CT signs of subarachnoid hemorrhage. Subarachnoid hemorrhage (SAH). Pathological anatomy of cerebral hemorrhage

With subarachnoid hemorrhage (SAH), blood flows into the space between the arachnoid membrane and the brain substance itself. The main causes of this condition are the rupture of the aneurysm (all of them are located subarachnoid) and head trauma, as well as the causes include dissection of the wall of the arterial vessel. Risk factors for spontaneous SAH: hypertension, significant daily fluctuations in blood pressure, oral contraceptives (in women), use of cocaine, amphetamine and other sympathomimetics, alcohol consumption, amyloid angiopathy, anticoagulant or thrombolytic therapy, vascular malformations, intracranial vein thrombosis.

Diagnosis of subarachnoid hemorrhage: CT is the method of choice

With subarachnoid hemorrhage, it is computed tomography that allows it to be most fully and reliably visualized. Here, there is a direct dependence of the reliability of visualization on the time elapsed after the moment of hemorrhage (if less than 12 hours have passed since the onset of SAH, the reliability will be very high; if 12-24 hours have passed, the reliability will be lower, since the blood can be partially lysed during this time and it will be difficult for the interpreter to come to a conclusion).

On the presented images, the signs of SAH are determined (in this case, of a traumatic nature). It can be seen that the density of the content of the Sylvian fissures is different - on the right it is much more due to the fact that the right Sylvian fissure contains hyperdense blood (marked by arrows in the images)

These images also show changes of a traumatic nature, different from those given above - this is an acute subdural hematoma (most pronounced on the left side), causing dislocation of the midline structures.

Rupture of an arteriovenous malformation as a cause of subarachnoid hemorrhage

Often the cause of SAH is the rupture of an arteriovenous malformation (AVM). In this case, the patient is also most often diagnosed with hypertension. The size of the malformation is usually small - no more than 2-3 cm in diameter, its drainage into deep veins is typical. The most common malformations of the posterior cranial fossa. All arteriovenous malformations have a typical structure: their structure includes adductor arteries, a "tangle" of pathologically tortuous, altered vessels (of a mixed - both arterial and venous - nature), as well as draining veins.

The following types of malformations are distinguished: arterial, arteriovenous fistulous, arteriovenous racemose, arteriovenous micromalformation, cavernous arteriovenous malformation, telangiectasia. There is also a classification of AVMs according to Spetzler-Martin, which is based, first of all, on the size of the arterio-venous node: according to this classification, AVMs less than 3 cm, 3-6 cm, more than 6 cm are distinguished; AVM localization (outside or inside a functionally significant area of ​​the brain); the nature of drainage (lack of deep draining veins or their presence). Rupture can cause hemorrhagic stroke, SAH. A lethal outcome in AVM rupture occurs in 10-15% of patients.

On native (without contrast) CT or MRI, the AVM looks like an intracerebral formation of increased density, irregular shape, with areas of calcification; there may also be noticeable individual convoluted vessels that have a different - incorrect - course.

Rupture of cerebral artery aneurysm as a cause of subarachnoid hemorrhage

An aneurysm of the cerebral arteries is a local expansion of the lumen of an artery due to a change or damage to its wall. Most often, aneurysms are formed in the area of ​​bifurcation of vessels or in the area of ​​discharge of daughter trunks. Typical localization sites of aneurysms: anterior cerebral, anterior communicating artery. Peak age for aneurysm formation: 20-40 years. The development of an aneurysm depends on the resistive properties of the vascular wall, as well as hemodynamic factors (defects in the muscular membrane of the vessel, defects in the discharge of daughter trunks, collagenization). At first, it is customary to talk about preneurysm, which over time becomes an aneurysm.

Classification of aneurysms: bifurcation-hemodynamic (congenital, saccular); aneurysms in systemic hypertension (hypertension, polycystic kidney dysplasia, aortic coarctation, and others); aneurysms in regional hypertension (arteriovenous malformation and others); aneurysms in hereditary mesenchymopathies (Maran's syndrome, Ehlers-Durso syndrome), atherosclerotic aneurysms (dolichoectasia of the basilar artery), hypertensive, radiation.

This patient has SAH caused by spontaneous rupture of an anterior cerebral artery aneurysm. Pay attention to the marked area, where blood is clearly visualized in the external cerebrospinal fluid spaces. In addition, the rupture of the aneurysm led to a hemorrhagic stroke - a parenchymal hemorrhage with deformation of the brain ventricles is clearly visible.

Radiation semiotics of aneurysms

CT in case of aneurysm rupture is characterized by the presence of a hematoma or subarachnoid hemorrhage of typical localization (the nature of hemorrhage in case of aneurysm rupture - SAH - in 30% of cases). Aneurysms can be saccular (small - less than 4 mm, medium - from 4 to 10 mm, large - more than 10 mm), fusiform aneurysms capture extended sections of blood vessels, aneurysm (dolichoectasia) of the great cerebral vein (Galen's vein) is often combined with arteriovenous malformation. Nonspecific arteritis occurs in the form of central hematomas, sometimes hemorrhages are bilateral (bilateral).

This patient has a hemorrhage from an aneurysm of the anterior communicating artery. Pay attention to the hyperdense (light) strip in the interhemispheric fissure - this is blood (marked with an arrow)

Less than a month later, the same patient had an aneurysm rupture and a hemorrhagic stroke. The changes compared to the previous images are pronounced - it is possible to visualize a parenchymal hematoma in the left frontal lobe, as well as a breakthrough of blood into the ventricles of the brain.

Malformations of arterial vessels as a cause of subarachnoid hemorrhage

Malformations of cerebral vessels are a heterogeneous group of dysembryogenetic formations of predominantly angiomatous nature. This also includes persistent embryonic vessels, various kinds of shunts and fistulas. Angiomatous malformations can be - cavernous, intermediate, racemose (telangiectasia, arteriovenous); mixed, combined (within the CNS, factomatosis). Non-angiomatous defects are: varicose veins (for example, varicose veins of the brain), arteriovenous sinuses and fistulas, persistent embryonic vessels, and some others.

Unclassified malformations: cavernous angiomas - 5-13% of all malformations of cerebral vessels. Clinically manifested by convulsive syndrome, progressive neurological deficit, symptoms of intracerebral hemorrhage (like diapedesis or hematoma). Venous angiomas (racemosis or varicose veins) are small dilated veins that pass through the parenchyma and flow into the draining collector vein). Telangiectasias are dilated capillaries located in the substance of the brain. Not visualized on CT. On MRI after injection of contrast, in some cases, a “gentle” cloud-like increase in signal intensity is observed.

The images presented show the classic signs of subarachnoid hemorrhage - note the area marked with a circle in the left image and arrows in the rest. One can see hyperdense blood in the subarachnoid CSF spaces; on the image in the axial plane, the difference between the right and left hemispheres of the brain is clearly visible.

FROM ubarachnoid hemorrhage(SAH) is a clinical syndrome characterized by known nosological independence and is caused by various etiological factors. Spontaneous SAH is considered hemorrhage non-traumatic nature (spontaneous SAH is a type of hemorrhagic stroke).

Etiology. The most common (80 - 85%) SAH occurs, which develop as a result of blood entering the subarachnoid space due to rupture of an aneurysm of a cerebral vessel. Aneurysms usually occur at the branching of the arteries, usually at the base of the brain.

Risk factors for SAH (which are not sufficiently specific): arterial hypertension, especially with significant daily fluctuations in blood pressure (BP), oral contraceptives, smoking, cocaine use, alcoholism, pregnancy and childbirth (modification of this risk factor requires the greatest responsibility). Among close relatives of patients with SAH, aneurysms are detected more often.

The most common causes of spontaneous non-aneurysmal SAH: small ruptures of intradural arteries, mycotic microaneurysms, immunodeficient arteritis or arteritis due to drug abuse. The recurrence rate is 1% per year.

Diagnostics. SAH should be suspected in the presence of characteristic clinical signs, confirmed by computed tomography (CT). If CT is not possible or if CT does not reveal SAH, a lumbar puncture (LP) is necessary. LP is also indicated for suspected inflammatory lesions of the meninges (with SAH, the temperature may rise to subfebrile numbers).

The most typical clinical sign of SAH is a sudden onset or developing within seconds or minutes of severe headache (often described by the patient as a "sharp blow to the head"). After a few seconds, about half of the patients lose consciousness, which in most cases recovers spontaneously. The clinical picture may resemble a syncopal state or an epileptic seizure. At the same time, one should not forget that epileptic seizures often develop with SAH, and a number of patients develop neurogenic cardiac arrhythmias. Focal neurologic deficits are often mild or moderate and may reflect the location of the aneurysm. Examples can be damage to the oculomotor nerve in case of rupture of an aneurysm of the posterior communicating artery, the development of contralateral hemiparesis in case of rupture of an aneurysm of the middle cerebral artery, abulia in case of aneurysms of the anterior communicating artery. Neck stiffness is often present and may appear several hours after SAH.

Differential diagnosis for sudden headache is carried out with cerebral venous thrombosis, migraine, meningoencephalitis, intracerebral hemorrhage, acute hypertensive encephalopathy, sinusitis.

To assess the severity of SAH, the Hunt and Hess scale was proposed (W. Hunt, R. Hess, 1968):

(*) - in the presence of significant systemic pathology or severe vasospasm, the gradation increases by one.

In 1988, the World Federation of Neurosurgeons proposed a new classification of SAH: World Federation of Neurological Surgeons (WFNS) grading scale of SAH:

(*) - gross neurological deficit is assessed - aphasia, hemiparesis, hemiplegia; cranial nerve paresis is not considered a neurological deficit.

The severity of SAH according to changes on CT is assessed using the Fisher scale:

Blood that is in the subarachnoid space may not be detected on CT scan after 24 hours, and after 5 days it is not detected already in 50% of cases. At a later date, LP and MRI are used to detect SAH. If occlusive hydrocephalus or hematoma of the temporal region is detected on CT need to consult a neurosurgeon and emergency surgical intervention. In addition to occlusive hydrocephalus caused by hemotamponade, at the end of the 1st, beginning of the 2nd week, aresorptive hydrocephalus may develop.

There is an option non-aneurysmal perimesencephalic hemorrhage. In this case, the outflow of blood is limited to cisterns around the midbrain, the center of bleeding is located directly in front of the midbrain, and in some cases traces of the presence of blood are found only in front of the brain bridge. This variant accounts for 10% of all SAH and 2/3 of all SAH with normal angiograms and is benign in terms of prognosis.

In patients with SAH, it is recommended to study the fundus, determine the sodium content in the blood, and evaluate the volume of circulating blood (CBV). Examination of the fundus reveals edema of the optic discs; hemorrhage into the vitreous body (Terson's syndrome); subhyaloid or preretinal hemorrhage (a highly specific but insensitive sign for SAH). The determination of sodium in the blood serum reveals hyponatremia, which occurs in combination with hypernatriuria against the background of a decrease in BCC. Another syndrome leading to a violation of the water and electrolyte balance is the syndrome of inappropriate secretion of antidiuretic hormone.

Treatment. Patients with SAH in a serious condition (depression of consciousness) should be placed in intensive care units, where tracheal intubation and artificial ventilation of the lungs are performed in patients in a coma and with respiratory failure, correction of electrolyte disorders. In all cases of SAH management, early provision of adequate intravenous access is necessary. The introduction of liquids should be carried out under the control of daily diuresis, plasma osmolality and sodium content in plasma. The basis should be balanced salt solutions. Adequate oxygenation is required. It is necessary to control blood pressure - avoid hypo- and hypertension.

All patients with SAH should consult a neurosurgeon. In a non-severe condition (I-III degree on the WFNS scale), clipping of the aneurysm is shown in the first 48-72 hours after its rupture. In more severe patients (grade III-IV on the WFNS scale, high surgical risk, with aneurysms with a narrow neck), endovasal intervention can be applied. If it is impossible to carry out an urgent operation, surgical treatment is carried out in the "cold period" - not earlier than after 2 weeks.

The main indications for surgery for ruptured aneurysms are :
1 . risk of rebleeding from the aneurysm (frequency 26% within 2 weeks, mortality - 76%);
2 . prevention of ischemic complications (64%, fatal - 14%);
3 . the presence of intracerebral hematoma with compression of the brain and dislocation (lethality without surgery 95%).

(! ) Radical exclusion of aneurysms by clipping is 98%, with endovasal intervention - 80%. Postoperative mortality ranges from 2 - 3 to 20%, depending on the severity of the condition.

To detect vasospasm, transcranial dopplerography is possible. Vascular spasm in SAH can be reflex at the time of aneurysm rupture and does not lead to cerebral infarction, as well as secondary, by the end of the 1st week, due to the effect of biologically active substances on the vascular wall (beginning on days 3-4, reaches a maximum on 7 - 12 days). Identification and assessment of the degree of vasospasm can be carried out by determining the peak systolic blood flow velocity according to ultrasound.

moderate vasospasm is determined when the blood flow velocity in the MCA is more than 140 cm/s, but up to 200 cm/s, while neurological symptoms may be reversible. Severe vasospasm is determined at a blood flow velocity of more than 200 cm/s and is accompanied by the detection of ischemia on CT. More precisely, the state of vasospasm is determined by the Lindegard index - the ratio of peak systolic velocity in the MCA and in the homolateral internal carotid artery. Vasospasm in the basilar artery is characterized by a ratio of peak systolic velocity to velocity in the extracranial vertebral artery of more than 2.

Applied "three G» therapy (induced hypervolemia, hemodilution, hypertension) to reduce vasospasm, which increases cerebral blood flow and prevents ischemic brain damage. It is noted that it is hypervolemic hemodilution that clearly reduces the severity of angiospasm, in contrast to isovolemic hemodilution, which negatively affects cerebral blood flow. It is proposed to maintain the SBP at the level of 160 ± 20 mm Hg. Art. (SBP up to 200 mm Hg in patients with clipped aneurysm), and the achievement of hypervolemia and hemodilution by intravenous administration of 5% human albumin or hydroxyethyl starch. The optimal central venous pressure is 10 - 12 mm Hg, hematocrit - 33 - 35%.

(! ) For the prevention of vasospasm, nimodipine a (Nimotop) IV or 60 mg every 4 hours for 3 weeks is recommended for all patients with SAH (Evidence A).

The most discussed adverse event with the use of nimodipine is the possibility of lowering blood pressure, which cannot be a serious limitation of its use. First, with a decrease in systolic blood pressure by more than 20 mm Hg. Art. from the initial on the background of taking nimodipine, in the absence of angiospasm or stable subcritical angiospasm, it is possible to reduce the dose of the drug. Secondly, the additional use of "three G" therapy allows you to maintain optimal blood pressure.

In patients with SAH, it is recommended to ensure complete bed rest before aneurysm surgery, and in the absence of aneurysm, at least 7 days, with a further staged expansion of the regime. If the etiology of SAH is not clear and / or the impossibility of surgical treatment, it is justified to comply with bed rest for 30 days. It is necessary to protect patients from stress and tension.

In SAH, early administration of analgesics to relieve pain is recommended. It is advisable to use analgesics that do not affect cyclooxygenase-1. The use of paracetamol is quite effective. Perfalgan is currently on the market for intravenous administration.

Contraindicated the use of epsilon-aminocaproic acid due to an increased risk of thrombosis. The use of hemostatic agents to prevent rebleeding from a ruptured aneurysm is not indicated. The efficacy of tranexamic acid in the preoperative period has been proven in one randomized prospective study.

Additional Information:

Symposium "Subarachnoid hemorrhage (clinic, etiology, diagnosis, treatment)" Simonyan V.A., Lutsky I.S., Grishchenko A.B., Donetsk National Medical University. M. Gorky (

Subarachnoid hemorrhage is a type of intracranial hemorrhage in which blood spreads into the subarachnoid space of the brain and spinal cord. Distinguish between subarachnoid hemorrhage in TBI and in acute cerebrovascular accident according to the hemorrhagic type. To designate the latter, the terms "spontaneous subarachnoid hemorrhage" and "non-traumatic subarachnoid hemorrhage" are used.

ICD-I0 codes: 160.0-160.9. Subarachnoid hemorrhage.

EPIDEMIOLOGY

According to the stroke registries of different countries, the incidence of subarachnoid hemorrhage is 14-20 per 100,000 population per year. The proportion of subarachnoid hemorrhage among other types of stroke does not exceed 5%.

Subarachnoid hemorrhage can occur at any age, but it most often occurs between the ages of 40 and 60.

ETIOLOGY

The causes of subarachnoid hemorrhage are diverse, but most often it is the result of rupture of aneurysms of cerebral vessels, it accounts for 70-80% of all subarachnoid hemorrhages. Diseases in which the development of subarachnoid hemorrhage is possible are listed below.

Primary vascular diseases of the CNS:
- arterial aneurysms of cerebral vessels;
- vascular malformations of the central nervous system (arteriovenous malformations, cavernomas, arteriovenous fistulas);
- anomalies of the vascular system of the brain (Nishimoto's disease, exfoliating aneurysms of cerebral vessels).
Secondary vascular pathology of the CNS:
- arterial hypertension;
- vasculitis;
- blood diseases;
- violation of the blood coagulation system when taking anticoagulants, antiplatelet agents, contraceptives and other drugs.

When it is not possible to establish the etiological factor of subarachnoid hemorrhage, the concept of "subarachnoid hemorrhage of unknown origin" is used. The share of such hemorrhages accounts for about 15%.

CLASSIFICATION

Subarachnoid hemorrhages are classified according to the etiological factor and prevalence. The latter is possible only on the basis of CT or MRI data. This takes into account both the massiveness of the hemorrhage, and its combination with other components of intracranial hemorrhage - parenchymal and ventricular. Depending on this factor, isolated subarachnoid hemorrhage, subarachnoid-parenchymal, subarachnoid-ventricular and subarachnoid-parenchymal-ventricular hemorrhage are distinguished (Fig. 30-6).

Rice. 30-6. Typical subarachnoid hemorrhage. You can see the symmetrical distribution of blood in the basal cisterns, interhemispheric fissure, convexital subarachnoid spaces (CT).

In world practice, the classification of subarachnoid hemorrhages proposed by M. Fisher (1980) has become widespread. It characterizes the prevalence of subarachnoid hemorrhage according to the results of CT (Table 30-1)

Table 30-1 . Classification of hemorrhage according to M. Fisher (1980)

CLINICAL PICTURE

Subarachnoid hemorrhage develops acutely, without any precursors and is characterized by the onset of a sudden intense diffuse headache of the type of "hit", "spreading of hot fluid in the head". nausea, vomiting. Typical short-term loss of consciousness and the rapid development of meningeal syndrome in the absence of focal neurological disorders.

A prolonged loss of consciousness indicates a severe hemorrhage, as a rule, with a breakthrough of blood into the ventricular system, and a rapid addition of focal symptoms indicates a subarachnoid-parenchymal hemorrhage.

Meningeal symptoms are the main differential diagnostic sign of subarachnoid hemorrhage. Depending on the massiveness of the subarachnoid hemorrhage, they can be expressed to varying degrees and persist from several days to 3-4 weeks.

Along with the development of neurological symptoms, subarachnoid hemorrhage may be accompanied by various viscerovegetative disorders. Most often, at the time of hemorrhage, an increase in blood pressure is recorded. An increase in blood pressure is a reaction to a stressful situation. at the same time having a compensatory character, since it ensures the maintenance of cerebral perfusion pressure in conditions of intracranial hypertension that occurs at the time of subarachnoid hemorrhage. High blood pressure at the time of hemorrhage, especially in patients suffering from arterial hypertension, can cause an erroneous interpretation of an acute condition as a hypertensive crisis.

In cases of severe subarachnoid hemorrhage, cardiac and respiratory disturbances may occur.

In the acute stage of subarachnoid hemorrhage, an increase in body temperature up to febrile numbers is often noted, as well as the development of leukocytosis.

These symptoms may be misinterpreted as signs of an infectious disease.

The severity of the patient's condition at the time of subarachnoid hemorrhage and the further course of the disease depend primarily on the massiveness of the hemorrhage and its etiology. The most severe subarachnoid hemorrhages occur when aneurysms of cerebral vessels rupture (see the section "Surgical treatment of cerebral aneurysms").

DIAGNOSTICS

The clinical diagnosis of subarachnoid hemorrhage must be confirmed by instrumental studies. Lumbar puncture still remains the most reliable and affordable method for diagnosing subarachnoid hemorrhage. Liquor in subarachnoid hemorrhage is intensely stained with blood. The admixture of blood in the cerebrospinal fluid, gradually decreasing. persists for 1-2 weeks from the onset of the disease. In the future, the liquor acquires a xanthochromic color.

In unconscious patients, lumbar puncture should be performed with great caution due to the risk of brain dislocation.

In recent years, CT has become the method of choice in the diagnosis of subarachnoid hemorrhage. CT not only detects and evaluates the prevalence of blood in the subarachnoid space, but also provides information on the presence of ventricular and parenchymal components of hemorrhage, edema and dislocation of the brain, and the state of the CSF system. Without these data, the correct management of a patient with subarachnoid hemorrhage at the present stage of development of neurosurgery is impossible. In some cases, even with conventional CT, it is possible to establish or suggest the cause of the hemorrhage. Modern computed tomographs also make it possible to perform a high-quality study of the vascular system of the brain (CT angiography), which provides more than 90% accuracy in diagnosing the source of bleeding.

In CT diagnostics of subarachnoid hemorrhage, it must be taken into account that the information content of the method is directly dependent on the time of CT (the time elapsed after the hemorrhage), which is due to a change in the radiopaque properties of the outflowing blood. Already a week after a subarachnoid hemorrhage, blood in the subarachnoid space is visible only in half of the cases. In this regard, with negative CT data, patients with a clinical picture of subarachnoid hemorrhage require a diagnostic lumbar puncture.

Diagnosis of subarachnoid hemorrhage using MRI is less accurate due to the rapid changes in signal intensity due to the transformation of hemoglobin molecules in the erupted blood. However, in the absence of CT, MRI can be successfully used not only to diagnose subarachnoid hemorrhage, but also to determine the source of bleeding (MRI angiography). For the diagnosis of angiospasm - one of the complications of subarachnoid hemorrhage - TKDG is used. This study allows to identify angiospasm in the vessels of the base of the brain, to determine its prevalence and severity.

PRINCIPLES OF MANAGEMENT

Primary hospitalization of patients with a clinical picture of subarachnoid hemorrhage is urgently carried out in a neurological hospital. With an incorrect interpretation of the symptoms or with an erased or atypical clinical picture of subarachnoid hemorrhage, patients are sometimes mistakenly hospitalized in therapeutic, infectious, neurotraumatological, toxicological and psychiatric departments.

In the hospital, it is necessary to conduct CT (MRI) of the brain to verify subarachnoid hemorrhage and determine the anatomical form of the hemorrhage, and if possible, a one-stage non-invasive study of the vascular system of the brain (CT -, MRI - angiography). In the absence of signs of hemorrhage on CT (MRI) or if these methods are not available, a lumbar puncture should be performed.

After instrumental confirmation of the diagnosis of subarachnoid hemorrhage, an urgent consultation with a neurosurgeon is necessary to resolve the following issues:

The need for angiographic examination in order to clarify the source of hemorrhage;

Indications for transfer to a neurosurgical hospital.

Medical tactics

Therapeutic tactics in patients with subarachnoid hemorrhage depends on the results of the angiographic examination.

When cerebral aneurysms (the most common and dangerous cause of subarachnoid hemorrhage) or other vascular pathology requiring neurosurgical intervention are detected, the decision on the timing and methods of the operation is made individually depending on the type of pathology, the general condition of the patient, age, severity of the existing neurological deficit, the prevalence of hemorrhage, severity of angiospasm associated with hemorrhage, equipment and experience of hospital specialists.

In the absence of indications for surgery, medical therapy is carried out. The main tasks are stabilization of the patient's condition, maintenance of homeostasis, prevention of recurrence of subarachnoid hemorrhage, prevention and treatment of vascular spasm and cerebral ischemia, specific therapy for the disease that caused the hemorrhage.

The amount of therapy depends on the severity of the patient's condition.

Protective mode.
Raising the head end of the bed by 30 0.
Analgesia and sedation during arousal and all manipulations.
Maintaining normothermia.
Placement of a gastric tube in patients who are in a state of stunning or coma, due to the threat of possible aspiration.
Installation of a urinary catheter in patients who are in a state of stunning or coma.
Appointment of anticonvulsants in cases of epileptiform seizure at the time of hemorrhage.

Normalization of respiration and gas exchange. Normalization and maintenance of stable hemodynamics. For patients without impaired consciousness, intubation and auxiliary ventilation are carried out in the presence of clinical signs of respiratory failure: cyanosis, tachypnea more than 40 per minute, with P and O 2 values ​​less than 70 mm Hg. Patients with impaired consciousness (stupor, coma) should be intubated and transferred to mechanical ventilation due to the risk of developing hypoxia and aspiration.

If arterial hypotension occurs, it is necessary to maintain a normovolemic or moderately hypervolemic state (central venous pressure 6-12 cm of water column), this is achieved by infusion of colloid and crystalloid solutions.

Therapy for cerebral edema. With clinical and CT signs of increasing cerebral edema, threatening the development of dislocation syndrome, along with the above measures, the use of osmodiuretics (15% mannitol) in combination with saluretics (furosemide) is recommended. Treatment should be carried out under the control of the electrolyte composition of the blood (at least 2 times a day). Treatment of cerebral edema, especially in severely ill patients, is desirable under conditions of intracranial pressure control using ventricular or subdural sensors.

Prevention and therapy of cerebral angiospasm and cerebral ischemia. There are currently no proven treatments for angiospasm. To prevent it, it is recommended to use calcium channel blockers (nimodipine) in tablet form, 60 mg every 4 hours orally. Treatment should be started before the appearance of instrumental or clinical signs of angiospasm, since the drug is ineffective with an already developed spasm. In the treatment of angiospasm and its consequences, maintaining adequate perfusion of the brain tissue is of great importance. This can be achieved using the so-called 3H-therapy (arterial hypertension, hypervolemia, hemodilution) or its elements. With the development of symptomatic segmental spasm, a positive effect can be achieved using balloon angioplasty in combination with intra-arterial administration of papaverine.

The indications for prescribing antioxidants and neuroprotectors for the prevention and treatment of ischemic complications of subarachnoid hemorrhage are controversial, since the clinical effect of these groups of drugs has not been proven.

Forecast

The prognosis of the disease in patients with subarachnoid hemorrhage depends on many factors. The most significant of them is the etiology of hemorrhage.

Subarachnoid hemorrhage from an arterial aneurysm is accompanied by high mortality and the frequency of re-hemorrhage. In the absence of surgical treatment of aneurysms, up to 60% of patients die within the first year from the onset of the disease. With timely surgical treatment of an aneurysm, the risk of death is reduced by a factor of three. With subarachnoid hemorrhage of another etiology, the prognosis is usually favorable.

Survivors of subarachnoid hemorrhage (SAH) describe it as the worst pain of their lives.

It leaves behind problems with speech and muscles, increases the possibility of heart attacks, and the survival of patients depends entirely on the timeliness of medical care.

How to understand that blood has entered the brain, what does it threaten and how to reduce the likelihood of its occurrence?

Subarachnoid hemorrhage is a type in which blood is ejected into the subarachnoid space of the brain (the area between its cavities that is filled with cerebrospinal fluid).

Ejection can occur as a result of the development of vascular pathologies, head injuries, and blood clotting disorders. In this case, the patient has a severe headache. The frequent absence of other symptoms can make the diagnosis difficult.

This condition also occurs as a result of damage to the brain parenchyma. In this case, specific neurological signs will be observed: disruption of the facial muscles (hemiparesis).

A complete list of possible causes of subarachnoid hemorrhage (SAH) is shown in the table below:

The pathogenesis of a hemorrhage can be described as a collection of fluid in the subarachnoid cavity - the space between the pia mater and the arachnoid membrane. This cavity contains cerebrospinal fluid, rising from the spinal cord, enveloping both hemispheres of the brain and descending back.

When bleeding begins, blood drains to the basal cisterns (located at the base of the brain). And it begins to flow into the cerebrospinal fluid, which leads to spasms of the arteries, the death of neurons and swelling of the brain. The amount of CSF due to blood increases, which leads to an increase in pressure in the brain cavity and can contribute to its displacement.

Classification

In neurology, three classifications of the severity of the course of the disease are used.

Hunt scale - Hess, according to which the severity is determined by the manifested symptoms:

• 1st: mild headache and increased tone of the neck muscles;
• 2nd: the headache intensifies. At this stage, neurological symptoms begin to appear (pain in the eyes, strabismus, paresis (partial impairment of motor function));
• 3rd: a slight neurological deficit is manifested, characterized by drowsiness, a decrease in the reaction rate;
• 4th: severe neurological deficit - stunning, loss of reaction, partial paralysis of one side of the body, lack of response to external stimuli;
• 5th: deep coma, a sharp increase in muscle tone.

Fisher scale, classifies the patient's condition according to the volume of hemorrhage, which appears on the results of computed tomography or MRI:

• hemorrhage is not detected;
• the size of the lesion is 1 mm;
• defeat more than 1 mm;
• intraventricular hemorrhage or damage to the brain parenchyma (the value does not matter).

Glasgow Coma Scale (GCS), determines the severity of the disease by neurological deficit (the condition is assessed by points, where 15 is a clear consciousness and 3 is a deep coma):

• 15 GCS - no neurological deficit;
• 13-14 GCS - moderate or deep stunning;
• 8-10 GCS - stupor (numbness, lethargy);
• 6-7 GCS - moderate coma;
• 4-5 GCS - thermal coma;
• 3 GCS - deep coma.

And there is also a classification that combines some of the factors from the above methods for assessing the patient's condition. The Ogilvie and Carter scale takes into account the age of the patient, the severity of the patient according to the Hunt-Hess and Fisher scales, and the size of the aneurysm. Severity is assessed by the number of features present and absent.

Symptoms

The symptoms of SAH come on suddenly. The clinic of the disease is characterized by a sharp and acute headache that cannot be tolerated. In a large number of people, headache is the only symptom of the disease. But pain can also appear in other diseases of the brain.

The remaining signs are divided as follows:

Most often, subarachnoid hemorrhage occurs against the background of physical or emotional outbursts.

Differential Diagnosis

The most effective method is computed tomography (CT).

It defines:

• place of hemorrhage;
• data on the liquor system;
• the presence of cerebral edema.

In addition, in order to detect hemorrhage, the following methods can be used, both partially and in combination (in each specific clinical case, the methods used may differ):

How is the treatment carried out?

Emergency care for a person with such bleeding can only be provided by physicians using intravenous injections to reduce arousal and headache. The introduction of any medication on its own can aggravate the situation (for example, aspirin is contraindicated for patients).

If there is a suspicion of bleeding, the patient must be taken to the hospital. Therapeutic actions should begin to be carried out by the ambulance team at the prehospital stage. Subarachnoid hemorrhage is fatal in 50% of cases, and a third of patients die in an ambulance.

The patient is taken to the neurological, neurosurgical department or intensive care unit.

After establishing or confirming the diagnosis, the patient is prescribed drugs that increase blood clotting and drugs that lower blood pressure.

Medical therapy

Drug treatment includes the primary stage (stopping the bleeding) and elimination of the headache.

If the course of the disease is accompanied by convulsions or seizures, medications can be used to reduce these manifestations of the disease.

During drug treatment, drugs are prescribed:

• reducing spasms of arteries;
• laxatives and diuretics (help reduce dropsy of the brain);
• painkillers;
• reducing convulsions;
• antiemetics;
• tranquilizers.

Surgical intervention

Brain surgery is performed if an intracerebral hemorrhage is caused by an aneurysm, as well as in case of a massive cerebral hemorrhage, characterized by impaired consciousness, loss of speech and motor function (in this case, the hematoma is removed).

There are two types of surgery:

• Neurosurgical clipping. The operation consists in applying a metal clip to the aneurysm, which will prevent growth and rupture. The operation is performed on the open brain under general anesthesia, in case of an aneurysm of the middle cerebral artery (occlusion has great risks, since access to the artery is difficult).
• Endovascular occlusion. The operation consists in introducing a spiral into the aneurysm, which, like a staple, prevents growth and rupture. The operation is performed on the closed brain (the coil is inserted through a catheter that leads from the femoral artery through the carotid and vertebral arteries to the aneurysm) and under general anesthesia. This type of surgery is performed more frequently, especially in cases where the patient's condition is unstable and open-brain surgery may worsen it. Also, preference is given to occlusion for aneurysms of the basilar artery and posterior cerebral artery, since clipping is not possible in this case.

In the case of an aneurysm of the anterior cerebral and anterior communicating artery, both operations can be performed.

Surgical intervention can also be called the removal of a hematoma through the holes in the skull. The operation is performed only if the blood clot is on the surface.

rehabilitation period

The recovery time after subarachnoid bleeding depends on the severity of its course, but takes at least 6 months.

Rehabilitation is carried out under the supervision of doctors in a hospital and directly depends on drug therapy, as well as on:

• patient hygiene;
• therapeutic gymnastics and physical education;
• sessions with a speech therapist.

Patients who have had a hemorrhage may face several problems that can significantly lengthen the rehabilitation period:

• constant fatigue (decided by walking, with a gradual increase in time);
• insomnia (sleep and rest schedule);
• persistent headaches (they are treated only with medication);
• problems with sensitivity and motor function (physiotherapy and physiotherapy exercises help);
• vision problems (a visit to an ophthalmologist is required);
• partial or complete loss of memory (its restoration is carried out with medication).

All emerging problems are solved with the attending physician, who will refer the patient to other specialists (for example, an ophthalmologist). As a preventive measure, both for the first and subsequent hemorrhages, it is recommended to eat well, stop smoking / alcohol / drugs, engage in physiotherapy exercises and monitor the level of pressure.

Possible complications and consequences

The possibility of complications and their severity depends on the causes of intracerebral hemorrhage and the timeliness of medical care. The faster the patient was taken to the hospital, the greater his chances of survival and successful treatment.

The most severe consequence is cerebral vasospasm (vasospasm leading to). This complication develops in a third of patients and can lead to cerebral infarction and death.

And also subarachnoid hemorrhage can provoke the development of:

• epilepsy (occurs in 5%);
• neurological defects (problems with speech/motor function)
  hydrocephalus;
• depression/anxiety and other mental problems.

Forecast

Subarachnoid hemorrhage is an extremely dangerous disease with a mortality rate of 50%.

Most patients die during the first month in the hospital, slightly less on the first day and before medical care.

The prognosis for the occurrence of complications and consequences is very unfavorable - most of the sick have a disability, and only 25% of all those who have undergone this condition fully recover.