The Jury recommended the use of newly described definitions. AKI significantly contributes to the morbidity and mortality of critically ill patients, and adequate volume repletion is of major importance for its prevention, though correction of fluid deficit will not always prevent renal failure. Fluid resuscitation with crystalloids is effective and safe, and hyperoncotic solutions are not recommended because of their renal risk. Renal replacement therapy is a life-sustaining intervention that can provide a bridge to renal recovery; no method has proven to be superior, but careful management is essential for improving outcome.

In this model of lung injury induced solely by mechanical forces, the prone position resulted in a less severe and more homogeneous distribution of ventilator-induced lung injury. These results parallel those previously obtained in oleic acid-preinjured animals ventilated with higher positive end-expiratory pressure.

To investigate whether respiratory acidosis modulates ventilator-induced lung injury (VILI), we perfused (constant flow) 21 isolated sets of normal rabbit lungs, ventilated them for 20 min (pressure controlled ventilation [PCV] = 15 cm H(2)O) (Baseline) with an inspired CO(2) fraction adjusted for the partial pressure of CO(2) in the perfusate (PCO(2) approximately equal to 40 mm Hg), and then randomized them into three groups. Group A (control: n = 7) was ventilated with PCV = 15 cm H(2)O for three consecutive 20-min periods (T1, T2, T3). In Group B (high PCV/normocapnia; n = 7), PCV was given at 20 (T1), 25 (T2), and 30 (T3) cm H(2)O. The targeted PCO(2) was 40 mm Hg in Groups A and B. Group C (high PCV/hypercapnia; n = 7) was ventilated in the same way as Group B, but the targeted PCO(2) was approximately equal to 70 to 100 mm Hg. The changes (from Baseline to T3) in weight gain (Delta WG: g) and in the ultrafiltration coefficient (Delta K(f) = gr/min/ cm H(2)O/100g) and the protein and hemoglobin concentrations in bronchoalveolar lavage fluid (BALF) were used to assess injury. Group B experienced a significantly greater Delta WG (14.85 +/- 5.49 [mean +/- SEM] g) and Delta K(f) (1.40 +/- 0.49 g/min/cm H(2)O/100 g) than did either Group A (Delta WG = 0.70 +/- 0.43; Delta K(f) = 0.01 +/- 0.03) or Group C (Delta WG = 5.27 +/- 2.03 g; Delta K(f) = 0.25 +/- 0.12 g/min/cm H(2)O/ 100 g). BALF protein and hemoglobin concentrations (g/L) were higher in Group B (11.98 +/- 3.78 g/L and 1.82 +/- 0.40 g/L, respectively) than in Group A (2.92 +/- 0.75 g/L and 0.38 +/- 0.15 g/L) or Group C (5.71 +/- 1.88 g/L and 1.19 +/- 0.32 g/L). We conclude that respiratory acidosis decreases the severity of VILI in this model.

BackgroundPatients undergoing alcohol withdrawal in the intensive care unit (ICU) often require escalating doses of benzodiazepines and not uncommonly require intubation and mechanical ventilation for airway protection. This may lead to complications and prolonged ICU stays. Experimental studies and single case reports suggest the α2-agonist dexmedetomidine is effective in managing the autonomic symptoms seen with alcohol withdrawal. We report a retrospective analysis of 20 ICU patients treated with dexmedetomidine for benzodiazepine-refractory alcohol withdrawal.MethodsRecords from a 23-bed mixed medical-surgical ICU were abstracted from November 2008 to November 2010 for patients who received dexmedetomidine for alcohol withdrawal. The main analysis compared alcohol withdrawal severity scores and medication doses for 24 h before dexmedetomidine therapy with values during the first 24 h of dexmedetomidine therapy.ResultsThere was a 61.5% reduction in benzodiazepine dosing after initiation of dexmedetomidine (n = 17; p < 0.001) and a 21.1% reduction in alcohol withdrawal severity score (n = 11; p = .015). Patients experienced less tachycardia and systolic hypertension following dexmedetomidine initiation. One patient out of 20 required intubation. A serious adverse effect occurred in one patient, in whom dexmedetomidine was discontinued for two 9-second asystolic pauses noted on telemetry.ConclusionsThis observational study suggests that dexmedetomidine therapy for severe alcohol withdrawal is associated with substantially reduced benzodiazepine dosing, a decrease in alcohol withdrawal scoring and blunted hyperadrenergic cardiovascular response to ethanol abstinence. In this series, there was a low rate of mechanical ventilation associated with the above strategy. One of 20 patients suffered two 9-second asystolic pauses, which did not recur after dexmedetomidine discontinuation. Prospective trials are warranted to compare adjunct treatment with dexmedetomidine versus standard benzodiazepine therapy.

After oleic acid-induced lung injury, animals ventilated with high tidal volume and PEEP undergo less extensive histologic change in the prone position than in the supine position. The prone position alters the distribution of histologic abnormalities.

We conclude that RM transiently but profoundly depressed cardiac output in three models of acute lung injury. The results imply that a lung recruiting maneuver should be used with caution, especially when using sustained inflation in the setting of pneumonia.

He/oxygen did not significantly reduce intubation rate or intensive care unit stay, but hospital stay was shorter and total costs were lower. He/oxygen NIPSV can be safely administered and could prove to be a cost-effective strategy.

To investigate whether the magnitude of blood flow contributes to ventilator-induced lung injury, 14 sets of isolated rabbit lungs were randomized for perfusion at either 300 (Group A: n = 7) or 900 ml/ min (Group B: n = 7) while ventilated with 30 cm H2O peak static pressure. Control lungs (Group C: n = 7) were ventilated with lower peak static pressure (15 cm H2O) and perfused at 500 ml/min. Weight gain, changes in the ultrafiltration coefficient (DeltaKf) and lung static compliance (CL), and extent of hemorrhage (scored by histology) were compared. Group B had a larger decrease in CL (-13 +/- 11%) than Groups A (2 +/- 6%) and C (5 +/- 5%) (p < 0.05). Group B had more hemorrhage and gained more weight (16.2 +/- 9.5 g) than Groups A (8.7 +/- 3.4 g) and C (1.6 +/- 1.0 g) (p < 0.05 for each pairwise comparison between groups). Finally, Kf (g . min-1 . cm H2O-1 . 100 g-1) increased the most in Group B (DeltaKf = 0.26 +/- 0. 20 versus 0.17 +/- 0.10 in Group A and 0.05 +/- 0.04 in Group C; p < 0.05 for B versus C). We conclude that the intensity of lung perfusion contributes to ventilator- induced lung injury in this model.