Polyposis is one of the most difficult diseases to treat, and there is no systematic and effective treatment method. (1) Fibrin sheath theory: In a series of studies, it was found that the “fibrin obstruction theory” of venous ulcer formation was proposed, also called the “fibrin sheath theory”. Many scholars found that the tissue-type fibrinogen activator (t-PA) of the lower extremity of ulcer patients was reduced, fibrinogen inhibitor (PAI) was increased, and the fibrinolytic capacity of the skin tissue in the ulcer area was significantly reduced. (2) Oxygen diffusion barrier: many scholars made transcutaneous oxygen partial pressure (P02) assay and found that venous ulcer or fatty scleroderma area almost always showed significantly lower P02 than normal skin area. (3) gastrocnemius muscle “pump” insufficiency: it is generally believed that the normal limb gastrocnemius muscle discharges 60-90ml of blood for each contraction, and the foot venous pressure thus decreases by 8kpa. when the gastrocnemius muscle contracts in patients with lower limb venous insufficiency, its “pump “The blood pumping function is abnormal. Under the pathological condition of lower gum venous valve insufficiency or deep vein obstruction, when the gastrocnemius muscle “pump” contraction function is incomplete, the degree of venous pressure decrease is greatly reduced and the time of venous pressure recovery is significantly shortened due to venous blood backflow or venous blood cannot pass through the obstructed deep vein. (4) “Leukocyte accumulation” theory: chronic lower limb venous insufficiency patients in standing or walking, lower limb venous pressure is bound to rise, so that the capillary perfusion pressure is reduced, the flow rate is reduced, thus causing the accumulation of leukocytes. The accumulated leukocytes can release toxic metabolites and protein hydrolases, which make the capillary wall suffer damage, resulting in increased capillary permeability and leukocyte accumulation, plus the former makes fibrinogen exude to form fibrin, which is deposited in the tissue interstitial, and the latter makes capillary embolism, resulting in regional tissue ischemia centered on the affected capillaries. In conclusion, the formation of chronic venous ulcers of the lower extremities is a complex process that is afraid to be explained by a single factor. As seen clinically, some people with severe venous reflux or gastrocnemius ‘pump’ insufficiency may not have ulcer formation. In general, when lower limb venous insufficiency and gastrocnemius “pump” damage exist simultaneously, the former causes lower limb venous system hypertension and aggravates the damage of gastrocnemius “pump” and then affects lower limb venous emptying, thus aggravating lower limb venous hypertension. The consequence is increased capillary wall permeability, which contributes to pathological deposition of fibrin around the capillaries and the formation of small emboli with leukocyte deposits, eventually forming ulcers. Obviously the establishment of the cause of venous ulcers of the lower extremities and the increasing clarity of the pathogenesis will certainly open new ways to improve the cure rate of ulcers, and the effectiveness of many methods and drugs that have been tried in recent years also fully illustrates the clinical significance of the study of the causes of ulcers.