Subarachnoid hemorrhage is a clinical syndrome caused by the rupture of a diseased blood vessel at the base or surface of the brain and the direct flow of blood into the subarachnoid space, also known as primary subarachnoid hemorrhage, which accounts for about 10% of acute strokes. The incidence rate in China is about 2.0/100,000 people per year according to the World Health Organization survey, and 6-20/100,000 people per year have also been reported. It is also seen as secondary subarachnoid hemorrhage due to intracerebral parenchymal, ventricular hemorrhage, rupture of the epidural or subdural vessels and blood penetrating the brain tissue into the subarachnoid space.
Causes
Any cause that can cause cerebral hemorrhage can cause this disease. The common causes are.
1, intracranial aneurysm accounts for 50-85% of the total number of aneurysms, which are usually found in the branches of the large arteries of the cerebral base artery ring, with the anterior half of the ring being more common.
2, cerebrovascular malformation mainly arteriovenous malformation, mostly seen in adolescents, accounting for about 2%, arteriovenous malformation is mostly located in the cerebral hemisphere middle cerebral artery distribution area.
3.Anomalous vascular network disease of the cerebral base (moyamoya disease) accounts for about 1%.
4.Other intercalated aneurysm, vasculitis, intracranial venous system thrombosis, connective tissue disease, hematological disease, intracranial tumor, coagulation disorders, complications of anticoagulation therapy, etc.
5. The cause of bleeding is unknown in some patients, such as: primary pericentral hemorrhage.
The risk factors for subarachnoid hemorrhage are mainly those that lead to intracranial aneurysm rupture, including hypertension, smoking, heavy alcohol consumption, previous history of aneurysm rupture, large aneurysm size, and multiple aneurysms. Compared to nonsmokers, smokers have larger aneurysm volumes and more frequently have multiple aneurysms.
Pathogenesis
An aneurysm is a localized lesion in the arterial wall (which may be due to weakness or structural damage) that bulges outward to form a permanent, confined dilatation. The formation of aneurysms may result from congenital defects in the muscular layer of the arterial wall or from acquired degeneration of the internal elastic layer or a combination of both. Therefore, there is a degree of genetic predisposition and familial aggregation for the occurrence of aneurysms. About 4% of first-degree relatives of patients with subarachnoid hemorrhage have aneurysms. However, intracranial aneurysms are not entirely caused by congenital anomalies; a significant proportion develop later in life, as the elasticity of the arterial wall gradually decreases with age and protrudes outward to form an aneurysm in response to factors such as blood flow impact.
Whether the aneurysm ruptures, the arteriovenous malformation lesion ruptures the vessel or a sudden increase in blood pressure causes the vessel to rupture in other cases, it causes blood to flow into the cerebral subarachnoid space and spread rapidly through the cerebrospinal fluid surrounding the brain and spinal cord, irritating the meninges and causing signs of meningeal irritation such as headache and cervical tonicity. The entry of blood into the subarachnoid space also increases the contents of the cranial cavity, increases pressure, and causes secondary cerebral vasospasm. The latter is due to extensive ischemic damage and edema of the neuromuscular junction formed between the smooth muscle cells of the vessel wall as a result of the traction of the blood clot and the fibrous cords surrounding the vessel wall (mechanical factors) after hemorrhage. In addition, a large amount of blood or clots deposited at the base of the skull, some of the agglutinated red blood cells can also block the small sulcus between the arachnoid villi, so that the back absorption of cerebrospinal fluid is blocked, thus acute traffic hydrocephalus or arachnoid adhesions can occur, causing a rapid increase in intracranial pressure, further reducing cerebral blood flow, aggravating cerebral edema, and even leading to the formation of brain herniation. All of the above can cause patients to become conscious again or develop limited neurological symptoms after their condition has stabilized and improved. The dilatation and hemorrhage of posterior communicating artery aneurysm may compress the adjacent arteriolar nerve and produce different degrees of arteriolar nerve palsy (manifested as impaired eye movement). The blood may also stimulate the hypothalamus, causing endocrine and autonomic dysfunction such as elevated blood glucose and fever.
Clinical manifestations
Sex and age
Aneurysm rupture is more common in young adults than in men, and vascular malformations are more common in adolescents.
Onset of disease
A sudden onset of headache that occurs in seconds or minutes is the most common mode of onset. Patients can often clearly describe the time and circumstances of onset. The onset is usually preceded by obvious triggers, such as strenuous exercise, emotional stress, exertion, defecation, coughing, and alcohol consumption; a few patients may have the onset in quiet conditions. About 1/3 of patients have headache, nausea, vomiting and other symptoms a few days or weeks before the rupture of aneurysm.
Clinical manifestations
The typical clinical manifestations of SAH are sudden onset of severe headache, nausea, vomiting and meningeal irritation with or without focal signs. Bursting severe head pain of limited or total head pain occurs during or after strenuous activity, which is unbearable, persistent or continuously progressive, and sometimes the pain may also occur in the upper cervical segment. The site of origin is often related to the site of aneurysm rupture. Common concomitant symptoms include vomiting, transient impaired consciousness, back of the neck or precinct pain, and photophobia. Meningeal irritation signs appear within a few hours after the onset of the disease in the majority of cases, with the most pronounced cervical ankylosis and positive Kernig and Brudzinski signs. Retinal hemorrhage and optic papillary edema can be seen on fundus examination. About 25% of patients may develop psychiatric symptoms, such as euphoria, delirium, and hallucinations. Seizures, focal neurological deficits such as actinic nerve palsy, aphasia, monoplegia or mild hemiplegia, and sensory deficits may also be present. Some patients, especially elderly patients, often have atypical clinical manifestations such as headache and meningeal irritation signs, while psychiatric symptoms are more pronounced. Patients with primary midbrain hemorrhage have milder symptoms, CT shows blood accumulation in the midbrain or the brain pool around the cerebral bridge, angiography does not reveal aneurysms or other abnormalities, rebleeding or delayed vasospasm generally do not occur, and the clinical prognosis is good.
Common complications
(1) Rehemorrhage: It is an acute and serious complication of SAH, and the morbidity and mortality rate is about 50%. The risk of rebleeding is greatest within 24 hours after hemorrhage, and the incidence of rebleeding is higher within 1 month after the onset of hemorrhage; the incidence of rebleeding is 20%-30% within 2 weeks and 30% within 1 month. The cause of rebleeding is mostly aneurysm rupture. Patients who are comatose on admission, elderly, female, and have a systolic blood pressure over 170 mmHg are at greater risk of rebleeding. The clinical manifestations are: sudden onset of severe headache, nausea and vomiting, deepening of consciousness, convulsions, and aggravation or reappearance of the previous symptoms and signs in the presence of stable or improving condition. Confirmation of diagnosis is mainly based on the above-mentioned manifestations, CT showing an increase in pre-existing hemorrhage or an increase in the amount of blood contained in the cerebrospinal fluid from lumbar puncture, etc.
(2) Cerebral vasospasm: It is an important cause of death and disability. About 20-30% of SAH patients develop cerebral vasospasm, which causes delayed ischemic injury and can be followed by cerebral infarction. Early cerebral vasospasm appears after the hemorrhage and lasts for several minutes or hours; late cerebral vasospasm starts 3-5 days after the hemorrhage, peaks at 5-14 days, and gradually decreases at 2-4 weeks. Clinical manifestations include altered consciousness, focal neurological impairment (e.g., hemiparesis, aphasia, etc.), and the symptoms of brain tissue damage near the aneurysm are usually the most severe.
(3) Hydrocephalus: Acute obstructive hydrocephalus occurs in about 15-20% of patients with SAH. Acute hydrocephalus occurs within 1 week after the onset of the disease and is caused by blood entering the ventricular system and subarachnoid space to form blood clots that obstruct the cerebrospinal fluid circulation pathway, which is a deformed obstructive hydrocephalus; mild cases show drowsiness, psychomotor retardation and memory impairment, swelling with headache, vomiting and impaired consciousness. Most of the acute obstructive hydrocephalus can be improved with the absorption of hemorrhage. Delayed hydrocephalus occurs 2~3 weeks after SAH and is traffic hydrocephalus. It is characterized by progressive mental retardation, gait abnormalities and urinary and bowel disorders. Cerebrospinal fluid pressure is normal, so it is also called normal cranial pressure hydrocephalus, and head CT or MRI shows enlarged ventricles.
(4) Other: convulsions may occur in 5-10% of patients, 2/3 of which occur within 1 month and the rest within 1 year. 5%-30% of patients may develop hyponatremia and hypovolemic cerebral salt consumption syndrome, or dilutional hyponatremia and water retention due to increased secretion of antidiuretic hormone, and the above two types of hyponatremia need to be distinguished clinically; cerebrocardiac syndrome and acute pulmonary dysfunction, associated with fluctuating catecholamine levels and sympathetic dysfunction. [1]
Ancillary examinations
Imaging examinations
1, cranial CT: is the preferred method to diagnose SAH, CT shows high-density shadow in the subarachnoid space can confirm the diagnosis of SAH. according to the CT results can initially determine or suggest the location of intracranial aneurysm: if located in the internal carotid artery segment is often asymmetric blood accumulation in the suprasellar pool; middle cerebral artery segment is mostly seen in the lateral fissure accumulation; the anterior communicating artery segment is the basal accumulation of blood in the anterior interstitial fissure; and the bleeding in the interpeduncular pool and circumferential pool, generally no aneurysm. The sensitivity of CT for the diagnosis of subarachnoid hemorrhage is 90-95% within 24 hours, 80% within 3 days, and 50% within 1 week.
2. Head MRI: When the sensitivity of CT decreases several days after the disease, MRI can play a greater role. 4 days later, T1 image can clearly show the extravasated blood, and the high signal of blood can last at least 2 weeks, and in 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 site of ruptured aneurysm.
Cerebrospinal fluid (CSF) examination
Usually, lumbar puncture is not used as a routine clinical examination if the diagnosis has been confirmed by CT examination. Lumbar puncture is best performed 12 hours after onset to facilitate identification of puncture misdiagnosis. Homogeneous bloody cerebrospinal fluid is a characteristic manifestation of subarachnoid hemorrhage and indicates fresh hemorrhage. If the CSF is yellowish or phagocytic red blood cells, phagocytes with iron-containing heme or bilirubin crystals are found, it suggests that SAH has been present for various times.
Cerebrovascular imaging
Cerebral angiography (DSA): It is the most valuable method to diagnose intracranial aneurysm, with a positive rate of 95%, and can clearly show the location, size, relationship with the aneurysm-carrying artery and the presence of vasospasm of the aneurysm. When conditions are available and the condition permits, whole brain DSA should be performed as soon as possible to determine the cause of hemorrhage, decide the treatment method and judge the prognosis. However, since angiography can aggravate neurological damage, such as cerebral ischemia, aneurysm rupture and bleeding again, the timing of angiography should avoid the peak of cerebral vasospasm and rebleeding, that is, within 3 days or 3~4 weeks after bleeding is appropriate.
2.CT angiography (CTA) and MR angiography (MRA): CTA and MRA are non-invasive methods of cerebral vascular imaging, but they are not as sensitive and accurate as DSA, and are mainly used for follow-up of aneurysm patients and patients who cannot tolerate DSA examination during the acute period.
3.Other: Transcranial ultrasound Doppler (TCD) dynamic detection of the flow velocity of major intracranial arteries is the most sensitive method for timely detection of cerebral vasospasm (CVS) tendency and the degree of spasm.
Laboratory tests
Routine blood count, coagulation function, liver function and immunological tests are helpful to find other causes of bleeding.
Diagnosis and differential diagnosis
Diagnosis
Patients with sudden onset of severe headache, nausea, vomiting and positive meningeal irritation signs, without signs of focal neurological deficit, with or without impaired consciousness should be highly suspected of the disease. Combining CT to confirm high density signs in the cerebral pool and subarachnoid space can diagnose subarachnoid hemorrhage. If CT examination does not reveal any abnormality or if CT examination is not available, the diagnosis of subarachnoid hemorrhage can be made based on the clinical manifestations combined with the uniform and consistent hemorrhage and increased pressure of CSF by lumbar puncture.
Differential diagnosis
1. Cerebral hemorrhage It is not easy to distinguish from SAH in deep coma. Cerebral hemorrhage is more often associated with hypertension, with symptoms and signs of focal neurological deficits such as hemiparesis and aphasia. Primary ventricular hemorrhage is clinically difficult to distinguish from severe SAH, and cerebellar hemorrhage and caudate nucleus head hemorrhage are easy to be confused with SAH because there is no obvious limb paralysis, and careful neurological function examination, cranial CT and DSA examination can be used for differentiation.
2, intracranial infection Various types of meningitis such as tuberculosis, fungal, bacterial and viral meningitis, although there are headache, vomiting and meningeal irritation signs, but often preceded by fever, the onset is not as acute as SAH, CSF shape suggests infection rather than hemorrhage, head CT without subarachnoid hemorrhage and other features can be distinguished.
3.Stroke or intracranial metastasis About 1.5% of brain tumors can occur as stroke, forming intra- or paratumoral hematoma combined with SAH, intracranial metastasis of carcinoma, meningeal carcinomatosis or CNS leukemia can sometimes be called hemorrhagic CSF, but it can be differentiated based on detailed medical history, detection of tumor/carcinoma cells in CSF and head CT.
4.Other elderly people with SAH mainly have psychiatric symptoms, and the onset of SAH is slow, and the signs of meningeal irritation such as headache and cervical tonicity are not obvious, or the symptoms of impaired consciousness and brain parenchymal damage are heavy, so it is easy to miss or misdiagnose the disease, so attention should be paid to the medical history and physical examination, and head CT or CSF examination to clarify the diagnosis.
Emergency treatment
1.Sudden severe headache and vomiting should be suspected as possible subarachnoid hemorrhage, and should be sent to hospital promptly.
2, try to keep the patient in a head-high lateral position to avoid posterior tongue root obstruction to ventilation, and promptly clean vomit from the mouth to avoid inadvertent aspiration into the airway.
3, try to avoid long-distance transfer, choose the nearest medical unit with conditions for treatment;
4, when transferring patients should be escorted by medical personnel and observe changes in condition at any time, and take the necessary measures at any time.
5, before transfer should be given dehydration, hypotension and other treatment, . Administer sedative, painkillers and absolute bed rest.
6, avoid vibration as much as possible during transport.
7.Ventricular puncture and drainage is feasible for large amount of bleeding, or lumbar puncture to release hemorrhagic cerebrospinal fluid; cranial CT or lumbar puncture can confirm.
8, actively look for the cause, for intracranial artery and intracranial vein malformation, after confirming the surgical radical treatment.
9, keep an eye on blood pressure changes.
10.Keep patients happy and avoid emotional tension.
Clinical treatment
After the diagnosis of SAH, cerebral angiography or CT angiography (CTA) should be performed as soon as possible, and once the rupture of intracranial aneurysm is confirmed, craniotomy or endovascular interventional embolization should be prepared as soon as possible. the main purpose of SAH treatment is to prevent and treat complications such as rebleeding, vasospasm and hydrocephalus, and to reduce the mortality and disability rate.
General treatment and symptomatic treatment
Monitor the changes of vital signs and neurological signs, keep the airway unobstructed, and maintain the stability of respiration and circulation. Stay quietly in bed, avoid agitation and exertion, keep bowel movement smooth, and apply sedative and antiepileptic drugs as appropriate.
Reduce intracranial pressure
Limit fluid intake appropriately to prevent hyponatremia. Mannitol, furosemide and other dehydrating agents are commonly used to reduce intracranial pressure, and albumin can also be used as appropriate. When there is a large intracerebral hematoma, surgical removal of the hematoma can be performed to lower the intracranial pressure to save life.
Prevention and treatment of rebleeding
(1) Quiet rest and absolute bed rest for 4-6 weeks; (2) Blood pressure control. Patients may have elevated blood pressure due to severe pain, so pay attention to removing pain and other triggers. (3) Apply anti-fibrinolytic drugs to prevent rebleeding caused by lysis of the clot around the aneurysm, commonly used drugs include aminohexanoic acid and aminomethylbenzoic acid, etc.; (4) Surgical elimination of the aneurysm is the best way to prevent rebleeding of aneurysmal SAH.
Prevention and treatment of cerebral vasospasm
(1) Maintain blood volume and blood pressure, if necessary, give colloid fluid expansion, dopamine drip, 3H therapy (hypervolemia, elevated blood pressure, hemodilution) is more often used to treat cerebral vasospasm after SAH in foreign countries. (2) Early use of calcium antagonists such as nimodipine. (3) Early surgical removal of aneurysm and removal of blood clot.
Prevention and treatment of hydrocephalus
(1) Give acetazolamide to inhibit cerebrospinal fluid secretion or apply dehydrating drugs such as mannitol and furosemide. (2) If internal treatment is ineffective, cerebrospinal fluid shunt: ventricular-atrial or ventricular-abdominal shunt is feasible to avoid aggravating brain damage.
Disease prognosis
About 10% of patients die before receiving treatment, and the death rate within 30 days is about 25% or higher. The death rate is approximately 50% for rebleeding, 20-25% for rebleeding within 2 weeks, and 2-4% for annual recurrence after 6 months. The most important factors affecting prognosis are the time interval after onset and the level of consciousness, with death and complications occurring mostly within 2 weeks of illness, and the morbidity and mortality rate at 6 months being 71% in comatose patients and 11% in awake 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 after cerebral subarachnoid hemorrhage depends on its etiology, condition, blood pressure status, age, and neurological signs. Subarachnoid hemorrhage due to ruptured aneurysm has a poor prognosis, while subarachnoid hemorrhage due to cerebrovascular malformation is often easier to recover from. Those with unknown causes have a better prognosis and less chance of recurrence. The prognosis is worse in elderly and frail patients with progressive worsening of consciousness, increased blood pressure and intracranial pressure, or hemiplegia, aphasia, or convulsions.