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Background: In recent years, the volume of medical knowledge and health data has increased rapidly. For example, the increased availability of electronic health records (EHRs) provides accurate, up-to-date, and complete information about patients at the point of care and enables medical staff to have quick access to patient records for more coordinated and efficient care. With this increase in knowledge, the complexity of accurate, evidence-based medicine tends to grow all the time. Health care workers must deal with an increasing amount of data and documentation. Meanwhile, relevant patient data are frequently overshadowed by a layer of less relevant data, causing medical staff to often miss important values or abnormal trends and their importance to the progression of the patient’s case.
Objective: The goal of this work is to analyze the current laboratory results for patients in the intensive care unit (ICU) and classify which of these lab values could be abnormal the next time the test is done. Detecting near-future abnormalities can be useful to support clinicians in their decision-making process in the ICU by drawing their attention to the important values and focus on future lab testing, saving them both time and money. Additionally, it will give doctors more time to spend with patients, rather than skimming through a long list of lab values.
Methods: We used Structured Query Language to extract 25 lab values for mechanically ventilated patients in the ICU from the MIMIC-III and eICU data sets. Additionally, we applied time-windowed sampling and holding, and a support vector machine to fill in the missing values in the sparse time series, as well as the Tukey range to detect and delete anomalies. Then, we used the data to train 4 deep learning models for time series classification, as well as a gradient boosting–based algorithm and compared their performance on both data sets.
Results: The models tested in this work (deep neural networks and gradient boosting), combined with the preprocessing pipeline, achieved an accuracy of at least 80% on the multilabel classification task. Moreover, the model based on the multiple convolutional neural network outperformed the other algorithms on both data sets, with the accuracy exceeding 89%.
Conclusions: In this work, we show that using machine learning and deep neural networks to predict near-future abnormalities in lab values can achieve satisfactory results. Our system was trained, validated, and tested on 2 well-known data sets to ensure that our system bridged the reality gap as much as possible. Finally, the model can be used in combination with our preprocessing pipeline on real-life EHRs to improve patients’ diagnosis and treatment.
Life-threatening cardiomyopathy is a severe, but common, complication associated with severe trauma or sepsis. Several signaling pathways involved in apoptosis and necroptosis are linked to trauma- or sepsis-associated cardiomyopathy. However, the underling causative factors are still debatable. Heparan sulfate (HS) fragments belong to the class of danger/damage-associated molecular patterns liberated from endothelial-bound proteoglycans by heparanase during tissue injury associated with trauma or sepsis. We hypothesized that HS induces apoptosis or necroptosis in murine cardiomyocytes. By using a novel Medical-In silico approach that combines conventional cell culture experiments with machine learning algorithms, we aimed to reduce a significant part of the expensive and time-consuming cell culture experiments and data generation by using computational intelligence (refinement and replacement). Cardiomyocytes exposed to HS showed an activation of the intrinsic apoptosis signal pathway via cytochrome C and the activation of caspase 3 (both p < 0.001). Notably, the exposure of HS resulted in the induction of necroptosis by tumor necrosis factor α and receptor interaction protein 3 (p < 0.05; p < 0.01) and, hence, an increased level of necrotic cardiomyocytes. In conclusion, using this novel Medical-In silico approach, our data suggest (i) that HS induces necroptosis in cardiomyocytes by phosphorylation (activation) of receptor-interacting protein 3, (ii) that HS is a therapeutic target in trauma- or sepsis-associated cardiomyopathy, and (iii) indicate that this proof-of-concept is a first step toward simulating the extent of activated components in the pro-apoptotic pathway induced by HS with only a small data set gained from the in vitro experiments by using machine learning algorithms.