I. What is arterial embolism? Arterial embolism is a blockage of blood flow caused by a blood clot or a foreign body that enters a blood vessel and becomes an embolus, stopping with blood flow in a peripheral artery of similarly small caliber or in an artery of a visceral artery. Arterial embolism is mainly caused by blood clots; in addition, foreign bodies such as tumors, air, and fat may also become emboli. Thrombus is the most common. Ninety percent of blood clots originate from the heart and are commonly seen in rheumatic heart disease, atrial fibrillation, and myocardial infarction. Embolism caused by blood clots often occurs in cardiovascular patients. The sources of embolism are as follows: cardiac origin Many reports indicate that the most frequent cause of peripheral artery embolism is cardiac. Embolism is of cardiac origin in 94% of cases, 77% of which are associated with atrial fibrillation. Atherosclerotic coronary heart disease, including myocardial infarction, atrial fibrillation, congestive heart failure, and ventricular wall aneurysms account for approximately 60% of cases, and rheumatic heart disease accounts for 20%. Rheumatic heart disease and coronary heart disease, both of which have thrombosis within the left heart. In rheumatic heart disease, especially in mitral stenosis, stagnant blood flow in the atria combined with rheumatic lesions in the endothelium predispose fibers in the blood to attach to the atrial wall and form thrombi. Coronary heart disease, especially when myocardial infarction, left ventricle enlargement, contraction weakness, blood can not empty, more prone to thrombus formation. Embolism formed by atheroma of vascular origin and atherosclerotic atheromatous material during atherosclerosis has been reported to increase recently. Large emboli can originate from a mixture of large atheromatous material, thrombus, and cholestyramine crystals that are shed into the arterial circulation. Small emboli are caused by the release of cholestrol crystals or by the shedding of ulcerated atherosclerotic plaques. In recent years, due to the widespread implementation of artificial heart valve conversion and artificial vessel transplantation, placement of pacemakers, arteriography, arteriovenous fistulas for hemodialysis, intra-arterial indwelling catheters, and the application of large arterial counterpulsation balloon catheters, all may cause arterial embolism. Acute arterial embolism can lead to ischemic necrosis of the distal limb, and if the embolism is not lifted in time, serious cases will lead to amputation, and even because of the necrosis of the limb after If the embolism is not released in time, serious cases will lead to amputation and even death due to systemic organ failure caused by the absorption of toxins after limb necrosis. Clinical manifestations Acute arterial embolism without collateral circulation compensation, the disease progresses rapidly. The typical symptoms of acute arterial embolism are pain, pallor, chills, numbness, motor disturbance and weakening and loss of arterial pulsation. The severity of symptoms depends on the location and degree of embolism, the amount of secondary thrombosis, the presence of previous atherosclerotic disease causing arterial stenosis, and the condition of collateral circulation. Pain, which is often the earliest symptom to appear, extends distally with the clasp. Numbness is the first symptom to appear in about 20% of patients, and pain is not obvious. The skin color and temperature change, the blood circulation of the limb is impaired, the skin is waxy pale. If a small amount of blood still accumulates in the blood vessels, scattered small islands of purple spots may appear between the pale skin. With further development of ischemia, the muscles may become rigid, the skin temperature of the affected limb may drop, and the skin may show florid changes or even purple and dark. It is most obvious in the distal part of the limb. The skin temperature change is actually one joint lower than the true embolic plane. In cases of terminal abdominal aortic embolism, the skin temperature changes are approximately in the bilateral thighs and buttocks, the common iliac artery approximately in the lower thigh, the common femoral artery approximately in the mid-thigh, and the N artery approximately in the lower calf. Weak or absent arterial pulsation: The patient’s dorsalis pedis artery and posterior tibial artery are usually palpated first, and if no pulsation is felt, the N artery is then palpated, and finally the femoral artery. This is used to initially confirm the location of the embolism. Numbness and motor impairment: The distal end of the affected limb shows a stocking-type zone of infection loss, which is due to dysfunction caused by peripheral nerve ischemia. Proximally, there is a hyperalgesia zone, and then proximally, there may be a sensory hypersensitivity zone. The affected limb may also have pins and needles-like sensation, muscle weakness, or even paralysis, and an undegraded hand and foot drop. Diagnosis (a) A history of cardiovascular system disease. (B) There are 5 “P” signs. 1. Pain (Pan): severe pain caused by ischemia and hypoxia of tissues. 2. Pallor (Pallor): with skin syncope. 3, numbness (Paresthesia): the distal end of the affected limb is stocking-type sensory loss area. 4.Motor impairment (Paraalysis): muscle strength is weakened or even paralyzed. 5.Weak or absent arterial pulsation (Pulselessness). (C) Angiographic ultrasound: no pulsation and blood flow in the distal artery at the embolization site. (4) CT artery (CTA) to clarify the embolism site, scope and degree. Treatment 1.Surgical treatment: For acute arterial embolism, surgery is the first choice. Once the cause is clear, the emergency operation of artery dissection and embolization surgery can effectively lift the embolism in the shortest time, restore the blood supply and maintain the limb to the greatest extent. Generally, the effect of emergency embolization is performed within 24 hours of embolism. 2. Non-surgical treatment: If there is no local surgical condition, or the diagnosis of the cause of embolism is not clear. Anticoagulation and thrombolytic therapy can be used first. Urokinase 20WU intravenous infusion twice a day + low molecular heparin calcium 4100U subcutaneous injection twice a day is usually used. Thrombolytic therapy is generally more effective for fresh thrombi occurring within 3 days and less effective for those older than 7 days; regional arterial catheter drips are more effective than systemic drugs.