Wearable Sensors and Machine Learning for Hypovolemia Problems in Occupational, Military and Sports Medicine: Physiological Basis, Hardware and Algorithms

Hypovolemia is a physiological state of reduced blood volume that can exist as either (1) absolute hypovolemia because of a lower circulating blood (plasma) volume for a given vascular space (dehydration, hemorrhage) or (2) relative hypovolemia resulting from an expanded vascular space (vasodilation) for a given circulating blood volume (e.g., heat stress, hypoxia, sepsis). This paper examines the physiology of hypovolemia and its association with health and performance problems common to occupational, military and sports medicine. We discuss the maturation of individual-specific compensatory reserve or decompensation measures for future wearable sensor systems to effectively manage these hypovolemia problems. The paper then presents areas of future work to allow such technologies to translate from lab settings to use as decision aids for managing hypovolemia. We envision a future that incorporates elements of the compensatory reserve measure with advances in sensing technology and multiple modalities of cardiovascular sensing, additional contextual measures, and advanced noise reduction algorithms into a fully wearable system, creating a robust and physiologically sound approach to manage physical work, fatigue, safety and health issues associated with hypovolemia for workers, warfighters and athletes in austere conditions.

Utilization and Efficacy of Resuscitation Endpoints in Trauma and Burn Patients: A Review Article

Shock is a sequelae in trauma and burn patients that substantially increases the risk for morbidity and mortality. The use of resuscitation endpoints allows for improved management of these patients, with the potential to prevent further morbidity/mortality. We conducted a review of the current literature on the efficacy of hemodynamic, metabolic, and regional resuscitation endpoints for use in trauma and burn patients. Hemodynamic endpoints included mean arterial pressure (MAP), heart rate (HR), urinary output (UO), compensatory reserve index (CRI), intrathoracic blood volume, and stroke volume variation (SVV). Metabolic endpoints measure cellular responses to decreased oxygen delivery and include serum lactic acid (LA), base deficit (BD), bicarbonate, anion gap, apparent strong ion difference, and serum pH. Mean arterial pressure, HR, UO, and LA are the most established markers of trauma and burn resuscitation. The evidence suggests LA is a superior metabolic endpoint marker. Newer resuscitation endpoint technologies such as point-of-care ultrasound (PoCUS), thromboelastography (TEG), and rotational thromboelastometry (ROTEM) may improve patient outcomes; however, additional research is needed to establish the efficacy in trauma and burn patients. The endpoints discussed have situational strengths and weaknesses and no single universal resuscitation endpoint has yet emerged. This review may increase knowledge and aid in guideline development. We recommend clinicians continue to integrate multiple endpoints with emphasis on MAP, HR, UO, LA, and BD. Future investigation should aim to standardize endpoints for each clinical presentation. The search for universal and novel resuscitation parameters in trauma and burns should also continue.

The changes of the tubular epithelium phenotype in the contralateral kidney nephrons while developing unilateral ureteral obstruction: an experimental study

Introduction. The high prevalence of renal diseases caused by urinary tract obstruction led to the need for experimental research of compensatory and pathological processes with kidney injury. It is also of relevance to study key mechanisms providing a compensatory function of the contralateral kidney for early diagnosis, treatment, and prognosis of obstructive renal diseases.Purpose of the study. To examine epithelial nephron cells phenotype dynamics changes in contralateral kidney using unilateral ureteral obstruction experimental model.Materials and methods. Model of unilateral ureteral obstruction was established using adult rabbits. The studies were carried out on days 7, 14 and 21 of complete obstruction of the left ureter. Immunophenotyping was performed on contralateral kidney tissue samples using epithelial (cytokeratin 7, E-cadherin) and mesenchymal (vimentin, α-smooth muscle actin) markers.Results. The contralateral kidney under additional load can maintain the morphological and functional characteristics of the nephron for a long time. The first transmogrify signs in the nephron epithelium phenotype were detected by day 21 as the diffuse appearance of mesenchymal marker vimentin with unaltered visualization of epithelial phenotype markers.Conclusion. The results obtained allow us to assume that the compensatory reserve of the contralateral kidney is gradually decreasing when the duration of the obstruction increases. Thus, the likelihood of developing negative disorders increases.

Age-associated determinants decompensation of the bladder in the conditions of prostate hyperplasia

Introduction. In conditions of long-term infravesical obstruction caused by prostate hyperplasia (РН), 15-30% of patients eventually experience decompensation of detrusor function. At the same time, the details of the adaptive transformation of the vascular bed of the bladder, as well as its correlation with the structural remodeling of this organ, which determine the decompensation of the lower urinary tract in conditions of chronic urinary retention, are still unclear. Aim. To study the role of vascular and age-related factors in the depletion of the compensatory reserve of detrusor in long-term РН in elderly and senile people. Material and methods. Autopsy material from 25 men who did not have urological pathology, from 25 men who had РН without signs of decompensation of the bladder and biopsy material from 25 patients operated on for РН in the decompensation stage were examined. The age of all persons ranged from 60 to 80 years. Control – 10 men aged 20-30 years, who died as a result of injuries. Histological sections of the areas of the bladder were stained with hematoxylin-eosin, according to Mason and Hart. Results. In conditions of long-term РН, the functioning of a locally hypertrophic detrusor occurs against the background of age-related atrophic-sclerotic changes in it, the cause of which is: atherosclerosis of large arteries, as well as hyalinosis of small arteries and arterioles, characteristic of arterial hypertension. The «working capacity» of the bladder under these conditions is provided by the activity of regulatory muscle formations in the arterial and venous basins, with the help of which the necessary level of oxygenation is achieved. However, progressive age-related changes in the cardiovascular system over time lead to an increase in chronic ischemia. Sclerotic changes develop in the regulatory structures of the arteries and veins. As a result, there is a gross diffuse sclerosis of the detrusor with atrophy of the muscle fibers. Conclusions. Decompensation of detrusor in РН is a consequence of earlier vascular decompensation, the morphological markers of which are: arteriosclerosis, phlebosclerosis and sclerosis of regulatory structures.

Intracranial pressure waveform characteristics in idiopathic normal pressure hydrocephalus and late-onset idiopathic aqueductal stenosis

Background Idiopathic normal pressure hydrocephalus (iNPH) and late-onset idiopathic aqueductal stenosis (LIAS) are two forms of chronic adult hydrocephalus of different aetiology. We analysed overnight intracranial pressure (ICP) monitoring to elucidate ICP waveform changes characteristic for iNPH and LIAS to better understand pathophysiological processes of both diseases. Methods 98 patients with iNPH and 14 patients with LIAS from two neurosurgical centres were included. All patients underwent diagnostic overnight computerised ICP monitoring with calculation of mean ICP, ICP heartbeat related pulse wave amplitude calculated in the frequency domain (AMP) and the time domain (MWA), index of cerebrospinal compensatory reserve (RAP) and power of slow vasogenic waves (SLOW). Results ICP was higher in LIAS than iNPH patients (9.3 ± 3.0 mmHg versus 5.4 ± 4.2 mmHg, p = 0.001). AMP and MWA were higher in iNPH versus LIAS (2.36 ± 0.91 mmHg versus 1.81 ± 0.59 mmHg for AMP, p = 0.012; 6.0 ± 2.0 mmHg versus 4.9 ± 1.2 mmHg for MWA, p = 0.049). RAP and SLOW indicated impaired reserve capacity and compliance in both diseases, but did not differ between groups. INPH patients were older than LIAS patients (77 ± 6 years versus 54 ± 14 years, p < 0.001). Conclusions ICP is higher in LIAS than in iNPH patients, likely due to the chronically obstructed CSF flow through the aqueduct, but still in a range considered normal. Interestingly, AMP/MWA was higher in iNPH patients, suggesting a possible role of high ICP pulse pressure amplitudes in iNPH pathophysiology. Cerebrospinal reserve capacity and intracranial compliance is impaired in both groups and the pressure-volume relationship might be shifted towards lower ICP values in iNPH. The physiological influence of age on ICP and AMP/MWA requires further research.