspondence: A. Kleyman \\u2013 University College London, Bloomsbury Institute of Intensive Care Medicine, London, United Kingdom\", \"text\": \"\\nResults: At 6\\u00a0h post-sepsis no differences were seen in renal and hepatic phosphorylation of AMPK, ACC, PDH and HSL between sham and septic animals. While cardiac ACC phosphorylation was strongly increased in septic rats, AMPK phosphorylation did not differ, suggesting that ACC phosphorylation was mediated not by AMPK but rather via the glucagon-PKA pathway. The biggest changes were observed in skeletal muscle. AMPK phosphorylation was increased in gastrocnemius and even more so in soleus in septic rats but this was not accompanied by a corresponding increase in ACC phosphorylation. In both muscles PDH phosphorylation markedly increased while PDH fell, suggesting a fall in pyruvate oxidative decarboxylation and glucose usage as a fuel. HSL phosphorylation was strongly increased in soleus in non-survivors. UCP2 and UCP3 levels were not altered in any organ. Table\\u00a031.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig31\"], \"section\": \"Correspondence: A. Ballin \\u2013 Azienda Ospedaliera di Padova, UOC Anesthesia and Intensive Care Unit, Padua, Italy\", \"text\": \"\\nResults: We found a progressive and significant reduction in both circulating EMPs (median 207, IQR 95-404 \\u00e8 median 64, IQR 45-90 MPs/mL, p\\u2009=\\u20090.013) and LMPs (median 432, IQR 93-479 \\u00e8median 39, IQR 35-282 MPs/mL, p\\u2009=\\u20090.044) between the start of ECMO support (T0) and soon after the decannulation (T2), as shown in Fig.\\u00a031. Survivors showed higer levels of LMPs (p\\u2009=\\u20090.034) compared to non survivors and almost significantly higher levels of EMPs (p\\u2009=\\u20090.062). Standard laboratory tests (i.e. CRP, PCT, and WBC) did not show any significant difference between the same time points, and between different outcomes. There was no correlation between level of any kind of MPs and heparin dose, bleeding episodes, and mortality.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab32\"], \"section\": \"Correspondence: J.F. Georger \\u2013 Centre Hospitalier Intercommunal de Villeneuve Saint Georges, Lucie et Raymond AUBRAC, Reanimation Polyvalente - Surveillance Continue, Villeneuve Saint Georges, France\", \"text\": \"The evolution of parameters was in the Table\\u00a032.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig33\", \"Fig34\"], \"section\": \"Correspondence: F. Zarantonello \\u2013 University of Padova, Department of Medicine (DIMED), Padova, Italy\", \"text\": \"\\nResults: We enrolled 15 severe ARDS patients requiring VV-ECMO. ECMO median duration was 9 (interquartile range 8-14.5) days. Mortality was 53.3\\u00a0%. We found a strong correlation between maximum clot firmness (MCF) and amplitude of the curve at 10\\u00a0minutes (A10) in all ROTEM tests (Rho\\u2009>\\u20090.96, p\\u2009<\\u20090.001). 67\\u00a0% of patients had at least one episode of bleeding. 30.5\\u00a0% of the hemorrhages were severe. PLT was lower in bleeding compared to non-bleeding group (p\\u2009=\\u20090.02). Among the ROTEM tests, heparinase modified thromboelastometry clotting time and clot formation time (HEPTEM CT and CFT) were significantly higher in bleeding group (p\\u2009<\\u20090.05) (Fig.\\u00a033). The POC tests evaluating the intrinsic and extrinsic coagulation pathways, as well as the thrombin receptor activating peptide-6 test (TRAP-AUC) assessing platelet aggregometry, were different between groups, even though not statistically significant (Fig.\\u00a034). There was no difference in PT, aPTT, anti-Xa activity, fibrinogen and ACT between groups.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig35\"], \"section\": \"Correspondence: M. Ostermann \\u2013 Guys and St Thomas' NHS Foundation Trust, London, United Kingdom\", \"text\": \"\\nResults: 1129 patients received RRT for AKI of whom 42\\u00a0% died in hospital. There was a significant difference in cumulative fluid balance at initiation of RRT between hospital survivors and non-survivors. (Fig.\\u00a035)\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab36\"], \"section\": \"Correspondence: M. Ostermann \\u2013 Guys and St Thomas' NHS Foundation Trust, London, United Kingdom\", \"text\": \"108 patients (9.6\\u00a0%) had FO >10\\u00a0%. They had a significantly higher hospital mortality (X2\\u2009=\\u20095,89; p\\u2009=\\u20090,015) and longer stay in ICU (19.6\\u00a0days versus 12.8; p\\u2009<\\u20090,001) but also higher SOFA score compared to patients with FO \\u226410\\u00a0%. (Table\\u00a036)\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig37\", \"Fig38\", \"Tab37\"], \"section\": \"Correspondence: R.E. Berthelsen \\u2013 Nordsj\\u00e6llands Hospital, Dept. of Anaesthesiology and Intensive Care, Hiller\\u00f8d, Denmark\", \"text\": \"\\nResults: We screened 4087 patients and identified 864 with AKI (Fig.\\u00a037) of whom 461 and 255 developed fluid overload above respectively 5\\u00a0% and 10\\u00a0% of bodywieght (BW) during their first 5\\u00a0days in ICU (Fig.\\u00a038). At day 28, 514 of the AKI patients had renal recovery and 282 had died (Table\\u00a037).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig39\"], \"section\": \"Correspondence: A.M.A. Liberatore \\u2013 Federal University of S\\u00e3o Paulo, Surgery, S\\u00e3o Paulo, Brazil\", \"text\": \"\\nResults and conclusions: SDF at T6h showed broadly distributed microcirculation and tissue dysfunction at both groups (Fig.\\u00a039). The outlining of tubules became blurred by their enlargement, with compression of tubular lumen and of the peritubular microvessels, suggesting an obstructive phenomenon by cellular edema. Histology. After 6\\u00a0hours of sepsis, animals treated with aggressive fluid infusionshowed less peritubular congestion, preserved mesangial space and lower areas with hyaline degenerations and better preservation of the tubular lumen compared to sepsis without aggressive overhydrating. PAS staining showed a very slight hyaline degeneration, better preservation of tissue architecture, lower occurrence of cellular death, suggesting that the aggressive fluid therapy in the early stage of sepsis minimizes the severity of vascular and tissue injury in the kidney. The live animals treated with the aggressive fluid showed less peritubularmicrovesselscongestion compared to S8, better preservation of the mesangial space, minor hyaline degeneration, and less cell death in deeper regions of the cortexafter a month of recovery. However, the general appearance showing a kidney limitation for venous blood drainage. Clearly, the aggressive-fluid therapy attenuates renal damage compared to S8. The results suggest that animals treated with aggressive fluid therapy, at the early stage of sepsis, have better conditions to respond against new harmful challenges to the kidney. Besides, the recover process after sepsis seems to be partial, justifying the occurrence of the post-sepsis syndrome.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig40\"], \"section\": \"Correspondence: D. Arias-Verd\\u00fa \\u2013 Complejo Universitario Carlos Haya, M\\u00e1laga, Spain\", \"text\": \"\\nResults: Age 41.13 (3.2) years, 50\\u00a0% men and base CrCl 163 (19.51) mL/min. Median percentage of change between base and maximum CrCl was 123.5\\u00a0% (78.2-143.2) and because a pick was detected between 3 and four hours after protein load we analysed these two hours together, finding a median change of 80.7\\u00a0% (69.95-144). Changes between the first and third hours were significant either for absolute values (p 0.023) or % (p 0.031). Hourly changes in CrCl are presented in Fig.\\u00a040\\n\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig41\"], \"section\": \"Correspondence: S. Rozemeijer \\u2013 VU University Medical Center Amsterdam, Department of Intensive Care, Adults, Amsterdam, Netherlands\", \"text\": \"\\nResults Forty patients with shock and 52 without shock were included. Patients with eGFR\\u2009<\\u200930\\u00a0mL/min were excluded. Mean age was 69 (60-76) vs. 67 (59-76) yrs. and APACHE III score was 81 (63-107) vs. 57 (45-70) (p\\u2009<\\u20090.001). Shock patients had a higher RRI than patients without shock (median, 0.751 (0.692-0.788) vs. 0.654 (0.610-0.686); p\\u2009<\\u20090.001), (Fig.\\u00a041). On univariate analysis, high age, APACHE III score, vasopressor support, pulse pressure index (PPI: (systolic-diastolic)/systolic blood pressure), central venous pressure and positive fluid balance, and low mean arterial pressure (MAP), reactance/m and creatinine clearance were the markers most significantly associated with high RRI (p\\u2009<\\u20090.01). Markers of the microcirculation were not. On multivariate analysis, vasopressor support, higher PPI, lower MAP and lower Xc/m remained as independent determinants of RRI (n\\u2009=\\u200989, Adj. R2\\u2009=\\u20090.472).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab42\"], \"section\": \"Correspondence: J.R. Goodall \\u2013 Salford Royal NHS Foundation Trust, Critical Care, Salford, United Kingdoms\", \"text\": \"Most of the staff were not aware of the time since the most recent infections, as can be seen in Table\\u00a042.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab44\"], \"section\": \"Correspondence: S. Houston \\u2013 St Mary's Hospital, Adult Intensive Care Unit, London, United Kingdom\", \"text\": \"\\nResults In total 50 patients were prescribed thiopentone. Eight received a bolus and three had other indications. A further 3 patients had a duration under 6\\u00a0hours and were excluded. Thirty-six patients were reviewed with 1 patient dying during infusion. Patient characteristics are shown in Table\\u00a044.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig49\"], \"section\": \"Correspondence: S. Houston \\u2013 St Mary's Hospital, Adult Intensive Care Unit, London, United Kingdom\", \"text\": \"Hypokalaemia (potassium\\u2009<\\u20093.5) developed in 25 patients (69.4\\u00a0%) during infusion with the mean lowest at 12\\u00a0hours (Fig.\\u00a049). Subsequently 11 (31.4\\u00a0%) patients developed hyperkalaemia (potassium\\u2009>\\u20095.5), mean peak 12\\u00a0hours after.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab45\", \"Tab46\"], \"section\": \"Correspondence: S. Houston \\u2013 St Mary's Hospital, Adult Intensive Care Unit, London, United Kingdom\", \"text\": \"Insulin use, duration of infusion, weight, potassium replacement or presence of hypokalaemia had no statistical significance relating to loss of regulation (Tables\\u00a045 and 46).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab48\"], \"section\": \"Correspondence: A. Gritsan \\u2013 Krasnoyarsk State Medical University, Krasnoyarsk Regional Hospital, Anaesthesiology and Intensive Care, Krasnoyarsk, Russian Federation\", \"text\": \"\\nResults In both groups assessed results are presented in Table\\u00a048. Starting ventilator patients in both groups were required at different times substantially on average, and the eighth day in both groups were diagnosed with pneumonia.The frequency of hemodynamic disturbances and duration of inotropic support were comparable in both groups. The mortality rate in group 1 was significantly lower than in group 2, which explains the increase in the period of mechanical ventilation and stay of patients in the ICU and in the hospital. Analysis on GOS the surviving patients showed no significant differences.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab48\"], \"section\": \"Correspondence: S. Spina \\u2013 University of Milan - Bicocca, School of Medicine and Surgery, Milan, Italy\", \"text\": \"\\nResults Preliminary data are based on 170 patients (58\\u00a0% male and 42\\u00a0% female, 67 (56-73) years old, GCS at admission 7 (6-9)) admitted for intracranial hemorrhage (29\\u00a0%), subarachnoid hemorrhage (22\\u00a0%), trauma (21\\u00a0%), stroke (12\\u00a0%). Tracheostomy was performed at 10 (7-13) days from admission for compromised neurological status (89\\u00a0%, GCS at tracheostomy 7 (6-8)). Direct laryngoscopy Fantoni\\u00b4s translaryngeal technique (TLT), Percutwist, surgical, standard TLT and Dolphin were used in 63\\u00a0%, 18\\u00a0%, 11\\u00a0%, 6\\u00a0% and 2\\u00a0% of the cases. ENT specialists and intenstivists performed 46\\u00a0% and 54\\u00a0% of the tracheostomy, respectively. No deleterious effect on recorded parameters was detected (see Table\\u00a048). Four lesions of the tracheal rings were documented.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig50\", \"Fig50\", \"Fig51\"], \"section\": \"Correspondence: R. van Groenendael \\u2013 Radboud University Medical Center, Intensive Care, Nijmegen, Netherlands\", \"text\": \"\\nResults EA-230 was well tolerated and showed an excellent safety profile. Treatment with the highest dose of EA-230, but not with lower doses, resulted in a significant attenuation of the endotoxin-induced increase in plasma levels of IL-6, IL-8, IL-1RA, MCP-1, MIP-1\\u03b1, and MIP-1\\u03b2 (IL-6, IL-8, and MCP-1 shown in Fig.\\u00a050a, b, and c), and the adhesion molecule VCAM-1 (Fig.\\u00a050d). Furthermore, the highest dose of EA-230 reduced fever and flu-like symptoms (Fig.\\u00a051). Endotoxemia resulted in a marked increase in GFR, but no differences between groups were observed.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig52\", \"Fig53\", \"Fig53\"], \"section\": \"Correspondence: R. Koch \\u2013 Radboud University Medical Center, Intensive Care, Nijmegen, Netherlands\", \"text\": \"\\nResults LPS administration resulted in a typical increase in plasma levels of cytokines, which was absent in the placebo group (Fig.\\u00a052). Following Fluenz challenge, viral shedding for at least one of the four influenza strains present in the vaccine was 12/15 (80\\u00a0%) in the LPS-Fluenz group compared with 13/15 (87\\u00a0%) in the placebo-Fluenz group. The increase in viral shedding of the influenza A and B strains was similar between groups (Fig.\\u00a053, upper panels). Likewise, the Fluenz-induced increase in levels of the chemokine IP-10 in nasal wash, as well as local symptoms, were not different between the LPS-Fluenz and placebo-Fluenz group (Fig.\\u00a053, lower panels).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig54\", \"Fig54\"], \"section\": \"Correspondence: J. Bringue \\u2013 Fundaci\\u00f3 Parc Taul\\u00ed, Sabadell, Spain\", \"text\": \"\\nResults Results show a decrease in circulating lymphocytes, Treg lymphocytes and lung weight in groups treated with MTX compared to the septic group (Fig.\\u00a054a-c). The cellular content in alveolus in the CLP MTX group shows a decrease in cell infiltration of polimorfonuclear cells and lymphocytes compared to CLP group, while the number of alveolar macrophages is not altered in the different groups (Fig.\\u00a054d-f).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig55\"], \"section\": \"Correspondence: J. Bringue \\u2013 Fundaci\\u00f3 Parc Taul\\u00ed, Sabadell, Spain\", \"text\": \"Expression of the inflammatory cells recruitment, matrix remodelling and proinflmatory markers show an increase in septic rats, while with MTX treatment exhibit a reduction. Finally, MTX cause an increase of the expression of the anti-inflammatory cytokine IL4 (Fig.\\u00a055).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig60\"], \"section\": \"Correspondence: S.J. Pollen \\u2013 UCL, Bloomsbury Institute of Intensive Care Medicine, London, United Kingdom\", \"text\": \"\\nMethods Live na\\u00efve kidney slices (200\\u00a0\\u03bcm thick) were exposed to serum from 24\\u00a0hour sham operated or septic rats for 90\\u00a0minutes and imaged with a confocal microscope using fluorescent dyes to detect dynamic changes in mitochondrial function (Fig.\\u00a060).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig61\"], \"section\": \"Correspondence: S.J. Pollen \\u2013 UCL, Bloomsbury Institute of Intensive Care Medicine, London, United Kingdom\", \"text\": \"\\nResults Septic serum caused a decrease in MMP, an increase in ROS, but no change in NADH at 90\\u00a0minutes exposure compared to baseline (Fig.\\u00a061). Sham serum did not cause any change from baseline and was comparable to slices exposed only to a physiological saline solution.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig62\", \"Fig62\", \"Fig62\"], \"section\": \"Correspondence: H.D. Torrance \\u2013 Barts Health NHS Trust, London, United Kingdom\", \"text\": \"\\nResults Ten polytrauma patients with a median Injury Severity Score (ISS) of 38 (IQR 29-50) were recruited. This cohort was 80\\u00a0% male with a median age of 27 (IQR 23-50). There was a decrease in antigen density of mHLA-DR on healthy donor PBMCs when incubated with admission (P\\u2009<\\u20090.01) or 24HR (P\\u2009<\\u20090.05) polytrauma serum, compared to incubation with serum from age and sex matched controls (Fig.\\u00a062a). Culturing in the presence of IFN-\\u03b3 (P\\u2009<\\u20090.01) or GM-CSF (P\\u2009<\\u20090.05) prevented this decrease in antigen density (Fig.\\u00a062b). Pre-incubation with an IL-10 neutralising antibody partially reversed the detrimental effects of the incubation with polytrauma trauma serum (P\\u2009<\\u20090.001; Fig.\\u00a062c).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab55\"], \"section\": \"Correspondence: M. Adriaanse \\u2013 Bravis Hospital, Department of Intensive Care, Roosendaal, Netherlands\", \"text\": \"\\nResults 4033 patients were included (before- and after-period: 1385 and 2632 patients, 15 patients had missing data on covariables). Delirium was independently associated with hospital mortality in crude analysis (OR 1.95, p\\u2009<\\u20090.001, Table\\n55). There was significant interaction between APACHE II and delirium (p\\u2009<\\u20090.001). After adjustment the OR for delirium was 8.61, but the effect was much stronger in the patients with a higher APACHE II score above the median value (\\u226415; OR 1.68, p\\u2009=\\u20090.07 versus >15; OR 19.0, p\\u2009<\\u20090.001). Mortality risk of delirium in the after-period compared with the before-period and with CAM-ICU versus ICDSC (after-period) did not differ (before versus after-period, OR 0.82, p\\u2009=\\u20090.079 and ICDSC versus CAM-ICU, OR 1.03, p\\u2009=\\u20090.831).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig67\", \"Fig67\"], \"section\": \"Correspondence: S. Funcke \\u2013 University Medical Center Hamburg-Eppendorf, Center of Anesthesiology and Intensive Care Medicine, Hamburg, Germany\", \"text\": \"\\nResults Under propofol sedation, sensitivity and specificity of ANI (AUC\\u2009=\\u20090.97 and 0.99), SPI (AUC\\u2009=\\u20090.86 and 0.90) and PRD (AUC\\u2009=\\u20091.00 and 0.96) for detecting both painful stimuli were high compared to HR, MAP and BIS (AUC\\u2009=\\u20090.75 and 0.74, 0.74 and 0.76 and 0.53 and 0.58, resp., Fig.\\u00a067a\\u2009+\\u2009b). Likewise, with propofol sedation and remifentanil 0.2 mcg/kg/min, sensitivity and specificity of ANI (AUC\\u2009=\\u20090.82 and 0.80.), SPI (AUC\\u2009=\\u20090.73 and 0.84) and PRD (AUC\\u2009=\\u20090.63 and 0.68) for detecting both painful stimuli were higher compared to HR, MAP and BIS (AUC\\u2009=\\u20090.52 and 0.51, 0.48 and 0.48 and 0.52 and 0.60, resp., Fig.\\u00a067c-f).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig69\", \"Fig70\", \"Fig71\"], \"section\": \"Correspondence: A. Messina \\u2013 AOU Maggiore della Carit\\u00e0, Novara, Italy\", \"text\": \"In non responders, PPV and dicrotic pressure did not change significantly during the FC while CCE was significantly reduced from baseline to minute 10 (p\\u2009<\\u20090.05) (Figs.\\u00a069, 70, 71).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig72\"], \"section\": \"Correspondence: J.A. Silversides \\u2013 Belfast Health and Social Care Trust, Critical Care, Belfast, United Kingdom\", \"text\": \"\\nResults In a meta-analysis of the 7 included randomised trials (n\\u2009=\\u20091390), we found a non-significant reduction in mortality with a conservative or deresuscitative fluid strategy (pooled odds ratio 0.86, 95\\u00a0% confidence interval (CI) 0.68-1.09) compared to a liberal strategy or usual care (Fig.\\u00a072). We found a non-significant reduction in RRT use with a conservative or deresuscitative fluid strategy (2 studies, pooled odds ratio 0.73, 95\\u00a0% CI 0.51-1.05). Four trials reported shorter length of ICU stay or increased number of ICU-free days, and 2 studies reported shorter duration of mechanical ventilation or increased ventilator-free days with a conservative or deresuscitative fluid strategy compared to a liberal strategy or usual care. Marked clinical heterogeneity was present.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab56\"], \"section\": \"Correspondence: A. Eladawy \\u2013 Kasr Alainy Medical School, Cairo University, Cairo, Egypt\", \"text\": \"There was no significant correlation between 3-day cumulative fluid balance with either LUS, Ee\\u00b4 ratio, or TFC (Table\\u00a056).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab57\"], \"section\": \"Correspondence: A. Eladawy \\u2013 Kasr Alainy Medical School, Cairo University, Cairo, Egypt\", \"text\": \"There was a significant correlation between TFC & LUS on day 1 & day 3 (r\\u2009=\\u20090.610, p\\u2009<\\u20090.01), (r\\u2009=\\u20090.4, p\\u2009=\\u20090.05) respectively. There was no relationship between Ee\\u00b4 ratio & both TFC & LUS on day 1, it became significant on day 3 (Table\\u00a057).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab58\"], \"section\": \"Correspondence: A. Eladawy \\u2013 Kasr Alainy Medical School, Cairo University, Cairo, Egypt\", \"text\": \"TFC correlated significantly with LUS in patients with negative fluid balance but not in those with positive fluid balance. By the same token, LUS was correlated significantly with Ee\\u00b4 in patients with negative balance only. However, no correlation was found between TFC & Ee\\u00b4 in patients with either negative or positive fluid balance (Table\\u00a058).\\n\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig75\"], \"section\": \"Correspondence: C. Lee \\u2013 Edwards Lifesciences, Critical Care, Irvine, United States\", \"text\": \"\\nResults / conclusions There were 25,419 total hypotensive events. Group 1 contained 1,200 events, 2 had 2,066, 3 had 7,290, and 4 had 5,283. 9,560 events were not used in analysis due to data outliers or meeting more than 1 group criteria. Overall, each group's 5\\u00a0minute\\u00a0% change profile was different at 5 and 10\\u00a0minutes (Fig.\\u00a075). % change in CO, SVV, and SV were significantly different when comparing Group 1 to 2, 3, and 4 at 10\\u00a0minutes. % change in Ea dyn and SVR were significantly different when comparing Group 2 to 1, 3, and 4 at 10\\u00a0minutes prior to event. % change in dP/dt were all significantly different when comparing Group 3 to 1, 2, and 4 at 10 and 5\\u00a0minutes prior to event. In conclusion, the underlying cause of a hypotensive event can potentially be classified into 1 of 4 prescriptive groups up to 10\\u00a0minutes prior to the start of an event.\\n\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig78\", \"Fig79\", \"Fig80\"], \"section\": \"Correspondence: S.D. Hutchings \\u2013 Kings College Hospital, London, United Kingdom\", \"text\": \"\\nResults During shock and early resuscitation Group A (n\\u2009=\\u200910) had a mean PVD of 10.5 (SD\\u2009\\u00b1\\u20092.5) mm/mm2, and Group B (n\\u2009=\\u200912) 5.5 (SD\\u2009\\u00b1\\u20094.1) mm/mm2. During the later resuscitation phases, Group A maintained a significantly higher PVD than Group B. Group A initially had a higher cardiac output but the difference between the groups narrowed as resuscitation progressed. At the end of resuscitation group A had significantly lower plasma lactate, higher lactate clearance, lower standard base deficit, and smaller mixed venous - arterial CO2 gradient. There was no significant difference in blood pressure between the two groups at any stage. There was a wide spread of PVD for a given blood pressure, especially during the shock and early (hypotensive) resuscitation phases (Fig.\\u00a078). The choice of initial resuscitation fluid appeared not to produce differing effects in terms of microcirculatory perfusion (Figs.\\u00a079 and 80).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab58\"], \"section\": \"Correspondence: Z. Jian \\u2013 Edwards Lifesciences, Irvine, United States\", \"text\": \"478 ICU patients from multiple clinical sites that were not used in the calibration set were used as a test set for the final validation of HPI\\u2122. Patients included septic shock (189), post cardiac surgery (208), cardiogenic shock (32), post liver transplantation (19), and others (30, respiratory failure, post non cardiac surgery, etc.). The patient demographics are listed in Table\\u00a058. Radial arterial pressure waveforms were recorded with a FloTrac\\u2122 sensor (Edwards Lifesciences, Irvine, CA). The waveforms were passed to the algorithm to calculate the hypotension probability. The receiver operating characteristic (ROC) analysis was used to assess algorithm performance.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig81\"], \"section\": \"Correspondence: Z. Jian \\u2013 Edwards Lifesciences, Irvine, United States\", \"text\": \"\\nResults 16,078 hypotensive events were registered, on average 34 events per patient with a duration of 11 (\\u00b189) minutes per event. The algorithm was able to predict hypotension with a sensitivity and specificity of 90\\u00a0%, 87\\u00a0% and 86\\u00a0%, for 5, 10, and 15\\u00a0minutes prior to the event, respectively. The area under the curve (AUC) is 0.96, 0.94, and 0.93, for 5, 10, and 15\\u00a0minutes prior to the event, respectively (Fig.\\u00a081).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig82\"], \"section\": \"Correspondence: M. Charlton \\u2013 University Hospitals of Leicester NHS Trust, Anaesthesia, Critical Care and Pain, Leicester, United Kingdom\", \"text\": \"\\nResults Data were collected from 34 healthy volunteers (19 male), mean age 23\\u00a0years [range 20-49] on 4 non-consecutive days. Two distinct stages of cooling and reheating were seen, with a rapid post-occlusion/reheating slope demonstrated at the end of the VOT in all volunteers [Fig.\\u00a082]. The mean rate of reheating in the palm was 0.015\\u00a0\\u00b0C.s-1 [SD 0.009\\u00a0\\u00b0C.s-1]. This is comparable to the mean gradient found when determining a linear model for the same stage, returning a result of 0.0148\\u00a0\\u00b0C.s-1 [SD 0.008\\u00a0\\u00b0C.s-1].\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab64\"], \"section\": \"Correspondence: P. Nuevo-Ortega \\u2013 University Hospital Virgen de la Victoria/IBIMA, Department of Intensive Care Unit, M\\u00e1laga, Spain\", \"text\": \"\\nResults We studied 2313 patients in UHVV group with a mean age of 61.8\\u2009\\u00b1\\u200912.2\\u00a0years old (61.3\\u2009\\u00b1\\u200912.3 vs. 61.9\\u2009\\u00b1\\u200912.5 vs. 62.2\\u2009\\u00b1\\u200911.69, p=\\u2009>\\u20090.05) and 23\\u00a0% were female (23\\u00a0% vs. 22\\u00a0% vs. 22\\u00a0%; p=\\u2009>\\u20090.05). In Andalusia group (n\\u2009=\\u200923167) mean age was 62.3\\u2009\\u00b1\\u200911.7\\u00a0years old (62.5\\u2009\\u00b1\\u200911.7 vs. 62.1\\u2009\\u00b1\\u200911.8 vs. 61.9\\u2009\\u00b1\\u200911.9; p=\\u2009>\\u20090.05) and 23\\u00a0% were female (24\\u00a0% vs. 23\\u00a0% vs. 22\\u00a0%; p=\\u2009>\\u20090.05). No significant differences between three periods in both groups The results we can see in the Table\\u00a064.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab64\"], \"section\": \"Correspondence: J. Aron \\u2013 Kings College Hospital, Intensive Care Unit, London, United Kingdom\", \"text\": \"(p 0.013) and ICU LOS (p 0.0009), with a trend towards a reduction in length of renal replacement therapy (p 0.06) (Table\\u00a064). Similar benefits were not demonstrated if levosimendan was introduced as a first or second vasoactive agent compared to a third or fourth agent. However survival to discharge was improved (41.5\\u00a0% vs 33.3\\u00a0% respectively).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab66\"], \"section\": \"Correspondence: M. Bottiroli \\u2013 Anesthesia and Critical Care Medicine, Cardiothoracic Department 'A. De Gasperis', ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy\", \"text\": \"\\nResults We recruited 80 patients. Etiologies of CS were: 33 acute decompensation of chronic cardiomyopathies, 16 acute myocarditis, 16 acute myocardial infarctions and 15 other causes. Baseline variables are reported in Table\\u00a066 (*p\\u2009<\\u20090,05).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab66\"], \"section\": \"Correspondence: P. Nuevo-Ortega \\u2013 University Hospital Virgen de la Victoria/IBIMA, Department of Intensive Care Unit, M\\u00e1laga, Spain\", \"text\": \"\\nResults We studied 946 patients with a mean age of 61.8\\u2009\\u00b1\\u200912.2\\u00a0years (61.3\\u2009\\u00b1\\u200912.3 vs. 61.9\\u2009\\u00b1\\u200912.5 vs. 62.2\\u2009\\u00b1\\u200911.69, p=\\u2009>\\u20090.05) and 22.7\\u00a0% were female (22\\u00a0% vs. 23\\u00a0% vs. 23\\u00a0%; p=\\u2009>\\u20090.05), no significant differences between three periods. The results we can see in the Table\\u00a066.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig86\"], \"section\": \"Correspondence: F. Galfo \\u2013 University College London, Bloomsbury Institute of Intensive Care Medicine, London, United Kingdom\", \"text\": \"\\nResults Ischaemia/reperfusion reduced cell viability from 94\\u00a0% to 79\\u00a0% (Fig.\\u00a086). MGC-0109 adminstered at the onset of reperfusion increased cell survival in a dose-dependent manner. At the highest concentration survival was similar to cells that did not undergo I/R. Protective effects were also seen with addition of MGC-0109 to H2O2-treated normoxic cells (data not shown).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig87\", \"Fig87\"], \"section\": \"Correspondence: A. Marino \\u2013 University College London, Bloomsbury Institute of Intensive Care Medicine, London, United Kingdom\", \"text\": \"\\nResults Insult severity (IA/LV ratio) was normally distributed with a mean\\u2009\\u00b1\\u2009SEM of 19\\u2009\\u00b1\\u200910\\u00a0%. The severe group (IA/LV\\u2009>\\u200919\\u00a0%) had significantly lower MAP and higher lactate values than the mild severity group (Fig.\\u00a087, top panel). Temporal changes in cardiac contractility and output did not however relate to insult severity (Fig.\\u00a087, bottom panel).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab69\", \"Tab69\"], \"section\": \"Correspondence: C.C. Chao \\u2013 Taipei Medical University Hospital, Emergency Department, Taipei, United States\", \"text\": \"(p\\u2009=\\u20090.13). The reduction in the D2B time was driven by a reduction in time from ECG interpretation to activate CCL (28.3\\u2009\\u00b1\\u20094.1 in the group 1 and 17.6\\u2009\\u00b1\\u20092.3\\u00a0minutes in the group 2) (p\\u2009=\\u2009.001) shown in Table\\u00a069. Mortality rate in group 1 is 12.5\\u00a0% compare to 2.2\\u00a0% in group 2 (p\\u2009=\\u2009.07), shown in Table\\u00a069.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig88\"], \"section\": \"Correspondence: A. Wilson \\u2013 Central Manchester Foundation NHS Trust, Adult Critical Care, Manchester, United Kingdom\", \"text\": \"We have reviewed over 4200 patient-days of data in a rolling audit of the effectiveness of our project. Fig.\\u00a088 demonstrates the percentage of patients for whom an IBW was recorded and for whom a target oxygen saturation was prescribed each month.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab70\", \"Tab71\"], \"section\": \"Correspondence: M.A. Leite \\u2013 Western Parana State University Hospital, Cascavel, Brazil\", \"text\": \"609 patients were admitted, 440 were discharged alive from the hospital. In the Outpatient Clinic, 126 patients were evaluated, 61\\u00a0% male, age 44\\u2009\\u00b1\\u200918.19\\u00a0years, 48\\u00a0% were smokers and 8\\u00a0% COPD. The main causes of admission were postoperative elective surgery (26\\u00a0%) and trauma with head injury (20\\u00a0%), mean APACHE II 19.08, ICU length of time 7.23\\u00a0days, hospital length of time 17.75\\u00a0days, MV\\u2009>\\u200924\\u00a0hours 47.62\\u00a0%, and mean MV time 86.45\\u00a0hours. The groups showed significant differences in spirometric data, shown in Table\\u00a070. In the SF-36 only the areas vitality and social aspects showed statistical difference (Table\\u00a071).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig95\"], \"section\": \"Correspondence: S. Bianzina \\u2013 Anesthesia and Intensive Care, Fondazione IRCCS Policlinico S. Matteo, University of Pavia, Pavia, Italy\", \"text\": \"Figure\\u00a095 shows the mean values of PaO2 during the different phases of WLL. During bipulmonary ventilation gas exchanges improved in response to FiO2 1 and PEEP. Monopulmonary ventilation, instead, induced a clear reduction of PaO2, which increased in lateral position and during liquid tidal ventilation, with a substantial effect of elevated hydrostatic lavage pressures. The wide SD indicates an uneven response of gas exchanges in the studied population.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig96\"], \"section\": \"Correspondence: T.S. Meyhoff \\u2013 Copenhagen University Hospital, Department of Intensive Care 4131, Copenhagen, Denmark\", \"text\": \"We included 690 patients with a 90-day mortality rate of 23\\u00a0%. During the first 3\\u00a0days in ICU, 65\\u00a0% of the patients received respiratory support, 57\\u00a0% circulatory support and 13\\u00a0% renal replacement therapy (RRT). Patients receiving 3\\u00a0days of RRT had the worst outcome (OR 6.5 [95\\u00a0% CI 1.3 - 32.8]) as compared to patients receiving 1\\u00a0day. For respiratory- and circulatory support the odds ratios were 2.2 [0.9 - 5.3] and 1.2 [0.5 - 2.6], respectively (Fig.\\u00a096).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig97\"], \"section\": \"Correspondence: T. \\u00d6hman \\u2013 Karolinska University Hospital, Department of Anaesthesiology, Surgical Services and Intensive Care Medicine, Stockholm, Sweden\", \"text\": \"Carbon dioxide levels raised from (mean (SD)) 5.6 kPa (0.40) to 9.2 kPa (0.47) during hypercapnia. The bias (limits of agreement, LoA) for ELV at normocapnia was 303 (131 to 476) ml, and percentage error (PE) was 31\\u00a0%. During hypercapnia, bias (LoA) decreased to -75 (-188 to 39) ml, and PE to 20\\u00a0%. The hemodynamic interventions resulted in significant changes in CO, i.e. a decrease by 41\\u00a0% (caval occlusion) followed by a 59\\u00a0% increase (dobutamine inf.). ELV and FRC remained stable throughout these changes (Fig.\\u00a097).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig98\"], \"section\": \"Correspondence: C. Chiurazzi \\u2013 Universit\\u00e0 degli Studi di Milano, Dipartimento di Fisiopatologia Medico-Chirurgica e dei Trapianti, Milano, Italy\", \"text\": \"Thirty-three ARDS patients were enrolled (5 mild, 10 moderate and 18 severe). As shown in Fig.\\u00a098, within a given class of severity, the grams of tissue undergoing the intratidal collapse did not change significantly between PEEP 5 or 15 cmH2O (63\\u2009\\u00b1\\u200926 vs 39\\u2009\\u00b1\\u200932, 92\\u2009\\u00b1\\u200953 vs 78\\u2009\\u00b1\\u2009142 and 123\\u2009\\u00b1\\u200994 vs 96\\u2009\\u00b1\\u200984 in mild, moderate and severe ARDS respectively). We observed a clear tendency to decrease from PEEP 5 to 15 cmH2O, though it was not statistically significant (p\\u2009=\\u20090.23, 0.76 and 0.27 respectively in mild, moderate and severe ARDS - paired t-test).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab72\"], \"section\": \"Correspondence: L.E. Brock \\u2013 Guys and St Thomas' NHS Foundation Trust, Physiotherapy, London, United Kingdom\", \"text\": \"Data was collected by retrospective casenote review during a 3\\u00a0week period in August 2015. The project was registered as a service evaluation and therefore ethics requirements were waived. Demographics, details of the PT assessment ,and outcomes following extubation were collected (Table\\u00a072). Extubation failure was defined as reintubation up to one week following extubation.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab75\"], \"section\": \"Correspondence: F.D. Simonis \\u2013 Academic Medical Center, Amsterdam, Netherlands\", \"text\": \"Of 7,784 patients, 693 patients had ARDS of which 164 patients with mild ARDS and on invasive ventilation were included in the analysis. Table\\u00a075 shows outcomes per group at the moment mild ARDS was diagnosed, and after 24\\u00a0hours. Reclassification after 24\\u00a0hours showed an improved prognostication with regard to hospital mortality, ICU- and 90-day mortality and the number of ventilator-free days and alive at day 28.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab76\"], \"section\": \"Correspondence: B. Llorente Ruiz \\u2013 Hospital Universitario Pr\\u00edncipe de Asturias, Intensive Care Unit, Madrid, Spain\", \"text\": \"The results of the demographic and clinical variables are shown in Table\\u00a076.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab77\"], \"section\": \"Correspondence: B. Llorente Ruiz \\u2013 Hospital Universitario Pr\\u00edncipe de Asturias, Intensive Care Unit, Madrid, Spain\", \"text\": \"Regarding the evaluation of HRQL by SGRQ, the mean scores were slightly higher in all domains with regard to the reference values from Spanish population by age and sex, indicating subjective respiratory problems with an impact on daily life. Only 7 of our 31 patients (22.6\\u00a0%) had scores normal in all domains and in the total scores. 18 patients (58.1\\u00a0%) had higher scores in all domains. The other 6 patients (19.3\\u00a0%) had a higher score in some of the domains. Table\\u00a077\\n\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig101\", \"Fig101\"], \"section\": \"Correspondence: C. Chiurazzi \\u2013 Universit\\u00e0 degli Studi di Milano, Dipartimento di Fisiopatologia Medico-Chirurgica e dei Trapianti, Milano, Italy\", \"text\": \"Twenty-seven ARDS patients were studied at PEEP 5 cmH2O. Age 58 [44-72] years (median [IQ range]), BMI 25 [22-29] kg/m2, PaO2/FiO2 105 [83-168], PaCO2 44 [40-51] mmHg, tidal volume 7 [5-8] ml/Kg IBW. Energy delivered per breath (J) was significantly related to lung strain (Fig.\\u00a0101, upper panel) and inhomogeneity (Fig.\\u00a0101, lower panel); the relationship between delivered energy and intratidal collapse-decollapse did not reach statististical significance (r2\\u2009=\\u20090.10, p\\u2009=\\u20090.11).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab80\"], \"section\": \"Correspondence: J. Mckinlay \\u2013 Royal Surrey County Hospital, ICU and SPACeR research group, Guildford, United Kingdom\", \"text\": \"95\\u00a0% of patients had a decrease in their L3MCSA during their ICU stay. See Table\\u00a080.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab81\", \"Fig103\"], \"section\": \"Correspondence: K.N. MacEachern \\u2013 Mount Sinai Hospital, Toronto, Canada\", \"text\": \"Ninety pH tests were done and 21 tests missed, for 12 patients. The overall mean pH was 5.2 and median pH\\u00a05.7. Stratification by drug therapy results can be found in Table\\u00a081. A cumulative percentile chart of pH with acid inhibitor Method is reported in Fig.\\u00a0103. All patients received EN. The mean calorie deficit observed was 1513 calories, for all reasons, not the gastric pH test alone. EN was held for 1\\u00a0h before the test. The lab reported results usually in 30\\u00a0minutes. Length of the feeding tube to insertion point was recorded for 1 patient.\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Tab82\"], \"section\": \"Correspondence: C.T. Anthon \\u2013 Copenhagen University Hospital - Rigshospitalet, Department of Intensive Care, Copenhagen, Denmark\", \"text\": \"Baseline characteristics were similar in the HES- and the Ringer's groups. By day 2, 13 (11\\u00a0%) patients in the HES group had died vs. 11 (10\\u00a0%) in the Ringer's group (P\\u2009=\\u20090.91). Plasma concentrations of TNF-\\u03b1, IL-6 and IL-10 decreased from baseline to day 2 in the HES- and the Ringer's groups, but mean delta cytokine concentrations did not differ between the groups (Table\\u00a082). Also, no associations were observed between changes in the cytokine plasma concentrations and 90-day mortality (TNF-\\u03b1: odds ratio for 1-unit increase, 1.000 (95\\u00a0% Confidence Interval, 0.998 - 1.003), P\\u2009=\\u20090.87; IL-6: 1.001 (0.999 - 1.002), P\\u2009=\\u20090.32; IL-10: 1.000 (0.999 - 1.001), P\\u2009=\\u20090.89).\"}, {\"pmc\": \"PMC5042924\", \"pmid\": \"\", \"reference_ids\": [\"Fig104\"], \"section\": \"Correspondence: J.C.F. Vieira \\u2013 Federal University of S\\u00e3o Paulo, Surgery, S\\u00e3o Paulo, Brazil\", \"text\": \"In sublingual, there was a significant reduction in vascular density of animals with sepsis only after 3\\u00a0hours of sepsis compared to the sham group. (Fig.\\u00a0104). This suggests that reducing the density in sepsis is only noticeable during periods of increased severity of sepsis. The comparison between the periods of sepsis showed that only the first two hours had a higher density compared to other periods of sepsis. These results have shown that in sepsis, the densi
Metadata
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