Stroke stroke

Stroke cerebral is an acute disorder of cerebral circulation.

Etiology, pathogenesis. In most cases, strokes are a complication of hypertension and atherosclerosis, less often they are caused by diseases of the valvular heart apparatus, myocardial infarction, congenital abnormalities of the brain vessels, hemorrhagic syndromes and arteritis. Approximately 90% of patients with stroke have some form of heart damage with symptoms of cardiovascular failure. An exception are only some variants of hemorrhagic strokes, for example, when an aneurysm ruptures in people of young age.

Symptoms, course. Acute cerebral vascular lesions are divided into five groups: 1) transient disorders of cerebral circulation; 2) cerebral infarction; 3) embolism of cerebral vessels; 4) bleeding in the brain; 5) subarachnoid hemorrhage. There is also a so-called small stroke, or a stroke with a reversible neurologic deficit, in which all focal symptoms disappear after 3 weeks.

Transitory disorders of cerebral circulation are acute circulatory disorders, in which focal and general cerebral symptoms last no more than 24 hours. The immediate cause is microembolism of clusters of cholesterol crystals, fragments of atheromatous plaques or conglomerates of platelets. Microemboli, brought by the current of blood into the small vessels of the brain, cause a regional spasm. Less often transient disorders are caused by microhemorrhagia. Dyscirculation in the pool of carotid arteries is manifested by numbness of half of the face, hemiparesis or hemiparesis. Insufficiency of blood flow in the vertebrobasilar system, which occurs much more often, is manifested by dizziness, vomiting and instability in walking, occasionally with focal signs. A frequent variant of transient cerebrovascular disorders is the hypertensive cerebral crisis, in which cerebral and vegetative symptoms predominate: headache, nausea, vomiting, ringing and tinnitus, dizziness, sweating, hyperemia of the face.

The cerebral infarction (thrombosis according to old classifications) is characterized by the presence in the anamnesis of transistor ischemic attacks, the gradual formation of focal signs (for several hours), the preservation of consciousness, the absence or low severity of cerebral symptoms, and the absence of blood in the cerebrospinal fluid.

However, with extensive heart attacks, cerebral symptoms may not be inferior to those with a cerebral hemorrhage. "Flickering" of focal symptoms before the final development of focal prolapse or "stupenoobraznoe" formation of a defect, the presence of noise in auscultation of the carotid artery or a decrease in its pulsation with a high degree of probability indicate extracerebral genesis of ischemia caused by atherosclerotic occlusion of the main vessels of the neck (at least half of all cases of brain Heart attacks). Contrary to the prevailing notions, relatively often cerebral infarction develops against a background of a sharp increase in blood pressure.

Embolism of cerebral vessels is characterized by apoplectiform development of a stroke, often loss of consciousness and the presence in most patients of rheumatic mitral disease, less recently, a recent myocardial infarction or prolapse of the mitral valve (echocardiography). "Paradoxical embolism" is an insult in case of congenital noninvasion of the interatrial septum, which causes emboli from the thrombosed veins of the lower extremities to enter the cerebral vessels. Infarction, resulting from embolism of the cerebral vessel, can be both ischemic and hemorrhagic in nature and varies widely in size. In some patients with embolic stroke, there is a stage of precursors ("stroke in progress"): in a few hours (less often days) there are local or diffuse headaches, and sometimes transient focal symptoms. In 5-10% of patients, repeated embolism, including other organs, is noted. In connection with this circumstance, the question arises of surgical correction of the defect and the removal of thrombotic masses from the cavities of the heart in each case of stroke in rheumatic heart disease.

Hemorrhage in the brain in typical cases is characterized by apoplectiform emergence of focal symptoms, the development of a coma and the impurity of blood to the cerebrospinal fluid. As a rule, cerebral hemorrhage occurs in patients with arterial hypertension; Isolated atherosclerosis without elevated blood pressure - a rare cause of hemorrhage. In some cases, the focus of hemorrhage is limited and does not communicate with either the ventricular system or the subsatellite space. In this situation, cerebrospinal fluid with a lumbar puncture does not contain blood. If, in addition, the hemorrhagic focus is small, the cerebral symptoms are not expressed and the clinical picture of the stroke repeats the picture of ischemic brain lesions. A serious complication of hemispheric hemorrhages is the development of tentorial cerebral hernias: an increase in the volume of the affected hemisphere due to edema or effusion leads to the fact that the medial parts of the temporal lobe are wedged into the incision of the cerebellar medulla and infringe the middle brain. An indicator of this complication is the appearance of oculomotor disorders in the patient with a coma (strabismus, ptosis, mydriasis). Hemorrhage in the cerebellum can cause compression of the medulla oblongata due to the displacement of the cerebellar tonsils into the large occipital orifice.

Subarachnoid hemorrhage usually (80% of cases) is caused by rupture of intracranial aneurysms, usually located in the region of the arterial circle of the large brain (the vilizian circle), less often they are caused by hypertension, hemorrhagic syndromes. In the clinical picture of such strokes, the paroxysmal symptomatic complex of stimulation of the meninges predominates: headache, vomiting, neck stiffness, Kernig symptom, and often psychomotor agitation. Sometimes there is a convulsive attack. On the 2-3rd day of the disease, the temperature rises. The basal location of the aneurysms, the main source of bleeding, explains the frequent damage to the cranial nerves, often oculomotor nerves. The consciousness is often broken. Approximately 1/3 of patients develop a spasm of individual intracranial vessels (usually on the 2nd-3rd day of the disease). A persistent vasospasm leads to ischemic foci of softening, in particular in the brainstem. In the first hours of hemorrhage on the fundus, hemorrhages in the retina or stagnant discs can be detected. Many cases of sheath hemorrhage proceed with a sharp increase in blood pressure, caused by stimulation of blood stem stem vegetative centers. This also explains the discirculation in the coronary vessels, usually leading to changes in the ECG. Demonstrativeness of the acute development of meningeal syndrome in combination with an intense admixture of blood in the cerebrospinal fluid makes the diagnosis of a hemorrhage one of the simplest among other forms of stroke. Equally, bloody cerebrospinal fluid makes it easy to distinguish hemorrhage from meningitis. The admixture of "pathway" blood in the cerebrospinal fluid during puncture can in most cases be correctly recognized on the basis of its clarification in the second and third test tubes and the absence of xanthochromia after centrifugation. Against the assumption of a random admixture of blood is indicated by the detection of macrophages (erythrophages) in the cerebrospinal fluid. Erythrocytes are found and fluid within 7-10 days after a stroke, and xanthochromy is kept up to the saloon.

Studies of blood and urine in the acute stage of stroke are mandatory. However, only the detection of significant leukocytosis on the first day of stroke can serve as an indirect sign of hemorrhage. Chest x-ray is very important for detecting left ventricular hypertrophy of the heart as an indicator of long-term arterial hypertension. A craniographic study is also very desirable, since with a fall at the time of an insult a patient can get a serious craniocerebral injury. It is necessary to consider as a rule the investigation of cerebrospinal fluid in all patients with acute impairment of cerebral circulation, admitted to the hospital. Contraindications to puncture in the acute stage of stroke occur relatively infrequently. From lumbar puncture should be abandoned with the agonal state, non-curable left ventricular failure with pulmonary edema and signs of cerebral hernia. Rapid reduction in pressure of cerebrospinal fluid as it is removed can serve as an indication of the tamponation of the large occipital opening by the shifting tonsils of the cerebellum. In such a situation, the liquid must be discontinued immediately. None of the modern methods of assessing hemocoagulation (including prothrombin index and developed coagulogram) does not provide any information about the nature of the stroke.

Differential diagnosis of cerebral stroke often requires the exclusion of inflammatory or neoplastic lesions of the brain. With the acute development of the shell syndrome, the detection of blood in the cerebrospinal fluid can confidently distinguish the hemorrhage from meningitis. One should only keep in mind the possibility of obtaining bloody fluid and with meningococcal meningitis, but the cytogram differs sharply and in these cases (thousands of neutrophils in meningitis). The cerebral hemorrhage flows in a stroke, but usually it is possible to find out with a brain tumor that the acute period was preceded by an increasing headache and focal symptoms. Particularly complex are cases of subacute (sometimes within a few days) development of a stroke. A significant help in diagnosis is the degree of displacement of the median structures on the echoencephalogram: the extreme degrees of displacement, as a rule, are typical for volumetric processes. The decisive role in all doubtful cases is computed tomography.

Treatment. Hospital conditions dramatically expand the range of therapeutic possibilities and provide constant monitoring of the patient's condition, therefore, most patients with cerebral stroke should be admitted to the hospital. Contraindications to transportation to the hospital are gross violations of breathing and cardiovascular activity, as well as pre-conditioning. It is inappropriate to send to the hospital elderly people with severe age-related somatic changes and signs of marasmus.

It is often impossible to establish the nature of a stroke in the first hours of the illness, so treatment should focus on normalizing breathing, cardiovascular activity, homeostasis and the prevention of pneumonia, thromboembolism, and pressure ulcers. Drug stimulation of the respiratory center in cerebral stroke is impractical; Lobelia and quotation because of their inefficiency and side effects do not apply. To compensate for cardiac activity, enter / in (slowly!) Strophanthin or other cardiac glycosides; Sulphocamphocaine, cordiamine. In the case of lung edema, diuretics are added: furosemide, ethacrynic acid (uretit), mannitol, and euphyllin. Increased blood pressure should be reduced to the usual numbers for the patient, and not to the standard values ​​of the norm. For rapid reduction in blood pressure, parenterally administered clonidine, reserpine (rausedil), diuretics (furosemide, ureitis), antipsychotics, dibazole and ganglion blockers are most effective. Papaverine, no-shpa, halidor, even with parenteral administration, have no significant hypotensive effect, as well as magnesium sulfate. In acute hypotonic reaction (collapse), hypertensive agents and intravenous fluid or drip fluid administration are used. An important place in the treatment of stroke is the fight against brain edema. All diuretic agents (furosemide, ureitis, euphyllin), hyperosmolar solutions, primarily a 20% mannitol solution, have a pronounced anti-edema effect. Dexamethasone IV in the 16 to 24 mg / day (in the absence of hypertension and diabetes). A powerful effect has the inside (or inserted through the probe) glycerin, a single dose of which is determined at a rate of 1 g / kg. Bloodletting during a cerebral crisis or stroke is excluded from medical practice.

From the first days with severe strokes, antibiotics should be prescribed to prevent pneumonia. In hyperthermia, a bubble with cold water or ice is used, etc. In cases of severe psychomotor agitation, parenteral administration of diazepam (seduxen) or sodium oxybutyrate (GHB) is most appropriate. To stop vomiting and hiccups are shown neuroleptics, antihistamines and cerucal. With the development of cardiovascular failure and associated circulatory disorders, most drugs must be administered intravenously, and not subcutaneously or intramuscularly. An important role in the acute and especially the recovery period of stroke is played by the struggle with hypodynamia; The patient has to rotate in bed every 2 hours every 2 hours in order to prevent pneumonia and decubitus. Essential is the toilet of the oral cavity (removal of removable prostheses!), Skin care and high-calorie and easily assimilated food. When the chair is delayed, laxatives are prescribed, with urinary retention - catheterization.

The question of the timing of activation is decided individually. With hemorrhagic and embolic strokes, the duration of strict bed rest should not be less than 3 weeks. On the contrary, with a favorable course of nonembolic infarctions and transient disorders of cerebral circulation of patients, it is possible to put it cautiously just a few days after the stroke. Especially poorly tolerated by elderly people; In the case of prolonged bed rest, their subsequent rehabilitation is extremely complicated because of the decompensation of the vestibular apparatus. Restorative gymnastics and especially massage with a satisfactory state of the patient can begin already in the first days of the disease. It is necessary to correlate the volume of loads with the severity of stroke and the state of the cardiovascular system.

Differential treatment of ischemic strokes. Drugs that dilate the cerebral vessels may not give the desired effect due to the pathological reaction of the vessels of the affected area, which sometimes further aggravates ischemia in the affected area (syndrome of intracerebral "stealing"). However, everyday practice certainly justifies the expediency of parenteral administration of xanthinal nicotinate, papaverine, no-shpa. Use low molecular weight dextran reopolyglucin. Indications are shown inside or in / in the infusion of Cavinton and Trental, the methods of curantyl and cinnarizine. Intravenous and (or) inside appoint piracetam (3-4 ampoules of 20% solution of 5 ml / day), pyriditol, cerebrolysin (5-10 ml iv or in / m).

Ischemic attacks are divided into transient ischemic attacks, a developing stroke and a completed stroke. Developing stroke is considered to be a period of increasing symptoms, usually not exceeding 48 hours, completed stroke - stage of a persistent neurological defect. Anticoagulants are most effective in developing a stroke. However, long-term use of them can cause hemorrhagic complications of micro- and macrohematuria, subcutaneous petechial hemorrhages, nasal and gastric bleeding, cerebral hemorrhages). Anticoagulants are contraindicated in diseases of the liver, kidneys, heart defects in the stage of decompensation, septic states, peptic ulcer of the stomach and duodenum, malignant neoplasms, blood diseases with hemostatic disorders, pregnancy, in the postpartum period. Contraindications are also a coma or condition of a deep sopor at the time of deciding the appointment of anticoagulants; High figures of blood pressure (systolic above 200, diastolic - above 100 mm Hg); Epileptic seizures after the onset of a stroke; Increased leukocytosis (over 10 103 103 / μl), detected during the first 24 hours after the onset of the stroke; Unexplained hemorrhagic stroke in the anamnesis. Anticoagulant therapy is certainly indicated for patients with cerebral embolisms of cardiac origin. It is started with heparin - 10 000 units 4-6 times a day for 3 days in / in or p / k. With iv administration gerapine acts immediately, with n / to the introduction - after 40-50 minutes. Treatment with heparin should be carried out under the control of clotting time. The optimal increase in clotting time is 2.5 times. To prevent hemorrhagic complications, the urine composition (the appearance of red blood cells) should be systematically monitored. Usually on the third day of treatment, anticoagulants of indirect action are injected in an increasing dose, and the dose of heparin is reduced. Treatment with anticoagulants of indirect action is carried out under the control of the prothrombin index, which should be reduced to more than 40-50%. Preference should be given to derivatives of indanedione-phenylene and omephene. Individual sensitivity of patients to anticoagulants of indirect action is different. Changing daily doses of anticoagulants depending on the prothrombin index (with daily monitoring), within a week you can choose a stable scheme for taking medications. Hemorrhagic complications caused by anticoagulants are treated according to the general principles of hemostatic therapy: epsilon-aminocaproic acid, hemofobin, fresh-frozen plasma 1-2 l / day. In case of an overdose of heparin, iv antagonist - protamine sulfate (5 ml of 1% solution) is administered.

Differential treatment of hemorrhagic stroke. Amino-caproic acid has the most pronounced coagulant and antifibrinolytic action. The maximum effect is achieved with its iv introduction again with intervals of 4-6 hours at a dose of 20-30 g / day. Inside the drug taken at intervals of 4 hours, pre-dissolved it in sweet water. Moderate haemostatic effect is administered by IV gluconate calcium, ascorbic acid, as well as intramuscular injections of vikasol. An exceptionally important role is played by correction of high blood pressure. It should be avoided drastically reducing it because of the risk of worsening brain perfusion.

The prognosis for a cerebral infarction is determined primarily by its localization and the vastness of the affected area of ​​the brain; The outcome of an embolic stroke largely depends, in addition, on embolism in other organs. Hemorrhage in the brain in 70-80% of cases leads to death of patients. About 50% of patients die from the first attack of spontaneous envelope hemorrhage. Active recovery treatment can achieve that patients with hemiplegia can walk alone; Movements in the hand are usually restored worse than in the leg.