How to treat cerebrovascular accident. Venous insufficiency of the brain Chronic cerebral insufficiency

Chronic cerebrovascular insufficiency (CCF) is a brain dysfunction characterized by slow progression. It is one of the most common pathologies in neurological practice.

Etiological factors

The cause of the development of insufficiency, which is especially common in elderly and senile patients, is small-focal or diffuse damage to brain tissue. It develops against the background of long-standing problems with cerebral circulation, since during ischemia the central nervous system does not receive enough oxygen and glucose.

The most common causes of chronic ischemia:

One of the etiological factors is considered to be anomalies in the development of the aortic arch and vessels of the neck and shoulder girdle. They may not make themselves felt until development and. Certain importance is attached to compression (squeezing) of blood vessels by bone structures (with spinal curvatures and osteochondrosis) or tumors.

Blood circulation may also be impaired due to deposits of a specific protein-polysaccharide complex, amyloid, on the vascular walls. Amyloidosis leads to dystrophic changes in blood vessels.

In older people, one of the risk factors for CNMC is often low blood pressure. It does not exclude arteriosclerosis, i.e. damage to the small arteries of the brain.

Symptoms of chronic cerebrovascular insufficiency

Important:The main clinical features of CNM include syndromicity, stages and a progressive course!

It is customary to distinguish 2 main stages of chronic cerebral ischemia:

1. initial manifestations;
2. encephalopathy.

The initial stage develops when the flow of blood decreases from normal levels of 55 ml/100 g/min to 45-30 ml.

Typical patient complaints:

In the early stages of development of cerebral blood flow insufficiency, symptoms appear after physical exertion or psycho-emotional stress, fasting and drinking alcohol.

During the examination, when determining the neurological status, no signs of focal changes in the central nervous system are revealed. Special neuropsychological tests can identify disorders of thinking functions (in a mild form).

Note:Every year in our country, up to 450 thousand cases of acute cerebrovascular accidents - strokes - are diagnosed. According to various sources, vascular dementia affects from 5% to 22% of elderly and senile people.

Discirculatory encephalopathy (DE) develops against the background of a decrease in blood flow to 35-20 ml/100 g/min. Changes, as a rule, occur due to general vascular pathologies.

Note:significant changes in hemodynamics are noted if there is a narrowing of the main vessels to 70-75% of normal.

DE forms:

• venous;
• hypertensive;
• atherosclerotic;
• mixed.

Discirculatory encephalopathy is divided into 3 stages depending on the severity of neurological symptoms.

Signs of stage 1:

• (problems with remembering new information are noted);
• decreased ability to concentrate;
• decreased mental and physical performance;
• high fatigue;
• dull (cephalgia), increasing with psycho-emotional experiences and mental stress;
• problems with switching from one task to another;
• frequent;
• unsteadiness when walking;
• worsening mood;
• emotional instability.

The working capacity of patients with stage 1 is preserved. A neurological examination reveals moderate memory impairment and decreased attention. Reflexes are moderately increased; their intensity on the right and left is slightly different.

Signs of stage 2:

• progression of memory disorders;
• severe deterioration in sleep;
• frequent cephalgia;
• transient dizziness and instability in a vertical position;
• darkening of the eyes when changing body position (standing up);
• touchiness;
• irritability;
• reduction of needs;
• slow thinking;
• pathological attention to minor events;
• obvious narrowing of the circle of interests.

Stage 2 is characterized not only by decreased ability to work (disability group II-III), but also by problems with the patient’s social adaptation. During the examination of the neurological status, vestibulo-cerebellar disorders, poverty and slowdown of active movements with a specific increase in muscle tone are revealed.

Signs of stage 3:

• thinking disorders increasing to dementia ();
• tearfulness;
• sloppiness;
• (not always);
• a pronounced decrease in self-criticism;
• pathological lack of will;
• weakening of sphincter control (involuntary urination and defecation);
• frequent drowsiness after eating.

Note:For patients at this stage of development of the pathology, the Winscheid triad is very characteristic, i.e., a combination of memory impairment, headaches and episodes of dizziness.

Patients with stage 3 discirculatory encephalopathy are disabled; they are given disability group I.

Diagnostics

The diagnosis is made based on the clinical picture, the patient’s complaints, and the results obtained from examining the brain and blood vessels.

Note:There is an inverse relationship between the number of patient complaints about decreased memory ability and the severity of chronic ischemia. The greater the impairment of cognitive functions, the fewer complaints.

During examination of the fundus, blanching of the optic nerve head and atherosclerotic changes in the vessels are detected. Upon palpation, compaction of the arteries supplying the brain - carotid and temporal - is determined.

The instrumental research methods necessarily used to verify the diagnosis include:

• dopplerography;
• angiography;
• rheoencephalography with additional tests;
• aorta and other great vessels;
• brain and vessels of the “cerebral basin” (the main method of neuroimaging);
• electroencephalography.

Additional data is obtained from laboratory tests for the metabolism of lipid compounds, an electrocardiogram and biomicroscopy of the conjunctival vessels.

Important:atherosclerosis of cerebral vessels is often combined with atherosclerotic lesions of the arteries of the legs and coronary vessels.

The task of differential diagnosis is to exclude brain diseases that do not have a vascular etiology. It is known that the functions of the central nervous system can be secondarily impaired due to diabetes mellitus, damage to the respiratory system, kidneys, liver and digestive tract.

Measures for the treatment and prevention of CNMK

When identifying the first symptoms of chronic cerebral ischemia, it is strongly recommended to periodically carry out a comprehensive course of treatment. It is necessary to prevent or slow down the development of pathological changes.

Primary prevention of CNM is within the competence of general practitioners - family doctors and local therapists. They must carry out explanatory work among the population.

Basic preventive measures:

• maintaining a normal diet;
• making adjustments to the diet (reducing the amount of carbohydrates and fatty foods);
• timely treatment of chronic diseases;
• rejection of bad habits;
• regulation of work schedule, as well as sleep and rest;
• combating psycho-emotional stress (stress);
• active lifestyle (with dosed physical activity).

Important:Primary prevention of pathology should begin in adolescence. Its main focus is eliminating risk factors. It is necessary to avoid overeating, and. Secondary prevention is needed to prevent episodes of acute cerebral blood flow disorders in patients with diagnosed chronic ischemia.

Treatment of vascular insufficiency involves rational pharmacotherapy. All medications should be prescribed only by a local doctor or specialist, taking into account the general condition and individual characteristics of the patient’s body.

Patients are advised to take a course of vasoactive drugs (Cinnarizine, Cavinton, Vinpocetine), antisclerotic drugs and antiplatelet agents to reduce blood viscosity (Acetylsalicylic acid, Aspirin, Curantil, etc.). Additionally, antihypoxants are prescribed (to combat oxygen starvation of brain tissue), and vitamin complexes (including and). The patient is recommended to take neuroprotective drugs that contain amino acid complexes (Cortexin, Actovegin, Glycine). To combat certain secondary disorders of the central nervous system, the doctor may prescribe drugs from the group of tranquilizers.

Important:is of great importance for maintaining blood pressure levels at the level of 150-140/80 mm Hg.

It is often necessary to select additional combinations of drugs if the patient is diagnosed with atherosclerosis, hypertension and (or) coronary insufficiency. Making certain changes to the standard treatment regimen is necessary for diseases of the endocrine system and metabolic disorders - diabetes mellitus, thyrotoxicosis and obesity. Both the attending physician and the patient must remember: the medications should be taken in full courses, and after a break of 1-1.5 weeks, begin a course of another medication. If there is an obvious need to use different drugs on the same day, it is important to maintain a time interval of at least half an hour between doses. Otherwise, their therapeutic activity may decrease, and the likelihood of developing side effects (including allergic reactions) may increase.

People who have clinical signs of cerebrovascular insufficiency are advised to refrain from visiting baths and saunas to avoid overheating of the body. It is also advisable to reduce your time in the sun. Climbing into the mountains and staying in areas at an altitude of over 1000 m above sea level poses a certain danger. It is necessary to completely abandon nicotine, and reduce the consumption of alcohol-containing drinks to a minimum (no more than 30 ml of “absolute alcohol” per day). The consumption of strong tea and coffee should be reduced to 2 cups (approximately 100-150 ml) per day. Excessive physical activity is unacceptable. You should not sit in front of a TV or PC monitor for more than 1-1.5 hours.

Plisov Vladimir, medical observer

Chronic cerebral circulatory failure (CCF) is a slowly progressive pathology leading to a constant lack of oxygen and nutrients in brain cells.

Depending on which parts of the brain are most affected, the disease manifests itself in various neurological and neuropsychiatric pathologies. Impairment of brain functions is secondary to changes in brain structures - focal or disseminated lesions appear in them.

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Causes and mechanism of development of the disease

When one of the cerebral vessels is narrowed or blocked by an atherosclerotic plaque or thrombus, blood flow is impaired. As a result, energy resources to ensure the functioning of the brain are depleted, and harmful substances accumulate. This leads to disruption of local metabolic processes. Subsequently, a zone of replacement of the medulla with scar tissue is formed.

The most common causes of chronic cerebral ischemia are:

• atherosclerotic damage to cerebral (brain) vessels;
• cardiac ischemia;
• hypertension or episodes of hypertension.

Secondary causes include pathological deformations of the cervical spine, diabetes mellitus and other endocrine disorders, blood diseases, cerebral rheumovasculitis, venous insufficiency, anomalies in the development of blood vessels in the brain and heart. Any pathological process that affects blood vessels and narrows their lumen is potentially the cause of the development of chronic CNM.

Clinical manifestations of pathology

Chronic cerebrovascular insufficiency differs from acute cerebrovascular accident in the diameter of the vessels affected. If one of the main arteries is involved in the pathology, then a vascular catastrophe develops - a cerebral stroke - a condition with severe manifestations and a poor prognosis. With CNMK, small arteries and capillaries are affected. As a result, many small lesions form at different times or the brain suffers as a whole. Clinical manifestations progress gradually as changes accumulate.



Based on patient complaints and objective research, the following syndromes are distinguished:

• asthenic syndrome – increased exhaustion, emotional lability, sleep disturbance;
• cephalgic – headaches that occur at least once a week for at least three months:
• syndrome of diffuse neurological symptoms - unexpressed neurological signs detected during a targeted examination: asymmetry of facial muscles, difference in the strength of tendon reflexes on the left and right, weakening of the pupillary reaction;
• vestibulocerebellar syndrome – instability when walking, dizziness, coordination disorders;
• pseudobulbar – symptoms associated with impaired swallowing and articulation;
• extrapyramidal syndrome - the section connecting the spinal cord and brain is affected, trembling of the head and hands appears, actions slow down, and muscle stiffness develops;
• vascular dementia syndrome (dementia) – impairment of intellect, memory, will.

With the development of chronic cerebrovascular insufficiency, one syndrome rarely develops in isolation. Since brain damage is associated with systemic vascular pathology, it is widespread. Therefore, when making a diagnosis, they speak of the predominant syndrome.





Stages of the disease

As individual small areas of the brain are damaged, their function is transferred to neighboring, normally functioning parts. Compensation occurs for impaired brain activity. When a large volume of brain matter is damaged, compensation is disrupted—symptoms appear and progress.

If the exacerbation of the underlying disease is eliminated in time (for example, blood pressure decreases during a crisis), and the brain cells are “maintained,” then the changes can be reversible. If assistance is provided later, the changes are saved.

There are three stages of chronic cerebrovascular insufficiency:

1. 1. Compensation – subjective symptoms are inherent. Complaints of prolonged headache, tinnitus, dizziness, fatigue, decreased memory and performance, inattention, depression, change in life values.
2. 2. Subcompensation - unsteadiness when walking, unclear speech, trembling of fingers, uncontrollable laughter and crying are added, professional memory suffers, orientation in the area is impaired, and self-criticism is noticeably reduced. The occurrence of transient ischemic attacks (attacks resembling a stroke, but passing during treatment without serious consequences), and fluctuations in blood pressure cannot be ruled out.
3. 3. Decompensation - at this stage, patients have very few complaints, due to the lack of criticism towards themselves. Sensitivity disorders, severe paralysis and paresis, dysfunction of the pelvic organs (frequent urination) are objectively determined. In most cases, there is a history of strokes.

Typically, the severity of the condition increases gradually over several years and decades. When examined by a neurologist, changes that are characteristic of both the first and second, or second and third stages are often revealed.



Examinations to detect pathology

When examining a patient with chronic cerebral insufficiency, one should initially determine the underlying pathological process that led to disturbances in the blood supply to the brain. Etiological treatment (aimed at eliminating the cause of the disease) depends on this.

The first stage of the examination is a thorough interview of the patient, as a result of which complaints, history of the development of the disease, life characteristics, concomitant pathologies, previous diseases, operations, injuries, and hereditary history are assessed. In laboratory data, determination of the lipid profile, blood glucose level, and coagulation parameters has diagnostic value.



Using instrumental research methods, changes in the cardiovascular system are determined using ECG and Echo-CG. To visualize the vessels of the brain, Doppler ultrasound should be performed, and for an in-depth analysis of the pathology of brain structures, computed tomography and magnetic resonance imaging should be performed.

There are a number of diseases that manifest themselves with similar syndromes.

Chronic cerebral ischemia should be differentiated from borderline mental disorders, endogenous psychoses in the early stages, consequences of brain injuries, and oncological diseases. The greatest difficulty for diagnosis is neurodegenerative diseases (not associated with vascular damage), especially if they are accompanied by changes in the psyche. These are Alzheimer's, Parkinson's and some others.

Treatment of CNMK

First of all, you should influence the patient’s lifestyle. It is necessary to comply with normal physical activity, quit smoking and drink alcohol.

Diet - table No. 10c according to Pevzner. According to this diet, the consumption of foods high in cholesterol (fatty meat, canned food, smoked meats, baked goods) is excluded, and foods rich in fiber (vegetables, fruits) are increased. Food is steamed or stewed. The amount of daily fluid and salt consumed is limited. A day requires 5-6 meals in moderate quantities. The last dose is 3 hours before bedtime.

Pathogenetic therapy consists of treating the underlying disease (coronary heart disease, arterial hypertension, diabetes mellitus) and includes several groups of drugs.

Antihypertensive drugs

They are intended to influence vascular risk factors and correct blood pressure. The drug or their combination, as well as the dose, is selected individually. This group of drugs includes:

• angiotensin-converting enzyme (ACE) inhibitors - captopril, lisinopril, enalapril, perindopril;
• beta blockers: anaprilin, metoprolol, oxprenolol, talinolol;
• calcium antagonists: verapamil, nifedipine, nimodipine;
• diuretics (spironolactone, hypothiazide).



Fight cholesterol and blood clots

Normalization of blood cholesterol levels involves reducing the level of low-density lipoproteins, correcting hypertriglyceridemia, and increasing the level of high-density lipoproteins. Particularly important is the atherogenic index, a calculated indicator that reflects the ability of cholesterol to form plaques. Statins are used for treatment - drugs that affect cholesterol (atorvastatin, rosuvastatin, simvastatin) and fatty acid sequestrants (cholestyramine).

The rheological properties of blood are improved through the use of antiplatelet agents (dipyridamole, small doses of acetylsalicylic acid), anticoagulants (warfarin). The use of these drugs should be carried out with regular monitoring of blood clotting parameters.

Restoration of cerebral blood flow, correction of symptoms

To improve blood supply, medications that dilate cerebral vessels are prescribed - Vinpocetine, Cinnarizine.

To improve metabolic processes in conditions of deficiency of nutrients and oxygen in the brain tissue, neuroprotectors are used - piracetam, biogenic stimulants, B vitamins.

For neurosis-like conditions and sleep disorders, drugs from the group of tranquilizers and sedatives are prescribed: Phenazepam, tinctures of valerian, motherwort, peony. To eliminate dizziness, betahistine drugs are used.

Surgical treatment of chronic cerebrovascular insufficiency is possible when a cerebral vessel is occluded by a thrombus or plaque. It is also recommended to eliminate provoking factors, such as deformities of the spine and chest.

Catad_tema Chronic cerebral ischemia - articles

Treatment of chronic brain failure

1. Brain damage of vascular etiology is one of the most common pathological conditions in neurological practice. It is customary to distinguish between acute and chronic cerebrovascular accidents (CVA). Acute NMCs include stroke and transient NMCs (TIMCs), while chronic ones include initial manifestations of NMCs (NIMCs) and dyscirculatory encephalopathy (DE). DE is a syndrome of chronic progressive diffuse and/or multifocal brain damage of vascular etiology, which develops as a result of repeated acute cerebrovascular accidents and/or chronic insufficiency of blood supply to the brain. Other terms proposed to denote this clinical condition (chronic cerebral ischemia, cerebrovascular disease, ischemic cerebral disease) are less successful. The term "dyscirculatory encephalopathy" reflects the morphology and possible pathogenetic mechanisms of the process.

2. In accordance with two main pathogenetic mechanisms (repeated acute disorders and chronic ischemia), DE at the morphological level is represented by two main forms: cerebral infarction and leukoaraiosis. Cerebral infarction can often develop without clinical stroke and is an incidental finding during neuroimaging. A marker of chronic cerebral ischemia is leukoaraiosis - diffuse changes in the deep parts of the white matter of the brain. Morphologically, leukoaraiosis is represented by demyelination, gliosis, expansion of the perivascular space, and sweating of the cerebrospinal fluid. The most common cause of these conditions is chronic uncontrolled arterial hypertension.

3. Arterial hypertension leads to damage to the subcortical basal ganglia and deep white matter of the brain. The subcortical basal ganglia are integrated into functional anatomical circles with the frontal cortex. The circulation of excitation through neuronal circles is necessary for tuning the frontal cortex. The frontal lobes are responsible for the regulation of voluntary activity: the formation of motivation, choosing the goal of the activity, building a program and monitoring its achievement. Disruption of connections between the frontal cortex and the subcortical basal ganglia (the “disconnection” phenomenon) leads to secondary dysfunction of the frontal cortex, which is the main pathogenetic mechanism of DE, at least at its initial stage.

Clinical manifestations Frontal dysfunction manifests itself in three areas: cognitive, emotional and neurological (motor disorders).

Disorders of regulation of voluntary activity

4. The first signs of cerebrovascular insufficiency are cognitive impairment of a frontal nature, which is evidenced by a decrease in reaction speed: the patient needs more time and attempts than normal to solve pressing intellectual problems. Fatigue and decreased performance are the most common patient complaints at this stage of the disease. With DE, operative memory is impaired, with relative preservation of memory for life events. Impaired episodic memory, if the patient forgets what happened yesterday, indicates the presence of a degenerative process.

Clock drawing test

5. Traditionally, neuropsychological scales are used to assess the cognitive sphere, of which the most popular is the Brief Mental Status Assessment Scale. Unfortunately, this scale was developed for the diagnosis of Alzheimer's disease, so its use does not allow for a sufficiently complete assessment of the functions of the frontal lobes for the diagnosis of DE. The clock drawing test assesses both spatial functions and the ability to organize activities. The figure shows a test of a patient with a severe frontal disorder: visuospatial impairment. In addition, to assess the function of the frontal lobes, frontal tests are used: generalizations, associations, “dynamic praxis”, Shulge’s test and composing a story from a picture. The most sensitive test for early diagnosis is the symbol-numeric combination test, which is performed over time and allows you to assess the severity of bradyphrenia.

6. A study of the frequency of cognitive impairment (CD) in dyscirculatory encephalopathy (DE) showed that 88% of patients at the initial stage of DE have cognitive impairment of varying severity (moderate - MCI and mild - MCI). Cognitive disorders are the most characteristic, objective and reproducible symptom of vascular lesions of the brain.

Prevalence of cognitive impairment in dyscirculatory encephalopathy without dementia

Yakhno N.N.. Zakharov V.V.. Lokshina A.B., 2005

7. Emotional and cognitive disorders are connected by the presence of common pathogenetic factors (the phenomenon of dissociation and frontal dysfunction), and are also capable of directly influencing each other. Thus, the control of a number of cognitive functions has an emotional mechanism. Cognitive impairment of control over the result of an activity in the form of impulsivity occurs against the background of the absence of such an emotional phenomenon as doubt about the correctness of the result obtained. The experience of one’s growing intellectual and, as a rule, motor inability contributes to the formation of depressive disorders. It is currently believed that depression in DE should be considered a separate form of the disease, since it has a number of pronounced features of the clinical course and response to therapy.

8. The main neurological disorders in DE are complex motor control disorders, pseudobulbar syndrome, pyramidal tetraparesis and pelvic disorders.

First of all, the functioning of complex motor control systems that are closed through the frontal cortex and include its connections with subcortical and brainstem structures is disrupted. Clinically, this is expressed in gait disturbances and frontal dysbasia.

It has been proven that there is a significant correlation between the severity of motor and cognitive impairments in DE (I.V. Damulin et al.).

Clinic of dyscirculatory encephalopathy: movement disorders
Gait disturbance
Frontal abasia

Parkinsonism of the lower body 9. Treatment of chronic cerebral vascular insufficiency (CVI) should include etiotropic, pathogenetic and symptomatic therapy. Etiotropic therapy for DE should be primarily aimed at the underlying pathological processes of CHMN, such as arterial hypertension, atherosclerosis of the great arteries of the head and other cardiovascular diseases. Treatment of chronic cerebral vascular insufficiency10. To optimize microcirculation, patients with cerebrovascular insufficiency are prescribed vasoactive drugs, which include phosphodiesterase inhibitors (aminophylline, pentoxifylline, vinpocetine, gingko biloba), calcium channel blockers (cinnarizine, flunarizine, nimodipine) and α2-adrenergic receptor blockers (nicergoline). In addition to their vasodilatory effects, many of them also have positive metabolic effects, which allows them to also be used as symptomatic nootropic therapy. Metabolic drugs include pyrrhodoline derivatives (piracetam, pramiracetam, oxiracetam), which have a stimulating effect on metabolic processes in neurons. Peptidergic and amino acid preparations (Cerebrolysin, Cortexin, Actovegin, glycine) contain biologically active compounds that have a multimodal positive effect on neurons. 11. Piracetam is one of the basic drugs used in the pathogenetic therapy of CHMN; it has long proven itself in clinical practice. The study of the mechanism of action of Nootropil continues to this day. Thus, recent studies have shown that Nootropil ® has a pronounced membrane-stabilizing effect, and this effect is non-specific for the brain. The effect of Nootropil on neurons causes an improvement in metabolism and neurotransmission, the effect on erythrocytes and platelets leads to increased plasticity and reduced aggregation (Moller WE. Int Acad Biomed Drug Res, Basel, Karger 1992;2:35-40. Nootropil ® monograph 2004). 12. The presented study shows the neuroprotective qualities of Nootropil. After artificial damage to a small area of ​​the cortex, the rats were divided into groups receiving Nootropil ® and placebo. Nootropil ® or placebo was given 1 hour after surgery; injections were given twice a day for 3 weeks, when the rats were kept in special conditions - improved (spacious cage, many moving and stationary objects, 10 other rats) and worse (small empty single cage). The damaged cortex was assessed after 3 weeks. As a result, it was revealed that in rats in the control group, the percentage of decrease in gray matter was higher than in rats receiving Nootropil, regardless of the conditions of detention. Thus, Nootropil ® has a neuroprotective effect after ischemic injury. Nootropil ® increases the survival of neurons under hypoxic conditions
Nootropil protects cells during ischemic damage 13. The effectiveness of Nootropil in the treatment of cognitive disorders in elderly patients was assessed in a meta-analysis of the results of 19 studies, which involved over 1,400 patients (665 patients took placebo and 753 Nootropil). All studies were conducted from 1972 to 1993. in parallel groups and had a double-blind design. The main evaluation criterion was the CGIC indicator (Clinical Global Impression of Change - global assessment of clinically significant changes). The meta-analysis data allowed the researchers to conclude: "The results clearly demonstrate the statistical superiority of piracetam over placebo when using a global assessment of clinically significant changes. These results provide compelling evidence of the global clinical effectiveness of piracetam in various groups of elderly subjects with cognitive impairment" (Waegemans T, Wilsher CR, Danniau A, Ferris SH, Kurz A, Winblad B Clinical efficacy of piracetam in cognitive impairment: a metaanalysis (Dement Geriatr Disord 2002;13:217-224). 14. A meta-analysis showed that more than 60% of patients reported clinically significant improvement at the end of treatment compared with 30% of patients receiving placebo. Thus, the results of the meta-analysis demonstrate the effectiveness of Nootropil ® in the treatment of cognitive disorders of varying severity. Meta-analysis: resultsThe results of a meta-analysis demonstrate the effectiveness of Nootropil in the treatment of cognitive disorders of varying severity

Waegemans T et al. Dement Geriatr Cogn Disord 2002.13:217-24.

15. A study of the effectiveness of Nootropil was conducted in 162 patients with age-related memory loss (without dementia or depression). Patients took Nootropil ® 2.4 g/day or 4.8 g/day or placebo for 12 weeks. Before and after treatment, patients completed a text recall test. The results of the study showed that Nootropil significantly improves memory performance in patients with age-related changes. The improvements were especially pronounced in the group of patients receiving Nootropil ® at a high dose of 4.8 mg/day. In conclusion, it should be emphasized that CSMN is a common complication of chronic uncontrolled arterial hypertension, cerebral atherosclerosis, and other cardiovascular diseases. The most common manifestation of CHMS is a combination of cognitive, emotional and motor disorders of a frontal nature. Treatment of CHF should be aimed at the underlying cardiovascular disease, optimizing microcirculation and maintaining neuronal metabolism. Use of Nootropil ® in patients with age-related memory loss

*R<0.05, **р<0,01, ***р<0.001

Nootropil causes a more significant improvement in the word reproduction test at a dose of 4.8 g

Israel L et al. Int Psychogeriatr 1994:6 155-70

Pathological deformation of the BCA (vertebral, carotid) arteries is a congenital or acquired change in the configuration of the brachiocephalic arteries (vessels supplying the brain), leading to disruption of the properties of blood flow and the development of acute cerebrovascular accident or chronic cerebral circulatory failure.

Types of pathological tortuosity of the internal carotid artery (pathological tortuosity of the ICA):

It is easier to imagine the mechanism of blood flow disturbance when a garden hose is compressed, twisted or bent - acceleration of fluid flow and loss of laminar properties leads to loss of kinetic energy of the blood and insufficient blood supply to the brain. Another mechanism is the narrowing of the lumen at the point where the artery bends - septal stenosis, which, under certain conditions, is an analogue of stenosis of the lumen of the vessel in atherosclerosis.

Pathological tortuosity of the internal carotid artery (ICA tortuosity)

Pathological tortuosity of the internal carotid artery (pathological tortuosity of the ICA) is the most common pathology among all deformities of the BCA.

Narrowing of the arteries supplying the brain with blood as a result of pathological deformation of the BCA leads to chronic disorders of cerebral circulation, which is a pre-stroke condition (stroke - cerebral infarction).

Chronic cerebrovascular insufficiency (CCF)

This is a state of constant lack of blood in the brain, continuous oxygen starvation of brain tissue, forcing neurons to be in constant tension of all intracellular systems and intercellular connections, which leads to disruption of the normal functioning of both brain cells and the organ as a whole.

Symptoms of cerebrovascular insufficiency

In almost half of the cases, symptoms are not detected, and tortuosity is discovered accidentally during examination and duplex scanning of the carotid arteries. Most often, the first manifestations of CNM are in the form of headaches in the frontal and temporal regions, attacks of dizziness, tinnitus, and memory loss. More severe neurological disorders are somewhat less common - in the form of transient ischemic attacks (TIA), sudden loss of consciousness. The main precursors to the development of a major stroke are TIA, with possible transient paralysis of the arms and/or legs (from several minutes to several hours), speech impairment, transient or sudden blindness in one eye, memory loss, dizziness, and fainting. Having a TIA is an alarming warning sign that your brain is in serious danger and you should get tested and treated as soon as possible.

Causes of CCI (chronic cerebrovascular insufficiency)

The cause of pathological deformations of the BCA is genetic and is associated with improper construction of the artery framework, consisting of structural proteins - collagen and elastin. With age, tortuosity increases, which often becomes the cause of complaints in old age, despite the congenital nature of the disease. Pathological tortuosities are inherited!

The main classification of CNMK used in Russia (according to A.V. Pokrovsky) contains 4 degrees:

I degree - asymptomatic course or absence of signs of cerebral ischemia against the background of proven, clinically significant cerebral vascular damage;

II degree - transient ischemic attack (TIA) - the occurrence of focal neurological deficit with complete regression of neurological symptoms within up to 1 hour, transient cerebrovascular accident (TCVA) - the occurrence of focal neurological deficit with complete regression of neurological symptoms within up to 24 hours;

III degree - the so-called chronic course of SMN, i.e. the presence of cerebral neurological symptoms or chronic vertebrobasilar insufficiency without a history of focal deficiency or its consequences. In neurological systematizations, this degree corresponds to the term “dyscirculatory encephalopathy”;

IV degree - previous, completed or complete stroke, i.e. the existence of focal neurological symptoms for more than 24 hours, regardless of the degree of regression of the neurological deficit (from complete to no regression).

Basic methods for diagnosing CNM:

• ultrasound duplex scanning of the brachiocephalic arteries,
• multislice computed tomography – angiography of the brachiocephalic arteries,
• angiography of the brachiocephalic arteries.

Chronic cerebrovascular insufficiency (CCF) treatment.

If there is a risk of developing a stroke in the area of ​​​​the blood supply to the artery, surgical treatment is recommended - elimination of tortuosity. The operation is a standard intervention with a proven technique. The elimination method is finally selected during surgery. The method according to Paulukas is reimplantation of the mouth of the internal carotid artery into the common carotid artery, the method according to E. Hurwitt is removal of the tortuous section with subsequent restoration of blood flow through the artery. In case of pathological tortuosity of the vertebral artery, reimplantation of the ostium of the vertebral artery is performed.

Important!

• Pathological tortuosity cannot be straightened with medicine!
• If you or your parents have tortuosity of the carotid arteries, get examined yourself and get your relatives examined.

In the cardiac surgery department of the Federal State Budgetary Institution "SPMC" of the Ministry of Health of Russia, surgical treatment of pathological deformation of the brachiocephalic (vertebral, carotid) arteries is carried out.

Our surgeons have developed and used a method for reconstructing arteries in case of pathological tortuosity of the ICA (internal carotid artery) while preserving the important anatomical glomerulus, which leads to a significant reduction in the incidence of postoperative instability of blood pressure.

Make an appointment with a cardiovascular surgeon: or on the website.

Cardiology online

Hello! I am concerned about the deterioration of memory, performance,

headaches, sometimes numbness of the limbs.

I contacted a vascular surgeon.

I present to you the results of duplex scanning of the brachiocephalic arteries,

internal carotid artery, 25 mm from the mouth. Along the course of the vessel

there is an increase in LSV from 0.5 m/s to 1.25 m/s and 0.5 m/s distally

Please note that in the patient’s position on the right side, tortuosity

becomes somewhat more pronounced both in form and in changes in the SDSC:

an increase in LSC to 160 cm/sec is recorded.

bending, and in terms of the nature of changes in the SDSCh, it is less pronounced than on the left:

on the back, the blood flow speed ranges from 0.5 m/s to 0.9 m/s, while

as in the position on the left side - 0.5 m/s - 1.1 m/s. Stenosis of the right ICA 30%.

There is a recording of MR agnography of the vessels of the head and neck on a disk (with description).

Diagnosed with grade 3 SMN, ischemia.

Is any further research needed?

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• Ilya: Is it possible to engage in professional biathlon with ischemia?
• ayqun: Hello. My dad had an incident a few days ago.
• Elena: My husband is 49 years old, no heart attack, but the test was positive, they did a co.

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Comparative analysis of long-term results of carotid endarterectomy depending on the surgical technique

A.V. Pokrovsky, G.I. Kuntsevich, D.F. Beloyartsev, I.E. Timina, R.V. Kolosov

Department of Vascular Surgery and Department of Ultrasound Diagnostics of the Institute of Surgery named after. A.V. Vishnevsky RAMS, Moscow, Russia

A comparative analysis of the long-term results of 105 carotid endarterectomies (EAE) was carried out in 89 patients operated on from 1997 to 2003. 90.5% of patients (95) were operated on for atherosclerotic stenosis of the internal carotid artery (ICA), in 6.6% (7 ) there was a combination of ICA tortuosity and stenosis. The initial degree of cerebrovascular insufficiency (CVI) was different: CVI degree 1 - in 22.8%, CCI degree 2 - in 12.4%, CCI degree 3 - in 25.7%, CCI degree 4 - in 38.1 % of patients. Depending on the method of carotid EAE, the distribution of patients was as follows: 50.4% - after eversion carotid EAE, after open (classical) EAE with plastic surgery with a PTFE patch - 49.6%. The average follow-up period after eversion EAE was 31.8 months, after open EAE with patch repair – 37 months, with a follow-up period from 3 to 72 months. 76.4% of patients were examined more than 1 year after surgery.

In the long term, all patients were examined clinically with color duplex scanning of the carotid arteries. The condition of the reconstruction zone of the carotid arteries, the diameter, thickness of the walls of the arteries, and the state of blood flow were assessed. TIA was observed in 1 patient in the eversion group and in 1 patient in the open EAE group. In fact, in the long-term period, 98% of the operated patients had no neurological complications.

The development of hemodynamically significant restenosis was noted in 8 cases (7.6%). Moreover, after eversion EAE in 4 patients, after open EAE - also in 4. Myointimal hyperplasia (more than 3 mm) with the development of hemodynamic changes was detected in 1 patient after eversion EAE and in 2 patients - after open EAE. In other cases, the development of restenosis in the reconstruction zone was associated with the presence of an atherosclerotic plaque.

Carotid EAE in the long-term period, regardless of the method of carotid artery repair, is an effective method for preventing cerebrovascular accidents.

In the long term after surgery, the frequency of restenosis after eversion and open EAE does not differ significantly. The use of both eversion and open EAE techniques with PTFE patch repair is a promising method of surgical treatment of carotid artery stenosis.

KEY WORDS: eversion, open carotid endarterectomy, long-term results, restenosis.

How long can you live with grade 3 dyscirculatory encephalopathy?

Discirculatory encephalopathy is characterized by the following symptoms:

• At stage 1 – headaches, dizziness, a feeling of “noise in the head”, memory and attention disorders, sleep disorders.
• At stage 2 – the symptoms indicated in the previous paragraph and various mental disorders (depressive and anxiety states), as well as decreased control over one’s own actions.
• At stage 3 – severe dementia, walking impairment, urinary incontinence, speech disorders, etc.

The progressive deterioration of the condition of a patient with dyscirculatory encephalopathy quite naturally provokes the emergence of both himself and his loved ones the question of how long can one live with this disease? There is only one answer to this question: the more advanced the disease, the worse the prognosis. That is, with the 3rd (last) degree of encephalopathy, there is practically no hope for improving the patient’s well-being and at least some positive dynamics, since changes in the brain matter are already irreversible. With the 1st degree of the disease, on the contrary, with the help of qualified treatment it is possible to restore a person’s health and stop the progression of pathological processes in the brain.

In general, the life expectancy of patients with DEP is influenced by various factors: the initial causes of the development of the disease, the depth of pathological changes, the treatment provided, the conditions in which the person lives, the presence of concomitant diseases, etc. It is impossible to single out any general time frame for all patients - everything very individual: some live for years with a diagnosis of stage 3 DEP, while others die suddenly from complications. Therefore, you should not despair and refuse medical help.

Causes of dyscirculatory encephalopathy

The occurrence of progressive cerebrovascular accidents is most often associated with the following reasons:

• Atherosclerosis.
• Hypertension.
• Pathological changes in veins.
• Vasculitis.
• Blood diseases.
• Neurocirculatory dystonia.

Doctors often fail to identify one cause, and then they talk about dyscirculatory encephalopathy of mixed origin. Doctors can influence some of these etiological factors with the help of medications, for example, to stabilize blood pressure, reduce inflammatory changes in blood vessels, normalize blood clotting, etc. If the patient has severe atherosclerosis of large and small vessels of the brain, it is much more difficult to restore cerebral circulation.

What is the treatment for stage 3 DEP?

In advanced forms of the disease, treatment is symptomatic and is aimed at alleviating the patient’s condition and prolonging his life as much as possible. The following groups of drugs are used as drug therapy for grade 3 DEP:

• Antihypertensive drugs. It is very important to keep blood pressure within normal limits, as this helps stop the progression of the disease and prevent the occurrence of complications (for example, ischemic and hemorrhagic strokes).
• Diuretics (to normalize blood pressure and eliminate swelling of the brain).
• Vasodilators (especially drugs that dilate intracerebral arteries) and anticoagulants.
• Neuroprotectors are drugs that protect the brain from damaging influences.
• Psychotropic drugs (prescribed depending on the patient’s symptoms).
• Anticonvulsants, etc.

In addition to drug therapy, patients with stage 3 DEP need proper care. Since people with this diagnosis often cannot take care of themselves, cannot control their actions, they cannot be left alone. If the patient is forced to lie down (due to severe movement disorders), it is necessary to take all measures to prevent the development of bedsores, inflammatory processes in the respiratory tract, and dysfunction of the digestive organs. All this greatly affects both the duration and quality of life of a person with dyscirculatory encephalopathy.

Classification of cerebrovascular insufficiency

We use the classification of SMN according to the severity of ischemic brain damage, proposed by A.V. Pokrovsky in 1978:

I degree - asymptomatic course or absence of signs of cerebral ischemia against the background of proven clinically significant damage to cerebral vessels;

II degree - transient cerebrovascular accident (TCI) or TIA, i.e. the occurrence of focal neurological deficit with complete regression of neurological symptoms within up to 24 hours;

III degree - the so-called chronic course of SMN, i.e. the presence of cerebral neurological symptoms or chronic vertebrobasilar insufficiency without a history of focal deficiency or its consequences. In neurological systematizations, this degree also corresponds to the term “dyscirculatory encephalopathy”;

IV - suffered a completed or complete stroke, i.e. the existence of focal neurological symptoms for more than 24 hours, regardless of the degree of regression of the neurological deficit (from complete to no regression). Among strokes, neurologists distinguish a minor stroke or a completely reversible neurological deficit within a period of 24 hours to 3 weeks, and completed strokes are divided according to the nature of the remaining moderate or severe neurological deficit.

In principle, such classifications are used everywhere, only often when describing lesions of the carotid areas, authors combine grades I and III of insufficiency, considering such patients as asymptomatic. From a modern point of view, there are two significant justifications for this point of view: firstly, the tactical approaches to the treatment of these groups of patients are identical, as are the treatment results, and, secondly, to differentiate the chronic course of SMN from cerebral symptoms in dyscirculatory or post-traumatic encephalopathy, degenerative diseases of the central nervous system, severe

arterial hypertension, migraine in some cases is difficult.

The clinical picture of SMN consists of three groups of symptoms: cerebral, ocular and/or hemispheric for lesions of the carotid area and symptoms of impaired blood supply to the VSB.

TO cerebral Symptoms include headache, decreased memory and intellectual abilities.

Ocular A manifestation of carotid lesions is homolateral permanent or transient blindness caused by embolism in the central retinal artery and known in the literature as amaurosis fugax, the onset of which is described by the patient as a flash in the eye.

Hemispheric manifestations of SMN are very diverse in manifestation and are determined by the localization of ischemic brain damage. The most common hemispheric focal symptoms are motor (hemiparesis) and sensory (hemianesthesia) disturbances in symmetrical limbs and, less commonly, the face on the side opposite to the localization of the ischemic focus, as well as speech disorders with damage to the left hemisphere. The duration of the presence of a neurological deficit determines the clinical form of SCI: for TIA - up to 24 hours, for small strokes - from 24 hours to 3 weeks, and if complete regression of focal symptoms does not occur, then we should talk about a completed stroke. Depending on the location of the area of ​​impaired blood flow in the brain, the clinical picture of SCI can vary significantly. When obstruction of the ICA occurs with the lack of sufficient compensation for blood circulation in the hemisphere of the same name, an extensive cerebral infarction develops through the circle of Wills system, often involving the entire hemisphere.

Clinically, this is manifested by the development of contralateral hemiplegia and pronounced depression of consciousness. If it is possible to assess sensory function, then contralateral hemianaesthesia and homonymous hemianopia (defect of the right or left halves of the visual fields) are identified. If adequate collateral inflow through the ACA and PCA on the affected side is maintained in the above situation, motor and sensory disturbances of the face, arms and legs are less severe (paresis). When the dominant hemisphere is involved, global aphasia develops; when the non-dominant right hemisphere is damaged, anosognosia develops (lack of a critical assessment of one’s defect: paralysis, decreased vision, hearing, etc.).

Acute occlusion of the main trunk of the MCA is accompanied by similar focal symptoms described above, as well as depression of consciousness in approximately 1/4 of the patients. When a more distal portion of the SMA is involved, damage occurs only to the cortical layers of the frontal and anterior parts of the parietal regions, which is manifested primarily by disturbances in the lower 2/3 of the face and arm and less pronounced in the leg. Damage to the dominant hemisphere is manifested by aphasia, which is predominantly motor in nature (Broca's aphasia: impairment of active speech while maintaining understanding of oral and written speech); Anosognosia with NMC in the non-dominant right hemisphere is characterized by less severity than with more proximal involvement of the SMA. More distal lesions of the SMA are accompanied by even less pronounced motor and sensory impairments, and visual deficits persist. When the dominant hemisphere is involved, it occurs

sensory transcortical Wernicke's aphasia (impaired understanding of oral speech with the ability to repeat what was said to others, copying and writing from dictation). Isolated damage to the non-dominant parietal lobe causes impairments in stereognosis (tactile recognition of objects) and graphesthesia (recognition of objects drawn on the skin). Damage to the parieto-occipital region of the dominant hemisphere leads to Gerst-Mann syndrome, which includes finger agnosia (inability to distinguish between one’s own fingers), acalculia (inability to count), agraphia (inability to write) and right-left disorientation (inability to distinguish between the right and left halves of the body) .

Acute occlusion of the ACA is accompanied by contralateral hemiparesis and hemianesthesia with a more frequent presence of motor disorders. Less extensive infarctions may be accompanied by motor-sensory disorders only in the contralateral lower limb with increasing muscle weakness in the distal direction. Bilateral strokes in the ACA basins can cause lower paraparesis, dysfunction of the pelvic organs, more often the bladder, less often akinetic mutism, i.e. absence of verbal communication of the patient with others while the speech apparatus is preserved against the background of inhibition of all motor functions, except for the fixing movements of the eyeballs, while consciousness is preserved.

Symptoms of circulatory disorders in the VBB. An infarction in the posterior hemispheric regions of the brain in the PCA territory leads to contralateral hemianopsia with preservation of the macula due to the mixed blood supply to the region of the latter of the MCA and PCA regions. At

In occipital hemianopsia, patients experience a visual field deficit, unlike midcerebral hemianopia, where the patient may not be aware of the visual defect until tests are performed. In addition, with occipital hemianopia, the upper and lower quadrants may be involved to varying degrees and optokinetic nystagmus persists, i.e. occurs when the gaze fixes on rapidly changing objects moving in one direction. With bilateral NMC in the PCA basins, bilateral homonymous hemi-anopsia may occur with or without preservation of the macula (cortical blindness). In addition, lesions of the occipital lobes of the cerebral hemispheres are characterized by metamorphopsia (distortion of the shape and size of visible objects), palinopsia (preservation or reappearance of an object after it disappears from the field of view), photopsia (appearance of a veil and grid before the eyes), ciliated scotomas (hemianoptic visual field defects, accompanied by a flickering sensation and migraine-like pain), amnesia and contralateral hemianesthesia.

Focal disturbances of the blood supply to the cerebellum and brainstem are accompanied by a combination of dysfunction of homolateral cranial nerves and cerebellar disorders with contralateral motor and sensory disorders of the limbs and trunk. For the specified localization of lesions, many syndromes associated with impaired patency of a particular branch of OA have been described. One of the most common symptom complexes is the lateral medulla oblongata syndrome, which develops, as a rule, with occlusion of the intraranial segment of the vertebral artery, less often when obstruction of the posterior inferior artery occurs.

teria cerebellum. Characteristic manifestations of the latter syndrome are homolateral plegia of the facial muscles, vocal cord paralysis, ataxia, Horner's syndrome and contralateral loss of pain and temperature sensation of half the body, often accompanied by nausea, vomiting, dizziness and facial pain. With cerebellar infarctions, both isolated ataxia and often in combination with dizziness, vomiting, nystagmus, diplopia, headache and depression of consciousness are possible. Occlusion of the OA causes coma, tetraparesis and ophthalmoplegia.

It should be remembered that fainting or loss of consciousness (drop attacks), systemic and non-systemic dizziness cannot be considered as focal manifestations of VBI in the absence of other focal manifestations of circulatory disorders in the VBI.

With damage to the BCS and proximal involvement of the RCA, in addition to the media clinic, brachial ischemia can be observed, which more often occurs during exercise. Critical ischemia of the upper extremities is rare and is usually associated with embolism into the distal arm from proximal arterial segments.

Lacunar strokes are characterized by isolated hemiparesis without sensory impairment with visual field defects or dysphasia when the internal capsule or base of the pons is affected, and isolated sensory impairment of the face, arms and legs without other focal lesions when the thalamus is affected. Other syndromes include ataxic hemiparesis (femoral paresis with homolateral ataxia) and dysarthria/clumsy hand syndrome. Sensorimotor impairments and other focal deficits are less commonly identified, depending on the location of the NMC.

Considering the variety of clinical manifestations of media, patients with BCA diseases must be examined by neurologists and ophthalmologists.

Physical assessment of the anthological status of patients with media consists of palpation and auscultation. The common carotid, temporal, axillary, brachial, radial and ulnar vessels are accessible to palpation. Standard points for auscultation are the right sternoclavicular joint (BCS projection), the angles of the lower jaw (bifurcations of the carotid arteries), and the supraclavicular fossa (ostia of the vertebral and subclavian arteries). If necessary, palpation and auscultation are carried out in the projection of the accessible BCA along its length. It is mandatory to measure blood pressure in your arms. The difference is more than 20 mm Hg. between the brachial arteries indicates hemodynamically significant damage to the brachiocephalic trunk or subclavian arteries, unless there is symmetrical damage on both sides. In the latter case, measuring blood pressure in your legs can help. If the thoracoabdominal aorta is not narrowed and there is no damage to the arteries of the lower extremities, blood pressure in the popliteal arteries is normal at 10-20 mm Hg. should exceed the blood pressure in the arms, and the blood pressure at the ankle should correspond to the blood pressure in the upper extremities.

Considering the high prevalence of patients with SMN and the enormous social and medical significance of this problem, we can distinguish groups of patients who must undergo a comprehensive instrumental examination to identify lesions of the BCA:

All patients who have had a stroke, TIA or VBI;

Patients who have a systolic murmur on the BCA, especially above the bifurcations of the carotid arteries, have asymmetry of the BCA pulsation, a blood pressure gradient between the arms of more than 20 mm Hg;

All patients over 50 years of age with other vascular lesions (ischemic heart disease, aortic aneurysm, vasorenal hypertension, chronic arterial insufficiency).

When the diagnosis of SMN is confirmed, such patients must be examined by a vascular surgeon to decide on treatment tactics.

The principal objectives of instrumental diagnostics in patients with chronic SMN are: assessment of the degree and nature of blood flow disturbances in the extra- and intracranial parts of the cerebral vessels, morphological study of the nature of changes in the vascular wall (localization, extent, structure and condition of the internal surface), identification of ischemic damage to the brain brain and a description of its location and volume. Today, among the various diagnostic techniques, the following are of greatest clinical importance and are used on a daily basis:

▲ Ultrasound research methods: continuous wave Doppler ultrasound, color duplex scanning with color and power Doppler mapping, transcranial Doppler ultrasound and duplex scanning;

▲ magnetic resonance imaging and angiography;

All of these methods, with the exception of the last one, are non-invasive (in some situations, contrast enhancement is required with CT).

Doppler ultrasound(USDG), which until the early 90s was the only ultrasound method for studying blood flow, is used today in a rather limited manner - only to assess the functional state of the circle of Willis using compression tests and to determine the direction of blood flow in the superficial arteries of the orbit in order to detect brain theft through ECA system during occlusion of the homolateral ICA.

Currently, the main ultrasound method for studying BCA is color duplex scanning(CDS). Its fundamental advantage in comparison with previously used ultrasound techniques (ultrasound, gray scale duplex scanning) was the ability to study the structure and surface of the atherosclerotic plaque, which made it possible to significantly expand knowledge about the pathogenesis of SMN (this statement mainly applies to lesions of the carotid bifurcation) and clarify the indications to surgical treatment for ICA stenosis.

CDS of the BCA (carotid, subclavian, vertebral arteries) before and after surgical reconstructions is carried out with a linear sensor with a scanning frequency of 5-10 MHz. To visualize the aortic arch and the proximal parts of its branches, a 3.5-5 MHz sector sensor is used.

Ultrasound examination is carried out in the following modes: two-dimensional scanning, color Doppler mapping (CDC), power Doppler mapping (EDC), pulse-wave Dopplerography.

All studies are performed with the patient lying on his back. When scanning the carotid and subclavian arteries, the patient's head is tilted back and turned

in the direction opposite to the one being studied. When examining the vertebral arteries, his head is positioned straight and moderately tilted back. For optimal visualization of the aortic arch and proximal portions of the BCA, the patient's neck should be in maximum extension as possible.

The aortic arch with the proximal parts of its branches is examined from the suprasternal position (with a sector sensor), the sensor is carefully inserted behind the sternum, the scanning plane is directed downward.

The BCS with the orifices of the right CCA and RCA is examined from the right medial supraclavicular approach (sensor behind the sternoclavicular joint); the scanning plane is directed down and to the right (Fig. 5.81). The intrathoracic sections of the left CCA and RCA are examined from the left medial supraclavicular approach, the sensor is placed parallel to the clavicle, the scanning surface is directed downward.

For reliable visualization of all the walls of the carotid arteries, it is necessary to scan in two planes - longitudinal and transverse (relative to the course of the vessel) from various approaches.

For longitudinal scanning of the carotid arteries, the following ultrasound approaches are used:

Anterior (anteromedial) - the sensor is located parallel to the SA projection along the anterior edge of the sternocleidomastoid muscle (between the muscle and the trachea) at an angle of 30-60° to the surface of the neck, the ultrasound beam is directed laterally and posteriorly;

Middle (lateral) - the sensor is located parallel to the SA projection on the sternocleidomastoid muscle (scanning is carried out through the muscle) at an angle of 60-90° to the surface of the neck, the ultrasound beam is directed medially;

Posterior (posterolateral) - sensor located parallel

8 years after balloon dilatation

1 - OSA; 2 - PKA; 3 - BCS.

projections of the SA posterior to the sternocleidomastoid muscle at an angle of 30-60° to the surface of the neck, the ultrasound beam is directed medially and anteriorly.

When scanning in the transverse plane, the same approaches are used, but the sensor is located perpendicular to the course of the SA and at an angle close to 90° to the surface of the neck. Initially, it is advisable to place the sensor on the sternocleidomastoid muscle, and then smoothly move it anterior and posterior to the specified muscle to achieve optimal visualization of the studied SA.

The study begins with the proximal part of the CCA, which is traced distally to the bifurcation. The ostium of the ICA and ECA is then identified and each of these arteries is examined (Fig. 5.82).

To visualize the ICA, the upper edge of the sensor must be moved laterally, to study the ECA - more medially. Longitudinal scanning of the CCA, ICA and ECA is carried out from the three indicated approaches.

Rice. 5.82.CDS of the bifurcation of the carotid artery in a longitudinal section.

Then the carotid arteries are examined in the transverse plane, moving the sensor from the proximal part of the CCA to its bifurcation and

visualization of the sections of the ICA and ECA (Fig. 5.83). After this, they return to longitudinal scanning and carry out color Doppler mapping and analysis of the Doppler frequency shift spectrum.

To study the subclavian artery, the sensor is placed parallel to the clavicle in the supraclavicular region, the scanning plane is directed downward. Less commonly, the subclavian artery can be optimally located by placing the sensor along the projection of the vessel under the collarbone, with the scanning plane directed upward. When examining the brachial, ulnar and radial arteries, the sensor is placed along the anatomical course of the artery at an angle close to 90° to the

Rice. 5.83.CDS of the bifurcation of the carotid artery in cross section. 750

surface of the skin. The main arteries of the upper extremities are accessible for ultrasound examination along almost their entire length, starting from the lower third of the shoulder. Ultrasound examination is supplemented by measuring systolic blood pressure in the main arteries of both upper extremities.

When examining the vertebral arteries, the patient lies on his back, his head is positioned straight and moderately tilted back. The sensor is placed parallel to the projection of the VA in front of the sternocleidomastoid muscle at an angle close to 90° to the surface of the neck, the ultrasound beam is directed posteriorly. This placement of the sensor directly above the clavicle (perpendicular to the clavicle) allows one to obtain an image of the subclavian artery in the transverse plane, a longitudinal image of the vertebral artery at the mouth and throughout the first segment. Gradually moving the sensor upward (without losing the image of the VA on the screen) allows you to visualize the VA in the interosseous spaces throughout segment II.

The study of the subclavian-carotid anastomosis is carried out from the medial supraclavicular approach. To search for the specified anastomosis, two methods are used:

First, a transverse section of the CCA is obtained proximal to its bifurcation, then, without losing the image of the CCA on the screen, the sensor is moved down towards the clavicle until the anastomosis is visualized;

From the supraclavicular approach, a longitudinal image of the RCA is obtained, then the sensor is moved medially along the RCA until the anastomosis is visualized (Fig. 5.84). Optimal visualization of the anastomosis, RCA, and CCA is achieved by minor image-guided changes in probe position.

Rice. 5.84.CDS of subclavian-carotid anastomosis in EDC mode. Patient S. 12 years after the operation of replantation of the RCA into the CCA on the left.

1 - OSA; 2 - RCA, arrows indicate the area of ​​anastomosis.

Search and examination of anastomoses (proximal and distal) of the subclavian-subclavian shunt are carried out from the supraclavicular, axillary-axillary shunt - from the subclavian access. The axillary-axillary shunt, located antesternally, is visualized along its entire length when the sensor moves from the anastomosis along the shunt under the control of the image of the shunt on the monitor screen.

The proximal anastomosis of the subclavian-extracarotid shunt is located from the supraclavicular approach by moving the sensor along the RCA. After examining the area of ​​the proximal anastomosis, it is necessary to move the probe along the shunt under image guidance to the distal anastomosis.

When describing plaques using CDS, three groups of morphological characteristics are classified:

▲ depending on the structure, plaques are divided into three types according to

transparency for ultrasound radiation: echo-negative (echo-transparent, hypoechoic), echo-positive (echo-dense, isoechoic) and hyperechoic (calcified);

▲based on the ratio of the above components in the plaque, the latter are divided into homogeneous (homogeneous echostructure) and heterogeneous (heterogeneous echostructure);

▲By the nature of the surface of the plaque, smooth, uneven and ulcerated surfaces are distinguished.

All plaques according to the first two criteria were divided into 4 types (Gray-Weale classification):

1) hypoechoic homogeneous, so-called soft plaques (morphologically represented by lipoidosis with areas of hemorrhage);

2) heterogeneous plaques, including hypo- and isoechoic areas with a predominance of the former (lipoids with areas of hemorrhage predominate over fibrous areas);

3) heterogeneous plaques, including hypo- and isoechoic areas with a predominance of the latter (areas of fibrosis predominate over areas of lipoidosis and hemorrhage);

4) homogeneous isoechoic plaques (entirely fibrous) with or without Ca inclusions (hyperechoic areas), in everyday practice they are simply called homogeneous, although it is terminologically correct to include soft plaques as the latter.

Plaques of types 1 and 2 were classified as unstable, i.e. prone to rapid growth, including due to massive hemorrhage into the plaque (especially soft ones); plaques of the 3rd and 4th types - stable, with a tendency to slower growth. Clinically, ulcerated plaques can also be classified as unstable plaques due to the high risk of brain embolization. We adhere to the following CDS protocol for BCA lesions.

Protocol for CDDS of BCA patients before and after reconstruction of the branches of the aortic arch.

1. Suprasternal access(sector

Longitudinal image of the aortic arch and the proximal parts of its branches;

Longitudinal image of the BCS and its bifurcation, the proximal parts of the right CCA and RCA.

2. Study of the carotid arteries in the longitudinal and transverse plane from the anterior, middle and posterior approaches (in relation to the sternocleidomastoid muscle).

3. Study of the vertebral arteries from anterior approach.

4. Supraclavicular approach along the long axis of the RCA:

Bifurcation of the BCS (right), proximal parts of the CCA and RCA;

b) median and lateral:

Proximal anastomosis of the subclavian-extracarotid shunt.

5. Short supraclavicular approach

Transverse section of the RCA, the mouth and segment I of the vertebral artery;

Anastomoses of subclavian-external carotid and subclavian-subclavian shunts.

6. Subclavian access by length

no and short axis of the PKA":

Longitudinal and transverse images of the RCA in segments I, II, III;

Anastomoses of the subclavian-subclavicular shunt.

7. Study of blood flow through the brachial, ulnar and radial arteries(in the projection of the anatomical course of the vessels), measuring blood pressure on both sides.

8. Studies of shunts throughout.

1. 2D scanning:

Anatomical course of the studied vessels;

The structure and thickness of the artery wall;

The presence, nature and extent of atherosclerotic plaques;

Degree (percentage) of lumen stenosis;

Homogeneity of the lumen, presence of blood clots.

2. Color Doppler modes.

Search for vessels, anastomoses and shunts and obtain the most informative sections;

Reliable determination of the presence or absence of blood flow;

Visualization of hypo- and isoechoic plaques, determination of the state of plaques and blood clots in the lumen;

Determination of the degree of stenosis;

Precise direction of the scanning beam and angle correction when recording the Doppler frequency shift spectrum.

Reliable determination of the direction of blood flow;

Assessing the nature of blood flow and identifying areas of turbulence.

Adequate staining of the lumen of hard-to-reach vessels (proximal branches of the aortic arch, vertebral artery);

Visualization of blood flow at an unfavorable scanning angle (BCS, BCS bifurcation, RCA, branching and tortuosity of vessels, all anastomoses);

Identification of low-speed flows.

3. Pulsed wave Doppler

Qualitative and quantitative

Doppler spectrum analysis

frequency shift for condition assessment

nia (clarification of the degree of stenosis)

proximal and distal (according to

in relation to the place of registration

spectrum) of the vascular bed.

Transcranial Dopplerography(TCD) allows, depending on the access, to locate the MCA, ACA, PCA and PCA (temporal window), the orbital artery and the siphon of the ICA (orbital window), OA and intracranial segments of the VA (suboccipital window), i.e. most of the intracranial arteries. The main parameters identifying

The main features of TCD are the determination of vessel patency and the presence of asymmetry of blood flow between the same paired intracranial arteries. TCD makes it possible to suspect damage to the intraranial segments of the BCA at the stage of non-invasive examination, which is impossible with CD. The disadvantages of the method include pronounced operator dependence and poor repeatability. Often, when the windows are completely or partially impenetrable to ultrasound beams due to the individual structural features of the skull bones, TCD is not informative, and due to difficulties in location due to the variant location of the vessel, a false conclusion can be made about the obstruction of the artery being studied. TCD is of greatest importance for monitoring cerebral blood flow during surgical interventions on the BCA (see below).

Transcranial duplex scanning(TDS), especially in EDC mode, has greater sensitivity than TCD and allows visualization of intracranial arteries over some extent. Due to the fragmentation of the located segments, it is difficult to create a holistic picture of the blood flow and the state of the lumen of intracranial vessels during TDS.

CT scan(CT) is one of the main methods for assessing the location and extent of ischemic brain damage. Based on CT data, the reliability of anamnestic information about the manifestations of SMN is assessed; in case of multiple lesions of the BCA, the tactics of surgical treatment are clarified by determining the clinically most significant blood supply to the brain; information about the size of the ischemic focus (cyst) influences the decision on the possibility of surgical intervention

Rice. 5.85. CT scan of the brain. On the left in the area of ​​the temporal lobe there is an ischemic cyst measuring 4.03; 55.0 cm, communicating with the anterior horn of the left lateral ventricle.

(Fig. 5.85). The advantages of CT are the accessibility and speed of the study, which can be repeated over time if necessary, including in patients in critical condition who require constant infusion and ventilation support. However, the method has some limitations. Thus, in the acute period of stroke, with the exception of hemorrhages and extensive ischemic damage, a small lesion is not visualized in the first hours and days. The use of contrast enhancement in such a situation is effective only a few days after an acute episode, when the lesion is saturated with a contrast agent due to extravasation of blood or plasmorrhagia. In addition, CT may miss small chronic infarcts at the base of the brain and in the posterior fossa. Benefits magnetic resonance imaging(MRI) in comparison with CT are the possibility of earlier, within

24 hours, detection of acutely developed ischemic foci, higher sensitivity in determining both fresh and chronic areas of ischemic damage, the ability to obtain brain sections in three projections, which facilitates the interpretation of data and makes them more visual. MRI, unlike CT, takes more time to conduct the study, which is also impossible in patients with incorporated metal objects (pacemaker) and in patients whose condition is unstable.

A very important advantage of magnetic resonance research methods is the possibility of simultaneous carrying out on the same machine as for MRI, MP angiography(MRA), i.e. non-invasive visualization of vessels along their length due to the difference in magnetic characteristics (signal intensity) of a moving medium (bright signal from blood) and stationary formations (dark signal). The semiotics of the data obtained with MRA is similar to those with contrast angiography: vessel occlusion is visualized as a complete disappearance of the signal, its “break,” and stenosis is manifested by a weakening of the signal intensity, narrowing of the image of the artery, or even local disappearance of the signal. Just like digital subtraction angiography, MRA allows you to subtract surrounding tissue and venous blood flow from the image. Obtaining an image of the BCA with MRA, depending on the selected mode, is possible throughout the entire length from the aortic arch to the intracranial segments, which gives this method an advantage over ultrasound. Taking into account the fact that the overwhelming majority of patients with SMN are patients with lesions of the carotid bifurcation, the importance of MRA as the only

the method of non-invasive detection of distal stenoses and high tortuosity of the ICA (inaccessible with CDS, especially in patients with a short neck, high location of the bifurcation of the ICA) is increasing immeasurably (Fig. 5.86). The sensitivity and specificity of MRA in diagnosing ICA lesions is 90-100%, which is not inferior to the capabilities of CD, and according to some authors, even surpasses the latter.

When interpreting two-dimensional MRA images, the degree of stenosis may be overestimated due to the fact that turbulent blood flow distal to the area of ​​even moderate stenosis can lead to a significant drop in signal intensity. In this mode, arterial narrowing of the carotid arteries is also possible when passing through the bones of the base of the skull. It is partially possible to prevent these disadvantages in three-dimensional imaging mode.

Vascular anatomy in MRA may change during swallowing, coughing, breathing, and due to arterial pulsation. The TOF MRA technique does not allow complete subtraction, which is why signals from adjacent tissues can mask the image of blood vessels. The last difficulty is partially overcome with the help of the RS MPA technique, in which subtraction is carried out better.

With MRA, unlike CDS, it is impossible to obtain information about the structure and condition of the surface of atherosclerotic plaques. In general, at present, MRA can be assessed as the only non-invasive method for obtaining images of the entire length of the BCA and as an extremely important method for outpatient screening that does not require hospitalization of the patient.

In cases where the most accurate and detailed

Rice. 5.86. MRA BCA. Bilateral ICA loops.

understanding of the relationship between the BCA and/or surrounding tissues (especially bone structures), the morphology of the vascular lesion, then to this day the gold standard for such diagnostics remains X-ray contrast angiography in a digital subtraction version. This technique makes it possible to obtain information about the state of the BCA along the entire length from the aortic arch to the cortical intracerebral branches, to identify ways of stealing cerebral blood flow, and also to assess the consistency of the collateral connections of the BCA.

To obtain complete information, contrasting of blood vessels is carried out in two projections. For the aortic arch and the initial sections of its branches, the left oblique is the basic projection; the second can be used as a straight or lateral one. For better contrast

When performing BCA in the neck, selective vascular catheterization is used; When using the subtraction technique, the choice of projections is not important. Intracranial blood flow is assessed in direct and lateral projections separately for each hemisphere when the contrast agent enters through the ICA and then through the VA.

The main disadvantage of X-ray contrast angiography is its invasiveness, which is accompanied by the risk of complications associated with the puncture site (bleeding, thrombosis), the possibility of damage to the vascular wall or embolism when inserting catheters and conductors, and the likelihood of neurological deficits due to persistent spasm of cerebral vessels upon administration of contrast agent. substances, as well as systemic complications due to the circulation of the contrast agent (allergic reactions, the occurrence or progression of renal failure, etc.). In connection with the above, standard angiography is permissible only in those patients who are expected to undergo surgery.

Indications for X-ray contrast angiography are gradually narrowing, and the frequency of its use in the diagnosis of SCI is decreasing every year against the backdrop of improvements in existing and the emergence of new methods of non-invasive instrumental diagnostics. Nevertheless, the significance of this method in a number of diagnostic situations remains significant, and taking into account the development of endovascular surgery and the specific growth of intraluminal interventions in the treatment of lesions of the BCA, it is very large.

Differential diagnosis of SMN should be carried out with degenerative and oncological diseases of the brain, hy-

pertensive encephalopathy, hysteria, functional disorders at the microcirculatory level (vegetative disorders, migraine, etc.). The main differential criterion is the absence or presence of signs of clinically significant damage to the main arteries of the brain, and the diagnostic method of choice in solving this problem is ultrasound diagnostic methods and, first of all, color duplex scanning.

Indications for surgical treatment and results of studies comparing the effectiveness of carotid EAE and drug treatment for ICA stenoses. From the mid-60s to the mid-80s, a number of retrospective studies were conducted around the world to compare the results of surgical treatment and conservative therapy for carotid stenoses . It turned out that in patients with TIA within a year after the onset of the first symptoms without surgical treatment, the risk of developing a stroke is 10%, decreasing further to an annual level of 6% and falling even lower after 3 years. Carotid EAE reduced the risk of developing stroke in the affected hemisphere to less than 1% per year.

In patients after strokes, the annual incidence of recurrent stroke was 9% and further decreased to 2% per year after carotid EAE.

In the second half of the 80s and early 90s, similar studies were devoted to studying the fate of patients with asymptomatic lesions of the ICA. It turned out that with stenoses of more than 75%, the risk of developing a stroke ranges from 3 to 5% per year, and in the vast majority of cases, stroke occurs without previous symptoms. The incidence of stroke after carotid EAE dropped to 0.3% per year.

The results obtained made it possible to formulate requirements for the quality of surgical treatment for ICA stenosis, which would make it effective in any case in comparison with drug therapy. Thus, the combined mortality rate + complications from stroke during carotid endarterectomy should not exceed 3% in asymptomatic patients, 5% in TIA, 7% after a stroke, 10% in carotid artery restenosis, and the mortality rate for all groups should not be higher 2% each. However, despite the external convincingness of the above data in favor of surgical treatment for carotid stenosis, the results obtained were criticized primarily by neurologists on the following grounds:

Conclusions were drawn retrospectively from groups of patients operated on and observed in different clinics, with different surgical experience, diagnostic capabilities and tactical approaches;

Due to the lack of a unified protocol, unequal indicators were assessed according to different principles, therefore the results of the studies are statistically unreliable and incomparable;

Strict principles of randomization were absent or not followed (milder patients were operated on, more severe patients were treated conservatively, or vice versa).

In order to overcome the received disagreements, prospective corporate randomized studies were conducted to definitively compare the results of surgical and conservative treatment for ICA stenoses.

matic Carotid Endarterectomy Trial) and ECST (European Carotid Surgery Trial). The first study randomized 659 patients at 50 centers in the United States and Canada. 2 years after inclusion in the study, the frequency of ipsilateral strokes in operated patients was 9% (including perioperative), and in those receiving conservative treatment (disaggregants) - 26%. Among them, the frequency of fatal and disabling strokes was 2.5 and 13.1%, respectively, i.e. with drug therapy, the share of such strokes accounted for half. The study was terminated due to ethical reasons.

In the European study, 778 symptomatic patients were randomized, and 3 years after randomization, the incidence of ipsilateral stroke in operated and non-operated patients was 12.3% (including perioperative) and 21.9%. The data obtained finally resolved the issue of the need for surgical treatment for ICA stenosis of more than 70%.

The first study to compare conservative therapy and surgical interventions in patients with asymptomatic stenoses, ACAS (Asymptomatic Carotid Atherosclerotic Study), was completed in 1995. It showed that within 5 years the risk of developing a stroke in non-operated patients is 11%, and after surgery over the same period - 5.1%, i.e. In absolute terms, the benefit per year was not as great as in studies of symptomatic lesions. Critics of surgical interventions for asymptomatic lesions should respond that the indicated difference in the effectiveness of the two treatment methods is not entirely reliable. Asymptomatic patients with ICA stenoses appear in

In the vast majority of cases, not on their own, but come to the doctor’s attention regarding diseases of other vascular systems: coronary, renal, arteries of the lower extremities, aortic aneurysms, etc., and the disease is at a stage that, as a rule, already requires surgical treatment itself. An assessment of the perioperative risk of stroke against the background of asymptomatic clinically significant lesions of the branches of the aortic arch in patients during revascularization of other arterial systems has never been carried out and has not been considered by supporters of conservative measures at all. Surgical teams are well aware of the clinical significance of this problem, and therefore it is necessary to take into account the fact that a huge number of such asymptomatic patients are operated on for BCA lesions preventively, as the first stage before reconstruction of other great vessels.

In order to explain and more accurately evaluate the results of ACAS, new studies have now begun and are ongoing in an attempt to identify risk groups among patients with asymptomatic lesions, including based on the structural features of atherosclerotic plaques in the carotid bifurcation, which was not previously taken into account.

Taking into account the above, indications for carotid endarterectomy today are based on 4 criteria, listed below in descending order of importance: clinical manifestations of SMN, the degree of ICA stenosis, the structural characteristics of the atherosclerotic plaque and the condition of its surface.

We define readings to carotid endarterectomy for ICA stenosis as follows:

▲ for symptomatic lesions (patients with TIA or after a stroke

t) surgery is indicated for all types of plaques (hypoechoic, heterogeneous and homogeneous), narrowing the lumen of the vessel by 60% or more, as well as for ulcerated plaques of 50% or more;

In patients with asymptomatic lesions or a chronic course of SMN, surgery is indicated for homogeneous plaques that narrow the lumen of the vessel by 70% or more, for heterogeneous and hypoechoic, as well as ulcerated plaques - from 60% or more.

Carotid EAE is contraindicated in patients up to 6 weeks after a stroke, in patients with persistent severe neurological deficit after a history of stroke with a brain cyst size of 3-4 cm or more. In the first case, there is a high risk of transformation of an ischemic stroke into a hemorrhagic one, and in the second, restoration of normal patency of the ICA does not lead to any regression of focal symptoms and is accompanied by a high probability of hemorrhage into the cyst. General contraindications for surgery are typical: 2-3 months after myocardial infarction, liver and kidney failure.

Principles of performing carotid endarterectomy. This surgical intervention is the second most common among operations on the cardiovascular system after coronary artery bypass grafting. Thus, in the USA in 1971, carotid endarterectomies were performed, in 1979, in 1984, their number was, and by the beginning of the 90s, the millionth carotid EAE was performed in the USA. Today, pericarotid endarterectomies are performed annually in this country.

The fundamental task that requires resolution during carotid endarterectomy is

protection of the brain from ischemic damage at the time of ICA clamping. Among patients with carotid stenosis, the majority tolerate clamping of the ICA well within a safe period (on average up to 60 minutes), but 10-15% of patients, due to functional or anatomical failure of the circle of Willis and/or against the background of impaired blood flow in several main arteries of the brain, are not able to compensate for the cessation of blood flow through the compressed ICA. In the latter case, 2-5 minutes after clamping the ICA, ischemic damage to the corresponding hemisphere begins to develop. Prevention of such a complication of carotid EAE requires determining the patient’s brain tolerance to ICA clamping and protecting the brain from ischemia during ICA clamping in intolerant patients.

Methods for determining the brain’s tolerance to ICA clamping are divided into preoperative (test with clamping of the carotid artery under TCD control) and intraoperative (operation under local anesthesia with the patient retained consciousness, measurement of the retrograde pressure index and TCD monitoring). In the first case, the patient undergoes the Matas test (3-minute compression of the common carotid artery to the transverse processes of the vertebrae in the middle third of the neck) with monitoring of blood flow along the homolateral MCA during TCD. A drop in mean blood flow velocity below 20 cm/s is critical, after which perfusion of the affected hemisphere becomes inadequate and the patient is considered intolerant. It should be noted that 20-30 s after the velocity drops below 20 cm/s, a slow increase in blood flow velocity to stable normal values ​​may begin.

ny. If confusion and focal neurological symptoms appear during the test, the study is immediately stopped and the patient is also considered intolerant. It must be taken into account that percutaneous compression of the carotid artery may be accompanied by compression of the glomus, manifested by nausea, blurred vision, dizziness, which can be regarded as the occurrence of a neurological deficit, but in reality is not such. To prevent the effect of irritation of the carotid body, the carotid artery should be clamped as low as possible at the angle of the lower jaw.

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internal shunt in the carotid artery (this is impossible or very difficult to do using other methods), evaluate the effectiveness of reconstruction immediately after restoration of blood flow along the ICA (by

increase in blood flow velocity in the MCA), take into account the likelihood of developing cerebral hyperperfusion in the postoperative period (with a significant increase in blood flow velocity after removing the clamp from the ICA) and take measures to prevent this syndrome, identify material emboli entering the intracranial vessels from the reconstruction zone.

The use of local anesthesia during carotid EAE allows one to quickly identify disturbances of consciousness and/or the development of focal deficits in the patient due to the latter’s constant contact with the anesthesiologist and the operating team and begin measures to protect the brain. The features of local anesthesia for this intervention will be discussed in more detail below.

Retrograde blood pressure index in the carotid artery reflects the degree of collateral compensation of blood flow in the selected hemisphere. If the ratio of retrograde blood pressure to antegrade blood pressure when directly measured in the common carotid artery is not less than 1/3, but the absolute value of retrograde blood pressure is higher than 40 mm Hg. and the curve of its image on the monitor screen has a distinct pulse character, and does not look like an isoline, then it is considered that the patient tolerates clamping of the ICA. The methodology for this measurement will be discussed in more detail below.

There are 6 methods of protecting the brain if it is intolerant to clamping the ICA: general and craniocerebral (local) hypothermia, pharmacoprotection (barbiturates, etc.), general anesthesia, artificial hypertension and internal shunting. The first four methods reduce the metabolic demands of the brain and/or increase the resistance of cell membranes to ischemic damage, the last two provide an influx of

blood to the brain by collateral or main route. Both types of hypothermia and drug protection today are of more historical interest and are not routinely used in carotid surgery for various reasons: due to labor intensity, low or unproven effectiveness.

By holding artificial hypertension it is possible to improve collateral compensation during ICA clamping with a retrograde pressure index close to 1/3 or its absolute value of about 40 mmHg. The optimal method of increasing blood pressure in this situation is the introduction of traces of mesatone, and the optimal level of blood pressure increase is an indicator that is 20% higher than the patient’s initial (“working”) blood pressure. In most situations, such an increase is sufficient to achieve adequate collateral compensation without the use of internal bypass and, at the same time, is not so significant as to contribute to the development of cardiac complications.

The most adequate method of protecting the brain from ischemic damage is to use temporary intraluminal (internal) shunting at the time of clamping of the ICA, allowing for antegrade blood flow to the corresponding hemisphere. The essence of the method is that after clamping the carotid arteries and performing an arteriotomy, a special silicone tube is inserted into the lumen of the internal and common carotid arteries, through which blood enters the brain at the stage of ICA reconstruction. The shunt is removed before allowing blood flow through the ICA upon completion of reconstruction. There are several types of internal shunts for carotid EAE (soft and hard, straight and loop-shaped, with end intraluminal fixatives).

frames and without them, with and without a side outlet), but we prefer straight, rigid, non-compressible bypasses without clamps for the reasons outlined below. Although it is tempting to use internal shunting in carotid surgery due to safety concerns, the insertion of a shunt itself carries the risk of complications and also limits exposure to the inner surface of the artery covered by the shunt itself.

The main complications associated with the use of internal bypass surgery arise at the stage of shunt insertion:

Material cerebral embolism as a result of plaque disorganization upon insertion of the distal portion of the shunt into the ICA;

Air embolism of the brain;

Dissection of the distal end of the internal carotid artery shunt with perfusion of the false canal, lack of perfusion of the brain and possible spread of the dissection into the intracranial parts of the ICA and its branches.

To prevent these complications, we adhere to the following principles of internal shunting during carotid EAE. A tourniquet is placed on the CCA holder, the carotid arteries are clamped and the lumen of the CCA is opened with a transition to the ICA. The length of the arteriotomy should be such that the arterial incision begins 0.5-1 cm proximally and ends 0.5-1 cm distal to the plaque. The surgeon should see a completely free lumen of the artery when inserting a shunt, which significantly reduces the possibility of material embolism and ICA dissection. Inserting a shunt through an arteriotomy site containing an atherosclerotic plaque is unacceptable and very dangerous due to the possibility of its fragmentation.

The second fundamental point is that first the shunt is inserted into the ICA, and blood from the brain begins to flow retrogradely through the proximal end of the shunt, washing out possible air and material emboli. Next, the tourniquet on the CCA is carefully partially released and the shunt is inserted into the CCA using a retrograde blood stream, and the tourniquet is finally tightened. This sequence completely eliminates the possibility of material and air emboli entering the brain, which is very likely during the initial introduction of a shunt into the CCA, when a powerful central blood stream is capable of washing away both air from the opened arterial segment and plaque particles into the distal channel.

Complications from an already installed shunt include its thrombosis and prolapse. To identify shunt blockage, we use TCD monitoring data - the only method that allows us to make a timely decision to change the shunt.

The final complication associated with internal shunting relates to the time of shunt removal. If you leave a significant portion of the artery suture line unstitched, then removing any type of shunt is quite easy. But in such a situation, suturing the arteriotomy may take a long time, while the absolutely safe period of time for insertion or removal of the shunt is 2 minutes. In the case of large carotid arteries, it is possible to apply a parietal clamp to the unstitched section of the suture line to complete the latter, but this technique is not always available. If you leave a short section of the suture line unstitched, which can be quickly sewn, then removing the shunt with force through a small hole is fraught with breaking the thread or cutting through it.

calling. To prevent this complication, we use the following technique.

The suture line is sutured all the way to the point where both threads are tied, which is marked in the CCA (its larger diameter makes it easier to remove the shunt than from the ICA). Next, at a distance sufficient for unhindered removal of the shunt (usually 1 cm for each of the threads), both threads are unraveled to such an extent as to form a free hole in the suture line. Once the shunt is removed, both sutures are fully tightened and tied, after which blood flow can be allowed to flow. If in such a situation you use not a straight, but a loop-shaped shunt or a shunt with a side outlet, then it becomes more difficult to bring both stitching threads as close as possible, since in these types of shunts either both legs of the loop or a side outlet, which are much larger in size, protrude from the lumen of the artery than a ligature holding a straight shunt. The order in which the shunt is removed from the ICA or CCA does not matter, since in any case, either through the shunt or through the ICA, possible emboli and air are washed out retrogradely; sometimes both ends of the shunt can be removed at the same time.

We believe that internal bypass for carotid EAE should be used only selectively, in patients who are not tolerant to ICA clamping. Despite the fact that with strict adherence to the described precautions, the threat of complications associated with the use of an internal shunt is minimal, expanding the indications for this method of brain protection to routine use increases the total risk of carotid EAE in the general group of patients with ICA stenoses.

Method of local anesthesia for carotid EAE, which is a combination of conductor

and infiltration anesthesia, A.Imparato was introduced. The concentration of the anesthetic used is 0.5%; in terms of the duration of the effect, it is preferable to use lidocaine.

The conduction component of anesthesia is aimed at blocking the cervical plexus at the Ci-Civ level, which provides pain relief to the neck tissue on the side of the operation. Using a syringe with a capacity of 2 ml, an anesthetic is injected through a hypodermic needle on the side of the operation at 4 points in the projection of the line connecting the transverse processes of the first four vertebrae. The distance between the points on the skin is approximately 1 - 1.5 cm. The transverse process of the first vertebra, inaccessible to palpation, is projected immediately below the lower point of the mastoid process. 2 ml of anesthetic is injected into each point. Next, using a 10-milliliter syringe, the needle is passed through points on the skin until it stops in the transverse process of each of the four indicated vertebrae, preceded by the introduction of a small amount of anesthetic. Next, the needle is slightly pulled up and directed 1-1.5 cm deep along the anterior surface of the transverse process in the same direction, also preceded by the introduction of an anesthetic. The piston is pulled towards itself to prevent the needle from entering one of the veins of the spinal plexus. The introduction of an anesthetic into these veins can lead to serious neurological disorders, including loss of consciousness and the appearance of focal symptoms. Next, at the reached depth, 10-15 ml of anesthetic is injected into each point.

Infiltration of anesthetic along the skin incision line is performed secondarily. When isolating the carotid arteries, the anesthetic is injected periadventitially into the CCA in the lower corner of the wound and into the carotid body to prevent reflex

noah bradycardia. It should be remembered that conduction anesthesia at the C I -C IV level does not lead to complete anesthesia of the upper parts of the sternocleidomastoid muscle, the muscles of the oral diaphragm and the digastric muscle. If it is necessary to carry out manipulations in this area (traction with hooks and retractors, muscle dissection), additional infiltration anesthesia is required.

If there is no tolerance to the test clamping of the CCA or the disappearance of the initial tolerance, at the main stage of the operation under local anesthesia, the patient is given an internal shunt, intubated, and the intervention is continued under general anesthesia. The need for emergency implementation of these measures sufficiently complicates the work of the operating room team, since both anesthesiologists and surgeons are forced to simultaneously manipulate almost the same anatomical area.

The advantages of local anesthesia for carotid EAE include the most accurate control over the state of consciousness and neurological status of the patient and the ability to maintain spontaneous breathing in patients with severe respiratory diseases. The most important disadvantage of this method of pain relief is the pronounced psycho-emotional depression of the patient, which forced us to limit the indications for local anesthesia due to the significant frequency of cardiac complications in comparison with the same operations under general anesthesia. In addition, modern inhalational anesthetics reduce the oxygen demand of neurons and increase cerebral blood flow, which helps protect the brain from ischemia (see above). When the operation time is extended by more than 1.5-2 hours, the effect of the local anesthetic weakens

continues or may end, requiring repeated tissue infiltration.

We are currently determining the indications for carotid EAE under local anesthesia in the absence of other (instrumental) options for determining the brain's tolerance to ICA clamping and in patients with severe respiratory distress that may worsen during mechanical ventilation and require continued respiratory support.

Carotid endarterectomy technique. The patient is on the operating table in a supine position with the head end slightly elevated (semi-seated position). A cushion is placed under the patient's shoulder blades and the head is turned as far as possible in the direction opposite to the side of the operation. The surgical field is covered with 4 sheets: the upper one - along the lower edge of the lower jaw so that the angle of the jaw acts as a guide to the surgical field; internal - along the midline of the neck from the chin to the jugular notch; the lower one - along the lower edge of the clavicle along its entire length and the outer one - from the mastoid process along the anterior edge of the trapezius muscle to the brachioclavicular joint so that the earlobe protrudes into the surgical field between the upper and lateral sheets as a guide.

The skin incision begins from the lower edge of the mastoid process (only behind the auricle, since damage to the branches of the facial nerve is possible in front) parallel and 1-2 cm below the lower jaw; having reached the projection of the inner edge of the sternocleidomastoid muscle at the angle of the lower jaw, smoothly rotate and extend the incision downwards along the projection of the specified edge to the border of the middle

Rice. 5.87. The bifurcation of the CCA is highlighted.

her and the lower third of the neck. The possibility of damage to the branches of the facial nerve (marginal mandibular nerve) should be taken into account, which is why the incision should not reach the borders of the lower jaw. At the same time, the subcutaneous tissue and subcutaneous muscle (m.platysma) are dissected with the skin. In the upper corner, the sensitive greater auricular nerve may pass through the wound, innervating the lower and posterior parts of the auricle and the parotid region at the back. If possible, its integrity should be preserved, since the intersection of this nerve is accompanied by the development of persistent numbness in this area. If the auricular nerve limits exposure, it is coagulated and divided. Access to the CCA requires intersection of the large facial vein, which flows into the internal jugular vein. Both ends of the crossed vein are sutured, since simple tying of ligatures, due to the large size of the facial vein, often leads to leakage of its stumps and is fraught with the development of heavy bleeding in the postoperative period. Periad-ventitially, 1 ml of 0.5% lidocaine solution is injected into the CCA (later the same amount is injected into the glomus to prevent reflex bradycardia), on the arterial

A holder is applied and after dissecting the fiber upward along the vessel, the carotid bifurcation is isolated. Before starting manipulations on the bifurcation of the CCA, it is necessary to get an accurate idea of ​​the location and direction of the hypoglossal nerve, usually located along the lower edge of the posterior belly of the digastric muscle 1-2 cm above the bifurcation, slanting from the outside inwards and from top to bottom through the initial sections of the ICA and ECA. Along the lateral edge of the ICA, a branch of the superior root (radix superior) departs from the hypoglossal nerve, heading down along the neurovascular bundle of the neck and forming the cervical loop (ansa cervicalis). Next, the superior thyroid artery, which arises in the initial section of the ECA, is isolated, and the latter is taken on a holder. The trunk of the ECA is usually isolated to the level of the origin of the lingual artery, but if the atherosclerotic lesion of the ECA extends higher, then the artery is mobilized along its length (Fig. 5.87).

The most important condition for isolating the ICA directly is minimal contact with the artery. We do not bypass the ICA with a hold, but move the artery in the wound

during mobilization, we carry it out with the help of supports on the ECA, and to a lesser extent on the OCA. If these techniques are not enough, then fixation of the ICA only at the adventitia is acceptable. After isolating the initial section of the ICA (2-3 cm), its patency and localization of the plaque are assessed by careful digital inspection, lightly running a finger along the surface of the artery. It is unacceptable to compress the artery with tweezers, rough pressure, etc., as this can lead to fragmentation of the atheromatous plaque and distal embolism. It is at the stage of isolating the ICA that the largest number of intraoperative cerebrovascular accidents is observed. If the ICA lesion extends higher, then further secretion of the

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Four (4) degrees of cerebral vascular insufficiency (Pokrovsky A.V., Kiyashko V.A., RMAPO, A.V. Vishnevsky Institute of Surgery, Moscow):

Ι degree– asymptomatic cerebral vascular insufficiency;

Asymptomatic course is those conditions when the patient completely lacks any complaints indicating cerebral circulatory insufficiency, but upon physical examination (auscultation) or according to instrumental diagnostic methods there are indications of varying degrees of damage to the arteries supplying blood to the brain.

ΙΙ degree– transient cerebrovascular accidents (TCI) or transient ischemic attacks (TIA) lasting no more than a day;

Transient cerebrovascular accidents - this group of patients is often encountered in the practice of a neurologist, since the patient develops clear neurological symptoms indicating ischemia of the carotid or vertebral basin. The frequency of episodes ranges from 10–20 times a day to 1–2 times a month and even less frequently. Paroxysms are provoked by physical activity and changes in body position. In addition to purely neurological symptoms, patients may also experience visual impairment. Transient blindness in one eye, that is, “amaurosis fugax,” is one of the leading symptoms of carotid artery stenosis, but, unfortunately, doctors (including ophthalmologists) are poorly aware of this.

ΙΙΙ degree– chronic brain failure – discirculatory encephalopathy;

Disculatory encephalopathy - characterized by constant headaches, a sharp decrease in performance, and sleep disorders. A neurological examination reveals pseudobulbar, pyramidal and extrapyramidal symptoms of varying severity.

ΙV degree– ischemic stroke and its consequences (circulatory disorders can occur in various vascular areas of the brain: carotid and vertebral).

Ischemic stroke in the carotid region develops much more often than in the vertebral region. It should be especially noted that in almost 70% of cases, a stroke in the carotid region develops suddenly, without any previous ischemic attacks. In case of stroke, symptoms persist for more than 24 hours. The clinical picture of severe residual symptoms of stroke is observed in patients with occlusion of the internal carotid artery and continued thrombosis from the bifurcation of the common carotid artery into its intracranial parts.

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