Subarachnoid hemorrhage (SAH): causes, symptoms and treatment principles
Cerebral hemorrhage Etiology of cerebral hemorrhages Cerebral hemorrhage most often develops in hypertension, as well as in arterial hypertension due to diseases of the kidneys, endocrine glands (pheochromocytoma, pituitary adenoma) and in systemic vascular diseases of an allergic and infectious-allergic nature, accompanied by an increase in AD (periarteritis nodosa, lupus erythematosus). Cerebral hemorrhage can occur with congenital angioma, with microaneurysms formed after traumatic brain injury or septic conditions, as well as with diseases accompanied by hemorrhagic diathesis – Werlhof’s disease, leukemia and uremia. Pathogenesis of cerebral hemorrhages It is now recognized that in the pathogenesis of hemorrhages, arterial hypertension is of greatest importance. Hypertension, especially in hypertensive disease, leads to vascular changes, fibrinoid degeneration and hyalinosis of the arteries of the kidneys, heart, and also inside the cerebral arteries. Vascular changes go through several stages: subendothelial serous infiltration with increased endothelial permeability for blood plasma is accompanied by perivascular transudation and further contributes to concentric compaction of the vessel walls due to fibrinoid substance. The rapid development of fibrinoid degeneration leads to the formation of dilated arterioles and aneurysm. At the same time, it can be observed that blood elements penetrate into the torn structures of the arterial walls, and thrombosis can form in these places. As a result of fibrinoid-hyaline degeneration of the arterial walls, dissecting aneurysms can develop, which are considered the cause of bleeding (per rexis) as a result of rupture of the vessel. The intensity and size of cerebral bleeding are determined by the size of the aneurysm, the pressure of the blood flowing from it and the speed of its thrombosis. Most often, hemorrhage develops in the area of the subcortical nodes, in the area of the putamen from the striatal arteries.
Hemorrhages in the overwhelming majority of cases develop in patients with essential hypertension and in all other diseases that are accompanied by arterial hypertension. In atherosclerosis without hypertension, hemorrhages are very rare. In diseases not accompanied by arterial hypertension (blood diseases, somatic diseases accompanied by hemorrhagic diathesis, uremia, etc.), the main mechanism for the development of hemorrhage is diapedesis due to increased permeability of the vessel walls. Pathological anatomy of cerebral hemorrhage Cerebral hemorrhage develops more often as a result of rupture of a vessel and much less often as a result of diapedesis. Morphologically, hematomas are distinguished, that is, cavities filled with liquid blood and clots, well delimited from the surrounding tissue, and hemorrhages with uneven contours, clearly not delimited – hemorrhagic sweating. Attention is drawn to the predominant localization of hematomas in the region of the subcortical nodes of the cerebral hemispheres. Much less often hematomas develop in the area of the dentate nuclei of the cerebellum and even less often in the area of the brain pons. The formation of a hematoma occurs mainly due to the spreading of the outflowing blood of the medulla and compression of the latter.
With a cerebral hemorrhage, in 85-90% of cases, blood breakthrough into the ventricular system or into the subarachnoid space is observed. The most typical breakthrough site is the lateral-basal part of the anterior horn of the lateral ventricle (head of the caudate nucleus). There are hemorrhages with a single-stage breakthrough, walls in different parts of the ventricular system. With hemorrhages of the type of hematoma, extensive cerebral edema, flattening of the convolutions and the development of hernial inclusions of the brain are often found. Hematoma of hemispheric localization causes a displacement of the brain stem with its insertion into the tentorial opening, which results in deformation of the brain stem and the development of secondary small hemorrhages in it. Hemorrhages of the type of hemorrhagic impregnation occur mainly in the optic hillocks, less often in the pons and white matter of the cerebral hemispheres. They are the result of the fusion of small foci of hemorrhage arising from small vessels by diapedesis. Classification of cerebral hemorrhages In clinical practice, the classification of hemorrhages, depending on the localization of the focus of hemorrhage, has become widespread. Among parenchymal hemorrhages, hemorrhages in the cerebral hemispheres, hemorrhages in the brain stem and cerebellum are distinguished. According to localization in the hemispheres, hemorrhages are divided into lateral – outward from the inner capsule, medial – inward from it and mixed, occupying the entire area of the subcortical ganglia.
Clinic of hemorrhages in the brain Hemorrhage develops, as a rule, suddenly, usually during the day, during the period of active activity of the patient, although in isolated cases hemorrhages are observed both during the patient’s rest period and during sleep. Hemorrhage in the brain is characterized by a combination of cerebral and focal symptoms. Sudden headache, vomiting, impaired consciousness, rapid loud breathing, tachycardia with the simultaneous development of hemiplegia or hemiparesis are common initial symptoms of hemorrhage. The degree of impairment of consciousness is different – from mild stunning to deep atonic coma. When determining the depth of the disturbance of consciousness, attention is paid to the possibility of contact with the patient, the patient’s fulfillment of simple and complex instructions, the ability to report anamnestic information, the speed and completeness of the patient’s responses, the safety of criticism, attitude to his condition, the patient’s orientation in the environment. With a deep loss of consciousness, there is no speech contact with the patient, only the patient’s reaction to loud sounds, to an injection or a series of injections is recorded. With a mild degree of stunning, both in answering questions and when executing orders (even if the patient does not have aphasia), slower reactions are visible, an increase in the latency period. The patient does not succeed in fulfilling difficult instructions, he is quickly “exhausted.” and “turns off”, although he can report information about himself, but confuses them, answers questions slowly and “out of place.” Motor restlessness, anxiety, underestimation of one’s condition are often noted; the reaction to the injection is preserved – there is a grimace of pain and withdrawal of an arm or leg. Stunning or stupor observed in the initial period can go to anybody after a few hours.
Coma is characterized by a deeper disturbance of all vital functions (respiration, cardiac activity), a decrease or loss of reactions to stimuli. The patient does not respond to a single injection, weak and medium sounds, to touch, but withdraws his healthy hand in response to a series of injections. With an atonic coma – an extreme degree of a terminal state – all reflexes (pupillary, corneal, pharyngeal, skin, tendon) are lost, blood pressure falls, the breathing rhythm is changed – breathing like Chain-I Stokes is replaced by breathing like Kussmaul. The general appearance of the patient with massive hemorrhage is characteristic: the eyes are closed, the skin is hyperemic, and profuse sweating is often observed. Pulse is tense, blood pressure is increased. The eyes are turned towards the affected hemisphere (paralysis of the cortical gaze center), the pupils can be of different sizes (anisocoria occurs in 60-70% of hemorrhage hemorrhages), usually the pupil is larger on the side of the focus. Often, there is a divergent (strabismus, caused, like anisocoria, by compression of the oculomotor nerve on the side of the hematoma, which is a symptom indicating the developing compression of the brain stem by hematoma and perifocal cerebral edema, originally arising in the hemisphere where the hemorrhage occurred. The most frequent focal symptom of hemorrhage is hemiplegia. Usually combined with central paresis of the facial muscles and tongue, as well as temihypesthesia in the contralateral extremities and hemianopsia. Focal symptoms (Hemorrhages in the cerebral hemispheres should include gaze palsy, seneoromotor aphasia (with left hemispheric localization) e. unawareness of the patient’s paralysis, with hemorrhage in the right hemisphere. With hemorrhages in the right hemisphere, violent movements are observed in healthy right limbs – parakinesis or automated movements.
Parakinesis can be noted shortly after a stroke in phases e psychomotor agitation, when consciousness is not completely lost. The patient moves his healthy arm and leg, as if gesturing, or touches the nose, chin, scratches the abdomen, flexes and unbends the leg. Outwardly, these movements resemble purposeful ones, however, as consciousness is disturbed, they become more and more automated. A significant place in the clinic of the acute period of hemorrhage is occupied by dystonia, various variants of muscle tone disorders, studied in detail by domestic neuropathologists: S.N.Davidenkov (1921), N.K.Bogolepov (1953), D.K.Lunev (1962), etc. At the first moment, an acute violation of cerebral circulation leads to the development of muscle hypotension on the side of the paralysis. An increase in muscle tone can develop immediately after a stroke or after a few hours or even a few days. For cerebral hemorrhage, the most characteristic increase in muscle tone is paroxysmal, in the form of paroxysms. A paroxysmal increase in muscle tone, called by S. N. Davidenkov hormone, is clinically manifested very clearly. Paroxysmal increase in muscle tone is more often observed in paralyzed limbs, but it can also be in the limbs homolateral to the focus. In the hands, tonic spasm usually involves the adductors of the shoulder, flexors and pronators of the forearm, in the legs – the adductors of the hip, extensors of the lower leg, and internal rotators of the foot. One can observe how, as tonic spasms in these muscles are relaxed, an increase in muscle tone occurs in the antagonist muscles. The duration of such paroxysms of muscle hypertension ranges from several seconds to several minutes. Attacks of hormonal convulsions are aggravated by various extra- and interoreceptive stimuli. Sometimes the seizures of hormetonia reach such intensity that they are accompanied by the movement of the limb. In some patients, there is partial hormetonia, that is, covering any one limb, in others – hemihormetonia. Particularly sharply paroxysmal increase in muscle tone is observed with nolispheric hemorrhages, accompanied by a breakthrough of blood into the ventricles of the brain. Changes in muscle tone in hemispheric hemorrhages are associated with dysfunction of the tonic structures of the brain stem, which regulate muscle tone, caused by compression and dislocation of the stem. With parenchymal hemorrhages, meningeal symptoms appear after a few hours (sometimes by the end of the first day). At the same time, the rigidity of the occipital muscles may not be at all, the upper Brudzinsky symptom is rarely caused, but Kernig’s symptom on the non-paralyzed side and the positive lower Brudzinsky symptom are noted with great constancy. The absence of Kernig’s symptom on the side of the paralysis is one of the criteria for determining the side of the lesion. An increase in body temperature is observed in patients with parenchymal hemorrhage in a few hours from the moment of illness and lasts for several days in the range of 37-38 ° C. With the breakthrough of blood into the ventricles and with the proximity of the focus of hemorrhage to the hypothalamic region, the body temperature reaches 40-41 ° C. As a rule, leukocytosis is observed in the peripheral blood, a slight shift in the leukocyte formula to the left, on the first day of the disease there is an increased sugar content, sometimes residual nitrogen. Often, there is an increased fibrinolytic activity of the blood, in most cases, platelet aggregation is reduced. Course and prognosis of cerebral hemorrhages With cerebral hemorrhages, there is a high mortality rate, which, according to different authors, ranges between 75-95%. Up to 42-45% of patients with massive cerebral hemorrhage die within 24 hours from the onset of stroke, the rest die on the 5-8th day of the disease and, in rare cases, on the 15-20th day. The most common cause of death in patients with hemorrhagic strokes is infringement of the trunk in hemispheric hemorrhage due to cerebral edema.
The second place in the frequency of causes of death is occupied by the focus itself with a massive breakthrough of blood into the ventricular system and destruction of vital formations. Treatment of cerebral hemorrhages A patient with cerebral hemorrhage must be properly put to bed, giving the head an elevated position, raising the head end of the bed.In case of cerebral hemorrhage, first of all, therapy is needed aimed at normalizing vital functions, stopping bleeding and combating cerebral edema, and then deciding on the possibility of removing the outflowing blood. First of all, it is necessary to ensure free patency of the respiratory tract, for which it is necessary to remove the liquid secretion from the upper respiratory tract using special suction, apply oral and nasal air ducts, wipe the patient’s oral cavity. With concomitant pulmonary edema, cardiotonics are recommended: 1 ml of a 0.06% solution of kargli, con a or 0.5 ml of a 0.05% solution of strophanthin with glucose iv, as well as inhalation of oxygen with alcohol vapors in order to reduce pricing in the alveoli. Atropine 1 is prescribed – 0.5 ml of 0.1% solution, furosemide (lasix) 1-2 ml of 1% solution, diphenhydramine 1 ml of 1% solution in / m. It is necessary to use funds aimed at preventing and eliminating hyperthermia. At a body temperature of about 39 ° C and above, 10 ml of a 4% solution of amidopyrine or 2-3 ml of a 50% solution of analgin i / m are prescribed. Regional hypothermia of large vessels is also recommended (ice bladders on the carotid arteries in the neck, axillary and groin areas). To stop bleeding and prevent its resumption, it is necessary to lower blood pressure and increase blood clotting. To lower blood pressure, use dibazol (2-4 ml of a 1% solution), Gemiton (1 ml of a 0.01% solution). In the absence of effect, aminazine is prescribed (2 ml of a 2.5% solution and 5 ml of a 0.5% solution of novocaine) i / m or as part of a mixture: chlorpromazine (2 ml of a 2.5% solution), diphenhydramine (2 ml of a 1% solution) , promedol (2 ml of 2% solution) in / m; ganglion blockers – pentamine (1 ml of a 5% solution in / m or 0.5 ml in 20 ml of 40%) glucose solution i.v., slowly under the control of blood pressure), benzohexonium (1 ml of a 2% solution i / m), arfonad (5 ml 5% solution in 150 ml of 5% glucose solution IV at a rate of 50-30 drops per minute).
Antihypertensive drugs should be used with caution. Ganglion blockers can drastically reduce blood pressure, so they should be prescribed in exceptional cases, with blood pressure exceeding 200 mm Hg. Art. Ganglion blockers should be administered carefully with constant monitoring of blood pressure every 20-30 minutes. In this case, it is necessary to achieve a decrease in pressure to the optimal level, individual for each patient. Shown are agents that increase blood coagulability and reduce vascular permeability: 2 ml of 1% solution of vicasol, calcium preparations (10 ml of 10% solution of calcium chloride i / v or calcium gluconate 10 ml of 0.25% solution of i / m). Apply 5% solution of ascorbic acid – 5-10 ml / m. Patients with hemorrhagic stroke should be prescribed drugs that inhibit the pathologically increased fibrinolytic activity of the blood. For this purpose, aminocaproic acid is used, injecting ep in the form of a 5% solution intravenously 100 ml dropwise under the control of the fibrinogen content and fibrinolytic activity of the blood during the first two days. To reduce intracranial hypertension and relieve cerebral edema, furosemide – laix (20-40 mg i.v. or i.m.), as well as mavnit (ready-made 10-15-20% solution at the rate of 1 g in 200 ml of isotonic sodium chloride solution or 5% glucose solution IV drip). The use of urea is undesirable, since the vicarious expansion of the cerebral vessels that follows a powerful anti-edema effect can lead to repeated even more severe edema and possible bleeding into the brain parenchyma. Glycerin has a dehydration effect, which increases the osmotic pressure of the blood without causing electrolyte imbalance. Infusion therapy should be carried out under the control of indicators of acid-base balance and electrolyte composition of plasma. With an increase in cerebral edema and a threat to the patient’s life, surgical treatment is indicated. Surgery. Surgical intervention for intracerebral hematoma is reduced to the removal of spilled blood and the creation of decompression. Currently, many years of experience has been accumulated in the surgical treatment of hemorrhagic strokes. It can be considered a generally accepted point of view of neurosurgeons that surgical treatment is indicated for lateral hematomas and inappropriate for medial and extensive hemorrhages.