Loop on the carotid artery. Deformation of the internal carotid artery - pathological tortuosity

CAROTID DISEASES

The blood supply to the brain is carried out by pairs of internal carotid and vertebral arteries. The internal carotid arteries supply large hemispheres brain, forming the so-called anterior circulatory system. The vertebral arteries form the posterior circulatory system, supplying the brainstem, cerebellum, and usually the occipital lobes.

Due to various reasons and diseases of the lumen of the vessel, and as a result, sufficient blood flow can decrease, which can lead to such serious consequences as transient ischemic attack and stroke.

Atherosclerosis

The carotid and vertebral arteries are usually smooth and unobstructed internally, but with age, the sticky substance that forms plaques can build up in the walls of the arteries. Plaque is made up of cholesterol, calcium, and fibrous tissue. The more plaques, the greater the percentage of narrowing of the artery and the less elastic they are. This process is called atherosclerosis. When the number of plaques increases, blood flow through the carotid arteries can decrease to critical levels and even lead to a complete cessation of blood supply - a stroke.

Atherosclerotic plaques develop in various ways. Fibrous protrusion usually forms first. As it grows, it protrudes more and more into the lumen of the vessel, which can create an obstacle to blood flow. Some of these plaques in their central part may disintegrate, and blood flows past the cavity containing cholesterol and thrombotic material. Upon contact with the flowing blood, these thrombotic and cholesterol particles are transported to the brain, where they become lodged in smaller arteries. These small emboli obstruct blood flow, causing ischemia or death of the tissue supplied by the small vessel. This is the mechanism of microembolization - transient ischemic attack.

Pathological tortuosity of the carotid arteries

Another disease leading to cerebral circulation is a pathological tortuosity of the carotid arteries. There are three types of deformation of the internal carotid arteries (ICA), designating them as tortuosity ("tortuosity"), looping ("coiling") and arterial kinking ("kinking"). By tortuosity is meant S- or C-shaped deformation ICA without sharp angles and visible blood flow disturbances. This type of ICA deformity is considered congenital and hemodynamically insignificant. Loop formation ("coiling") is characterized by a congenital circular deformity with the formation of a loop, which can lead to impaired cerebral blood flow. Kinking is an acquired, hemodynamically significant angulation of the ICA with stenosis of its lumen.

SYMPTOMS OF THE DISEASE

Diseases of the carotid arteries in the early stages of development generally do not provoke the manifestation of noticeable symptoms, in most cases the first symptom of damage to the carotid arteries is a stroke. But still, with a careful attitude to the state of one's own body, a person can note some signs that precede the development of an acute violation of cerebral blood flow. Symptoms characteristic of this condition usually last no more than an hour. During such attacks, the patient feels severe weakness, a state of numbness. In one half of the body, he may feel itching, tingling. Often these manifestations occur in the leg or arm. For the duration of such an attack, a person may lose control of a limb, sometimes vision in one eye disappears, speech becomes slurred. As a rule, signs of a transient ischemic attack completely disappear in a day. But the manifestation of such a “signal” cannot be ignored in any case, since this is a sign that a person will have a stroke in the near future. Therefore, it is extremely important to immediately contact a specialist and undergo a complete examination.

Risk Factors for Carotid Stenosis

Carotid artery stenosis is caused by factors that are largely responsible for the development of most cardiovascular diseases. These include:

Age (risk increases with age)
Smoking
Arterial hypertension (high blood pressure)
High levels of lipids or cholesterol in the blood
Diet with high content saturated fat
Heredity
Diabetes
Obesity
Sedentary lifestyle

Carotid stenosis before the age of 75 is more common in men than in women. Women have a higher risk over the age of 75. People who have coronary artery disease (CHD) have an increased risk of developing carotid artery disease.

DIAGNOSIS OF CAROTID DISEASES

To diagnose diseases of the carotid arteries, the doctor necessarily conducts a detailed survey of the patient in order to find out about all the symptoms that appear, the history of the disease and the characteristics of the patient's health. Most important information in this case, information about the patient's smoking, as well as about the features of his blood pressure. After that, the doctor examines the patient. Auscultation of the carotid arteries is mandatory to detect arterial murmur, which indicates the presence of constrictions, as well as measurement of blood pressure. Currently, it is mandatory to use special instrumental diagnostic methods.

Doppler and duplex ultrasound of the carotid arteries. Ultrasound allows you to give an adequate assessment of the structure of the vessel and the blood flow in it. As a rule, such a study allows you to accurately determine the presence of carotid artery disease. The study evaluates the shape of the convoluted carotid artery and characterizes the state of hemodynamics. In accordance with this, all types of violations of the straightness of the ICA course can be divided into "hemodynamically significant" and "hemodynamically insignificant".

CT angiography, MR angiography. Tomographic studies allow obtaining a visual image of the course of the vessel, identifying the localization of stenocclusive lesions, as well as obtaining a layered image vascular wall. To improve the diagnostic value of the study, the introduction of a contrast agent is used.

Lengthening of 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 for concern and is usually found on accidental examination. With age, the elasticity of the arterial wall changes and the smooth bends of the artery can become kinks, with the development of a pattern of cerebrovascular accidents. When lengthening arteries without kinks at ultrasound examination blood flow disorders are not determined.

Kinking is the kink of an artery at an acute angle. Kinking can be congenital, when cerebrovascular accidents are determined from early childhood and develop over time from an elongated carotid artery. Contributes to the formation of folds arterial hypertension, progression of atherosclerosis in the internal carotid artery. Clinically, kinking of the internal carotid artery is manifested by transient disorders of cerebral circulation. With kinking of the vertebral artery, vertebrobasilar insufficiency develops. Detection of kinking with brain symptoms the question of surgical repair

Coiling is the formation of a loop of an artery. Despite the smooth running of the loop, changes in blood flow in it are very significant. The nature of the bends during coiling can change depending on the position of the body, blood pressure. There is a chaotic nature of the blood flow, 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 in himself. The appearance of symptoms of cerebrovascular insufficiency indicates violations of blood flow compensation and dictates the need for a detailed examination and treatment.

Selective angiography. It is an invasive x-ray research technique in which the doctor through a puncture in the femoral or radial artery using special catheters selectively catheterizes the artery under study and injects a contrast agent. At the same time, an accurate image of the internal lumen of the vessel is obtained on the monitor screen.

TREATMENT OF CAROTID DISEASES

Treatment of pathology of the carotid arteries directly depends on how pronounced the stenosis of the carotid artery, what is the severity of atherosclerosis or the degree of blood flow disturbance due to pathological tortuosity. Also, the doctor must pay attention to the symptoms of the disease and general state sick. If, during the diagnostic process, atherosclerotic lesions of the carotid arteries were detected in a person, then it is extremely important for the patient to immediately change his lifestyle, guided by the doctor's recommendations, and be sure to undergo a course of treatment with medications.

People with hypertension should take drugs to normalize blood pressure. Be sure to stop smoking, follow a diet, eating foods with low content cholesterol. Sometimes treatment with statins, drugs that lower blood cholesterol levels, will be appropriate.

In the case of severe atherosclerotic lesions of the carotid arteries, it is advisable to carry out surgical treatment, the purpose of which is to restore adequate blood flow through the affected vessel. The attending physician decides which method of surgical therapy to choose in each case. At present, there are three active surgical techniques for the treatment of hemodynamic significant diseases carotid arteries: carotid endarterectomy, carotid resection with redress, balloon angioplasty and stenting.

CAROTID ENDARTERECTOMY

The operation consists in the open removal of plaque from the carotid artery. Pain relief -

general anesthesia, monitoring of the state of the brain is carried out on the basis of cerebral oximetry (measurement of the level of oxygen in the brain blood). If necessary, a special temporary shunt is used so that the blood circulation of the brain is not disturbed during the operation. Indications for surgery:

Atherosclerotic plaque narrowing the carotid artery by 70% or more
Stroke or transient brain disorders in the basin of the affected artery
Atherosclerotic plaque in the vertebral artery in the presence of symptoms of vertebrobasilar insufficiency and the absence of other causes of neurological disorders;
Occlusion (blockage) of the internal carotid artery with poor reserves of cerebral circulation

"Classic endarterectomy"

With a long atherosclerotic plaque, the "classic" technique of endarterectomy is used. An incision is made along the entire length of the altered artery. A special tool is used to peel off the plaque and remove it. The operation site is well washed to remove small particles of atherosclerotic plaque. Inner shell, if necessary, fixed with separate seams. The opening in the carotid artery is then sutured with a special patch to prevent it from re-narrowing later.

"Eversion endarterectomy"

If an atherosclerotic plaque is located at the very beginning of the internal carotid artery, then it is removed by the method of "eversion", the so-called eversion carotid endarterectomy. The internal carotid artery is cut off, the plaque is exfoliated, the artery is everted like a stocking until the plaque is removed. The artery is then sutured back into place. This technique is much faster and simpler than the "classical" one, but is feasible only on a short atherosclerotic plaque - up to 2.5 cm.

Currently, operations on the carotid arteries are safe and short. The risk of complications does not exceed 3%. Hospitalization in most cases is necessary for 4-5 days

SURGICAL TREATMENT OF PATHOLOGICAL TWIST OF THE CAROTID ARTERIES

The operation consists in cutting off the excess of the tortuous artery, after which the carotid vessel straightens, the patency is restored (reconstruction by the method of resection of the excess with redressing and reimplantation of the ICA into the old mouth. In case of extended fibrous transformation, insufficient diameter of the artery, the presence of aneurysms or thinning of the walls outside the tortuosity zone, resection of the internal carotid artery with prosthetics.The great saphenous vein or PTFE prostheses are used as a plastic material.The results of surgical treatment are good.Symptoms of cerebral vascular insufficiency are completely resolved in 96% of patients. Drug treatment pathological tortuosity is not effective, since the artery cannot heal from drugs. It is important to clearly define the diagnosis of pathological tortuosity and prove its significance for cerebral circulation.

Scheme of the operation of resection of a pathological deformity of the internal carotid artery with redressing and reimplantation into the old mouth: a - stage of isolation of the carotid arteries; b - resection of pathological tortuosity; c - the internal carotid artery after resection is implanted into the old mouth; d - schematic representation of the result of the operation

Scheme of resection of pathological tortuosity of the ICA with prosthetics

ENDOVASCULAR TREATMENTS

Angioplasty - the operation of restoring the lumen of an artery affected by an atherosclerotic plaque involves the introduction of a special silicone balloon through the narrowed lumen, which, when inflated, creates high pressure causing compression of atherosclerotic plaque and restoration of arterial patency.

Stenting - is usually performed together with angioplasty and involves strengthening the wall of the stretched artery with a special mesh (stent). The stent is pressed against the vascular wall and maintains the patency of the artery. Stents are usually made of inert metals and have a honeycomb structure. According to the installation method, there are balloon-expandable and self-expanding. Stents and balloons can be covered with a film of medicinal product that improves the results of the intervention.

Stent grafts (endoprostheses) These are stents lined from the inside with a thin layer of polytetrafluoroethylene. Unlike simple stents, stent grafts are airtight and are used to close the cavity of the aneurysm, and also have a longer patency. In fact, these are vascular prostheses installed inside the lumen of the artery.

Place in the "Articles" section

Is a pair: left side begins in the region of the brachial trunk, the right one - in the region of the aortic arch. In this case, both vessels end in the chest. The internal carotid artery contributes to the blood supply and nutrition of all organs of the head, so any pathology can provoke serious consequences for the whole organism.

Kinking of the internal carotid artery is a phenomenon of its pathological tortuosity in the form of an inflection.

Anatomical features

The carotid arteries are not absolutely symmetrical - the left one is always several centimeters larger than the right one. These vessels are responsible for the blood supply to the brain, eyes, etc. At the same time, for normal functioning, the brain needs to receive blood at the rate of 3.7 grams per minute for every 100 grams of this organ.

In the region of the cartilage of the thyroid gland, this vessel forms several branches, and is divided into the external carotid and internal carotid arteries.

Norm

In the normal state, it does not have constrictions that prevent the flow of blood to the head. However, if the lumen in one of its parts is narrowed, a violation of the blood supply to the organs of the head develops. Common cause of ischemic stroke, hypertension or nervous disorders is a violation of this physiological process due to tortuosity or kinks of the internal carotid artery.

Varieties of vascular pathologies

One of the most common causes of cerebral blood flow disorders is the tortuous structure of the carotid artery. More than 28% of patients who died from a stroke were found to have this pathology. Almost every fourth comprehensive examination the elongation or tortuosity of this vessel is determined.

Specialists highlight the following varieties tortuosity of the internal carotid artery:

Reasons for the development of kinking

In most cases, kinking of the internal carotid artery is a pathology of a congenital nature, but often the development similar disease other factors contribute, including:

age-related vascular changes;
persistent high blood pressure;
smoking;
diabetes;
unhealthy diet with a lot of fats and carbohydrates;
overweight.

The hereditary factor also plays a huge role in the development of the disease. If relatives have been diagnosed with this pathology, it is necessary to undergo a diagnosis. A sedentary lifestyle can provoke the development of kinking.

Symptoms of a pathological phenomenon

Most often, people with kinking of the internal carotid artery complain of the following symptoms:

frequent occurrence headache that does not go away after taking painkillers;
periodically amplifying noise and sound phenomena in the ears;
periodic fainting, which can last a couple of seconds;
fog or flickering goosebumps before the eyes;
violations of coordination of movements;
in more complex cases - speech disorders and weakness of the upper limbs.

Thus, the symptoms of kinking of the left internal carotid artery or the right one are very similar to a number of other vascular diseases, for example, vascular atherosclerosis common among the elderly. To determine the disease, it is necessary to carry out a number of necessary diagnostic procedures.

Kinking diagnostics

To detect kinking - pathological tortuosity of the internal carotid artery, complex diagnostic measures. To begin with, the specialist conducts a survey of the patient, determining the situation and identifying the moments when his health worsened. Auscultation (listening with a phonendoscope) of the carotid arteries is mandatory to determine the presence or absence of pathological noises and measurement of blood pressure.

In addition, one of the instrumental diagnostic methods should be used:

Treatment of the disease

the only effective methodology kinking therapy is considered surgery. In this case, surgeons cut off an extra section of the artery, straightening the vessel. As a result of such an operation, the blood supply to the head and brain is completely restored.

Since such surgery, thanks to modern medical techniques, is the least traumatic, and its implementation rarely takes more than 20 minutes, in most cases it is carried out under local anesthesia. After the operation, the patient is sent to the hospital, and he is discharged for outpatient treatment in the absence of complications in one to two days.

The efficiency of the operation is very high. All pathological symptoms disappear completely in about 95% of patients. The probability of occurrence of complications is not more than 1%.

Drug therapy in this situation is ineffective, since it only alleviates the symptoms, but does not eliminate the problem itself - the pathological bending of the vessel.

Treatment in childhood

Carotid kinking therapy in childhood has some features. In general, this disease began to be detected in children relatively recently, which is due to the lack of the necessary diagnostic equipment in most medical institutions.

Most often, a very effective method of treating kinking in children is surgery. But, given the fact that the child is in constant development, sometimes it is possible to eliminate and cure such a pathology without surgical procedures. In some cases, the tortuosity resolves on its own as the child grows. This phenomenon is observed in almost 30% of cases. It is possible to improve the blood supply to the brain and prevent the development of ischemic disorders with the help of special exercises shown by a specialist. If such exercises do not give a positive effect, doctors resort to surgical intervention especially in situations where the child feels very unwell.

Preventive measures

To avoid the development of such a pathology, it is necessary:

stick to the basics healthy eating;
control body weight, exercise moderately;
give up bad habits;
exclude weight lifting, as a result of which the pressure on the vessels increases, and the internal carotid artery begins to gradually deform.

The article briefly reviewed the kinking of the carotid artery. What is it and how to get rid of this pathology, you now know.

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

Hello!
I fell from the tree with the back of my head, there was a short loss of consciousness. He did not go to the hospital, after 5 years attacks began, at first the objects he looked at partially disappeared, then a strong headache. In the future, he prevented the onset of an attack by taking lingonberries. After a while, 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 seizures.

Already as a student, after I had blown up a few balloons, the attack arose again, I was lucky - I found lingonberries. Until the age of 57, 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 competent specialists, I ask you to tell me: what is the algorithm of my actions to cure such a phenomenon?

- Evgeny Nikolaevich Zverkov

Hello, Evgeny Nikolaevich!

The fact that you lost consciousness indicates that you suffered a concussion at that time. Most likely, then you had both nausea and retrograde amnesia (you may not remember this now). And then your body gradually coped (not fully, of course) with this situation ... And there was a lull until the pathological tortuosity of the vertebral arteries arose ... However, let me explain everything to you, Evgeny Nikolaevich, in order... So...

Pathological tortuosity of the vertebral arteries: condition analysis

What is happening to you now, Evgeny Nikolaevich, can happen according to different reasons as extracerebral (narrowing or complete closure-occlusion of the brachiocephalic or vertebral arteries - the so-called vertebral artery syndrome, or chronic disorder cerebral circulation in the vertebrobasilar basin), and intracerebral (discoordination in the activity of the circle of Willis, sclerosis of the intracerebral arteries, etc.). You can write 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 (a state of the so-called “floating anxiety”) is the “vertebral artery syndrome” ... What is it? And here's what ... As the destruction of the intervertebral discs in cervical region of the spine, 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 inevitably occurs. plexus, which leads to pain in the muscles of the neck, to the so-called myogelosis of the muscles of the neck, that is, to their excessive tension, as well as to a feeling of numbness in the hands ...

Peel all the cloves of garlic, rub them, put them in a jar and pour 1 cup of unrefined sunflower oil. You can find the recipe and scheme for taking this wonderful remedy in my article "".
3 tablespoons dry chopped herb St. John's wort Pour in a thermos with 1 cup of boiling water. Insist 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.
Drink daily for 3 months tea from the herb Origanum vulgaris. A break of 1 month and again a course of 3 months.
Take 0.2 g daily Mumiyo(in the morning on an empty stomach, drinking a 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.
Propolis-garlic tincture
Rosehip decoction. You can find the recipe and scheme for taking this wonderful remedy in my article "".
Tinctures (pharmacy) 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.
Thrombo ASS- 1 tablet (50 mg) 1 time per day after meals. Courses prescribed by a doctor.
5 lemons with peel (without seeds - remove them) and 5 heads of garlic(not teeth, namely heads) grind and mix very carefully with 0.5 kg. honey (preferably sweet clover). Infuse 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.
20 g of dry crushed roots of calamus pour 0.5 l of vodka. Insist in a dark warm place for 7 days, shaking the contents every other day. Strain. Drink with dropsy and edema cardiac origin 1 teaspoon 3 times a day 30 minutes before meals. Course 1 month. Break 1 month and again course 1 month.
Hawthorn tincture (pharmacy drug) 15-18 drops 3 times a day, 20 minutes before meals, with a small amount of water. Courses of 3 months with breaks of 1.5 months for 1 year. This is a must do!
Fir baths, which are taken according to the methodology presented in my article "".
It is advisable to take courses of a drug containing Omega-3 acids- one of the most powerful means of protecting the aorta and its main branches, including the arterial vessels of the heart and brain.
Old doctors and healers advised and advise to use this remedy: once every two weeks, put on yourself before going to bed, soaked in lightly salted water (in a concentration similar to sea water) and a well-wrung shirt. You can find a description of this procedure in my article "".
In nutrition, it is desirable to refuse milk (but not fermented milk products), from sugar, from white bread, from pasta. You can find nutrition recommendations in my article "".
There is such an old and effective tincture, known as the "Spirit of Melissa". You can find the recipe for this excellent remedy in the same article of mine "".
1 tablespoon herb Thyme (Bogorodskaya herb) pour 1 cup boiling water. You can find the recipe and regimen for this useful tool in the same article of mine "".
"Nervochel" in tablets(pharmaceutical preparation) - 5 mg (under the tongue) 3 times a day. Course 4 weeks.

It is necessary to draw up a treatment plan with the alternation of funds among themselves (no more than 2-3 at the same 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) with barely warm boiled water(80-100 ml, i.e., about half a glass) and cover. In the morning, add to the volume of a full glass of the same boiled water and stir to drink. Start taking food gelatin with daily dose in 2-3 grams, gradually bringing to 4-5 grams.

And more importantly...

Necessarily use an orthopedic soft neck brace(Schanz collar) and orthopedic silicone insoles in any shoes (including home shoes - do not forget to shift them!). And also beautiful Gel "Doctor Khoroshev" with amaranth oil for the spine and joints.
High quality orthopedic insoles, an excellent neck 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 such a prayer in case of a painful condition. After all, prayer in illness (any prayer is not a simple set of words) is an amazing, centuries-old rhythmic of words that has a very beneficial effect on the activity of brain structures and subcortical structures; this prayer has helped so many people if it is repeated several times a day:

Prayer in Sickness:
Lord God, Lord of my life, You, in Your goodness, said: I do not want the death of a sinner, but that he turn and live. I know that this sickness with which I suffer is Your punishment for my sins and iniquities; I know that for my deeds I deserved the gravest punishment, but, 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 test I deserve, and after healing from it, turn with all my heart, with all my soul and all my feelings to You, the Lord God, my Creator, and be alive for fulfillment your holy commandments, for the peace of my family and for my well-being. Amen.

Now you know what will help alleviate your condition. Health to you, Evgeny Nikolaevich, and many years of life!

One of the most poorly understood and mysterious diseases of the carotid and vertebral arteries is pathological tortuosity (kinking). In every third person who died from a stroke, pathological bends of the carotid or vertebral arteries were found.

In 16-26% of the adult population, various options elongation and tortuosity of the carotid or vertebral arteries in the neck.

The cause of the tortuosity is most often congenital, but often the lengthening of the artery develops with hypertension. For a long time tortuosity may not give any symptoms, but at some point the patient begins transient cerebrovascular accident. Angiosurgeons of our clinic are focused on developing the problem of pathological tortuosity of the carotid and vertebral arteries.

Types of pathological tortuosity of the carotid arteries

Lengthening of 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 for concern and is usually found on accidental examination. Arterial lengthening is important for ENT doctors, since the wall of the artery 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 the smooth bends of the artery can become kinks, with the development of a pattern of cerebrovascular accidents. When the arteries are lengthened without kinks, ultrasound examination of the blood flow does not reveal any disturbances.

Kinking is the kink of an artery at an acute angle. Kinking can be congenital, when cerebrovascular accidents are determined from early childhood and develop over time from an elongated carotid artery. The formation of kinks is promoted by arterial hypertension, the progression of atherosclerosis in the internal carotid artery. Clinically, kinking of the internal carotid artery is manifested by transient disorders of cerebral circulation. With kinking of the vertebral artery, vertebrobasilar insufficiency develops. Identification of kinking with brain symptoms raises the question of surgical correction of tortuosity.

Clinical manifestations

The manifestations of pathological tortuosity are diverse, the most common are:
- A picture of transient ischemic attacks in the blood supply pool of the convoluted artery with temporary paralysis of half of the body or arm (hemiparesis), speech impairment, etc.);
- Temporary blindness in one eye;
- Noise in the head;
- Dizziness;
- Flashing before the eyes;
- Headaches without a clear localization;
- Short-term loss of consciousness;
- Falls without loss of consciousness;
- Temporary imbalance;
- Migraine attacks.

Treatment of pathological tortuosity

Pathological tortuosity is subject to surgical treatment. The artery straightens out, its excess is cut off, the patency is restored. The results of surgical treatment are good. Symptoms of cerebral vascular insufficiency completely disappear in 96% of patients. The risk of operations is less than 1%. Operations can be performed under local anesthesia. Drug treatment of pathological tortuosity is not effective, since the artery cannot heal from drugs. It is important to clearly define the diagnosis of pathological tortuosity and prove its significance for cerebral circulation. Then the results of treatment will please both patients and their doctors.

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

pathological physiology blood circulation in the area of bends

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 violation of hemodynamics is observed at the site of the inflection, where an acute angle is formed. Then there is a turbulent blood flow and a velocity gradient between the adductor and efferent knees, the linear velocity of the blood flow increases, and the diameter of the lumen at the bend decreases. Tortuosity at a right or obtuse angle, as a rule, is not hemodynamically significant. The study of pathologically tortuous arteries is greatly facilitated by three-dimensional CT and MR images.

Treatment. Operations for pathological tortuosity consist in 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 of hemangiomas.

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

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

Racemose hemangiomas are an anomaly in the development of vessels in the form of a plexus of thickened, dilated and serpentine vessels, among which extensive cavernous cavities are often found. Both the latter forms of hemangiomas are located not only in the skin and subcutaneous tissue, but also in deeper tissues, including muscles and bones. Possible malignancy of hemangiomas.

The color of the skin in the hemangioma changed from red to dark purple. With capillary hemangiomas, it is bright red, and with superficially located cavernous and racemous angiomas, it varies from cyanotic to bright purple. The temperature of the skin in the area of hemangiomas is increased, which is explained by increased inflow arterial blood and more vascularity. Superficially located cavernous and racemose hemangiomas are usually soft in consistency, resembling 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 is significant if the tumor communicates with large vessels.

The main symptoms of deep hemangiomas, sprouting muscles and

bones, are pain in the affected limb, due to compression or involvement in the pathological process of the nerve trunks. Palpation reveals a tumor of soft elastic or dense elastic consistency without clear boundaries. With arterial racemostic hemangiomas, it is sometimes possible to notice a pulsation of swelling, to palpate to determine the symptom of "cat's purr". Extensive hemangiomas are often combined with congenital arteriovenous fistulas, accompanied by soft tissue hypertrophy, some lengthening of the limb, and a violation of its function.

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

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 contours of the bone, thinning of the cortical layer, bone defects, and sometimes osteoporosis with small foci of rarefaction.

Treatment. With conservative treatment, cryotherapy, electrocoagulation are used, sclerosing drugs are injected directly into the hemangioma. Surgical treatment consists in 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 that feed the vascular "tumor", stitching and sheathing 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, repeated embolization of the adducting vessels.

18.6. Arterial injury

It is customary to distinguish between open and closed vascular injuries. With open injuries, the integrity of the skin or mucous membranes is disturbed, there is infected wound. Usually, open lesions are accompanied by more or less profuse external bleeding. Wounds of arteries by firearms are fundamentally different from stab and cut wounds by the mechanism of damage and more extensive destruction of soft tissues and dysfunction of adjacent nerves and organs. A gunshot wound needs 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.

More often than others, the femoral, brachial and forearm arteries are damaged.

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

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

II degree. Injury to all layers of the wall with opening of the lumen of the vessel, but without complete intersection of the latter. A wound in the vessel wall may be accompanied by life-threatening bleeding or thrombosis, leading to bleeding arrest;

III degree. Complete intersection of arteries with massive bleeding. In some cases, bleeding can be stopped by screwing the intima.

With closed injuries of the arteries due to blunt trauma, they also distinguish:

damage only to the intima (I degree);

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

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

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

Clinical picture and diagnosis. The main symptom of open arterial injury is bleeding. With damage to the main arteries of the II-III degree, bleeding becomes threatening and can lead to hemorrhagic shock. When the size of the defect in the vessel wall is small (II degree of damage), the hole can close with 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 impair blood circulation in the limbs and increase the symptoms of ischemia. Limb ischemia is most pronounced with a 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 limbs, pallor and coldness of the skin, absence of a peripheral pulse, impaired sensitivity (from hypesthesia to complete anesthesia). With severe ischemia, paralysis and muscle contracture occur. In a number of victims in the area of damage, it is possible to determine a pulsating swelling (pulsating hematoma), which indicates the presence of a hematoma communicating with the lumen of the artery. Above the projection of a pulsating hematoma, a blowing systolic murmur is heard.

Closed damage to the arteries is also accompanied by symptoms of ischemia. Its cause can be thrombosis of the lumen of the vessel due to damage to the intima (I and II degree), compression of it by an extensive hematoma in cases of rupture or crushing of the artery (III degree).

Diagnosis of open arterial injuries is usually not difficult. However, with closed injuries, combined with bone fractures, 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, the disappearance of the peripheral pulse. Diagnosis is greatly facilitated by ultrasound and arteriography.

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

tic pressure bandage, in others - tamponade of the wound, finger pressing of the bleeding artery, application of a tourniquet. It is unacceptable to leave a tourniquet for 2 hours or more, as this aggravates the severity of ischemia of the affected limb. It must be removed hourly, while pressing the artery with a finger. In a medical institution, if necessary, measures should be taken to combat blood loss (blood transfusion and plasma-substituting solutions), according to indications, heart and painkillers, oxygen inhalations are prescribed. If the conditions for surgical intervention allow, but there is no way to apply a vascular suture, then sometimes they resort to a temporary connection of 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.

Surgery for traumatic injuries of the arteries involves the primary surgical treatment of the wound and the restoration of the main blood flow through the damaged vessel. For small stab and incised 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, hands, forearms, lower legs) is possible only with the use of microsurgical techniques, when the vascular suture is performed under a microscope.

The results of surgical treatment of arterial injuries 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 guided by when providing timely surgical care to most 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 time elapsed since the injury. Only the presence of irreversible ischemia, which is primarily evidenced 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 impaired blood flow through the vessels due to obliterating (stenotic) or dilating (aneurysmal) lesions. The most common causes of obliteration or stenosis of the arteries are: 1) obliterating atherosclerosis, 2) nonspecific aortoarteritis, 3) thromboangiitis obliterans (endarteritis). Regardless of the cause of vessel obliteration, sometimes more or less pronounced tissue ischemia appears, to eliminate which reconstructive operations are used, taking into account the characteristics of the pathological process. The general characteristics of obliterating vascular diseases are given below.

18.7.1. Obliterating atherosclerosis

It is the most common disease and occurs mainly in men over 40 years of age. The process is localized mainly in the arteries of large and medium caliber. The main cause of this disease is hypercholesterolemia. In the bloodstream, cholesterol circulates in a bound state with 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. Individuals with high levels of these atherogenic lipoprotein fractions are more likely to suffer from atherosclerosis.

Pathological picture. The main changes develop in the intima of the arteries. Pathological changes in the intima are usually distinguished as fatty stripes, fibrous plaques and complicated lesions (plaque ulceration, blood clots). Fat streaks are the earliest manifestation of atherosclerosis, characterized by focal accumulation in the intima of macrophages filled with lipids, 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 localization and distribution of aortic fatty streaks and fibrous plaques do not match. It is widely believed that the fat streaks undergo regression, but the evidence is inconclusive.

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

Fibrous atherosclerotic plaques, called mother-of-pearl, rise above the surface of the intima, represent its thickening, which can be determined by palpation. In typical cases, the fibrous plaque has a domed shape, a dense texture, protrudes into the lumen of the artery and narrows it. The plaque consists of extracellular fat located in the central part, the remnants of necrotic cells (detritus), covered with a fibromuscular layer, or a peak 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 the plaques is disturbed. The cells that make up the plaque structure undergo necrosis, hemorrhage occurs in the thickness of the plaque, and cavities appear filled with amorphous fat and tissue detritus. Often this is 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, getting into the distal bed with blood flow, can cause microembolism. In fabric elements

Organization * Ulceration

Atheromatosis CR™ effusion

Rice. 18.8. Changes that develop in the wall of arteries in atherosclerosis (schematic representation). Explanation in the text.

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

The favorite localization of atherosclerotic lesions are the places of division of the main arteries: the brachiocephalic trunk, the orifices of the vertebral arteries, the bifurcation of the aorta, the common carotid, common iliac, femoral and popliteal arteries. This phenomenon is explained by the peculiarities of hemodynamics. In the zone of bifurcations of the arteries, the intima experiences a blow from the main blood flow, here there is some slowdown and division of the blood flow along the arterial branches. The main blood flow deviates from a rectilinear trajectory, forms eddies that damage the intima and favor the formation of plaques. This suggests that atherosclerotic lesions of arterial walls are, 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 occurring against the background of such adverse factors as hypertension, diabetes mellitus, obesity, and smoking. From the moment the first clinical symptoms appear, 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 limb ischemia. The abdominal aorta is usually affected distal to the renal arteries. Approximately one-third of patients are affected by the aortoiliac (Lerish syndrome), and in 2/3 patients, the femoral-popliteal segments are affected.

18.7.2. Nonspecific aortoarteritis

A disease of autoimmune genesis, belonging to the group of non-specific inflammatory diseases, affects the aorta and its large branches. Synonyms of nonspecific aortoarteritis are: pulseless disease, Takayasu's syndrome, aortic arch syndrome, arteritis of young women. The disease is more common in women under the age of 30.

Pathological picture. Morphologically non-specific

aortoarteritis is a systemic chronic productive process in the wall of the aorta and its large branches, beginning with inflammatory infiltration of the adventitia and media. In the middle layer, a pattern of productive inflammation is observed, smooth muscles and elastic fibers undergo destruction. A pronounced periprocess occurs around the vessel due to the thickening of the adventitia and its adhesion to the surrounding tissues. The intima is affected a second time, there is a reactive thickening in it, which entails a sharp narrowing or complete closure of the mouth and lumen of the affected arteries, fibrin deposition is often observed on the surface of the intima. The media atrophies and is compressed by a wide fibrous intima and a thickened adventitia muff. In the late 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 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 the 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 sections of the branches extending from the aorta. The disease is characterized by a slowly progressive course.

There are three stages of the course 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. In the blood, an increase in ESR, leukocytosis, an increase in the level of y-globulins, C-reactive protein are found. After a few weeks or months, the disease acquires a subacute course, and after 6-10 years from its onset, symptoms of damage to one or another vascular pool appear.

Involvement in the pathological process of the aortic arch and its branches leads to chronic ischemia of the brain and upper extremities. The defeat of the mesenteric arteries is accompanied by ischemia of the digestive system. With the defeat of the bifurcation of the abdominal aorta and iliac arteries, ischemia of the lower extremities occurs. With stenosis of the descending aorta, co-arctation syndrome develops, and with stenosis of the renal arteries, a syndrome of vasorenal hypertension 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(Winivarter's disease)-Burger)

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

common thromboangiitis refers to allergic autoimmune diseases. 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 antielastin antibodies and an increased content of class A and M immunoglobulins are also found. Young men under the age of 40 are most often ill. The development of thromboangiitis is facilitated by factors that cause persistent vasospasm (smoking, hypothermia, repeated minor injuries). A long-term spasm of the arteries and vasa vasorum leads to chronic ischemia of the vascular wall, resulting in intimal hyperplasia, adventitia fibrosis and degenerative changes in the own nervous apparatus of the vascular wall. In the late stage of the development of the disease, atherosclerotic changes are often found in the walls of large vessels. Against the background of the 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 in the thrombosis zone, and calcium salts are deposited.

If at the beginning of the disease the distal parts of the vessels of the lower extremities, in particular the arteries of the lower leg and foot, are affected, then later larger arteries (popliteal, femoral, iliac) are also involved in the pathological process. The disease can be combined with migrating thrombophlebitis of 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. With atherosclerosis, the bifurcation of the common carotid artery is most often affected, less often - the mouth of the brachiocephalic trunk, subclavian, vertebral artery. Nonspecific aortoarteritis affects the branches of the aortic arch (common carotid and subclavian arteries). More rarely, extravasal compressions lead to violations of the patency of the branches of the aortic arch: compression of the subclavian artery by a highly located 1st rib or additional cervical rib, hypertrophied anterior scalene or pectoralis minor muscle, compression of the vertebral artery by osteophytes in severe cervical osteochondrosis, etc. One of the causes of impaired patency of brachiocephalic arteries may be their deformation - pathological tortuosity and kinks.

With stenosis narrowing 70-80% of the lumen of the vessel, the volumetric blood flow decreases and turbulent flows appear. In post-stenotic areas, blood flow slows down, favoring platelet aggregation at the locations of atherosclerotic plaques and thrombus formation. Separation of thrombus particles leads to microembolism of cerebral vessels. Embolism can occur when the brain vessels are blocked by fragments of an atherosclerotic plaque that collapses due to ulceration or hemorrhage.

In the pathogenesis of disorders associated with circulatory disorders, the main role belongs to ischemia of brain regions that are supplied with blood from the affected artery. With the defeat of one of the four arteries of the brain (internal carotid or vertebral), blood

the supply of the corresponding parts 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, in case of occlusion of a segment of the subclavian artery, medial to the origin of the vertebral artery, blood 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 vertebral artery, impoverishing cerebral blood flow, especially during exercise (subclavian-vertebral steal syndrome). The vertebral artery becomes, as it were, a collateral for the blood supply to the upper limb on the side of the lesion.

Diseases of the vessels of the brain. About 80% of occlusive diseases of the branches of the aortic arch, causing a violation of the arterial blood supply to the brain, are due to atherosclerotic lesions. Less common is aortoarteritis (giant cell arteritis - Takayasu's disease), fibromuscular dysplasia. Acute symptoms of cerebrovascular accident may occur due to vascular embolism. Embolism of cerebral vessels is often caused by atherosclerosis of the carotid arteries. With ulceration and destruction of an atheromatous plaque, its particles (atheromatous detritus, small blood clots, microparticles of dead tissue) are transferred by blood flow to small vessels of the brain and cause their 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 disorders (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. An instrumental study (ultrasound, angiography) allows you to identify the degree of narrowing of the artery. With a significant narrowing of the lumen, surgical treatment is indicated to prevent stroke - severe, irreversible changes in the brain. Patients with a sustained stroke after recovery also need surgical treatment to prevent a recurrence of a stroke.

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

Transient ischemic attacks are usually caused by microembolism of small branches of the cerebral vessels, which occurs during ulceration and decay 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 occlusion of the vessel and the presence of collaterals. Hypoperfusion resulting from microembolism causes temporary visual impairment and associated neurological symptoms.

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

need urgent treatment to prevent the development of persistent ischemic stroke.

Patients with chronic vascular insufficiency often complain of headache, dizziness, tinnitus, memory impairment. They have short-term bouts of loss of consciousness, staggering when walking, double vision. Sometimes you can observe lethargy, decreased intelligence, dysarthria, aphasia, dysphonia. An objective examination often reveals weakness of convergence, nystagmus, changes in coordination of movements, sensitivity disorders, short-term mono- and hemiparesis, 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 affected. They range from mild visual impairment to complete loss of vision. There are frequent complaints of patients about the presence of a veil, a grid before the eyes.

Insufficiency of blood supply to the upper extremities manifested by their weakness, increased fatigue, 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 the lesion of the vessel, as a rule, is absent or weakened. With damage to the subclavian artery, blood pressure on the corresponding arm decreases to 80-90 mm Hg. Art., a systolic murmur is heard over the stenotic arteries. With stenosis of the bifurcation and the internal carotid artery, it is clearly defined at the angle of the lower jaw; with narrowing of the brachiocephalic trunk - in the right supraclavicular fossa behind the sternoclavicular joint. The degree of violation of the blood supply to the upper limbs can be determined by a test that resembles a test that causes intermittent claudication. In the sitting position, the patient is offered to raise his hands up and make a quick clenching of the hands into a fist and unclenching. Note the time of onset of hand fatigue and the time of onset of pain. The symptom is positive with stenosis of the subclavian artery distal and proximal to the branches 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).

The syndrome of compression of the subclavian vessels and nerves can be caused by an additional 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). With these 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 muscles of the hand, often note acrocyanosis, swelling of the hand. It is characteristic that at certain positions of the hand and head, the symptoms of arterial insufficiency are aggravated. This is manifested by increased pain and paresthesia, the appearance of a feeling of heaviness in the arm, a sharp weakening or disappearance of the pulse in the radial artery. So, in patients suffering from the syndrome of the anterior scalene muscle and the cervical rib, the most significant compression of the subclavian artery and the deterioration of blood supply occur when the arm raised and bent at a right angle at the elbow joint is retracted back while a sharp turn of the head with a raised chin

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 the arm is abducted backwards and downwards, and in patients with Wright's syndrome - when raising and abducting the diseased arm, as well as throwing it back on the back of the head. Constant traumatization of the artery and nerves leads to cicatricial changes around these anatomical formations and pronounced 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 gives reason to believe that changes in the relationship between the structures between the collarbone and the upper chest, which develop gradually with age, are the main cause of the disease. Symptoms of the disease are caused not so much by recurrent 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 a change 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, which determines the direction and speed of blood flow, the presence of overflow from one pool to another. With duplex scanning using modern ultrasound devices, it is possible to establish with great accuracy the localization and extent of pathological changes, the degree of damage to the arteries - occlusion, stenosis, the nature of the pathological process - atherosclerosis, aorto-arteritis (Fig. 18.9). When planning surgical interventions, panarteriography of the aortic arch according to Seldinger or selective arteriography of its branches is performed. Traditional radiopaque 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 in occlusive lesions of brachiocephalic vessels is dictated by the frequent development of 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 intracranial artery embolism (unstable plaques complicated by hemorrhage or ulceration).

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

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

In patients with vascular patency disorders caused by extravasal compression, it is necessary to eliminate the cause of compression. According to the indications, a scalenotomy, resection of the 1st rib, intersection of the pectoralis minor or subclavian muscle, etc., are performed.

If it is impossible to perform a reconstructive operation, 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 are manifested by pain after eating, weight loss, systolic murmur in the epigastric region above the projection of the aorta.

Etiology and pathogenesis. The most common causes of damage to the mesenteric vessels and the celiac trunk are atherosclerosis and nonspecific aortoarteritis, less often - fibromuscular dysplasia, anomalies in the development of visceral arteries. Violation of their patency also occurs with extravasal compression, which is more often exposed to the celiac trunk. Its compression can be caused by the falciform ligament and the medial pedicle 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, less often the celiac trunk. Nonspecific aortoarteritis of this localization, as a rule, occurs in young age; visceral branches are always affected along with the corresponding segment of the aorta. The defeat is longer. Extravasal vascular compression is observed equally often in any age group.

Into the notion chronic ischemia organs of digestion" combines signs of circulatory disorders in three vascular basins: the celiac trunk, superior and inferior mesenteric arteries. The lack of blood flow in the basin of the affected artery for a certain time is compensated by the redistribution of blood from other vascular basins. However, as the disease progresses, a decrease in compensatory capabilities occurs collateral circulation.

serious hemodynamic disturbances occur with simultaneous damage to several visceral arteries. 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 parts 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 malabsorption. At the same time, the function of the liver and pancreas is impaired. One of the consequences of chronic abdominal ischemia is an acute violation of visceral circulation, which occurs due to thrombosis of the affected artery and often ends in intestinal gangrene.

clinical picture. Chronic abdominal ischemia is characterized by a triad of symptoms: pain, bowel dysfunction, and weight loss. According to the predominant clinical manifestations, 4 forms of the disease are distinguished: celiac (painful), 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. With damage to the superior mesenteric artery, 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 that affect the intraorgan nerve endings.When the inferior mesenteric artery is affected, only 8% of patients experience aching pain in the left iliac region.Patients notice a decrease in pain with restriction of food intake.Intestinal dysfunction is expressed in bloating, unstable stool, constipation.In the feces, the remains of undigested food, mucus are often found.

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

An isolated lesion of the visceral arteries is rare, more often it is combined with lesions of other vascular beds, therefore, in differential diagnosis, the correct interpretation of patient complaints is of great importance.

During auscultation of the abdomen in the epigastric region, a characteristic systolic murmur is often heard due to stenosis of the celiac trunk or superior mesenteric artery.

Data from laboratory studies 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.

An x-ray examination reveals a slow passage of barium through the intestines, flatulence, segmental spasms of the intestines. Colonoscopy reveals diffuse or segmental colitis, atrophy of the

viscous shell, less common erosion, segmental stenosis with the disappearance of haustration. Histological examination of biopsy specimens reveals edema of the lamina propria, a decrease in the number of crypts, areas of fibrosis, dilatation 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 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 organs is necessary in order to exclude them. organic lesions in the genesis of abdominal pain syndrome.

Ultrasound duplex scanning allows visualization of the abdominal aorta and the initial sections of the celiac trunk and its branches (the common hepatic and splenic arteries), as well as the superior mesenteric artery. With stenosing lesions in the mouths of these arteries, turbulent high-speed blood flow appears, the diameter of the affected vessel decreases, and post-stenotic expansion is observed.

Aortography, performed in the anteroposterior and lateral projections, allows you to assess the condition of the orifices of the celiac and mesenteric arteries. The angiogram in chronic abdominal ischemia reveals both direct signs of damage to the visceral arteries (filling defects, narrowing, occlusion, post-stenotic vasodilation) and indirect signs (retrograde filling, collateral expansion, poor contrasting of the affected artery). CT or MR angiography can be used to assess the condition of the mesenteric vessels.

Treatment. In mild cases, they are limited to conservative treatment, including diet, antispasmodic and antisclerotic drugs, agents that improve tissue metabolism and blood rheology. The progression of the disease is an indication for surgical treatment.

To eliminate external compression of the celiac trunk, it is sufficient to dissect the cicatricial-modified medial crura of the diaphragm, the falciform ligament of the liver, or the fibers of the celiac plexus. With stenosis and occlusion in the region of the mouths of the visceral arteries, endarterectomy is effective, and in cases of widespread lesions, the operations of choice are either resection of the affected area with its subsequent prosthesis, or shunting.

78.7.6. Diseases of the renal arteries. Vasorenal hypertension

Secondary symptomatic arterial hypertension develops as a result of stenosis of the renal artery, disturbance of the main blood flow and blood circulation in the kidneys without primary damage to the parenchyma and urinary tract. Characteristic of this disease are high blood pressure, impaired renal function, suspicion of involvement in the pathological process of the renal artery. 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, fibroid

musculoskeletal dysplasia, thrombosis and embolism, compression of arteries by tumors, etc. Atherosclerosis ranks first in frequency (40-65%), fibromuscular dysplasia ranks second (15-30%), and nonspecific aortoarteritis ranks third (16 -22%. Atheromatous plaque is usually located in the aorta and extends to the mouth of the 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 branches. In 50% of patients, the lesion is bilateral). Narrowing of the artery occurs due to hyperplasia, which in the form of a ring covers 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, aortic coarctation, and Takayasu's aortoarteritis.

The 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 the angiotensinogen circulating in the blood into angiotensin I, which quickly turns into angiotensin II with the help of angiotensin-converting enzyme. Angiotensin II constricts arterioles, causes hypoperfusion of the kidney, increases the secretion of aldosterone and sodium retention in the body. Hypertension occurs in response to renal hypoperfusion. A certain importance in the development of vasorenal hypertension is also given to a decrease in the level of certain depressant and vasodilator substances that can be produced by the kidneys (prostaglandins, kinins, etc.).

Clinical picture and diagnostics. At the beginning of the disease, most patients do not show symptoms of the disease. Only a few have headaches, irritability, 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 both sides of the midline. If the cause of vasorenal hypertension is an atherosclerotic lesion of the arteries, then other symptoms of atherosclerosis can be detected in patients. The absence of hypertension in the family and 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 rise to the assumption of the presence of vasorenal 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, flushing, heaviness in the head, blurred vision); 2) overload of the left parts of the heart and coronary insufficiency (aching pains in the region of the heart, 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 pools are often also affected, so patients may have symptoms due to a different localization of the pathological process.

Blood pressure in patients is sharply increased: systolic pressure



		" " f

Rice. 18.10. Bilateral critical stenosis of the renal arteries, a - before treatment; b - after endovascular stent placement. Angiograms.

leniya in most patients above 200 mm Hg. Art., and diastolic - 130-140 mm Hg. Art. Hypertension is persistent and does not respond well to conservative therapy. The boundaries of the heart are expanded to the left, the apex beat is strengthened; on the aorta, the accent of the II tone is determined. 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 angiopathy of the retina, coronary and renal insufficiency.

Urography and radioisotope renography are of great importance for diagnosis. On a series of urograms, a slow flow of a 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, delayed excretion of the isotope from the kidney on the side of the lesion is noted. During the examination, it is necessary to exclude other causes of symptomatic arterial hypertension (adrenal diseases, damage to the kidney parenchyma, central nervous system, brachiocephalic arteries). When the diagnosis is unclear, a kidney biopsy is used; determine the activity of renin in the peripheral blood and in the blood flowing from the kidneys.

Angiography, being the final stage of diagnosis, is indicated with an increase in diastolic blood pressure above 10 mm Hg. Art. and a rapid increase in signs of impaired renal function. With atherosclerotic vascular lesions, an angiogram reveals a characteristic narrowing of the mouth or initial section of the renal artery over 1.5-2 cm. At the same time, the abdominal aorta and its visceral branches are affected. With fibromuscular dysplasia, the narrowing is localized in the middle and distal parts of the renal artery; areas of expansion usually alternate with zones of annular narrowing, resembling a thread with beads.

Treatment. Despite the emergence of modern antihypertensive drugs with a pronounced inhibition of the renin-angiotensin-aldosterone system (angiotensin-converting enzyme inhibitors - captopril, enalapril, etc.), drug therapy, even successful, is not physiological, since a decrease in blood pressure in conditions of renal artery stenosis leads to decompensation circulation and kidney failure.

Rice. 18.11. Methods of reconstruction of the renal artery.

G _ transaortal endarterectomy; 6 - suture of the aorta after endarterectomy; c - resection of the renal artery with prosthetics with a venous graft.

Therefore, conservative treatment is used in the elderly and in case of systemic damage to the arterial bed. In patients with a high operational risk, percutaneous endovascular dilatation and stent placement in the renal arteries are used (Fig. 18.10). The volume of surgical intervention depends on the location of the lesion.

With isolated atherosclerotic lesions of the renal arteries, transaortic endarterectomy is usually performed. From a small incision in the aortic wall, the altered intima is removed along with an atherosclerotic plaque. Removal of the intima is facilitated by eversion of the wall of the renal artery into the lumen of the aorta (Fig. 18.11, a, b). Good results can be obtained in more than 60% of patients.

With fibromuscular dysplasia, resection of the affected area of the artery is performed, followed by prosthetics with a segment of the great saphenous vein or a. hypogastrica. With a small extent of the lesion, the altered section of the artery is resected and its distal part is reimplanted into the aorta according to the end-to-side type or the patency of the vessel is restored by an end-to-end anastomosis (Fig. 18.11, c). A decrease in blood pressure is observed in more than 90% of operated patients.

Treatment of vasorenal hypertension due to nonspecific aortoarteritis is difficult. As a rule, it is necessary to perform a corrective operation not only on the renal arteries, but also on the aorta. Therefore, resection of the renal arteries with prosthetics is more often used.

With a wrinkled kidney, damage to the intrarenal branches, organized blood clots in the renal artery and its branches, a nephrectomy is performed.

18.7.7. Obliterating diseases of the arteries of the lower extremities

Occlusion or stenosis of the vessels of the lower extremities most often occurs due to atherosclerosis of the arteries, thromboangiitis obliterans (endarteritis), aortoarteritis, fibromuscular dysplasia. These diseases are the main cause of peripheral arterial insufficiency.

Narrowing and obliteration of arteries cause a sharp decrease in blood flow, impair blood circulation in the vessels of the microvasculature, reduce oxygen delivery to tissues, cause tissue hypoxia and impaired

tissue exchange. The latter worsens due to the disclosure of arteriolo-venular anastomoses. A decrease in oxygen tension in tissues leads to the accumulation of incompletely oxidized metabolic products and metabolic acidosis. Under these conditions, the adhesive and aggregation properties increase and the disaggregation properties of platelets decrease, erythrocyte aggregation increases, blood viscosity increases, which inevitably leads to hypercoagulation and the formation of blood clots. Thrombi block the microvasculature, exacerbate the degree of ischemia of the affected organ. Against this background, disseminated intravascular coagulation develops.

Activation of macrophages, neutrophilic leukocytes, lymphocytes and endothelial cells under conditions of ischemia is accompanied by the release of pro-inflammatory cytokines from them (IL-1, IL-6, IL-8, TNF), which play an important role in the regulation of microcirculatory circulation, increased capillary permeability, in vascular thrombosis, damage (necrosis) of tissues by active oxygen radicals. In the tissues, the content of histamine, serotonin, prostaglandins, which have a membrane-toxic effect, increases. Chronic hypoxia leads to the breakdown of lysosomes and the release of hydrolases that lyse cells and tissues. The body is sensitized by the breakdown products of proteins. There are pathological autoimmune processes that exacerbate microcirculation disorders and increase local hypoxia and tissue necrosis.

Clinical picture and diagnosis. Depending on the degree of insufficiency of the arterial blood supply to the affected limb, four stages of the disease are distinguished (according to the Fontaine-Pokrovsky classification).

Stage I - functional compensation. Patients note chilliness, convulsions and paresthesias in the lower extremities, sometimes tingling and burning in the fingertips, fatigue, fatigue. When cooled, the limbs become pale in color, become cold to the touch. During the march test, after 500-1000 m, intermittent claudication occurs. In order to standardize the march test, the patient is recommended to move at a speed of 2 steps per second (according to the metronome). The length of the traveled path is determined before the appearance of pain in the calf muscle and the time until it is completely impossible to continue walking. The test is conveniently carried out on a treadmill. According to the indicators of the march test, one can judge the progression of the disease and the success of treatment. Intermittent claudication occurs due to insufficient blood supply to the muscles, impaired oxygen utilization, and accumulation of under-oxidized metabolic products in the tissues.

Stage II - subcompensation. The intensity of intermittent claudication is increasing. At the indicated pace of walking, it occurs already after overcoming a distance of 200-250 m (Pa stage) or somewhat less (116 stage). The skin of the feet and legs loses its inherent elasticity, becomes dry, flaky, hyperkeratosis is revealed on the plantar surface. The growth of nails slows down, they thicken, become brittle, dull, acquiring a matte or brown color. The growth of hair on the affected limb is also disturbed, which leads to the appearance of areas of baldness. Atrophy of the subcutaneous adipose tissue and small muscles of the foot begins to develop.

Stage III - decompensation. IN pain at rest appears on the affected limb, walking becomes possible only at a distance of 25-50 m. The color of the skin changes dramatically depending on the position of the affected limb: when lifting, its skin turns pale, when lowered, reddening of the skin appears, it becomes thinner and becomes easily vulnerable. Not-

significant trauma due to abrasions, bruises, cutting nails lead to the formation of cracks and superficial painful ulcers. Progressive atrophy of the muscles of the lower leg and foot. Employability is significantly reduced. In severe pain syndrome, to alleviate suffering, patients take a forced position - lying with their legs down.

StageIV- destructive changes. Pain in the foot and fingers become constant and unbearable. The resulting ulcers are usually located in the distal extremities, more often on the fingers. Their edges and bottom are covered with a dirty gray coating, there are no granulations, there is an inflammatory infiltration around them; edema of the foot and lower leg joins. Developing gangrene of the fingers and feet often proceeds according to the type of wet gangrene. The ability to work at this stage is completely lost.

The level of occlusion leaves a certain imprint on the clinical manifestations of the disease. For the defeat of the femoral-popliteal segment is characterized by "low" intermittent claudication - the appearance of pain in the calf muscles. For atherosclerotic lesions of the terminal abdominal aorta and iliac arteries(Lerish syndrome) are characterized by "high" intermittent claudication (pain in the gluteal muscles, in the muscles of the thighs and hip joint), atrophy of the muscles of the leg, impotence, a decrease or absence of a pulse in the femoral artery. Impotence is caused by a violation of blood circulation in the system of internal iliac arteries. Occurs in 50% of observations. It occupies an insignificant place among other causes of impotence. In some patients with Leriche's syndrome, the skin of the extremities becomes ivory, areas of baldness appear on the thighs, hypotrophy of the muscles of the extremities becomes more pronounced, sometimes they complain of pain in the umbilical region that occurs during exercise. These pains are associated with switching blood flow from the mesenteric artery system to the femoral artery system, i.e., with the "mesenteric steal" syndrome.

In most cases, the correct diagnosis can be established using a routine clinical examination, and special research methods, as a rule, only detail it. When planning a conservative therapy, with the correct use of clinical methods, a number of instrumental studies can be abandoned. Instrumental diagnostics has an undoubted priority in the period of preoperative preparation, during the operation and postoperative observation.

Inspection provides valuable information about the nature of the pathological process. In chronic ischemia of the lower extremities, patients usually develop muscle hypotrophy, the filling of the saphenous veins decreases (a symptom of a groove or a dry river bed), the skin color changes (pallor, marbling, etc.). Then trophic disorders appear in the form of hair loss, dry skin, thickening and brittle nails, etc. In severe ischemia, blisters filled with serous fluid appear on the skin. More often there is dry (mummification) or wet (wet gangrene) necrosis of the distal segments of the limb.

Palpation and auscultation of the vessels of the leg give essential information about the localization of the pathological process. Thus, the absence of a pulse on the popliteal artery indicates obliteration of the femoral-popliteal segment, and the disappearance of a pulse on the thigh indicates damage to the iliac arteries. In a number of patients with high occlusion of the abdominal aorta, pulsation cannot be detected even with palpation of the aorta through the anterior abdominal wall. In 80-85% of patients with obliterating atherosclerosis, the pulse is not detected on the popliteal artery, and in 30% - on the femoral one. Should

remember that a small number of patients (10-15%) may have an isolated vascular lesion of the lower leg or foot (distal form). All patients should perform auscultation of the femoral, iliac arteries and abdominal aorta. Above the stenotic arteries, a systolic murmur is usually heard. With stenosis of the abdominal aorta and iliac arteries, it can be well defined not only above the anterior abdominal wall, but also on the femoral arteries under the inguinal ligament.

The selective lesion of the distal arteries is the reason that in patients with obliterating thromboangiitis, the pulsation of the arteries on the feet first of all disappears. At the same time, it should be borne in mind that in 6-25% of practically healthy people, the pulse on the dorsal artery of the foot may not be determined due to anomalies in its position. Therefore, a more reliable sign is the absence of a pulse in the posterior tibial artery, the anatomical position of which is not so variable.

functional tests. The symptom of plantar ischemia of O p -pel consists in blanching of the sole of the foot of the affected limb, raised up at an angle of 45 °. Depending on the speed of blanching, one can judge the degree of circulatory disorders in the limb. In severe ischemia, it occurs within 4 -6 s. Later, changes were made to the Goldflam and Samuels test, which made it possible to more accurately judge the time of appearance of blanching and restoration of blood circulation. In the supine position, the patient is asked to raise both legs and hold them at a right angle in the hip joint. Within 1 min, they offer to bend and unbend the feet in the ankle joint. Determine the time of appearance of blanching of the feet. Then the patient is offered to quickly take a sitting position with his legs down and note the time until the filling of the veins and the appearance of reactive hyperemia. The data obtained can be digitally processed, making it possible to judge the change in blood circulation during the treatment.

Goldflam test. In the position of the patient on his back with his legs raised above the bed, he is offered to perform flexion and extension in ankle joints. In violation of blood circulation, after 10-20 movements, the patient experiences fatigue in the leg. At the same time, the color of the plantar surface of the feet is monitored (Samuels test). With severe circulatory failure, blanching of the feet occurs within a few seconds.

The Sitenko-Shamova test is carried out in the same position. A tourniquet is applied to the upper third of the thigh until the arteries are completely clamped. After 5 minutes, the bandage is removed. Normally, no later than 10 s, reactive hyperemia appears. In case of insufficiency of arterial circulation, the time for the appearance of reactive hyperemia is lengthened several times.

Panchenko's knee phenomenon is determined in a sitting position. The patient, throwing his sore leg over the healthy knee, soon begins to experience pain in the calf muscles, a feeling of numbness in the foot, a crawling sensation in the fingertips of the affected limb.

The symptom of compression of the nail bed is that when the terminal phalanx of the first toe is compressed in the anteroposterior direction for 5-10 s in healthy people, the resulting blanching of the nail bed is immediately replaced by a normal color. In violation of blood circulation in the limb, it lasts for several seconds. In cases where the nail plate is changed, it is not the nail bed that is squeezed, but the nail fold. In patients with impaired peripheral circulation

Rice. 18.12. Atherosclerosis of the aortoiliac segment.

a - occlusion of the infrasternal aorta (angiogram); b - occlusion of the external iliac artery (CT-ashiogram); V - bilateral isolated sgenoses of the common iliac arteries (MR angiogram).

the white spot on the skin formed as a result of compression disappears slowly, within a few seconds or more.

Rheography, Doppler ultrasound, transcutaneous determination of p0 2 and pCO 2 of the lower extremities help to establish the degree of ischemia of the diseased limb.

Obliterating lesions are characterized by a decrease in the amplitude of the main wave of the rheographic curve, the smoothness of its contours, the disappearance of additional waves, and a significant decrease in the value of the rheographic index. Rheograms recorded from the distal parts of the affected limb in case of circulatory decompensation are straight lines.

Doppler ultrasound data usually indicate a decrease in regional pressure and linear blood flow velocity in the distal segments of the affected limb, a change in the blood flow velocity curve (the so-called main-altered or collateral type of blood flow is recorded), a decrease in the ankle systolic pressure index, which is derived from the ratio

systolic pressure at the ankle to pressure at the shoulder.

Using ultrasound duplex scanning in patients with Leriche's syndrome, it is possible to clearly visualize changes in the terminal abdominal aorta and iliac arteries, occlusion or stenosis of the femoral, popliteal artery, determine the nature and duration of the lesion in the main collateral arteries (in particular, in deep artery hips). It allows you to determine the localization and extent of the pathological process, the degree of damage to the arteries (occlusion, stenosis), the nature of changes in hemodynamics, collateral circulation, the state of the distal bloodstream.

Rice. 18.13. Distal vascular lesions.

a - occlusion of the superficial femoral artery (MR angiogram); b - multiple stenoses of the arteries of the lower leg (angiogram).

Verification of the topical diagnosis is carried out using angiography (traditional radiopaque, MR or CT angiography) - the most informative method for diagnosing obliterating atherosclerosis.

Angiographic signs of atherosclerosis include marginal filling defects, corroded contours of vessel walls with areas of stenosis, the presence of segmental or widespread occlusions with filling of the distal sections through a network of collaterals (Fig. 18.12; 18.13).

With thromboangiitis, angiograms determine good patency of the aorta, iliac and femoral arteries, conical narrowing of the distal segment of the popliteal artery or proximal segments of the tibial arteries, obliteration of the lower leg arteries in the rest of the length with a network of multiple, small tortuous collaterals. The femoral artery, if involved in the pathological process, appears to be evenly narrowed. It is characteristic that the contours of the affected vessels are usually even.

Surgery. Indications for performing reconstructive surgeries in case of segmental lesions can be determined starting from the Pb stage of the disease. Contraindications are severe concomitant diseases internal organs- heart, lungs, kidneys, etc., total calcification of the arteries, lack of patency of the distal bed. Restoration of the main blood flow is achieved with the help of endarterectomy, bypass grafting or prosthetics.

In case of obliteration of the artery in the femoral-popliteal segment, femoral-popliteal or femoral-tibial shunting is performed with a segment of the great saphenous vein. The small diameter of the great saphenous vein (less than 4 mm), early branching, varicose veins, phlebosclerosis limit its use for plastic purposes. As a plastic material, the vein of the umbilical cord of newborns, allovenous grafts, lyophilized xeno-

Rice. 18.14. Femoral-popliteal shunting.

nografts from the arteries of cattle. Synthetic prostheses are of limited use, as they often thrombose in the very near future after surgery. In the femoro-popliteal position, polytetrafluoroethylene prostheses have proved to be the best (Fig. 18.14).

In atherosclerotic lesions of the abdominal aorta and iliac arteries, aortofemoral bypass (Fig. 18.15) or resection of the aortic bifurcation and prosthesis (Fig. 18.16) using a bifurcation synthetic prosthesis are performed. If necessary, the operation can be completed by excision of necrotic tissues.

In recent years, in the treatment of atherosclerotic lesions of the arteries, the method of X-ray endovascular dilation and retention of the lumen of a dilated vessel using a special metal stent has become widespread. The method is quite effective in the treatment of segmental atherosclerotic occlusions and stenoses of the femoropopliteal segment and iliac arteries. It is also successfully used as an addition to reconstructive operations, in the treatment of "multi-story" lesions. In case of diabetic macroangiopathies, reconstructive operations allow not only to restore the main blood flow, but also to improve blood circulation in the microvasculature. Due to the defeat of vessels of small diameter, as well as the prevalence of the process, reconstructive

Rice. 18.15. Aortic bypass grafting with a synthetic prosthesis.

Rice. 18.16. Resection of aortic bifurcation with prosthetics.

operations with thromboangiitis obliterans are of limited use.

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

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

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

With necrosis or gangrene, there are indications for amputation of the limb. At the same time, the level of amputation depends on the level and degree of damage to the main arteries and the state of the collateral circulation.

The volume of surgical intervention should be strictly individualized and performed taking into account the blood supply of the limb and the convenience of subsequent prosthetics. With isolated necrosis of the fingers with a clear demarcation line, exarticulation of the phalanges with resection of the head of the tarsal bone or necrectomy is performed. With more common lesions, amputations of the fingers, transmetatarsal amputations and amputation of the foot in the transverse - Chopar joint are performed. The spread of the necrotic process from the toes to the foot, the development of wet gangrene, 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 should 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 conservative treatment: 1) elimination of the impact of adverse factors (prevention of cooling, prohibition of smoking, drinking alcohol, etc.); 2) training walking; 3) elimination of vasospasm with the help of antispasmodics (pentoxifylline, complamin, cinnarizine, vazaprostan, nikospan); 4) pain relief (nonsteroidal analgesics); 5) improvement of metabolic processes in tissues (group 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,

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

In patients with an autoimmune genesis of the disease, it becomes necessary to use corticosteroids, immunostimulants. Most patients with atherosclerosis require correction of lipid metabolism, which must be made on the basis of 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), 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, persistently seeking from patients a sharp reduction in the consumption of animal fats, a complete cessation of smoking. It is necessary to regularly and correctly take medicines prescribed for the treatment of concomitant diseases (diabetes mellitus, hypertension, hyperlipoproteinemia), as well as diseases associated with impaired lung and heart functions: an increase in cardiac output leads to an increase in tissue perfusion below the site of occlusion, and therefore, and improve their oxygen supply.

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

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 such patients, along with drug therapy using hemosorption.

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

18.8. Aneurysms of the aorta and peripheral arteries

A vessel aneurysm is commonly 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's 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 non-specific - aortoarteritis; mycotic lesions).

Erdheim's idiopathic median necrosis, median necrosis during pregnancy, may be the cause of aneurysm formation.

18.8.1. Aortic aneurysms

Most aortic aneurysms are atherosclerotic in origin. Macroscopically, the inner surface of an atherosclerotic aneurysm is represented by atheromatous plaques, ulcerated and calcified in places. Inside the cavity of the aneurysm, compacted masses of fibrin are located near the wall. They make up 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. In connection with the deterioration of the trophism, instead of the expected organization of the "thrombotic cup", its 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.

Aneurysms are divided into saccular and fusiform according to their shape. The former are characterized by local protrusion of the aortic wall, while the latter are characterized by a diffuse expansion of the entire circumference of the aorta.

pathological physiology. With an aneurysm, there is a sharp slowdown in the linear velocity of blood flow in the sac, its turbulence. Only about 45% of the volume of blood in the aneurysm enters the distal bed. The mechanism of slowing blood flow in the aneurysmal sac is due to the fact that the main blood flow, passing through the aneurysmal cavity, rushes along the walls. In this case, the central flow slows down due to the return of blood due to the turbulence of the blood flow, the presence of thrombotic masses in the aneurysm.

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