Utilising novel interventions to enhance vascular function with applications for pressure injury prevention

The purpose of this thesis was to identify and investigate novel approaches to enhance vascular function and subsequently delay the onset of pressure injuries in vulnerable populations. Pressure injuries, also known as pressure ulcers or bedsores, represent a significant cost within healthcare settings due to their high prevalence and associated complications. Despite various preventative measures and guidelines in place, the challenge of delaying their onset remains ever present and in recent years could be seen to have lacked innovation. Hence, this thesis comprises of a multifaceted exploration aimed at investigating innovative interventions targeting vascular function to mitigate the risk of developing pressure injuries.

A review of the current literature inspired the design and manufacture of a custom skin deformation device which would be used throughout the thesis to measure the vascular health of both healthy and clinical populations. To complement the device, a novel stepwise pressure application protocol was developed to measure various aspects of skin blood flow, these being (1) baseline skin blood flow; (2) blood flow at 42°C; (3) skin blood flow under increasing externally applied pressures; (4) post direct pressure reactive skin blood flow. Throughout the thesis, this combination of device and protocol were employed to assess the efficacy of three physiological interventions thought to be able to improve vascular health and delay the onset of pressure injuries in an at-risk clinical population. These interventions were (1) improved diet via acute nitrate supplementation (Chapter 4); (2) passive heating via localised hot water immersion of the lower legs (Chapter 5); (3) increased exercise levels in a spinal cord injured population via neuromuscular electrical stimulation resistance training (Chapter 7). While the main body of the experimental studies revolved around assessing the three novel interventions, work was also carried out quantifying how different levels of externally applied heat and pressure affected both loaded and reactive skin blood flow (Chapter 3) and comparing the skin blood flow at the sacrum of a healthy and spinal cord injured population (Chapter 6).

While the novel interventions did not improve vascular health to a degree which may delay the onset of pressure injuries, there were novel findings throughout the thesis. Namely, how direct pressure reactive hyperaemia continues to increase in magnitude under increasing levels of externally applied pressure, despite a plateau in ischaemia. Basal levels of nitrite in venous blood differs depending on anatomical location. Direct pressure reactive hyperaemia in a spinal cord injured population is significantly larger than that of a healthy population following the same pressure application stimulus. Finally, decreased soft tissue mass leads to skin blood flow having a lower resistance to externally applied pressure.

In the future, these novel findings will help researchers better understand the complex aetiology of pressure injury genesis, and hopefully inform the design of pressure injury prevention technology, methodologies, or interventions.