No abstract

Change in carotid corrected flow time can predict fluid responsiveness status after a passive leg raise maneuver. Using point-of-care ultrasound to assess change in carotid corrected flow time is an acceptable and reproducible method for noninvasive identification of fluid responsiveness in critically ill patients with undifferentiated shock.

Purpose Sepsis is a devastating condition with considerable mortality. The causes of long-term mortality are poorly understood. To test the hypothesis that septic patients are more susceptible to recurrent infections and death due to infectious complications, we investigated the outcomes of patients who survived sepsis, with regards to incidence of recurrent infections and mortality. Material and Methods A retrospective study of subjects admitted to the intensive care unit (ICU) for sepsis from 2001–2 who achieved 30-day survival (“SS”, N=78) and a control group of subjects admitted to the ICU for non-infectious conditions with a similar severity of illness (N=50) was performed. The primary endpoint was the number of recurrent infections in the first year post-hospitalization. Results The SS group had higher rates of infections following hospital discharge compared to controls. Using a multivariable model, having survived sepsis was the strongest predictor of the development of subsequent infections (rate ratio [RR] 2.83, P=0.0006), the need for re-hospitalization for infection in the year after the initial hospitalization (RR 3.78, P=0.0009), and post-discharge mortality (hazard ratio=3.61, P=0.003). Conclusions Critically ill patients who survive sepsis have an increased risk of recurrent infections in the year following their septic episode, which is associated with increased mortality.

Pulmonary alveolar proteinosis (PAP) is a syndrome of reduced GM-CSF-dependent, macrophage-mediated surfactant clearance, dysfunctional foamy alveolar macrophages, alveolar surfactant accumulation, and hypoxemic respiratory failure for which the pathogenetic mechanism is unknown. Here, we examine the lipids accumulating in alveolar macrophages and surfactant to define the pathogenesis of PAP and evaluate a novel pharmacotherapeutic approach. In PAP patients, alveolar macrophages have a marked increase in cholesterol but only a minor increase in phospholipids, and pulmonary surfactant has an increase in the ratio of cholesterol to phospholipids. Oral statin therapy is associated with clinical, physiological, and radiological improvement in autoimmune PAP patients, and ex vivo statin treatment reduces cholesterol levels in explanted alveolar macrophages. In Csf2rb−/− mice, statin therapy reduces cholesterol accumulation in alveolar macrophages and ameliorates PAP, and ex vivo statin treatment increases cholesterol efflux from macrophages. These results support the feasibility of statin as a novel pathogenesis-based pharmacotherapy of PAP.