Acute cerebrovascular accident clinical guidelines. New European guidelines for the treatment and prevention of stroke and transient ischemic attacks

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Clinical guidelines for the diagnosis and management of stroke in general medical practice, including primary and secondary prevention 2013

Association of General Practitioners (Family Doctors) of the Russian Federation

Diagnosis and tactics in stroke

in general medical practice, including primary and secondary prevention

1. Methodology

When preparing clinical guidelines on stroke, a search was made for the most reliable scientific information in electronic databases, as well as an analysis of printed publications published on this topic over the past 5 years. The main evidence base for the recommendations was the following electronic resources: MEDLINE, Cochrane Collaboration Library, European Stroke Organization website, American Heart Association / American Stroke Association website, scientific electronic library eLIBRARY.RU. A table of levels of evidence was used to assess the quality and strength of the evidence (Table 1).

High-quality meta-analysis, systematic review of randomized clinical trials (RCTs), or large RCTs with very low bias that can be generalized to an appropriate population.

High-quality systematic review of cohort or case-control studies, or high-quality cohort or case-control studies with a very low risk of bias, or RCTs with a low risk of bias, the results of which can be generalized to the appropriate population.

Cohort or case-control or controlled trial without randomization with a low risk of bias, the results of which can be generalized to the appropriate population, or RCTs with a very low or low risk of bias, the results of which cannot be directly generalized to the appropriate population.

Case series or uncontrolled study or expert opinion. Indicates a lack of high-level evidence.

Corresponds to the level of evidence III and IV

Reviews of published meta-analyses and systematic reviews with tables of evidence were used to analyze the evidence. Expert consensus was used in formulating recommendations. When presenting the text of the recommendations, levels of evidence (A, B, C, D) are given, the criteria for which are indicated in Table 1.

2. Definition and general characteristics

Stroke is an acute cerebrovascular accident (CVC), which is characterized by a sudden (within minutes, less often - hours) onset of focal neurological symptoms (motor, speech, sensory, coordinator, visual and other disorders) and / or cerebral disorders (changes in consciousness, headache, vomiting, etc.), which persist for more than 24 hours or lead to the death of the patient in a short period of time due to a cause of cerebrovascular origin.

There are two clinical and pathogenetic forms of stroke:

1) ischemic stroke (brain infarction). due to acute focal cerebral ischemia, leading to a heart attack (zone of ischemic necrosis) of the brain;

2) hemorrhagic stroke(non-traumatic intracerebral hemorrhage) caused by rupture of an intracerebral vessel and penetration of blood into the brain parenchyma or rupture of an arterial aneurysm with subarachnoid hemorrhage.

ONMK also includes transient disorders of cerebral circulation. which are characterized by the sudden onset of focal neurological symptoms that develop in a patient with a cardiovascular disease (arterial hypertension, atherosclerosis, atrial fibrillation, vasculitis, etc.), last several minutes, less than hours, but not more than 24 hours and end with a complete restoration of impaired functions .

Transient disorders of cerebral circulation include: 1) transient ischemic attack (TIA), which develops as a result of short-term local ischemia of the brain and is characterized by sudden transient neurological disorders with focal symptoms;

2) hypertensive cerebral crisis, which is a condition associated with an acute, usually significant rise in blood pressure (BP) and is accompanied by the appearance of cerebral (rarely focal) neurological symptoms secondary to hypertension. The most severe form of hypertensive crisis is acute hypertensive encephalopathy, the basis of the pathogenesis of which is cerebral edema.

A cerebral infarction is, as a rule, the result of the interaction of many diverse etiopathogenetic factors, which can be divided into local and systemic: 1) local: morphological changes in the brachiocephalic or intracerebral arteries, atherosclerotic lesions of the vessels of the aortic arch and cerebral arteries, heart damage as a source of thromboembolic cerebral infarctions , fibromuscular dysplasia of the walls of the brachiocephalic and cerebral arteries, arteritis, changes in the cervical spine, anomalies in the structure of the vessels of the neck and brain, etc .; 2) systemic factors: disorders of central and cerebral hemodynamics, coagulopathy, polycythemia, certain forms of leukemia, hypovolemia, etc.

In every second case, the cause of intracerebral non-traumatic hemorrhage is arterial hypertension, about 10-12% is due to cerebral amyloid angiopathy, about 10% is due to anticoagulants, 8% - tumors, all other causes account for about 20%. Intracerebral hemorrhages can develop either as a result of rupture of the vessel, or by diapedesis, usually against the background of previous arterial hypertension.

Spontaneous subarachnoid hemorrhage in most cases (70-85%) is caused by rupture of a saccular aneurysm, the size of which can vary from 2 mm to several centimeters in diameter, more often 2-10 mm. Saccular aneurysms most commonly occur in the arteries of the circle of Willis and appear to be due to a congenital defect in the vessel wall, usually occurring at a bifurcation or branching of the artery. Over time, there is a gradual increase in the size of the aneurysm. Approximately 30% of all aneurysms are localized on the posterior communicating artery (at the site of its origin from the internal carotid artery), 20-25% - on the middle cerebral artery, 10-15% - on the arteries of the vertebrobasilar system (mainly the basilar and inferior cerebellar arteries). The main risk factor (RF) for rupture of saccular aneurysm is arterial hypertension, additional ones are smoking and alcohol abuse.

In the clinical course of a stroke, the following periods are distinguished: 1) 1-3 days - the most acute period; 2) up to 28 days - acute period; 3) up to 6 months - early recovery period; 4) up to 2 years - late recovery period; 5) after 2 years - a period of residual effects.

3 . Epidemiology

More than 500,000 people have a stroke every year in the Russian Federation. According to the data of the domestic national register conducted between 2001 and 2005, the incidence of stroke in the Russian Federation is 3.48 ± 0.21 cases per 1000 population. The incidence of various types of stroke varies widely, in particular, cerebral infarctions account for 65-75%, hemorrhages (including subarachnoid) - 15-20%, and transient cerebrovascular accidents account for 10-15%. The frequency of cerebral strokes in the population of people older than 50-55 years increases by 1.8-2 times in each subsequent decade of life.

The socio-economic consequences of stroke are extremely high, in particular: death in the acute period of a stroke occurs in 34.6%, and during the first year after the end of the acute period - in 13.4%; severe disability with the need for constant care is present in 20.0% of stroke patients; 56.0% have limited ability to work and only 8.0% return to their previous work activities. Disability due to stroke ranks first among all causes of primary disability, accounting for 3.2 per 10,000 population. Disability after a stroke on average in the country is 56-81%.

Mortality from stroke among people of working age has increased in the Russian Federation over the past 10 years by more than 30%. The annual death rate from stroke in our country is 175 per 100,000 population.

4. Classifications of stroke

I. International classification of stroke according to ICD-10:

G45 - Transient transient cerebral ischemic attacks (attacks) and related syndromes

I60 Subarachnoid hemorrhage

I61 - Intracerebral hemorrhage

I62 Other non-traumatic intracranial hemorrhage

I63 - Cerebral infarction

I64 Stroke, not specified as haemorrhage or infarction.

II. Classification of stroke (Odinak M.M. et al. 1998):

A. With the preservation of neurological deficit up to 24 hours:

2. Hypertensive crises.

B. With the preservation of neurological deficit from 24 hours to 3 weeks:

1. Acute hypertensive encephalopathy.

2. Minor stroke (with reversible neurological deficit).

B. With the preservation of neurological deficit for more than 3 weeks:

1. Hemorrhagic stroke (non-traumatic hemorrhage):

1.1. parenchymal hemorrhage;

1.2. intraventricular hemorrhage;

1.3. subarachnoid hemorrhage;

1.4. subdural hemorrhage;

1.5. extradural hemorrhage;

1.6. mixed forms of hemorrhages.

2. Ischemic stroke:

2.1. Embolic

2.2. Non-embolic (thrombosis, non-thrombotic softening).

III. International etiopathogenetic classification of ischemic stroke TOAST (Adams H.P. et al, 1993): 1) atherothrombotic; 2) cardioembolic; 3) lacunar; 4) associated with other, rarer causes (vasculitis, hypercoagulable syndromes, coagulopathy, arterial dissection, etc.); 5) of unknown origin.

IV. Classification of ischemic stroke according to pathogenetic subtypes (Vereshchagin N.V. et al. 2000): 1) atherothrombotic (34% of cases), including arterio-arterial embolism (13%) and cerebral thrombosis (21%); 2) cardioembolic (22%); 3) hemodynamic (15%); 4) lacunar (22%); 5) stroke according to the type of hemorheological microocclusion (7%).

5. Risk factors for stroke

The most important modifiable risk factors that increase the risk of stroke are: arterial hypertension of any origin, heart disease, atrial fibrillation, lipid metabolism disorders, diabetes mellitus, pathology of the main arteries of the head, hemostatic disorders. The main non-modifiable risk factors include: gender, age, ethnicity, heredity. There are also risk factors associated with lifestyle: smoking, overweight, low level of physical activity, unhealthy diet (in particular, insufficient consumption of fruits and vegetables, alcohol abuse), long-term psycho-emotional stress or acute stress.

The prevalence of the main risk factors in Russia is quite high: 59.8% of adult men and 9.1% of women smoke; have arterial hypertension 39.9% and 41.1%; hypercholesterolemia - 56.9% and 55.0%; obesity - 11.8% and 26.5%, respectively; 12.0% of men and 3.0% of women consume excessive alcohol.

6. Stroke screening is an active prophylactic detection of the main modifiable risk factors (arterial hypertension, cardiac arrhythmias, intravascular thrombosis, atherosclerotic stenosis of the carotid arteries), including in asymptomatic patients. The most widely used diagnostic methods that form the basis of screening for stroke in the population include the following:

1) control of blood pressure, keeping a diary of blood pressure / heart rate, if necessary, performing daily monitoring of blood pressure (level of evidence A);

2) lipid profile (level of evidence A);

3) coagulogram (level of evidence C);

4) blood glucose level (level of evidence A);

5) auscultation of the carotid arteries (level of evidence C);

6) duplex scanning of brachiocephalic arteries (level of evidence B);

7) ECG, if necessary, Holter ECG monitoring and ultrasound of the heart (level of evidence A).

7. Diagnosis of stroke at the prehospital stage

The main task of a general practitioner at the prehospital stage is the correct and rapid diagnosis of stroke, which is possible on the basis of clarifying complaints, anamnesis and conducting a somatic and neurological examination. An exact definition of the nature of the stroke (hemorrhagic or ischemic) is not required, it is possible only in a hospital after CT or MRI studies of the brain. To make the right tactical decision on the targeted hospitalization of a patient in a regional vascular center or a specialized hospital, it is desirable to determine the probable type of stroke already at the prehospital stage. In particular, this is necessary in case of subarachnoid hemorrhage (Department of Neurosurgery - urgent endovascular embolization of cerebral artery aneurysm) and ischemic stroke, which according to its characteristics corresponds to the protocol of thrombolytic therapy (regional vascular center - urgent intravenous systemic thrombolysis).

A presumptive diagnosis of the ischemic or hemorrhagic nature of a stroke is possible by a combination of certain signs. The clinical picture of the development of stroke is characterized, as a rule, by a sudden (within minutes, less often hours) onset of focal (or cerebral, and in the case of subarachnoid hemorrhage - meningeal) symptoms. For the correct and timely diagnosis of stroke, a family doctor needs to know and be able to identify the main clinical and neurological syndromes (focal, cerebral, meningeal) characteristic of this disease during a neurological examination.

8. Clinical manifestations

Stroke should be suspected in all cases in the presence of acute development of focal neurological symptoms or a sudden change in the level of consciousness. Among the disorders of the brain functions that develop during a stroke, there are: focal symptoms, meningeal syndrome (signs of involvement of the meninges), cerebral disorders. The most frequent signs and focal symptoms of a stroke depend on the damage to the vascular pools of the blood supply to the brain.

I. Carotid circulatory system (arteries: carotid, middle cerebral, anterior cerebral):

1. Hemiparesis on the side opposite the lesion: weakness, awkwardness, heaviness in the arm (in the shoulder girdle), in the hand, face or leg. More often there is a combination of damage to the hands and face. Sometimes one half of the face may be involved (facial paresis). The involved side of the body is opposite to the side of the affected artery.

2. Sensory disturbances: sensory disturbances, paresthesias, altered sensation only in the arm, hand, face or leg (or various combinations), most often the arm and face are involved. It usually occurs simultaneously and on the same side as hemiparesis.

3. Speech disorders: difficulty in finding the right words, slurred and fuzzy speech, difficulty understanding the speech of others (aphasia), writing difficulties (dysgraphia) and reading (dyslexia). Slurred and slurred speech, impaired pronunciation of words and articulation (dysarthria).

4. Visual disturbances: blurred vision within the field of view of both eyes. The involved visual field is opposite to the side of the affected artery.

5. Monocular blindness: visual disturbances in one eye. All or part of the visual field may suffer, often these disorders are described as disappearance, blanching, a gray spot, a black spot in the visual field. The eye suffers, on the side of the affected carotid artery.

II. Vertebrobasilar circulatory system (arteries: vertebral, basilar, posterior cerebral):

1. Vertigo: Feeling unsteady and spinning. May be associated with nystagmus. Isolated dizziness is a common symptom of a number of non-vascular diseases.

2. Visual disturbances: blurred vision on the right or left, both eyes are involved at the same time.

3. Diplopia: the feeling of two images instead of one. There may be a sensation of movement of the objects being examined, a violation of the movement of the eyeballs to the side (oculomotor paresis), or asynchronous movement of the eyeballs.

4. Movement disorders: weakness, clumsiness, heaviness or dysfunction in the hand, leg, arm or face. One half of the body or (rarely) all four limbs may be involved. The face may be involved on one side, the limbs on the other (alternating stem syndromes). Drop attacks (sudden fall without loss of consciousness) are a common symptom of the onset of paralysis of all four limbs without loss of consciousness.

5. Sensitivity disorders: sensory disturbances, paresthesias. One half of the body or all four limbs may be involved. It usually occurs simultaneously with movement disorders.

6. Dysarthria: slurred and indistinct speech, poor articulation, pronunciation.

7. Ataxia: violation of statics, unsteady gait, throwing to the side, discoordination on one side of the body.

Following the confirmation of the main diagnosis, the most difficult and responsible task is to accurately and quickly diagnose the nature of the stroke (ischemic, hemorrhagic), since in the acute period of the disease, further treatment tactics largely depend on this. Along with a thorough neurological examination, this requires a detailed analysis of the anamnesis, the course of development of stroke. Ischemic stroke (cerebral infarction) is characterized by:

1) previous TIA or transient monocular blindness;

2) previously identified angina pectoris or symptoms of ischemia of the lower extremities;

3) pathology of the heart (heart rhythm disturbances, most often in the form of atrial fibrillation, the presence of artificial heart valves, rheumatism, infective endocarditis, acute myocardial infarction, mitral valve prolapse, etc.);

4) development during sleep, after taking a hot bath, physical fatigue, as well as during an attack of atrial fibrillation, including against the background of acute myocardial infarction, collapse, blood loss;

5) the gradual development of neurological symptoms, in some cases, its flickering, i.e., the increase, decrease and again increase in clinical symptoms;

6) age over 50;

7) prevalence of neurological focal symptoms over cerebral symptoms.

Cerebral hemorrhage is characterized by:

1) long-term arterial hypertension, often with a crisis course;

2) the development of a stroke during emotional or physical overstrain;

3) high blood pressure in the first minutes, hours after the onset of a stroke;

4) the age of patients is not a determining factor, however, the older age range is more typical for cerebral infarctions compared to hemorrhages;

5) the rapid development of neurological and cerebral symptoms, often leading after a few minutes to a coma of the patient (this is especially true for hemorrhage in the brain stem or cerebellum, although occasionally it is also observed with extensive infarcts of the brain stem due to blockage of the main artery, however, for it typical precursors - blurred vision, fog before the eyes, doubling, violations of phonation, swallowing, statics, etc.);

6) a characteristic appearance of some patients is a purple-cyanotic face, especially with a hypersthenic constitution, and at the same time nausea or repeated vomiting;

7) the rarity of transient disorders of cerebral circulation in history and the absence of transient monocular blindness;

8) severe cerebral symptoms, complaints of headache in a certain area of ​​the head, preceding (in a few seconds or minutes) the development of focal neurological symptoms.

Subarachnoid hemorrhage is characterized by:

1) relatively young age of patients (usually up to 50 years);

2) the onset of the disease is sudden, among full health, during active, especially physical activity;

3) the initial symptom is a severe headache, often described by patients as "unbearable", with a possible loss of consciousness;

4) frequent development of emotional arousal, rise in blood pressure, subsequently sometimes hyperthermia;

5) the presence of a pronounced meningeal syndrome: stiff neck, positive symptoms of Brudzinsky and Kernig, photophobia and increased sensitivity to noise, often in the absence of focal symptoms;

6) always - the presence of blood in the cerebrospinal fluid (lumbar puncture).

A METHOD FOR ASSESSING COMPLIANCE WITH MODERN CLINICAL RECOMMENDATIONS OF DRUG THERAPY AIMED TO REDUCE THE RISK OF REPEATED STROKE (ACCORDING TO THE LIS-2 REGISTER)

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Over the past five years, a lot of evidence has accumulated that has caused significant changes in approaches to treatment. Much of this change is reflected in the recent American Heart Association/American Stroke Association Guidelines for Early Care of Patients with Acute Ischemic Stroke, published in Stroke in March 2018. The aim of their development is to provide a holistic complex for the management of adult patients with acute ischemic stroke. These recommendations are addressed to first- and second-level physicians, allied professionals, and hospital administrators and supersede the 2013 Recommendations with all subsequent updates.

Prehospital care

1. Heads of structural divisions of the health care system, along with medical workers, are encouraged to develop and implement health education programs on stroke issues. Programs should remain relevant for a long time and ensure maximum coverage of various groups of the population, taking into account ethnic, age, gender and other differences. (I; B-R)

2. Patients who show signs of a stroke or are in the vicinity are strongly advised to notify the emergency medical service as soon as possible, and the dispatchers of this service are to ensure priority and speed in transporting these patients to the clinic. (I;B-NR)

3. Stroke education programs for doctors, medical staff and emergency medical teams contribute to improving the quality of care in the clinic. (I;B-NR)

Emergency Assessment and Stroke Care

1. Primary care providers and emergency medical dispatchers are encouraged to use the Stroke Severity Rating Scale. (I;B-NR)

2. Since the initial medical intervention for stroke is carried out by the emergency medical team, it is highly recommended to implement an appropriate treatment protocol. (I;B-NR)

3. It is recommended that emergency medical personnel provide the receiving hospital with prehospital notification that a suspected stroke patient is on the way. In this way, appropriate resources can be mobilized before he arrives. (I;B-NR)

Stroke emergency system

1. Emergency medical service managers, in coordination with local, regional and national agencies, with the advice of health experts, are encouraged to develop triage algorithms and protocols for the rapid identification and evaluation of patients with overt or suspected stroke using validated, standardized diagnostic tools such as the FAST, LAPSS, CPSS. (I;B-NR)

2. It is recommended to create regional structures for stroke management from institutions providing primary emergency care (including intravenous alteplase) and centers on the basis of which it is possible to provide comprehensive periprocedural treatment. (I;A)

3. Patients with positive screening results and/or suspected stroke should be transported as soon as possible to clinics with staff experienced in the use of intravenous alteplase. (I;B-NR)

4. When choosing among several clinics offering intravenous alteplase, it is debatable to prioritize a facility offering a higher level of care, including mechanical thrombectomy, over nearby clinics. (IIb; B-NR)

Certification of specialized centers

1. It is recommended that specialized stroke centers be certified by an independent external body such as the Center for Improvement in Healthcare Quality (USA), Det Norske Veritas (Norway), the Healthcare Facilities Accreditation Program or The Joint Commission, or local health authorities. Medical centers should be interested in certification. (I;B-NR)

Teamwork in the clinic

1. Rapid evaluation of patients with suspected stroke is recommended following an organized clinical protocol. (I;B-NR)

3. It is reasonable to further reduce the target door-to-needle time to 45 minutes for ≥50% of patients with acute ischemic stroke. (IIb; C-EO)

5. Multidisciplinary teams trained in emergency care, provided they have access to expert information in neurology, are advised to be cautious about scaling up intravenous thrombolytic therapy for acute ischemic stroke. (I; A)

1. For areas where there are no own capabilities for visual examination and timely interpretation, it is recommended to transmit data from patients with suspected acute stroke using teleradiology. (I;A)

2. Expert evaluation of teleradiology data can be effective for making an adequate decision on the acceptability of prescribing intravenous alteplase. (IIa; B-R)

5. The teleradiology-guided prescribing approach of intravenous alteplase may also be reliable and beneficial for ischemic stroke patients in specialized treatment centers. (IIb; B-NR)

6. It is advisable to use the teleradiology system when considering interhospital transportation of patients with acute ischemic stroke to perform mechanical thrombectomy. (IIb; B-NR)

Organization and integrated collaboration

1. The issue of organization and integrated interaction may be relevant for specialized treatment centers and medical institutions providing primary emergency care for ischemic stroke, including intravenous administration of alteplase. Its essence lies in the development of competencies for performing emergency non-invasive intracranial vascular imaging, more accurate selection of patients for endovascular intervention and reduction in the duration of endovascular therapy. (IIb; C-LD)

2. For mechanical thrombectomy, it is recommended that the patient be in a specialized treatment center where cerebral angiography can be performed promptly, where there are qualified interventionists and a multidisciplinary peri-procedural care team. When developing, monitoring and operating a system of their interaction, it is recommended to focus on prompt assessment and treatment, which requires tracking results. Institutions are encouraged to define criteria for the accreditation of professionals performing safe and timely intra-arterial revascularization procedures. (I; C-EO)

3. All clinics providing specialized care for stroke patients are encouraged to develop, adopt and adhere to statutory treatment protocols that reflect the current recommendations of national and international professional organizations, as well as government health authorities. (I; C-EO)

4. It is also recommended to adopt protocols and work out in advance the procedures for transferring patients inside and outside the hospital in the process of continuous treatment, which will effectively solve these problems at any time of the day. (I; C-EO)

5. Government agencies and third party payers are encouraged to develop and implement acute stroke patient reimbursement schedules consistent with experience in achieving optimal patient outcomes, whether or not patients receive specific drugs and procedures. (IIb; C-EO)

Clinical databases

1. Participation in the completion of the Stroke Database is recommended as it contributes to the consistent adherence to current clinical guidelines and the process of continuous improvement in the quality and outcomes of care. (I;B-NR)

Improving the quality of specialized care

1. Healthcare institutions are encouraged to establish a multidisciplinary quality improvement committee to review and monitor benchmarks, indicators, and issues of evidence-based clinical practice and outcomes in stroke. The formation of a clinical practice improvement working group and the creation of an appropriate database will help maintain established quality standards. In addition, the database can be used to identify gaps or differences in the quality of medical services provided and address them in a timely manner. (I;B-NR)

2. A continuous process of quality improvement, carried out both by individual elements and by the system as a whole, can positively affect the complex of treatment and its results. (IIa; B-NR)

3. Stroke outcome assessment should take into account the patient's baseline severity. (I;B-NR)

Emergency evaluation and treatment

Stroke Severity Scale

Table 1. NIHSS Stroke Severity Scale

Imaging methods for studying the brain

1. All patients admitted to hospital with suspected acute stroke are advised to have a brain imaging study assessed immediately upon arrival at the clinic. In most cases, an assessment of the results of non-contrast computed tomography is sufficient to make a decision on further treatment. (I;B-NR)

2. It is recommended that the clinic be organized so that brain imaging results can be obtained within 20 minutes of delivery in at least 50% of patients who may need intravenous alteplase or mechanical thrombectomy. (I;B-NR)

3. Currently, there is insufficient evidence to determine the threshold values ​​for the stiffness of CT hypoattenuation (permeability) in patients with ischemic stroke, so it cannot be considered as a criterion for postponing intravenous alteplase. (III: not recommended; B-R)

4. Signs of hyperdense middle cerebral arteries according to computed tomography data are not a criterion for late administration of intravenous alteplase to patients who meet other criteria for this appointment. (III: not recommended; B-R)

5. The routine use of magnetic resonance imaging to rule out microbleeding in the brain after intravenous alteplase is not recommended. (III: not recommended; B-NR)

6. The use of imaging study criteria to select patients for treatment with intravenous alteplase for stroke of unknown onset (sleep-onset) is not recommended outside the scope of research studies. (III: not recommended; B-NR)

7. Performing multimodal computed tomography and magnetic resonance imaging should not delay the initiation of intravenous alteplase. (III: harmful; B-NR)

8. For patients eligible for endovascular therapy, non-invasive intracranial vascular testing is recommended at the time of initial evaluation of imaging data, but intravenous alteplase should not be delayed. (I; A)

9. Computed angiography to detect large vessel occlusion is recommended for patients who meet the criteria for endovascular therapy, without waiting for the determination of serum creatinine levels, if there is no history of renal failure. (IIa; B-NR)

10. Imaging of the extracranial internal carotid and vertebral arteries, in addition to the intracranial circulation, is recommended for planning mechanical thrombectomy and evaluating patient suitability. (IIa; C-EO)

11. The use of imaging modalities other than computed tomography and angiography or magnetic resonance imaging and angiography (such as perfusion testing) to select applicants for mechanical thrombectomy less than 6 hours before the procedure is not recommended. (III: not recommended; B-R)

12. In acute ischemic stroke with occlusion of large vessels of the carotid artery basin between the 6th and 24th hour from the onset of symptoms, diffusion-weighted magnetic resonance imaging, computed tomographic perfusion or magnetic resonance perfusion is recommended to be performed exclusively with an auxiliary purpose, for selection of patients for mechanical thrombectomy, provided that the rules for standard imaging and other selection criteria, the effectiveness of which has been confirmed in randomized clinical trials, have been strictly observed. (I; A)

13. Assessment of the state of collateral circulation can be a criterion for the suitability of patients to perform mechanical thrombectomy. (IIb; C-LD)

Other types of diagnostics

1. The appointment of alteplase in all patients is preceded only by the determination of the level of glucose in the blood. (I; B-R)

2. Baseline evaluation of an electrocardiographic study in patients with acute ischemic stroke is recommended, but should not influence the initiation of intravenous alteplase. (I;B-NR)

3. Evaluation of baseline blood troponin levels in acute ischemic stroke is recommended, but should not influence the initiation of intravenous alteplase. (I;B-NR)

4. The practical value of the results of chest x-ray in the hyperacute period of ischemic stroke in the absence of evidence of acute pulmonary, cardiac or vascular disease is unclear. But if results are obtained, their interpretation should not delay intravenous administration of alteplase. (IIb; B-NR)

Basic supportive and intensive care

Respiratory tract, respiration and oxygenation

1. Airway management and assisted ventilation are recommended for acute stroke patients with impaired consciousness or bulbar dysfunction that threatens airway function.

2. Maintaining arterial saturation >94% may require supplemental oxygen. (I; C-LD)

1. Maintaining the level of systemic perfusion requires the correction of the state of hypotension and hypovolemia. (I; C-EO)

2. Eligible patients for intravenous alteplase with elevated blood pressure need to carefully lower their systolic and diastolic blood pressure levels to<185 и <110 мм рт. ст. соответственно перед началом фибринолитической терапии. (I; B-NR)

3. In patients who have not received thrombolytic therapy, unless additional data are available, it is recommended to maintain blood pressure at a level of ≤185/110 mm Hg before planned intra-arterial therapy. Art. before performing the procedure. (IIa; B-R)

4. The usefulness of drug-induced hypertension in acute ischemic stroke has not been established. (IIb; C-LD)

Table 2 Treatment options for hypertension in patients with acute ischemic stroke requiring reperfusion therapy

6. Early treatment of hypertension in patients with acute ischemic stroke may be necessary for comorbidities (acute coronary event, acute heart failure, dissecting aortic aneurysm, post-thrombotic symptomatic intracerebral hemorrhage, or preeclampsia/eclampsia). A 15% reduction in blood pressure is considered safe. (I; C-EO)

7. With blood pressure<220/120 мм рт. ст. у пациентов, не получавших альтеплазу или эндоваскулярную терапию при отсутствии сопутствующих заболеваний, требующих интенсивной антигипертензивной терапии, начало и возобновление лечения при артериальной гипертензии в течение первых 48–72 ч после наступления инсульта не снижает уровень смертности. (III: не рекомендуется; А)

Body temperature

2. The usefulness of active hypothermia in the treatment of patients with ischemic stroke has not been established and can only be considered in the context of clinical trials. (IIb; B-R)

blood glucose

1. Patient data suggest that persistent hyperglycemia observed within the first 24 hours of the onset of acute ischemic stroke is associated with worse outcomes compared with normoglycemia, therefore it is recommended to control glucose levels in the range of 140-180 mg / dl, preventing possible hypoglycemia . (IIa; C-LD)

2. In patients with acute ischemic stroke, hypoglycemia (<60 мг/дл) требует лечения. (I; A)

3. After an acute ischemic stroke, it makes sense to screen all patients for fasting plasma glucose, glycated hemoglobin, or a glucose tolerance test. The choice of screening methods and timing of testing is based on clinical judgment, bearing in mind that the acute condition itself can cause changes in blood glucose levels. A relatively more accurate test is the determination of the level of glycated hemoglobin. (IIa; C-EO)

Intravenous administration of alteplase

Table 3 Criteria for prescribing intravenous alteplase (grade of recommendation; level of evidence)

2. Abciximab should not be given concomitantly with intravenous alteplase. (ІІа; B-NR)

3. Given the extremely low incidence of unexpected abnormal platelet counts or coagulation function in the population, it is prudent not to withhold intravenous alteplase until appropriate studies are available. (ІІа; B-NR)

4. Clinicians should be aware that hypo- and hyperglycemia can mimic symptoms of acute stroke, so blood glucose levels should be determined prior to initiating intravenous alteplase, which should not be administered in clinical conditions of extravascular origin. (III: not recommended; B-NR)

5. Clinicians should be aware of the side effects of fibrinolytic therapy, including bleeding and angioedema, which can cause partial airway obstruction. (I; B-NR) (If severe headache, acute hypertension, nausea, vomiting, or worsening neurological symptoms occur, stop alteplase and perform an emergency head CT scan.)

Symptomatic intracranial bleeding within 24 hours of intravenous alteplase in acute ischemic stroke (IIb, C-EO)

1. Stop the administration of alteplase.

2. Perform a complete blood count, determine INR, activated partial thromboplastin time, fibrinogen level, blood group and blood compatibility.

3. Urgently perform a computed tomography examination of the head without intravenous contrast enhancement.

4. Assign intravenous infusion of cryoprecipitate (including blood coagulation factor VIII): 10 units. within 10–30 min; prescribed for fibrinogen levels<200 мг/дл.

5. Give intravenous infusion of tranexamic acid 1000 mg over 10 minutes or ε-aminocaproic acid 4–5 g over 1 hour followed by 1 g until bleeding stops.

6. Consult a hematologist and a neurosurgeon.

7. Maintenance therapy should provide control of arterial, intracranial, cerebral perfusion pressure, mean arterial pressure, body temperature and blood glucose levels.

Orolingual angioedema (IIb; C-EO)

1. It is necessary to maintain the functionality of the respiratory tract:

1) If the edema is limited to the front of the tongue and lips, then there is no need for endotracheal intubation.

2) Rapidly progressing (within 30 minutes) swelling of the larynx, palate, oral cavity, or oropharynx indicates a high risk of needing intubation.

3) For conscious patients, fiber optic intubation is the best option. Nasotracheal intubation may be necessary but increases the risk of epistaxis after intravenous alteplase.

2. Interrupt intravenous administration of alteplase and stop taking angiotensin-converting enzyme inhibitors.

3. Prescribe methylprednisilone (125 mg).

4. Prescribe diphenhydramine (50 mg).

5. Give ranitidine (50 mg) or famotidine (20 mg) intravenously.

6. With a further increase in angioedema, adrenaline (0.1%) is prescribed 0.3 ml subcutaneously or inhaled 0.5 ml.

7. Prescribe icatibant, a selective B 2 receptor antagonist of bradykinin, 3 ml (30 mg) subcutaneously in the abdomen; an additional injection (30 mg) may be given at 6-hour intervals, but no more than 3 injections in 24 hours; Plasma C1-esterase inhibitor (20 IU/kg) has been successfully used in hereditary and angiotensin-converting enzyme-dependent angioedema.

8. Carry out maintenance therapy.

Other thrombolytics and sonothrombolysis

1. Benefits of intravenous defibrogenesis and fibrinolytic agents other than alteplase and tenecteplase have not been proven and therefore their use outside of clinical trials is not recommended. (III: not recommended; B-R)

2. Since there is no evidence of benefit or equivalence of the effect of tenecteplase 0.4 mg/kg intravenous bolus over alteplase, this option may be considered as an alternative for patients with mild neurological impairment without significant intracranial occlusion. (IIb; B-R)

3. The use of sonothrombolysis as adjuvant therapy with intravenous thrombolysis is not recommended. (III: not recommended; B-R)

Mechanical thrombectomy

1. In patients who meet the criteria for alteplase, it is recommended that it be administered, even if mechanical thrombectomy is being considered. (I;A)

2. In the process of considering mechanical thrombectomy, patients treated with alteplase do not need to evaluate the clinical response to its administration. (III: harm; B-R)

3. Mechanical thrombectomy using a stent retriever is indicated for patients who meet all of the following criteria: 1) a pre-stroke score on a modified Rankin scale from 0 to 1; 2) pathological occlusion of the internal carotid artery or M1 segment of the middle cerebral artery; 3) age ≥18 years; 4) NIHSS score ≥6; 5) CT score ASPECTS ≥6; 6) treatment can be started (puncture of the femoral artery) within 6 hours from the onset of symptoms. (I;A)

4. Mechanical thrombectomy using a stent retriever can also be considered for patients with pathological M2 or M3 occlusion of the middle cerebral artery provided they meet other criteria, but the benefit of this approach has not been determined. (IIb; B-R)

5. Mechanical thrombectomy using a stent retriever may also be considered for patients with pathologic anterior, vertebral, basilar, or posterior cerebral artery occlusion, provided they meet other criteria, but the benefit of this approach has not been determined. (IIb; C-EO)

6. Mechanical thrombectomy using a stent retriever may also be appropriate for patients with a pre-stroke Modified Rankin score >1 as an ASPECTS CT score.<6 или значением оценки по шкале NIHSS <6 и патологической окклюзией внутренней сонной артерии или проксимального М1-сегмента средней мозговой артерии при условии, что они соответствуют прочим критериям, но преимущества этого подхода не определены. (IIb; B-R)

7. For selected patients with acute ischemic stroke within 6-16 hours from the last known time before the onset of symptoms, with occlusion of a large carotid basin, provided that they meet other criteria (DAWN or DEFUSE 3), mechanical thrombectomy is recommended. (I;A)

8. The technical goal of mechanical thrombectomy according to the Modified Perfusion Recovery Score for Ischemic Stroke (mTICI) is to achieve a 2b/3 angiographic result to maximize a favorable clinical outcome. (Ib; B-R)

10. The use of devices other than stent retrievers is allowed, but the choice of the latter is a priority. (IIb; B-R)

11. The use of a proximal balloon guiding catheter or a large peripheral access catheter rather than a single guiding cervical catheter in combination with stent retrievers is preferred. (IIa; C-LD)

12. The use of adjuvants, including intra-arterial thrombolysis, may be appropriate to achieve an mTICI 2b/3 angiographic outcome. (IIb; C-LD)

13. Endovascular therapy for tandem occlusion (both extracranial and intracranial during thrombectomy) is reasonable. (IIb; B-R)

14. When choosing an anesthesia method during endovascular therapy, it is advisable to be guided by the results of an individual risk assessment, technical and other characteristics of the procedure. (IIa; B-R)

15. During mechanical thrombectomy, it is advisable to maintain blood pressure at ≤180/105 mm Hg. Art. and hold it for another 24 hours (IIa; B-R)

16. In case of mechanical thrombectomy with successful reperfusion, it is advisable to maintain blood pressure at the level<180/105 мм рт. ст. (IIb; B-R)

Other types of endovascular therapy

1. In the presence of contraindications to the use of alteplase, intra-arterial thrombolysis may be considered in carefully selected patients, starting within 6 hours after the onset of a stroke, but the consequences are unknown. (IIb; C-EO)

Antiplatelet therapy

1. In acute ischemic stroke, the appointment of acetylsalicylic acid is recommended within 24-48 hours from its onset. For patients treated with intravenous alteplase, acetylsalicylic acid administration is usually delayed up to 24 hours, but the decision to use it may be considered, given the concomitant circumstances that determine a significant benefit. However, this option is a source of significant risk. (I;A)

2. It is not recommended to consider the use of acetylsalicylic acid as an alternative treatment for patients with acute ischemic stroke if they meet the criteria for intravenous alteplase or mechanical thrombectomy. (III: not recommended; B-R)

3. Further studies are needed to determine the efficacy of tirofiban and eptifibatide. (IIb; B-R)

4. The use of glycoprotein IIb/IIIa receptor antagonists in acute ischemic stroke is potentially hazardous and should not be used. (III: dangerous; B-R)

5. To prevent early secondary stroke for up to 90 days in patients with mild ischemic stroke, it is recommended to prescribe dual antiplatelet therapy (acetylsalicylic acid and clopidogrel) starting 24 hours after the onset of symptoms. (IIa; B-R)

Anticoagulants

1. In the treatment of patients with acute ischemic stroke, emergency anticoagulation therapy to prevent early recurrent stroke, stop the worsening of neurological symptoms, or improve post-treatment outcomes is not recommended. (III: not recommended; A)

2. The acceptability of emergency anticoagulation therapy in patients with severe ipsilateral stenosis of the internal carotid artery leading to ischemic stroke has not been determined. (IIb; B-NR)

3. The safety and benefit of short-term anticoagulant therapy for non-occlusive, extracranial intraluminal thrombosis in patients with stroke has not been determined. (IIb; C-LD)

4. Currently, the possibility of using argatroban, dabigatran or other thrombin inhibitors as a treatment for patients with acute ischemic stroke requires further clinical studies. (IIb; B-R)

5. The safety and benefit of factor Xa inhibitors in ischemic stroke have not been determined and further studies are required. (IIb; C-LD)

Hemodilution, vasodilators and hemodynamic augmentation

1. Expansion of circulating blood volume due to hemodilution is not recommended in the treatment of patients with acute ischemic stroke. (III: not recommended; A)

2. Administration of high-dose albumin in the treatment of patients with acute ischemic stroke is not recommended. (III: not recommended; A)

3. The use of vasodilators such as pentoxifylline in the treatment of patients with acute ischemic stroke is not recommended. (III: not recommended; A)

4. Currently, equipment for cerebral blood flow augmentation in the treatment of patients with acute ischemic stroke can only be used in clinical trials. (IIb; B-R)

Neuroprotective effect

1. Current pharmacological and non-pharmacological treatments with purported neuroprotective properties have not been shown to be effective in improving outcomes after ischemic stroke, so other neuroprotective agents are not recommended. (III: not recommended; A)

Emergency carotid endarterectomy/carotid angioplasty and stenting

1. Justification for urgent or emergency carotid endarterectomy in the presence of a small infarct with a large area at risk (for example, detection of penumbra on imaging and relevant clinical signs), due to critical stenosis or occlusion of the carotid arteries, or acute neurological deficit as a result of thrombosis after carotid endarterectomy has not been established. (IIb; B-NR)

2. For patients with unstable neurological status (for example, with a stroke), the effectiveness of urgent or emergency carotid endarterectomy has not been established. (IIb; B-NR)

Other therapies

1. The use of transcranial shortwave infrared laser therapy in the treatment of acute ischemic stroke is not recommended. (III: not recommended; B-R)

Dysphagia

1. Prior to feeding, it is advisable to identify patients at increased risk of aspiration. (IIa; C-LD)

3. An instrumental assessment with a high probability of aspiration is appropriate to check for its presence or absence and clarify the physiological causes of dysphagia when choosing a treatment approach. (IIa; B-NR)

4. The choice of the method of instrumental evaluation of the swallowing function (fiber optic endoscopy, video fluoroscopy, etc.) depends only on the availability and other factors in the individual situation. (IIb; C-LD)

Nutrition

1. Enteral nutrition in acute ischemic stroke should be started within 7 days. (I; B-R)

2. In case of dysphagia in the early stages of a stroke (during the first 7 days), it is advisable to install nasogastric tubes for feeding, and in patients with expected prolonged dysphagia (> 2–3 weeks), percutaneous gastrostomy is recommended. (IIa; C-EO)

3. The introduction of nutritional supplements into the diet is advisable at a high risk of malnutrition. (IIa; B-R)

4. To reduce the risk of developing pneumonia after a stroke, it is advisable to introduce an oral hygiene protocol. (IIb; B-NR)

Prevention of deep vein thrombosis

1. In immobilized patients, to reduce risk in the absence of contraindications, it is recommended to use intermittent pneumocompression in addition to standard therapy (acetylsalicylic acid and hydration). (I; B-R)

2. The benefits of prophylactic subcutaneous heparin (unfractionated or low molecular weight) in immobilized patients with acute ischemic stroke have not been determined. (IIb; A)

3. During anticoagulation, the benefits of prophylactic use of unfractionated or low molecular weight heparin have not been established. (IIb; B-R)

4. In case of ischemic stroke, elastic compression stockings should not be used. (III: harmful; B-R)

Depression control

1. The appointment of a detailed study to identify post-stroke is recommended, but the optimal timing has not been determined. (I;B-NR)

2. In the absence of contraindications for post-stroke depression, antidepressants are prescribed and the effectiveness of treatment is monitored. (I; B-R)

Other types of treatment

1. Prophylactic use of antibiotics in ischemic stroke is not recommended. (III: not recommended; B-R)

2. Placement of indwelling bladder catheters carries a risk of urinary tract infections. (III: harmful; C-LD)

4. It is recommended to minimize or eliminate skin friction, reduce pressure on the surface of the skin, provide adequate support, avoid excessive moisture and dryness, and maintain an adequate level of skin nutrition. Regular cleaning, a high level of hygiene, and the use of special mattresses and cushions for wheelchairs and seats are also recommended until patients regain mobility. (I; C-LD)

5. As needed, it is advisable for patients and their families to use palliative care resources. Caregivers may need assistance in making patient-centered decisions about the extent of medical interventions or restrictions on care given the prognosis of the disease. (IIa; C-EO)

Rehabilitation

3. Too early mobilization of patients (24 hours) from the onset of stroke may reduce the likelihood of a favorable outcome after 3 months. (III: harmful; B-R)

4. It is recommended that all stroke patients be given a formal assessment of their daily living and self-care activities, communication abilities, and functional mobility. The results of the assessment should be taken into account when planning the scope of further care. (I;B-NR)

6. The efficacy of fluoxetine or other selective serotonin reuptake inhibitors to improve motor response has not been reliably established. (IIb; C-LD)

Treatment for severe complications

Edema of the cerebellum and brain

1. Ventriculostomy is recommended for obstructive hydrocephalus after cerebral infarction. The need to perform an associated or subsequent decompression craniotomy depends on the size of the infarct, the neurological condition, the degree of brain compression and the effectiveness of treatment. (I; C-LD)

2. Decompression suboccipital craniotomy with opening of the dura mater is recommended for cerebellar infarction, leading to worsening of neurological symptoms, despite the maximum medical effect. If indicated, and if this does not involve additional risk, treatment for obstructive hydrocephalus is recommended at the same time as ventriculostomy. (I;B-NR)

3. It is recommended to inform family members of a patient with cerebellar infarction about the likelihood of a positive outcome due to suboccipital craniotomy, which will facilitate the decision to perform it. (IIb; C-LD)

4. Patients with extensive supratentorial infarction are at high risk for complications such as cerebral edema and increased intracranial pressure. Therefore, discussion of treatment options and possible outcomes with patients or their caregivers is recommended to be carried out promptly. In making consensus decisions about the prognosis of the disease and limitations in the choice of interventions, a patient-centered approach is recommended. (I; C-EO)

5. In the first days after a stroke, patients with extensive cerebral infarction should be treated to reduce the risk of edema and carefully monitored for signs of neurological deterioration. At a high risk of malignant cerebral edema, the expediency of a quick transfer of these patients to a neurosurgical clinic should be considered. (I; C-LD)

6. In patients over 60 years of age with unilateral infarction of the middle cerebral artery basin, with worsening neurological symptoms within 48 hours, despite medical therapy, it is recommended to perform decompression craniotomy with opening of the dura mater, since this can reduce mortality by almost 50% and improve results of subsequent rehabilitation. (IIa; A)

7. As a criterion for selecting patients for decompression craniotomy, it is currently recommended to consider the syndrome of decreased level of consciousness caused by cerebral edema. (IIa; A)

8. Osmotic therapy in patients with postinfarction cerebral edema is recommended when the clinical picture worsens. (IIa; C-LD)

9. Short-term mild hyperventilation (target pCO 2 = 30-34 mm Hg) in patients with acute severe neurological impairment due to cerebral edema is recommended as a transitional therapy. (IIa; C-EO)

10. In case of ischemic edema of the brain or cerebellum, the use of hypothermia or barbituric acid derivatives is not recommended. (III: not recommended; B-R)

11. Due to lack of evidence of efficacy and increased potential risk of infectious complications, the use of corticosteroids (usually given in high doses) is not recommended in the treatment of patients with cerebral edema and increased intracranial pressure observed in ischemic stroke. (III: harm; A)

convulsive syndrome

1. For recurrent seizures after a stroke, the recommended treatment is the same as for seizures due to other neurological causes, and anticonvulsants are recommended to be selected individually. (I; C-LD)

2. Prophylactic use of anticonvulsants is not recommended. (III: not recommended; BR)

Prevention of secondary consequences of a stroke

brain imaging

1. Standard use of magnetic resonance imaging for all patients with acute ischemic stroke is not economically feasible and is not recommended for initial diagnosis or treatment planning. (III: not recommended; B-NR)

2. Magnetic resonance imaging may be useful in selected cases to obtain additional information, but its effect on the results has not been determined. (IIb; C-EO)

Vascular imaging

1. For non-disabled patients (Modified Rankin score 0-2) with acute ischemic stroke in the carotid artery, in which carotid endarterectomy or stenting is indicated, non-invasive visualization of the cervical vessels should be performed within 24 hours of admission to the hospital. clinic. (I;B-NR)

2. In patients with acute ischemic stroke, it is not recommended to plan prophylactic treatment based on the results of standard computed tomography angiography and magnetic resonance angiography performed to detect stenosis or occlusion of intracranial arteries. (III: not recommended; A)

3. For selected patients with acute ischemic stroke, prophylactic treatment planning based on the results of standard computed tomography and magnetic resonance angiography may be useful, but its effectiveness has not been determined. (IIb; C-EO)

Heart function test

1. Monitoring of cardiac function can detect fibrillation and other serious arrhythmias requiring emergency intervention. It is recommended that cardiac monitoring be performed for at least the first 24 hours after the patient arrives at the clinic. (I;B-NR)

2. The clinical benefit of long-term monitoring of cardiac function after acute ischemic stroke has not been determined. (IIb; B-R)

3. For selected patients, long-term monitoring of cardiac function after an acute ischemic stroke may be useful to provide additional information when planning subsequent prophylactic treatment, but its impact on outcomes has not been determined. (IIb; C-EO)

4. Standard echocardiography for all patients with acute ischemic stroke during the planning of subsequent prophylactic treatment is not reasonable and is not recommended. (III: not recommended; B-NR)

5. Standard echocardiography may be appropriate for selected patients with acute ischemic stroke during planning for subsequent preventive treatment. (IIb; B-R)

1. For patients not on intensive statin therapy with ischemic stroke, presumably of atherosclerotic origin, regular cholesterol levels are not recommended. (III: not recommended; B-R)

2. Measurement of blood cholesterol levels in patients with ischemic stroke, presumably of atherosclerotic origin, provided that they comply with the optimal regimen of statin therapy, may be useful in the appointment of subtilisin-kexin type 9 proprotein convertase inhibitors in order to reduce mortality from myocardial infarction, stroke and cardiovascular disease. (IIb; B-R)

Other Assessment Methods for Prevention of Secondary Consequences of Stroke

1. Standard screening for hyperhomocysteinemia in recent ischemic stroke is not applicable. (III: not recommended; C-EO)

2. Routine screening for antiphospholipid antibodies in patients with ischemic stroke is not recommended unless there are other manifestations of the antiphospholipid syndrome and there is an alternative explanation for the ischemic event, such as atherosclerosis, carotid stenosis, or atrial fibrillation. (III: not recommended; C-LD)

Antithrombotic therapy

1. For patients with non-cardioembolic acute ischemic stroke, it is recommended to use antiplatelet agents instead of oral anticoagulant therapy to reduce the risk of recurrent stroke and other cardiovascular events. (I; A)

2. For patients with non-cardioembolic acute ischemic stroke, additional benefits from increasing the amount of acetylsalicylic acid taken or choosing another antiplatelet agent have not been established. (IIb; B-R)

3. For patients with non-cardioembolic acute ischemic stroke, switching from antiplatelet therapy to the use of warfarin to prevent secondary stroke is not clinically beneficial. (III: not recommended; B-R)

4. The choice of antiplatelet agent for early prevention of secondary effects in patients with non-cardioembolic acute ischemic stroke should be optimized taking into account individual risk, cost, tolerability, relative efficacy and other clinical characteristics. (I; C-EO)

5. For patients with ischemic stroke, atrial fibrillation and coronary heart disease, the use of additional antiplatelet agents together with oral anticoagulants to reduce the risk of ischemic cardiovascular and cerebrovascular events has no definite clinical benefit. Unstable angina and coronary artery stenting represent special circumstances in which dual antiplatelet/oral anticoagulant therapy may be indicated. (IIb; C-LD)

6. For most patients with acute ischemic stroke after atrial fibrillation, it is reasonable to prescribe oral anticoagulant therapy within 4-14 days after the onset of neurological symptoms. (IIa; B-NR)

7. For patients with acute ischemic stroke and hemorrhagic transformation, the question of starting or resuming antiplatelet or anticoagulant therapy is considered depending on the specific clinical course and leading symptoms. (IIb; B-NR)

8. For patients with acute ischemic stroke and dissection of the carotid or vertebral arteries with established recurrent cerebral ischemic events that are not amenable to treatment, the value of stenting has not been determined. (IIb; C-LD)

statin therapy

1. Prescribing statins to patients with acute ischemic stroke who have previously taken statins is reasonable. (IIa; B-R)

3. In the presence of contraindications to the use of high-intensity statin therapy, if permissible, patients with atherosclerotic cardiovascular pathology are prescribed moderate-intensity statin therapy. (I; A)

4. For patients with atherosclerotic cardiovascular pathology aged >75 years, it is advisable to evaluate the benefits and possible risks of adverse effects, interaction with other drugs and the wishes of the patients themselves before prescribing statin therapy. It is advisable to continue statin therapy in patients with known tolerance. (IIb; C-EO)

Revascularization of the carotid arteries

1. When revascularization is indicated to prevent secondary events in non-disabled minor stroke patients (modified Rankin score 0–2), the optimal time to perform it is 48 h–7 days from the onset of the event. (IIa; B-NR)

Smoking cessation

1. All smokers who have had an acute ischemic stroke are strongly advised to stop smoking. (I; C-EO)

2. Counseling, nicotine replacement products and medications are promoted. (I; A)

3. For smoking patients with acute ischemic stroke, it is recommended to start intensive behavioral therapy in the clinic. (IIa; B-R)

4. For patients with acute ischemic stroke who smoke, varenicline may be prescribed. (IIb; B-R)

5. Interventions for smoking patients with acute ischemic stroke may include pharmacological and behavioral methods aimed at smoking cessation. (IIb; B-R)

6. Patients who have had an acute ischemic stroke are advised to avoid side (passive) smoking. (IIa; B-R).

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A stroke (its synonym is the term "apoplexy") is an acute violation of cerebral circulation, and as a result, a violation of the brain functions. The disease is divided into two large groups: hemorrhagic and ischemic.

A hemorrhagic stroke is a hemorrhage into the substance of the brain as a result of a rupture of a blood vessel. The most common cause of such a gap is high blood pressure (read more).

Ischemic stroke. in fact, a cerebral infarction is the result of insufficient blood flow to areas of the brain. The cause may be a narrowing or spasm of the blood vessel, its complete blockage. In some cases, there is a combination of these two types of stroke.

Most often, apoplexy occurs in middle-aged and elderly people. It should be noted that according to statistics, mortality from vascular diseases of the brain ranks second, second only to diseases of the circulatory system after coronary heart disease.

Depending on the localization of the lesion, a stroke can manifest itself with cerebral and focal neurological symptoms. General cerebral symptoms include such symptoms as: impaired consciousness, stupor, loss of orientation in time, etc. (read more). Focal symptoms depend on the function that the affected area of ​​the brain carries. For example, if the site provides the function of movement, then weakness in the limb may develop, up to paralysis (read more).

Hemorrhagic stroke occurs suddenly, often after physical overexertion, strong excitement, or stress. Harbingers of this type of disease can serve as a headache, flushing of the face. Ischemic stroke develops within a few hours, more often at night. The growing symptomatology of apoplexy depends on the localization of the process (read more).

In the event of a stroke, the patient needs urgent hospitalization. It should be borne in mind that therapy is most effective for the first minutes and hours of the disease. A contraindication to hospitalization is an unconscious state with a violation of important vital functions. In this case, intensive drug therapy is in place (read more). After the condition improves, the patient is hospitalized. Stroke treatment is based on a course of vascular, restorative and rehabilitation therapy (read more).

The outcome of an apoplexy, as well as the likelihood of relapse (recurrence), depends on its type, location and nature of the lesion. Directly from the stroke itself, patients die relatively rarely, more often from associated diseases, such as congestive pneumonia. It becomes obvious that a patient with this diagnosis needs the closest, constant care. Care should include such activities as: feeding the patient, fighting pressure sores, cleansing the intestines, vibromassage of the chest. When caring for a stroke patient, it is necessary to take into account many little things that are ignored in everyday life, being taken for granted (read more).

Stroke and atherosclerosis are interrelated diseases in which urgent hospitalization and appropriate drug therapy are indicated.

Read more about atherosclerosis here.

In the best way treatment of damage to large vessels- cervical portion of the carotid artery, available malformations and ruptured aneurysms - is surgical. However, large ABA often manifest in infancy as persistent heart failure and are not subject to surgical correction. In such cases, embolization of the feeding arteries is first resorted to in order to reduce the volume of the anomaly.

Aneurysms in children are much less common than in adults. The question of when it is better to have an operation for a ruptured aneurysm - sooner or later - is not decided unambiguously. Currently, the possibility of conservative treatment is being studied in adult patients in order to improve the clinical condition, prevent re-hemorrhage and vasospasm.

To evaluate the effectiveness similar approaches in children. controlled studies are needed that have not yet been conducted. In some institutions, adult patients are given antifibrinolytic substances such as episilon aminocaproic acid (amicar). The likelihood of rebleeding may be reduced, but all possible consequences of hypercoagulability, including embolism, are noted.

Accepted in our clinic tactics for children with a ruptured aneurysm or ABA includes: careful monitoring of fluid and electrolyte balance to avoid complications associated with inadequate secretion of ADH; the introduction of corticosteroids, if the hematoma is accompanied by a volumetric effect and there is a threat of wedging; bed rest and as early as possible surgical intervention if the patient's clinical condition is stable.

Patients with telangiectasias by type Nishimoto's disease. and also for those in whom direct reconstruction of the carotid artery is not feasible (for example, after irradiation of the head and neck with a large dose of X-rays), it is possible to create anastomoses between the external and internal carotid arteries (ECA-ICA). In the early 1960s, microsurgery began to develop, putting stereoscopic magnifying instruments and coaxial illumination in the hands of neurosurgeons, which made it possible to operate through small holes, avoid extensive retraction, and thereby minimize tissue and blood vessel injury.

New technique improved results surgical correction of aneurysms and vascular malformations and cerebral revascularization. The creation of microvascular anastomoses between the external carotid artery and the internal one improves the blood supply to the ischemic areas. It is indicated in the presence of hypoperfusion and insufficiency of collateral circulation with reversible ischemic neurological disorders, i.e., with transient attacks of ischemia, but is useless in a completed stroke. The issue of accessibility of the lesion to surgical treatment is solved with the help of arteriography.

The increasingly widespread positron emission tomography(PET) measures cerebral blood flow and helps select those patients who are eligible for ECA-ICA anastomoses. Usually an anastomosis is made between the superficial temporal artery and the middle cerebral artery. The temporal artery is mobilized and passed through a small burr hole into the temporal lobe, sutured to one of the cortical branches of the middle cerebral artery.

In young children, the vessels are thin and the operation is technically more difficult. In the clinic mayo. making such anastomoses since 1975. 90% of operated patients are still older than 2 years. Clinical improvement was noted in 75% of cases. There were 2 children among 56 patients who underwent CHA-ICA anastomosis according to the Yasergill method in this clinic. One of them is a six-year-old girl with Nishimoto's telangiectasias; at follow-up, the anastomosis remained functional and her clinical condition stabilized and improved.

Other was a 5 year old boy with a giant aneurysm of the internal carotid artery, manifested by proptosis and headache. He was ligated with the ICA and anastomosis of the ECA-ICA was performed; the result is excellent. Another, simpler technique has also been proposed: transplantation of the scalp artery, together with the adjacent strip of aponeurosis, into a narrow linear foramen of the dura mater. With such encephaloduroarteriosyangiosis, the proximal and distal ends of the scalp artery remain intact. Indications for bypass surgery include progressive occlusion, intractable stenosis, giant aneurysms, and musculoskeletal disease.

Recommendations for the prevention of stroke in patients with cerebrovascular accident

The main provisions of the new American guidelines for the prevention of recurrent stroke are presented. They affect the control of risk factors (arterial hypertension, diabetes mellitus, dyslipidemia, etc.), the use of interventional approaches in patients with atherosclerosis of large arteries, the principles of treatment for cardiogenic embolism, antithrombotic therapy for non-cardioembolic stroke, and the treatment of stroke in a number of specific conditions (arterial dissection, open foramen ovale, hypercoagulation syndromes, etc.). The problem of using anticoagulants after cerebral hemorrhage is considered.

New guidelines from the American Heart Association and the American Stroke Association Council on Stroke for the prevention of ischemic stroke (IS) in IS or transient cerebrovascular accident (TICH) survivors have been published in Stroke Journal. The following is a summary of these evidence-based recommendations. The definition of the class and levels of evidence used in the recommendations is given in the table.

Risk factor management required for all patients with IS or TNMK

Arterial hypertension

Antihypertensive therapy is recommended to prevent recurrent stroke and other vascular complications in all non-hyperacute survivors of IS or TNMC (Class I, Level of Evidence A). Because both patients with and without a history of hypertension benefit from antihypertensive therapy, this recommendation applies to all patients with IS and TNMK, regardless of a history of hypertension (Class I, Level of Evidence B). The absolute level of target blood pressure (BP) and the degree of its reduction is not clear and should be individualized, but the benefit is associated with an average reduction in blood pressure of about 10/5 mmHg. Art. and the normal level of blood pressure, according to the recommendations of JNC-7, is< 120/80 мм рт. ст. (класс IIа, уровень доказательности В).

Several lifestyle modifications have been associated with BP reduction and should be used as part of general antihypertensive therapy (Class IIb, Level of Evidence C). The optimal drug regimen remains unclear, but evidence supports the use of diuretics and a combination of diuretics and ACE inhibitors (Class I, Level of Evidence A). The choice of specific drugs and targets should be individualized based on analysis of data and specific patient characteristics: eg, extracranial cerebrovascular occlusive disease, renal dysfunction, heart disease, and diabetes (Class IIb, Level of Evidence C).

Diabetes

Patients with diabetes mellitus (DM) should have tighter control of blood pressure and lipids (class IIa, level of evidence B). Although all major classes of antihypertensive drugs are suitable for BP control, most patients require more than one drug. ACE inhibitors and angiotensin II receptor antagonists are most effective in slowing the progression of kidney disease and are recommended as first choice in diabetic patients (Class I, Level of Evidence A).

To reduce the risk of microvascular (class I, level of evidence A) and possibly macrovascular (class IIb, level of evidence B) complications in patients with IS or TNMC and diabetes, glycemic control at a level close to normoglycemic is recommended. Target hemoglobin A 1c ≤ 7% (class IIa, level of evidence B).

Patients with IS or TNMK with elevated cholesterol levels, concomitant coronary artery disease, or symptoms of atherosclerotic origin should be managed according to the recommendations of the National Cholesterol Education Program III - NCEP III (Class I, Level of Evidence A). They are advised to prescribe statins. Target LDL cholesterol reduction for individuals with coronary heart disease or symptomatic atherosclerotic disease is less than 100 mg/dL, for patients with multiple risk factors, less than 70 mg/dL (Class I, Level of Evidence A).

In patients with IS or TNMC of presumably atherosclerotic origin, but with no previous indications for statin use (normal cholesterol levels, no concomitant coronary heart disease or signs of atherosclerosis), it is reasonable to prescribe statins to reduce the risk of vascular complications (class IIa, level of evidence B).

Niacin or gemfibrozil can be given to patients with IS or TMJ with low HDL cholesterol levels (Class IIb, Level of Evidence B).

All healthcare professionals should actively encourage smoking patients with IS or TNMK to stop smoking (Class I, Level of Evidence A). Avoidance of tobacco smoke in the environment is recommended (Class IIa, Level of Evidence C). Counseling and use of nicotine and smoking cessation drugs should be used to help patients stop smoking (Class IIa, Level of Evidence B).

Alcohol consumption

Alcohol abusers should completely stop or reduce alcohol consumption (Class IIb, Level of Evidence C). Consideration may be given to drinking small to moderate amounts of alcohol - no more than two drinks per day for men and one drink for non-pregnant women (Class IIb, Level of Evidence C).

Obesity

In all patients with IS and TNMC who are overweight, weight loss should be considered to maintain a body mass index between 18.5 and 24.9 kg/m 2 (Class IIb, Level of Evidence C). Clinicians should advise patients to maintain weight through an adequate balance of calories, physical activity, and behavioral counseling.

Physical activity

For patients with IS or TNMC who may be involved in physical activity, in order to reduce the influence of risk factors and comorbidities that increase the likelihood of stroke recurrence, consideration should be given to performing at least 30 minutes of moderate-intensity exercise on most days (class IIb , level of evidence C). For stroke-disabled patients, a therapeutic regimen of supervised exercise is recommended.

Interventional approaches to patients with atherosclerosis of large arteries

Extracranial lesion of the carotid artery

Surgical carotid endarterectomy (CE) is recommended for patients who have had TNMC or IS less than 6 months ago with severe (70-90%) stenosis of the ipsilateral carotid artery. Perioperative morbidity and mortality in CE is less than 6% (Class I, Level of Evidence A). In patients with recent TNMV or IS and moderate (50-69%) ipsilateral carotid artery stenosis, CE may be recommended based on patient-specific factors such as age, gender, presence of comorbidities, and severity of initial symptoms (Class I, Level of Evidence A). With carotid artery stenosis less than 50%, there is no indication for CE.

For patients with TNMC or IS who are eligible for CE, it is recommended that CE be performed for 2 weeks (Class IIa, Level of Evidence B).

In patients with symptomatic severe stenosis (> 70%) who have difficult surgical access to the site of the stenosis, in patients with medical conditions that significantly increase the risk of surgery, or in other specific circumstances such as radiation-induced stenosis after CE , balloon angioplasty and carotid stenting (ALS) can be considered, which are as effective as CE (Class IIb, Level of Evidence B). ALS is reasonable when performed by surgeons with established periprocedural morbidity and mortality of 4-6%, i.e., similar to those observed in clinical studies of TE and ALS (Class IIa, Level of Evidence B).

In patients with symptomatic carotid occlusion, routine extracranial-intracranial bypass surgery is not recommended (Class III, Level of Evidence A).

Extracranial vertebrobasilar disease

Endovascular treatment of patients with extracranial symptomatic vertebral stenosis may be considered when symptoms persist despite therapy with antithrombotics, statins, and other treatments for risk factors (Class IIb, Level of Evidence C).

Intracranial atherosclerosis

The benefit of endovascular therapy (angioplasty and/or stent placement) for patients with hemodynamically significant intracranial stenosis who remain symptomatic despite treatment (antithrombotics, statins, and other treatments for risk factors) is unclear and is considered exploratory (grade IIb, level of evidence C).

Medical treatment of patients with cardiogenic embolism

Atrial fibrillation

Patients with IS or TNMC with persistent or paroxysmal atrial fibrillation (AF) are recommended anticoagulation with an adjusted dose of warfarin with a target international normalized ratio (INR) of 2.5 (2.0–3.0) (Class I, Level of Evidence A).

For patients unable to take oral anticoagulants, aspirin 325 mg/day is recommended (Class I, Level of Evidence A).

Acute myocardial infarction and left ventricular thrombosis

In patients with IS or TNMC associated with acute myocardial infarction in whom an intramural left ventricular thrombus is identified by echocardiography or other methods, it is reasonable to take oral anticoagulants from 3 months to 1 year to maintain the INR at a level of 2.0 to 3.0 ( class IIa, level of evidence B). During anticoagulant therapy for coronary artery disease, concomitant therapy with aspirin at a dose of 162 mg / day should be carried out (class IIa, level of evidence A).

cardiomyopathy

In patients with IS or TNMK with dilated cardiomyopathy, warfarin therapy (INR 2.0-3.0) or antiplatelet therapy (class IIb, level of evidence C) may be considered to prevent recurrence.

Valvular heart disease

Rheumatic disease of the mitral valve. Patients with IS or TNMK and rheumatic mitral valve disease, regardless of the presence of AF, are indicated for long-term warfarin therapy with a target INR of 2.5 (2.0-3.0) (class IIa, level of evidence C). Antiplatelet agents should not be routinely added to warfarin to avoid additional risk of bleeding (Class IIb, Level of Evidence C).

In patients with IS or TNMK and rheumatic mitral valve disease who have experienced recurrent embolism while taking warfarin, regardless of the presence of AF, it is recommended to add aspirin - 81 mg / day (class IIa, level of evidence C).

Mitral valve prolapse. Patients with IS or TNMC and mitral valve prolapse may benefit from antiplatelet therapy (Class IIa, Level of Evidence C).

Mitral ring calcification. In patients with IS or TNMC and mitral annular calcification, antiplatelet therapy or warfarin may be considered (Class IIb, Level of Evidence C).

Aortic valve disease. In patients with IS or TNMC and aortic valve disease without AF, antiplatelet therapy may be considered (Class IIb, Level of Evidence C).

Prosthetic heart valves. For patients with modern mechanical prosthetic heart valves who have had IS or TNMC, oral anticoagulant therapy is recommended with an INR target of 3.0 (2.5-3.5) (Class I, Level of Evidence B).

In patients with mechanical prosthetic heart valves who have had IS or systemic embolism, despite adequate oral anticoagulant therapy, it is advisable to add aspirin at a dose of 75-100 mg/day to oral anticoagulants and maintain the INR at the target level of 3.0 (2.5-3. 5) (class I, level of evidence B).

In patients with IS or TNMK with bioprosthetic heart valves and no other sources of thromboembolism, warfarin anticoagulant therapy (INR 2.0-3.0) may be considered (Class IIb, Level of Evidence C).

Antithrombotic therapy for non-cardioembolic stroke or TNMK (atherosclerosis, lacunar or cryptogenic infarcts)

In patients with non-cardioembolic IS or TNMK, antiplatelet drugs rather than oral anticoagulants are recommended to reduce the risk of recurrent stroke and other CV events (Class I, Level of Evidence A). Acceptable options for initial therapy are aspirin (50 to 325 mg/day), a long-acting combination of aspirin and dipyridamole, and clopidogrel (Class IIa, Level of Evidence A).

Compared with aspirin alone, the combination of aspirin with long-acting dipyridamole and clopidogrel is safe. The combination of aspirin with long-acting dipyridamole has been suggested instead of aspirin alone based on evidence from head-to-head comparative clinical trials (Class IIa, Level of Evidence A), and clopidogrel may also be considered instead of aspirin alone (Class IIb, Level of Evidence B). The data currently available are insufficient to form evidence-based recommendations for choosing between other antiplatelet agents besides aspirin. The choice of antiplatelet drug should be individualized based on the patient's risk factor profile, tolerability, and other clinical characteristics.

The addition of aspirin to clopidogrel increases the risk of bleeding and is not recommended for routine use in IS or TNMC (Class III, Level of Evidence A).

In patients allergic to aspirin, it is reasonable to prescribe clopidogrel (class IIa, level of evidence B).

There is no evidence that increasing the dose of aspirin in patients who have had an IS while taking it is of additional benefit. Although patients without cardioembolism are often offered alternative antiplatelet drugs, none of them, alone or in combination, has been studied in patients who developed a complication while taking aspirin.

Treatment of stroke in patients with other specific conditions

Dissection of the arteries

For patients with IS and extracranial arterial dissection, warfarin for 3–6 months or antiplatelet agents is reasonable (Class IIa, Level of Evidence B). Most patients with stroke or TNMK require long-term antiplatelet therapy - more than 3-6 months. Anticoagulant therapy for more than 3–6 months may be considered in patients with recurrent ischemic events (Class IIb, Level of Evidence C).

In patients with well-established recurrent ischemic events despite adequate antithrombotic therapy, endovascular therapy (stenting) may be considered (Class IIb, Level of Evidence C). In patients who are not candidates for, or fail, endovascular therapy, surgery may be considered (Class IIb, Level of Evidence C).

Open foramen ovale

In patients with IS or TNMC and patent foramen ovale, antiplatelet therapy is reasonable to prevent recurrence (Class IIa, Level of Evidence B). In high-risk patients who have other indications for oral anticoagulants, such as hypercoagulability or evidence of venous thrombosis, warfarin may be considered (Class IIa, Level of Evidence C).

Data on the need to close the foramen ovale in patients with a first stroke are insufficient. Its closure may be considered in patients who experience recurrent cryptogenic stroke despite optimal treatment (Class IIb, Level of Evidence C).

Hyperhomocysteinemia

For patients with IS or TNMK and hyperhomocysteinemia (levels > 10 µmol/l), it is advisable to take daily standard multivitamin preparations with adequate content of vitamins B 6 (1.7 mg / day), B 12 ( 2.4 µg/day) and folate (400 µg/day) (class IIa, level of evidence B). However, lowering homocysteine ​​levels has not been proven to reduce stroke recurrence.

Hypercoagulable states

hereditary thrombophilia. Patients with IS or TNMK and established hereditary thrombophilia should be evaluated for deep vein thrombosis, which is an indication for short-term or long-term anticoagulant therapy, depending on clinical and hematological parameters (Class I, Level of Evidence A). The likelihood of alternative stroke mechanisms should also be carefully assessed. In the absence of venous thrombosis, long-term use of anticoagulants or antiplatelet therapy is reasonable (Class IIa, Level of Evidence C). In patients with a history of recurrent thrombotic events, long-term anticoagulant therapy may be considered (Class IIb, Level of Evidence C).

Antiphospholipid antibodies. Patients with cryptogenic IS or TNMK and antiphospholipid antibodies are indicated for antiplatelet therapy (class IIa, level of evidence B).

Patients with IS or TNMK who meet the criteria for antiphospholipid syndrome with multiple organ occlusive vein or artery disease, miscarriage, and livedo (marbled skin) are eligible for oral anticoagulant therapy with an INR target of 2.0 to 3.0 (Class IIa, Level evidence B).

sickle cell anemia

For patients with sickle cell anemia and IS or TNMK, the general treatment recommendations above apply in combination with risk factor control and the use of antiplatelet agents (Class IIa, Level of Evidence B). In these patients, adjunctive therapy may also be considered, including regular blood transfusions to lower hemoglobin S levels to< 30-50 % от общего уровня гемоглобина, гидроксимочевину или хирургическое шунтирование при наличии тяжелой окклюзивной болезни (класс IIb, уровень доказательности C).

Thrombosis of the sinuses of the brain

In patients with cerebral sinus thrombosis, even in the presence of hemorrhagic infarction, it is advisable to prescribe unfractionated or low molecular weight heparin (class IIa, level of evidence B). Anticoagulant therapy should be carried out for 3-6 months, followed by a switch to antiplatelet therapy (class IIa, level of evidence C).

stroke in women

Pregnancy

In pregnant women with IS or TNMK and high risk factors for thromboembolic events such as coagulopathy or mechanical heart valves, the following options may be considered:

• the use of unfractionated heparin at adapted doses throughout pregnancy - for example, subcutaneously every 12 hours under the control of partial thromboplastin time;
• the use of low molecular weight heparin in adapted doses throughout pregnancy under the control of factor Xa;
• use of unfractionated or LMWH up to 13 weeks, followed by warfarin until the middle of the third trimester, and then switching back to unfractionated or LMWH until delivery (Class IIb, Level of Evidence C).

In pregnant women with fewer risk factors, consideration may be given to starting unfractionated or low molecular weight heparin in the first trimester, followed by low-dose aspirin until the end of pregnancy (Class IIb, Level of Evidence C).

Hormone therapy in postmenopausal women

Hormone replacement therapy is not recommended for postmenopausal women with IS or TNMK (Class III, Level of Evidence A).

The use of anticoagulants after cerebral hemorrhage

Patients with intracranial and subarachnoid bleeding or subdural hematoma should stop all anticoagulants and antiplatelet agents in the acute period for at least 1-2 weeks after bleeding and prescribe the necessary drugs to eliminate the anticoagulant effect - for example, vitamin K, fresh frozen plasma (class III, level of evidence IN).

For patients who need hypocoagulation shortly after cerebral bleeding, intravenous heparin may be safer than oral anticoagulants. The use of oral anticoagulants can be resumed after 3-4 weeks under strict monitoring and maintaining the INR at the lower limit of the therapeutic level (class IIb, level of evidence C).

Special circumstances: Anticoagulant therapy should not be restarted after subarachnoid bleeding until the acute effects of the ruptured aneurysm have been completely resolved (Class III, Level of Evidence C). In patients with intracranial lobar bleeding or microhemorrhages and suspected cerebral amyloid angiopathy on magnetic resonance imaging, the risk of recurrent intracranial bleeding may be higher if anticoagulant therapy is restarted (Class IIb, Level of Evidence C). In patients with hemorrhagic infarction, the possibility of continuing anticoagulant therapy is determined by the characteristics of the clinical course and indications for the use of anticoagulants (class IIb, level of evidence C).

"APPROVE"

First Deputy Minister

healthcare of the Russian

Federations

A.I. VYALKOV

December 26, 2000 No. 2510/14162-34

"AGREED"

Head of department

medical care organizations

population and prevention

noncommunicable diseases

A.A. Karpeev

December 18, 2000

"PRINCIPLES OF DIAGNOSIS AND TREATMENT OF ACUTE DISORDERS

CEREBRAL CIRCULATION"

The guidelines were prepared by a group of highly qualified specialists - neurologists and neuroresuscitators of our country, who have been working on the problem of acute cerebrovascular accidents for many years. Organizational issues related to diagnostic and therapeutic measures at the prehospital and hospital stages are clearly stated. Indications for hospitalization of patients in intensive care units, intensive care units, angioneurological departments are given. An algorithm of diagnostic measures necessary for adequate therapy of hemorrhages and cerebral infarctions, including neurosurgical methods of treatment, is described. Particular emphasis is placed on targeted diagnosis and treatment of various subtypes of ischemic stroke. Much attention is paid to the treatment of severe forms of stroke, including its complications such as cerebral edema and acute obstructive hydrocephalus. Special sections are devoted to the rehabilitation of patients with acute disorders of cerebral circulation and measures of secondary prevention of various types of stroke. The classification of acute cerebrovascular accidents according to the ICD X revision, the main drugs used in the treatment of stroke is given.

The guidelines are written in a clear and understandable language for doctors, based on the positions of evidence-based medicine. The text is well structured. This document can be recommended for printing without making any changes or additions.

and neurosurgery

St. Petersburg State

medical university named after acad. I.P. Pavlova

Corr. member RAMS, professor

A.A. SKOROMETS

"PRINCIPLES OF DIAGNOSIS AND TREATMENT OF PATIENTS WITH ACUTE

CEREBRAL CIRCULATION DISORDERS"

Recommendations "Principles of diagnosis and treatment of patients with acute cerebrovascular accident" were compiled by the staff of the Research Institute of Neurology of the Russian Academy of Medical Sciences - leading experts in the problems of emergency angioneurology.

The recommendations contain comprehensive information on the diagnosis and management of patients with stroke at all stages of treatment, and also consider the main areas of secondary prevention. The approach used by the authors to the presentation of the material, taking into account the pathogenetic features of various forms and subtypes of stroke, made it possible to develop the optimal tactics of the treatment and diagnostic process, which meets international standards.

The recommendations also present the main criteria for determining the pathogenetic subtypes of ischemic cerebrovascular accidents, the timely diagnosis of which is an indispensable condition not only for adequate therapy, but also the basis for successful prevention of recurrent stroke.

"Principles of diagnosis and treatment of patients with acute disorders of cerebral circulation" should be published in the form of methodological recommendations for subsequent immediate wide distribution among both neurologists and physicians of therapeutic departments who supervise patients with stroke.

Head of the Department of Neurology

Educational - scientific medical center

Office of the President of the Russian Federation

doctor of medical sciences, professor

V.I.SHMYREV

The guidelines were prepared by the Research Institute of Neurology of the Russian Academy of Medical Sciences (RAMS Academician Professor N.V. Vereshchagin, Professors Z.A. Suslina, M.A. Piradov, Candidate of Medical Sciences L.A. Geraskina), Corresponding Member of the Russian Academy of Medical Sciences Professor N.N. .Yakhno, Candidate of Medical Sciences V.A. Valenkova, with the participation of the departments of the Russian State Medical University (Professors V.I. Skvortsova, A.I. Fedin), Moscow State Medical and Dental University of the Ministry of Health of Russia (Professor I.D. Stulin) , Moscow Research Institute of Emergency Medicine named after N.V. Sklifosovsky (Professor V.V. Krylov).

Reviewers: Corresponding Member of the Russian Academy of Medical Sciences Professor A.A. Skoromets -

Head of the Department of Neurology and Neurosurgery

St. Petersburg State

I.P. Pavlov Medical University;

Doctor of Medical Sciences Professor V.I. Shmyrev -

Head of the Department of Neurology, Educational and Scientific

Medical Center of the Office of the President

RF.

Acute cerebrovascular accidents (ACC) are the most important medical and social problem. The incidence of stroke is 2.5 - 3 cases per 1000 population per year, mortality - 1 case per 1000 population per year. Mortality in the acute period of stroke in Russia reaches 35%, increasing by 12-15% by the end of the first year after a stroke. Post-stroke disability ranks first among all causes of disability and is 3.2 per 10,000 population. 20% of stroke survivors return to work, while one third of those with stroke are people of working age. Thus, in Russia, stroke develops annually in 400-450 thousand people, approximately 200 thousand of them die. More than 1 million stroke survivors live in the country, and 80% of them are disabled.

Despite the fact that primary prevention plays a decisive role in reducing mortality and disability due to stroke, a significant effect in this regard is the optimization of the system of care for patients with stroke, the introduction of therapeutic and diagnostic standards for these patients, including rehabilitation measures and prevention of recurrent strokes.

The European Regional Office of the World Health Organization (WHO) believes that the creation of a modern system of care for patients with stroke will reduce mortality during the first month of the disease to the level of 20% and ensure independence in everyday life 3 months after the onset of the disease for at least 70% of surviving patients.

The development and implementation of common principles for the management of patients with acute cerebrovascular accident should help optimize the diagnostic approach and the choice of therapeutic measures to ensure the best outcome of the disease.

I. DIAGNOSIS CRITERIA FOR CERTAIN CVA

Stroke includes acute disorders of cerebral circulation, characterized by a sudden (within minutes, less often - hours) appearance of focal neurological symptoms (motor, speech, sensory, coordinating, visual, and other disorders) and / or cerebral disorders (changes in consciousness, headache, vomiting, etc.), which persist for more than 24 hours or lead to the death of the patient in a shorter period of time due to a cause of cerebrovascular origin.

Stroke is divided into hemorrhagic and ischemic (cerebral infarction). A small stroke is distinguished, in which the impaired functions are completely restored during the first 3 weeks of the disease. However, such relatively mild cases occur only in 10-15% of stroke patients.

Transient cerebrovascular accidents (TIMC) are characterized by a sudden onset of focal neurological symptoms that develop in a patient with a vascular disease (arterial hypertension, coronary artery disease, rheumatism, etc.) and last several minutes, less often hours, but no more than a day and end with a complete restoration of impaired functions. Transient neurological disorders with focal symptoms, which developed as a result of short-term local ischemia of the brain, are also referred to as transient ischemic attacks (TIA). A special form of PNMK is acute hypertensive encephalopathy. More often, acute hypertensive encephalopathy develops in patients with malignant arterial hypertension and is clinically manifested by a severe headache, nausea, vomiting, impaired consciousness, convulsive syndrome, in some cases accompanied by focal neurological symptoms.

The appearance of a TIA or a small stroke indicates a high risk of recurrent and, as a rule, more severe stroke (since the pathogenetic mechanisms of these conditions are largely similar) and requires prevention of recurrent stroke.

II. STAGE MANAGEMENT OF PATIENTS WITH CVA

Basic principles of organization of medical care for stroke.

I. Diagnosis of stroke at the prehospital stage.

II. The earliest possible hospitalization of all patients with stroke.

III. Diagnosis of the nature of a stroke.

IV. Clarification of the pathogenetic subtype of stroke.

V. The choice of optimal treatment tactics.

VI. Rehabilitation and activities for secondary prevention of stroke.

III. ACTIVITIES AT THE PRE-HOSPITAL STAGE

Main goals:

1. Diagnosis of stroke.

2. Carrying out a complex of urgent therapeutic measures.

3. The implementation of emergency hospitalization of the patient.

Assistance is provided by linear or specialized neurological ambulance teams.

1. CVA is diagnosed with the sudden appearance of focal and / or cerebral neurological symptoms in a patient with a general vascular disease and in the absence of other causes (trauma, infection, etc.)

2. Urgent therapeutic measures are determined by the need to ensure sufficient lung ventilation and oxygenation, maintain the stability of systemic hemodynamics, and relieve convulsive syndrome.

Assessment: the number and rhythm of respiratory movements, the state of visible mucous and nail beds, participation in the act of breathing of auxiliary muscles, swelling of the cervical veins.

Measures: if necessary - cleansing the upper respiratory tract, setting up an air duct, and if indicated (tachypnea 35-40 per 1 minute, increasing cyanosis, arterial dystonia) - transferring the patient to artificial lung ventilation (ALV). Manual breathing apparatuses (ADR-2, Ambu type), apparatuses with automatic drive are used.

2.2. Maintaining an optimal level of systemic arterial pressure.

Emergency parenteral administration of antihypertensive drugs should be avoided if systolic BP does not exceed 200 mm Hg, diastolic BP does not exceed 120 mm Hg, and the calculated mean BP does not exceed 130 mm Hg. (mean BP = (systolic BP - diastolic BP) : 3 + diastolic BP). Reduce blood pressure should not be more than 15-20% of the original values. It is preferable to use drugs that do not affect the autoregulation of cerebral vessels - alpha - beta - blockers, beta - blockers, angiotensin-converting enzyme (ACE) inhibitors.

In case of arterial hypotension, the use of drugs that have a vasopressor effect (alpha-agonists), drugs that improve myocardial contractility (cardiac glycosides), volume-replacing agents (dextrans, plasma, saline solutions) is recommended.

2.3. Relief of convulsive syndrome (anticonvulsants - tranquilizers, neuroleptics; if necessary - muscle relaxants, inhalation anesthesia).

3. Stroke is a medical emergency, so all patients with stroke should be hospitalized.

The time of hospitalization should be minimal from the onset of development of focal neurological symptoms, preferably within the first 3 hours from the onset of the disease.

A contraindication for hospitalization of a patient with stroke is only an agonal state.

IV. ACTIONS AT THE HOSPITAL STAGE

IV.1. Organizational events

Hospitalization of patients with stroke is carried out in a multidisciplinary hospital that has the necessary X-ray - radiological (including computed tomography (CT), magnetic resonance imaging (MRI), angiography) and ultrasound equipment, as well as:

a) a department for patients with cerebral circulation disorders with an intensive care unit;

b) a neuro intensive care unit or an intensive care unit with specially allocated beds and trained personnel for the management of patients with stroke;

c) department of neurosurgery.

Patients who have:

Altered level of wakefulness (from mild stupor to coma);

Breathing and swallowing disorders;

Severe violations of homeostasis;

Decompensation of cardiac, renal, hepatic, endocrine and other functions against the background of stroke.

Patients with stroke who do not require emergency resuscitation and neurosurgical care are hospitalized in the department for patients with cerebral circulation disorders. At the same time, patients are admitted to the intensive care unit:

With unstable (progressive) neurological symptoms ("stroke in development");

With a pronounced neurological deficit, requiring intensive individual care;

With additional somatic disorders.

IV.2. Diagnostic measures

IV.2.1. STAGE OF HOSPITAL DIAGNOSIS

The goal is to confirm the diagnosis of stroke and determine its nature (ischemic, hemorrhagic).

Requirements:

1. Assistance to patients with stroke is provided by a neurologist, resuscitator, therapist and neurosurgeon.

2. Patients with stroke should have the right of priority instrumental and laboratory examination so that the diagnostic process is as complete and fast as possible (within an hour from the moment of hospitalization).

3. For patients with TIA, diagnostic examinations are also carried out in a hospital and in the same volume as for patients with stroke.

All patients with a presumptive diagnosis of stroke are shown to have computed tomography (CT) of the head, which in most cases allows distinguishing hemorrhagic stroke from ischemic stroke and excluding other diseases (tumors, inflammatory diseases, CNS injuries). Magnetic resonance imaging (MRI) of the head is a more sensitive method for diagnosing cerebral infarction at an early stage. However, it is inferior to CT in detecting acute hemorrhages, therefore it is less suitable for emergency diagnosis.

In the case when CT or MRI is not available, echoencephaloscopy (M-ECHO) is mandatory, in the absence of contraindications - lumbar puncture and CSF examination.

Lumbar puncture is contraindicated in inflammatory changes in the lumbar region and in case of suspected intracranial volumetric process (risk of dislocation disorders).

MAIN DIAGNOSTIC MEASURES FOR PATIENTS WITH CVA

(regardless of the nature of the stroke)

1. Clinical blood test with platelet count, hematocrit.

2. Blood type, Rh factor.

3. Blood test for HIV.

4. Blood test for HBs antigen.

5. Wasserman reaction.

6. Biochemical blood test: sugar, urea, creatinine, bilirubin, ACT, ALT, cholesterol, triglycerides, high and low density lipoproteins.

7. Electrolytes (potassium, sodium), plasma osmolality.

8. Gas composition of blood, acid-base balance.

9. Screening - study of the hemostasis system: fibrinogen, fibrinolytic activity (euglobulin lysis), thrombin time, activated partial thrombin time (APTT), prothrombin test with calculation of international normalized ratio (MHO), blood clotting time, bleeding time, D - dimer, platelet aggregability (adrenaline-, ADP-, collagen-induced), blood viscosity.

10. Clinical urinalysis.

11. ECG.

12. X-ray of the chest.

13. X-ray of the skull.

14. Consultation of a therapist.

15. Consultation with an ophthalmologist.

Additional diagnostic measures (according to indications)

1. Glycemic profile.

2. Glucosuric profile.

3. Consultation with an endocrinologist.

4. EEG (in the presence of a convulsive syndrome).

5. Study of markers of intravascular activation of the hemostasis system: fragments of prothrombin I+II, thrombin-antithrombin complex (TAT) and protein C system, fibrin-peptide A, soluble complexes of fibrin-monomer, D-dimer, plasmin-antiplasmin complex (PAP).

6. Assessment of intravascular platelet aggregation: platelet factor 4, thromboxane B2, beta thrombomodulin.

Result: verification of the diagnosis of stroke and the nature of the stroke (ischemic, hemorrhagic).

IV.2.2. STAGE "IN-DEPTH" HOSPITAL DIAGNOSIS is a direct continuation of the previous stage.

PURPOSE: clarification of the pathogenetic subtype of stroke:

A. Ischemic stroke:

Atherothrombotic (includes stroke due to arterio - arterial embolism);

Cardioembolic;

hemodynamic;

Lacunar;

Stroke by the type of hemorheological microocclusion.

B. Hemorrhagic stroke:

Non-traumatic subarachnoid hemorrhage (hypertensive, aneurysm rupture);

Parenchymal hemorrhage;

Hemorrhage in the cerebellum;

Subarachnoid - parenchymal;

Ventricular hemorrhage;

Parnchymal-ventricular.

A. ISCHEMIC STROKE.

Compulsory examinations (conducted within an hour from the moment of hospitalization):

1. Ultrasound examination of extra- and intracranial vessels, including duplex scanning.

2. Emergency cerebral angiography - performed only in cases where it is necessary to make a decision on drug thrombolysis.

3. Echocardiography.

Additional studies (conducted during the first 1 - 3 days):

1. Planned cerebral angiography:

It is carried out to clarify the cause of ischemic stroke,

The scope of the study includes angiography of the branches of the aortic arch, the main arteries of the head, intracranial vessels.

2. Holter ECG monitoring.

3. Daily monitoring of blood pressure.

Special studies are carried out if there are indications during the acute period of the disease, their types and volume are determined by a council with the participation of relevant specialists - a hematologist, a cardiologist - a rheumatologist, etc.

Result: clarification of the leading mechanism for the development of stroke and the pathogenetic subtype of ischemic stroke, the choice of tactics for managing the patient, including the decision on the need for surgical correction.

B. HEMORRHAGIC STROKE.

Purpose: clarification of the pathogenetic basis of hemorrhage (hypertensive, due to aneurysm rupture or arteriovenous malformation)

Diagnostic measures:

1. Cerebral angiography:

1.1 Indications:

Subarachnoid hemorrhage;

Atypical localization of intracerebral hematoma (according to CT, MRI);

Ventricular hemorrhage.

1.2 Scope of study: bilateral carotid and vertebral angiography.

2. Transcranial dopplerography - to identify and assess the severity of cerebral vasospasm, its dynamics during treatment.

Emergency consultation of a neurosurgeon is indicated:

1. Hemorrhagic stroke:

a) supra- and subtentorial hematoma;

b) subarachnoid hemorrhage.

2. Cerebellar infarction.

3. The presence of acute obstructive hydrocephalus.

A scheduled consultation with a neurosurgeon and/or a vascular surgeon is indicated for ischemic stroke, MI in the presence of hemodynamically significant stenosis, occlusion of the main arteries of the head, tortuosity of the arteries of the neck, stenosis/occlusion of the cerebral arteries.

Indications for surgical treatment of patients with stroke.

A. Hemorrhagic stroke.

1. Intracerebral hemispheric hemorrhages with a volume of more than 40 ml (according to CT of the head).

2. Hemorrhage in the cerebellum.

3. Obstructive hydrocephalus.

B. Aneurysms, arterio - venous malformations, arterio - sinus fistulas, accompanied by various forms of intracranial hemorrhage and / or cerebral ischemia.

B. Ischemic stroke.

1. Cerebellar infarction with severe secondary stem syndrome, deformity of the brain stem (according to CT/MRI of the head), obstructive hydrocephalus.

IV.3. Management of patients with various forms of stroke (see Appendix III)

General principles for the treatment of patients with stroke include basic therapy (regardless of the nature of stroke) and differentiated therapy, taking into account the nature and pathogenetic subtype of stroke.

IV.3.1. Activities of basic therapy for stroke

1. Measures aimed at normalizing the function of external respiration and oxygenation (rehabilitation of the respiratory tract, installation of an air duct, tracheal intubation, if necessary, mechanical ventilation).

2. Regulation of the function of the cardiovascular system:

a) maintenance of blood pressure by 10% above the numbers to which the patient is adapted (when conducting antihypertensive therapy, beta-blockers, ACE inhibitors, calcium channel blockers are preferred, with arterial hypotension - agents that have a vasopressor effect (dopamine, alpha-adrenergic agonists) and volume-replacing therapy (dextrans, single group fresh frozen plasma);

b) antiarrhythmic therapy for cardiac arrhythmias;

c) with IHD (post-infarction cardiosclerosis, angina pectoris) - antianginal drugs (nitrates);

d) drugs that improve the pumping function of the myocardium - cardiac glycosides, antioxidants, optimizers of tissue energy metabolism.

3. Control and regulation of homeostasis, including biochemical constants (sugar, urea, creatinine, etc.), water-salt and acid-base balance.

4. Neuroprotection - a complex of universal methods for protecting the brain from structural damage - begins at the prehospital stage (may have some features in various subtypes of stroke).

5. Measures aimed at reducing cerebral edema (they have features depending on the nature of the stroke).

6. Measures for the prevention and treatment of somatic complications: pneumonia, bedsores, uroinfection, DIC, phlebothrombosis and pulmonary embolism, contractures, etc.

7. Symptomatic therapy, including anticonvulsant, psychotropic (with psychomotor agitation), muscle relaxants, analgesics, etc.

IV.3.2. General principles of pathogenetic treatment for ischemic stroke

The modern strategy for the treatment of patients with ischemic stroke is based on the early diagnosis of the pathogenetic subtype of stroke.

The main principles of pathogenetic treatment of ischemic stroke include:

1) restoration of blood flow in the ischemic zone (recirculation, reperfusion).

2) maintaining the metabolism of the brain tissue and protecting it from structural damage (neuroprotection).

Basic recycling methods

1. Restoration and maintenance of systemic hemodynamics.

2. Drug thrombolysis (recombinant tissue plasminogen activator, alteplase, urokinase).

3. Hemangiocorrection - normalization of the rheological properties of blood and the functionality of the vascular wall:

a) antiplatelet agents, anticoagulants, vasoactive agents, angioprotectors;

b) extracorporeal methods (hemosorption, ultrahemofiltration, laser blood irradiation);

c) gravitational methods (cyt-, plasmapheresis).

4. Surgical methods of recirculation: extra-intracranial microanastomosis, thrombectomy, reconstructive operations on arteries.

Basic methods of neuroprotection

1. Restoration and maintenance of homeostasis.

2. Drug protection of the brain.

3. Non-drug methods: hyperbaric oxygen therapy, cerebral hypothermia.

Antiedematous therapy for ischemic stroke

1. Osmotic diuretics (under the control of plasma osmolality).

2. Hyperventilation.

3. An additional anti-edematous effect is provided by the use of neuroprotectors, maintaining homeostasis.

4. With the development of occlusive hydrocephalus in cerebellar infarction, surgical treatment is performed according to indications (decompression of the posterior cranial fossa, ventricular drainage).

IV.3.2.1. Features of the treatment of various pathogenetic subtypes of ischemic stroke

When verifying a stroke due to obstruction of the afferent artery (atherothrombotic, including due to arterio-arterial embolism, cardioembolic infarction) upon admission of the patient in the first 3-6 hours from the onset of the disease and no changes in CT examination of the head (hemorrhagic changes, mass effect) , with stable blood pressure not higher than 185/100 mm Hg. it is possible to carry out drug thrombolysis: recombinant tissue plasminogen activator (rt-PA) at a dose of 0.9-1.1 mg/kg of the patient's weight, 10% of the drug is administered intravenously as a bolus (when the intra-arterial catheter is standing - in/a), the remaining dose - in / in drip for 60 minutes). However, the need for a highly specialized preliminary examination of a potential recipient, including CT of the head, angiography, and a significant risk of hemorrhagic complications of thrombolytic therapy currently do not allow recommending this treatment method for widespread use and force it to be limited to specialized angioneurological centers.

1. CARDIOEMBOLIC STROKE:

a) anticoagulants - direct action in the acute period, followed by a transition to long-term maintenance therapy with indirect anticoagulants;

b) antiaggregants;

c) neuroprotectors;

d) vasoactive drugs;

e) adequate treatment of cardiac pathology (antiarrhythmic drugs, antianginal drugs, cardiac glycosides, etc.).

2. ATHEROTROMBOTIC STROKE:

a) antiplatelet agents (platelet, erythrocyte);

b) with a progressive course of the disease (increasing thrombosis), direct-acting anticoagulants are indicated with a transition to indirect ones;

c) hemodilution (low molecular weight dextrans, single group fresh frozen plasma);

d) angioprotectors;

e) neuroprotectors.

3. HEMODYNAMIC STROKE:

a) restoration and maintenance of systemic hemodynamics:

Preparations of vasopressor action, as well as - improving the pumping function of the myocardium;

Volume-substituting agents, mainly biorheological preparations (plasma), low molecular weight dextrans;

With myocardial ischemia - antianginal drugs (nitrates);

With dysrhythmia - antiarrhythmics, with conduction disorders (bradyarrhythmias) - implantation of a pacemaker (temporary or permanent);

b) antiaggregants;

c) vasoactive drugs (taking into account the state of systemic hemodynamics, blood pressure, cardiac output, the presence of dysrhythmias);

d) neuroprotectors.

4. LACUNARY STROKE:

a) the basis is the optimization of blood pressure (ACE inhibitors, angiotensin II receptor antagonists, beta-blockers, calcium channel blockers);

b) antiaggregants (platelet, erythrocyte);

c) vasoactive agents;

d) antioxidants.

5. STROKE BY THE TYPE OF HEMOROHEOLOGICAL MICROOCCLUSION:

a) hemangiocorrectors of various groups (antiplatelet agents, angioprotectors, vasoactive drugs, low molecular weight dextrans);

b) with insufficient efficiency, the development of DIC - the use of direct anticoagulants, and then - and indirect action;

c) vasoactive drugs;

d) antioxidants.

6. ACUTE HYPERTENSION ENCEPHALOPATHY:

a) a gradual decrease in blood pressure by 10-15% of the initial level (preferably the use of easily dosed ACE inhibitors, alpha - beta - blockers, beta - blockers, the use of vasodilating drugs is contraindicated);

b) dehydrating therapy (saluretics, osmotic diuretics);

c) hyperventilation;

d) neuroprotectors;

e) angioprotectors;

f) hemangiocorrectors (mainly biorheological preparations - plasma, low molecular weight dextrans);

g) symptomatic treatment (anticonvulsants, antiemetics, analgesics, etc.).

IV.3.3. General principles for the treatment of hemorrhagic stroke

Basics of basic therapy for hemorrhagic stroke have some features.

1. Regulation of the function of the cardiovascular system:

a) in hypertensive hemorrhages, optimization of blood pressure is of pathogenetic importance;

b) in some cases, patients need long-term controlled arterial hypotension. The drug of choice for this treatment is sodium nitroprusside, which is administered through an infusion pump with continuous monitoring of blood pressure.

2. Measures aimed at reducing cerebral edema:

a) the use of membrane stabilizers (dexazone 4-8 mg intramuscularly 4 times a day);

b) hyperventilation;

c) the use of neuroprotectors;

d) restoration and maintenance of homeostasis;

e) surgical methods - hematoma removal, ventricular drainage, decompression.

3. Neuroprotection (see Ischemic stroke).

4. Measures for the prevention and treatment of somatic complications: DIC - syndrome, phlebothrombosis and pulmonary embolism (use of hemangiocorrectors - antiplatelet agents, anticoagulants, low molecular weight dextrans). The decision on their appointment should be made by a council with the participation of a therapist - a hematologist.

Pathogenetic treatment of hemorrhagic stroke (conservative)

1. The use of angioprotective agents that help strengthen the vascular wall.

2. With subarachnoid hemorrhage and intracerebral hematomas with a breakthrough of blood into the cerebrospinal fluid system - prevention of vascular spasm (vasoselective calcium channel blockers - nimodipine up to 25 mg / day. IV drip or 0.3-0.6 every 4 hours inside; vasoactive drugs).

3. To improve microcirculation and prevent secondary ischemic lesions of the brain tissue, low molecular weight dextrans, antiplatelet agents are used in conditions of continuous monitoring of blood pressure, parameters of the hemostasis system.

V. Rehabilitation of patients with stroke

V.1. The main tasks of rehabilitation.

1. Restoration (improvement) of impaired functions.

2. Mental and social readaptation.

3. Prevention of post-stroke complications (spasticity, contractures, etc.).

V.2. Indications and contraindications for rehabilitation.

All patients with stroke require rehabilitation measures.

Contraindications to active rehabilitation are:

1. severe somatic pathology in the stage of decompensation;

2. mental disorders.

V.3. Basic principles of rehabilitation.

The main principles of rehabilitation are: early start, duration and systematic, stages, complexity, active participation of the patient.

The duration of rehabilitation is determined by the timing of the restoration of impaired functions: the maximum improvement in motor functions is noted in the first 6 months, household skills and ability to work - within 1 year, speech functions - over 2-3 years from the moment of stroke.

V.4. Organization of staged care for patients with stroke.

1. Angioneurological department of a multidisciplinary hospital.

2. Department of early rehabilitation of a multidisciplinary hospital:

Patients are transferred, as a rule, 1 month after the onset of a stroke,

A full course of rehabilitation treatment is carried out,

The duration of the course is 1 month.

3. Further treatment is determined by the severity of the neurological defect:

A) in the presence of motor, speech and other disorders, the patient is sent to a rehabilitation center or a rehabilitation sanatorium;

B) in the absence of severe neurological disorders, the patient is sent to a local neurological or cardiovascular sanatorium;

B) Patients with severe residual neurological impairment or who have contraindications for active rehabilitation are discharged home or transferred to a specialized nursing hospital.

4. Patients with moderate severity of residual neurological disorders continue their rehabilitation on an outpatient basis (rehabilitation departments or outpatient clinics).

5. Repeated courses of inpatient rehabilitation are indicated in the ongoing recovery of impaired functions and the prospect of recovery.

VI. Prevention of repeated strokes

The risk of stroke in reversible forms of cerebrovascular pathology (TIA, minor stroke) is high and amounts to at least 5% per year. Prevention of repeated stroke should be carried out taking into account the pathogenetic mechanisms of their development.

If a cardiogenic embolism turned out to be the cause of a TIA or a small stroke, in addition to correcting (medical, surgical) cardiac pathology, indirect anticoagulants or antiplatelet agents are indicated. In the case of a small deep (lacunar) infarction pathogenetically associated with hypertension, the main direction in preventing recurrent stroke is to conduct adequate antihypertensive therapy.

It is more difficult to prevent stroke in patients with atherosclerotic changes in the carotid arteries (atherothrombotic, hemodynamic stroke, as well as due to arterio-arterial embolism). The significance of the pathology of the carotid artery for a particular patient is determined by the individual characteristics of the structure of the vascular system of the brain, the severity and prevalence of its damage, as well as the structure of atherosclerotic plaques.

Currently, in patients with TIA and a small stroke in the pathology of the carotid arteries, two directions for preventing stroke are generally recognized:

1. the use of antiplatelet agents;

2. angiosurgical operation: elimination of carotid artery stenosis, if there are contraindications to it, cranio-cerebral bypass can be performed.

Prescribing antiplatelet agents to patients who have had a TIA or a minor stroke reduces their risk of developing a second stroke by 20-25%. In the case of significant stenosis of the carotid artery (more than 70% of the lumen of the vessel) on the side of the affected hemisphere of the brain, carotid endarterectomy as a means of preventing recurrent stroke is much more effective than the use of antiplatelet agents. A prerequisite is the operation in a specialized clinic, in which the level of complications associated with the operation does not exceed 3-5%. With carotid stenosis up to 30%, drug prevention is preferred. Surgery may become necessary if a complicated medium-sized plaque becomes a source of recurrent cerebral embolism.

Prevention of recurrent stroke in patients with hemorrhagic stroke is:

1. in patients with arterial hypertension - in conducting adequate antihypertensive therapy;

2. in patients with hemorrhage due to rupture of an arterial aneurysm or arteriovenous malformation - in an angiosurgical operation.

APPS

APPENDIX I. Classification of stroke according to ICD-10

G45 TRANSIENT CEREBRAL ISCHEMIC

SEIZURES (ATTACKS) AND RELATED SYNDROMES

G45.0 Syndrome of vertebrobasilar arterial system

G45.1 Carotid artery syndrome (hemispheric)

G45.2 Multiple and bilateral syndromes of cerebral

Arteries

G45.3 Transient blindness

G45.4 Transient global amnesia

G45.8 Other transient cerebral ischemic attacks and

Associated Syndromes

G45.9 Transient cerebral ischemic attack

unspecified

G46<*>VASCULAR BRAIN SYNDROMES IN CEREBROVASCULAR

DISEASES (I60 - I67+)

G46.0<*>Middle cerebral artery syndrome (I66.0+)

G46.1<*>Anterior cerebral artery syndrome (I66.1+)

G46.2<*>Posterior cerebral artery syndrome (I66.2+)

G46.3 Stroke syndrome in brainstem (I60-I67+)

Syndrome:

Benedict

Claude

Fauville

Miyara - Jublé

Wallenberg

Weber

G46.4<*>Cerebellar stroke syndrome (I60 - I67+)

G46.5<*>Pure motor lacunar syndrome (I60 - I67+)

G46.6<*>Purely sensitive lacunar syndrome (I60 - I67+)

G46.7<*>Other lacunar syndromes (I60 - I67+)

G46.8<*>Other cerebrovascular syndromes

Cerebrovascular diseases (I60 - I67+)

CEREBROVASCULAR DISEASES (I60-I69)

I60 Subarachnoid hemorrhage

I60.0 Subarachnoid haemorrhage from carotid sinus and

Bifurcations of the internal carotid artery

I60.1 Subarachnoid hemorrhage from middle cerebral

arteries

I60.2 Subarachnoid haemorrhage from anterior

Connecting artery

I60.3 Subarachnoid haemorrhage from posterior

Connecting artery

I60.4 Subarachnoid haemorrhage from basilar artery

I60.5 Subarachnoid haemorrhage from vertebral artery

I60.6 Subarachnoid haemorrhage from other

intracranial arteries

I60.7 Subarachnoid hemorrhage from intracranial

Artery, unspecified

I60.8 Other subarachnoid haemorrhage

I60.9 Subarachnoid hemorrhage, unspecified

I61 Intracerebral hemorrhage

I61.0 Intracerebral haemorrhage in hemisphere

subcortical

I61.1 Intracerebral hemorrhage in cortical hemisphere

I61.2 Intracerebral hemorrhage, unspecified

I61.3 Intracerebral hemorrhage in brainstem

I61.4 Intracerebral hemorrhage in cerebellum

I61.5 Intracerebral hemorrhage, intraventricular

I61.6 Multiple intracerebral hemorrhage

I61.8 Other intracerebral haemorrhage

I61.9 Intracerebral hemorrhage, unspecified

I62 Other non-traumatic intracranial hemorrhage

I62.0 Subdural hemorrhage (acute) (non-traumatic)

I62.1 Non-traumatic extradural hemorrhage

I62.2 Intracranial hemorrhage (non-traumatic)

Unspecified

I63 Cerebral infarction

I63.0 Cerebral infarction due to precerebral thrombosis

Arteries

I63.1 Cerebral infarction due to precerebral embolism

Arteries

I63.2 Cerebral infarction due to obstruction unspecified or

Stenosis of the precerebral arteries

I63.3 Cerebral infarction due to thrombosis of cerebral arteries

I63.4 Cerebral infarction due to cerebral artery embolism

I63.5 Cerebral infarction due to obstruction unspecified or

Stenosis of the cerebral arteries

I63.6 Cerebral infarction due to cerebral vein thrombosis

Non-pyogenic

I63.8 Other cerebral infarction

I63.9 Cerebral infarction, unspecified

I64 Stroke, not specified as haemorrhage or infarction

APPENDIX II. Key criteria for diagnosing the main pathogenetic subtypes of ischemic stroke

I. ATHEROTROMBOTIC STROKE (including arterio - arterial embolism)

1. The onset is often intermittent, step-like, with a gradual increase in symptoms over hours or days. Often debuts during sleep.

2. The presence of atherosclerotic lesions of extra- and / or intracranial arteries (pronounced stenosing, occlusive process, atherosclerotic plaque with an uneven surface, with an adjacent thrombus) corresponding to a focal brain lesion.

3. Often preceded by ipsilateral transient ischemic attacks.

4. The size of the lesion may vary from small to extensive.

II. CARDIOEMBOLIC STROKE

1. Onset - usually the sudden onset of neurological symptoms in an awake, active patient. The neurological deficit is most pronounced at the onset of the disease.

2. Localization - mainly the zone of vascularization of the middle cerebral artery. Heart attack - more often medium or large, cortical - subcortical. The presence of a hemorrhagic component is characteristic (according to head CT).

3. Anamnestic indications and CT signs of multiple focal lesions of the brain (including "silent" cortical infarcts) in various pools that are not areas of adjacent blood supply.

4. The presence of cardiac pathology - the source of embolism.

5. Absence of gross atherosclerotic lesion of the vessel proximal to the blockage of the intracranial artery. Symptom of "disappearing occlusion" during dynamic angiographic examination.

6. History of thromboembolism of other organs.

III. HEMODYNAMIC STROKE

1. The onset is sudden or step-like, both in an active patient and in a resting patient.

2. Localization of the focus - a zone of adjacent blood supply, including cortical infarctions, foci in the periventricular and white matter of the semioval centers. The size of the heart attack - from small to large.

3. The presence of pathology of extra- and / or intracranial arteries:

a) atherosclerotic lesion (multiple, combined, layered stenosis);

b) deformities of the arteries (angular bends, looping);

c) anomalies of the vascular system of the brain (dissociation of the circle of Willis, hypoplasia of the arteries).

4. Hemodynamic factor:

a) decrease in blood pressure (physiological - during sleep, as well as orthostatic, iatrogenic arterial hypotension, hypovolemia);

b) a drop in cardiac output (decrease in stroke volume due to myocardial ischemia, a significant decrease in heart rate).

IV. LACUNARY STROKE

1. Previous arterial hypertension.

2. Onset - more often intermittent, symptoms increase over hours or days. BP is usually elevated.

3. Localization of the infarction - subcortical nuclei, adjacent white matter of the semioval center, internal capsule, base of the brain bridge. The size of the focus is small, up to 1-1.5 cm in diameter, and may not be visualized on head CT.

4. The presence of characteristic neurological syndromes (purely motor, purely sensitive lacunar syndrome, atactic hemiparesis, dysarthria and monoparesis; isolated monoparesis of the arm, leg, facial and other syndromes). The absence of cerebral and meningeal symptoms, as well as violations of higher cortical functions when localized in the dominant hemisphere. The course is often of the type of "small stroke".

V. STROKE BY THE TYPE OF HEMOROHEOLOGICAL MICROOCCLUSION

1. The absence of any vascular disease of established etiology (atherosclerosis, arterial hypertension, vasculitis, vasculopathy, cardiac, coronary pathology).

2. Absence of hematological pathology of established etiology (erythremia, secondary erythrocytosis, coagulopathy, antiphospholipid syndrome).

3. The presence of pronounced hemorheological changes, disturbances in the system of hemostasis and fibrinolysis.

4. Severe dissociation between the clinical picture (moderate neurological deficit, small lesion size) and significant hemorheological disorders.

5. The course of the disease - according to the type of "small stroke".

VI. ACUTE HYPERTENSION ENCEPHALOPATHY

1. More often develops in patients with malignant arterial hypertension.

2. Clinical manifestations: severe headache, nausea, vomiting, impaired consciousness, convulsive syndrome.

3. Ophthalmoscopy reveals edema of the optic disc, angioretinopathy.

4. With CT of the head - expansion of the ventricular system, a decrease in the density of white matter.

5. The presence of increased CSF pressure during lumbar puncture and signs of intracranial CSF hypertension according to echoencephaloscopy.

APPENDIX III. The main drugs used in the treatment of patients with stroke

III.1. Preparations of hemangiocorrective action

1. Antiplatelet agents (under the control of platelet aggregation):

Aspirin 1 mg/kg x day;

Dipyridamole 25-50 mg 3 times a day;

Aspirin 1 mg/kg + dipyridamole 25-50 mg twice a day;

Ticlid (ticlopidine) 250 mg twice a day;

Pentoxifylline 200 mg intravenously 2 times a day or 1200 mg / day orally.

2. Anticoagulants:

a) direct action (under the control of platelet count, antithrombin III level, blood clotting time and APTT, clinical urinalysis to exclude microhematuria):

Fraxiparine 7500 s/to the abdomen 2 times a day;

Heparin 5-10 thousand units 4 times a day s / c of the abdomen or intravenously;

b) indirect action (under the control of the prothrombin test and MHO):

Phenylin at 0.015-0.03 per day;

Warfarin 5-6 mg/day.

3. Vasoactive drugs:

Vinpocetine / Cavinton 10-20 mg IV drip 2 times a day or 5-10 mg 3 times inside;

Nicergoline 4 mg IM or IV drip 2 times a day or 10 mg 3 times inside;

Instenon 2 ml intravenously or intramuscularly;

Euphyllin 2.4%, 10 ml intravenously by stream or drip, into 250 ml of isotonic sodium chloride solution 2 times a day;

Cinnarizine 0.025 2 tablets 3 times a day;

Xanthinol nicotinate 15% 2 ml / m or 0.15 3 times a day.

3. Angioprotectors:

Anginin (parmidin, prodectin) 0.25 1 tab. 3 times a day,

Askorutin 2 tablets. 3 times a day,

Troxevasin 0.3 1 caps. 2 times a day or 5 ml intravenously,

Etamzilat 12.5% ​​2 ml intravenously or intravenously,

Dobesilat 0.25 1 tab. 3 times a day,

Wobenzym 1 tab. 3 times a day.

5. Biorheological preparations:

a) plasma, albumin,

b) low molecular weight dextrans:

Reopoliglyukin (rheomacrodex) 400 ml IV drip 1-2 times a day.

III.2. Neuroprotective drugs.

1. Calcium channel blockers:

Nimodipine (Nimotop) IV drip up to 25 mg/day. through an infusomat or inside at 0.3 - 0.6 every 4 hours - with continuous monitoring of blood pressure, heart rate.

2. Antioxidants:

Emoksipin 25-50 mg/day IV drip in 250 ml isotonic sodium chloride solution 2 times a day,

Mildronate 10% 5-10 ml intravenously by stream or drip in isotonic sodium chloride solution,

Vitamin E 200 mg 2 times a day orally,

Ascorbic acid 5% 6-8 ml IV drip or 0.5-0.8 inside.

3. Preparations of predominantly neurotrophic action:

Piracetam 12 g per day intravenously or orally,

Cerebrolysin 15 - 20 ml IV drip,

Semax 1% 2 drops in each nasal passage 4-6 times a day,

Glycine 0.7 - 1.0 g per day sublingually,

Picamilon 10% 2 ml 2 times a day IM or IV or 0.05 3 times a day inside.

4. Drugs that improve energy tissue metabolism:

Cytochrome C 5 ml IM,

Cyto - poppy 15 mg IV,

Actovegin 10% or 20% 250 ml IV drip or 5 ml IM,

Riboxin 2% 10 ml IV bolus or drip or 0.4 3 times a day inside,

ATP 1%, 2 ml IM,

Aplegin 10 ml per 250 ml isotonic sodium chloride solution IV drip.

To achieve the best effect, it is advisable to use simultaneously the combined use of various groups of neuroprotective, hemangiocorrective agents. The choice of specific drugs is made taking into account the leading pathogenetic mechanism of ischemic stroke.

APPENDIX IV. Rehabilitation activities

IV.A. Basic methods of rehabilitation.

A.1. For movement disorders:

1. Kinesiotherapy, including learning to walk.

2. Household rehabilitation, including training in self-care skills (may be included in the course of kinesiotherapy).

3. Electrical stimulation of the neuromuscular apparatus.

4. The fight against spasticity, including the use of muscle relaxants (sirdalud, baclofen, mydocalm), thermal procedures (paraffin, ozokerite applications), selective or acupressure massage.

5. Prevention of contractures that occur against the background of post-stroke trophic changes in the joints (arthropathies), including heat therapy (paraffin, ozocerite applications), analgesic electrophysiotherapy (SMT, DD currents, TENS, electro- or phonophoresis of medicinal substances).

6. Orthopedic measures: the use of splints, special devices for walking, orthopedic shoes.

A.2. In case of speech disorders - classes with a speech therapist - aphasiologist to restore speech, reading, writing, counting.

A.3. With central post-stroke pain syndrome - the appointment of antidepressants (amitriptyline) and carbamazepine (tegretol, finlepsin) in an individual dosage.

A.4. Neurotrophic drug therapy. It is especially indicated for speech disorders, cognitive disorders, reduced mental and motor activity:

Cerebrolysin 5 ml intramuscularly or 10-15 ml intravenously in drops per 200 ml isotonic sodium chloride solution N 20-30 daily 2-3 times during the first year,

Piracetam 2.4 - 4.8 g per day for several months,

Semax 0.1% 2 drops in each nasal passage 3-6 times a day for 2 months.

A.5. Psychotherapy (elements of psychotherapy are included in kinesiotherapy classes, in the practice of a speech therapist - aphasiologist, neurologist - rehabilitologist).

IV.B. Additional methods of rehabilitation.

B.1. Biofeedback with electrokymogram feedback in hemiparesis.

B.2. Biofeedback with stabilogram feedback for balance and walking disorders.

B.3. Acupuncture and/or electroacupuncture for muscle spasticity and pain syndromes.

B.4. Occupational therapy in specially equipped workshops.

B.5. Psychotherapy conducted by a specialist - a psychotherapist.

Some additional rehabilitation methods can only be used in specialized rehabilitation centers due to their complexity, high cost and lack of the necessary qualified specialists.

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