Lower extremity arteriosclerosis obliterans

Introduction to lower extremity arteriosclerosis obliterans Lower Extremity Arterial Disease (PAD) is an important manifestation of atherosclerosis. Arteriosclerosis obliterans is a degenerative disease, which is the basic pathological process of the large and middle arteries, mainly the abnormal deposition of cells, fibrous stroma, lipids and tissue fragments, complex pathology in the process of proliferation of the intima or middle layer of the arteries. Changes, in peripheral vascular disease, arterial stenosis, occlusion or aneurysmal lesions, almost all caused by arteriosclerosis. Arteriosclerotic lesions are generally systemic disorders that occur in some large, medium-sized arteries, such as the lower aorta, the radial artery, the femoral artery, and the radial artery. The upper extremity arteries are rarely involved. The diseased artery is thickened, hardened, accompanied by atheromatous plaque and calcification, and may be followed by thrombosis, resulting in stenosis or occlusion of the arterial lumen, ischemic symptoms in the limb, chills, numbness, pain, intermittent Clinical manifestations such as ulceration or necrosis of the sacral and toe or foot, sometimes stenotic or occlusive lesions are segmental and multiplanar, occurring in the bifurcation of the artery and the posterior wall of the lumen, and the curved portion of the trunk of the artery More often, the distal side of the lesion often has a smooth outflow tract. basic knowledge Sickness ratio: 0.0001% Susceptible people: the elderly Mode of infection: non-infectious Complications: arterial embolism

Causes of lower extremity arteriosclerosis obliterans

(1) Causes of the disease

Epidemiological survey results show that the three high risk factors of arteriosclerosis are: high blood pressure, high cholesterol and smoking, which are related to the occurrence and development of arteriosclerosis occlusion.

The cause of arteriosclerosis is multi-sourced, according to the American Heart Association's epidemiological survey, the primary and secondary risk factors for arteriosclerosis.

Arteriosclerosis obliterans is the result of the gradual development of arteriosclerosis. The true cause of the disease is not fully understood. There are some related factors between various etiological theories. In the high risk factors of atherosclerosis, arteriosclerotic lesions in different parts of the body may be It is more closely related to certain high-risk factors. For example, plasma cholesterol and low-density lipoprotein levels are significantly associated with coronary heart disease, but only moderately related to cerebrovascular and peripheral vascular arteriosclerosis. Cerebrovascular diseases are mainly associated with hypertension. The main risk factor for peripheral vascular occlusive disease is smoking.

(two) pathogenesis

Pathogenesis

The main pathogenesis of arteriosclerosis obliterans can be as follows.

(1) Injury and smooth muscle cell proliferation theory: Rokitansky first proposed the injury response theory in the pathogenesis of arteriosclerosis in 1852. The arterial intimal injury caused by various causes is the initiating factor of arteriosclerosis. These damage factors mainly include: Hypertension, hemodynamic changes, thrombosis, hormonal and chemical stimuli, immune complexes, bacterial viruses, diabetes and hypoxemia, after arterial intimal injury, stimulate smooth muscle cells to migrate to the intima, followed by proliferation The smooth muscle cells of the arterial membrane are a multifunctional cell that synthesizes collagen, elastin and aminoglucan (GAGs), and forms a middle membrane with larger arterial smooth muscle cells and elastin and collagen. In the smooth muscle cell layer, the surface of the lumen is covered by a single layer of endothelial cells, which can promote the proliferation of arterial smooth muscle cells under the action of hypertension, hyperlipidemia or injury.

In the process of smooth muscle cell proliferation, the first process of the injury process itself and the basic fibroblast growth factor (bFGF) released by endothelial cells and smooth muscle cells stimulate the first proliferation of smooth muscle cells, and the platelet-promoting platelet growth factor (PDGF) stimulates smooth muscle cells to migrate to the intima, and smooth muscle cell migration to the intima is mainly regulated by angiotensin II and PDGF, which promotes smooth muscle cell proliferation (Fig. 1). These proliferating cells form a large number of extracellular cells. Matrix and lipid accumulation eventually form atherosclerotic plaque, and the arterial wall at the plaque plaque stops the normal diffusion around the lumen or reduces oxygen transmission through the vasotrophic tube, which can lead to hypoxemia of the local arterial wall. The hypoxic state of cellular metabolism in atherosclerotic plaques can cause necrosis and inflammation in the lesion.

(2) Lipid infiltration theory: Blood lipids infiltrate into the endothelium through the endovascular space, and then clear into the lymphatic circulation through the middle and outer membranes. Lipids are present in plasma in the form of lipoproteins, which are lipids. Complex with protein, the more fat content in lipoprotein, the lower the density, according to its density can be divided into high density lipoprotein (HDL), low density lipoprotein (LDL), very low density lipoprotein (VLDL) And chylomicrons (CM), in the process of arteriosclerosis, low-density lipoprotein mainly accumulates in the intima of the arteries, leading to the accumulation of low-density lipoprotein in the intima of the arteries: 1 changes in arterial infiltration Increased LDL infiltration; 2 increased interstitial tissue space; 3 decreased ability of vascular cells to metabolize LDL; 4 blocked transmission of LDL from the inner membrane to the middle membrane; 5 increased plasma LDL concentration; 6 in the arterial intimal LDL Specific binding to the connective tissue complex, the reduction of mucopolysaccharide in the arterial wall of the elderly, helps LDL to penetrate into the arterial wall, and the enzyme activity in the arterial wall is reduced, which is also conducive to the deposition of cholesterol. Various lipoproteins are easy to be included. Membrane lag , Accumulate, eventually will form atherosclerotic plaques.

In addition, Brown et al first reported the presence of LDL receptors on the cell surface. LDL binds to the receptor and is transported into the cell for proteolysis, then releases the amino acid to the middle membrane. Normally, the LDL receptor is synthesized in the inner lipid network. Insertion in the plasma membrane through the Golgi apparatus, genetic abnormalities can lead to receptors unable to recognize proteins or abnormal receptors can not bind to LDL, in patients with type IIa hypercholesterolemia associated with LDL receptor deficiency, leading to LDL Reduced intake, so that the body's blood LDL increased, therefore, familial hypercholesterolemia patients are at high risk of arteriosclerosis.

In the process of arteriosclerotic lesions, HDL has a protective effect on the arterial wall. LDL hydrolyzes protein components in lysosomes to be hydrolyzed into amino acids, cholesterol is hydrolyzed into free cholesterol, part is used, and part of it is stored. The main function of HDL is to eliminate cholesterol. It is sent to the liver for metabolism. The balance between LDL and HDL determines the metabolism of cholesterol in the arterial wall. When atherosclerosis occurs, the amount of LDL increases, and the activity of cholesterol esterase increases significantly. Therefore, the lipid metabolism in the arterial wall is disordered. Both are involved in the process of atherosclerotic lesions.

(3) Hemodynamics: In the pathogenesis of arteriosclerosis, hemodynamic changes and special vascular anatomy are two interrelated pathogenic factors, and hardened plaques often occur in specific parts of the vascular bed.

1 Hemodynamic factors: Hemodynamic factors leading to the formation of sclerosing plaque include: Shear Stress, blood flow separation, stasis, swing of shear vector, turbulence and hypertension.

A. Shear force: Wall shear force is the tangential pulling force generated by the movement of blood flow along the surface of vascular endothelial cells. The gradient is proportional to blood flow and blood viscosity, and inversely proportional to the cube of blood vessel radius (r3). A slight change in radius can have a significant effect on the wall shear force. Current studies have confirmed that arteriosclerotic plaques are mainly located in the low shear zone of the vessel wall rather than in the high shear zone, although experimental results indicate acute Increased wall shear force can cause vascular endothelial cell destruction, desquamation and smooth muscle cell proliferation, but no vascular endothelial cell damage is seen in the process of increased chronic wall wall shear. Arteriosclerotic plaque occurs in low blood vessel The mechanism of the force region is that the low shear force slows the process of transporting arteriosclerotic substances from the vessel wall, leading to an increase in lipid deposition. In addition, the low shear force interferes with the normal transformation of blood vessel wall and endothelial cell metabolism-related substances, blood flow. Stratification and stasis, in the bifurcation of the artery, for example, at the bifurcation of the carotid artery, the blood flow velocity is slow and blood flow stratification occurs, so that the blood vessel wall contacts the arteriosclerosis in the blood flow. Longer quality time, which contributes to the formation of atherosclerotic plaque. In addition, stratification of blood flow makes platelets easy to deposit. Studies on radiology and ultrasonography have confirmed the existence of blood flow stratification on the lateral wall of the cervical branch bifurcation. Blood stasis.

B. Turbulence: This kind of random disordered blood flow phenomenon is rarely seen in the normal vascular system. It is currently considered that turbulence is not directly related to the formation of atherosclerotic plaque. The turbulence occurs at the distal end of the lesion, and it is on the atherosclerotic plaque. Block rupture or thrombosis plays a role.

2 vascular anatomical factors: in the process of lower extremity arteriosclerosis, the most common site of arteriosclerosis is the bifurcation, the infrarenal abdominal aorta and the iliac femoral artery, which has a certain relationship with its anatomical features.

The infrarenal abdominal aorta is particularly prone to arteriosclerotic lesions, which can lead to the formation of occlusive sclerosing plaques or aneurysmal changes. The difference between the abdominal aorta and the thoracic aorta is the blood flow state wall structure and nourish blood vessels, kidney. The blood flow of the abdominal aorta below the arteries depends mainly on the degree of lower extremity movement. The reduction in the life and physical activity of the case can lead to a decrease in the blood flow velocity in the abdominal aorta. Compared with the thoracic aorta, there are few nourishing vessels in the abdominal aorta wall. Therefore, the slowing of the abdominal aorta blood flow velocity and the difference in arterial intima and medial nutrients, these two factors make the arteriosclerosis substance accumulate in the intima of the abdominal aorta.

The superficial femoral artery is the most common site of atherosclerotic stenosis, but it is rare in the deep femoral artery. The superficial femoral artery plaque is not better than the branch, and the plaque caused by plaque is the earliest. The site is the iliac crest, and the mechanical stimulation of the tendon near the superficial femoral artery makes it easy to form atherosclerotic plaque, which causes occlusion of the lower part of the superficial femoral artery. However, some scholars hold different views. Blair believes that the adductor is in the adductor. The superficial femoral artery is not very prone to form sclerosing plaque, but the ability of vascular dilatation to increase the intimal plaque is limited. Therefore, the same degree of endometrial plaque as other parts of the femoral artery in the adductor canal Can produce more severe stenosis.

(4) Genetics: Genetic investigations show that the family history of this disease is 2 to 6 times higher than that of the general population. It may be due to genetic control of cell-induced cholesterol synthesis, which leads to excessive accumulation of cholesterol.

2. Good hair

The majority of arteriosclerotic occlusive disease occurs in the lower limbs. Because the lower extremity arteries are thick and long, the pressure of receiving blood is large, and the endometrium of the arteries is more likely to be damaged by internal and external injuries. The three vulnerable parts of the lower extremity arteries are: calf iliac artery, femoral hernia Arterial and main iliac arteries, the highest incidence of femoral condyle, which is related to repeated mechanical contraction of muscles around the adductor muscles of the thigh. Servell reported 5100 cases of surgery, the occlusion site was distributed: 14% of the main iliac artery Femoral artery 49%; radial artery 16%; anterior tibial artery 21%, the disease is characterized by stenosis or occlusive disease often segmental, limited to the arterial bifurcation, involving one or both lower extremities Arteries, upper limbs are rarely involved, the length of the lesion is generally 4 ~ 10cm, the distal artery of the lesion is more smooth, can be used as an outflow channel of vascular bypass graft surgery, so that most cases can be treated surgically.

3. Pathophysiology

After arteriosclerosis occlusion can cause a variety of pathophysiological changes.

(1) Limb ischemia: Limb ischemia can be divided into functional and critical ischemia.

1 Functional Ischemia: In the resting state, the blood supply to the limbs can be ensured, but with the movement of the limbs, the blood flow cannot be increased, and the clinical manifestations are intermittent claudication. The main performance characteristics are three: A. The muscle group shows pain; B. A certain amount of exercise can make the pain repeat; C. The movement can stop the pain quickly after stopping.

2 Chronic Critical Limb Ischemia: The diagnostic criteria for chronic critical limb ischemia need to have the following points: A. Recurrent resting pain for more than 2 weeks, regular painkillers should be taken, with crotch Arterial systolic pressure 6.67kPa (50mmHg), toe systolic pressure 4.0kPa (30mmHg), B. Foot or toe ulcer and gangrene, with iliac artery pressure 6.67kPa (50mmHg), or toe systolic pressure 4.0 kPa (30mmHg), unlike the way in which pain is performed, ischemic rest pain is not manifested in the muscle group but in the foot, especially the toe and humeral head.

3 Pathophysiological mechanism of critical limb ischemia: When the arterial trunk is stenosis or occlusion, the distal end can cause local hypotension, release vasoactive substances, cause small arteries to dilate, maintain nutritional blood flow through microvascular expansion, and further develop the lesion. Capillary arterioles collapse due to low transmural pressure, small arteriospasm, microthrombus formation, interstitial edema can cause capillary collapse, endothelial cell swelling, platelet accumulation, leukocyte adhesion and local immune system activation, these factors ultimately lead to Limb distal microcirculation perfusion disorders.

(2) changes in arterial blood flow: arteriosclerotic plaque occurs in the posterior wall of the lower extremity artery, and at the beginning or bifurcation of the aorta. The superficial femoral artery is often extensively affected. As the plaque builds up, the thrombus can be deposited. In the lesion and adjacent arterial wall, the blood flow can be blocked, the artery is completely blocked, the limb blood flow is proportional to the arterial pressure, and the peripheral resistance is inversely proportional. After the main artery is occluded, the distal perfusion pressure of the obstruction is reduced. Peripheral resistance increases and limb blood flow decreases.

According to the Bursa equation.

It can be seen from the above formula that when blood flow passes through the narrow main artery or collateral circulation, it is mainly affected by the radius of the artery and the length of the stenotic blood vessel.

When the main blood vessels of the limb are occluded, the total resistance of the blood flow is the parallel resistance of the collateral vessels. If the occlusion of the same artery occurs, the total resistance is added by the series resistance, so the vascular resistance of multiple arterial occlusions is blocked by one artery. The resistance is large, the compensatory capacity of the artery itself is reduced, and even the minimum requirement is not met, leading to tissue necrosis.

(3) collateral circulation: collateral circulation is present in the blood vessels of the main blood vessels, usually not open. When the main blood vessels are narrow or occluded, the collateral vessels gradually expand due to the pressure difference between the two ends of the blood vessels. When exercising, the tissue is hypoxic, acid. Poisoning, the surrounding resistance is further reduced, and the pressure difference is increased.

The collateral circulation usually provides adequate blood flow for chronic single vessel occlusion, can meet the needs of the limb at rest and the extra blood flow maintains a moderate amount of movement, but sudden arterial occlusion such as embolism, collateral circulation is not sufficient Time compensation can lead to limb tissue necrosis. On the other hand, if the development of collateral circulation is consistent with the progression of arterial occlusive disease, the patient's clinical symptoms may not change, or there may be severe limb ischemia, with collateral circulation. The development has gradually eased.

Lower extremity arteriosclerosis obliterans can occur in different parts of the following collateral circulation network:

1 When the end of the abdominal aorta is occluded: the intercostal artery, the lumbar artery and the iliac crest, the buttocks, the circumflex and the abdominal wall arteries may be anastomosis, and the other collateral branch is the left colon branch of the superior mesenteric artery and the mesenteric arterioles. Finally, the rectal blood vessels enter the inferior epigastric artery.

2 When the common artery of the external iliac artery is occluded: the anastomosis between the hip branch of the inferior epigastric artery and the branch of the femoral artery of the deep femoral artery is called "cross anastomosis".

When 3 superficial arteries are occluded: the collateral circulation between the penetrating branch of the deep femoral artery and the knee joint of the radial artery is open and compensated.

Lower extremity arteriosclerosis obliteration prevention

The prevention of this disease is mainly to strictly control the risk factors of atherosclerosis, such as strict monitoring, control of blood pressure, blood sugar, blood lipids, strict smoking cessation, can delay the progression of atherosclerosis, reduce the incidence of lower extremity arteriosclerosis, And prevent the occurrence of cardiovascular and vascular adverse events.

1. Patients with one or more of the above risk factors should be monitored to detect and diagnose possible arterial stenosis and occlusive disease.

2. For patients with lower extremity arteriosclerosis obliterans, early exercise should be strengthened, strict medication should be used, and foot care should be strengthened to avoid skin damage and trauma, so as to prevent the disease from worsening.

3. For patients who have undergone surgery or treatment, the above preventive measures still need to be applied to prevent vascular restenosis at the surgical site and arterial lesions in other parts of the body.

Lower extremity arteriosclerosis obliterans complications Complications, arterial embolism

There are also limb pain, joint contracture, pulmonary embolism and so on.

Symptoms of lower extremity arteriosclerosis obliterans Common symptoms Arteries are stretched and twisted in the elderly. Legs cramps, weakness, fatigue, skin temperature, decreased blood viscosity, increased area, feeling of tissue necrosis

The clinical symptoms of patients with atherosclerosis mainly depend on the speed and extent of limb ischemia. The extent of occlusive lesions is extensive, as long as the lesions of arterial occlusion develop slowly, the collateral circulation can be effectively established. The flow is correspondingly increased, the blood supply can be compensated, so that the degree of ischemia and hypoxia can be alleviated, and there is no obvious ischemic symptom in the clinic. If the lesion develops rapidly, the collateral circulation is incomplete and the compensation is limited. Patients may have obvious symptoms such as intermittent claudication and limb pain. According to the severity of the patient's symptoms, according to the Fontaine staging, the clinical manifestations are generally divided into 4 stages.

In the first period, during the minor complaint period, the patient only felt that the skin temperature of the affected limb was reduced, cold, or mildly numb, fatigue after the activity, and the foot was prone to foot and foot infection and was not easy to control.

In the second phase, intermittent claudication, when the patient is walking, due to ischemia and hypoxia, the more common part is the muscles of the calf, which are painful and fatigued. It is necessary to stop walking. After a short break, the symptoms are relieved. In order to continue activities, if you walk a distance, the symptoms reappear, and intermittent calf is the most common symptom of ischemic lesions of the lower extremities.

In the third period, the resting pain period, when the lesion develops further, and the collateral circulation is seriously deficient, the limb is in a rather severe ischemic state, even when resting, it feels pain, numbness and paresthesia, and the pain is generally limb Mainly.

In the fourth stage, the tissue necrosis period mainly refers to the continuous development of the lesion to the occlusion phase. The collateral circulation is very limited, and the symptoms of nutritional disorders appear. Before the ulcer or gangrene occurs, the skin temperature decreases, the color is dark purple, and early gangrene and ulcer often occur in On the toe, as the lesion progresses, the infection and gangrene can gradually develop upward to the foot, ankle, or calf. In severe cases, symptoms of systemic poisoning may occur.

Examination of lower extremity arteriosclerosis obliterans

1. General inspection

Because the patients are mostly elderly, there may be a variety of concomitant diseases and risk factors for atherosclerosis, which require comprehensive examination, including blood pressure, blood sugar, blood lipid determination, and heart and cerebrovascular assessment.

2. Special inspection

(1) Segmental arterial systolic pressure measurement: measuring the pressure level of different planes of lower extremity arteries and bilateral contrast, if the arteries have obvious stenosis, the distal pressure is significantly reduced, and the presence or absence of lesions and their sites can be initially determined.

(2) Ankle index (ABI): The ratio of the systolic blood pressure of the lower extremity to the systolic blood pressure of the upper extremity was measured using a Doppler flowmeter and a pressure gauge. At rest, ABI is generally between 0.91 and 1.30. Above 1.30, the arterial wall is stiff and not easy to be compressed. ABI between 0.90 and 0.41 suggests mild to moderate ischemia; ABI 0.40, suggesting severe ischemia. . There is also a toe-arm index (TBI) to understand the condition of the terminal artery.

(3) Percutaneous oxygen partial pressure measurement: by measuring the partial pressure of oxygen in the local tissue, the blood perfusion of local tissue can be indirectly understood, and the degree of ischemia can be evaluated; and it can be used to determine the healing tendency of the extremity ulcer and wound, percutaneous The oxygen partial pressure is too low, suggesting that the wound is not easy to heal.

(4) Color Doppler ultrasound: for common screening methods, atherosclerotic plaque, stenosis, occlusion, etc. can be seen. This method is non-invasive, convenient, and inexpensive, but has little meaning for treatment guidance.

(5) CT angiography (CTA): It has become the first choice for lower extremity arteriosclerosis obliterans, which can clearly show the location, extent and extent of arterial lesions; confirm the diagnosis and help to determine the treatment plan. The shortcoming is due to the need to use iodine-containing contrast agents, which may affect kidney function, and those with renal insufficiency should be used with caution.

(6) Magnetic resonance angiography (MRA): with CTA, it can also provide a clear imaging diagnosis for lower extremity arteriosclerosis obliterans. The advantage is that there is no need to use iodine-containing contrast agent, but the resolution of calcification is poor, and may Overestimate the severity of the lesion.

(7) Digital subtraction angiography (DSA): for the diagnosis of lower extremity arteriosclerosis obliterans gold standard, can accurately show the location, extent, extent, collateral circulation, delay phenomenon can evaluate the distal outflow tract. DSA is of great significance for the assessment of lesions and the choice of surgical methods. At the same time, in the hospitals with conditions, intravascular treatment can be performed simultaneously with angiography, and arterial lesions can be resolved at the same time.

Diagnosis and identification of lower extremity arteriosclerosis obliterans

diagnosis

Most patients with arteriosclerotic occlusion can make a diagnosis based on medical history and physical examination, and detailed medical history; careful physical examination, such as pulse palpation of the limb and auscultation of the abdomen and femoral-iliac artery are necessary for diagnosis. According to the strength or disappearance of the pulse and the appearance of murmur, it can also be based on resting pain, paresthesia or numbness, as well as limb tissue dystrophy, ulcers or gangrene, etc., can initially make diagnosis of arteriosclerosis obliteration, X-ray Tablets showed atherosclerotic calcification of the arteries, / index of non-invasive vascular examination can be <1, and severe cases can reach below 0.5. Arteriography can show that the artery is elongated and twisted, and the lumen is diffuse irregularly narrow or segmental. Sexual occlusion can be clearly diagnosed. Patients may be accompanied by hypertension, hyperlipidemia, hyperglycemia, coronary heart disease, stroke, etc., which is helpful for diagnosis. However, X-ray films without arterial calcification and normal blood lipids cannot exclude arteriosclerosis. The existence of sexual occlusion.

Differential diagnosis

Lower extremity arteriosclerosis obliterans still need to be differentiated from the following diseases.

1. Thromboangiitis obliterans: This disease is more common in male young adults, more than 90% of patients have a history of smoking, it is a chronic, periodic increase in systemic, small movements, venous occlusive disease, mainly involving the lower limbs The arteries such as the dorsal artery of the foot, the posterior tibial artery, the radial artery or the femoral artery, etc., about 40% of patients in the early stage of the onset or during the onset of the disease, recurrent thrombophlebitis and vasculitis Generally, there is no history of hypertension, history of diabetes, history of coronary heart disease, etc. Arterial angiography shows that the artery is segmental stenosis or occlusion, the lesion is near, the distal artery is smooth, flat, no distortion and expansion, according to the age of onset, And the contrast can be distinguished from AS0.

2. Multiple arteritis: more common in young women, mainly invading the beginning of the aorta and its branches, such as the carotid artery, subclavian artery, renal artery, etc. The lesion causes arterial stenosis or obstruction, and the brain, upper limb or lower limb appears. Ischemic symptoms, clinical manifestations of memory loss, headache, dizziness, fainting, cold limbs, numbness, soreness, fatigue, intermittent claudication, but no lower extremity rest pain and gangrene, arterial pulsation can be weakened or disappeared, blood pressure is reduced Or can not be measured, renal artery stenosis that occurs renal hypertension, such as combined with bilateral subclavian artery stenosis, may have upper limb hypotension, lower extremity hypertension; thoracic and abdominal aortic stenosis, upper extremity hypertension, lower limb hypotension, in There is systolic murmur near the artery stenosis, fever and erythrocyte sedimentation rate during the active period of the disease. According to the age and symptoms of the patient, signs and angiography are easier to distinguish from AS0.

3. Nodular arterial inflammation: There may be symptoms of lower limb pain when walking, skin often has scattered purple spots, ischemia or necrosis, often fever, fatigue, weight loss, increased erythrocyte sedimentation rate, etc., often accompanied by Visceral organ lesions rarely cause large arterial occlusion or arterial pulsation to disappear, to confirm the diagnosis of this disease requires biopsy.

4. Idiopathic arterial thrombosis: this disease is rare, often complicated by other diseases such as collagen disease (systemic lupus erythematosus, nodular arteritis, rheumatoid arthritis, etc.) and polycythemia, can also occur in After surgery or arterial injury, the incidence is more acute, and can cause limb gangrene.

5. Acute lower extremity arterial embolism: rapid onset, sudden pain in the affected limb, pale, cold, numbness, dyskinesia and arterial pulsation weakened or disappeared, more common in heart disease, most of the embolus formed in the heart, falling off to the lower limbs In the arteries, according to the previous no intermittent claudication and rest pain, the onset is rapid, and it is easier to distinguish it from ASO.

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