Subarachnoid hemorrhage.

Subarachnoid hemorrhage is a sudden bleeding into the subarachnoid space. The most common cause of spontaneous bleeding is a ruptured aneurysm. Subarachnoid hemorrhage is characterized by sudden acute headache, usually with loss or impairment of consciousness. Secondary vascular spasm (causing focal cerebral ischemia), meningismus, and hydrocephalus (leading to persistent headache and lethargy) are often observed. Diagnosis is based on CT and CSF analysis. Medical care - neurosurgery and symptomatic treatment - is provided in specialized centers.

Subarachnoid hemorrhage occurs when blood leaks from a ruptured aneurysm into the space between the arachnoid and pia mater. The most common cause of subarachnoid hemorrhage is craniocerebral trauma, but traumatic subarachnoid hemorrhage is considered an independent nosology. Spontaneous (primary) subarachnoid hemorrhage in approximately 85% of cases is caused by rupture of intracranial aneurysms, most often congenital saccular or grape-like. Bleeding may stop spontaneously. Aneurysm rupture can occur at any age, but most often occurs between the ages of 40 and 65. Less common causes are mycotic aneurysms, arteriovenous malformations, and diseases with hemorrhagic syndrome.

Blood entering the subarachnoid space causes irritation of the meninges, aseptic meningitis, and increased intracranial pressure over several days or weeks. Secondary vascular spasm may lead to focal cerebral ischemia; approximately 25% of patients develop symptoms of TIA or ischemic stroke. The maximum pronounced cerebral edema and the risk of vascular spasm with subsequent formation of infarction areas (brain swelling) is observed between 72 hours and 10 days after the hemorrhage. Secondary acute hydrocephalus often develops. Sometimes the aneurysm ruptures again and the bleeding recurs, most often during the first week of the disease.

ICD-10 codes:

I60.0-I60.9. Subarachnoid hemorrhage.

According to stroke registries in different countries, the incidence of subarachnoid hemorrhage is 14-20 per 100,000 population per year. The share of subarachnoid hemorrhage among other types of stroke does not exceed 5%. Subarachnoid hemorrhage can occur at any age, but most often it occurs at 40-60 years of age.

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What causes subarachnoid hemorrhage?

The causes of subarachnoid hemorrhage are varied, but most often it is a consequence of ruptured cerebral aneurysms, accounting for 70-80% of all subarachnoid hemorrhages. Diseases that can cause subarachnoid hemorrhage are listed below.

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

When it is not possible to establish the etiologic factor of subarachnoid hemorrhage, the term "subarachnoid hemorrhage of unknown genesis" is used. Such hemorrhages account for about 15%.

Symptoms of subarachnoid hemorrhage

Acute, intense headache reaches its peak within a few seconds. At the moment of aneurysm rupture or immediately after it, there is often a short-term loss of consciousness; sometimes this occurs after a few hours. Patients behave very restlessly, convulsions are possible. Sometimes focal neurological symptoms join the picture of the lesion, which can become irreversible within a few minutes or hours. In the first hours of the disease, in the absence of pronounced edema and syndrome of herniation of the cerebellar tonsils, rigidity of the neck muscles is not expressed. But during the first 24 hours, with the development of chemical meningitis and increasing irritation of the meninges, moderate or pronounced symptoms of meningism, vomiting, bilateral pathological plantar reflexes, changes in pulse rate and respiration appear. High temperature, prolonged headaches and confusion may persist for 5-10 days. Secondary hydrocephalus can cause headache, confusion, and motor impairment that persist for weeks. Recurrent bleeding can worsen existing symptoms and add new ones.

Subarachnoid hemorrhage develops acutely, without any precursors and is characterized by the occurrence of sudden intense diffuse headache of the "blow" type, "spreading of hot liquid in the head", nausea, vomiting. Short-term loss of consciousness and rapid development of meningeal syndrome in the absence of focal neurological disorders are typical. Long-term loss of consciousness indicates severe hemorrhage, usually with a breakthrough of blood into the ventricular system, and the rapid addition of focal symptoms indicates subarachnoid-parenchymatous hemorrhage.

Meningeal symptoms and meningeal syndrome 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 visceral autonomic disorders.

Most often, an increase in arterial pressure is recorded at the time of hemorrhage. An increase in arterial pressure is a reaction to a stressful situation, which at the same time has a compensatory nature, since it ensures the maintenance of cerebral perfusion pressure in conditions of intracranial hypertension that occurs at the time of subarachnoid hemorrhage. High arterial 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 problems may occur.

In the acute stage of subarachnoid hemorrhage, an increase in body temperature up to febrile numbers, as well as the development of leukocytosis, are often noted. These symptoms can be misinterpreted as signs of an infectious disease.

The severity of the patient's condition at the time of subarachnoid hemorrhage and the subsequent course of the disease depend primarily on the massiveness of the hemorrhage and its etiology. Subarachnoid hemorrhages are most severe when aneurysms of the brain vessels rupture.

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Classification of subarachnoid hemorrhage

Subarachnoid hemorrhages are classified by etiologic factor and prevalence. The latter is possible only on the basis of CT or MRI data. In this case, both the massiveness of the hemorrhage and its combination with other components of intracranial hemorrhage - parenchymatous and ventricular - are taken into account. Depending on this factor, isolated subarachnoid hemorrhage, subarachnoid-parenchymatous, subarachnoid-ventricular and subarachnoid-parenchymatous-ventricular hemorrhage are distinguished. In world practice, the classification of subarachnoid hemorrhages proposed by M. Fisher (1980) has become widespread. It characterizes the prevalence of subarachnoid hemorrhage based on CT results.

Classification of hemorrhage according to M. Fisher (1980)

Gradation	Blood on CT
1	No signs of blood
2	Diffuse or vertical clots less than 1 mm thick
3	Localized clot or vertical layers more than 1 mm thick
4	Intracerebral or intraventricular clot with or without diffuse subarachnoid hemorrhage

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Diagnosis of subarachnoid hemorrhage

The clinical diagnosis of subarachnoid hemorrhage must be confirmed by instrumental studies. The most reliable and accessible method for diagnosing subarachnoid hemorrhage to date remains lumbar puncture. The cerebrospinal fluid in subarachnoid hemorrhage is intensely colored with blood. The admixture of blood in the cerebrospinal fluid, gradually decreasing, remains for 1-2 weeks from the onset of the disease. Later, the cerebrospinal fluid acquires a xanthochromic color.

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

The diagnosis is based on characteristic symptoms and confirmed by computed tomography performed as quickly as possible before the damage becomes irreversible. The sensitivity of CT without contrast in detecting subarachnoid hemorrhage exceeds 90%. False negative results are possible only with a small volume of spilled blood. If the CT examination result is negative or it is impossible to perform it in a patient with a clinical diagnosis of subarachnoid hemorrhage, a lumbar puncture is performed. However, lumbar puncture is contraindicated if increased intracranial pressure is suspected, since a sudden decrease in CSF pressure can neutralize the tamponade effect of the thrombus on the ruptured aneurysm, causing bleeding.

In cases of subarachnoid hemorrhage, the CSF is leaking under increased pressure, contains a large number of red blood cells, or has a xanthochromic color. Red blood cells may also enter the CSF after a traumatic lumbar puncture, as evidenced by a gradual decrease in the color intensity in each subsequent tube with CSF obtained during a single lumbar puncture. Six or more hours after the hemorrhage, the red blood cells are destroyed, due to which the CSF acquires a xanthochromic color, and microscopic examination of the CSF centrifugate reveals jagged red blood cells. If the results are equivocal, the lumbar puncture should be repeated in 8 to 12 hours, assuming that hemorrhage has occurred. If subarachnoid hemorrhage is confirmed, immediate cerebral angiography is indicated to evaluate all 4 major arterial vessels of the brain, since multiple aneurysms are possible.

Subarachnoid hemorrhage may cause ECG changes (elevation or depression of the ST segment) that mimic myocardial infarction, which is facilitated by the patient's syncope. Other variants of neurogenic ECG changes may include prolongation of the QRS or QT intervals and symmetrical inversion of peaked or deep T waves.

Transcranial Dopplerography is used to diagnose angiospasm, one of the complications of subarachnoid hemorrhage. This study allows us to identify angiospasm in the vessels of the base of the brain, and determine its prevalence and severity.

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Treatment of subarachnoid hemorrhage

Subarachnoid hemorrhage should be treated in a specialized center whenever possible. The patient is prescribed strict bed rest, symptomatic treatment of agitation and headache. High blood pressure is controlled if the mean value exceeds 130 mm Hg; sufficient fluid is administered orally or intravenously to maintain euvolemia. Nicardipine is titrated as in ischemic stroke. Constipation is prevented to avoid any physical effort and strain. The use of anticoagulants and antiplatelet drugs is contraindicated.

To prevent vascular spasm and prevent ischemic damage, nimodipine is prescribed orally at 60 mg 6 times a day for 21 days, while maintaining blood pressure at the desired level. Clinical signs of acute hydrocephalus are an indication for ventricular drainage.

Obliteration of the aneurysm reduces the risk of recurrent bleeding, so if there is access to the aneurysm, surgical intervention is recommended. The preferred method is aneurysm clipping, but others are also used, such as providing a bypass blood flow in patients with acute hydrocephalus or with hematomas that can be emptied. If the patient is conscious, most neurosurgeons prefer to perform surgery on the first day to minimize the risk of rebleeding, postoperative vasospasm, cerebral infarction and other secondary complications. If the first day is missed, the operation is performed 10 days or later, which reduces the surgical risks, but increases the risk of rebleeding, which occurs more often, which ultimately increases overall mortality. Angiographic intravascular embolization of the aneurysm with coils is used as an alternative intervention, especially when the aneurysm is localized in the anterior cerebral artery basin or in the posterior vascular basin.

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

In hospital, it is necessary to perform CT (MRI) of the brain to verify subarachnoid hemorrhage and determine the anatomical form of hemorrhage, and if possible, a one-time 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 unavailable, 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 an angiographic examination to determine the source of the hemorrhage;
• indications for transfer to a neurosurgical hospital.

Treatment tactics for subarachnoid hemorrhage

Treatment tactics in patients with subarachnoid hemorrhage depend on the results of 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 surgery is made individually depending on the type of pathology, the general condition of the patient, age, severity of the existing neurological deficit, prevalence of hemorrhage, severity of angiospasm accompanying the hemorrhage, equipment and experience of hospital specialists.

In the absence of indications for surgery, drug therapy is administered. The main tasks are to stabilize the patient's condition, maintain homeostasis, prevent recurrence of subarachnoid hemorrhage, prevent and treat vascular spasm and cerebral ischemia, and provide specific therapy for the disease that caused the hemorrhage.

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

Recommendations

• Protective regime.
• Raise the head end of the bed by 30°.
• Analgesia and sedation during arousal and all manipulations.
• Maintaining normothermia.
• Insertion of a gastric tube into patients who are in a state of stupor or coma due to the risk of possible aspiration.
• Insertion of a urinary catheter into patients who are in a state of stupor or coma.
• Prescription of anticonvulsants in cases of epileptiform seizure at the time of hemorrhage.

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Normalization of breathing and gas exchange

In patients without impaired consciousness, intubation and auxiliary mechanical ventilation are performed in the presence of clinical signs of respiratory failure: cyanosis, tachypnea over 40 per minute, with paO2 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 hypoxia and aspiration. The recommended level of systolic blood pressure is 120-150 mm Hg. In arterial hypertension, oral and intravenous antihypertensive drugs are used. If arterial hypotension occurs, it is necessary to maintain a normovolemic or moderately hypervolemic state (central venous pressure 6-12 cm H2O), this is achieved by infusion of colloidal and crystalloid solutions.

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Treatment of cerebral edema

In case of clinical and CT signs of increasing cerebral edema threatening the development of dislocation syndrome, along with the above measures, it is recommended to use osmotic diuretics (15% mannitol) in combination with saluretics (furosemide). Treatment should be carried out under control of the electrolyte composition of the blood (at least 2 times a day). Treatment of cerebral edema, especially in severe patients, is preferably carried out under conditions of intracranial pressure control using ventricular or subdural sensors.

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Prevention and therapy of cerebral angiospasm and cerebral ischemia

There are currently no proven methods for treating angiospasm. For its prevention, calcium channel blockers (nimodipine) in tablet form are recommended at 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 if the spasm has already developed. 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 method of so-called ZN-therapy (arterial hypertension, hypervolemia, hemodilution) or its elements. In the development of segmental symptomatic spasm, a positive effect can be achieved using balloon angioplasty in combination with intra-arterial administration of papaverine.

Indications for the use of antioxidants and neuroprotectors for the prevention and treatment of ischemic complications of subarachnoid hemorrhage are contradictory, since the clinical effect of drugs in these groups has not been proven.

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Forecast

The prognosis of patients with subarachnoid hemorrhage depends on many factors. The mortality rate for the first aneurysm hemorrhage is about 35%, and another 15% of patients die from a second rupture in the following weeks. After 6 months, the probability of a second rupture is about 3% per year. In general, the prognosis for cerebral aneurysms is quite serious, somewhat better for AVMs, and most favorable in cases where four-vessel angiography does not reveal pathology, probably because the bleeding source was small and was able to close on its own. Surviving patients often have a residual neurological defect, even after optimal treatment in the acute period.

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