How does the diabetic foot develop? Why do so many diseases, such as hypertension, coronary artery disease or cerebral infarction, only call the foot injury of diabetic patients diabetic foot? And not called hypertensive foot, coronary heart disease foot or cerebral infarction foot? The diabetic foot has its distinctive features. The first complication that generally occurs in diabetic patients is peripheral neuropathy, for example, the patient feels numbness, ants walking, insect crawling, heat, electric shock-like sensation in the lower limbs, often from the distal toes up to the knee, and the patient has a sock and glove-like sensation. That suggests that there are already early symptoms of peripheral neuropathy. As the disease progresses, patients with motor nerve, sensory nerve and autonomic nerve damage, the foot once the loss of nerve protection is vulnerable to injury, or the damage is already there, but the patient can not feel it until very serious. The blood vessels of the lower limbs of diabetic patients are prone to macroangiopathy, microangiopathy and microcirculatory disorders, resulting in narrowing of the vascular cavity and even blockage, which block the blood supply to the foot, so that the oxygen and nutrients needed by the body do not easily reach the foot, and as a result, the tiny injuries to the foot do not easily heal, but instead ulcerate to the deep part of the foot. Infection adds to the damage of the foot, so serious diabetic foot is the result of the interaction of diabetic lower limb peripheral neuropathy, lower limb vasculopathy and infection. Suffice it to say that almost every diabetic foot patient has diabetic peripheral neuropathy, which includes motor neuropathy, sensory neuropathy and autonomic neuropathy. As a result of motor nerve damage in diabetic patients, the imbalance between the extensor and flexor muscles of the foot often causes the plantar fat pad and metatarsal head to sink, even forming a “bowed foot” or “chicken claw toe” deformity. Due to the atrophy of the foot muscles, the normal posture and elasticity of the foot is lost, and the metatarsal area endures heavy pressure when walking. The fat pad that normally protects the metatarsal head is pulled forward by the subluxation of the toes, and the dorsiflexion of the toes at the metatarsophalangeal joint and the bending of the interphalangeal joint form a typical claw toe, which is easily damaged and leads to gangrene due to the poor protection of the soft pad in the small area when walking. After injury to the autonomic nerve of the lower extremity, the skin of the extremity has little or no sweating, and the patient’s foot skin is dry and cracked, which is susceptible to bacterial infection causing ulcers, cellulitis, and deep abscesses. In addition, the autonomic nerve can control skin microbleeds, and the autonomic-mediated physiological effects of changes in peripheral temperature are regulated by insulation or heat dissipation. When the autonomic nerve is injured, which leads to increased skin blood flow especially in the hypophysis, it can lead to edema or atrophy of the skin of the lower extremity, and gangrene can occur. Sensory abnormalities include mainly numbness, pain, burning or radiating pain in the tissues, and impaired or absent sensation in the foot, often leading to penetrating neuropathic ulcers. The foot is dulled and often painless after trauma, and the patient is unaware of the injury or has known the injury but suffers no pain and is negligent and is infected by bacteria to develop severe extremity gangrene. Most local infections in diabetic patients are secondary. Localized infections can have many causes, both local and systemic. For example, skin injury, high-risk foot, foreign body retention in the wound, dead space, and poor drainage. Systemic factors, often related to metabolic disorders, vascular and neurological lesions, malnutrition, decreased immune function and resistance of the body, etc. There are conditions suitable for bacterial growth and reproduction throughout the body or locally for bacteria to survive. Due to the toxic products produced by bacterial toxins or their destroyed necrotic tissues, a series of local or systemic pathophysiological changes can be caused.