The blood glucose level in acute cerebral infarction and the prognosis of type 2 diabetes mellitus can involve medium and small arteries, capillaries, and veins. On this basis, multiple organ damage is often complicated. If blood glucose is inadequately controlled, blood viscosity, erythrocyte aggregation enhancement, coagulation factors, and fibrinogen increase the extent of atherosclerosis and accelerate thrombosis. Diabetic patients are in a hypercoagulable state with enhanced platelet activation due to diabetes, which may be repeated as a concurrent pathological factor for cerebral infarction. Additionally, acute cerebral infarction can cause stress-induced hyperglycemia, leading to a vicious cycle. Therefore, the higher the blood sugar, the more severe the condition. The data also indicate that: the recovery of blood glucose levels correlates with prognosis; continued rise in blood sugar leads to poor prognosis and high mortality. This may be due to cerebral ischemia in the hyperglycemic state causing excessive sugar and oxygen deficiency in the affected area. Anaerobic metabolism increases, leading to the accumulation of lactic acid and other acidic substances, decreasing the pH value, causing vasodilation, over-perfusion syndrome, and failure of brain energy metabolism. Brain edema increases, expanding the infarction area, resulting in exacerbation. Monitoring and timely control of blood glucose levels can help with the severity and prognosis of acute cerebral infarction in type 2 diabetes mellitus.