First of all, cerebral embolism refers to various kinds of emboli in blood (such as attached thrombus in the heart, atherosclerotic plaque, fat, tumor cells, fibrocartilage or air, etc.) entering the cerebral artery with blood and blocking the blood vessel, causing ischemic necrosis of brain tissue in the blood supply area of that artery and focal neurological deficits when the collateral circulation cannot compensate. Cerebral embolism accounts for about 15-20% of strokes. It can develop at any age and usually has no obvious cause and few prodromal symptoms before onset. The onset is very rapid, with symptoms often peaking within seconds or minutes, and the rate of disability and death is very high. So what kind of patients are prone to this condition? There are many types of emboli in cerebral embolism, which can be induced by emboli produced by various diseases entering the bloodstream and blocking blood vessels. And heart disease is the most common cause of cerebral embolism. Rheumatic heart disease mitral valve stenosis, enlarged left atrium, slow and stagnant blood flow in the heart, easy to make blood clotting and thrombus formation. When the blood flow is irregular or atrial fibrillation occurs, this attached thrombus is easily dislodged to form emboli and cerebral embolism occurs. In bacterial endocarditis, due to endothelial or subendothelial lesions, bacteria often attach to the endothelium and multiply, and collect with platelets, red blood cells, hemoglobin, etc. to form bacterial redundancies, which are dislodged and enter the skull with the blood, and cerebral embolism can also occur. In myocardial infarction, the endocardium of atria and ventricles can be injured, and the injured endocardium is prone to wall thrombus, and under the action of atrial fibrillation and other factors, the thrombus is dislodged to form emboli, which also often causes cerebral embolism. In addition, congenital heart disease, cardiac mucinous tumor, and cardiac surgery are also causes of cardiogenic cerebral embolism. The more common non-cardiogenic emboli are fat emboli and air emboli. When long bone fracture, or due to fracture surgery, the fat globules in bone marrow enter the blood, which is easy to form fat embolism; while gas embolism is common in open trauma and surgery of chest and neck, artificial pneumothorax, pneumoperitoneum and improper decompression of divers and pilots, which forms nitrogen embolism; in addition, pulmonary vein embolism, cerebral vein embolism are also causes of non-cardiogenic cerebral embolism. How to prevent the occurrence of cerebral embolism? Most patients, their relatives and friends, and some medical personnel think or expect more about better drugs (in fact, the role of drugs used for cerebral embolism treatment is very limited) to make patients recover sooner, but neglect other aspects of treatment. For example, the patient’s diet, because a considerable number of cerebral embolism patients can’t take care of themselves and even can’t eat (because of swallowing difficulty), if they are not given nasal feeding (a tube is inserted into the stomach through the nose and food is injected directly into the stomach through this tube), the patient’s nutrition and body metabolism will have new problems soon, so it is difficult to receive good treatment effect even if the treatment of cerebral embolism itself is good with drugs. Therefore, the patient’s life care, diet, and the management of other comorbidities should be given top priority. The treatment principle of cerebral embolism itself is to improve cerebral circulation, prevent re-embolism, eliminate cerebral edema, and protect cerebral function. Anticoagulation, thrombolysis and other treatments are only useful in the early stage of the disease, so early treatment is more emphasized. Anticoagulants such as subcutaneous injection of low-molecular heparin (less side effects) have certain therapeutic effects on early cerebral embolism. Because anticoagulants (especially heparin) cause side effects of bleeding, cerebral hemorrhage should be excluded when applying them, and attention should be paid to monitoring patients’ blood coagulation status. Thrombolytic drugs (such as urokinase, streptokinase, etc.) may also work only in the early stage. When using vasodilators and blood pressure-lowering drugs, the patient’s blood pressure must be paid attention to, as low blood pressure caused by such drugs will lead to further worsening of cerebral ischemia, which should be paid great attention to. Low molecular dextran can help reduce blood viscosity, and hypertonic dehydrating agents such as mannitol can relieve cerebral edema, but attention should be paid to the patient’s heart function and kidney function when applying them to avoid losing sight of this.