Predictive Ability of the Stability and Workload Index for Transfer Score to Predict Unplanned Readmissions After ICU Discharge

Objective: Unplanned readmission of hospitalized patients to an ICU is associated with an increased mortality and hospital length of stay. The ability to identify patients at risk, who would benefit from prolonged ICU treatment, is limited. The aim of this study is to validate a previously published numerical index named the Stability and Workload Index for Transfer in a heterogeneous group of ICU patients. Design: In this retrospective data analysis, the Stability and Workload Index for Transfer score was calculated for all patients, and the ability of the score to predict readmission was compared with the original publication. Setting: Four ICUs, one intermediate care unit, and one postanesthesia care unit of the department of anesthesia and intensive care of a university hospital. Patients: All consecutive patients treated in one of the units. Interventions: None. Measurements and Main Results: Unplanned ICU readmissions or unexpected death within 7 days of ICU discharge. The data of 7,175 patients were included in the analysis. Five hundred ninety-six patients were readmitted or died within 7 days of discharge. The patients who are readmitted to the ICU are significantly older and have significantly higher scores that define the severity of disease at the time of admission and discharge of their first ICU stay. The source of admission for the initial ICU stay did not differ (p = 0.055), and the last Glasgow Coma Scale and the last Pao(2)/Fio(2) ratio before discharge from the ICU were higher in patients who did not need a readmission to the ICU. The performance of the Stability and Workload Index for Transfer score is poor with an area under the receiver operator curve of 0.581 (95% CI, 0.556-0.605; p < 0.001). Conclusions: Based on the data from our patients, the proposed Stability and Workload Index for Transfer score by Gajic et al is not ideal in aiding the clinician in the decision, if a patient can be discharged safely from the ICU and further research is necessary to define the patients at risk for readmission

ApoE attenuates unresolvable inflammation by complex formation with activated C1q

Apolipoprotein-E (ApoE) has been implicated in Alzheimer's disease, atherosclerosis, and other unresolvable inflammatory conditions but a common mechanism of action remains elusive. We found in ApoE-deficient mice that oxidized lipids activated the classical complement cascade (CCC), resulting in leukocyte infiltration of the choroid plexus (ChP). All human ApoE iso-forms attenuated CCC activity via high-affinity binding to the activated CCC-initiating C1q protein (K-D similar to 140-580 pM) in vitro, and C1q-ApoE complexes emerged as markers for ongoing complement activity of diseased ChPs, A beta plaques, and atherosclerosis in vivo. C1q-ApoE complexes in human ChPs, A beta plaques, and arteries correlated with cognitive decline and atherosclerosis, respectively. Treatment with small interfering RNA (siRNA) against C5, which is formed by all complement pathways, attenuated murine ChP inflammation, A beta-associated microglia accumulation, and atherosclerosis. Thus, ApoE is a direct checkpoint inhibitor of unresolvable inflammation, and reducing C5 attenuates disease burden

ApoE attenuates unresolvable inflammation by complex formation with activated C1q

Apolipoprotein-E (ApoE) has been implicated in Alzheimer's disease, atherosclerosis, and other unresolvable inflammatory conditions but a common mechanism of action remains elusive. We found in ApoE-deficient mice that oxidized lipids activated the classical complement cascade (CCC), resulting in leukocyte infiltration of the choroid plexus (ChP). All human ApoE iso-forms attenuated CCC activity via high-affinity binding to the activated CCC-initiating C1q protein (K-D similar to 140-580 pM) in vitro, and C1q-ApoE complexes emerged as markers for ongoing complement activity of diseased ChPs, A beta plaques, and atherosclerosis in vivo. C1q-ApoE complexes in human ChPs, A beta plaques, and arteries correlated with cognitive decline and atherosclerosis, respectively. Treatment with small interfering RNA (siRNA) against C5, which is formed by all complement pathways, attenuated murine ChP inflammation, A beta-associated microglia accumulation, and atherosclerosis. Thus, ApoE is a direct checkpoint inhibitor of unresolvable inflammation, and reducing C5 attenuates disease burden