Head CT often reveals subarachnoid hemorrhage. Computed tomography in the diagnosis of subarachnoid hemorrhage

Vomiting, loss of consciousness, loss of consciousness and a coma are possible, especially severe with aneurysms of the arteries of the base of the brain or posterior cranial fossa, when the outflow of blood can block the cerebrospinal fluid spaces, which leads to the acute development of intracranial hypertension.

Upon restoration of consciousness, photophobia, hyperesthesia occur, a positive symptom of Burdenko-Kramer (symptom of cerebellar occlusion) - pain in the fronto-occipital-orbital region, blepharospasm, sharp soreness of the eyeballs when pressed. Radicular pains, distal painful paresthesias (Wakez symptom) are often noted. When examining a patient, stiff neck muscles and other meningeal symptoms are determined.

When an aneurysm ruptures, located in the area where the posterior communicating artery originates from the ICA, there are signs of compression of the oculomotor nerve passing in the immediate vicinity of these vessels. This symptom is not a sign of brain dislocation. Rupture of an aneurysm at the branching site of the ICA and ophthalmic artery causes optic nerve and chiasm symptoms and homolateral blindness.

Diagnostics

Subarachnoid hemorrhage causes a fairly vivid and typical clinical picture, so its diagnosis “in fact” usually does not cause difficulties and is confirmed by the results of a CSF study. Further diagnostics is carried out in order to detect the source of bleeding, i.e., as a rule, an aneurysm, arterial or venous, to determine its localization and treatment tactics.

This requires angiography in any available option - MRI, CT angiography or radiopaque (the best option). All vascular pools of the brain are examined, since in 15-20% of cases aneurysms are multiple.

Neuroimaging methods also help to determine the size of the hematoma, its localization, the spread of blood in the CSF spaces, as well as the detection of brain dislocation and angiospasm - a typical and dangerous complication of subarachnoid hemorrhage. On the first day after aneurysm rupture, CT detects blood accumulation in the subarachnoid space in 90% of patients.

With approximately the same frequency, erythrocytes are found in large numbers in the cerebrospinal fluid, 4-10 hours after centrifugation, cerebrospinal fluid xanthochromia is detected due to the formation of free hemoglobin.

Treatment

Treatment consists in preventing re-rupture of the aneurysm, preventing and eliminating angiospasm as the main complication of subarachnoid hemorrhage, intracranial hypertension and cerebral edema, and resuscitation, if required. Further, the issue of choosing the direction of treatment is decided, while much is determined by the general condition of the patient and the neurological syndrome. To assess the severity of the patient's condition, the Hunt-Hess scale can be used (W. Hunt, T. Hess, 1968):

	Clinical manifestations
	Moderate headache and mild neck stiffness
	Severe headache, severe neck stiffness, cranial nerve involvement
	Focal neurological deficit, impairment of consciousness to the level of stupor
	Initial coma, hemiparesis or hemiplegia, initial decerebrate rigidity
	Deep coma, decerebrate rigidity, muscular hypotension

Conservative treatment is an independent task or is carried out in terms of preoperative preparation, if for some reason an urgent surgical intervention is impossible. The patient's usual level is maintained HELL. Reducing it in order to prevent re-hemorrhage is impractical and even dangerous, since under conditions of possible diffuse arterial spasm it threatens with ischemic brain damage.

Water-electrolyte balance is maintained, blood glucose is controlled, meaning that moderate hyperglycemia may develop in subarachnoid hemorrhage, as in any form of stroke. It is carried out, as with GI, the prevention of acute ulcerative bleeding.

Prevention and treatment of vasospasm. Generalized arteriolospasm occurs due to the effect on the reactivity of the cerebral arteries of hemolysis products penetrating into the substance of the brain and perivascular spaces. Vasospasm causes cerebral hypoxia and persists for 1-2 weeks. Treatment is with calcium antagonists (nimodipine 60 mg every 4 hours for 3-4 weeks). Hemodilution (rheopolyglucin, 5% glucose solution in a large volume), especially hypervolemic, cannot be used due to the threat of an uncontrolled increase in blood pressure and the possibility of re-hemorrhage. The exception is WHO the possibility of using mannitol.

There is no specific conservative therapy for GI. An alternative to surgery for small aneurysms can be narrowly focused gamma therapy, which in 80-90% of cases causes thrombosis and obliteration of aneurysms.

When deciding on conservative therapy of a patient, it should be borne in mind that 30-40% of aneurysms within a month after the first subarachnoid hemorrhage give a second rupture, which, as a rule, is much more severe than the first.

Surgery. Surgical treatment is the only radical way to help the patient. Intervention is most justified on the first day after aneurysm rupture. This prevents re-rupture of the aneurysm, which is usually fatal, and complications such as cerebral angiospasm and cerebral edema. If for some reason such an early operation is not possible, it is performed after 1.5-2 weeks.

Surgical intervention, regardless of the time elapsed before admission to the hospital, is indicated for I-II severity of the patient's condition on the Hunt-Hess scale. With III degree of severity, the decision to operate is made taking into account the localization of the aneurysm, the volume of the hematoma, and the qualifications of the surgeon.

Arteriovenous aneurysms are conservatively treated in the same way as arterial aneurysms. Indications for surgery are less certain than for arterial aneurysms. In case of malformations, manifested only by epileptic seizures and moderate focal symptoms, without bleeding, the tactics of waiting with symptomatic treatment is considered justified. Recurrent subarachnoid hemorrhages make surgery necessary.

Postoperative mortality is about 15% (A. N. Konovalov), which is significantly less than with conservative treatment, when mortality is 50-60%. The prognosis of the outcome of subarachnoid hemorrhage (before treatment and subsequently) can be generally determined according to the criteria of the World Federation of Neurosurgeons scale based on the Glasgow Coma Severity Scale:

A more detailed and balanced assessment of the severity of subarachnoid hemorrhage and other strokes can be given using the US National Health Stroke Severity Scale, which includes 11 criteria and their multiple gradations (www.ninds.nih.gov/doctors/NIN_Stroke_Scale.pdf; or www.ninds .nih.gov/doctors/NIN_Stroke_Scale_Booklet.pdf).

Surgical treatment of unruptured aneurysms. If an aneurysm is detected in a patient outside the acute period of subarachnoid hemorrhage, the decision on surgical treatment and its methodology is made taking into account a number of factors:

• unruptured ICA aneurysms located in the cavernous sinus and having a diameter of less than 5-7 mm are not subject to surgical treatment;
• unruptured aneurysms larger than 7 mm located in the anterior part of the circle of Willis are clipped;
• unruptured aneurysms with a diameter of more than 7 mm and located in the back of the circle of Willis are subject to embolization.

The content of the article

To hemorrhagic stroke include hemorrhages in the substance of the brain (hemorrhage in the brain or parenchymal hemorrhage) and in the intrathecal spaces (subarachnoid, subdural, epidural). Combined forms of hemorrhage are also observed - subarachnoid-parenchymal, parenchymal-subarachnoid and parenchymal-ventricular.

Hemorrhage in the brain

Etiology of cerebral hemorrhage

Hemorrhage in the brain most often develops with hypertension, as well as with arterial hypertension caused by diseases of the kidneys, endocrine glands (pheochromocytoma, pituitary adenoma) and with systemic vascular diseases of an allergic and infectious-allergic nature, accompanied by an increase in blood pressure (periarteritis nodosa, lupus erythematosus ). Hemorrhage in the brain can occur with congenital angioma, with microaneurysms formed after a traumatic brain injury or septic conditions, as well as with diseases accompanied by hemorrhagic diathesis - Werlhof's disease, leukemia and uremia.

The pathogenesis of cerebral hemorrhage

It is now recognized that arterial hypertension is of the greatest importance in the pathogenesis of hemorrhages. Hypertension, especially in hypertension, 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 to blood plasma is accompanied by perivascular extravasation and further contributes to the concentric thickening of the vessel walls due to the fibrinoid substance. The rapid development of fibrinoid degeneration leads to the formation of dilated arterioles and to 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 region of the subcortical nodes, in the region of the putamen from the striatal arteries.

Hemorrhages in the vast majority of cases develop in patients with hypertension and in all other diseases that are accompanied by arterial hypertension. In atherosclerosis without arterial 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 walls of blood vessels.

Pathological anatomy of cerebral hemorrhage

Hemorrhage in the brain develops more often as a result of rupture of the vessel and much less frequently due to 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, not clearly 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 region of the dentate nuclei of the cerebellum, and even more rarely in the region of the brain bridge. The formation of a hematoma occurs mainly due to the expansion of the medulla by the outflow of blood and compression of the latter.

With cerebral hemorrhage, in 85-90% of cases there is a breakthrough of blood into the ventricular system or into the subarachnoid space. The most typical site of a breakthrough is the lateral-basal part of the anterior horn of the lateral ventricle (head of the caudate nucleus). There are hemorrhages with a one-stage breakthrough, walls in different parts of the ventricular system. With hemorrhages of the type of hematoma, extensive cerebral edema, flattening of the gyri and the development of hernial herniation of the brain are often found. A hematoma of hemispheric localization causes a displacement of the brain stem with its wedging into the tentorial foramen, resulting in deformation of the brain stem and the development of secondary small hemorrhages in it.

Hemorrhagic impregnation type hemorrhages occur mainly in the visual tubercles, less often in the pons of the brain and the white matter of the cerebral hemispheres. They are the result of the fusion of small foci of hemorrhage arising from diapedesis from small vessels.

Classification of cerebral hemorrhages

In clinical practice, the classification of hemorrhages has become widespread depending on the location of the hemorrhage focus. Among parenchymal hemorrhages, hemorrhages in the cerebral hemispheres, hemorrhages in the brain stem and cerebellum are distinguished. By localization in the hemispheres, hemorrhages are divided into lateral - outward from the internal capsule, medial - inward from it and mixed, occupying the entire area of ​​the subcortical ganglia.

Cerebral hemorrhage clinic

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 simultaneous development of hemiplegia or hemiparesis are the usual initial symptoms of hemorrhage. The degree of impairment of consciousness is different - from a slight stun to a deep atonic coma. When determining the depth of the disorder of consciousness, attention is paid to the possibility of contact with the patient, the patient's compliance with simple and complex instructions, the ability to provide 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 verbal 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 response to questions and in the execution of orders (even if the patient does not have aphasia), slow reactions and an increase in the latent period are visible. The patient does not succeed in fulfilling complex instructions, he quickly "exhausted." and “turns off”, although he can report information about himself, but confuses them, answers questions slowly and “out of place”. Often noted motor restlessness, anxiety, underestimation of their condition; the reaction to the injection is preserved - there is a grimace of pain and withdrawal of the arm or leg.

Stunning or stupor noted in the initial period can pass into a coma after a few hours.. Coma is characterized by a deeper violation 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. In atonic coma - the extreme degree of the terminal state - all reflexes (pupillary, corneal, pharyngeal, skin, tendon) are lost, blood pressure drops, the breathing rhythm is changed - Cheyne-I Stokes type breathing is replaced by Kussmaul type breathing. The general appearance of a patient with a massive hemorrhage in the hemispheres is characteristic: the eyes are closed, the skin is hyperemic, and profuse sweating is often observed. The pulse is tense, blood pressure is elevated. The eyes are turned towards the affected hemisphere (paralysis of the cortical center of gaze), the pupils can be of different sizes (anisocoria occurs in 60-70% of cases of hemorrhages of hemispheric localization), 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 developing compression of the brainstem by the hematoma and perifocal cerebral edema, which initially occurred in the hemisphere where the hemorrhage occurred.

The most common focal symptom of hemorrhage is hemiplegia. Usually associated with central paresis of the facial muscles and tongue, as well as hypoesthesia in the contralateral limbs and hemianopsia. Focal symptoms (Hemorrhages in the cerebral hemispheres should include gaze paralysis, sensory-motor aphasia (with left-hemispheric localization of the hemorrhage), anosognosia, i.e., the patient’s unawareness of his paralysis, with hemorrhage in the right hemisphere. With hemorrhages in the right hemisphere, violent movements in healthy right limbs - parakinesis or automated movements. Parakinesis can be noted shortly after a stroke in the phase of psychomotor arousal, when consciousness is not yet completely lost. The patient moves a healthy arm and leg, as if gesticulating, or touches his nose, chin, scratches his stomach, flexes and unbends the leg.Outwardly, these movements resemble purposeful ones, however, as consciousness is disturbed, they become more and more automated.Dystonia, various variants of muscle tone disorders, studied in detail by Russian neuropathologists, occupy a significant place in the clinic of the acute period of hemorrhage: S.N. Davidenkov (1921), N. K. Bogolepov (1953), D. K. Lunev (1962) and others.

Increased muscle tone may 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. The paroxysmal increase in muscle tone, called hormetonia by S. N. Davidenkov, is clinically manifested very clearly.

A paroxysmal increase in muscle tone is more often observed in paralyzed limbs, but it can also be in the limbs that are homolateral to the focus. In the arms, tonic spasm usually involves the adductors of the shoulder, flexors, and pronators of the forearm; in the legs, the adductors of the thigh, extensors of the lower leg, and internal rotators of the foot. It can be observed how, as the relaxation of tonic spasms in these muscles, an increase in muscle tone occurs in the muscles - antagonists. The duration of such paroxysms of muscular hypertension ranges from a few seconds to several minutes. Attacks of hormetonic convulsions are aggravated by various extra- and interoreceptive stimuli. Sometimes convulsions of hormetonia reach such intensity that they are accompanied by movement of the limb. Some patients have partial hormetonia, that is, covering any one limb, while others have hemihormetonia.

A particularly sharp paroxysmal increase in muscle tone is observed with noluspheric 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 that regulate muscle tone, due to compression and dislocation of the brain stem.

With parenchymal hemorrhages, meningeal symptoms appear after a few hours (sometimes by the end of the first day). At the same time, there may be no stiff neck at all, the upper Brudzinsky symptom is rarely caused, but Kernig's symptom on the non-paralyzed side and a positive lower Brudzinsky symptom are noted with great constancy. The absence of Kernig's symptom on the side of 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 a few hours after the onset of the disease and lasts for several days within 37-38 ° C. With a 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 of the leukocyte formula to the left, on the first day of the disease there is an increased content of sugar, sometimes residual nitrogen. Often there is an increased fibrinolytic activity of the blood, in most cases, platelet aggregation is reduced.

The 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 a 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 the incarceration of the trunk with 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 the destruction of vital formations.

Treatment of cerebral hemorrhages

A patient with a cerebral hemorrhage must be properly put to bed, giving the head an elevated position, raising the head end of the bed. With a cerebral hemorrhage, first of all, therapy is needed aimed at normalizing vital functions, stopping bleeding and combating cerebral edema, and then resolving the issue of ability to remove spilled blood.

First of all, it is necessary to ensure the free patency of the respiratory tract, for which it is necessary to remove the liquid secret from the upper respiratory tract using special suction, use the oral and nasal air ducts, and wipe the patient's oral cavity. With concomitant pulmonary edema, cardiotonic drugs are recommended: 1 ml of a 0.06% solution of karg li, cona or 0.5 ml of a 0.05% solution of strophanthin with glucose IV, as well as inhalation of oxygen with alcohol vapor in order to reduce pricing in the alveoli. Assign atropine 1 - 0.5 ml of a 0.1% solution, furosemide (lasix) 1-2 ml of a 1% solution, diphenhydramine 1 ml of a 1% solution in / m.

It is necessary to use means 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 packs on the region of the carotid arteries in the neck, in the axillary and inguinal regions).

To stop bleeding and prevent its resumption, it is necessary to lower blood pressure and increase blood clotting. To reduce blood pressure, dibazol (2-4 ml of a 1% solution), hemiton (1 ml of a 0.01% solution) are used. If there is no effect, chlorpromazine (2 ml of a 2.5% solution and 5 ml of a 0.5% solution of novocaine) is prescribed intramuscularly 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; ganglionic blockers - pentamine (1 ml of 5% solution i / m or 0.5 ml in 20 ml 40%) glucose solution i / v, slowly under the control of blood pressure), benzohexonium (1 ml 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.

Ganglioblockers can dramatically reduce blood pressure, so they should be prescribed in exceptional cases, with blood pressure exceeding 200 mm Hg. Art. Ganglioblockers 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.

Means that increase blood clotting and reduce vascular permeability are shown: 2 ml of a 1% solution of vikasol, calcium preparations (10 ml of a 10% solution of calcium chloride in / in or calcium gluconate 10 ml of a 0.25% solution in / m). Apply a 5% solution of ascorbic acid - 5-10 ml / m.

Patients with hemorrhagic stroke need prescribe drugs that inhibit pathologically increased fibrinolytic activity of the blood. For this purpose, aminocaproic acid is used, administering ep in the form of a 5% solution of intravenous drip, 100 ml, under the control of fibrinogen content and fibrinolytic activity of the blood during the first two days. To reduce intracranial hypertension and relieve cerebral edema, furosemide is used - laaix (20-40 mg intravenously or intramuscularly), as well as mavnit (prepared 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 cerebral vessels following a powerful anti-edematous effect can lead to repeated, even coarser edema and possible bleeding into the brain parenchyma. Glycerin has a dehydrating 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 life of the patient, surgical treatment is indicated.

Surgery.
Surgical intervention for intracerebral hematoma is reduced to the removal of the outflow of blood and the creation of decompression. At present, many years of experience in the surgical treatment of hemorrhagic strokes have been accumulated. It can be considered a generally accepted point of view of neurosurgeons that surgical treatment is indicated for lateral hematomas and is inappropriate for medial and extensive hemorrhages. Surgical treatment for lateral hematomas should be carried out on the first day of a stroke before the development of displacement, deformation and compression of the brain stem. In the surgical treatment of hematoma, mortality compared with conservative therapy decreases from 80% to 50-40% [Arutyunov A.I., Romodanov A.P., Pedachenko G.A., 1967; Bogatyrev Yu. V., 1968].

subarachnoid hemorrhage

Etiology of subarachnoid hemorrhages

In most cases, the cause of spontaneous subarachnoid hemorrhage is a ruptured intracranial aneurysm. Arterial aneurysms of the brain, as well as aneurysms of other localization, are a limited or diffuse expansion of the lumen of the artery or a protrusion of its wall. Most aneurysms of the arteries of the brain have the characteristic appearance of a small thin-walled sac, in which one can usually distinguish the bottom, middle part and the so-called neck.

Due to these anatomical features, such aneurysms are often referred to as saccular aneurysms. Less commonly, an aneurysm has the form of a large spherical formation or a diffuse expansion of an artery over a considerable length (the so-called S-shaped aneurysms).
Most aneurysms are located in the arteries at the base of the brain. Their favorite localization is the place of division and anastomosis of the arteries of the brain. Especially often, aneurysms are localized on the anterior communicating artery at the place where the posterior communicating artery originates from the internal carotid artery or in the region of the branches of the middle cerebral artery. A relatively small part of aneurysms is localized in the system of vertebral and basilar arteries. Aneurysms are more common in women than in men.

The question of the origin of saccular aneurysms, which make up the vast majority of aneurysms, remains largely open to date. According to most authors, the formation of aneurysms is based on defects in the development of the vascular system of the brain; another (less numerous) group of researchers emphasizes the role of atherosclerosis and hypertension as one of the main causes of saccular aneurysms.

The concept of traumatic genesis of cerebral aneurysms was proposed by M. B. Kopylov (1962), who believes that at the time of injury, pressure in the arteries of the brain increases sharply. Under the influence of such a hemohydraulic shock, damage to the arterial wall may occur with the subsequent development of an aneurysm. A small part of aneurysms develops due to the entry of infected emboli into the artery of the brain. These so-called mycotic aneurysms are characterized by a predominant location on the convexital surface of the brain. They most often develop in young people suffering from prolonged septic endocarditis. Atherosclerosis undoubtedly plays a leading role in the origin of large spherical and S-shaped aneurysms.

Not all aneurysms cause clinical symptoms. Most aneurysms are an incidental finding during post-mortem examination. Aneurysms are found in people of all ages, from infancy to old age. Clinically, aneurysms manifest themselves as subarachnoid hemorrhage in the fourth and fifth decades of life.

Among other causes of subarachnoid hemorrhage, atherosclerotic and hypertensive vascular changes, primary and metastatic brain tumors, inflammatory diseases, uremia, and blood diseases are noted.

Clinic of subarachnoid hemorrhages

Usually subarachnoid hemorrhage develops suddenly, without any precursors. Only a small part of patients before hemorrhage have symptoms caused by the presence of an aneurysm - limited pain in the fronto-orbital region, paresis of the cranial nerves (often the oculomotor nerve). A rupture of an aneurysm can occur at a time of physical or emotional stress.

First symptom of subarachnoid hemorrhage- a sudden acute headache, which the patients themselves define as a “hit”, as a sensation of “hot liquid spreading in the head”. At the first moment of the disease, the pain may be local in nature (in the forehead, back of the head), then it becomes diffuse. In the future, the patient develops pain in the neck, back and legs. Nausea and repeated vomiting occur almost simultaneously with the headache. The onset of headache is followed by loss of consciousness. In mild cases, the loss of consciousness is short-lived (10-20 minutes), in severe cases, the unconscious state lasts for many hours and even days. At the time of rupture of the aneurysm or shortly after it, epileptic seizures may occur.

For hemorrhages from arterial aneurysms, it is especially characteristic rapid development of the meningeal symptom complex. Examination of the patient revealed stiff neck, symptoms of Kernig and Brudzinsky, photophobia, general hyperesthesia. Only in the most seriously ill patients with inhibition of reflex activity, meningeal symptoms may be absent.

A frequent symptom that accompanies subarachnoid hemorrhage is a mental disorder. The degree of mental disorder can be different - from a little confusion, disorientation to severe psychosis. Often, after a hemorrhage, psychomotor agitation is observed or memory impairments characteristic of the Korsakoff syndrome develop.

As a reaction to the outflow of blood into the hypothecal space, as well as as a result of irritation of the hypothalamic region, in the acute period there is an increase in body temperature to 38-39 ° C, changes in the blood in the form of moderate leukocytosis and a shift of the leukocyte formula to the left. Along with this, in many patients who do not suffer from hypertension, there is a rise in blood pressure. In severe cases, with massive hemorrhages, there are pronounced violations of vital functions: cardiovascular activity and respiration.

In the acute stage of subarachnoid hemorrhage, a number of symptoms are due to a rapid increase in intracranial pressure (headache, vomiting). An increase in intracranial pressure and the resulting difficulty in venous outflow lead to the development of congestion in the fundus. In addition to the expansion of the veins and swelling of the nipples of the optic nerves, hemorrhages in the retina of the eye can be detected.

In a large percentage of cases with subarachnoid hemorrhage, cranial nerve paresis and symptoms of focal brain damage are also observed. Cranial nerve lesions in patients with spontaneous subarachnoid hemorrhages are pathognomonic for ruptured basal arterial aneurysms. Most often, isolated paresis of the oculomotor nerve occurs at the time of aneurysm rupture or shortly after it. In the overwhelming majority of cases, an isolated unilateral lesion of the oculomotor nerve is observed with hemorrhage from an aneurysm located at the point where the posterior communicating artery originates from the internal carotid.
Hemorrhages from aneurysms of the internal carotid and anterior communicating arteries near the optic nerves and chiasm are relatively often accompanied by visual impairment. Dysfunction of other cranial nerves is less common.

There are two main causes of cranial nerve damage in patients with arterial aneurysms. Firstly, direct compression of the nerve by the aneurysm and, secondly, hemorrhage into the nerve and its membranes at the time of aneurysm rupture, followed by the formation of connective tissue perineural adhesions.

Many patients develop symptoms of focal brain damage: paresis of the extremities, sensory disturbances, speech disorders, etc. The occurrence of these symptoms is most often due to concomitant cerebral hemorrhage or local cerebral ischemia caused by arterial spasm or ischemia due to aneurysm thrombosis.

A lot of work is currently devoted to the study of the clinical manifestations of arterial spasm in the rupture of arterial aneurysms, pathoanatomical changes in the brain caused by spasm. According to angiographic data, the most pronounced spasm of the arteries is noted near the aneurysm, however, in some cases, spasm of the arteries located at a distance from it can also be detected. The duration of spastic contraction of the arteries most often does not exceed 2-4 weeks.

It has been suggested that acute ischemia of the brain stem resulting from spasm is the most likely cause of a number of severe symptoms that accompany an aneurysm rupture, such as loss of consciousness, respiratory and cardiac disturbances. Of interest is the fact that arterial spasm can cause not only cerebral ischemia near a ruptured aneurysm, but also a distant hemispheric lesion. So, with aneurysms of the anterior communicating artery, it is often possible to detect local symptoms caused by circulatory disorders in the basin of the anterior cerebral arteries - paresis of the legs, mental changes, praxis defects. Spasm of the middle cerebral artery leads to paresis of the opposite limbs, impaired sensitivity in them and aphasic phenomena. The causes of arterial spasm in ruptured arterial aneurysms are not well understood. It is suggested that such factors as damage to the wall of the artery and its segmental nervous apparatus by toxic products of the breakdown of blood cells are of great importance.

The course and prognosis of subarachnoid hemorrhages

The prognosis of intracranial hemorrhages caused by rupture of arterial aneurysms is unfavorable. In most cases, the case is not limited to a single hemorrhage. Repeated hemorrhages from aneurysms are especially difficult. With them, paresis, paralysis are more often observed, and mortality is approximately twice as high as with primary hemorrhages.

Observation of patients who have undergone subarachnoid hemorrhage has made it possible to establish that the main part of relapses occurs 2-4 weeks after the first hemorrhage. 2 months after the rupture of the aneurysm, repeated hemorrhages occur relatively rarely. During the first 4-6 weeks, up to 60% of patients with hemorrhages from arterial aneurysms die.

Diagnosis of subarachnoid hemorrhage

The clinic of subarachnoid hemorrhage can be considered well studied, and in typical cases the diagnosis does not cause serious difficulties. However, in some cases, at the onset of the disease, when the meningeal symptom complex has not yet fully developed and symptoms such as vomiting, headache, fever come to the fore, acute intoxication, food poisoning can be erroneously diagnosed.
In other cases, with a relatively mild gradual development of the syndrome of subarachnoid hemorrhage, a suspicion of cerebrospinal meningitis arises. Diagnostic difficulties in most cases can be easily eliminated with the help of a lumbar puncture. The diagnosis of subarachnoid hemorrhage is confirmed by the presence of blood in the cerebrospinal fluid. It is necessary to examine the liquid quickly in order to avoid (incorrect therapeutic measures.

In the first days after a subarachnoid hemorrhage, the cerebrospinal fluid is more or less intensely stained with blood. However, macroscopic analysis of the bloody fluid is not sufficient to confirm the diagnosis. It is recommended to centrifuge the taken liquid. In the fluid obtained after centrifugation with subarachnoid hemorrhage, xanthochromia is determined. In addition, the diagnosis of subarachnoid hemorrhage in the first hours of the disease can be confirmed by the presence of leached erythrocytes during microscopic examination of the cerebrospinal fluid. A day or more after subarachnoid hemorrhage, macrophages and lymphocytic cytosis appear in it.

The final diagnosis of an aneurysm of the arteries of the brain, determining its exact localization, shape and size is possible only with the help of angiography. Even the most thorough neurological examination in most cases allows only more or less likely to suggest an aneurysm of the cerebral arteries, and accurate topical diagnosis of aneurysms, especially multiple ones, is practically impossible.
The dangers associated with transporting a patient to specialized neurosurgical hospitals are exaggerated in many cases. Often difficulties for the differential diagnosis arise with subarachnoid hemorrhages from brain tumors that have previously been asymptomatic. However, the increase in focal symptoms of damage to the brain substance, as well as neutrophilic cytosis in the cerebrospinal fluid, observed during the entire period of the disease in brain tumors, make it possible to make a correct diagnosis.

Treatment of subarachnoid hemorrhages

Treatment of subarachnoid hemorrhage includes conservative and surgical methods, depending on the etiology that caused subarachnoid hemorrhage.

Strict bed rest is required for 6 weeks. The duration of this period is due to the fact that the vast majority of repeated hemorrhages from aneurysms occur within 1-11/2 months after the first one. In addition, a significant period is required for the formation of strong connective tissue adhesions near the ruptured aneurysm.

In the acute stage of hemorrhage, in order to create conditions for aneurysm thrombosis, drugs are indicated that increase blood clotting (vikasol, calcium chloride), as well as agents aimed at inhibiting the fibrinolytic activity of the blood. For this purpose, aminocaproic acid 10-15 g is used daily for the first 3-6 weeks, which are dangerous for re-hemorrhage.

Since even slight tension or excitement can cause an increase in blood pressure and provoke re-hemorrhage, the use of sedatives is necessary. The appointment of these drugs in the acute period of hemorrhage is all the more indicated that many patients who have had hemorrhage from aneurysms are excited. With strong excitement, the use of drugs such as diazepam (seduxen), chlorpromazine, etc. is required. It is important to control bowel function.

Rupture of an aneurysm is often accompanied by an increase in blood pressure, so there is a need to prescribe drugs that reduce blood pressure. In cases where aneurysm rupture is accompanied by a widespread and persistent spasm of the cerebral arteries, it becomes necessary to use drugs that eliminate spastic contraction of the arteries and improve collateral circulation. Unfortunately, existing vasodilators are ineffective in arterial spasm caused by aneurysm rupture.

Also shown is therapy aimed at combating cerebral edema and intracranial hypertension. For this purpose, repeated spinal punctures, saluretics, glycerol and barbiturates are used parenterally.

The radical method of treatment of arterial aneurysms is surgical. Until recently, surgery was considered an indication to prevent recurrent hemorrhage, which usually develops within 2-6 weeks after aneurysm rupture. However, in recent years, this issue has been revised, since, according to a number of observations, conservative therapy aimed at inhibiting fibrinolysis and carried out for a period dangerous for the development of relapse reliably prevents recurrent subarachnoid hemorrhages.

Subarachnoid hemorrhage is a diagnosis that shocks both the patient affected by such an ailment, and his friends and relatives. Like any pathological process in the brain, the disease has an etiology dangerous for human health, it can threaten not only the loss of capacity, but also death.

In this article, we will talk about the features of the disease, its root causes and symptoms, knowledge of which will help you seek medical help in time, and also consider the specifics of the diagnosis, therapy and rehabilitation of the disease, effective ways to prevent it.

Features of the disease

To understand what a subarachnoid cerebral hemorrhage is, a small digression into physiology will help, namely, into the structure of the cover of the hemispheres. Physiologically, the meninges consist of three balls:

• external, solid configuration;
• medium, spider type;
• internal, which is a vascular cover.

There is a space between all the balls: the zone between the first two balls is called the subdural, and the area between the choroid and the middle membrane is called the subarachnoid.

In the normal state, all membranes have an integral structure, which ensures the protection of the hemispheres and normal brain activity. The precedent in which, due to difficulties in blood circulation, vasospasm or traumatic cases, there is an outpouring of blood into the subarachnoid zone, is identified as subarachnoid. Subarachnoid hemorrhage, abbreviated as SAH, may also be referred to as intracranial outpouring of blood or stroke.

Hemorrhage of the subarachnoid type is often characterized by spontaneity, occurs against the background of a segmental or large-scale rupture of the cerebral blood vessels, is accompanied by sharp and intense headaches, bouts of vomiting, and loss of consciousness. This is a very dangerous condition, often causing a sudden death for the patient, and the chances of saving a person directly depend on the promptness of first aid and the intensity of filling the subarachnoid zone with blood.

Causes of outpouring

A help for the progression of the pathology is a violation of the tightness of the walls of the vascular highways of the hemispheres. The causes of subarachnoid hemorrhage can have different etiologies, mainly are as follows:

1. Complicated head injuries, which are accompanied by craniocerebral injuries, brain contusions or direct rupture of arteries in the hemispheres.
2. Sudden rupture of the wall of an artery, which can be triggered by infectious diseases, a rapid increase in pressure, and also occur due to the use of alcoholic beverages or drugs.
3. Deformation of a vascular malformation.

Symptoms of pathology

Often, the progression of the pathology begins to make itself felt to a person with unpleasant symptoms with its etiology of a neuralgic nature a few days before the onset of a massive outpouring. During this period, thinning of the vessel wall is characteristic, through which blood begins to seep in small volumes. This condition is accompanied by nausea and dizziness, visual impairment. In the absence of timely diagnosis and adequate treatment, the disease progresses, one or more vessels rupture, and blood begins to intensively fill the subarachnoid segments of the brain. Similar symptoms may be accompanied by traumatic subarachnoid hemorrhage, if the head injury is not characterized by particular intensity.

Symptoms of extensive bleeding are pronounced, accompanied by sharp, explosive pains of a diffuse type in the head area, followed by irradiation to the shoulders, neck and occipital region. Subarachnoid hemorrhage in the brain of a progressive type is often accompanied by nausea with bouts of vomiting, photophobia, impaired consciousness, often with fainting precedents and coma. The period from the beginning of a massive outpouring to coma can range from several minutes to half a day.

In newborns, subarachnoid hemorrhage is mainly a consequence of traumatism during childbirth, characterized by the formation of hematomas in the hemispheres. Cerebral effusion of blood in newborns is accompanied by the following symptoms:

• piercing, intense crying of the child against the background of increased motor activity;
• convulsive attacks;
• lack of sleep;
• involuntary eye movement, visual strabismus;
• extreme severity of congenital reflexes;
• increased muscle tone;
• bulge of the fontanel with intense pulsation;
• icteric shade of the body.

Symptoms of pathology in a newborn can appear both immediately after birth and within a few days, depending on the magnitude of the outpouring into the hemispheres. With timely identification of the problem, modern medicine allows you to resuscitate the child, in most cases without negative consequences for his future life.

The prevalence of the disease and the stages of its progression

Precedents associated with SAH of the brain are quite common. According to statistics, the most common are the precedents of subarachnoid effusion against the background of traumatism, accounting for about sixty percent of all cases.

Less common are precedents for the development of pathology due to changes in blood circulation in the cerebral vessels, diagnosed in seven percent of patients with this pathology. Most often these are patients of solid and retirement age, as well as people with alcohol or drug addiction. The rarest are the cases of spontaneous progression of the disease, their prevalence is less than one percent.

As for the etiology of the disease, the most common in medical practice is the occurrence of SAH due to rupture of the arteries located in the circle of Vizilli. About eighty-five percent of all registered cases fall to the share of such precedents, half of them end in death, while fifteen percent of patients do not even have time to get to a medical facility.

Cerebral hemorrhage is a disease that most often affects the adult population, however, the children's category is no exception. In children, this pathology often occurs against the background of injuries. Subarachnoid hemorrhage in newborns can be the result of prolonged or too rapid natural childbirth, with a discrepancy between the birth canal of the mother and the head of the child, and also as a result of the baby being without oxygen for a long time. Provoke the progression of pathology in a child can be infectious diseases of the mother, pathology of brain activity in a child of a congenital category, fetal hypoxia.

SAH of traumatic origin medicine classifies into three stages of development:

1. Progression of intracranial hypertension against the background of mixing of outflowing blood with cerebrospinal fluid, an increase in the latter in volume.
2. An increase in hypertension of the hemispheres to extreme maxima, due to the formation of blood clots in the cerebrospinal fluid channels, their blocking and impaired circulation of the cerebrospinal fluid.
3. Dissolution of blood clots, followed by intensification of inflammatory processes in the hemispheres.

Classification of the severity of the disease

To assess the severity of the patient's condition, medical specialists use three methodologies for ranking the course of the pathology.

Most often in practice, the Hunt-Hess scale is used to categorize the patient's condition, which has five degrees of damage to the human brain:

1. The first degree of the disease is considered the least life-threatening with timely initiation of therapy, characterized by a high percentage of patient survival. At this stage, the disease is asymptomatic with minor headaches and the onset of neck stiffness.
2. The second degree of the disease is characterized by a distinct loss of mobility of the occipital muscles, intense headaches, paresis of the nerves of the hemispheres. The prospects for a favorable outcome do not exceed sixty percent.
3. The third degree of the disease is manifested for a person by a moderate deficiency of the neuralgic category, stunning. The chances of surviving the patient do not exceed fifty percent.
4. The fourth level of pathology is characterized by the patient's stop state, a coma of the first degree may occur. Typical for this stage are failures of the autonomic system, severe hemiparesis. The chances of life are about twenty percent.
5. Last degree of progression: coma of the second or third level. The prognosis for the patient is disappointing, the survival rate is no more than ten percent.

The second, no less popular in medical practice for assessing the patient's condition, is Fisher's gradation, which is based on the results of computed tomography:

1. If the CT scan does not visually determine the outpouring of blood, the disease is assigned the first degree of severity.
2. The second stage is assigned to pathology if the scale of the outpouring does not exceed one millimeter in thickness.
3. With a lesion size of more than one millimeter, the third level of pathology progression is diagnosed.
4. With the spread of blood inside the ventricles and in the parenchyma, the fourth degree of SAH progression is diagnosed.

The SAH severity scale according to the World Federation of Neurosurgeons ranks the disease as follows:

1. The first stage - fifteen points on the GCS, no neurological deficit.
2. The second level - from thirteen to fourteen points, with no neurological insufficiency.
3. The third level - points are similar to the previous option, with the presence of signs of disorders from the nervous and peripheral systems.
4. The fourth stage of progression - according to the Glasgow Coma Scale, from seven to twelve points were assigned.
5. The last stage of the disease: less than seven points were diagnosed according to the GCS.

Diagnosis of pathology

Subarachnoid hemorrhage belongs to the category of the most difficult and life-threatening precedents. Its diagnosis involves a complex of hardware examinations of the patient in order to confirm the diagnosis, as well as determine the stage of development, localization of the hemorrhage, the degree of disturbances in the vascular system and hemispheres.

The main examination procedures are:

1. Primary examination of the patient, analysis of his complaints.
2. Visual assessment of a person's condition, monitoring of his consciousness and the presence of neurological abnormalities.
3. A laboratory blood test, with which you can determine the criteria for its coagulability.
4. Puncture of cerebrospinal fluid. If about twelve hours have passed since the beginning of the hemorrhage, according to its results, namely the presence of blood in the cerebrospinal fluid, it is possible to confirm the progression of SAH.
5. or computed tomography allows you to identify the presence and localization of the effusion, as well as assess the general condition of the brain. More informative in the situation with SAH is CT, therefore, this type of study is often prescribed to patients.
6. If a brain displacement is suspected as a result of an injury, echoencephalography is prescribed to confirm or refute this fact.
7. Dopplerography of the transcranial type is performed in order to monitor the quality of blood flow in the cerebral arteries, its deterioration as a result of narrowing of the blood channels.
8. Magnetic resonance angiography of the arteries helps to assess their integrity and patency.

Based on the results of the study, the patient will be diagnosed in accordance with the International Classification of Diseases of the tenth revision. SAH is included in the section "Diseases of the circulatory system", a subgroup of cerebrovascular diseases, may have an ICD-10 code from I160.0 to I160.9, depending on the localization of the source of the outpouring.

Treatment Methods

The methodology of pathology therapy provides for both drug treatment and surgical intervention, depending on the stage of the disease and its complexity. The expediency of therapy and its direction can only be determined by a qualified specialist solely on the basis of diagnostic results. Primary measures should be focused on stopping bleeding, stabilizing, preventing or reducing the volume of cerebral edema.

First aid

First aid for subarachnoid hemorrhage does not provide for any specific procedures, it consists in the immediate call of an "ambulance". It is strictly forbidden to give the patient any drugs to eliminate the symptoms, as this can cause unpredictable consequences.

If a patient has an epileptic seizure, you should try to create comfortable conditions for him by placing soft things under his head and other parts of the body. After the seizure ends, you need to put the sick person on their side, try to fix the limbs and wait for the ambulance to arrive.

When a person is in an unconscious state as a result of cardiac arrest, it is necessary to perform resuscitation of the cardiopulmonary type, with proportionality of compressions on the thoracic region to breaths thirty to two.

With an outpouring into the hemispheres, the only rational help to the patient is his hospitalization as soon as possible. All restorative and therapeutic procedures in the future are carried out exclusively under the guidance of specialists, based on the results of diagnosing the patient's condition.

Medical treatment

Conservative therapy can be used in situations where there are no indicators for surgical intervention, as well as to normalize the patient's condition in the preoperative and postoperative period.

The main objectives of drug treatment of subarachnoid hemorrhage are:

• achieving stability of the patient's condition;
• prevention of relapse;
• stabilization of homeostasis;
• elimination of the primary source of outpouring;
• carrying out therapeutic and preventive measures focused on prevention.

Depending on the complexity of the disease and its manifestations, the following drugs may be prescribed to the patient:

The expediency, dosage and duration of taking the drugs are determined solely by the attending doctor, based on medical indicators. In the process of treatment, the doctor traces the dynamics, can change the quantitative and qualitative composition of drugs in the absence of positive results.

Surgery

Surgical intervention is often prescribed by medicine for existing intracranial hematomas of a significant scale or when SAH occurs as a result of a serious head injury. In a situation where the patient has massive bleeding, emergency surgical procedures are performed. In other cases, the timing of the operation may vary and depend on the condition and age of the patient, the volume of the effusion and the complexity of the symptoms.

Medicine provides for the following types of surgical intervention for subarachnoid effusion:

1. Removal of hemorrhagic contents by introducing a syringe or a specific needle.
2. Elimination of hematoma with opening of the cranium.
3. Laser coagulation of blood vessels, if the effusion cannot be stopped with medications, sometimes with the application of specific clips to the damaged areas of the artery.

After surgery, the patient will have to undergo a mandatory course of drug therapy.

Rehabilitation procedures

Measures to restore the patient after subarachnoid hemorrhage are a mandatory continuation of therapy in the postoperative period. Depending on the complexity of the disease, rehabilitation can last from six months to several years, it has a complex structure.

After the precedent, it is important for the patient to completely abandon bad habits, try to avoid stressful situations and maintain a healthy lifestyle. In addition, during the rehabilitation period, medicine provides for the intake of medications, the action of which is aimed at preventing relapses.

Rehabilitation of the patient, depending on the severity of the experienced illness, may include the following areas:

• specific massages and hardware procedures to restore the patient's muscle and motor activity;
• health procedures in special centers;
• therapeutic exercises to restore walking and coordination skills;
• classes with a psychologist to restore the psycho-emotional state of the patient.

In the process of recovery at home, the patient will need proper care, as well as the support of loved ones and relatives.

Prognosis and possible complications

Subarachnoid hemorrhage of the brain is an insidious disease that very rarely passes without a trace for a person. The most harmless are complications in the form of frequent migraines and hormonal imbalances in the body. Additionally, after an experienced illness, the patient may experience a deterioration in brain activity, manifested in the form of psycho-emotional disorders, deterioration of attention and memory. However, such manifestations of the body after SAH are not considered particularly dangerous. Dangerous consequences include:

• vasospasm, which often provokes ischemic processes in the hemispheres;
• delayed ischemia, which affects more than a third of all patients, entails irreversible starvation of the brain with all the ensuing consequences;
• recurrent exacerbation of pathology;
• hydrocephalus;
• rare complications include pulmonary edema and heart attacks.

The chances of a patient recovering after SAH depend on many factors, such as the general physical health of a person, his age, the stage of the disease and the extent of the outpouring, and the promptness of first aid.

Often, it is a belated visit to a medical institution against the background of an abundant outpouring that causes a fatal outcome for the patient or serious complications that do not allow a person to return his life to its usual course.

Preventive measures

Prevention of SAH, like many other diseases of the cardiovascular system, is not particularly difficult. The main rule, the observance of which helps to prevent cerebral hemorrhage, in addition to precedents with injuries, is a healthy lifestyle. Rational nutrition, giving up bad habits, regular walks in the fresh air and moderate physical activity to keep the body in excellent condition, timely treatment of vascular and heart problems under the supervision of doctors are the primary and effective preventive measures against the development of SAH and other complex ailments.

If a person has the prerequisites for the development of SAH caused by problems of a cardiological nature, it is worth regularly undergoing examinations, taking, if necessary, preventive drugs prescribed by doctors to normalize pressure, heart rate, and monitor their health.

In this case, it is an attentive attitude to one’s body and a correct way of life that are the most important preventive measures that help to avoid a difficult and life-threatening precedent.

Summing up

Hemorrhage of the subarachnoid type belongs to the category of the most dangerous diseases, which very often cause death. Of course, it is better to prevent such situations, however, if such a precedent takes place, it is worthwhile to immediately deliver the patient to a medical facility: a person’s life depends on the speed of diagnosis and the provision of proper assistance.

Lead a full, healthy and correct lifestyle - this will help you avoid many health problems, is the key to the proper functioning of the body, reduces the risk of developing not only SAH, but also other diseases.

Subarachnoid hemorrhage (SAH) ranks third in the structure of cerebral stroke and accounts for about 10% of all forms of acute cerebrovascular accident with an incidence of 6 to 16 cases per 100,000 population per year. SAH most often develops in people aged 30 to 60 years. Mortality up to 28 days from the moment of onset is 30%.

Etiology

The main reason for the development of SAH is the rupture of the saccular aneurysm of the cerebral vessels, which occurs in 50-90% of cases. In 15% of cases, the cause remains unknown, arteriovenous malformations account for 5-7% of cases (Table 1). A significantly smaller share in the etiology of SAH belongs to brain tumors, hypertension, arteriosclerosis, amyloid angiopathy, cerebral angiomatosis, exogenous intoxications, blood diseases, coagulopathy, thrombolytic and anticoagulant therapy (Table 2). The frequency of occurrence of aneurysms of cerebral vessels is: in women - 12.2%, in men - 7.6% per 100 thousand population per year. The annual risk of an aneurysm rupture is 1-5%, during life - 10-30%.

Diseases often associated with saccular aneurysms:

- Marfan's syndrome;

- Ehlers-Danlos syndrome - type IV;

— insufficiency of alpha-antitrypsin;

- elastic pseudoxanthoma;

- neurophacomatosis (neurofibromatosis);

- congenital hemorrhagic telangiectasia;

- anomalies of the circle of Willis;

- moya-moya syndrome;

- coarctation of the aorta;

- polycystic kidney disease.

Given a certain genetic predisposition to the formation of aneurysms, it is believed that in first-degree relatives of patients with SAH, the risk of developing SAH is 3-7 times higher than in second-degree relatives or in the general population.

Aneurysmal SAH is most often caused by lesions of the following vascular beds: anterior communicating and anterior cerebral artery - 40-50%, internal carotid and posterior connective artery - 15-20%, middle cerebral artery - 15-20%, basilar and posterior cerebral artery - 3-5%, other arteries - 4-9%. Risk factors contributing to aneurysm rupture and the development of SAH are: arterial hypertension, smoking, chronic alcoholism, overweight, drug use. There are several different types of SAH, depending on the massiveness of the hemorrhage and the exit of blood outside the subarachnoid space: subarachnoid-parenchymal, subarachnoid-ventricular, subarachnoid-parenchymal-ventricular hemorrhage. All of these forms of hemorrhage can lead to occlusion of the CSF pathways, dislocation of the brain, and the formation of an occlusive-hydrocephalic syndrome. Depending on the shape, saccular, fusiform and fusiform aneurysms are distinguished. By size, they are divided into miliary (up to 3 mm in diameter), ordinary (4-15 mm), large (16-25 mm), giant (more than 25 mm). Aneurysms can be single or multi-chamber, single or multiple.

Nonaneurysmal perimesencephalic hemorrhage is a favorable and safe variant of SAH (Table 3), which accounts for 10% of all SAH and up to 2/3 of all SAH with normal cerebral angiograms. Blood flows into cisterns around the middle pons or ventral to the pons; aneurysms are not detected on angiograms. Clinical manifestations are much milder than with aneurysm rupture. The headache is not so intense, develops gradually (within minutes and hours), focal neurological symptoms are not observed.

Dissection of the arteries can lead to the development of SAH. The most common cause of SAH is a dissection of the vertebral artery, which begins in its extracranial part with a possible spread to the intradural part. Dissection of the intracranial part of the internal carotid artery as a cause of SAH is much less common than its defeat in the neck.

The most common causes of arterial dissection are:

- excessive rotation in the cervical spine;

- hyperextension injury;

– osteopathic manipulations;

- surgical intervention.

Currently, it has been proven that cerebral AVMs in very rare cases are the cause of isolated SAH, parenchymal-subarachnoid hemorrhages and isolated intraventricular hemorrhages occur more often in subependymal AVMs. Rarely, SAH occurs on the basis of the brain from dural AVMs, but they are marked by a recurrent course. Mycotic aneurysms are more often complicated by parenchymal hemorrhage and rarely cause basal SAH. The most common causes of mycotic aneurysms include infective endocarditis and aspergillosis. Sufficiently rare causes of SAH can be considered myxoma of the heart, sickle cell anemia, severe coagulopathy associated with the use of anticoagulants or congenital nature.

Clinical picture of SAH: acute and acute onset, often against the background of emotional and / or physical overstrain. The main debut clinical syndrome is an intense headache, depression of consciousness (from mild stunning to coma), psychomotor agitation often occurs, severe sympathicotonia, the appearance and growth of meningeal syndrome is observed.

Severe and unusual headache that develops within seconds of onset is a characteristic symptom of aneurysmal SAH. Biphasic headache is noted in patients with SAH due to dissection of the vertebral arteries. Spinal SAH may debut with acute, sudden pain in the lower part of the neck, spreading to the interscapular region, shoulder girdle, and arm.

More than 60% of patients with SAH have impaired consciousness: confusion, agitation, delirium, coma.

In 10% of patients, epileptic seizures are noted, in the vast majority of cases developing on the first day of the disease.

Meningeal symptoms in the form of neck stiffness, Brudzinski's and Kernig's symptoms are common signs of SAH, but they form within a few hours from the onset of the disease, may be absent in patients in a coma or suffering from myasthenia gravis. Meningeal syndrome is a symptom complex of irritation of the meninges in the form of the presence of meningeal symptoms in combination with changes in pressure and composition of the cerebrospinal fluid (Table 4). Syndrome of irritation of the meninges - headache, pain and tension of the muscles of the neck, irritability, hyperesthesia, photo- and phonophobia, nausea, vomiting, impaired consciousness in combination with muscle contractures in the form of stiff neck and neck muscles, Kernig's symptom, Brudzinsky's symptoms, Bikel's symptoms , Guillain and Edelman.

In the acute period of SAH, focal neurological symptoms are usually not detected, but they can form after 2-3 weeks due to secondary cerebral ischemia (Table 5).

Arterial hypertension is determined in about half of patients in the acute period of SAH, however, less than 25% of patients with SAH have a history of arterial hypertension.

The described typical clinical picture of the disease occurs in 2/3 of patients. In 1/3 of cases, the so-called atypical course of SAH is observed. There are several atypical clinical variants of SAH: migraine-like, pseudomeningitis, pseudohypertensive, pseudoradicular and pseudopsychotic. Features of the clinical picture of atypical variants of SAH are determined by their name, i.e. SAH proceeds under the clinical "masks" of a migraine or hypertensive crisis, acute psychosis, meningitis, and acute radicular pain syndrome. Meningeal signs are often delayed in time of onset and dissociated.

The clinical picture of aneurysmal SAH is largely determined by the topical location of the aneurysm.

Aneurysm of the anterior cerebral and anterior communicating artery: psychotic disorders, impaired memory, intelligence, akinetic mutism, confabulatory-akinetic Korsakoff syndrome, crural type of hemiparesis.

Aneurysm of the internal carotid artery: periorbital pain syndrome, eye symptoms (decreased visual acuity, loss of visual fields), damage to the III, IV and VI pairs of cranial nerves, damage to the I and II branches of the trigeminal nerve.

Aneurysm of the middle cerebral artery: "3 hemi" syndrome (hemiparesis, hemihypesthesia, hemianopsia) in combination with speech disorders in case of damage to the dominant hemisphere.

An aneurysm of the basilar artery may present as symptoms of damage to the upper and lower segments of the basilar artery. With aneurysms of the upper segment - one- or two-sided lesion of the third pair of cranial nerves, Parino's symptom, ophthalmoplegia, vertical and rotatory nystagmus.

With aneurysms of the lower segment: mydriasis, coma, respiratory disorders.

Clinical assessment of the severity of SAH.

The most significant prognostic criterion for the outcome of the disease is the severity of neurological disorders present at the time of the initial examination. Two rating scales are most commonly used: the Hunt-Hess scale (W. Hunt and R. Hess), which is comparable to the Glasgow coma scale, and the World Federation of Neurosurgeons (WFNS) scale (Tables 6-8).

Diagnosis of SAH is based on a comparison of the clinical picture of the disease, the results of neuroimaging and the study of cerebrospinal fluid.

Computed tomography (CT) of the brain has a high sensitivity (> 95%) in detecting blood in the subarachnoid space. The most common causes of negative CT results are minor hemorrhages and late examinations. After 48 hours from the onset of hemorrhage, the sensitivity of CT examination is 80-85%, on days 3-5 - 75%, on days 6-21< 30 %.

CT examination in the early period of the disease provides important information for assessing the risk of delayed vasospasm according to the classic and modified Fisher rating scale (Table 9).

The risk of vasospasm increases in the presence of blood not only in the cisterns, but also in the ventricles of the brain.

Magnetic resonance imaging (MRI) is much less commonly used for early diagnosis of SAH, but MRI is more sensitive than CT for delayed diagnosis of hemorrhage after several days.

In the presence of clinical symptoms of SAH and negative results of CT examination, examination of cerebrospinal fluid (CSF) is an obligatory diagnostic method. Xanthochromia after CSF centrifugation is detected after 6 hours from the onset of the disease and always after 12 hours. The most characteristic changes in CSF in various brain diseases are shown in Table. ten.

Vascular imaging is an important and mandatory diagnostic tool for clarifying the cause of SAH and detecting cerebral vasospasm.

Catheter cerebral angiography remains the gold standard, with 3D rotational projections of angiograms being particularly effective. If it is impossible to perform catheter angiography, it is advisable to perform non-invasive (CT or MRI) angiography, which has a fairly high sensitivity in detecting aneurysms of 4 mm or more.

Complications of SAH

The most severe and frequent complication is cerebral vasospasm and ischemic brain damage. According to the Fisher rating scale, in type II basal hemorrhage, cerebral vasospasm develops in 100% of cases, and cerebral ischemia in more than 50% of patients.

Cerebral vasospasm is formed from 3-4 days from the onset of the disease with a maximum development by 7-14 days with subsequent regression or leads to complete obliteration of the vascular bed in 20% of cases. Cerebral infarction develops in more than 60% of patients with cerebral vasospasm.

Recurrence of aneurysmal SAH, the second most common and severe complication, develops in 17-26% of patients with aneurysm, in 5% of patients with AVM, and very rarely in SAH of other etiologies. Most often, repeated hemorrhage occurs due to thrombus lysis at the site of aneurysm rupture, most often on the first day (4%) and in the next 4 weeks (1-2% per day). Risk factors for the development of repeated hemorrhages are the duration of the disease, the severity of the patient's condition, the level of blood pressure and the fibrinolytic activity of the CSF.

Common early complications of SAH are acute occlusive hydrocephalus and diffuse cerebral edema. Diffuse cerebral edema, confirmed by CT scan, serves as a marker of poor prognosis and treatment failure.

In 10-20% of patients, despite the improvement in hemodynamics, extracerebral complications may also develop, such as pulmonary edema, myocardial ischemia, cardiac arrhythmia, non-infectious hyperthermia, venous thrombosis with complications, hyponatremia. Rare complications are progressive cerebral edema, reversible posterior encephalopathy syndrome, and hemorrhagic transformation of cerebral infarction.

Treatment

Therapeutic tactics in SAH is largely determined by the etiology of hemorrhage and the severity of the course of the disease. If an aneurysm is detected, the patient is shown surgical treatment within the first three days from the onset of the disease. Most often, an aneurysm is repaired within the first 24 hours after hospitalization.

Basic principles for managing patients with SAH:

- urgent (emergency) hospitalization in an intensive care unit with special nursing care: in the first 12-24 hours, intensive care and resuscitation should be carried out;

- assessment and monitoring of somatic (cardiovascular and pulmonary) and neurological status;

— optimization of oxygenation;

- the appointment of nimodipine;

- immediate aggressive treatment of hydrocephalus;

— the fastest possible elimination of the aneurysm;

- with a significant increase in intracranial pressure - consideration of the issue of early surgical decompression;

- maintenance of normovolemia;

- in the presence of hypoperfusion - an increase in blood pressure;

- maintaining normal body temperature of the patient;

- control of the concentration of glucose in the patient's blood (4.4-8.3 mmol / l);

- control of the concentration of sodium in the blood plasma, the use of hypertonic solutions for hyponatremia;

- prevention of deep vein thrombosis of the lower extremities;

- do not use frequently and do not use high doses of sedatives or narcotic drugs, do not prescribe phenytoin;

- do not prescribe infusion of hypotonic solutions;

- do not carry out preventive hypervolemia;

- do not limit fluid intake, but do not overload patients with fluid;

- do not reduce blood pressure after surgical removal of the aneurysm;

- do not use glucocorticosteroids for a long time.

At an early stage in the care of patients with SAH, analgesic antiemetics, laxatives, H2 receptor blockers or proton pump inhibitors are prescribed, and measures are taken to reduce the risk of deep vein thrombosis of the extremities. Systolic blood pressure should be kept at numbers not exceeding 160 mm Hg, to avoid a sharp sudden decrease in perfusion pressure. With a significant increase in blood pressure, a bolus administration of labetalol is indicated.

Upon admission, patients are prescribed nimodipine (60 mg every 4 hours for 21 days), if arterial hypotension occurs, the single dose is halved (30 mg) and administered at intervals of 2 hours. Antiepileptic drugs are not prescribed for prophylactic purposes.

Antifibrinolytic agents (aminocaproic acid) are currently used very limitedly, only in carefully selected cases: with a very high risk of recurrent hemorrhage, the impossibility of prompt removal of an aneurysm, subject to measures to prevent arterial hypotension and hypovolemia, when prescribing individual doses of APS with a duration of use no more than 72 hours.

An important area of ​​conservative treatment of cerebral vasospasm is the correction of hemodynamic disorders, improvement of cerebral perfusion, and reduction of increased vascular resistance. It is necessary to assess the volemic status and take measures to prevent hypovolemia by prescribing isotonic or hypertonic (1.5, 3, 7.5%) sodium chloride solution and, as an addition, 5% (25%) albumin solution. The main goal of infusion therapy is to achieve zero fluid balance.

Therapy that improves hemodynamics is also known as "3G therapy": hypervolemia, hypertension and hemodilution. However, at present there are no convincing advantages of hemodilution, hypervolemia is possible only in patients in whom true normovolemia was determined before the development of vasospasm, and only induced hypertension improves regional cerebral blood flow and brain tissue oxygenation.

In cases where cerebral vasospasm is not amenable to conservative treatment, it is advisable to consider the use of endovascular intervention - transluminal balloon angioplasty and superselective intra-arterial administration of vasodilators; with an increase in body temperature in patients with SAH, it is necessary to exclude the infectious nature of hyperthermia (pneumonia, bacteremia, ventriculitis, and etc.), which requires the appointment of antibiotic therapy. In order to prevent infectious complications in immunocompetent patients, antibiotics are not prescribed. Non-infectious (so-called central) hyperthermia is corrected by the appointment of antipyretics and physical methods of hypothermia.

Prevention of venous thrombosis and its complications is carried out by the combined use of stockings and intermittent air compression. The safety of heparin use has not been proven.

Currently, further study of modern pharmacological possibilities of influence on delayed cerebral ischemia due to vasospasm in SAH is underway. Proven agents include oral nimodipine, and research is ongoing on endothelin antagonists (clososentan), statins (simvastatin), magnesium sulphate, albumin, and lumbar drainage. Experimental studies confirm the effectiveness of the widespread clinical use of magnesium sulfate as a cerebral vasodilator and neuroprotector.

Surgical treatment of a ruptured aneurysm is possible by surgical clipping and endovascular occlusion. Both methods are considered not as alternative, but as complementary. The choice of method depends on the location and size of the aneurysm, as well as on the age of the patients.

Hemorrhagic processes, that is, the outflow of blood into the meninges, occur in the practice of neurologists and specialized surgeons in 27-30% of cases of common lesions of cerebral structures. The condition requires urgent medical correction, possibly surgical methods.

Subarachnoid hemorrhage is an acute hemorrhagic process, the outflow of liquid connective tissue into brain structures with the development of neurocyte cell death. Complications dangerous to life and health are possible, the probability of death varies from 20 to 70%, depending on the extent of the lesion and the location of bleeding.

The symptoms are not typical, at first it is difficult to understand what happened, both for the patient and the specialist doctor. An examination is required.

Signs are limited to intense headache and initial neurological deficits. The full clinical picture unfolds after a few hours from the onset, when irreversible changes begin in the brain.

Recovery is possible, forecasts vary from case to case. Urgent hospitalization required.

To understand the essence of the pathological process, you need to learn some anatomical information. The brain and its surrounding tissues are not a homogeneous structure. It consists of several, conditionally speaking, "layers".

The deepest one is the soft shell. It is located especially close to the cerebral tissues; hemorrhages in this area quickly lead to compression and death of neurons with the development of severe neurological deficit.

Subarachnoid hemorrhage carries a colossal danger. Liquid connective tissue comes out into the space between the two "layers".

A rough accumulation or hematoma is formed. The clot pushes through the middle and soft membranes, compresses the brain and surrounding structures diffusely, that is, along its entire diameter.

If the subarachnoid space is not drained in a timely manner and the hematoma is not eliminated, ischemia of the brain tissues begins as a result of vascular compression.

This is a direct path to secondary necrosis of cerebral structures. The result of cell death is a persistent neurological deficit or death of the patient.

Subarachnoid hemorrhages are considered a form of stroke, but it is not always of internal, organic origin. It is necessary to understand the causes separately, as part of the diagnosis.

Classification

Typification is carried out for several reasons. At the same time, only the etiological criterion matters for a simple patient.

In accordance with it, the process is divided into:

• traumatic form. As follows from the description, it is provoked by a mechanical factor: a blow with a blunt object, a fall, and other moments can cause a rupture of the vessel and bleeding.
• Spontaneous (non-traumatic) or organic variety. It occurs much less frequently. Mainly in patients with reduced vascular elasticity, tumors of cerebral structures and other diseases.

Depending on the form of the violation, one or another treatment is carried out. In the case of trauma, no additional etiotropic measures are required, the factor arises suddenly and disappears just as quickly, leaving a consequence that needs to be dealt with.

The second classification pays attention to the localization of the hemorrhage.

Accordingly, allocate:

• isolated form. Blood is within the subarachnoid space. There is no compression of the brain, the symptoms are minimal. This variety carries a lesser danger to health and life.
• Diffuse or combined type. 3-4 more subspecies of this pathological process are called. But the names do not play a big role for the patient. They are named depending on the direction of the negative impact.

Fisher's classification is generally accepted. It is based on the results of computed tomography and echoes the previous subdivision method. Subarachnoid hemorrhage exists in three forms:

• First grade. No signs of violation. That is, the reference point that is used to describe the norm.
• Second class. The total thickness of the released blood layer is 1 mm or less. It is considered a relatively mild form of the condition, rarely leads to compression of cerebral tissues and even more fatal complications.
• Third class. The layer of blood is over 1 mm, pronounced neurological symptoms are noted. Urgent treatment is needed. Possible death of the patient from a violation of vital functions.
• Fourth grade. Massive bleeding. Compression of cerebral structures. Severe symptoms, severe neurological deficit. Surgery required.

Attention:

It is advisable to start treatment within the first hour after the onset of the disorder. Further, the chances of success fall.

Symptoms

Manifestations depend on the amount of blood released, the size of the hematoma. The cerebral components come first.

• Headache. Extremely intense, unbearable character. It occurs abruptly, similar to a hammer blow on the back of the head. Accompanied by a feeling of intense distension somewhere in the skull.

Baling, shooting, does not depend on the heart rate. The reason for such a pronounced moment is the stretching of the subarachnoid space and tissue compression, as well as rupture of the vessel. All three of these structures are richly innervated, which leads to an unbearable pain syndrome.

• Double vision. Unable to focus on subject, blurred vision. This is a temporary phenomenon. It lasts the first few tens of minutes if the visual pathways are not affected.
• Dizziness. Expressed, a person is not able to navigate in space. He takes a forced prone position in order to somehow compensate for the violation of well-being.
• Nausea and vomiting are possible, but relatively rare. Such a symptom is not considered long-term. This is a short term occurrence.
• Pain in one eye. From the side of defeat. It rarely occurs, no more than 3-5% of situations.
• Possible loss of vision. The so-called monocular blindness (on the one hand). The manifestations are also relatively rare.
• Seizures. Tonic-clonic. By nature, they resemble an epileptic seizure, which in essence the condition is. The episode lasts several minutes, may recur, which is considered an unfavorable sign. Speaks of a massive lesion of cerebral tissues.

This is the main clinical picture. The leading symptoms of subarachnoid hemorrhage in the brain are pain and vertigo.

Other possible signs:

• Loss of consciousness. Deep fainting, it is difficult to get a person out of such, standard methods do not help. Occurs in 3-5% of cases. Perhaps less often.
• Speech disorders. By type of partial or complete paralysis of the muscles involved in articulation.
• Weakness in half of the body.
• Painful reaction to light or sound. Moreover, the intensity of the stimulus can be minimal. The threshold is significantly reduced.
• Weakness in the muscles of the neck against the background of hyperkinesis (pathological tension).

Clinical signs overlap each other gradually. In some cases, the complex is limited to severe severe headache.

Causes

Development factors are multiple. The classic situation is a traumatic brain injury. In this case, the subarachnoid hematoma is large, because the mechanical effect is rarely small in intensity.

Among the organic factors, the leader is an arterial aneurysm - a vascular protrusion of a wall nature.

The rupture leads to massive bleeding. Moreover, the pathology itself does not go away. Requires treatment. Possible relapse and death of the patient.

Other options are much less common. These are benign or malignant brain tumors, encephalitis, meningitis, inflammatory pathologies of cerebral structures, arteriovenous malformations (connections between vessels of different types), past neck injuries can also become a factor in the development of the disorder.

There are also rare genetic, autoimmune pathologies that are not of great importance - including vasculitis, however, they are described in the clinical literature. Therefore, doctors evaluate the likelihood of rare violations, but they begin to search for them at the end.

Diagnostics

The examination is carried out urgently within the framework of a neurological hospital. Transportation is immediate, the sooner therapy is started, the higher the chances of a successful outcome.

There is no time for long explorations. If the patient is conscious, he is interrogated for complaints. When fainting or coma, they talk with relatives. An assessment of basic reflexes is mandatory.

Immediately after admission, doctors seek the possibility of an MRI diagnosis. This is the basis that allows you to visualize tissues, detect the location of the hemorrhage, assess the size of the hematoma, and also work out the tactics of therapy and operational access, if there are indications for surgical treatment.

Verification is carried out using tomography, this is a key event. However, it is not always possible to establish a diagnosis even in such a sensitive and informative way.

Then resort to spinal puncture. A typical sign of an emergency is blood in the fluid. Then measures are taken to stabilize the patient's position.

At the end, you can understand in more detail.

The following methods are shown:

• Study of reflexes (routine neurological). Provides information on the safety of higher nervous activity.
• Repeat MRI as indicated.
• Questioning the patient if he is conscious about the current state of health.

The survey is carried out on an urgent basis. The probable outcome depends on the rate of detection of the pathological process. Usually the diagnosis of SAH is assumed after routine measures, MRI puts everything in its place. There are no difficulties in identifying, except for rare clinical cases.

Treatment

Therapy is surgical or conservative. At the discretion of the specialist, based on the nature and severity of the pathological process.

The scheme of drug correction is standard, only the names of the drugs and dosages differ:

• Antihypertensive. Reduce blood pressure. Beta-blockers, calcium antagonists, centrally acting drugs, ACE inhibitors. A cardiologist must be connected to the treatment, because an incorrectly selected combination can put an end to the condition of the kidneys and heart.
• Narcotic painkillers such as morphine. Stop discomfort. Since they are extremely intense, improvised medicines will not help the cause.
• Cerebrovascular. To ensure normal cerebral circulation. Actovegin, Piracetam, Nimodipine. They are prescribed on a long-term basis, until the patient fully recovers.
• Anticonvulsant according to indications. As well as drugs for vomiting.

Surgical treatment is prescribed, if there are grounds for such. This is a large hematoma that compresses the brain tissue or an aneurysm of one of the vessels.

In the first case, the accumulation of blood is removed by open access, thereby nullifying the damaging factor. This is a severe traumatic operation, but there are no alternatives to it.

In the second situation, options are possible. Clip-on clips are used to eliminate wall protrusion or endovascular occlusion. These techniques are somewhat easier and less in terms of intervention.

Rehabilitation

Therapy continues after discharge from the hospital. At the end of the transferred subarachnoid stroke, the patient acquires a lot of negative symptoms. These are short-term complications or neurological deficits.

Among these unpleasant phenomena: headache of a regular nature, severe weakness, insomnia, partial or complete loss of sensitivity, visual impairment. To solve these problems, third-party specialized specialists are involved.

Among the methods of correction in the rehabilitation period:

• Taking non-narcotic analgesics according to indications. Pentalgin as the main one, drugs based on metamizole sodium.
• Therapeutic exercise for the normalization of motor activity, motor functions.
• Establishing a clear schedule for sleep and wakefulness. According to indications, short-term use of special drugs.
• Hiking for 40-50 minutes a day, preferably twice: in the morning and in the evening. Gradually, time can be increased.

Forecast

If the vital centers are not affected, the amount of bleeding is insignificant, the outcome is most often favorable. Factors that improve the likely outcome of an emergency:

• Young age. Up to 40 years old.
• A relatively mild variant of the pathological process. According to the described classification of Fisher - 2nd grade.
• The absence of a pronounced symptomatic complex. Not counting the headache, which is always noted.
• Mild neurological deficit, especially if there is none. It says that the important centers of the brain are normal.
• Lack of compression of cerebral structures.

Traumatic subarachnoid hemorrhage is usually more severe than other options, because the mechanical factor leads to extensive vascular destruction and massive bleeding.

Classic provocateurs are a car accident, a fall from a motorcycle, a bicycle, a great height in other situations.

As for the statistics, approximately 40% of patients die in the pre-hospital and hospital stages.

Only a quarter of the victims can count on a full recovery. During the first year, 40% of patients die or a little more.

The statistics are depressing. A lot depends on when you start treatment.

Possible consequences

The list of complications is wide, the phenomena are not always obvious enough.

• Cognitive impairment is the main consequence of SAH. Manifested as a decrease in the productivity of thinking and the speed of mental activity. Memory suffers especially, the full recovery of which is rarely achieved.
• Emotional deviations. An implicit violation that does not always go out to be associated with the transferred pathology. Anxiety syndrome, phobia. Against the backdrop of the expectation of re-hemorrhage. It is treated with psychotherapeutic methods and with the help of sedatives.
• Epilepsy. After damage to the hippocampus, temporal or frontal lobes of the brain.
• Hydrocephalus. An increase in the amount of liquor due to the deterioration of the drainage system.
• Ischemic stroke. As a result of compression of blood vessels by hematoma. It occurs as a complication in 15-20% of clinical cases.
• Recurrent bleeding. Happens in the first few days as an early consequence. Dramatically increases the risk of death of the patient or severe disability.

Prevention of negative consequences after suffering an emergency is part of the structure of therapeutic measures. The task is solved in parallel with others.

Subarachnoid hemorrhage (SAH) is a fatal condition in many cases. Requires urgent hospitalization and assistance. The sooner the better.

The chances of survival are about 60%, the probability of complete recovery is 20-25% on average.

The general trend is death in the first days, if the patient survived - a gradual compensation of functions in the initial six months or 12 months.