**2. Pathophysiology**

Diabetic peripheral neuropathy (loss of sensation) occurs typically 8–12 years after the onset of type 2 diabetes and is a tolerant factor for the development of ulcers. Diabetic peripheral neuropathy is a disorder of normal nerve activity throughout the body and can alter autonomic, motor, and sensory function [6]. Hyperglycemic conditions increase the production of several enzymes such as aldose reductase and sorbitol dehydrogenase. These enzymes convert glucose into sorbitol and fructose. The accumulation of these sugar products interferes with the synthesis of myo-inositol in nerve cells and impairs nerve conduction. In addition, hyperglycemic-induced microangiopathy results in reversible metabolic, motor and sensory nerve, immunological and ischemic damage leads to the autonomic nervous system dysfunction. It provokes low peripheral sensation and compensates for fine vasomotor control of pedal circulation and innervation of the small foot muscles. If the nerve is damaged, there is a risk of minor injuries, and when it is unnoticed an ulcer develops [7].

The microcirculation of the skin is controlled by the autonomic nervous system, when disturbed in Diabetes causes dryness and cracking of the skin, making it more susceptible to infections. These changes can help spread gangrene, ulcers, and loss of limbs [8, 9]. Hyperglycemia causes endothelial cell dysfunction, and smooth cell abnormalities in peripheral dysfunction include altered endothelial cell proliferation, basal membrane thickening, decreased nitrogen monoxide synthesis, increased blood density, altered microvascular tone, and blood flow. Clinically the case may have signs of vascular insufficiency such as claudication, night pain or rest pain, absent peripheral pulses, thinning of the skin, loss of limb hair, etc. [6].
