Table of contentsP001 - Sepsis impairs the capillary response within hypoxic capillaries and decreases erythrocyte oxygen-dependent ATP effluxR. M. Bateman, M. D. Sharpe, J. E. Jagger, C. G. EllisP002 - Lower serum immunoglobulin G2 level does not predispose to severe flu.J. Solé-Violán, M. López-Rodríguez, E. Herrera-Ramos, J. Ruíz-Hernández, L. Borderías, J. Horcajada, N. González-Quevedo, O. Rajas, M. Briones, F. Rodríguez de Castro, C. Rodríguez GallegoP003 - Brain protective effects of intravenous immunoglobulin through inhibition of complement activation and apoptosis in a rat model of sepsisF. Esen, G. Orhun, P. Ergin Ozcan, E. Senturk, C. Ugur Yilmaz, N. Orhan, N. Arican, M. Kaya, M. Kucukerden, M. Giris, U. Akcan, S. Bilgic Gazioglu, E. TuzunP004 - Adenosine a1 receptor dysfunction is associated with leukopenia: A possible mechanism for sepsis-induced leukopeniaR. Riff, O. Naamani, A. DouvdevaniP005 - Analysis of neutrophil by hyper spectral imaging - A preliminary reportR. Takegawa, H. Yoshida, T. Hirose, N. Yamamoto, H. Hagiya, M. Ojima, Y. Akeda, O. Tasaki, K. Tomono, T. ShimazuP006 - Chemiluminescent intensity assessed by eaa predicts the incidence of postoperative infectious complications following gastrointestinal surgeryS. Ono, T. Kubo, S. Suda, T. Ueno, T. IkedaP007 - Serial change of c1 inhibitor in patients with sepsis – A prospective observational studyT. Hirose, H. Ogura, H. Takahashi, M. Ojima, J. Kang, Y. Nakamura, T. Kojima, T. ShimazuP008 - Comparison of bacteremia and sepsis on sepsis related biomarkersT. Ikeda, S. Suda, Y. Izutani, T. Ueno, S. OnoP009 - The changes of procalcitonin levels in critical patients with abdominal septic shock during blood purificationT. Taniguchi, M. OP010 - Validation of a new sensitive point of care device for rapid measurement of procalcitoninC. Dinter, J. Lotz, B. Eilers, C. Wissmann, R. LottP011 - Infection biomarkers in primary care patients with acute respiratory tract infections – Comparison of procalcitonin and C-reactive proteinM. M. Meili, P. S. SchuetzP012 - Do we need a lower procalcitonin cut off?H. Hawa, M. Sharshir, M. Aburageila, N. SalahuddinP013 - The predictive role of C-reactive protein and procalcitonin biomarkers in central nervous system infections with extensively drug resistant bacteriaV. Chantziara, S. Georgiou, A. Tsimogianni, P. Alexandropoulos, A. Vassi, F. Lagiou, M. Valta, G. Micha, E. Chinou, G. MichaloudisP014 - Changes in endotoxin activity assay and procalcitonin levels after direct hemoperfusion with polymyxin-b immobilized fiberA. Kodaira, T. Ikeda, S. Ono, T. Ueno, S. Suda, Y. Izutani, H. ImaizumiP015 - Diagnostic usefullness of combination biomarkers on ICU admissionM. V. De la Torre-Prados, A. Garcia-De la Torre, A. Enguix-Armada, A. Puerto-Morlan, V. Perez-Valero, A. Garcia-AlcantaraP016 - Platelet function analysis utilising the PFA-100 does not predict infection, bacteraemia, sepsis or outcome in critically ill patientsN. Bolton, J. Dudziak, S. Bonney, A. Tridente, P. NeeP017 - Extracellular histone H3 levels are in...
Research demonstrates that the majority of alarms derived from continuous bedside monitoring devices are non-actionable. This avalanche of unreliable alerts causes clinicians to experience sensory overload when attempting to sort real from false alarms, causing desensitization and alarm fatigue, which in turn leads to adverse events when true instability is neither recognized nor attended to despite the alarm. The scope of the problem of alarm fatigue is broad, and its contributing mechanisms are numerous. Current and future approaches to defining and reacting to actionable and non-actionable alarms are being developed and investigated, but challenges in impacting alarm modalities, sensitivity and specificity, and clinical activity in order to reduce alarm fatigue and adverse events remain. A multi-faceted approach involving clinicians, computer scientists, industry, and regulatory agencies is needed to battle alarm fatigue.
OBJECTIVE Use machine-learning (ML) algorithms to classify alerts as real or artifacts in online noninvasive vital sign (VS) data streams to reduce alarm fatigue and missed true instability. METHODS Using a 24-bed trauma step-down unit’s non-invasive VS monitoring data (heart rate [HR], respiratory rate [RR], peripheral oximetry [SpO2]) recorded at 1/20Hz, and noninvasive oscillometric blood pressure [BP] less frequently, we partitioned data into training/validation (294 admissions; 22,980 monitoring hours) and test sets (2,057 admissions; 156,177 monitoring hours). Alerts were VS deviations beyond stability thresholds. A four-member expert committee annotated a subset of alerts (576 in training/validation set, 397 in test set) as real or artifact selected by active learning, upon which we trained ML algorithms. The best model was evaluated on alerts in the test set to enact online alert classification as signals evolve over time. MAIN RESULTS The Random Forest model discriminated between real and artifact as the alerts evolved online in the test set with area under the curve (AUC) performance of 0.79 (95% CI 0.67-0.93) for SpO2 at the instant the VS first crossed threshold and increased to 0.87 (95% CI 0.71-0.95) at 3 minutes into the alerting period. BP AUC started at 0.77 (95%CI 0.64-0.95) and increased to 0.87 (95% CI 0.71-0.98), while RR AUC started at 0.85 (95%CI 0.77-0.95) and increased to 0.97 (95% CI 0.94–1.00). HR alerts were too few for model development. CONCLUSIONS ML models can discern clinically relevant SpO2, BP and RR alerts from artifacts in an online monitoring dataset (AUC>0.87).
Tachycardia is a strong though non-specific marker of cardiovascular stress that proceeds hemodynamic instability. We designed a predictive model of tachycardia using multi-granular intensive care unit (ICU) data by creating a risk score and dynamic trajectory. A subset of clinical and numerical signals were extracted from the Multiparameter Intelligent Monitoring in Intensive Care II database. A tachycardia episode was defined as heart rate ≥ 130/min lasting for ≥ 5 min, with ≥ 10% density. Regularized logistic regression (LR) and random forest (RF) classifiers were trained to create a risk score for upcoming tachycardia. Three different risk score models were compared for tachycardia and control (non-tachycardia) groups. Risk trajectory was generated from time windows moving away at 1 min increments from the tachycardia episode. Trajectories were computed over 3 hours leading up to the episode for three different models. From 2809 subjects, 787 tachycardia episodes and 707 control periods were identified. Patients with tachycardia had increased vasopressor support, longer ICU stay, and increased ICU mortality than controls. In model evaluation, RF was slightly superior to LR, which accuracy ranged from 0.847 to 0.782, with area under the curve from 0.921 to 0.842. Risk trajectory analysis showed average risks for tachycardia group evolved to 0.78 prior to the tachycardia episodes, while control group risks remained < 0.3. Among the three models, the internal control model demonstrated evolving trajectory approximately 75 min before tachycardia episode. Clinically relevant tachycardia episodes can be predicted from vital sign time series using machine learning algorithms.
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