Etiology, pathogenesis of obliterating endarteritis

Etiology, pathogenesis of obliterating endarteritis

The development of endarteritis is promoted by prolonged hypothermia, frostbite, injuries of the lower extremities, smoking, vitamin deficiencies, severe shock, mental disorders, infections, disorders of autoimmune processes and other factors that cause persistent spasm of the vessels. Long-term spasm of the arteries and their accompanying vasa vasorum leads to chronic and walls, resulting in intimal hyperplasia, adventitious fibrosis and degenerative changes in the nervous system of the vascular wall. Against the background of altered intimacy, a blood clot forms, narrowing and obliteration of the lumen of the vessel occur. If at the beginning of the disease mainly the distal vessels of the lower extremities (lower leg and foot) are affected, then subsequently larger arteries (popliteal, femoral, iliac) are involved in the pathological process. A sharp weakening of blood flow through the arteries leads to a deterioration in blood flow in the vessels of the microvasculature providing tissue metabolism, reduced oxygen delivery to tissues and tissue hypoxia develops, which is enhanced by the opening of arteriovenular anastomoses. Under these conditions, blood viscosity increases, erythrocyte aggregation increases, the adhesion-aggregation increases, and the disaggregation properties of platelets decrease . Formed platelet agreganty that block the microvasculature. Chronic hypoxia leads to the disintegration of the lysosomes with the release of hydrolases, Lizzie – ruyuschih cells and tissues. Tissue necrosis, the accumulation of proteolytic enzymes. The body is sensitized to protein breakdown products. Pathological autoimmune processes occur, exacerbating microcirculation disorders and enhancing local hypoxia and tissue necrosis.

Clinic of obliterating endarteritis

Depending on the degree of insufficiency of arterial blood supply to the affected limb, 4 stages of obliterating endarteritis are distinguished:
Stage I – functional compensation. Patients note chilliness, sometimes tingling and burning at the fingertips, increased fatigue. When cooled, the limbs become pale, cold to the touch. When passing at a speed of 4-5 km / h a distance of more than 1000 m in patients with intermittent claudication. It lies in the fact that the patient begins to experience pain in the calf muscles or foot, causing him to stop. In the pathogenesis of this symptom, a number of factors are important, in particular, insufficient blood supply to the muscles, impaired oxygen utilization, and the accumulation of under-oxidized metabolic products in the tissues. The pulse on the arteries of the feet in this stage is weakened or not determined; Stage II – subcompensation . Intermittent claudication increases and at the indicated pace of walking it occurs already after passing 200 m or a little earlier, the skin of the feet and lower legs loses its inherent elasticity, it becomes dry, flaky, hyperkeratosis develops on the plantar surface. Nail growth slows down, they thicken, become brittle, dull, acquire a matte or brown color. Disturbed and hair growth on the affected limb, which leads to the appearance of areas of baldness. Atrophy of the subcutaneous base and small muscles of the foot begins to develop. Ripple in the arteries of the feet is not determined; Stage III – decompensation. There is pain in the affected limb at rest. Walking becomes possible at a distance of 25-50 m. The color of the skin changes dramatically depending on the position of the affected limb. Her rise is accompanied by blanching, lowering – by redness of the skin. The skin becomes thinner and easily vulnerable. Minor injuries – scuffs, bruises, after cutting off nails – lead to the formation of cracks and superficial painful ulcers. To alleviate the suffering, patients give the limb a forced position, lowering it down, sitting asleep. Atrophy of the muscles of the leg and foot progresses. Disability of patients is significantly reduced; IV stage – destructive changes. Pain in the foot and fingers becomes constant and unbearable. The resulting ulcers are usually located in the distal extremities, often on the fingers. Their edges and bottom are covered with a dirty gray coating, there are no granulations, and there is inflammatory infiltration in the circle. Swelling of the foot and lower leg joins. Developing gangrene of the fingers and feet often proceeds as wet. Ripple may be absent due to ascending arterial thrombosis. Disability in patients at this stage is completely lost.

The course of obliterating endarteritis is usually long, over several years. It is characterized by periods of exacerbation and remission. Exacerbation is more often observed in autumn and spring. There are two main clinical forms of the course of the disease: 1) limited, in which, as a rule, arteries of one or both lower extremities are affected. This form is benign, changes progress slowly; 2) generalized , characterized by damage not only to the vessels of the limbs, but also to the visceral vessels of the abdominal part of the aorta, branches of the aortic arch, coronary and cerebral arteries.

Diagnosis of obliterating endarteritis

Diagnosis of obliterating endarteritis is based on the clinic of the disease, the results of functional tests and special research methods. Among the functional tests, indicating a lack of arterial blood supply is certainly the most revealing symptom of plantar ischemia Oppel , sample Goldflama , Samuels and Shamova , knee phenomenon Panchenko. Rheovasography , ultrasound flowmetry , thermography and angiography of the lower extremities help to establish the diagnosis . Obliterating endarteritis is characterized by a decrease in the amplitude of the main wave of the rheographic curve in the leads from the lower leg and especially the foot, smoothness of its contours, the disappearance of additional waves, a significant decrease in the value of the rheographic index. Rheograms recorded from the distal sections of the affected limb are straight lines. Ultrasound findings usually indicate a marked decrease in pressure in the arteries of the feet, a decrease in the linear velocity of blood flow, and help to clarify the level of vascular damage.
A thermographic study reveals a decrease in the intensity of infrared radiation in the distal extremities. On angiograms , normal patency of the aorta, iliac and femoral arteries is usually visible, the popliteal artery is narrowed, often occluded , the leg arteries are usually obliterated , and a network of small corkscrew collaterals is traced. If the contrast medium fills the affected vessels, then their contours are even, there is no scalloped edges, so characteristic for obliterating atherosclerosis.

Etiology, pathogenesis of Raynaud’s disease

The disease is characterized by spasm of the vessels of the fingers of the upper and lower extremities and very rarely – the tips of the ears and nose. The process is localized mainly on the upper limbs, the lesion is usually bilateral and symmetrical. The main reasons for the development of Raynaud’s disease are prolonged hypothermia, chronic trauma to the fingers, impaired functions of some endocrine organs (thyroid, genital glands), severe emotional stress. Triggers in the development of the disease are disorders of the vascular innervation.

Raynaud’s Clinic

There are three stages of the disease:
stage I – angiospastic . It is characterized by a pronounced increase in vascular tone. There is a short-term spasm of the vessels of the terminal phalanges. Fingers (often II and III hands and I-III feet) become pale, cold to the touch and insensitive. After a few minutes, the spasm is replaced by vasodilation. Due to active hyperemia, redness occurs and the fingers darken. Patients notice a strong burning sensation and sharp pain in them, swelling appears in the area of ​​interphalangeal joints. When the vascular tone normalizes, the color of the fingers becomes normal and the pain disappears. Stage II – angioparalytic . Attacks of pallor of the “dead finger” in this stage are rarely repeated, the brush and fingers become bluish. When lowering the arms down, it intensifies and acquires a purple hue. Swelling and pastiness of the fingers become permanent. The indicated stages last on average 3 years — 5 years. Stage III – trophoparalytic . At this stage, panaritiums and ulcers appear on the fingers. Foci of necrosis are formed, capturing the soft tissues of 1-2 terminal phalanges, less often of the entire finger. With the development of demarcation, necrotic areas are rejected, after which slowly healing ulcers remain, the scars from which are pale in color, painful, fused to the bone.

Differential diagnosis of Raynaud’s disease

Differential diagnosis includes obliterans endarte – Riitta and diseases in which circulatory disorder in the upper limb caused extravasal compression subclavian artery.
In contrast to obliterating endarteritis in Raynaud’s disease, pulsation in the arteries of the feet and radial arteries persists. The disease is more benign. Compression of the subclavian artery can be caused by an additional cervical rib or a highly located I rib (costoclavicular syndrome), a hypertrophied anterior scalene muscle, or its tendon (anterior scalene syndrome), or a pathologically altered pectoral muscle (pectoralis minor syndrome). With the above syndromes, both arteries and brachial plexus are compressed, so their clinic consists of vascular and neurological disorders. Constant trauma to the artery leads to cicatricial changes in its wall, periarteritis and may result in vascular thrombosis. The result of severe disturbances in the blood supply to the upper limb are trophic disorders. The correct assessment of the clinical picture, the results of samples with a change in the position of the limb allows you to differentiate these syndromes from Raynaud’s disease . In patients with an additional VI rib, as well as costal-clavicular syndrome, an x-ray study is important in the diagnosis.

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