Background Burnout syndrome has reached epidemic levels among physicians (reported around 50%). Anesthesiology is among the most stressful medical disciplines but there is paucity of literature as compared with others. Analysis of burnout is essential because it is associated with safety and quality of care. We summarize evidence on burnout in anesthesiology. Methods We conducted a systematic review (MEDLINE up to 30.06.2017). We included studies reporting burnout in anesthesiology with no restriction on role or screening test used. Results Fifteen surveys/studies described burnout in anesthesiology, including different workers profiles (nurses, residents, consultants, and directors). All studies used the Maslach Burnout Inventory test but with significant differences for risk stratification. Burnout prevalence greatly varied across studies (10%–41% high risk, up to 59% at least moderate risk). Factors most consistently associated with burnout were strained working pattern, working as younger consultant, and having children. There was no consistent relationship between burnout and hospital characteristics, gender, or marital status. Conclusions Burnout prevalence among anesthesiologists is relatively high across career stages, and some risk factors are reported frequently. However, the small number of studies as well as the large differences in their methodology and in reporting approach warrants further research in this field.

Bivalirudin loading dose was not always used; infusion range and anticoagulation targets were different. In this systematic review, we discuss the reasons for this variability. Larger studies are needed to establish the optimal approach with the use of bivalirudin for ECMO.

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Recent growing evidence suggests that beta-blocker treatment could improve cardiovascular dynamics and possibly the outcome of patients admitted to intensive care with severe sepsis or septic shock

Objectives: Propofol-based sedation may increase hemodynamic instability by decreasing vascular tone and venous return. Incremental exogenous catecholamines doses may be required to counteract such effects, aggravating the deleterious effects of sympathetic overstimulation. α-2 adrenergic agonists have been reported to decrease norepinephrine requirements in experimental septic shock. The aim of the present study is to test the hypothesis that switching from sedation with propofol to the α-2 agonist dexmedetomidine may decrease norepinephrine doses in septic shock. Design: Prospective open-label crossover study. Settings: University hospital, ICU. Patients: Thirty-eight septic shock patients requiring norepinephrine to maintain adequate mean arterial pressure and needing deep sedation with propofol and remifentanil to maintain a Richmond Agitation-Sedation Scale score between –3 and –4. Interventions: An initial set of measurements including hemodynamics, norepinephrine doses, and depth of sedation were obtained during sedation with propofol. Propofol was then replaced by dexmedetomidine and a second set of data was obtained after 4 hours of dexmedetomidine infusion. Sedation was switched back to propofol, and a final set of measurements was obtained after 8 hours. A Richmond Agitation-Sedation Scale score between –3 and –4 was maintained during the study period. Measurements and Main Results: Norepinephrine requirements decreased from 0.69 ± 0.72 μg/kg/min before dexmedetomidine to 0.30 ± 0.25 μg/kg/min 4 hours after dexmedetomidine infusion, increasing again to 0.42 ± 0.36 μg/kg/min while on propofol 8 hours after stopping dexmedetomidine (p < 0.005). Dexmedetomidine dosage was 0.7 ± 0.2 μg/kg/hr. Before and after dexmedetomidine infusion, sedative doses remained unchanged (propofol 2.6 ± 1.2 vs 2.6 ± 1.2 mg/kg/hr; p = 0.23 and remifentanil 1.27 ± 0.17 vs 1.27 ± 0.16 μg/kg/hr; p = 0.52, respectively). Richmond Agitation-Sedation Scale was –4 (–4 to –3) before, –4 (–4 to –3) during, and –4 (–4 to –4) after dexmedetomidine (p = 0.07). Conclusions: For a comparable level of sedation, switching from propofol to dexmedetomidine resulted in a reduction of catecholamine requirements in septic shock patients.

Implementation of a comprehensive protocol for anticoagulation and transfusions in VV-ECMO for ARDS resulted in a low PRBC requirement, and an ECMO survival comparable to data in the literature. Lower ATIII emerged as a factor associated with increased need for transfusions. Higher PRBC transfusions were associated with ECMO mortality. Further investigations are needed to better understand the right level of anticoagulation in ECMO, and the factors to take into account in order to manage personalized transfusion practice in this select setting.

Cardiac arrest (CA) is a major health and economic problem. Management of patients resuscitated from CA is challenging for clinicians, and the mortality rate of those who achieve return of spontaneous circulation remains high. Hypoxic brain injury, cardiovascular abnormalities and systemic ischemia/reperfusion response characterize the so-called 'postcardiac arrest syndrome', which could lead to multiple organ failure and poor outcome after CA. The magnitude of these disorders differs in individual patients, mainly based on the cause and duration of CA and on the severity of the ischemic episode. Prognostication of outcome after CA is of importance because it could help physicians on triage decisions and readdress the overall management. A number of factors are thought to influence the prognosis of patients after CA, but due to the heterogeneity of CA population and scenarios no single factor has been identified as a reliable predictor of outcome and the timing and optimal approach to prognostication is still controversial. Biomarkers represent a growing area of interest in this field, as they may provide clinicians with early information on the severity of organ dysfunction to make a decision on clinical strategies and prognosticate outcome. In this article, the authors will focus on cardiac, neurological and inflammatory biomarkers as potential predictors of outcome after CA.