Chronic arterial occlusive disease

Arterial occlusion is a disease that can occur in any artery in the human body. Once arterial occlusion occurs, it will affect the normal blood delivery, which will cause many other human diseases. The most common arterial occlusive disease is carotid artery occlusion, which may cause a series of cardiovascular and cerebrovascular diseases. But what causes a person to develop chronic arterial occlusive disease?

Causes of Disease

The exact cause of this disease has not yet been determined. It may be related to a variety of factors, which can be roughly summarized into two aspects:

External factors

The main ones are smoking, cold and humid living environment, chronic injuries and infections.

Internal factors

Autoimmune disorders, sex hormone and prostaglandin imbalances, and genetic factors. Among the above factors, active or passive smoking is an important link in the occurrence and development of this disease. Most of the patients have a history of smoking. Nicotine can cause blood vessels to constrict, and tobacco extract can cause inflammatory lesions in the arteries of experimental animals. Quitting smoking can alleviate the condition, but the condition often relapses if smoking again.

Antinuclear antibodies are present in the patient's serum, and immunoglobulins and C3 complexes are found in affected arteries. Therefore, the importance of immune dysfunction in the pathogenesis of this disease has attracted more attention.

Pathophysiology

The pathological progression of this disease has the following characteristics:

(1) It usually starts in the artery and then may affect the vein, generally progressing from distal to proximal.

(2) The lesions are distributed segmentally, and the blood vessels between the two segments are relatively normal.

(3) The active phase is characterized by non-purulent inflammation of the entire vascular layer, with proliferation of endothelial cells and fibroblasts; infiltration of lymphocytes, less infiltration of neutrophils, and occasional giant cells; the lumen is blocked by thrombus.

(4) In the later stage, inflammation subsides, thrombus organization occurs, and new capillaries are formed. Extensive fibrous tissue forms around the arteries, often enveloping veins and nerves.

(5) Although collateral circulation is gradually established, it is insufficient to compensate, so ischemic changes may occur in the nerves, muscles, and bones. The pathological changes when veins are affected are generally the same as those when arteries are affected.

Symptoms and signs

The disease has an insidious onset, slow progression, and often cyclical attacks. After a long period of time, the symptoms gradually become more obvious and severe. Main clinical manifestations:

(1) The affected limb is sensitive to cold and the skin temperature decreases.

(2) Pale skin or cyanosis.

(3) Abnormal sensation.

(4) Pain in the affected limb is initially caused by inflammation of the blood vessel wall and stimulation of the adjacent peripheral nerves. Later, it causes ischemic pain due to arterial blockage, namely intermittent claudication or rest pain.

(5) Long-term chronic ischemia leads to changes in tissue nutritional disorders.

(6) The distal arterial pulsation of the affected limb is weakened or disappears.

(7) Recurrent migratory superficial phlebitis occurs in the affected limb before or during the onset of the disease.

(8) Severe ischemia at the extremities of the affected limbs causes dry gangrene, which then falls off and forms ulcers that do not heal for a long time.

Clinically, limb ischemia can be divided into three stages according to the degree of limb ischemia:

First ischemic phase

The affected limb is numb, cold, and afraid of cold, with mild intermittent claudication, which can be relieved after a short rest. Examination revealed that the skin temperature of the affected limb was slightly lower and the color was paler, the pulsation of the dorsalis pedis or posterior tibial artery was weakened, and migratory superficial phlebitis may occur repeatedly. The causes of ischemia are more functional (spasm) than organic (occlusion).

The second stage of nutritional disorder

The above symptoms become increasingly severe, and the distance of intermittent claudication becomes shorter and shorter until persistent resting pain occurs, which is more severe at night. The skin temperature of the affected limb drops significantly, becomes noticeably pale, or purple spots appear. Dry skin, no sweat, thickened and deformed toenails, calf muscle atrophy, and disappearance of dorsalis pedis artery and/or posterior tibial artery pulsation. At this stage, arterial lesions are mainly organic changes, and the limbs rely on collateral circulation to remain alive. During the lumbar sympathetic nerve block test, the skin temperature may still rise, but it will not reach the normal level.

The third necrosis stage

As the symptoms continue to worsen, the tips of the toes (fingers) of the affected limbs become black, shriveled, gangrenous, and ulcers form. The pain is severe and persistent, forcing the patient to sit with his knees bent and his feet touched day and night, or to lower his limbs to relieve the pain, and the limbs are accompanied by obvious swelling. The patient cannot sleep due to the pain and becomes emaciated and anemic. If secondary infection occurs, dry gangrene will turn into wet gangrene, and symptoms of systemic toxemia such as high fever and irritability will appear. In the third stage, the artery is completely blocked, the blood provided by the collateral circulation is insufficient to compensate for the necessary blood supply, and the necrotic extremity cannot survive.