Disease Overview Atherosclerotic occlusive disease is a localized manifestation of systemic atherosclerosis in the limbs, in which the endothelium of the arteries and its middle layer show degenerative and proliferative changes, causing the walls of the arteries to harden and shrink, losing elasticity, and leading to thrombosis, resulting in the progressive reduction or interruption of distal blood flow. It can occur in all major arteries of the body, mostly in the lower end of the abdominal aorta and the middle and large arteries of the lower limbs. Leriche syndrome occurs in the abdominal aorta and both common iliac arteries below the renal arteries. Leriche syndrome occurs in people over 50 years of age, with a male-to-female ratio of 6:1-9:1 and a prevalence of about 0.74%. Etiology of the disease The exact cause of the disease is not yet clear, and may be related to a variety of factors, which can be broadly categorized into two aspects: (1) External factors: mainly smoking, cold and damp living environment, chronic injury and infection. (2) Intrinsic factors: autoimmune dysfunction, dysregulation of sex hormones and prostaglandins, and genetic factors. Among the above factors, active or passive smoking is an important link in the occurrence and development of the disease. The majority of patients have a history of smoking, nicotine can cause vasoconstriction, tobacco leachate can cause inflammatory lesions in the arteries of experimental animals, smoking cessation can lead to remission of the disease, and the disease often recurs when smoking again. Antinuclear antibodies are present in the patient’s serum, and immunoglobulins and C3 complexes are found in the affected arteries, thus the importance of immune dysfunction in the pathogenesis of the disease has attracted more attention. Pathophysiology The pathological progression of the disease is characterized by the following features: (1) It usually begins in the arteries and then may involve the veins, generally progressing from distal to proximal. (2) The lesions have a segmental distribution, with relatively normal vascularity between segments. (3) The active stage is a non-suppurative inflammation of the entire vascular layer, with endothelial cell and fibroblast proliferation; lymphocyte infiltration, less neutrophilic infiltration, and occasional giant cells; the lumen is occluded by thrombus. (4) In the late stage, the inflammation subsides, the thrombus is mechanized, and there is neonatal capillary formation. There is extensive fibrous tissue formation around the artery. Often encapsulating veins and nerves. (5) Although there is a gradual establishment of collateral circulation, it is not sufficient to compensate, and thus ischemic changes may occur in nerves, muscles, and bones. The pathologic changes in venous involvement are much the same as in arterial. Symptoms and signs The disease has an insidious onset and progresses slowly, often with periodic episodes, and the symptoms gradually become obvious and aggravated after a long period of time. The main clinical manifestations are: (1) fear of cold in the affected limbs and decrease in skin temperature. (2) Pale skin color, or cyanosis. (3) Abnormal sensation. (4) Pain in the affected limb, which is caused by inflammation of the vessel wall and irritation of the adjacent peripheral nerves at an early stage, and later ischemic pain due to arterial obstruction, i.e. intermittent claudication or rest pain. (5) Long-term chronic ischemia leads to changes in tissue nutritional disorders. (6) Weakened or absent distal arterial pulsations in the affected limb. (7) Recurrent wandering superficial phlebitis of the affected limb before or during the onset of the disease. (8) Severe ischemia at the end of the affected limb . Dry gangrene is produced, and a long-lasting ulcer is formed after shedding. Clinically, according to the degree of ischemia of the limb, it can be divided into three phases: Phase I Local ischemia phase: the affected limb is numb, cold, afraid of cold, mild intermittent claudication, which can be relieved after a short rest. Examination reveals that the skin temperature of the affected limb is slightly lower, the color is paler, the pulsation of the dorsal foot or posterior tibial artery is weakened, and there may be recurrent superficial phlebitis of the wandering veins. The causes of ischemia are more functional (spasm) than organic (occlusion). Stage 2: Nutritional disorders: the above symptoms worsen, and intermittent claudication shortens the distance until persistent resting pain occurs, which is more intense at night. The skin temperature of the affected limb decreases significantly and is markedly pale, or purple spots appear. The skin is dry and sweatless, the toe (finger) nails are thickened and deformed, the calf muscles are atrophied, and the pulsations of the dorsalis pedis artery and/or posterior tibial artery have disappeared. At this stage, the arterial lesions have been mainly organic changes, and the limbs rely on collateral circulation to remain alive. In the lumbar sympathetic nerve block test, the skin temperature can still be elevated, but not to the normal level. Stage III Necrotic stage: symptoms continue to aggravate, and the toe (finger) ends of the affected limb become black, dried, gangrenous, and ulcers are formed. The pain is severe and persistent, forcing the patient to sit with knees bent and feet stroked day and night, or with the help of a drooping limb to relieve pain, with obvious swelling of the limb. The patient is unable to sleep because of the pain, and is lethargic and anemic. If secondary infection occurs, dry gangrene turns into wet gangrene, and systemic toxaemia symptoms such as high fever and irritability appear. In the third stage, the arteries are completely occluded, the blood supplied by collateral circulation is insufficient to compensate for the necessary blood supply, and the necrotic limb does not survive. Diagnostic examination Clinical diagnosis is generally not difficult. Diagnostic points include: (1) most patients are young men, most of whom are smokers; (2) different degrees of ischemic symptoms in the affected limb; (3) history of wandering superficial phlebitis; (4) weakened or absent pulsation of the dorsalis pedis artery or posterior tibial artery in the affected limb; and (5) no factors predisposing to atherosclerosis, such as hypertension, hyperlipidaemia, diabetes mellitus, or other factors, other than smoking. The following tests are helpful in determining the diagnosis. Observe the site, nature and degree of occlusion. l. General examination (1) Record the claudication distance and claudication time. (2) Skin temperature measurement. Bilateral limb corresponding part of the skin temperature difference of more than 2 ℃, suggesting that the lower skin temperature side of the arterial blood flow reduction. (3) Limb elevation test (Buerger test). If the test is positive, it suggests that the affected limb has serious blood supply deficiency. (4) Detension test. Make subarachnoid or epidural block anesthesia, and then in the same position of the lower limb, compare the temperature change before and after the block. The higher the skin temperature after block anesthesia, the more obvious. The higher the proportion of arterial spasm factor. If there is no obvious change, it means that the diseased artery is in severe stenosis or has been completely occluded. 2.Special examination (1) limb hemogram: electrical impedance and photoelectric hemodynamics show that the peak value decreases and the descending branch decreases at a slower rate. The former suggests a decrease in blood flow, and the latter indicates an increase in outflow tract resistance, which is proportional to the severity of the lesion. (2) Ultrasound Doppler examination: applying Doppler stethoscope to determine the strength of arterial blood flow according to the strength of arterial tone. The ultrasound Doppler flow meter can record the waveform of arterial blood flow. A decrease in the amplitude of the waveform or a straight line indicates that the arterial blood flow has decreased or the artery has been occluded. Segmental arterial pressure can also be measured to understand the location of the lesion and the severity of ischemia. The ankle-brachial index, i.e., the ratio of ankle pressure (systolic pressure of anterior or posterior tibial artery at the ankle) to that of the brachial artery on the same side of the ankle, with a normal value of >1.0, e.g., >0.5.