S bend of the internal carotid artery. Types of pathological tortuosity of blood vessels

Non-straightness vertebral arteries is a disease that occurs as a result of pathologies of the cervical spine such as curvature, osteochondrosis, scoliosis, and so on. Physiologically, the vertebral arteries pass in the protected area of ​​the cervical spine. As a result of its destruction, they shift or narrow, reducing blood permeability and further pathologies of the brain.

The vertebral arteries are the main suppliers of blood to the brain. Statistics show that more than 50 percent of strokes occur due to pathologies associated with the vertebral arteries. For this reason, they must be treated with full responsibility and, if symptoms of illness occur, immediately seek medical help.

Timely identification of the problem can significantly speed up the diagnostic and treatment processes. For this reason, it is worth remembering a number of symptoms, if they occur, you should contact a neurologist and orthopedist.

• Frequent headaches in the back of the head;
• Neck pain;
• The appearance of a pre-fainting state with sudden movements;
• Increased intracranial pressure;
• Constant or intermittent weakness in the arms, legs, or fingers;
• Spontaneous attacks of nausea;
• Loss of coordination and problems with the vestibular system;
• Systematic visual impairment.

These symptoms do not directly indicate that the problem lies specifically in the vertebral arteries, they just indicate. However, it is often associated with the vertebral arteries.

The non-linearity of the stroke means that instead of a straight and very shortcut to the brain, the artery is located along a convoluted trajectory. To correct the pathology, it is necessary to act not on the arteries, but on the primary problem - the cervical spine. Let's look at the causes of the disease in more detail.

Causes

Modern medicine shares the causes of non-straightness of the arteries in cervical spine spine into 2 categories – vertebrogenic and non-vertebrogenic.

Vertebrogenic causes are associated with pathologies of the development of the spine or changes in its structure, both in children and adults. In children this pathology may occur for the following reasons:

• Cervical spine injuries. They can occur at any age, including birth process, which is quite dangerous for a child;
• Pathological muscle spasms. Often droops as a result of hypothermia. Changes in the tone and location of the muscle affect the position of the artery, as a result of which the capacity of the latter decreases.

Vertebrogenic causes of pathology in adults arise for other reasons, among which the main ones are the following diseases:

• Swellings of the cervical spine or occipital part of the brain;
• Osteochondrosis;
• Ankylosing spondylitis;
• Trauma, as in children, can also affect the condition and location of the artery.

• Interesting read:

Among non-vertebral causes, it is worth noting the following groups of diseases:

• Inflammation, atherosclerosis, embolism and other diseases that cause loss of artery elasticity and tone;
• Diseases affecting the shape of the arteries, kinks, and so on;
• Pathologies associated with changes in the shape of arteries as a result of compression. Among the reasons are anomalous location ribs, tissue scarring as a result surgical intervention and so on.

The danger of non-straightness of both arteries is that it increases the likelihood of ischemic attacks in various areas brain. If you ignore the symptoms of the disease, there is a risk of cerebral stroke. Rehabilitation after a stroke is not always possible, and complete correction of its consequences is impossible.

Diagnostics

At the first manifestation of symptoms, you should contact your physician for an initial examination. After this, he gives a referral to a neurologist, who deals with further diagnostics and treatment of the disease. Most effective diagnostic methods when this problem occurs are:

• Ultrasound Dopplerography. This method examines both vertebral arteries for blood flow wave velocity to determine effectiveness. cerebral circulation and its reserve;
• MRI of the vessels of the cervical spine and brain. MRI allows you to determine the presence of aneurysms and inflammation in the arteries, including places where blood flow is disrupted;
• An X-ray of the cervical spine is also necessary, since with this method it is possible to see the condition of the bone tissue, the position of the vertebrae and processes, on the basis of which conclusions are drawn about possible;
• The use of a contrast agent, which is injected into the subclavian artery. This method called vascular angiography. It allows you to determine the presence of kinks or changes in the position of the arteries.

Advantages of treatment at the Innovative Vascular Center

The vascular surgeons of our clinic have significant experience in unique operations on the carotid arteries with pathological tortuosity. The main problem for surgical treatment is determining clear indications for surgical treatment. Our clinic has developed a clear diagnostic protocol that allows us to determine the clinical significance of a particular tortuosity and the degree of its effect on cerebral blood flow. The experience of successful operations in our clinic for pathological tortuosity exceeds 200 cases.

Causes and prevalence of pathological tortuosity

Pathological tortuosity always develops due to lengthening of the internal carotid artery, which is forced into bends or even loops. Excessive length of the internal carotid artery is often formed during embryonic development, that is, the tortuosity of the artery is most often congenital. With age, further twisting of the redundant carotid artery into a loop may occur. According to some researchers, pathological tortuosity may be the cause of neurological and intellectual problems in children of preschool and primary school age.

Lengthening of the internal carotid artery can also develop as a result of advanced hypertension, when constantly elevated blood pressure causes changes in the artery wall and its bends. Such tortuosity rarely affects cerebral hemodynamics and is more often a phenomenon detected incidentally by ultrasound of the great arteries.

Pathological tortuosity of the carotid arteries was detected in 16% of patients who died from ischemic stroke, more than 23% of children who suffered an ischemic stroke had pathological tortuosity. When examining patients undergoing treatment for cerebrovascular accidents, pathological tortuosity was detected by ultrasound angioscanning in 12%. Various violations the course of the internal carotid arteries, according to pathological studies, were identified in 40% of people.

Clinical forms

Lengthening the artery. The most common is elongation of the internal carotid or vertebral artery, which leads to the formation of smooth bends along the course of the vessel. An elongated artery is rarely a cause of concern and is usually discovered during random examination. Lengthening the artery is important for ENT doctors, since the artery wall may be abnormally close to the palatine tonsils and may be accidentally damaged during tonsillectomy. With age, the elasticity of the arterial wall changes and smooth bends of the artery can become kinks, with the development of a picture of cerebral circulation disorders. When lengthening the arteries without kinks during ultrasound examination blood flow disturbances are not determined.

- bending of the artery at an acute angle. Kinking can be congenital, when cerebral circulation disorders are detected from early childhood and develop over time from an elongated carotid artery. The formation of kinks is promoted arterial hypertension, progression of atherosclerosis in the internal carotid artery. Clinically, kinking of the internal carotid artery manifests itself transient disturbances cerebral circulation. With kinking of the vertebral artery, vertebrobasilar insufficiency develops. Detection of kinking with brain symptoms The question arises about surgical correction of tortuosity.

- formation of an artery loop. Despite the smooth movement of the loop, changes in blood flow in it are very significant. The nature of the bends during coiling may change depending on the position of the body, blood pressure. A chaotic nature of the blood flow is observed, which leads to a decrease in blood pressure after the loop and, accordingly, to a decrease in blood flow through the cerebral arteries. If a person has a well-developed circle of Willis on the lower surface of the brain, then he will never know about the existence of a loop or inflection. The appearance of symptoms of cerebral circulatory failure indicates disturbances in blood flow compensation and dictates the need for detailed examination and treatment.

Complaints and symptoms

Manifestations of pathological tortuosity are varied, the most common are:

• A picture of transient ischemic attacks in the blood supply of a tortuous artery with temporary paralysis of half the body or arm (hemiparesis), speech impairment, etc.);
• Temporary blindness in one eye;
• Noise in the head;
• Dizziness;
• Flashing before the eyes;
• Headaches without clear localization;
• Short-term loss of consciousness;
• Falls without loss of consciousness;
• Temporary imbalances;
• Migraine-like attacks.

Course and complications

If tortuosity of the carotid artery becomes symptomatic, then it is quite painful for the patient. Minor signs and symptoms of the disease gradually intensify and lead to decreased ability to work. The presence of pathological tortuosity can lead to symptomatic hypertension, which in turn contributes to the progression of tortuosity and the formation of kinks. In places where the carotid artery is bent, adhesions can form, which further disrupts the nature of blood flow, making it turbulent. Ultimately, these processes can lead to transient ischemic attacks or stroke.

The disease is characterized by elongation and sharp tortuosity of the arteries with the formation of kinks and impaired patency. Based on the shape, it is customary to distinguish between C-shaped, S-shaped tortuosity and looping (Fig. 18.7). The latter is the most unfavorable in terms of the development of hemodynamic disorders. Typically, kinking occurs when atherosclerosis and arterial hypertension and is most often localized in the internal carotid artery, usually before the entrance to the skull. In addition, the vertebral, subclavian arteries and brachiocephalic trunk may be affected. In the arteries lower limbs this type of circulatory disorder is much less common and has less clinical significance than in the brachiocephalic vessels.

Pathological physiology blood circulation in the area of ​​bends of the characteristic

Rice. 18.7. Pathological tortuosity (loop) of the internal carotid artery. MR angiogram.

is caused by the acceleration of particles moving along the outer edge of the vessel. A significant hemodynamic disturbance is observed at the point of inflection, where an acute angle is formed. Then a turbulent blood flow and a velocity gradient between the adductor and abducent knees appear, the linear speed of the blood flow increases, and the diameter of the lumen at the bend decreases. Tortuosity at right or obtuse angles is usually not hemodynamically significant. The study of pathologically tortuous arteries is greatly facilitated by three-dimensional CT and MR images.

Treatment. Surgeries for pathological tortuosity involve resection of the affected segment followed by direct end-to-end anastomosis.

18.5. Hemangiomas

Hemangiomas - benign tumors, developing from small blood vessels.

There are capillary, cavernous, racemose and mixed forms hemangiomas.

Capillary hemangiomas affect only the skin of the extremities and other parts of the body and consist of dilated, tortuous, closely spaced capillaries lined with well-differentiated endothelium.

Cavernous hemangiomas consist of dilated blood vessels and many cavities of varying sizes, lined with a single layer of endothelium, filled with blood and communicating with each other by anastomoses.

Racemotic hemangiomas are an anomaly of vascular development in the form of a plexus of thickened, dilated and serpentinely tortuous vessels, among which extensive cavernous cavities are often found. Both of the latter forms of hemangiomas are located not only in the skin and subcutaneous tissue, but also in deeper tissues, including muscles and bones. Malignancy of hemangiomas is possible.

The color of the skin in the area of ​​the hemangioma changes from red to dark purple. With capillary hemangiomas it is bright red, and with superficial cavernous and racemosa angiomas it varies from bluish to bright purple. The skin temperature in the area where hemangiomas are located is increased, which is explained by the increased influx of arterial blood and greater vascularization. Superficially located cavernous and racemosa hemangiomas are usually of a soft consistency, reminiscent of an easily compressible sponge.

Complications of hemangiomas located in the thickness of the skin and subcutaneous tissue are trophic changes and bleeding, which occur more often with injuries. Bleeding can be significant if the tumor communicates with large vessels.

The main symptoms of deep hemangiomas growing into muscles and

bones are pain in the affected limb caused by compression or involvement in pathological process nerve trunks. Palpation reveals a tumor of soft-elastic or dense-elastic consistency without clear boundaries. With arterial racemonic hemangiomas, it is sometimes possible to notice the pulsation of the swelling and palpation to determine the symptom of “cat purring”. Extensive hemangiomas are often combined with congenital arteriovenous fistulas and are accompanied by hypertrophy of soft tissues, some lengthening of the limb, and disruption of its function.

Diagnosis of hemangiomas is based on clinical data and the results of additional research methods, among which the most informative is arteriography. It allows you to identify the structure of the tumor, its extent and connection with the main arteries. To clarify the condition of the deep veins of the affected limb and their possible connection with hemangiomas, venography is used.

During an X-ray examination of the bones of the limb, in the case of pressure of a vascular tumor on the bone tissue, the radiographs reveal uneven bone contours, thinning of the cortical layer, bone defects, and sometimes osteoporosis with small foci of rarefaction.

Treatment. For conservative treatment, cryotherapy, electrocoagulation are used, and sclerosing drugs are injected directly into the hemangioma. Surgical treatment consists of excision of hemangiomas. Removal of deeply located and extensive hemangiomas is associated with the risk of massive bleeding, therefore, for preventive purposes, preliminary ligation or embolization of the arteries feeding the vascular “tumor”, suturing and suturing of hemangiomas is justified. In some cases, combined treatment is carried out, which begins with the introduction of sclerosing agents into the vascular tumor, followed by cryotherapy and repeated embolization of afferent vessels.

18.6. Arterial injuries

It is customary to distinguish between open and closed vascular injuries. In case of open injuries, the integrity of the skin or mucous membranes is compromised, there is infected wound. Typically, open injuries are accompanied by more or less profuse external bleeding. Injuries to arteries from firearms are fundamentally different from stab and cut wounds in the mechanism of injury and more extensive destruction of soft tissue and disruption of the functions of nearby nerves and organs. A gunshot wound requires urgent surgical treatment with intervention on the damaged vessel.

Closed injuries occur with blunt soft tissue trauma. They are characterized by hemorrhages along the neurovascular bundle, the formation of extensive hematomas, which can compress surrounding structures and cause additional functional disorders.

The most commonly damaged arteries are the femoral, brachial, and forearm arteries.

Pathological picture. In case of open injuries, the wound hole in the vessel wall is a direct continuation of the wound channel. There are three degrees of damage:

I degree. Injury to the wall of a vessel without opening its lumen (arterial contusion) and bleeding. An aneurysm may later develop at the site of wall damage;

II degree. Injury to all layers of the wall with opening of the lumen of the vessel, but without completely crossing the latter. A wound in the wall of a vessel can be accompanied by life-threatening bleeding or become thrombosed, which leads to stopping the bleeding;

III degree. Complete intersection of arteries with massive bleeding. By screwing in the intima, in some cases the bleeding can stop.

In case of closed arterial injuries due to blunt trauma, they are also distinguished:

damage to the intima only (grade I);

damage to the intima and muscle membrane (II degree);

damage to all layers of the vascular wall - ruptures, crushing (III degree).

Damage of the I-II degree is accompanied by arterial thrombosis or compression of collaterals, limb ischemia. Open and closed wounds of arteries are often combined with extensive damage to soft tissues, veins, fractures and dislocations of bones, contusion or injury to nerve trunks.

Clinical picture and diagnosis. The main symptom of open arterial injuries is bleeding. In case of damage to the main arteries of the II-III degree, the bleeding becomes threatening and can lead to hemorrhagic shock. When the size of the defect in the vessel wall is small (grade II damage), the hole can be closed by a thrombus. In such cases, damage to the artery is recognized only on the 2-3rd day after the injury. The accumulation of blood in the surrounding tissues leads to the formation of a tense hematoma, which can put pressure on the vascular bundle and thereby worsen blood circulation in the limb and increase the symptoms of ischemia. Limb ischemia is most pronounced with complete rupture of the vessel (III degree) as a result of both open and closed trauma.

The main symptoms of ischemia are pain in the distal parts of the limb, pallor and coldness of the skin, absence of a peripheral pulse, and impaired sensitivity (from hypoesthesia to complete anesthesia). With severe ischemia, paralysis and muscle contracture occur. In a number of victims, it is possible to detect a pulsating swelling (pulsating hematoma) in the area of ​​injury, which indicates the presence of a hematoma communicating with the lumen of the artery. A blowing systolic murmur is heard above the projection of the pulsating hematoma.

Closed arterial injuries are also accompanied by symptoms of ischemia. Its cause may be thrombosis of the lumen of the vessel due to damage to the intima (I and II degrees), compression by an extensive hematoma in cases of rupture or crush of the artery (III degree).

Diagnosis of open arterial injuries is usually not difficult. However, with closed injuries combined with bone fractures and nerve damage, recognition of vascular injuries is difficult. The main clinical signs indicating damage to the artery, in this case, are pain distal to the site of injury, which does not disappear after immobilization, reposition of fragments or reduction of dislocation; pallor (cyanosis) of the skin; lack of movement and sensitivity, disappearance of peripheral pulse. Diagnosis is greatly facilitated by ultrasound and arteriography.

Treatment. It is extremely important to temporarily stop the bleeding at the scene. In some cases, asep-

tic pressure bandage, in others - wound tamponade, digital pressure on the bleeding artery, application of a tourniquet. It is unacceptable to leave the tourniquet in place for 2 hours or more, as this aggravates the severity of ischemia of the affected limb. It must be removed hourly, and the artery must be pressed with a finger. IN medical institution if necessary, measures should be taken to combat blood loss (blood transfusions and plasma-substituting solutions); cardiac and painkillers and oxygen inhalations are prescribed according to indications. If conditions allow for surgical intervention, but it is not possible to apply a vascular suture, then sometimes they resort to temporarily connecting the ends of the damaged artery with a silicone tube to restore the main blood flow, after which the wounded person is urgently sent to a specialized department for final intervention on the damaged vessel.

Operation for traumatic injuries arteries provides for primary surgical treatment of the wound and restoration of the main blood flow through damaged vessel. For small stab and cut wounds of the arteries, a lateral vascular suture is applied using an atraumatic needle; for longitudinal wounds, a patch from a vein is used. When the size of the defect in the vessel wall with its complete rupture (III degree) reaches 1-3 cm, the vessel is mobilized, the damaged section of the artery is excised and a circular vascular suture is applied. A significant discrepancy between the ends of the damaged artery is an indication for plastic replacement of the resulting defect with an autovenous graft from the great saphenous vein or a synthetic prosthesis. Reconstruction of small-caliber arteries (fingers, hand, forearm, leg) is only possible using microsurgical techniques, when the vascular suture is performed under a microscope.

The results of surgical treatment of arterial wounds are largely determined by the severity of limb ischemia. Due to the fact that irreversible changes in muscle tissue often occur after 6-8 hours of hypoxia, this period of time should be targeted when providing timely surgical care to the majority of victims. However, if the viability of the limb is preserved, then restoration of blood flow through the damaged artery should be achieved regardless of the period that has passed since the injury. Only the presence of irreversible ischemia, as evidenced primarily by the disappearance of deep sensitivity and contracture of the muscles of the distal limbs, is an indication for amputation.

18.7. Obliterating diseases

Chronic diseases of the aorta and arteries lead to disruption of blood flow through the vessels due to obliterating (stenotic) or dilating (aneurysmal) lesions. The most common causes of arterial obliteration or stenosis are: 1) obliterating atherosclerosis, 2) nonspecific aortoarteritis, 3) thromboangiitis obliterans (endarteritis). Regardless of the cause of vessel obliteration, more or less pronounced tissue ischemia appears, to eliminate which reconstructive operations are used, taking into account the characteristics of the pathological process. General characteristics of obliterating vascular diseases are given below.

18.7.1. Obliterating atherosclerosis

It is the most common disease and is observed mainly in men over 40 years of age. The process is localized mainly in large and medium-sized arteries. The main cause of this disease is hypercholesterolemia. In the bloodstream, cholesterol circulates bound to proteins and other lipids (triglycerides, phospholipids) in the form of complexes called lipoproteins. Depending on the percentage of the components of these complexes, several groups of lipoproteins are distinguished, two of which (low and very low density lipoproteins) are active carriers of cholesterol from the blood to the tissues and are therefore called atherogenic. Atherosclerosis more often affects individuals with high levels of these atherogenic lipoprotein fractions.

Pathological picture. The main changes develop in the intima of the arteries. Pathological changes in the intima it is customary to distinguish between fatty streaks, fibrous plaques and complicated lesions (ulceration of plaques, formation of blood clots). Fatty streaks are the earliest manifestation of atherosclerosis, characterized by focal accumulation in the intima of lipid-filled macrophages, smooth muscle cells (foam cells) and fibrous tissue. On the intima they look like whitish or yellowish spots, clearly visible on preparations stained with fat-soluble dyes. Initial signs of damage may appear in childhood. Then their development stops. Despite the likely association of fatty streaks with fibrous atherosclerotic plaques, the location and distribution of aortic fatty streaks and fibrous plaques do not coincide. It is widely believed that fatty streaks undergo regression, but the evidence is inconclusive.

The formation of an atherosclerotic plaque begins with the accumulation of lipids in the intima (stage of lipoidosis). In the circumference of the foci of lipoidosis, proliferation of intima and smooth muscle fibers develops, young connective tissue appears, the maturation of which leads to the formation of a fibrous atherosclerotic plaque (stage of liposclerosis).

Fibrous atherosclerotic plaques, called pearlescent, rise above the surface of the intima and represent its thickening, which can be determined by palpation. In typical cases, the fibrous plaque has a dome-shaped shape, a dense consistency, protrudes into the lumen of the artery and narrows it. The plaque consists of extracellular fat located in the central part, the remains of necrotic cells (detritus), covered with a fibromuscular layer, or visor, containing a large number of smooth muscle cells, macrophages and collagens. The thickness of the plaque significantly exceeds the normal thickness of the intima. The extracellular fat of plaques is similar in composition to plasma lipoproteins.

With abundant accumulation of lipids, blood circulation in the tissue membrane of plaques is disrupted. The cells included in the structure of the plaques undergo necrosis, hemorrhage occurs in the thickness of the plaque, cavities appear filled with amorphous fat and tissue detritus. This is often accompanied by the formation of a defect on the surface of the intima, plaques ulcerate, and atheromatous masses and parietal thrombotic deposits are rejected into the lumen of the vessel and, entering the distal bloodstream with the bloodstream, can cause microembolism. In tissue elements

Rice. 18.8. Changes developing in the arterial wall during atherosclerosis (schematic representation). Explanation in the text.

plaques and calcium salts are deposited in areas of degenerating elastic fibers (atherocalcinosis). These processes occur in waves and lead to thrombosis and obliteration of the vessel (Fig. 18.8).

The favorite localization of atherosclerotic lesions is the division of the main arteries: the brachiocephalic trunk, the mouth of the vertebral arteries, the bifurcation of the aorta, the common carotid, the common iliac, the femoral and popliteal arteries. This phenomenon is explained by the peculiarities of hemodynamics. In the zone of arterial bifurcations, the intima experiences a blow from the main blood flow; here there is some slowing down and separation of the blood flow along the arterial branches. The main blood flow deviates from a straight path, forms turbulences that damage the intima and favor the formation of plaques. This suggests that atherosclerotic damage to arterial walls is, in to a certain extent, a chronic regenerative process in response to chronic trauma to the intima by turbulent and direct blood flow.

Obliterating atherosclerosis of the main arteries of the lower extremities is the most common disease of peripheral arteries, often arising against the background of such unfavorable factors like hypertension, diabetes, obesity, smoking. Since the appearance of the first clinical symptoms the disease progresses rapidly. The process is localized mainly in large vessels (aorta, iliac arteries) or in medium-sized arteries (femoral, popliteal). Narrowing and obliteration of these arteries cause severe ischemia of the limbs. The abdominal aorta is usually affected distal to the renal arteries. In approximately one third of patients the aortoiliac segment is affected (Leriches syndrome), and in 2/3 patients the femoral-popliteal segments are affected.

18.7.2. Nonspecific aortoarteritis

A disease of autoimmune origin, belonging to the group of nonspecific inflammatory diseases, affects the aorta and its large branches. Synonyms for nonspecific aortoarteritis are: pulseless disease, Takayasu syndrome, aortic arch, arteritis of young women. The disease occurs more often in women under 30 years of age.

Pathological picture. Morphologically nonspecific

aortoarteritis is a systemic chronic productive process in the wall of the aorta and its large branches, starting with inflammatory infiltration of the adventitia and media. In the middle layer, a picture of productive inflammation is observed, smooth muscles and elastic fibers are subject to destruction. A pronounced peri-process occurs around the vessel due to the thickening of the adventitia and its fusion with the surrounding tissues. The intima is affected secondarily, reactive thickening is observed in it, which entails sharp narrowing or complete closure of the mouth and lumen of the affected arteries, fibrin deposition is often observed on the intimal surface. The media atrophies and is compressed by the wide fibrous intima and the sleeve of thickened adventitia. In the later stages of nonspecific aortoarteritis, secondary atherosclerotic changes may appear: obliteration, fibrosis and calcification of the main arteries. In this case, even histologically it can be difficult to distinguish arteritis from atherosclerotic vascular lesions.

The pathological process in 70% of patients is localized in the aortic arch and its branches, in 30-40% - in the interrenal segment of the abdominal aorta and renal arteries. The process is equally often observed in the descending thoracic aorta and the bifurcation of the abdominal aorta (18 %). In 10% of patients the process is localized in the coronary arteries, in 9% - in the mesenteric vessels, in 5% - in pulmonary artery. In this case, the same patient may have damage to several arteries. The lesion, as a rule, is segmental in nature and is limited to the mouths and proximal parts of the branches extending from the aorta. The disease is characterized by a slowly progressive course.

There are three stages of the disease: acute, subacute and chronic. The disease begins in childhood or adolescence. Patients develop weakness, fatigue, low-grade fever, sweating, weight loss, joint pain, tachycardia, shortness of breath, and sometimes cough. An increase in ESR, leukocytosis, and an increase in the level of γ-globulins and C-reactive protein are detected in the blood. After a few weeks or months, the disease takes on a subacute course, and after 6-10 years from its onset, symptoms of damage to one or another vascular system appear.

Involvement of the aortic arch and its branches in the pathological process leads to chronic ischemia of the brain and upper extremities. Damage to the mesenteric arteries is accompanied by ischemia of the digestive organs. When the bifurcation of the abdominal aorta and iliac arteries is damaged, ischemia of the lower extremities occurs. With stenosis of the descending aorta, coarctation syndrome develops, and with renal artery stenosis, vasorenal hypertension syndrome develops. The disease can be complicated by the formation of an aneurysm. Clinical picture of these syndromes is described in the relevant sections.

18.7.3. Thromboangiitis obliterans(Winiwarter's disease-Burger)

Synonyms of the disease are: obliterating endarteritis, obliterating endocrine-vegetative arteriosis [Oppel V.A., 1928], spontaneous gangrene. Thromboangiitis obliterans (endarteritis) is an inflammatory chronic, recurrent, segmental, multilocular disease of nonspecific origin, which affects the walls of small and medium-sized arteries. Obliterate-

Common thromboangiitis is an allergic autoimmune disease. It is characterized by the presence of autoantibodies and circulating immune complexes in the blood, which confirms the autoimmune genesis of the disease. Antiphosphorus and anti-elastin antibodies and increased levels of immunoglobulins class A and M are also detected. Young men under 40 years of age are most often affected. The development of thromboangiitis is facilitated by factors that cause persistent vasospasm (smoking, hypothermia, repeated minor injuries). Long-term spasm of the arteries and vasa vasorum leads to chronic ischemia of the vascular wall, resulting in intimal hyperplasia, adventitial fibrosis and degenerative changes in the intrinsic nervous system of the vascular wall. In the late stages of disease development in the walls large vessels Atherosclerotic changes are often found. Against the background of altered intima, a parietal thrombus is formed, narrowing and obliteration of the lumen of the vessel occurs, which often ends in gangrene of the distal part of the limb. In the final stage of the disease, fibrous tissue grows and calcium salts are deposited in the area of ​​thrombosis.

If at the onset of the disease the distal sections of the vessels of the lower extremities are affected, in particular the arteries of the leg and foot, then later larger arteries (popliteal, femoral, iliac) are also involved in the pathological process. The disease can be combined with migrating thrombophlebitis of the superficial veins.

18.7.4. Obliterating lesions of the branches of the aortic arch

Chronic obstruction of the patency of the brachiocephalic vessels causes ischemia of the brain and upper extremities.

Etiology and pathogenesis. The most common causes of damage to the branches of the aortic arch are nonspecific aortoarteritis and atherosclerosis. In atherosclerosis, the bifurcation of the common carotid artery is most often affected, and less often - the mouth of the brachiocephalic trunk, subclavian, and vertebral arteries. Nonspecific aortoarteritis affects the branches of the aortic arch (common carotid and subclavian arteries). Less commonly, extravasal compression leads to disturbances in the patency of the branches of the aortic arch: compression of the subclavian artery by a highly located 1st rib or accessory cervical rib, hypertrophied anterior scalene or pectoralis minor muscle, compression of the vertebral artery by osteophytes in severe cervical osteochondrosis, etc. One of the reasons for the disturbance of the patency of the brachiocephalic arteries may be be their deformation - pathological tortuosity and kinks.

With stenosis, which narrows 70-80% of the lumen of the vessel, volumetric blood flow decreases and turbulent flows appear. In post-stenotic areas, a slowdown in blood flow occurs, which favors platelet aggregation at the locations of atherosclerotic plaques and thrombus formation. The detachment of thrombus particles leads to microembolism of cerebral vessels. Embolism can occur when cerebral vessels are blocked by fragments of an atherosclerotic plaque that is collapsing due to ulceration or hemorrhage.

In the pathogenesis of disorders associated with circulatory disorders, the main role is played by ischemia of areas of the brain that are supplied with blood from the affected artery. If one of the four arteries of the brain (internal carotid or vertebral) is damaged,

supply to the corresponding areas of the brain is compensated by retrograde blood flow through the circle of Willis and the inclusion of extracranial collaterals. However, such a restructuring of blood flow sometimes leads to a paradoxical effect - a deterioration in cerebral circulation. So, for example, with occlusion of a segment of the subclavian artery medial to the origin of the vertebral artery, blood flows into the distal segment subclavian artery and, consequently, it begins to flow into the upper limb from the circle of Willis of the brain through the vertebral artery, depleting cerebral blood flow, especially during physical activity (subclavian-vertebral steal syndrome). The vertebral artery becomes a collateral for blood supply to the upper limb on the affected side.

Diseases of the cerebral vessels. About 80% of occlusive diseases of the branches of the aortic arch, causing disruption of the arterial blood supply to the brain, are caused by atherosclerotic lesions. Less common are aortoarteritis (giant cell arteritis - Takayasu's disease) and fibromuscular dysplasia. Acute symptoms of cerebrovascular accident may occur due to vascular embolism. Cerebral embolism is often caused by atherosclerosis of the carotid arteries. When an atheromatous plaque is ulcerated and destroyed, its particles (atheromatous detritus, small blood clots, microparticles of dead tissue) are transferred by the blood stream to small vessels brain and cause embolism, manifested by ischemia of the corresponding part of the brain and stroke.

It is customary to distinguish 4 degrees of cerebrovascular accident: asymptomatic, transient ischemic attacks (transient ischemic attacks), chronic vascular insufficiency, stroke and its consequences.

The asymptomatic stage of the disease is manifested only by systolic murmur over the carotid or other arteries. Instrumental examination (ultrasound, angiography) allows us to determine the degree of narrowing of the artery. If the lumen is significantly narrowed, surgical treatment is indicated to prevent stroke - severe, irreversible changes in the brain. Patients who have developed a persistent stroke after recovery also need surgical treatment to prevent stroke recurrence.

Vertebrobasilar insufficiency occurs as a result of microembolism or hypoperfusion of the vertebral or basilar arteries and is manifested by transient attacks of sensory disturbances, awkward movements and other symptoms that can be bilateral. The appearance of only one of the symptoms (dizziness, diplopia, dysphagia, imbalance) is rarely caused by vertebrobasilar insufficiency, but if they simultaneously occur in a certain combination, then its presence can be assumed.

Transient ischemic attacks are usually caused by microembolism of small branches of cerebral vessels, which occurs during ulceration and disintegration of atherosclerotic plaques in the carotid arteries. Neurological symptoms depend on the location of the embolus in the vascular bed of the brain or the vessels of the eyes, the size, structure of the microembolus, its ability to undergo lysis, as well as the degree of blockage of the vessel and the presence of collaterals. Hypoperfusion resulting from microembolism causes temporary visual impairment and associated neurological symptoms.

Acute unstable neurological disorders refer to the category of rapidly increasing transient episodes of cerebral ischemia, causing a mild stroke with gradually decreasing symptoms. These patients

require urgent treatment to prevent the development of permanent ischemic stroke.

Patients with chronic vascular insufficiency often complain of headaches, dizziness, ringing in the ears, and memory impairment. They experience short-term attacks of loss of consciousness, staggering when walking, and double vision. Sometimes one can observe lethargy, decreased intelligence, dysarthria, aphasia, and dysphonia. An objective examination often reveals weakness of convergence, nystagmus, changes in motor coordination, sensitivity disorders, short-term mono- and hemiparesis, and unilateral Bernard-Horner syndrome. Depending on the degree of vascular insufficiency of the brain, these neurological disorders are transient or permanent.

Visual impairment occurs when both the carotid and vertebral arteries are damaged. They range from slight decrease in vision to complete loss of vision. Patients often complain of the presence of a veil or a grid before the eyes.

Insufficient blood supply to the upper extremities manifested by their weakness, increased fatigue, and chilliness. Severe ischemic disorders appear only with occlusion of the distal vessels of the arm. The pulsation of the arteries distal to the site of vessel damage is usually absent or weakened. When the subclavian artery is damaged, blood pressure in the corresponding arm decreases to 80-90 mmHg. Art., a systolic murmur is heard over the stenotic arteries. With stenosis of the bifurcation and internal carotid artery, it is clearly defined at the angle of the lower jaw; when the brachiocephalic trunk is narrowed - in the right supraclavicular fossa behind the sternoclavicular joint. The degree of impairment of the blood supply to the upper extremities can be determined by a test reminiscent of the test that causes intermittent claudication. In a sitting position, the patient is asked to raise his hands up and quickly clench and unclench his hands into a fist. The time of onset of hand fatigue and the time of onset of pain are noted. The symptom is positive when there is stenosis of the subclavian artery distal and proximal to the branch of the vertebral artery (steal syndrome, in which blood enters the subclavian artery from the circle of Willis through the vertebral artery).

Compression of the subclavian vessels and nerves (thoracicoutletsyndrome).

Compression syndrome of the subclavian vessels and nerves can be caused by an accessory cervical rib (cervical rib syndrome) or a highly located 1st rib (costoclavicular syndrome), hypertrophied anterior scalene muscle and its tendon (anterior scalene syndrome), pathologically altered pectoralis minor muscle (syndrome) Wright, or pectoralis minor muscle). With the listed syndromes, compression of both the artery and the brachial plexus occurs, so the clinical picture consists of vascular and neurological disorders. Patients usually complain of pain, chilliness, paresthesia, weakness of the arm muscles, and often note acrocyanosis and swelling of the hand. It is characteristic that in certain positions of the arm and head the symptoms of arterial insufficiency worsen. This is manifested by increased pain and paresthesia, the appearance of a feeling of heaviness in the arm, and a sharp weakening or disappearance of the pulse in the radial artery. Thus, in patients suffering from the syndrome of the anterior scalene muscle and cervical rib, the most significant compression of the subclavian artery and deterioration in blood supply occur when the raised arm, bent at a right angle at the elbow joint, is moved back while simultaneously turning the head sharply with the chin raised

Rice. 18.9. Atherosclerotic plaque causing stenosis of the internal carotid artery. Sonogram.

in the opposite direction and holding it in this position (Adson test); in patients suffering from costoclavicular syndrome - when abducting the arm backwards and downwards, and in patients with Wright's syndrome - when raising and abducting the affected arm, as well as throwing it back to the back of the head. Constant trauma to the artery and nerves leads to cicatricial changes around these anatomical formations and severe functional disorders. Symptoms of the disease rarely occur in childhood and adolescence. Even the cervical rib does not cause noticeable disorders in young men. This suggests that changes in the relationship of the structures between the collarbone and the upper chest, which develop gradually with age, are the main cause of the disease. The symptoms of the disease are caused not so much by periodically occurring disorders of the blood supply to the upper limb, but by transient compression of one or more trunks of the brachial plexus. A number of patients develop noticeable trophic disorders on the affected side.

Correct assessment clinical picture, the results of tests with changes in the position of the limb, instrumental studies allow for a differential diagnosis of these syndromes with Raynaud's disease.

Among the non-invasive research methods used in the diagnosis of lesions of the branches of the aortic arch, Doppler ultrasound is the most informative, with the help of which the direction and speed of blood flow and the presence of flow from one pool to another are determined. With duplex scanning using modern ultrasound devices, it is possible to accurately determine the localization and extent of pathological changes, the degree of arterial damage - occlusion, stenosis, the nature of the pathological process - atherosclerosis, aortoarteritis (Fig. 18.9). When planning surgical interventions, panarteriography of the aortic arch according to Seldinger or selective arteriography of its branches is performed. Traditional X-ray contrast angiography can be replaced by CT or MR angiography.

In patients with an additional cervical rib, as well as costoclavicular syndrome, radiographic data are of particular value.

Treatment. The need for reconstructive interventions for occlusive lesions of the brachiocephalic vessels is dictated by frequent development ischemic strokes. Indications for surgery are hemodynamically significant (more than 60-70%) stenoses or occlusions, as well as lesions that can become a source of embolism of intracranial arteries (unstable plaques complicated by hemorrhage or ulceration).

For isolated lesions of the brachiocephalic arteries, X-ray endovascular procedures are currently being introduced - balloon dilatation, endovascular stent installation. With segmental occlusions of the common carotid and initial segment of the internal carotid arteries, bifurcation

carotid artery, stenosis of the vertebral artery mouth, open endarterectomy is performed. In case of proximal occlusion of the subclavian artery, leading to the development of subclavian steal syndrome, the operation of choice is carotid-subclavian bypass with an autovein or synthetic prosthesis, or resection of the subclavian artery with implantation of its end into the common carotid. In case of widespread damage to the main arteries of the aortic arch, their resection with prosthetics or bypass surgery is performed. In case of multiple lesions of the branches of the aortic arch, simultaneous reconstruction of several arteries is performed. In the case of pathological tortuosity of vessels, the best type of operation is considered to be resection followed by direct end-to-end anastomosis.

In patients with vascular obstruction caused by extravasal compression, it is necessary to eliminate the cause of compression. According to indications, scalenotomy, resection of the first rib, intersection of the pectoralis minor or subclavian muscle, etc. are performed.

If it is impossible to perform reconstructive surgery, surgical interventions on the sympathetic nervous system are advisable: upper cervical sympathectomy (C, -C and), stellectomy (C VII) (removal or destruction of the cervicothoracic (stellate) ganglion (ganglion stellatum) and thoracic sympathectomy (Th n -Th IV) After surgery, peripheral resistance decreases and blood circulation in the collaterals improves.

18.7.5. Obliterating diseases of the visceral branches of the aorta

Chronic abdominal ischemia. The disease is caused by occlusive lesions of the visceral branches of the abdominal aorta, which manifest themselves as pain after eating, weight loss, and systolic murmur in the epigastric region above the aorta projection.

Etiology and pathogenesis. The most common causes of damage to the mesenteric vessels and celiac trunk are atherosclerosis and nonspecific aortoarteritis, less often - fibromuscular dysplasia, anomalies of the visceral arteries. Violation of their patency also occurs with extravasal compression, to which the celiac trunk is often subjected. Its compression can be caused by the falciform ligament and the medial crus of the diaphragm, neurofibrous tissue of the celiac (solar) plexus.

Atherosclerotic lesions of the mesenteric arteries are more often observed in middle-aged and elderly people. Atherosclerotic plaques, as a rule, are located in the proximal arterial segments; the inferior mesenteric artery is most often affected, and less often the celiac trunk. Nonspecific aortoarteritis of this localization usually occurs in at a young age; the visceral branches are always affected together with the corresponding segment of the aorta. The defeat may be more extensive. Extravasal compression of blood vessels is observed equally often in any age group.

The concept of “chronic ischemia of the digestive organs” combines signs of circulatory disorders in three vascular systems: the celiac trunk, the superior and inferior mesenteric arteries. The deficiency of blood flow in the affected artery basin is compensated for a certain time by the redistribution of blood from other vascular basins. However, as the disease progresses, the compensatory capabilities of collateral circulation decrease. Most

Serious hemodynamic disturbances occur when several visceral arteries are simultaneously damaged. Then hemodynamic disorders become especially pronounced at the height of digestion, when the existing blood flow is not able to provide normal blood supply to certain areas of the gastrointestinal tract, in which ischemia develops. The mucous layer and submucosa of the digestive tract are most sensitive to hypoxia, therefore its glandular apparatus undergoes dystrophy, which leads to a decrease in the production of digestive enzymes and impaired absorption. At the same time, the function of the liver and pancreas is impaired. One of the consequences of chronic abdominal ischemia is an acute disturbance of visceral circulation, which occurs as a result of thrombosis of the affected artery and often ends in intestinal gangrene.

Clinical picture. Chronic abdominal ischemia is characterized by a triad of symptoms: pain, intestinal dysfunction, and weight loss. Based on the predominant clinical manifestations, 4 forms of the disease are distinguished: celiac (pain), proximal mesenteric (small intestine dysfunction), distal mesenteric (colon dysfunction) and mixed.

The main symptom of the disease is abdominal pain. When the celiac trunk is damaged, the pain is intense, localized in the epigastrium and occurs 15-20 minutes after eating. When the superior mesenteric artery is damaged, the pain is less intense, appears in the mesogastrium 30-40 minutes after eating, usually lasts 2-2 "/ 2 hours, i.e. throughout the entire period of maximum functional activity of the digestive tract. Pain is associated with accumulation in ischemic tissues of under-oxidized metabolic products affecting intraorgan nerve endings. When the inferior mesenteric artery is damaged, only 8% of patients develop It's a dull pain in the left iliac region. Patients note a decrease in pain when limiting food intake. Intestinal dysfunction is expressed in bloating, unstable stools, and constipation. Remnants of undigested food and mucus are often found in the stool.

Progressive weight loss is explained by a violation of the secretory and absorption capacity of the intestines, as well as by the fact that patients limit themselves in food for fear of an attack of pain.

Isolated damage to the visceral arteries is rare; more often it is combined with damage to other vascular areas, therefore in the differential diagnosis great importance acquires the correct interpretation of patient complaints.

When auscultating the abdomen in the epigastric region, a characteristic systolic murmur is often heard, caused by stenosis of the celiac trunk or superior mesenteric artery.

Laboratory data indicate a decrease in the absorption and secretory functions of the intestine. The coprogram reveals a large amount of mucus, neutral fat and undigested muscle fibers. With the progression of the disease, dysproteinemia develops, characterized by a decrease in the content of albumin in the blood and an increase in the level of globulins, the activity of ALT and LDH increases, and the thymol test indicators increase.

X-ray examination reveals slow passage of barium through the intestines, flatulence, and segmental intestinal spasms. Colonoscopy reveals diffuse or segmental colitis, atrophy of the ligament

zestous membrane, erosions and segmental stenoses with the disappearance of haustration are less common. Histological examination of biopsy specimens reveals swelling of the lamina propria of the mucous membrane, a decrease in the number of crypts, areas of fibrosis, dilation and ectasia of the vessels of the submucosal layer, and focal lymphoid cell infiltrates. The results of radioisotope studies usually indicate a decrease in the absorption of I" 31 -triolion and the absorption of 1 13 | -butyric acid.

If an occlusive lesion of the mesenteric arteries is suspected, a thorough X-ray, endoscopic and ultrasound examination of the gastrointestinal tract is necessary in order to exclude them organic lesions in the genesis of abdominal pain syndrome.

Duplex ultrasound scanning allows you to visualize the abdominal aorta and the initial parts of the celiac trunk and its branches (common hepatic and splenic arteries), as well as the superior mesenteric artery. With stenotic lesions, turbulent high-speed blood flow appears at the mouths of these arteries, the diameter of the affected vessel decreases, and post-stenotic expansion is observed.

Aortography performed in anteroposterior and lateral projections allows one to assess the condition of the orifices of the celiac and mesenteric arteries. An angiogram for chronic abdominal ischemia reveals both direct signs of damage to the visceral arteries (filling defects, narrowing, occlusion, poststenotic vasodilation) and indirect signs (retrograde filling, dilation of collaterals, poor contrast of the affected artery). CT or MR angiography can be used to assess the condition of the mesenteric vessels.

Treatment. In mild cases, conservative treatment is limited, including diet, antispasmodic and antisclerotic drugs, agents that improve tissue metabolism and the rheological properties of blood. Progression of the disease is an indication for surgical treatment.

To eliminate external compression of the celiac trunk, it is sufficient to dissect the scarred medial crura of the diaphragm, the falciform ligament of the liver, or the fibers of the celiac plexus. For stenoses and occlusions in the area of ​​the ostia of the visceral arteries, endarterectomy is effective, and in cases of widespread lesions, the operations of choice are either resection of the affected area followed by its prosthetics, or bypass surgery.

78.7.6. Diseases of the renal arteries. Vasorenal hypertension

Secondary symptomatic arterial hypertension develops as a result of stenosis of the renal artery, disruption of the main blood flow and blood circulation in the kidneys without primary lesion parenchyma and urinary tract. Characteristics of this disease are high blood pressure, impaired renal function, and suspicion of involvement of the renal artery in the pathological process. Vasorenal hypertension occurs in 3-5% of patients suffering from arterial hypertension. Most often the disease affects young and middle-aged people.

Etiology and pathogenesis. The causes of damage to the renal arteries are diverse: atherosclerosis, nonspecific aortoarteritis, fibrous

heteromuscular dysplasia, thrombosis and embolism, compression of arteries by tumors, etc. The first place in frequency is atherosclerosis (40-65%), the second is fibromuscular dysplasia (15-30%), the third is nonspecific aortoarteritis (16 -22%). Atheromatous plaque is usually located in the aorta and extends to the ostium renal artery. Much less often, atheroma is located directly in the renal artery (in 90% of patients, the lesion is bilateral. Fibromuscular dysplasia usually affects the middle or distal part of the renal artery and can spread to the branches. In 50% of patients, the lesion is bilateral). Narrowing of the artery occurs due to hyperplasia, which in the form of a ring surrounds the artery and concentrically narrows its lumen. The disease occurs predominantly in women under the age of 45; is the cause of hypertension in 10% of children with arterial hypertension. The most common causes of hypertension in children are renal artery hypoplasia, coarctation of the aorta, and Takayasu aortoarteritis.

Narrowing of the lumen of the renal arteries leads to hypoperfusion of the kidneys, a decrease in pulse pressure in its vessels. In response to these changes, hyperplasia of juxtaglomerular cells occurs. The latter, under these conditions, secrete a large amount of renin, which converts angiotensinogen circulating in the blood into angiotensin I, which is quickly converted into angiotensin II using angiotensin-converting enzyme. Angiotensin II constricts arterioles, causes hypoperfusion of the kidney, increases aldosterone secretion and sodium retention in the body. Hypertension occurs in response to renal hypoperfusion. A certain importance in the development of renovascular hypertension is also attached to a decrease in the level of some depressor and vasodilator substances that can be produced by the kidneys (prostaglandins, kinins, etc.).

Clinical picture and diagnosis. At the onset of the disease, most patients do not show symptoms of the disease. Only a few experience headaches, irritability, and emotional depression. A constant increase in diastolic pressure is sometimes the only objective symptom of the disease. On auscultation, a persistent systolic murmur may be heard in the upper abdomen on either side of the midline. If the cause of renovascular hypertension is atherosclerotic damage to the arteries, then other symptoms of atherosclerosis can be detected in patients. The absence of hypertension in the family and in close relatives, the early onset of hypertension (especially in childhood or in women during the transition to adulthood), its rapid increase in its degree, resistance to antihypertensive drugs and the rapid deterioration of renal function give grounds for the assumption of the presence of renovascular hypertension.

In the late stage of the disease, the symptoms of renovascular hypertension can be classified as follows: 1) symptoms of cerebral hypertension (headaches, dizziness, tinnitus, hot flashes, heaviness in the head, blurred vision); 2) overload of the left parts of the heart and coronary insufficiency(aching pain in the heart area, palpitations); 3) symptoms of kidney infarction (pain in the lumbar region, hematuria); 4) signs of secondary hyperaldosteronism (muscle weakness, paresthesia, polyuria). With atherosclerosis and nonspecific aortoarteritis, other vascular beds are often affected, so patients may have symptoms due to another localization of the pathological process.

Blood pressure in patients is sharply increased: systolic pressure

Rice. 18.10. Bilateral critical renal artery stenosis, a - before treatment; b - after endovascular installation of stents. Angiograms.

in most patients the temperature is above 200 mm Hg. Art., and diastolic - 130-140 mm Hg. Art. Hypertension is persistent and difficult to respond to conservative therapy. The borders of the heart are expanded to the left, the apical impulse is strengthened; an accent of the second tone is determined on the aorta. In some patients, a systolic murmur is heard in the projection of the abdominal aorta and renal arteries. The disease is characterized by a rapidly progressive course, leading to impaired cerebral circulation, severe retinal angiopathy, coronary and renal failure.

Urography and radioisotope renography are of great importance for diagnosis. A series of urograms reveal a slow flow of contrast agent into the calyces of the pelvis of the affected kidney, a slow release of contrast compared to a healthy kidney, which often has big sizes due to compensatory hypertrophy. The diseased kidney is reduced in size.

With isotope renography, a slow release of the isotope from the kidney on the affected side is noted. During the examination, it is necessary to exclude other causes of symptomatic arterial hypertension (diseases of the adrenal glands, damage to the renal parenchyma, central nervous system, brachiocephalic arteries). If the diagnosis is unclear, a kidney biopsy is used; determine renin activity in peripheral blood and in the blood flowing from the kidneys.

Angiography, being the final stage of diagnosis, is indicated when diastolic blood pressure increases above PO mm Hg. Art. and rapid increase in signs of renal dysfunction. With atherosclerotic vascular lesions, the angiogram reveals a characteristic narrowing of the mouth or initial section of the renal artery over 1.5-2 cm. In this case, the abdominal aorta and its visceral branches are simultaneously affected. In fibromuscular dysplasia, the narrowing is localized in the middle and distal parts of the renal artery; areas of expansion usually alternate with areas of annular contraction, resembling a thread with beads.

Treatment. Despite the emergence of modern antihypertensive drugs with pronounced inhibition of the renin-angiotensin-aldosterone system (angiotensin-converting enzyme inhibitors - captopril, ena-lapril, etc.), drug therapy, even successful, is non-physiological, since a decrease in blood pressure in conditions of renal artery stenosis leads to decompensation blood circulation and kidney shrinkage.

Rice. 18.15. Coronary artery bypass grafting with a synthetic prosthesis.

Rice. 18.16. Resection of the aortic bifurcation with prosthetics.

Operations for thromboangiitis obliterans are of limited use.

Currently, for occlusions of the distal bed (arteries of the leg and foot), methods of so-called indirect revascularization of the limb are being developed. These include types of surgical interventions such as arterialization of the venous system and revascularizing osteotrephination.

In the case of diffuse atherosclerotic damage to the arteries, when it is impossible to perform reconstructive surgery due to the severe general condition of the patient, as well as in distal forms of damage, spasm of the peripheral arteries is eliminated by performing a lumbar sympathectomy, as a result of which collateral circulation improves. Currently, most surgeons are limited to resection of two or three lumbar ganglia. Either unilateral or bilateral lumbar sympathectomy is performed. To isolate the lumbar ganglia, extraperitoneal or intraperitoneal access is used.

Modern equipment allows performing endoscopic lumbar sympathectomy. The effectiveness of the operation is highest in patients with a moderate degree of ischemia of the affected limb (stage II of the disease), as well as in lesions localized below the inguinal ligament.

With necrosis or gangrene, indications for limb amputation arise. In this case, the level of amputation depends on the level and degree of damage to the main arteries and the state of collateral circulation.

The scope of surgical intervention must be strictly individualized and performed taking into account the blood supply to the limb and the convenience of subsequent prosthetics. For isolated necrosis of the fingers with a clear demarcation line, disarticulation of the phalanges with resection of the head of the tarsal bone or necrectomy is performed. For more common lesions, amputations of the fingers, transmetatarsal amputations and amputation of the foot at the transverse chopard joint are performed. The spread of the necrotic process from the toes to the foot, the development of wet gangrene, and the increase in symptoms of general intoxication are indications for limb amputation. In some cases it can be performed at the level of the upper third of the leg, in others - within the lower third of the thigh.

Conservative treatment indicated in the early (I-Pa) stages of the disease, as well as in the presence of contraindications to surgery or the absence of technical conditions for its implementation in patients with severe ischemia. It must be complex and pathogenetic in nature. Treatment with vasoactive drugs is aimed at improving intracellular oxygen utilization, improving microcirculation, and stimulating the development of collaterals.

Basic principles of conservative treatment: 1) elimination of exposure to adverse factors (prevention of cooling, prohibition of smoking, drinking alcohol, etc.); 2) training walking; 3) elimination of vascular spasm with the help of antispasmodics (pentoxifylline, complamin, cinnarizine, vazaprostan, nikoshpan); 4) pain relief (non-steroidal analgesics); 5) improvement of metabolic processes in tissues (B vitamins, nicotinic acid, solcoseryl, anginine, prodectin, parmidin, dalargin); 6) normalization of blood coagulation processes, adhesive and aggregation functions of platelets, improvement of the rheological properties of blood (indirect anticoagulants,

for appropriate indications - heparin, rheopolyglucin, acetylsalicylic acid, ticlid, chimes, trental). The most popular drug in the treatment of patients with chronic occlusive arterial diseases is trental (pentoxifylline) at a dose of up to 1200 mg/day orally and up to 500 mg intravenously. In patients with critical ischemia (stages III-IV), vasaprostan is most effective.

In patients with autoimmune origin of the disease, there is a need to use corticosteroids and immunostimulants. Most patients with atherosclerosis require correction of lipid metabolism, which must be done based on data on the content of total cholesterol, triglycerides, high and low density lipoproteins. If diet therapy is ineffective, cholesterol synthesis inhibitors (enduracin), statins (Zocor, Mevacor, Lovastatin), calcium ion antagonists (verapamil, cinnarizine, Corinfar), and garlic preparations (Allicor, Alisat) can be used. Physiotherapeutic and balneological procedures can be used (UHF, microwave, low-frequency DMV therapy, magnetotherapy, low-frequency pulsed currents, electrophoresis of medicinal substances, radioactive, iodine-bromine, sulfide baths), hyperbaric oxygenation, sanatorium treatment are advisable.

It is especially important to eliminate risk factors by persistently seeking from patients a sharp reduction in the consumption of animal fats and a complete cessation of smoking. Regular and correct use of medications prescribed for the treatment of concomitant diseases (diabetes mellitus, hypertension, hyperlipoproteinemia), as well as diseases associated with dysfunction of the lungs and heart is necessary: ​​an increase in cardiac output leads to an increase in tissue perfusion below the site of occlusion, and therefore, and improving their oxygen supply.

Training walking is essential for the development of collaterals, especially with occlusion of the superficial femoral artery, when the patency of the deep femoral artery and popliteal artery is preserved. The development of collaterals between these arteries can markedly improve the blood supply to the distal parts of the limb.

The issues of treatment and rehabilitation of patients with obliterating atherosclerosis of the lower extremities are inextricably linked with the problem of treating general atherosclerosis. The progression of the atherosclerotic process sometimes significantly reduces the effect of reconstructive vascular operations. In the treatment of this kind of patients, along with drug therapy hemosorption is used.

Forecast disease largely depends on the preventive care provided to patients with obliterating diseases. They must be under clinical supervision (control examinations every 3-6 months). Courses of preventive treatment, which should be carried out at least 2 times a year, allow you to maintain the limb in a functionally satisfactory condition.

18.8. Aneurysms of the aorta and peripheral arteries

An aneurysm of a vessel is usually understood as a local or diffuse expansion of the lumen, exceeding the normal diameter by 2 times or more.

Classification of aneurysms by etiology:

1. Congenital aneurysms observed in diseases of the aortic wall (Marfan disease, fibrous dysplasia, Ehlers-Danlos syndrome).

2. Acquired aneurysms resulting from: 1) non-inflammatory diseases (atherosclerotic, postoperative, traumatic aneurysms); 2) inflammatory diseases (specific - tuberculosis and syphilis and nonspecific - aortoarteritis; mycotic lesions).

The cause of aneurysm formation may be idiopathic Erdheim's medionecrosis or medionecrosis during pregnancy.

18.8.1. Aortic aneurysms

Most aortic aneurysms are of atherosclerotic origin. Macroscopically, the inner surface of an atherosclerotic aneurysm is represented by atheromatous plaques, sometimes ulcerated and calcified. Inside the cavity of the aneurysm, compacted masses of fibrin are located near the wall. They constitute the "thrombotic cup". There is damage to the muscular membrane with degeneration and necrosis of the elastic and collagen membranes, a sharp thinning of the media and adventitia and thickening of the intima due to atheromatous masses and plaques - the elastic frame of the wall is practically destroyed. Gradually accumulating and compressing under blood pressure, thrombotic masses can almost completely fill the aneurysmal sac, leaving only a narrow lumen for blood flow. Due to the deterioration of trophism, instead of the expected organization of the “thrombotic cup”, necrosis occurs at the site of contact with the walls of the aneurysm, and the wall itself is damaged. Thus, fibrin deposits lead not to strengthening, but to weakening of the aneurysm wall.

According to the morphological structure, the walls of the aneurysm are divided into true and false.

The formation of true aneurysms is associated with damage to the vascular wall by various pathological processes (atherosclerosis, syphilis, etc.). With true aneurysms, the structure of the vascular wall is preserved. The wall of false aneurysms is represented by scar connective tissue formed during the organization of a pulsating hematoma. Examples of false aneurysms are traumatic and postoperative aneurysms.

Based on their shape, aneurysms are divided into saccular and fusiform. The former are characterized by local protrusion of the aortic wall, while the latter are characterized by diffuse expansion of the entire circumference of the aorta.

Pathological physiology. With an aneurysm, there is a sharp slowdown in the linear speed of blood flow in the sac and its turbulence. Only about 45% of the blood volume in the aneurysm enters the distal channel. The mechanism for slowing blood flow in the aneurysmal sac is due to the fact that the main flow of blood, passing through the aneurysmal cavity, rushes along the walls. The central flow slows down due to the return of blood caused by turbulence of the blood flow and the presence of thrombotic masses in the aneurysm.

According to the clinical course, it is customary to distinguish uncomplicated, complicated, dissecting aneurysms. The most common complications of aneurysms are: 1) rupture of the aneurysm sac with profuse, life-threatening bleeding and the formation of massive hematomas, 2) thrombosis of the aneurysm, arterial embolism with thrombotic masses, 3) infection of the aneurysm with the development of phlegmon of surrounding tissues.

People who have hypertension and other work problems of cardio-vascular system, they do not always know the exact cause of such disorders. In some cases, these problems are associated with the development of a special type of pathology - tortuosity of the vertebral arteries.

With it, a person’s risk of ischemic stroke increases many times over. At severe consequences a person may experience disruptions in cerebral circulation.

This pathology is characterized by deformation of the vertebral artery, due to which the speed of blood flow supplying the brain decreases. The disease is predominantly genetic in nature. Its characteristic feature is the predominance in arterial tissue elastic fibers.

At normal development arteries, their tissues predominantly contain collagen fibers. Elastic fibers are not durable. When they predominate, rapid wear and tear of the vessel walls occurs.

For this reason, they quickly become thin and instantly deform. Thinning of blood vessels against the background of progression of pathology becomes common cause development of ischemic stroke in humans.

Reference. The death of 30% of patients from stroke is associated with the development of this type of disease.

Causes of pathology

Tortuosity and asymmetry of the diameters of the vertebral arteries mainly arises as a result of the action hereditary factors. The pathology may be acquired. IN special group at risk include people suffering from arterial hypertension.

One of the likely factors in the formation of arterial tortuosity is atherosclerosis. Given this chronic disease due to a malfunction in lipid and protein metabolism, cholesterol deposits occur on vascular walls. Risk factors for the development of atherosclerosis and accompanying arterial tortuosity include:

• overweight;
• smoking;
• unhealthy diet;
• constant stress;
• concomitant diseases associated with metabolic disorders (diabetes mellitus, hypothyroidism).

Symptoms

The disease is similar in its symptoms to a number of other pathologies, including:

• stroke;
• vascular dystonia;
• bulging of the arterial wall (aneurysm);
• atherosclerosis.

Important! In the disease there are two specific symptoms, manifested in humans. He may have sudden paralysis and arm weakness, as well as temporary speech impairment.

Various symptoms are possible, and treatment for tortuosity of the vertebral arteries will be prescribed taking into account the nature of their manifestation. Associated signs of pathology may also be:

The symptoms of the disease depend on the type and form of tortuosity of the arteries:

1. C-shaped tortuosity of the right vertebral artery, like the left one, in the first stages of its occurrence it does not show any signs. Often, as a result of progressive deformation and kinking of the artery, a violation occurs cerebral blood supply. The symptoms are identical to those of a stroke.
2. Loop crimp provokes sharp attacks of headaches, signs of stroke and disruption of blood circulation in the brain appear.
3. Deformation of the artery at an acute angle in some cases it occurs against the background of an existing c-shaped tortuosity arteries. A person develops symptoms over a long period of time characteristic symptoms hypertension and atherosclerosis. Associated signs of these phenomena are dizziness, nausea with vomiting and tinnitus.

Diagnostics

The following diagnostic methods are used to recognize the disease:

Treatment

There are several options for how to treat congenital tortuosity vertebral arteries:

• conservative method by taking medications to reduce blood pressure and eliminating symptoms in case of disruption of the vestibular apparatus;
• surgical intervention.

Treatment in the form of surgery is used only in extreme cases at high probability development of acute ischemic stroke in the patient, during which serious damage to the first arterial segment occurs.

The indication for surgery is stenosis of blood vessels, as well as their severe bending. During the intervention, metal awnings are used, fixed in the vessel and preventing it from narrowing again. Balloon-type catheters are also used during operations. With their help, it is possible to expand certain areas of blood vessels in which there is a risk of dangerous narrowing.

Often the operation is performed on a child after birth or during childhood, when the pathology is especially manifested in the form of a life-threatening cerebrovascular accident.

If tortuosity is not fatal dangerous threat for the life of the patient, he is prescribed symptomatic treatment.

Drugs are more commonly used to lower blood pressure and prevent stroke. Since the pathology is accompanied by a malfunction in the functioning of the vestibular apparatus, then additionally within the framework drug therapy Medicines may be prescribed to eliminate the manifestations of such disorders.

Attention! Drug treatment does not eliminate the pathology completely, but it can significantly improve a person’s quality of life and reduce the likelihood of developing a stroke.

Danger of pathology

There are several reasons why tortuosity of the vertebral artery is dangerous:

• it leads to a disruption in cerebral circulation;
• provokes constant headaches and attacks, accompanied by a sudden loss of consciousness;
• leads to the development of sudden ischemic stroke, which becomes a harbinger of lifelong disability or death.

Disease Prevention

Since pathological tortuosity of the left vertebral artery, like the right, more often occurs as a result of the influence of a genetic factor, prevention of the disease includes compliance with a number of rules to alleviate existing symptoms and prevent the development of stroke. For this it is important:

Conclusion

Tortuosity of the vertebral arteries is a hereditary disease and is manifested by numerous symptoms similar to other diseases.

Surgical treatment of arterial pathology is used in in case of emergency when there is a risk of the patient developing an ischemic stroke. In other cases, conservative treatment is carried out, which does not eliminate the disease, but helps to improve the patient’s condition.

Pathological tortuosity of the vertebral arteries causes problems in the body. An analysis of such a painful condition and recommendations for its relief in response to this letter...

Hello!
I fell from the tree on the back of my head and there was a brief loss of consciousness. I didn’t go to the hospital, after 5 years the attacks began, at first the objects I was looking at partially disappeared, then a severe headache began. Subsequently, he prevented the onset of an attack by taking lingonberries. After some time, my mother brought a grayish-brown powder, which I sniffed and then sneezed for a minute. I don’t remember how long I did this, but there were no more attacks.

Already as a student, after I inflated several balloons, the attack occurred again, I was lucky - I found lingonberries. Until I was 57 years old, there were no attacks, but for 3 days in a row everything is fine in the morning, at 10-11 o’clock the attack begins, I take lingonberries, there are no severe headaches, my head is heavy all day.

Dear Vladimir Stepanovich! Due to the fact that the town is small, therefore there may not be any competent specialists, I ask you, tell me: what is the algorithm for my actions to cure this phenomenon?

- Evgeniy Nikolaevich Zverkov

Hello, Evgeniy Nikolaevich!

The fact that you lost consciousness indicates that you then suffered a concussion. Most likely, at that time you had both nausea and retrograde amnesia (you may no longer remember this now). And then your body gradually coped (not fully, of course) with this situation... And there was a lull until pathological tortuosity of the vertebral arteries arose... However, let me tell you everything, Evgeniy Nikolaevich, in order... So...

Pathological tortuosity of the vertebral arteries: analysis of the condition

What is happening to you now, Evgeniy Nikolaevich, can happen according to various reasons, as extracerebral (narrowing or complete closure-occlusion of the brachiocephalic or vertebral arteries - the so-called vertebral artery syndrome, or chronic disturbance of cerebral circulation in the vertebrobasilar region), and intracerebral (discoordination in the activity of the circle of Willis, sclerosis of intracerebral arteries, etc.). You can write a lot about this for a long time.

Perhaps the most common cause of noise in the head, a feeling of heaviness in it, dizziness, an anxious and suspicious state (the state of the so-called “floating anxiety”) is “vertebral artery syndrome”... What is it? But here's what... As the intervertebral discs in the cervical spine are destroyed, their height decreases, which leads to pathological tortuosity of the vertebral arteries, which pass in the transverse processes of the cervical vertebrae (with the exception of the 7th). This leads to a deterioration in the blood supply to the brain, especially its stem structures and the cerebellum... In response to this, the brain responds with heaviness in the head, noise in it, dizziness and headache... And with all this, compression (compression) of the sympathetic cervical nerve plexus, which leads to pain in the neck muscles, to the so-called myogelosis of the neck muscles, that is, to their excessive tension, as well as to a feeling of numbness in the hands...

1. Peel all the cloves of garlic, wipe them, put them in a jar and pour in 1 cup of unrefined sunflower oil. You can find a recipe and regimen for taking this wonderful remedy in my article "".
2. 3 tablespoons of dry crushed St. John's wort herb pour 1 cup of boiling water into a thermos. Leave for 2 hours, strain. Take 1/3 cup 3 times a day before meals. The course is 1.5 months, the break is 1 month and again the course is 1.5 months.
3. Drink daily for 3 months Oregano herb tea. A break of 1 month and again a course of 3 months.
4. Take 0.2 g daily Mumiyo(in the morning on an empty stomach, washed down with low-fat warm milk or warm grape juice – 2-3 sips) for 10 days. A break of 7 days and again a course of 10 days. Conduct 4-5 such courses.
5. Propolis-garlic tincture
6. Rose hip decoction. You can find the recipe and regimen for taking this wonderful remedy in my article “”.
7. Tinctures (pharmacy) of Rhodiola rosea and Eleutherococcus, 6-8 drops 2 times a day, morning and afternoon (no later than 15 hours); courses for 2 months, alternating them with each other.
8. Thrombo ACC– 1 tablet (50 mg) 1 time per day after meals. Courses prescribed by a doctor.
9. 5 lemons with peel (without seeds - remove them) and 5 heads of garlic(not cloves, but heads) grind and mix very thoroughly with 0.5 kg. honey (preferably sweet clover). Leave for 7 days, stirring the contents every other day. Keep refrigerated. Take 1 teaspoon 3 times a day, on an empty stomach. The course of treatment is 2 months.
10. 20 g of dry crushed roots of Calamus, pour 0.5 liters of vodka. Leave in a dark, warm place for 7 days, shaking the contents every other day. Strain. For dropsy and cardiac edema, drink 1 teaspoon 3 times a day 30 minutes before meals. Course 1 month. A break of 1 month and again a course of 1 month.
11. Hawthorn tincture (pharmaceutical drug) 15-18 drops 3 times a day, 20 minutes before meals, washed down a small amount water. Courses of 3 months with breaks of 1.5 months for 1 year. This is a must!
12. Fir baths, which are accepted according to the method presented in my article “”.
13. It is advisable to take courses of a drug containing Omega-3 acids- one of the most powerful means, protecting the aorta and its main branches, including the arterial vessels of the heart and brain.
14. Old doctors and healers advised and still recommend using this remedy: once every two weeks, put on a shirt soaked in slightly salted water (the concentration is similar to sea water) and a well-wrung out shirt before going to bed. You can find a description of this procedure in my article "".
15. It is advisable to avoid milk in your diet (but not fermented milk products), from sugar, from white bread, from pasta. You can find nutritional recommendations in my article "".
16. There is such an ancient and effective tincture known as the “Spirit of Melissa”. You can find the recipe for this excellent remedy in the same article of mine “”.
17. 1 tablespoon Thyme herb ( Bogorodskaya grass) pour 1 cup of boiling water. You can find a recipe and regimen for taking this useful remedy in the same article of mine “”.
18. "Nervochel" tablets(pharmaceutical drug) – 5 mg (under the tongue) 3 times a day. Course 4 weeks.

A treatment plan should be drawn up with alternating means between each other (no more than 2-3 at a time).

Should carry out 4-5 courses of treatment with gelatin 1 month with breaks of 3 weeks.
Pour a portion of edible gelatin (4 - 5 grams) lukewarm boiled water(80-100 ml, i.e., about half a glass) and cover. In the morning, add the same boiled water to a full glass and stir to drink. You should start taking edible gelatin with daily dose at 2-3 grams, gradually increasing to 4-5 grams.

And it’s also very important...

Necessarily use an orthopedic soft cervical brace(Shants collar) and orthopedic silicone insoles in any shoes (including house shoes - don’t forget to change them!). And also beautiful gel "Doctor Khoroshev" With amaranth oil for the spine and joints.
High-quality orthopedic insoles, an excellent cervical brace and Doctor Khoroshev gel can be ordered by phone: 495-744-33-66.

And one more thing... If you are a believer, I would advise you to painful condition this is the prayer. After all, prayer in illness (any prayer is not a simple set of words) is an amazing, centuries-old rhythm of words, which has a very beneficial effect on the activity of brain structures and subcortical structures; This prayer has helped many people if it is repeated several times a day:

Prayer in illness:
Lord God, Master of my life, in Your goodness You said: I do not want the sinner to die, but for him to turn and live. I know that this disease from which I suffer is Your punishment for my sins and iniquities; I know that for my deeds I have deserved the heaviest punishment, but, O Lover of Mankind, deal with me not according to my malice, but according to Your boundless mercy. Do not wish my death, but give me strength so that I patiently endure the disease as a well-deserved test, and after healing from it I turn with all my heart, with all my soul and with all my feelings to You, the Lord God, my Creator, and live to fulfill Your holy commandments, for the peace of my family and for my well-being. Amen.

Now you know what will help alleviate your condition. I wish you health, Evgeniy Nikolaevich, and many years of life!