During the study period, about 15,200 patients were admitted to participating ICUs. Among them, 757 patients were treated with RRT sometime during the ICU stay (Figure (Figure1).1). Of the 757 enrolled patients, thenthereby we excluded patients (n = 19) who received concomitant extracorporeal treatments (e.g. endotoxin adsorption) other than those specified in the methods of this report, and those with incomplete data (n = 117). The majority of incomplete data was due to one missing datapoint needed to calculate RRT dose on a specific day, such as percentage pre-dilution or actual start or stop time. Complete data on pre-specified outcomes were not available for 11 patients (1.4%).Among the remaining 553 AKI patients, 419 received CRRT only, 88 received IRRT only and 46 were treated with mixed RRT schedules (IRRT, CRRT, coupled plasmafiltration adsorption).

As patients in this last group crossed over from one RRT modality to another, delivered dose could not be calculated due to lack of clinically validated models, and they were excluded from the analysis. Among patients treated on only one RRT schedule (either continuous only or intermittent only), 82% received CRRT. This proportion represents current practice in Europe as previously reported. Out of 419 CRRT patients, 81 patients had at least one interruption of 18 hours or more, and then resumed CRRT [14]. The median interruption time was 49 hours (IQR = 29 to 113), predominantly due to filter clotting, disconnection for procedures and change in patient clinical status (e.g. CRRT not required in a window period).

As daily CRRT dose would appear artificially low in this situation, such patients were not included in the analysis. Eighty eight patients (18%) were treated exclusively with IRRT. One patient had only three IRRT sessions over a span of 146 days, and was excluded from analysis (Figure (Figure11).Characteristics of the study population are described in Table Table1.1. CRRT patients were younger, more likely to have sepsis, more likely to have been admitted directly into the ICU from the emergency room and less likely to be surgical patients. The mean serum creatinine at RRT initiation was 265 ��mol/L. Nearly 60% of all patients were in RIFLE class Failure at RRT initiation. A small minority of patients did not meet criteria even for Risk, and were labelled as a non-renal indication (e.g.

volume overload). Among the reasons cited to start RRT, azotaemia was significantly more common in the IRRT group, and oliguria in the CRRT group. Crude ICU mortality was 54% in the CRRT group, 22% in the IRRT group and 45% in the mixed group.Table 1Clinical characteristics of ICU patients receiving RRTPatient characteristics by RRT doseCRRTIn the CRRT group, the median delivered RRT dose was Brefeldin_A 27.1 ml/kg/hour (IQR = 22.1 to 33.9). Only 75 patients (22%) received more-intensive dose (�� 35 ml/kg/hour), while 262 (78%) received less-intensive CRRT.

58) (Figure (Figure1).1). In both groups, blood glucose rose after nutrient administration (P <0.001). Despite insulin use, post-pyloric delivery of nutrient was associated with greater glycaemic excursions in the 'early' period (AUC60: intragastric 472 (425, 519) vs. post-pyloric 534 (501, 569) mmol/l.min; P = 0.03), and there was a trend for an increase in the www.selleckchem.com/products/ABT-888.html peak excursion (9.2 (8.4, 10.1) vs. 10.2 (9.5, 10.8) mmol/l; P = 0.09). Blood glucose concentrations at t60 (8.2 (7.3, 9.2) vs. 9.0 (8.3, 9.8) mmol/l; P = 0.19) and ‘overall’ glycaemia (AUC240: 1,875 (1,674, 2,075) vs. 1,898 (1,755, 2,041) mmol/l.min; P = 0.85) were similar in the two groups.Figure 1Blood glucose concentrations following administration of nutrient via intragastric and post-pyloric routes.

For the initial 60 minutes after the infusion, glycaemic excursions were greater following post-pyloric administration of nutrient (*P = 0.03), …Serum 3-OMG concentrations (glucose absorption)In all patients, 3-OMG concentrations increased after both infusions, and at study end (t240), remained greater than zero in all patients (Figure (Figure2).2). However, administration of nutrient directly into the small intestine resulted in increased glucose absorption during the ‘early’ period when compared with intragastric feeding (AUC60 intragastric 7.3 (4.3, 10.2) vs. post-pyloric 12.5 (10.1, 14.8) mmol/l.min; P = 0.008). Small intestinal feeding was also associated with a reduced time to peak (Time to Peak 3-OMG: 132 (100, 164) vs. 78 (61, 95) minutes; P = 0.001), although there was no difference in 3-OMG peak concentrations in the two groups (0.

29 (0.20 to 0.39) vs. 0.37 (0.31 to 0.43) mmol/l; P = 0.13). ‘Overall’ glucose absorption (AUC240) was similar between intragastric and post-pyloric feeding route (AUC240 49.1 (34.8, 63.5) vs. 56.6 (48.9, 64.3) mmol/l.min; P = 0.31).Figure 2Glucose (3-OMG) absorption following administration of nutrient via intragastric and post-pyloric routes. ‘Early’ glucose absorption was increased following post-pyloric delivery (* P = 0.008). While ‘overall’ glucose absorption was similar between intragastric …Relationships between 3-OMG and blood glucose concentrationsIn the whole group there was a relationship between rise in glycaemia and glucose absorption (3-OMG AUC60 and �� blood glucose concentration at t60 when compared to fasting glucose, r = 0.

50; P <0.001, and serum 3-OMG and blood glucose concentrations at t60 r = 0.41; P <0.001). There was also an association between the maximum increment in blood glucose and the rate of glucose absorption (for example, 3-OMG Batimastat peak and ��max in blood glucose, r = 0.37; P = 0.02).DiscussionThe key observation in this study is that small intestinal delivery of nutrient, when compared to intragastric administration, appeared to have little effect on ‘overall’ glucose absorption over 240 minutes.

Table selleck chemicals llc 2Underlying conditions and mechanism for patients with acute lung injury/acute respiratory distress syndromeComparison of extravascular lung water index and pulmonary vascular permeability indexThe EVLWI on the day of enrollment was significantly higher in ALI/ARDS patients than in patients with pleural effusion with atelectasis (18.5 �� 6.8 vs. 8.3 �� 2.1; P < 0.01) or cardiogenic edema (14.4 �� 4.0; P < 0.01) (Figure (Figure2).2). The PVPI on the day of enrollment was higher in the ALI/ARDS patients than in cardiogenic edema or pleural effusion with atelectasis patients (3.2 �� 1.4, 2.0 �� 0.8, and 1.6 �� 0.5, respectively). Although the EVLWI was higher in the cardiogenic edema than in pleural effusion with atelectasis patient (Figure (Figure2),2), there was no significant difference in PVPI between those groups (Figure (Figure33).

Figure 2Comparison of extravascular lung water indexed to predicted body weight. Comparison of extravascular lung water indexed to predicted body weight of patients with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), cardiogenic edema, and …Figure 3Comparison of pulmonary vascular permeability index. Comparison of pulmonary vascular permeability index (PVPI) of patients with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), cardiogenic edema, and pleural effusion with atelectasis …These differences were also noted when the maximal values of EVLWI and PVPI recorded during the study period were compared among the three groups (Figures (Figures22 and and33).

Relationship among EVLWI, PVPI, and intrathoracic blood volumeFor this analysis, cardiogenic edema and pleural effusion with atelectasis patients were considered non-ALI/ARDS patients because increased pulmonary vascular permeability is not the pathogenetic mechanism of these conditions and was not elevated compared with that in ALI/ARDS patients.In the ALI/ARDS patients, a strong correlation between EVLWI and PVPI (r = 0.729, P < 0.01) and a weak correlation between EVLWI and ITBV (r = 0.236, P < 0.01) were noted on the day of enrollment (Figure (Figure4).4). In the non-ALI/ARDS patients, moderate correlations between EVLWI and PVPI (r = 0.464, P < 0.01) and between EVLWI and ITBV (r = 0.493, P < 0.01) were noted (Figure (Figure55).Figure 4Extravascular lung water index and pulmonary vascular permeability index/intrathoracic blood volume correlation in ALI/ARDS patients.

Correlation between extravascular lung water index (EVLWI) and pulmonary vascular Entinostat permeability index (PVPI) and that …Figure 5Extravascular lung water index and pulmonary vascular permeability index/intrathoracic blood volume correlation in non-ALI/ARDS patients. Correlation between extravascular lung water index (EVLWI) and pulmonary vascular permeability index (PVPI) and that …