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Put Patients on Better Care Trajectories

Circulatory and pulmonary breakdowns in critical care are key drivers of adverse events and prolonged lengths of stay

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Circulatory breakdown occurs because the blood vessels become compressed, restricting blood flow

Research has demonstrated
a variety of harmful physiological effects resulting from circulatory and pulmonary breakdown

Higher adverse event risk
Prolonged length of stay
Inflammatory mediator release
Increased pain and discomfort

Introducing Vasotactic™ technology

We at TurnCare developed a patented Vasotactic™ technology, which provides precise, anatomy-specific therapy.
 
Our Vasotactic™ support therapy prevents vessels in the sacral region from becoming compressed, thereby avoiding circulatory breakdown.

Vasotactic™ works in all positions to enable improved pulmonary health 
with no trade off to circulatory health.

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A Different Approach

Geometry

Support surface that knows bony prominence location

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Algorithm

Non-repeating therapy algorithm that gives sacral vessels time to spring back to shape

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Precision

Adapts uniquely to each patient and underlying surface in real time

Traditional pressure redistribution beds, overlays, and cushions were not designed to prevent sacral-region vascular compression

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These surfaces were designed to spread pressure across pre-set locations without understanding the characteristics of the patients' sacral anatomy, the location of the bony prominences, or the physiology of human vasculature

References:

Bharucha JB, Seaman L, Powers M, Kelly E, Seaman R, Forcier L, ... & Wang L. A prospective randomized clinical trial of a novel, noninvasive perfusion enhancement system for the prevention of hospital-acquired sacral pressure injuries. Journal of Wound Ostomy & Continence Nursing. 2018;45(4);310-318.

 

Doll DN, Barr TL, Simpkins JW. Cytokines: Their role in stroke and potential use as biomarkers and therapeutic targets. Aging and Disease. 2014;5(5);294-306.

Eltzschig HK, Eckle T. Ischemia and reperfusion–from mechanism to translation. Nature medicine. 2011;17:1391–1401.

Kalogeris T, Baines CP, Krenz, M, Korthuis, RJ. Cell biology of ischemia/reperfusion injury. Int Rev Cell Mol Biol. 2012;298;229-317. 

Needham DM. Mobilizing patients in the intensive care unit: improving neuromuscular weakness and physical function. JAMA. 2008;300:1685–1690.

Parker A, Sricharoenchai T, Needham DM. Early rehabilitation in the intensive care unit: preventing physical and mental health impairments. Curr Phys Med Rehabil Rep. 2013;1(4):307–314.

Payen D, Lukaszewicz AC, Legrand M, Gayat E, Faiyre V, et al. A multicentre study of acute kidney injury in severe sepsis and septic shock: Association with inflammatory phenotype and HLA genotype. PLos ONE. 2012;7(6);e35838.

Pierce SM, Skalak TC, Rodeheaver GT. Ischemia-reperfusion injury in chronic pressure ulcer formation: a skin model in the rat. Wound Repair and Regeneration. 2000;8(1);68-76.

Truong A, Fan E, Brower R, Needham D. Bench-to-bedside review: mobilizing patients in the intensive care unit—from pathophysiology to clinical trials. Crit Care. 2009;13:216.

Zhang JM, An J. Cytokines, inflammation, and pain. International anesthesiology clinics. 2007;45(2);27-37.

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