Occlusion of the main arteries leads to acute or chronic disorders of the blood supply to the anatomical region or organ. Acute circulatory disorders are caused by embolism or thrombosis of the vessel. In 95%, the cause of embolism is a pathology of the heart: defects of the mitral or aortic valves, atrial fibrillation, a condition after myocardial infarction with the formation of parietal thrombi, aneurysm of the heart, septic endocarditis. In 5% of cases, the source of embolism is the formation of thrombotic masses in arterial aneurysms (especially often in aneurysms of the thoracic and abdominal aorta), after surgical interventions on the vascular system, with injuries, thrombosis of venous vessels with an open foramen ovale with increased pressure in the right atrium (paradoxical embolism). Embolism often occurs in places of physiological or secondary narrowing of arterial vessels, mainly in the area of bifurcation of large vessels. This leads to the simultaneous shutdown of at least two large areas of blood flow, which is accompanied by blockade of the collateral circulation. In 45% of cases, the embolus blocks the femoral artery, in 15% – the iliac and subcalcified, in 8% – the bifurcation of the aorta, rarely – the vessels of the hands, lower leg, brain, mesenteric vessels.
In acute embolism, the ischemia time of 4-6 hours is critical, with long periods of the disease, it is usually not possible to completely restore the function of the limb. With an increase in the duration of embolism, thrombosis occurs in the distal parts of the artery, which greatly complicates the surgical intervention and worsens the prognosis of the disease. At the final stage, thrombosis also occurs in the venous system; surgical treatment of this stage is ineffective.
The second cause of acute occlusion of arterial vessels is thrombosis, which occurs in the area of the altered arterial wall (atheromatosis, endarteritis). Less commonly, thrombosis occurs as a result of an arterial collapse from the outside with fractures, dislocations, hematomas, and thrombocytopathies of various origins. Very rarely, a sharp spasm of the artery after the introduction of contrast agents, poisoning with nicotine and er-gotamine can become the cause of arterial circulation disorders. The diagnosis is complicated when a fracture is combined with compression of an arterial vessel and secondary thrombosis.
Since acute thrombosis often occurs on the basis of an atherosclerotic lesion of the vessel, in which there is already a developed network of collaterals, the clinical picture of the disease is not as acute as in embolism, and the timing of reversible limb ischemia is longer.
Some types of acute occlusion of the main arteries. Acute vascular occlusion of the extremities is caused by embolism or vascular thrombosis. The clinical picture is characterized by sudden pain in the limb (75-80%). Pain may be absent in cases where full anesthesia develops rapidly from the outset, pain may be minimal if collateral circulation is maintained. The pallor of the skin in the initial stage is replaced by cyanosis with a marble pattern and a sharp decrease in skin temperature. This is an important sign that determines the degree of decrease in the blood supply to the limb. Paralysis and paresthesia (or anesthesia) are important in determining the severity of ischemia because peripheral nerve endings are very sensitive to anoxia. In the presence of paralysis and paresthesia, as a rule, there is gangrene and, conversely, while maintaining the motor and sensory function of the limb, despite the presence of signs of ischemia, gangrene is usually not detected. The absence of a pulse confirms the diagnosis and allows you to determine the location of the occlusion. With limb edema, the absence of a pulse can be determined using Doppler ultrasonography.
Diagnosis is based on history and identification of cardio-ape pathology. There are 3 degrees of ischemia of the affected limb (V. S. Savelyev): with ischemia of la degree, a feeling of numbness, coldness, paresthesia appears; with ischemia I6 degree – pain. With II degree ischemia, there are violations of sensitivity and active movements in the joints of the extremities (from paresis with H degree to paralysis with Hb degree). Ischemia of the III degree is characterized by the beginning of necrobiotic phenomena – subfascial edema in Ilia degree and muscle contracture in III6 degree. The end result of ischemia is gangrene of the limb. Angiography provides the most information about the nature and extent of the pathological process, the state of collateral blood flow.
Treatment. Anti-shock measures, low position of the limb, ppasmapheresis with the introduction of large amounts of fresh frozen plasma (see Compression syndrome), in the later stages – heparin to reduce the intensity of thrombus formation. Surgical intervention should be carried out within the first 6 hours from the onset of the disease: an arteriotomy is performed and the embolus is removed using a Fogarty probe; in case of arterial thrombosis, thrombo-bintimectomy is performed. After surgery, heparin therapy and treatment of cardiopathology are indicated to reduce the recurrence of embolism and retrombosis. At the III stage of ischemia, operations on the vessels are contraindicated due to the danger of tourniquet syndrome (similar to the syndrome of prolonged crushing). With embolism of arterial vessels distal to the knee or elbow joint, conservative therapy is indicated: antispasmodics, antiplatelet agents, heparin.
The prognosis depends on the timeliness of the surgical intervention and the nature of the changes in the vessel. With early surgery and good condition of its wall, it is possible to restore blood flow in the limb in 96% of cases.
Acute occlusion of the mesenteric vessels. Causes: embolism, thrombosis, dissecting aneurysm of the abdominal aorta, trauma. Intestinal necrosis can also occur when cardiac output falls below a critical level without mesenteric vascular occlusion. In 90% of cases, occlusion of the superior mesenteric artery occurs, in 10% of the inferior. With thrombosis, occlusion of the main trunk of the superior mesenteric artery often occurs, which is complicated by necrosis of the entire small intestine and colon to the splenic angle. With embolism, occlusion of more distal parts of the vessel occurs, while the necrosis zone is smaller.
Symptoms, course. The clinical picture of the disease depends on the time elapsed since its onset. There are 3 stages: I – the initial stage. The clinical picture is dominated by a triad of symptoms: abdominal pain, shock, and diarrhea. There is a characteristic discrepancy between the severe general condition of the patient and relatively minor changes detected during examination of the abdomen: swelling and moderate pain without symptoms of peritoneal irritation. On auscultation, there is decreased intestinal peristalsis. The blood picture is not changed. X-ray examination determined pneumatization and thickening of the wall of the small intestine. Duration of stage I-6 hours. Stage II (7-12 hours): severe pain in the abdomen, with palpation there is an increase in soreness, but there are no peritoneal symptoms, the patient’s condition gradually worsens. On digital examination of the rectum, there may be bloody discharge. In the blood, an increase in leukocytosis, x-ray changes are the same; Stage III – the stage of intestinal necrosis (after 12 hours). Symptoms of diffuse peritonitis and paralytic intestinal obstruction, high leukocytosis in the blood, multiple levels of fluid in the X-ray examination of the abdominal organs.
Diagnosis is based on anamnesis data, search for the source of embolism (atrial fibrillation, rheumatic heart disease), clinical manifestations of shock, intestinal paresis. An angiographic examination is desirable. Late surgical intervention causes the development of severe complications. In the 3rd stage of the disease, mesenteric venous thrombosis joins the arterial occlusion.
Treatment is only surgical. In stage I, intestinal revascularization is performed by removing a thrombus or thrombinthymectomy; in stage II, in the presence of focal necrosis of the intestinal wall, revascularization is supplemented with intestinal resection; in stage III, only a massive bowel resection can save the patient’s life. As a rule, surgery is performed in the II-III stages of the disease; postoperative mortality is 90%.
Chronic occlusions of arterial vessels lead to a decrease in blood flow in the anatomical region or organ. With a constant perfusion pressure, i.e., uniform blood flow, the pressure below the occlusion site decreases only when the vessel lumen is narrowed by more than 50%. This pattern becomes relative due to the presence of peripheral resistance. With high peripheral resistance, even a narrowing of the lumen by 50% does not lead to a decrease in blood flow with a decrease in pressure in the occlusion zone. With a slight peripheral resistance in the same situation, there is a decrease in pressure in the occlusion zone with a decrease in blood flow. With stenosis, organ blood flow depends on the inflow to the occluded area (i.e., perfusion pressure), the degree of constriction (percentage of vessel constriction), the magnitude of peripheral resistance, and blood viscosity. The morphological result of occlusion (i.e., increased blood flow velocity and blood flow eddies) is post-stenotic dilatation, the development of aneurysms, thrombi and peripheral embolism, collaterals. Collateral blood flow is a consequence of significant stenosis with a large pressure gradient between the pre- and post-stenotic segments of the vessel. There is an expansion of small preformed vessels with their true anatomical growth and the formation of sufficient roundabout blood flow. Organic vasoconstriction is not fully compensated, clinical manifestations occur initially during exercise.
Chronic disorders of arterial blood flow are divided into 3 groups: angioneuropathy (Raynaud’s disease, etc.); angiopathy; angioorganopathy. In the first two forms, in the absence of the effect of conservative measures, lumbar or thoracic sympathectomy is used. In angioorganopathies, which account for up to 90% of all obliterating diseases, surgical methods of treatment play the main role. The most common among organopathies is obliterating atherosclerosis and less often obliterating endarteritis and thromboangiitis.
Obliterating atherosclerosis is one of the main causes of peripheral blood flow disorders. Its development is promoted by diabetes mellitus, hyperlipidemia, hypertension, weight gain, nicotine intoxication, advanced and senile age. Risk factors include polycythemia, chronic infections, psychosocial stressful situations, treatment with strogens. The lesion is usually universal and concerns the narrowing of the lumen of the arteries not only of the extremities, but also of the brain, heart, and kidneys.
Classification of the severity of insufficiency of arterial blood flow of the limb: Stage I is clinically asymptomatic. There is a lack of pulse on the vessels of the limb, with angiography – narrowing or blockage of the vessel; Stage II – ischemic pain during exercise in the gluteal region and calf muscles (intermittent claudication), on the arteriogram – narrowing of the femoropopliteal or aortopod-iliac segment with sufficient development of collaterals; when at the stage, pain occurs when walking more than 100 m, at stage II6, less than 100 m; Stage III – pain at rest and at night of increasing intensity, physical activity sharply increases pain; Stage IV – significant pain at rest, physical activity is almost impossible; pronounced trophic disorders, necrosis on the fingers and feet, the development of gangrene.
There are 3 main localizations of atherosclerotic occlusion; pelvic, or aortoiliac type; femoral, or femoral-popliteal type; peripheral – damage to the vessels of the lower leg.
Clinical manifestations depend on the level of the lesion and the degree of vasoconstriction, the severity of collateral blood flow.
Aortoiliac type. Depending on the degree of blockage, intermittent claudication occurs with pain in the buttocks and hamstrings, later – pain at rest and gangrene of the peripheral limbs. Chilliness, increased sensitivity of the lower extremities to cold are common; the color of the skin of the legs changes; in the initial stages of the disease, they are pale, in the later stages they acquire a purple-bluish color. Skin atrophy with impaired hair and nail growth, hyperkeratosis. There is no pulsation on the femoral artery, often the lesion is bilateral (Lerish’s syndrome). On the survey radiograph, calcifications are determined in the wall of the aorta and iliac vessels. Angiography determines the location, extent and extent of the lesion.
Bucket-popliteal type. Blockage or narrowing of the superficial femoral artery up to the adductor canal (gunter’s canal). The nature and intensity of complaints depend on the presence of damage to the distal parts of the artery, the degree of vasoconstriction, and collateral blood flow. The pulse on the femoral artery is determined, but on the popliteal and arteries of the foot, it is sharply weakened or absent. With narrowing of the vessel with a sharp violation of hemodynamics in the zone of occlusion and immediately below, you can hear a systolic murmur. Angiography is needed.
Peripheral type: pain and paresthesia on the foot and fingers, difficult to treat interdigital fungal infections, prolonged wound healing after finger injuries. Pulsation on the femoral and popliteal arteries is preserved, but on the arteries of the foot is absent. In the diagnosis, you can use rheophagia, ultrasonic dopplerography, angiography.
With all types of localization of occlusion, it is necessary to carry out a differential diagnosis with radicular syndrome of the spinal cord, osteochondrosis, Raynaud’s disease, diabetic angiopathy, etc.
Treatment in the initial stage is conservative: elimination of adverse factors (cooling, smoking, drinking alcohol), antispasmodic therapy (no-shpa, halidor, etc.), ganglioblockers (diprofen, dikolin, etc.), painkillers. To improve metabolic processes in tissues, vitamins, complamin, solcoseryl are prescribed. It is advisable to prescribe drugs that normalize blood coagulation, reduce platelet affegation (reopoliglyukin, trental, chimes, fresh frozen plasma). Physiotherapeutic treatment is carried out, hyperbaric oxygenation, sanatorium-and-spa treatment is advisable.
The goal of surgical treatment is to restore blood flow in the affected limb. Indications for surgery depend on the stage of the disease (they are absolute at III-TV stages and relative at stage Pa), the technical feasibility of the operation (length and localization of blockage), the severity of concomitant pathology (myocardial infarction, diabetes mellitus, kidney damage, etc.). ).
Intervention options for arterial occlusion: with limited stenoses, balloon dilatation can be used, with extended lesions, thrombin-thymectomy. When arterial stenosis is localized above the inguinal ligament, bypass shunting with a synthetic graft is used, and when artery obstruction is located below, a graft from an autovein or a heterologous material is used. In case of generalized atherosclerotic vasoconstriction, lumbar sympathectomy with removal of 4 ganglia is indicated.
Complications: bleeding from the anastomosis area after surgery, early thrombosis of the operated vessel or graft, infection. Prevention of these complications consists in careful observance of the technique of applying a vascular suture, mandatory early gelarinization.
Forecast. The best prognosis was obtained with non-extended occlusions of large arteries. A five-year follow-up shows a good effect of surgical treatment in aortoiliac type in 90%, in femoral-popliteal type – in 60%.
Occlusion of branches of the aortic arch leads to ischemia of the brain and upper extremities. Etiology: atherosclerosis, nonspecific aorto-arteritis, compression by osteophytes, I rib, etc., congenital vascular anomalies, fibromuscular dysplasia. The main link in the pathogenesis of the disease is hypoxia of the brain regions supplied with blood by the affected artery. If one of the 4 arteries of the brain (internal carotid or vertebral) is damaged, blood supply to the corresponding part of the brain becomes possible due to blood flow through the arterial circle of the cerebrum (circle of Willis). However, this sometimes leads to a paradoxical effect. With occlusion of the proximal subclavian artery, blood enters the upper limb from the system of the arterial circle of the cerebrum, impoverishing the blood supply to the latter, especially during exercise (subclavian steal syndrome). The most common localization of occlusion is the bifurcation of the carotid arteries (50%), less often the common carotid artery, brachiocephalic trunk, subclavian and vertebral arteries.
Occlusion of the carotid arteries leads to impaired blood flow in the basin of the internal carotid and middle cerebral arteries. Symptoms: Stage I – asymptomatic, arteriography reveals arterial stenosis, the danger of which is thromboembolism, stage II – a high degree of vasoconstriction with intermittent ischemia with syncope, lasting several minutes, hemiparesis, aphasia, impaired gait and sensitivity (transient ischemic attack). Complications – thrombosis of small cerebral vessels; Stage III – complete occlusion of the artery, manifested by sudden apoplexy with loss of consciousness, a complete picture of apoplexy stroke; Stage IV – remaining neurological signs after a stroke.
Indications for surgery in stage I are relative (narrowing of the lumen by more than 50%, simultaneous stenosis or occlusion on the other side); in stage II they are absolute and in stage III they are relative (only in the first 6 hours, while consciousness is preserved).
Occlusion of the subclavian artery is caused by a stenop of the subclavian artery proximal to the origin of the vertebral artery; it manifests itself with physical tension of the upper shoulder girdle (steal syndrome). Changes in blood flow through the subclavian and vertebrobasilar vessels are pathogenetically important (see above). Symptoms: loss of consciousness, dizziness, paresis, weakness of the oculomotor muscles, speech and swallowing disorders, recurrent pain in the back of the head. Neurological symptoms are provoked by the work of the hand. The quality of the pulse and blood pressure is different on the right and left hands. Stenotic murmur is determined along the course of the subclavian artery. Angiography determines the narrowing, occlusion of the II steal effect, which is recognized by the retrograde contrast current in the Vertebral artery of the affected side.
Takayasu syndrome (pulseless disease) – degenerative or inflammatory diseases of the aortic wall: atherosclerosis, aortoarteritis or supravalvular aortic stenosis with stenosis and obliteration of large vessels extending from the aortic arch. It mainly affects women aged 25-50 years. A combination of intermittent neurological symptoms with “intermittent claudication” on the hands is characteristic. With a pronounced clinical picture, there is no pulse in the neck and both arms, but in most cases there is only a difference in blood pressure in the arms and legs.
Surgical treatment – restoration of blood flow by endarterectomy or segmental resection of the vessel with aploprosthesis.
Chronic occlusion of mesenteric vessels (abdominal toad). Causes: atherosclerosis of mesenteric vessels, arteritis, fibromuscular hyperplasia of the wall or compression of the artery from the outside (by the legs of the diaphragm, fibers of the nerve plexuses, fibrous cords). The most common localization is the superior mesenteric artery. Symptoms: severe pain 2-4 hours after eating, malabsorption, diarrhea, vascular noise. Abdominal pain is usually severe, prolonged, accompanied by weight loss (due to malabsorption due to hypoxic mucosal atrophy or as a result of fasting due to severe abdominal pain). Abdominal auscultation reveals stenotic vascular murmurs above the umbilicus. The main diagnostic method is angiography. Severe pain is an indication for surgery; in advanced cases, ischemic enteritis and enterocolitis occur.
Surgical treatment – endarterectomy or aorto-mesenteric bypass autovein.
Renal artery stenosis is caused by fibromuscular or atherosclerotic changes in the renal artery, which lead to narrowing of the vessel with a decrease in renal blood flow. As a result, the renin-angiotensin-aldosterone mechanism is activated, causing renal hypertension. Symptoms: high blood pressure, especially diastolic. Fibromuscular hyperplasia is characterized by young age, sudden onset of hypertension with severe pain in the lateral parts of the abdomen. In 30-50% of cases, stenotic noises over the renal vessels are determined. With intravenous urography, a decrease in the size of the kidney is detected, a slowdown in the release of a contrast agent, with radionuclide scanning, a decrease in blood flow in the renal parenchyma and vein. With aortography and selective renal angiography, the type, location and degree of vasoconstriction are determined.
Indications for surgery: proven arterial stenosis, juvenile hypertension and increased plasma renin activity in the affected kidney. Possible options for surgical treatment: balloon vasodilatation of the stenotic artery, endarterectomy, resection of the stenotic part of the vessel, implantation of the renal artery to a new part of the aorta, resection of the vessel with prosthesis with an autovein or allograft, bypass bypass grafting.
Prognosis: with fibromuscular stenosis of the renal artery, normalization of pressure can be achieved in 80-90%, with atherosclerosis and arteritis – 40-50%.
Thromboangitis obliterans is an inflammatory systemic disease of the arteries and veins with segmental obliteration and thrombosis, first of medium and small, and then of large vessels. It almost always occurs in young men. Factors predisposing to the disease are: smoking, cooling and especially frostbite, autoimmune diseases (rheumatism).
Morphologically, inflammation is determined with subintimal proliferation and narrowing of the lumen. Symptoms: clinical manifestations of circulatory failure of the limb (see Atherosclerosis). In about 10% of cases, there is damage to the venous vessels with their thrombosis. The course of the disease is long. There are two forms of the course of the disease: limited, in which the arteries of one or both lower extremities are affected, changes progress slowly, and generalized, in which the vessels of the extremities, visceral branches of the abdominal aorta, branches of the aortic arch, coronary and cerebral arteries are affected.
In the diagnosis, anamnesis, complaints, data from a clinical study, rheography, Doppler ultrasound, and angiography, if indicated, are important. Treatment is conservative (see above). With limited lesions, bypass shunting is possible. According to indications, sympathectomy, the purpose of which is to improve collateral circulation and eliminate vasospasm.
The prognosis is poor, there is no cure.
Raynaud’s disease – angiotrophoneurosis with a primary lesion of small terminal arteries and arterioles. The process is localized on the upper extremities, the lesion is usually symmetrical and bilateral, young women are more likely to get sick.
Etiology: prolonged chills, chronic traumatization of the fingers, endocrine disorders (thyroid gland, gonads), severe emotional stress.
Symptoms: there are 3 stages of the disease: angiospastic (short-term spasms of the vessels of the terminal phalanges of 2-3 fingers or 1-3 toes; the spasm is quickly replaced by vasodilation with reddening of the skin, warming of the fingers); angioparalytic (the hand and fingers acquire a cyanotic color, swelling and pastosity of the fingers); trophoparalytic (the tendency to develop panaritiums and ulcers, foci of superficial necrosis of the soft tissues of the terminal phalanges, after rejection, long-term non-healing ulcers).
Differential diagnosis is carried out with obliterating endarteritis and circulatory disorders in the limb due to compression of the subclavian artery (additional cervical rib, high-lying 1st rib – costoclavicular syndrome; hypertrophied anterior scalene muscle – syndrome of the anterior scalene muscle; pathologically altered pectoralis minor muscle). With these syndromes, there is compression of the subclavian artery and brachial plexus, hence the symptoms of vascular and neurological disorders: pain, chilliness, paresthesia, weakness of the muscles of the arm. At certain positions of the hand, there is an increase in symptoms and a decrease in the pulsation of blood vessels in the hand. Constant traumatization of the artery leads to cicatricial changes in its wall, periarteritis and may result in thrombosis.
Treatment of Raynaud’s disease is conservative, as in other obliterating vascular diseases. In the absence of effect, chest sympathectomy is performed, with necrosis – necrectomy. Courses of plasmapheresis with complete replacement of the removed plasma with fresh frozen plasma are shown.
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