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BackgroundExtracorporeal membrane oxygenation (ECMO) is a life-saving therapy in acute respiratory distress syndrome (ARDS) patients but is associated with complications and costs. Here, we validate various scores supposed to predict mortality and develop an optimized categorical model.MethodsIn a derivation cohort, 108 ARDS patients (2010–2015) on veno-venous ECMO were retrospectively analysed to assess four established risk scores (ECMOnet-Score, RESP-Score, PRESERVE-Score, Roch-Score) for mortality prediction (receiver operating characteristic analysis) and to identify by multivariable logistic regression analysis independent variables for mortality to yield the new PRESET-Score (PREdiction of Survival on ECMO Therapy-Score). This new score was then validated both in independent internal (n = 82) and external (n = 59) cohorts.ResultsThe median (25%; 75% quartile) Sequential Organ Failure Assessment score was 14 (12; 16), Simplified Acute Physiology Score II was 62.5 (57; 72.8), median intensive care unit stay was 17 days (range 1–124), and mortality was 62%. Only the ECMOnet-Score (area under curve (AUC) 0.69) and the RESP-Score (AUC 0.64) discriminated survivors and non-survivors. Admission pHa, mean arterial pressure, lactate, platelet concentrations, and pre-ECMO hospital stay were independent predictors of death and were used to build the PRESET-Score. The score’s internal (AUC 0.845; 95% CI 0.76–0.93; p < 0.001) and external (AUC 0.70; 95% CI 0.56–0.84; p = 0.008) validation revealed excellent discrimination.ConclusionsWhile our data confirm that both the ECMOnet-Score and the RESP-Score predict mortality in ECMO-treated ARDS patients, we propose a novel model also incorporating extrapulmonary variables, the PRESET-Score. This score predicts mortality much better than previous scores and therefore is a more precise choice for decision support in ARDS patients to be placed on ECMO.

These data support the beneficial effects of ventilation with use of low VT in patients undergoing surgery. Further trials are necessary to define the role of intraoperative higher PEEP to prevent PPC during nonopen abdominal surgery.

The objective of this study was to assess the required dose and anticoagulatory effect of argatroban (Mitsubishi, Pharma Deutschland GmbH, Düsseldorf, Germany), a direct thrombin inhibitor approved for anticoagulation in patients with heparin-induced thrombocytopenia (HIT) undergoing extracorporeal membrane oxygenation (ECMO). Nine consecutive patients undergoing ECMO for severe acute respiratory distress syndrome (ARDS) and presenting with suspected HIT were treated with a continuous argatroban infusion. Coagulation variables were measured and dose adjustments of argatroban were performed to target for an activated partial thromboplastin time (aPTT) of 50 to 60 s. The first patient received argatroban 2 microg/kg/min as recommended by the manufacturer. This resulted in excessive anticoagulation and severe bleeding. The consecutive eight patients received a 10-fold lower dose (0.2 microg/kg/min). This dose sufficiently increased aPTT time from 46 +/- 6 s to 65 +/- 14 s (P < 0.001) and thrombin time from 18 +/- 8 s to 45 +/- 11 s (P = 0.001). The maintenance dose averaged 0.15 microg/kg/min. Duration of argatroban infusion for ECMO averaged 4 +/- 1 days and no oxygenator or extracorporeal system clotting was observed. In three of nine patients (33%), HIT was confirmed. Argatroban is a feasible and effective anticoagulant for patients with suspected HIT undergoing ECMO. However, a dose 10-fold lower than that recommended by the manufacturer is sufficient to achieve appropriate anticoagulation in critically ill patients undergoing ECMO.

In critically ill patients with MODS, argatroban 2 microg/kg/min, as recommended by the manufacturer, resulted in extensive anticoagulation. A tenfold lower starting dose is sufficient and safe for effective anticoagulation in this specific patient population.

Prolonged impaired lung function after major abdominal surgery is not ameliorated by low tidal volume ventilation.

The intrapulmonary renin-angiotensin system via tissue concentration of angiotensin II or bradykinin may have multiple effects on pulmonary pathophysiology. Therefore, it was investigated whether the presence of the D allele of the angiotensinconverting enzyme (ACE) insertion/deletion (I/D) polymorphism or the A allele of angiotensinogen (AGT) promoter polymorphism (-6)A/G are independent risk factors for 30-day survival in acute respiratory distress syndrome (ARDS) patients.In a prospective study, adults (Germans of Caucasian ethnicity) with ARDS (n584) were recruited from the current authors' intensive care unit and genotyped for the ACE I/D and the AGT (-6)A/G polymorphisms, as were 200 healthy Caucasian controls.Mortality was increased in the ACE DD genotype compared with the I allele, and the ACE I/D polymorphism was an independent prognostic factor for 30-day survival. Patients with a homozygous DD genotype were at highest risk for death (hazard ratio 5.7; 95% confidence interval 1.7-19.2) compared with the II genotype. In contrast, the AGT (-6)A/G polymorphism was neither associated with an increased risk for development of ARDS nor with outcome.In patients with acute respiratory distress syndrome, the angiotensin-converting enzyme insertion/deletion polymorphism but not the angiotensinogen (-6)A/G promoter polymorphism is an independent risk factor with a pronounced effect on 30-day survival.