What Is a Subarachnoid Hemorrhage?

Subarachnoid hemorrhage (SAH) refers to a clinical syndrome caused by the rupture of diseased blood vessels at the bottom of the brain or on the surface of the brain. It accounts for 10% of acute stroke and is a very serious common disease. The World Health Organization survey shows that the incidence rate in China is about 2.0 per 100,000 person-years, and there are also reports of 6-20 per 100,000 persons per year. It can also be seen that due to intraventricular hemorrhage, epidural or subdural blood vessel rupture, blood penetrates the brain tissue and flows into the subarachnoid space, which is called secondary subarachnoid hemorrhage.

Martial arts sword	(Chief physician)	Department of Neurology, Xuanwu Hospital, Capital Medical University
Liu Chenyu	(Resident)	Department of Neurology, Xuanwu Hospital, Capital Medical University

Subarachnoid hemorrhage (SAH) refers to a clinical syndrome caused by the rupture of diseased blood vessels at the bottom of the brain or on the surface of the brain. It accounts for 10% of acute stroke and is a very serious common disease. The World Health Organization survey shows that the incidence rate in China is about 2.0 per 100,000 person-years, and there are also reports of 6-20 per 100,000 persons per year. It can also be seen that due to intraspinal hemorrhage, epidural or subdural rupture of blood, blood penetrates the brain tissue and flows into the subarachnoid space, which is called secondary subarachnoid hemorrhage.

Western Medicine Name

Subarachnoid hemorrhage

English name

subarachnoid hemorrhage, SAH

Affiliated Department

Internal Medicine-Neurology

Disease site

Intracranial

Contagious

Non-contagious

Whether to enter health insurance

Yes

Causes of subarachnoid hemorrhage

Any cause of cerebral hemorrhage can cause this disease. Common causes are:

1. Intracranial aneurysms account for 50-85%, and they occur in the aortic branches of the cerebral arterial ring, which is more common in the first half of the ring;

2. Cerebrovascular malformations are mainly arteriovenous malformations, which are more common in adolescents, accounting for about 2%. Arteriovenous malformations are mostly located in the middle cerebral artery distribution area of the cerebral hemisphere;

3. Anomalous vascular network disease of the brain (moyamoya disease) accounts for about 1%;

4. Other dissecting aneurysms, vasculitis, intracranial venous system thrombosis, connective tissue disease, blood disease, intracranial tumors, coagulopathy, and complications of anticoagulation therapy.

5. The cause of bleeding is unknown in some patients, such as: primary midbrain hemorrhage.

The risk factors of subarachnoid hemorrhage are mainly the factors that cause intracranial aneurysm rupture, including hypertension, smoking, heavy drinking, previous history of aneurysm rupture, large aneurysm volume, multiple aneurysms, etc. Compared to nonsmokers, smokers have larger aneurysms and more frequently have aneurysms.

Pathogenesis of subarachnoid hemorrhage

Aneurysms are arterial walls that bulge outward due to local lesions (which can be weak or structurally damaged), forming a permanent, limited expansion. The formation of aneurysms may be caused by congenital myometrial defects or acquired inner elastic layer degeneration of the arterial wall or a combination of the two. Therefore, the occurrence of aneurysms has a certain degree of genetic predisposition and familial aggregation. Approximately 4% of first-degree relatives of patients with subarachnoid hemorrhage have aneurysms. However, intracranial aneurysms are not entirely caused by congenital anomalies, and a considerable part of them develop in life. As the age increases, the elasticity of the arterial wall gradually weakens, and aneurysms protrude outward under the impact of blood flow and other factors.

Whether it is an aneurysm rupture, arteriovenous malformation, vascular rupture, or sudden increase in blood pressure that ruptures the blood vessel, other conditions cause blood to flow into the subarachnoid space of the brain. The cerebrospinal fluid surrounding the brain and spinal cord rapidly diffuses, stimulating the meninges, causing headache Meningeal irritation and neck stiffness. After the blood enters the subarachnoid space, it will also increase the contents of the cranial cavity, increase the pressure, and secondary cerebral vasospasm. The latter is due to traction (mechanical factors) of blood clots and fibrous cords surrounding the vessel wall after bleeding, and neuromuscular junctions formed between smooth muscle cells of the vessel wall produce extensive ischemic damage and edema. In addition, a large amount of blood or blood clots are deposited at the base of the skull. Part of the agglutinated red blood cells can also block the small grooves between the arachnoid villi and block the resorption of the cerebrospinal fluid. As a result, acute traffic hydrocephalus or arachnoid adhesions can occur. The sudden increase in intracranial pressure further reduced cerebral blood flow, exacerbated cerebral edema, and even caused the formation of cerebral hernia. All of the above can make the patient's condition stable and improve, and then there will be recurrent consciousness disturbance or limited neurological symptoms. The expansion and hemorrhage of the posterior communication aneurysm can compress the adjacent oculomotor nerve and produce oculomotor nerve paralysis (expressed as eye movement disorder) to varying degrees. It may also be caused by blood stimulating the hypothalamus, causing endocrine and autonomic nervous system disorders such as elevated blood sugar and fever.

Clinical manifestations of subarachnoid hemorrhage

Subarachnoid hemorrhage sex, age

It can occur at any age. Young adults are more common. Aneurysm rupture is more common in 30 to 60 years. There are more women than men and vascular malformations are more common in adolescents.

Onset of subarachnoid hemorrhage

Sudden onset, headaches that occur in seconds or minutes are the most common way to start. Patients can often clearly describe the time and context of the onset. There are obvious causes before the onset, such as strenuous exercise, emotional excitement, exertion, defecation, cough, drinking, etc .; a few can develop the disease in a quiet situation. About 1/3 of the patients had symptoms such as headache, nausea and vomiting a few days or weeks before the aneurysm ruptured.

Clinical manifestations of subarachnoid hemorrhage

The typical clinical manifestations of SAH are sudden severe headache, nausea, vomiting, and meningeal irritation, with or without focal signs. Bursting limitations or severe head pain during or after strenuous activities, unbearable, persistent or progressive aggravation, and sometimes pain in the upper neck. Its origin is often related to the site of aneurysm rupture. Common concomitant symptoms include vomiting, transient disturbances of consciousness, back or control pain, and photophobia. Meningeal irritation appears within a few hours after the onset of most cases, with neck stiffness being the most pronounced. Kernig sign and Brudzinski sign can be positive. Fundus examination revealed retinal hemorrhage and optic nipple edema, and about 25% of patients may develop psychiatric symptoms such as euphoria, delirium, and hallucinations. There may also be seizures, signs of focal neurological deficits such as oculomotor nerve palsy, aphasia, monoplegia or hemiplegia, and sensory disorders. Some patients, especially elderly patients, often have atypical clinical manifestations such as headache and meningeal irritation, and their mental symptoms are more obvious. Patients with primary midbrain hemorrhage have milder symptoms, CT manifestations of hemorrhage in the cerebellum around the midbrain or pontine, no aneurysms or other abnormalities found on angiography, and generally no rebleeding or delayed vasospasm occurs. good.

Common complications of subarachnoid hemorrhage

(1) Rebleeding: It is an acute serious complication of SAH, with a mortality rate of about 50%. The risk of rebleeding within 24 hours after bleeding is the highest, and the rebleeding points within 1 month after the onset are all higher. The incidence of rebleeding within 2 weeks was 20% to 30%, and 1 month was 30%. The cause of rebleeding is mostly aneurysm rupture. At the time of admission, coma, elderly women, and patients with systolic blood pressure over 170 mmHg were at greater risk for rebleeding. The clinical manifestations are: when the condition is stable or improved, sudden severe headache, nausea and vomiting, deepening of consciousness, convulsions, exacerbation or reappearance of original symptoms and signs. The diagnosis is mainly based on the above manifestations, CT shows an increase in original bleeding or an increase in blood volume in the cerebrospinal fluid of lumbar puncture.

(2) Cerebral vasospasm: an important cause of death and disability. Cerebral vasospasm occurs in about 20-30% of patients with SAH, causing late ischemic injury and secondary cerebral infarction. Early-onset cerebral vasospasm occurs after bleeding, which lasts for several minutes or hours; late-onset cerebral vasospasm begins at 3 to 5 days after bleeding, peaks at 5 to 14 days, and gradually decreases in 2 to 4 weeks. The clinical manifestations are changes in consciousness, focal nerve function damage (such as hemiplegia, aphasia, etc.), and the symptoms of brain tissue damage near the aneurysm are usually the most severe.

(3) Hydrocephalus: About 15-20% of SAH patients will develop acute obstructive hydrocephalus. Acute hydrocephalus occurs within 1 week after the onset. It is caused by blood entering the ventricular system and subarachnoid space to form a blood clot that blocks the cerebrospinal fluid circulation pathway. It is a deformed obstructive hydrocephalus; mild cases are lethargy and mental retardation And memory impairment, headache, vomiting, and disturbance of consciousness. Most of the acute obstructive hydrocephalus can be improved as the bleeding is absorbed. Delayed hydrocephalus occurs 2 to 3 weeks after SAH, and it is traffic hydrocephalus. Presented as progressive mental retardation, abnormal gait, and urinary and stool disorders. Cerebrospinal fluid pressure is normal, so it is also called normal intracranial hydrocephalus. CT or MRI of the head shows enlarged ventricles.

(4) Others: Convulsions can occur in 5% to 10% of patients, 2/3 of which occur within 1 month, and the rest occur within 1 year. 5% to 30% of patients can develop hyponatremia and reduced blood volume of cerebral salt wasting syndrome, or dilute hyponatremia and water retention caused by increased antidiuretic hormone secretion, the above two types of hyponatremia It needs to be identified clinically; brain-heart syndrome and acute pulmonary dysfunction can also occur, which are related to fluctuations in catecholamine levels and sympathetic nerve dysfunction. ^[1]

Auxiliary examination of subarachnoid hemorrhage

Imaging examination of subarachnoid hemorrhage

1. Skull CT: the preferred method for diagnosing SAH. CT shows that high density imaging in the subarachnoid space can confirm SAH. According to the CT results, the location of the intracranial aneurysm can be initially determined or suggested: if it is located in the internal carotid artery segment, it is often asymmetrical hemorrhage in the upper saddle pool; Hemorrhage at the base of the fissure; bleeding in the foot pool and annulus, usually without aneurysms. Dynamic CT examination also helps to understand the absorption of bleeding, the presence or absence of rebleeding, secondary cerebral infarction, hydrocephalus and its extent. The sensitivity of CT for the diagnosis of subarachnoid hemorrhage is 90-95% within 24 hours, 80% at 3 days, and 50% at 1 week.

2. Head MRI: When the sensitivity of CT decreases a few days after the disease, MRI can play a greater role. After 4 days, the T1 image can clearly show the extravasated blood, the blood high signal can last for at least 2 weeks, and the FLAIR image lasts longer. Therefore, when CT does not provide evidence of subarachnoid hemorrhage 1-2 weeks after the disease, MRI can be an important method for diagnosing subarachnoid hemorrhage and understanding the location of ruptured aneurysms.

CSF Subarachnoid hemorrhage cerebrospinal fluid (CSF) examination

Usually, CT examination has confirmed the diagnosis, lumbar puncture is not a routine clinical examination. If the amount of bleeding is small or the onset time is long, there is no positive detection on CT examination, and clinically suspicious inferior cavity bleeding requires a lumbar puncture examination for CSF. It is best to perform a lumbar puncture 12 hours after the onset of the disease to facilitate the identification of accidental puncture injuries. Uniform blood cerebrospinal fluid is a characteristic manifestation of subarachnoid hemorrhage and shows fresh bleeding, such as CSF yellowing or the discovery of phagocytic cells phagocytic red blood cells, hemosiderin or bilirubin crystals, etc., suggesting that SAH has existed at different times. .

Cerebrovascular imaging examination of subarachnoid hemorrhage

1. Cerebral angiography (DSA): It is the most valuable method for diagnosing intracranial aneurysms. The positive rate is 95%. It can clearly show the location and size of the aneurysm, the relationship with the tumor-bearing artery, and the presence or absence of vasospasm. Vascular malformations and moyamoya disease are also clearly visible. When conditions are available and the disease permits, a whole-brain DSA examination should be sought as soon as possible to determine the cause of bleeding, determine treatment methods, and determine prognosis. However, because angiography can aggravate neurological damage, such as cerebral ischemia, aneurysm rupture and bleeding, etc., the timing of angiography should avoid the peak period of cerebral vasospasm and rebleeding, that is, within 3 days or 3 to 4 weeks after bleeding. should.

2. CT angiography (CTA) and MR angiography (MRA): CTA and MRA are non-invasive methods of cerebral angiography, but their sensitivity and accuracy are not as good as DSA. It is mainly used for follow-up of patients with aneurysms and patients who cannot tolerate DSA in the acute stage.

3. Others: Transcranial ultrasound Doppler (TCD) dynamic detection of intracranial arterial flow velocity is the most sensitive method to find the tendency and degree of cramps of cerebral vasospasm (CVS) in time.

Subarachnoid hemorrhage laboratory test

Blood routine, blood coagulation, liver function, and immunological tests can help find other causes of bleeding.

Diagnosis and differential diagnosis of subarachnoid hemorrhage

Diagnosis of subarachnoid hemorrhage

Sudden severe headache, nausea, vomiting, and positive meningeal irritation in patients with no signs of focal nerve defect with or without disturbance of consciousness. The disease should be highly suspected. Combined with CT, it is confirmed that there is an intracranial and subarachnoid space. High-density signs can be diagnosed as subarachnoid hemorrhage. If the CT examination does not find abnormalities or there is no condition for CT examination, the diagnosis of subarachnoid hemorrhage can be made based on clinical manifestations combined with lumbar puncture CSF showing uniform bloody and increased pressure.

Differential diagnosis of subarachnoid hemorrhage

1. Cerebral hemorrhage is not easy to distinguish from SAH in deep coma. Cerebral hemorrhage is more than hypertension, and it is accompanied by symptoms and signs of focal neurological deficit such as hemiplegia and aphasia. Primary ventricular hemorrhage is difficult to distinguish from severe SAH clinically. Cerebellar hemorrhage and caudate nucleus hemorrhage are easy to be confused with SAH due to no obvious limb paralysis. Careful neurological examination, skull CT and DSA examination can be distinguished.

2. Intracranial infections of various types of meningitis such as tuberculous, fungal, bacterial, and viral meningitis. Although there are headaches, vomiting, and meningeal irritation, they often have fever first, and their symptoms are not as rapid as SAH and CSF. It suggests that the infection is not hemorrhage. The CT of the head without subarachnoid hemorrhage can be distinguished.

3. Approximately 1.5% of brain tumors may develop stroke after tumor stroke or intracranial metastases, which may form intratumoral or paratumor hematomas with SAH. Intracranial metastases, meningeal carcinomatous disease, or CNS leukemia can sometimes be described as bloody CSF, but according to the detailed Medical history, CSF detection of tumor / cancer cells, and head CT can be identified.

4. Other elderly patients with SAH are mainly caused by psychiatric symptoms. The onset is relatively slow. Meningeal irritation signs such as headache and neck stiffness are not obvious, or symptoms of impaired consciousness and brain parenchymal damage are serious. It is easy to miss or misdiagnose. Ask for medical history and physical examination, and then perform a skull CT or CSF examination to confirm the diagnosis. ^[2]

Emergency management of subarachnoid hemorrhage

1. Sudden severe headache and vomiting. Suspected of the possibility of subarachnoid hemorrhage, they should be sent to the hospital for treatment in time;

2. Try to keep the patient on the side with the head on the high side, avoid the back of the tongue to hinder ventilation, and clean up the vomit in the mouth in time to avoid inhaling the airway by mistake;

3. Try to avoid long-distance transfers and choose the nearest qualified medical unit for treatment;

4. Medical personnel should be escorted when transferring patients and observe changes in the condition at any time, and take necessary measures at any time:

5. Dehydration and antihypertensive treatment should be given before transfer, sedative and painkillers should be given, and absolute bed rest should be provided;

6. Avoid vibration during transportation as much as possible;

7. Ventricular puncture and drainage can be performed when there is a large amount of bleeding, or hemorrhagic cerebrospinal fluid can be placed by lumbar puncture; skull CT or lumbar puncture can be confirmed;

8. Actively search for the cause, and confirm the radical operation for those with intracranial arterial and intracranial venous malformations;

9. Pay attention to blood pressure changes at any time;

10. Keep the patient happy and avoid emotional tension. ^[3]

Clinical treatment of subarachnoid hemorrhage

After the diagnosis of SAH, cerebral angiography or CT angiography (CTA) should be performed as soon as possible. Once it is confirmed that the intracranial aneurysm has been ruptured, prepare for craniotomy and intravascular embolization as soon as possible. The purpose of SAH treatment is to prevent complications such as rebleeding, vasospasm, and hydrocephalus, and to reduce mortality and disability.

General and symptomatic treatment of subarachnoid hemorrhage

Monitor vital signs and changes in nervous system signs to keep airways open and maintain breathing and circulation stability. Stay in bed quietly, avoid excitement and exertion, keep the stool open, and apply sedative and antitussive and antiepileptic drugs symptomatically.

Subarachnoid hemorrhage reduces intracranial pressure

Appropriately limit the amount of liquid to prevent hyponatremia. Dehydrating agents such as mannitol and furosemide are commonly used in clinical practice to reduce intracranial pressure. Albumin can also be used as appropriate. When accompanied by a large intracranial hematoma, the hematoma can be removed surgically to reduce intracranial pressure and save lives.

Prevention and treatment of subarachnoid hemorrhage

(1) Rest quietly and stay in bed for 4-6 weeks absolutely; (2) Control blood pressure. Patients may have high blood pressure due to severe pain. Pay attention to removing the incentives such as pain. (3) Application of anti-fibrinolytic drugs to prevent rebleeding caused by the dissolution of blood clots around the aneurysm. Common drugs are aminocaproic acid and aminotoluic acid; (4) Elimination of aneurysms by surgery is the best way to prevent rebleeding of aneurysmal SAH Approach.

Prevention and treatment of cerebral vasospasm with subarachnoid hemorrhage

(1) To maintain blood volume and blood pressure, expand colloidal fluid, dopamine intravenously if necessary, and 3H therapy (high blood volume, elevated blood pressure, and blood dilution) are mostly used abroad to treat cerebral vasospasm after SAH. (2) Early use of nimodipine calcium antagonists. (3) Early surgery to remove aneurysms and blood clots.

Prevention and treatment of hydrocephalus in subarachnoid hemorrhage

(1) Inhibit cerebrospinal fluid secretion by acetazolamide, or use dehydration drugs such as mannitol and furosemide. (2) Cerebrospinal fluid shunt is feasible when medical treatment is not effective: ventricle-atrium or ventricle-peritoneal shunt to avoid aggravating brain damage.

Prognosis of subarachnoid hemorrhage disease

About 10% of patients die before receiving treatment. The case fatality rate within 30 days is about 25% or higher. The mortality of rebleeding is about 50%, the rebleeding rate within 20 weeks is 20-25%, and the annual recurrence rate after 6 months is 2-4%. The most important factor affecting the prognosis is the time interval and level of consciousness after the onset. Death and complications mostly occur within 2 weeks after the illness. The mortality rate at 6 months is 71% in comatose patients and 11 in conscious patients %. Other factors, such as older patients, have a worse prognosis than younger patients; aneurysmal SAH has a worse prognosis than non-aneurysmal SAH.

The course and prognosis of cerebral subarachnoid hemorrhage depend on its etiology, condition, blood pressure, age and neurological signs. Subarachnoid hemorrhage caused by aneurysm rupture has a poor prognosis, and subarachnoid hemorrhage caused by cerebral vascular malformations is often easier to recover. Unexplained people have a better prognosis and less chance of recurrence. The elderly and infirm have progressively worsening consciousness, increased blood pressure and significantly increased intracranial pressure or hemiplegia, aphasia, and convulsions. The prognosis is poor.