Publications

Massive hemorrhage remains the primary cause of potentially preventable death in traumatic injuries. Monitoring hemorrhage and resuscitation accurately can improve outcomes but continues to be challenging since traditional vital signs are highly compensated by the body. Previous work has developed physiologically interpretable algorithms to assess volume status in simulated models of hemorrhage and resuscitation. In this paper, we further develop these algorithms to assess volume status in a nonhuman primate model of controlled blood loss and subsequent whole-blood resuscitation. We acquired arterial blood pressure (ABP) waveform data on 12 adult male baboons during a step-and-hold protocol for hemorrhage and a constant resuscitation rate. A gradient-boosted regression tree model trained on only the ejected-wave pulse area (EWPA) feature yielded a 19% root-mean-square-error (RMSE), 0.71 R2, and an area under the receiver operating characteristic curve of ≥ 0.9 for key operating points of volume status. The performance of this model with a single feature compares well to results reported previously from single-feature machine-learning (ML) models as well as more complex machine learning models that are difficult to interpret and computationally intensive. This study is the first investigation of these physiologically interpretable models on invasively measured ABP waveforms.

Goal: Non-compressible torso hemorrhage represents a category of lethal injuries in both civilian and military traumatically injured populations that with proper intervention, training, or technological advancements are survivable. Endovascular localization of active bleeding in the pre-hospital setting can allow faster, less invasive, and more accurate applications of life-saving interventions. In this paper, we report initial in vivo and in silico experimental results to test the feasibility of endovascular localization of hemorrhage. Methods: Endovascular pressure waveforms were acquired on five pigs with an induced aortic injury via a custom intra-aortic catheter instrumented with four pressure sensors. Pressure and velocity data were then simulated on an in silico human aortic model with the same kind of injury. Results: A decrease in pulse pressure across the injury (proximal to distal) reliably indicated the injury location to within a few centimeters. The simulated model showed a similar decrease in pulse pressure as well as an increase in velocity. Conclusions: With additional refinement, localization accuracy may be sufficient for application of a modern covered stent to stop bleeding. The simulated model results indicate relevance for humans and provide guidance for future experiments.

Assessment of trauma-induced hemorrhage with ultrasound is particularly challenging outside of the clinic, where its detection is crucial. The current clinical standard for hematoma detection – the focused assessment with sonography of trauma (FAST) exam – does not aim to detect ongoing blood loss, and thus is unable to detect injuries of increasing severity. To enhance detection of active bleeding, we propose the use of ultrasound contrast agents (UCAs), together with a novel flow phantom and contrast-sensitive processing techniques, to facilitate efficient, practical characterization of internal bleeding. Within a the custom phantom, UCAs and processing techniques enabled a significant enhancement of the hemorrhage visualization (mean increase in generalized contrast-to-noise ratio of 17 %) compared to the contrast-free case over a range of flow rates up to 40 ml/min. Moreover, we have shown that the use of UCAs improves the probability of detection: the area under the receiver operating characteristic curve for a flow rate of 40 ml/min was 0.99, compared to 0.72 without contrast. We also demonstrate how additional processing of the spatial and temporal information further localizes the bleeding site. UCAs also enhanced Doppler signals over the non-contrast case. These results show that specialized nonlinear processing (NLP) pipelines together with UCAs may offer an efficient means to improve substantially the detection of slower hemorrhages and increase survival rates for trauma-induced injury in pre-hospital settings.

Hemorrhage is the leading cause of preventable death from trauma. Accurate monitoring of hemorrhage and resuscitation can significantly reduce mortality and morbidity but remains a challenge due to the low sensitivity of traditional vital signs in detecting blood loss and possible hemorrhagic shock. Vital signs are not reliable early indicators because of physiological mechanisms that compensate for blood loss and thus do not provide an accurate assessment of volume status. As an alternative, machine learning (ML) algorithms that operate on an arterial blood pressure (ABP) waveform have been shown to provide an effective early indicator. However, these ML approaches lack physiological interpretability. In this paper, we evaluate and compare the performance of ML models trained on nine ABP-derived features that provide physiological insight, using a database of 13 human subjects from a lower-body negative pressure (LBNP) model of progressive central hypovolemia and subsequent progressive restoration to normovolemia (i.e., simulated hemorrhage and whole blood resuscitation). Data were acquired at multiple repressurization rates for each subject to simulate varying resuscitation rates, resulting in 52 total LBNP collections. This work is the first to use a single ABP-based algorithm to monitor both simulated hemorrhage and resuscitation. A gradient-boosted regression tree model trained on only the half-rise to dicrotic notch (HRDN) feature achieved a root-mean-square error (RMSE) of 13%, an R2 of 0.82, and area under the receiver operating characteristic curve of 0.97 for detecting decompensation. This single-feature model's performance compares favorably to previously reported results from more-complex black box machine learning models. This model further provides physiological insight because HRDN represents an approximate measure of the delay between the ABP ejected and reflected wave and therefore is an indication of cardiac and peripheral vascular mechanisms that contribute to the compensatory response to blood loss and replacement.