Both neuropathy and microvascular complications are major contributors to poor outcomes of diabetic foot disease. The interplay between this neural and microvascular dysfunction in diabetes is elaborate, but poorly understood. A new Australian study observed relationships between clinically apparent peripheral sensory neuropathy, cardiac autonomic function and microvascular reactivity (post-occlusive reactive hyperaemia). They found evidence that those with peripheral sensory neuropathy have a sluggish reactive hyperaemia response to occlusion in the toe.
In a cross-sectional study, the researchers studied 99 people with type 2 diabetes. They identified the presence of peripheral sensory neuropathy with standard clinical tests, and measured cardiac autonomic function and peripheral post-occlusive reactive hyperaemia response. Reactive hyperaemia is the increase in skin and muscle blood flow following release of occlusion. It is one of many measures of microvascular function that are thought to reflect and precede clinically apparent cardiovascular disease. In the feet, increases in blood flow thanks to the microvasculature are required when there is an ulcer, and it may reflect the ability of the skin to mount inflammatory responses. These responses have also been shown to be of interest in the development of Charcot foot.
Surprisingly, this study found the timing to peak response response to be slower in the presence of neuropathy, but the magnitude was similar. This result suggests a co-existing relationship of nerve dysfunction (albeit in those with quite advanced neuropathy determined with unsophisticated testing) and altered microvascular reactivity. The response itself is likely to be the summation of multiple mechanisms, not just neural, and a causal relationship cannot be concluded from this observational study. However, the relationships found may prove to have implications for wound healing and other diabetic foot pathology in the presence of neuropathy, and are another step forward to better understanding the complex interplay between neural and microvascular complications in our patients.
This summary has been written by Alex Barwick