Subarachnoid hemorrhage

Subarachnoid hemorrhage - sudden bleeding into the subarachnoid space. The most common cause of spontaneous bleeding is aneurysm rupture. Subarachnoid hemorrhage is manifested by a sudden acute headache, usually with loss or impairment of consciousness. Often, secondary vascular spasm (causing focal cerebral ischemia), the phenomena of meningism and hydrocephalus (leading to persistent headache and lethargy) are often noted. The diagnosis is made on the basis of CT results and analysis of CSF. Medical care - neurosurgical intervention and symptomatic treatment - is provided in specialized centers.

Subarachnoid hemorrhage occurs as a result of the release of blood from a ruptured aneurysm into the space between the arachnoid and the pia mater. The most common cause of subarachnoid hemorrhage is a traumatic brain injury, but traumatic subarachnoid hemorrhage is considered as an independent nosology. Spontaneous (primary) subarachnoid hemorrhage in approximately 85% of cases is due to a rupture of intracranial aneurysms, most often congenital saccular or threatening like. Bleeding can stop spontaneously. Aneurysm rupture can occur at any age, but more often occurs between the ages of 40-65 years. Less common causes are mycotic aneurysms, arteriovenous malformations and diseases with hemorrhagic syndrome.

Blood entering the subarachnoid space causes irritation of the meningeal membranes, aseptic meningitis, and an increase in intracranial pressure over several days or weeks. Secondary vascular spasm can lead to focal cerebral ischemia; about 25% of patients develop symptoms of TIA or ischemic stroke. The most pronounced cerebral edema and the risk of vascular spasm with the subsequent formation of infarction sites (brain swelling) is observed between 72 hours and 10 days after hemorrhage. Often develops secondary acute hydrocephalus. Sometimes there is a repeated aneurysm rupture and recurrence of bleeding, most often during the first week of the disease. 

ICD-10 codes:

I60.0-I60.9. Subarachnoid hemorrhage.

According to the stroke registers of 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 in 40-60 years.

[1]

What causes subarachnoid hemorrhage?

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

• Primary vascular diseases of the central nervous system:
  • arterial aneurysm of cerebral vessels;
  • vascular malformations of the central nervous system (arterio-venous malformations, cavernomas, arterio-venous fistulas);
  • abnormalities of the vascular system of the brain (Nisimoto disease, exfoliating cerebral aneurysm).
• 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 drugs.

When it is not possible to establish the etiological factor of subarachnoid hemorrhage, use the concept of "subarachnoid hemorrhage of unknown origin." Such hemorrhages account for about 15%.

Symptoms of subarachnoid hemorrhage

Acute intense headache peaks in a few seconds. At the time of aneurysm rupture or immediately after it there is often a short-term loss of consciousness; sometimes it happens after a few hours. Patients behave very restlessly, convulsive seizures are possible. Sometimes focal neurological symptoms join the picture of the lesion, which may become irreversible within a few minutes or hours. In the first hours of the disease in the absence of pronounced edema and cerebellar tonsil penetration syndrome, the stiffness of the neck muscles is not pronounced. But during the first days with the development of chemical meningitis and the increase in irritation of the meninges, moderate or severe symptoms of meningism, vomiting, bilateral pathological plantar reflexes, changes in the frequency of the pulse and respiration appear. Fever, prolonged headaches and confusion may persist for 5–10 days. Secondary hydrocephalus can cause headaches, stunning and motor disturbances that persist for several weeks. Recurrent bleeding can aggravate existing symptoms and add new ones.

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

Meningeal symptoms and meningeal syndrome is the main differential diagnostic sign of subarachnoid hemorrhage. Depending on the massiveness of subarachnoid hemorrhage, they can be expressed in 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 viscero-vegetative disorders.

Most often at the time of hemorrhage, an increase in blood pressure is recorded. An increase in arterial pressure is a reaction to a stressful situation, at the same time having a compensatory nature, since it ensures the maintenance of cerebral perfusion pressure under 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 the acute condition as a hypertensive crisis.

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

In the acute stage of subarachnoid hemorrhage, an increase in body temperature up to febrile numbers and the development of leukocytosis are often noted. 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. Subarachnoid hemorrhages are most severe when the aneurysms of the brain vessels rupture.

[2], [3], [4], [5], [6], [7], [8]

Classification of subarachnoid hemorrhage

Subarachnoid hemorrhages are classified according to 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 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 hemorrhages are isolated. In world practice, widespread classification of subarachnoid hemorrhage, proposed by M. Fisher (1980). It characterizes the prevalence of subarachnoid hemorrhage according to the results of CT

Classification of hemorrhage by M. Fisher (1980)

Gradation	Blood CT
One	No blood signs
2	Diffuse or vertical clots with a thickness of less than 1 mm
3	Local clot or vertical layers more than 1 mm thick
Four	Intracerebral or intraventricular clot in the presence or absence of diffuse subarachnoid hemorrhage

[9], [10], [11], [12]

Diagnosis of subarachnoid hemorrhage

The clinical diagnosis of subarachnoid hemorrhage must be confirmed by instrumental studies. The most reliable and affordable method of diagnosis of subarachnoid hemorrhage so far remains lumbar puncture. Liquor with 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, CSF gets xanthochromic color.

Patients with unconscious lumbar puncture should be carried out with great caution because of the risk of dislocation of the brain.

The diagnosis is made on the basis of characteristic symptoms and is confirmed by the results of computed tomography carried out as quickly as possible before the damage becomes irreversible. The sensitivity of CT without contrast in the detection of subarachnoid hemorrhage exceeds 90%. False negative results are possible only with a small amount of blood that has poured out. If the CT scan is negative, or it is impossible to conduct it in a patient with a clinical diagnosis of subarachnoid hemorrhage, lumbar puncture is performed. However, lumbar puncture is contraindicated in case of suspected increased intracranial pressure, since a sudden decrease in pressure of CSF can level the tampon effect of a blood clot on a torn aneurysm, causing bleeding.

In the case of subarachnoid hemorrhage, CSF leaks under increased pressure, contains a large number of red blood cells, or has a xanthochromic stain. The erythrocytes in the CSF can get after the traumatic lumbar puncture, as evidenced by the gradual decrease in the intensity of the color in each subsequent test tube with the cerebrospinal fluid obtained in the course of one lumbar puncture. After 6 or more hours after hemorrhage, the erythrocytes are destroyed, and therefore the cerebrospinal fluid acquires xanthochromic coloration, and microscopic examination of the CSF centrifugate reveals jagged erythrocytes. If the results are dubious, the lumbar puncture should be repeated after 8-12 hours, assuming that hemorrhage has occurred. When a subarachnoid hemorrhage is confirmed, an immediate cerebral angiography is indicated to evaluate all 4 major arterial vessels of the brain, since multiple aneurysms are possible.

Subarachnoid hemorrhage can lead to changes in the ECG (elevation or depression of the ST segment), imitating myocardial infarction, which is facilitated by the patient's fainting. Other options for neurogenic ECG changes can be lengthening of the QRS or QT intervals and the symmetrical inversion of pointed or deep T teeth .

For the diagnosis of angiospasm - one of the complications of subarachnoid hemorrhage - apply transcranial Doppler. This study allows you to identify angiospasm in the vessels of the base of the brain, to determine its prevalence and severity.

[13], [14], [15], [16], [17], [18],

Treatment of subarachnoid hemorrhage

If possible, subarachnoid hemorrhage should be treated in a specialized center. The patient is prescribed strict bed rest, symptomatic treatment of arousal and headache. Increased blood pressure is stopped if the average value exceeds 130 mm Hg; A sufficient amount of fluid is injected or intravenously injected to maintain euvolemia. Titration of nicardipine is carried out as in ischemic stroke. In order to avoid any physical effort and stress, they prevent constipation. Contraindicated Prima nenie anticoagulants and antiplatelet tare preparations .

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

Obliteration of the aneurysm reduces the risk of recurrence of bleeding, therefore, if there is access to the aneurysm, surgical intervention is recommended. The preferred method is clipping of the aneurysm, but others are also used, such as bypassing blood flow in patients with acute hydrocephalus or with hematomas that can be emptied. If the patient is conscious, most neurosurgeons prefer to have surgery on the first day to minimize the risk of rebleeding, postoperative vasospasm, brain infarction, and other secondary complications. If the first days are missed, the operation is carried out 10 days later and later, which reduces operational risks, but increases the risk of re-bleeding, which happens more often, which ultimately increases the overall mortality rate. As an alternative intervention, angiographic intravascular embolization of the aneurysm with spirals is used, especially when the aneurysm is localized in the anterior cerebral artery pool or in the posterior vascular pool.

Primary hospitalization of patients with the clinical picture of subarachnoid hemorrhage 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, neurotraumatic, toxicological and psychiatric departments.

In the hospital it is necessary to conduct CT scan (MRI) of the brain to verify the 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, lumbar puncture should be performed.

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

• the need for an angiographic examination to clarify the source of hemorrhage;
• indications for transfer to a neurosurgical hospital.

Therapeutic tactics for subarachnoid hemorrhage

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

When cerebral aneurysms are detected (the most frequent and dangerous cause of subarachnoid hemorrhage) or another vascular pathology requiring neurosurgical intervention, decisions on the terms and methods of surgery are taken individually depending on the type of pathology, general condition of the patient, age, severity of the existing neurological deficit, prevalence of hemorrhage, the severity of concomitant hemorrhage angiospasm, equipment and experience of inpatient 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 of the disease that caused the hemorrhage.

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

Recommendations

• Protective mode.
• Raising the head end of the bed by 30 °.
• Analgesia and sedation during the excitation and conduct all manipulations.
• Maintain normothermia.
• Installing the gastric probe in patients in a state of stunning or coma, due to the threat of possible aspiration.
• Installing 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.

[19], [20], [21],

Normalization of respiration and gas exchange

Patients without impairment of consciousness intubation and auxiliary IVL are performed in the presence of clinical signs of respiratory failure: cyanosis, tachypnea more than 40 per minute, with p _a O ₂ less than 70 mm Hg. Patients with impaired consciousness (sopor, coma) should be intubated and transferred to a ventilator due to the risk of hypoxia and aspiration. The recommended systolic blood pressure level is 120-150 mm Hg. In hypertension, oral and intravenous antihypertensive drugs are used. If arterial hypotension occurs, it is necessary to maintain the normovolemic or moderately hypervolemic state (central venous pressure 6-12 cm of water), this is achieved by infusion of colloidal and crystalloid solutions.

[22], [23], [24], [25]

Brain Edema Therapy

With clinical and CT signs of increasing brain edema that threaten the development of dislocation syndrome, along with the above measures, use of osmodiuretiki (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 severe patients, is desirable to perform under conditions of monitoring intracranial pressure using ventricular or subdural sensors.

[26], [27], [28], [29], [30], [31], [32], [33], [34]

Prevention and therapy of cerebral angiospasm and cerebral ischemia

There are currently no proven methods for treating angiospasm. For prophylaxis, it is recommended to use calcium channel blockers (nimodipine) in tablet form, 60 mg every 4 hours orally. Treatment should begin before the appearance of instrumental or clinical signs of angiospasm, since the drug is ineffective in an already developed spasm. In the treatment of angiospasm and its effects, maintaining adequate perfusion of 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. With the development of segmental symptomatic spasm, a positive effect can be achieved with the help of balloon angioplasty in combination with intra-arterial administration of papaverine.

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

[35], [36], [37], [38], [39], [40], [41], [42]

Forecast

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

[43], [44], [45], [46], [47]