Dataset Information

Enabling the assessment of trauma-induced hemorrhage via smart wearable systems.

ABSTRACT: As the leading cause of trauma-related mortality, blood loss due to hemorrhage is notoriously difficult to triage and manage. To enable timely and appropriate care for patients with trauma, this work elucidates the externally measurable physiological features of exsanguination, which were used to develop a globalized model for assessing blood volume status (BVS) or the relative severity of blood loss. These features were captured via both a multimodal wearable system and a catheter-based reference and used to accurately infer BVS in a porcine model of hemorrhage (n = 6). Ultimately, high-level features of cardiomechanical function were shown to strongly predict progression toward cardiovascular collapse and used to estimate BVS with a median error of 15.17 and 18.17% for the catheter-based and wearable systems, respectively. Exploring the nexus of biomedical theory and practice, these findings lay the groundwork for digital biomarkers of hemorrhage severity and warrant further study in human subjects.

SUBMITTER: Zia J

PROVIDER: S-EPMC7375804 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Enabling the assessment of trauma-induced hemorrhage via smart wearable systems.

Zia Jonathan J Kimball Jacob J Rolfes Christopher C Hahn Jin-Oh JO Inan Omer T OT

Science advances 20200722 30

As the leading cause of trauma-related mortality, blood loss due to hemorrhage is notoriously difficult to triage and manage. To enable timely and appropriate care for patients with trauma, this work elucidates the externally measurable physiological features of exsanguination, which were used to develop a globalized model for assessing blood volume status (BVS) or the relative severity of blood loss. These features were captured via both a multimodal wearable system and a catheter-based referen ...[more]

PMID: 32766449

Similar Datasets

Project description:Complex biological processes such as acute inflammation induced by trauma/hemorrhagic shock/ (T/HS) are dynamic and multi-dimensional. We utilized multiplexing cytokine analysis coupled with data-driven modeling to gain a systems perspective into T/HS.Mice were subjected to surgical cannulation trauma (ST) ± hemorrhagic shock (HS; 25 mmHg), and followed for 1, 2, 3, or 4 h in each case. Serum was assayed for 20 cytokines and NO(2) (-)/NO(3) (-). These data were analyzed using four data-driven methods (Hierarchical Clustering Analysis [HCA], multivariate analysis [MA], Principal Component Analysis [PCA], and Dynamic Network Analysis [DyNA]). Using HCA, animals subjected to ST vs. ST + HS could be partially segregated based on inflammatory mediator profiles, despite a large overlap. Based on MA, interleukin [IL]-12p40/p70 (IL-12.total), monokine induced by interferon-? (CXCL-9) [MIG], and IP-10 were the best discriminators between ST and ST/HS. PCA suggested that the inflammatory mediators found in the three main principal components in animals subjected to ST were IL-6, IL-10, and IL-13, while the three principal components in ST + HS included a large number of cytokines including IL-6, IL-10, keratinocyte-derived cytokine (CXCL-1) [KC], and tumor necrosis factor-? [TNF-?]. DyNA suggested that the circulating mediators produced in response to ST were characterized by a high degree of interconnection/complexity at all time points; the response to ST + HS consisted of different central nodes, and exhibited zero network density over the first 2 h with lesser connectivity vs. ST at all time points. DyNA also helped link the conclusions from MA and PCA, in that central nodes consisting of IP-10 and IL-12 were seen in ST, while MIG and IL-6 were central nodes in ST + HS.These studies help elucidate the dynamics of T/HS-induced inflammation, complementing other forms of dynamic mechanistic modeling. These methods should be applicable to the analysis of other complex biological processes.

Project description:The etiology of trauma-hemorrhage shock-induced acute lung injury has been difficult to elucidate due, at least in part, to the inability of in vivo studies to separate the non-injurious pulmonary effects of trauma-hemorrhage from the tissue injurious ones. To circumvent this in vivo limitation, we utilized a model of trauma-hemorrhagic shock (T/HS) in which T/HS-lung injury was abrogated by dividing the mesenteric lymph duct. In this way, it was possible to separate the pulmonary injurious response from the non-injurious systemic response to T/HS by comparing the pulmonary molecular response of rats subjected to T/HS which did and did not develop lung injury as well as to non-shocked rats. Utilizing high-density oligonucleotide arrays and treatment group comparisons of whole lung tissue collected at 3 hours after the end of the shock or sham-shock period, 139 of the 8,799 assessed genes were differentially expressed. Experiment Overall Design: Four groups of rats (n=3) were studied in order to identify changes in pulmonary gene expression associated with T/HS, both in the presence and absence of lung injury. These included trauma-sham shock (T/SS) rats which had a laparotomy (trauma) but were not subjected to hemorrhagic shock. These rats had no lung injury and served as controls for rats which were subjected to T/HS (laparotomy plus 90 min of shock) and had lung injury. Differences in gene expression between these two groups would represent both the effects of hemorrhagic shock as well as lung injury. To distinguish the gene response of hemorrhagic shock from the gene response associated with lung injury, gene expression was also compared between T/HS rats (hemorrhage and lung injury) and rats subjected to T/HS plus lymph duct ligation (T/HS-LDL), since the T/HS-LDL rats experienced hemorrhagic shock but had no measurable lung injury. Lastly, to identify hemorrhagic shock- modified genes, the pulmonary gene response of T/HS-LDL (hemorrhage without lung injury) were compared to rats subjected to T/SS plus LDL (no hemorrhage or lung injury). Three hours after the end of the 90 min shock or sham-shock period (i.e. 4.5 hrs after the induction of T/HS), the rats were sacrificed and specimens harvested for genechip analysis and histology.

Dataset Information

Enabling the assessment of trauma-induced hemorrhage via smart wearable systems.

Publications

Enabling the assessment of trauma-induced hemorrhage via smart wearable systems.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets