Overview
Hypertensive cerebral hemorrhage (HCH) is a disorder with a high mortality and disability rate among cerebrovascular diseases. Although many medical institutions at home and abroad have studied it in the past hundred years, the death rate remains high and more than 3/4 of the survivors are left with different degrees of disability. According to the statistics in 2000, the elderly (>60 years old) population in China has exceeded 1.3 billion, and this disease, which mainly affects the elderly, is seriously threatening people’s health. Therefore, it is necessary to pay attention to it and continuously study effective measures for its prevention and treatment.
Causes
Hypertension can lead to pathological changes in the blood vessels of various organs throughout the body. Cerebral blood vessels undergo degeneration and atherosclerosis under prolonged high pressure to accommodate hypertension. Among them is the thickening of the walls of the small cerebral arteries, which counteracts the high pressure and prevents an increase in cerebral microcirculatory perfusion pressure. These changes are particularly severe in the penetrating arteries at the base of the brain.
Pathogenesis
Hypertensive cerebral hemorrhage is 80% supratentorial and 20% infratentorial. Hemorrhage in the cerebral hemispheres is most common in the basal nucleus and optic thalamus, followed by the brainstem and cerebellum. After cerebral hemorrhage, hematomas tend to expand in the direction of white matter fibers, and the early posthemorrhagic neural tissue is mainly affected by compression, separation and displacement. Most of the shell nucleus hemorrhages are caused by bleeding from the ductus arteriosus, among which bleeding from the lateral ductus arteriosus is common, and the hematoma tends to develop in the direction of the external capsule after hemorrhage; after bleeding from the medial ductus arteriosus, it tends to expand in the direction of the internal capsule. The hematoma tends to be larger and increases the size of the cerebral hemisphere. The cerebral hemisphere is swollen, the cerebral gyrus is flattened, and the cerebral sulcus is narrowed. The hippocampal herniation causes compression of the brainstem and the ipsilateral posterior cerebral artery and the arteriolar nerve, while the small median collateral artery of the midbrain and the cerebral bridge is dislocated and dissected, causing bleeding in the midbrain and the cerebral bridge. Sometimes the hematoma progresses medially from the cerebral hemisphere downward into the optic thalamus and midbrain. The hematoma may also disrupt the caudate nucleus and enter the lateral ventricle, which then flows into the subarachnoid space, called secondary subarachnoid hemorrhage. These secondary subarachnoid hemorrhages tend to accumulate in the middle and lateral foramina ventral to the cerebellum and in the subarachnoid space at the base. If the hemorrhage is in the cerebellar hemisphere, the hemisphere is enlarged and tends to compress the brainstem, which also tends to break into the subarachnoid space. Thalamic hemorrhage is usually due to rupture of the deep branches of the posterior cerebral artery, the thalamic geniculate artery and the thalamic perforating artery, and the blood may invade the internal capsule and the ventricles. The incidence of thalamic hemorrhage with blood invasion into the ventricles can be as high as 40% to 70%.
Brain stem hemorrhage is most common in the pons, often expanding from the middle to the sides, or invading upward into the midbrain, and often breaking into the fourth ventricle. Cerebellar hemorrhage mostly originates from the dentate nucleus, mainly from the superior cerebellar artery, and the posterior inferior cerebellar artery and anterior cerebellar artery can also be sources of hemorrhage; after hemorrhage in the cerebellar hemispheres, it can cross the midline to involve the contralateral side and invade the fourth ventricle, and it is not uncommon to extend into the cerebellar peduncle.
Usually, in patients with hypertensive cerebral hemorrhage, a hematoma can be formed 20-30 min after the onset of hemorrhage, and the hemorrhage gradually stops; 6-7 h after the hemorrhage, serous exudate and cerebral edema begin to appear around the hematoma, and with the prolongation of time, this secondary change is constantly aggravated, and even a vicious cycle occurs. Therefore, irreversible brain parenchymal damage caused by hematoma mostly occurs about 6h after hemorrhage.
Under microscopic observation, cerebral hemorrhage can be divided into three phases.
1, hemorrhagic phase A large area of hemorrhage can be seen. Red blood cells are mostly intact, softened brain tissue often appears at the edge of the hemorrhagic foci, nerve cells disappear or show local ischemic changes, and astrocytes also have dendritic destruction. There is often infiltration of polymorphonuclear leukocytes, capillary congestion and swelling of the canal walls, and sometimes punctate hemorrhage due to canal wall disruption. It should be noted that there is a circle of hypodense area outside the high-density area seen in CT examination, which is different from the hypodense area around the tumor, not edema but softened necrotic tissue. Because most of the cerebral hemorrhage is arterial rupture, the hematoma is large to a considerable volume within a short period of time, and the pressure on the surrounding brain tissue is very high, so it is easy to cause necrosis and softening of brain tissue.
2.Absorption period Glial cell proliferation can appear 24~36h after hemorrhage, especially microglia and some cells from the outer membrane of blood vessels form lattice cells. In addition to phagocytosis of lipids, a small number of lattice cells accumulate iron-containing heme, which often accumulate in sheets or around the hematoma. Astrocytes also have proliferation and obesity degeneration.
3.Recovery period After the blood and damaged tissues are gradually removed, the defective part is replaced by glial cells, glial fibers and collagen fibers, forming a scar. Smaller bleeding can be completely repaired, if bleeding is larger often left cystic cavity. This is the same as the softening outcome, except that the hemoglobin metabolites remain in the scar tissue for a long time, giving the tissue a brownish-yellow color.
Clinical presentation
Hypertensive cerebral hemorrhage occurs most frequently in hypertensive patients aged 50 to 60 years and usually develops during emotional stress, overexcitement, defecation, breath-holding exertion, or mental stress. Cerebral hemorrhage is often unpredictable and occurs suddenly, with a rapid onset, often developing to a peak within minutes to hours. It is less common for the disease to progress to a severe level over a longer period of time. The clinical manifestations depend on various factors such as the site of hemorrhage, the extent of hemorrhage, the body’s response, and the general condition. The onset of the disease is usually characterized by sudden and severe head pain, followed by frequent vomiting, systolic blood pressure of 180
mmHg or more, occasionally convulsions, etc. In severe cases, the consciousness often turns into coma within minutes or tens of minutes, accompanied by fecal and urinary incontinence. If the pulse rate is rapid and the blood pressure drops, it is a sign of endangerment. Focal neurological symptoms and signs are often described clinically according to the site of hemorrhage.
1. Hemorrhage in the nucleus accumbens and basal ganglia region. It is the most common site of hypertensive cerebral hemorrhage, mostly affecting the internal capsule. Patients often have head and eyes turned to the side of the hemorrhagic lesion, showing “staring at the lesion” and “three partial” symptoms, i.e. hemiparesis, hemianesthesia and hemianopia. In the early stage, the muscle tone and tendon reflexes of the limb on the side of hemorrhage decreased or disappeared, and then gradually became higher, the upper limb was flexed and inward, the lower limb was extended and straightened, the tendon reflexes became hyperactive, ankle clonus could appear, and the pathological reflexes were positive, which was typical of upper motor neuron hemiparesis. The hemorrhagic foci have hyperalgesia on the contralateral side of the hemiplegia, and there is no response when needling the limb or face or the response is slower than the other side. If the patient is clearly conscious and cooperates with the examination, the patient may also be found to have ipsilateral hemianopia contralateral to the hemorrhagic focus. If the hematoma breaks into the lateral ventricle, or even fills the whole lateral ventricle, it is called lateral ventricular cast, and its prognosis is poor.
2. Cerebral bridge hemorrhage. It often starts suddenly and enters deep coma within a few minutes, and the condition is critical. Cerebral bridge hemorrhage often starts from one side of the cerebral bridge, and then spreads to both sides quickly, resulting in bilateral limb paralysis. Most of them are flaccid, a few are spastic or decorticate tonic, and bilateral pathological reflexes are positive. The characteristic sign is extreme narrowing of the pupils on both sides in a “pinpoint” fashion. Some patients may develop central hyperthermia, irregular breathing and respiratory distress, and often die within 1 to 2 days.
3. Cerebellar hemorrhage. Patients with mild type have clear consciousness at the onset, often complaining of severe headache and vertigo on one side of the posterior occipital region, frequent vomiting, slurred pronunciation, and nystagmus. The limbs are often not paralyzed, but the limb on the side of the lesion appears to be ataxic. When the hematoma gradually enlarges and breaks into the fourth ventricle, it may cause acute hydrocephalus. In severe cases, herniation of the foramen magnum occurs, and the patient suddenly falls into coma, has irregular breathing or even stops, and eventually dies due to respiratory and circulatory failure.
4. Subcortical hemorrhage in the cerebral lobe. The symptoms are related to the size of the hematoma. Symptoms such as headache, vomiting, photophobia and irritability are usually present, and the corresponding neurological deficits in the cerebral lobes are more prominent. The hematoma is enlarged and the symptoms of cranial hypertension are obvious.
5. Thalamic hemorrhage. Most patients present with coma and hemiparesis after the onset of the disease. The typical ocular signs may appear in patients with medial or inferior thalamic hemorrhage, i.e. vertical gaze paralysis, mostly upward gaze disorder, both eyes inward and downward gaze nasal tip; eye oblique gaze, downward medial gaze on the hemorrhagic side; pupil narrowing, not equal in size, slow response to light; eye inability to converge and gaze disorder, etc. If the hemorrhage extends outward, the internal capsule may be affected and the “three deviations” sign may appear. If thalamic hemorrhage invades into the ventricle, the condition can be aggravated with high fever and tonic convulsions of the limbs, and the incidence of cerebral visceral syndrome can be increased.
Subcortical hemorrhage (lobar hemorrhage) is second only to basal ganglia hemorrhage and is similar to thalamic hemorrhage. Most scholars believe that lobar hemorrhage occurs in the parietal, temporal and occipital lobes, that is, the posterior half of the brain. The clinical manifestations of lobar hemorrhage are different from those of basal ganglia hemorrhage. Lobar hemorrhage tends to break into the adjacent subarachnoid space, but is less likely to break into the ventricular system because it is farther from the midline, so the meningeal irritation is severe but the impairment of consciousness is mild, and the prognosis is generally good. Its clinical manifestations are characterized by.
(1) Impaired consciousness is rare and relatively mild.
(2) Hemiparesis and isotropic gaze are less frequent and less severe because lobar hemorrhage is not as likely to involve the internal capsule as basal ganglia hemorrhage.
(3) Meningeal irritation is more common.
(4) Occipital lobe hemorrhage may have transient black and cortical blindness. Parietal-temporal lobe hemorrhage may have isotropic hemianopia and mild hemiparesis, and in the dominant hemisphere, aphasia. Frontal lobe hemorrhage may have mental retardation, urinary incontinence, and less severe hemiparesis.
7. Intraventricular hemorrhage. Primary intraventricular hemorrhage is rare, and most common cases are secondary to thalamic hemorrhage or basal ganglia hemorrhage. The clinical manifestations of these patients are closely related to the site of primary hemorrhage, the amount of hematoma, and the extent of ventricular involvement. The more the primary hemorrhage site is adjacent to the ventricles, the more the hemorrhage has the opportunity to extend into the ventricles and invade them. Therefore, the condition of patients with intraventricular hemorrhage is more serious. In addition to the symptoms and signs of the primary lesion, there are also a series of manifestations of brainstem involvement and rapid increase of intracranial pressure, more severe impairment of consciousness, obvious changes in vital signs, and often accompanied by high fever and tonic attacks.
Laboratory tests: When bleeding enters the subarachnoid space and secondary subarachnoid hemorrhage occurs, lumbar puncture may reveal bloody cerebrospinal fluid.
Other ancillary tests.
Cranial CT plain scan is the preferred examination, which can quickly clarify the site and extent of intracerebral hemorrhage and the amount of hematoma, as well as whether the hematoma breaks into the ventricles and whether it is accompanied by subarachnoid hemorrhage, etc. It can also identify cerebral edema and cerebral infarction. The occupying effect of the hematoma can be inferred from the displacement of the lateral ventricles by pressure, displacement of the falx and loss of the basal pool, which can help in the selection of treatment plan and prognosis. Other etiologies, such as vascular malformation, aneurysm and tumor, can also be identified based on the site of the hematoma and the enhanced CT performance.
When the cause of cerebral hemorrhage is suspected to be a factor other than hypertension, MRI examination is valuable to differentially diagnose cerebrovascular malformations, tumors, and giant intracranial aneurysms. However, MRI examinations are time-consuming, and in acute cases with severe disease, the patient’s vital signs and ventilation tract must be monitored during the examination to prevent accidents. In addition, the MRI manifestations of hematomas at different times are more complicated, which sometimes makes the diagnosis difficult instead.
Cerebral angiography can clearly diagnose aneurysm or vascular malformation, but when cerebral angiography is negative, especially when the intracerebral hematoma is large, it should be considered that the ruptured aneurysm or vascular malformation is temporarily compressed and obstructed without visualization; for tiny vascular malformation, angiography can also be falsely negative.
Diagnosis
The main points of diagnosis of hypertensive cerebral hemorrhage are: (1) it is mostly seen in hypertensive atherosclerotic patients over 50 years of age; (2) it often develops suddenly during daytime activities and exertion; (3) the course of the disease progresses rapidly and complete stroke manifestations such as impaired consciousness and hemiparesis appear soon; (4) the cerebrospinal fluid is homogeneous and bloody; (5) it is confirmed by CT or MRI scan.
Differential diagnosis
There are many causes of cerebral hemorrhage that can be differentiated from hypertensive cerebral hemorrhage, and the differentiation should be based on the patient’s age, past history and imaging examination. Younger patients tend to bleed from cerebrovascular malformations. A history of chronic hypertension supports hypertensive hemorrhage, and cerebral hemorrhage can also occur occasionally during long-term anticoagulant medication or during anticoagulation therapy for myocardial infarction, and the site of bleeding is also important. A typical shell nucleus or thalamic hemorrhage can basically be identified as hypertensive cerebral hemorrhage; subcortical hemorrhage in the cerebral lobes is mostly suggestive of vascular malformation; obvious subarachnoid hemorrhage suggests a high possibility of aneurysm. Brain metastases, especially melanoma, choriocapillary epithelial carcinoma, adrenal carcinoma, breast cancer, brain metastases of lung cancer, and glioblastoma in primary brain tumors are also prone to spontaneous hemorrhage. Other causes of bleeding include cerebral venous thrombosis, bleeding after cerebral infarction, blood disorders, and arteritis.
Treatment
The first step is to keep quiet, reduce unnecessary moving, keep the airway open, gradually lower the excessive blood pressure, treat cerebral edema, and lower the intracranial pressure. The surgical treatment of hypertensive cerebral hemorrhage is still controversial and should be analyzed according to the patient’s general condition, the location of the hematoma, its size and the evolution of the disease.
1. Indications for surgery. The main purpose of surgery is to remove the hematoma, reduce the intracranial pressure, make it possible to recover the compressed (not destroyed) neurons, prevent and alleviate a series of secondary pathological changes after hemorrhage, and break the life-threatening vicious circle. However, based on different data and different units, the choice of surgical indications varies. As a result, the treatment results obtained vary widely and are not comparable.
The current indications for surgery that have been accepted by most are broadly as follows.
(1) Preservation of a certain degree of consciousness and neurological function after hemorrhage, followed by gradual deterioration, but the manifestation of brain herniation is not yet obvious, indicating that there is still a possibility of reversal of the primary damage, and the deterioration is often closely related to the increase of intracranial pressure. Therefore, surgery is likely to be life-saving and should be actively considered.
(2) Cerebellar hemorrhage: Because the hemorrhage is close to the brainstem, and because there is no obvious aura before irreversible deterioration occurs. To prevent the above, surgery is the only effective treatment. Unless the clinical symptoms are mild and the bleeding volume is small (<10 ml).
(3) In cases where the diagnosis of the cause of bleeding is unclear and suspected to be a vascular malformation or aneurysm, surgical exploration is appropriate for further clarification.
(4) The evaluation of surgical removal of hematoma on the recovery of neurological function is uncertain and theoretically meaningful, but it cannot be fully confirmed in clinical aspects. Therefore, it is important to think about this point when choosing surgery.
(5) Brainstem hemorrhage is usually less likely to be considered for direct surgery and can be treated by stereotactic puncture. If complicated by ventricular hemorrhage, the presence of hydrocephalus can be treated with extraventricular drainage or shunt depending on the situation.
For those who have indications for surgery after the onset, if the hematoma can be removed under direct vision and the bleeding can be completely stopped, the chance of rebleeding after surgery will be greatly reduced, and early surgery should be advocated to break the vicious circle as soon as possible, reduce the morbidity and mortality rate and improve the quality of life of patients.
2.Surgical methods
(1) Craniotomy to remove the hematoma: The traditional practice can be divided into craniotomy with skin and bone flap formation and drilling to enlarge the bone window method. In the case of shell nucleus hemorrhage, for example, a horseshoe-shaped incision is usually made in the frontotemporal or temporal area, and the bone flap is opened. After entering the skull, the dura mater is cut open and the cortical area is cut at the shallowest point of the hematoma from the cortex (superior temporal or middle temporal gyrus), or the lateral fissure is separated to reveal the insula, and a 1 cm incision is made in the insula cortex to enter the hematoma cavity and remove the hematoma. For cerebellar hemorrhage, depending on the site of hemorrhage, a midline or paramedian incision can be made in the suboccipital area, and after drilling and enlarging the bone window, the dura mater can be cross-cut and confirmed by puncture, and then the cerebellum can be incised and the hematoma can be removed. In case of arterial bleeding, bipolar electrocoagulation can be used to deal with the small clots that are too tightly adhered, which are mostly primary bleeding points and can be retained; for the formed hematoma envelope, it is not necessary to deal with it unless it is necessary for diagnosis, so as not to aggravate the injury.
Cortical flap formation for cranial removal of hematoma mostly requires general anesthesia, which is traumatic and increases the burden of patients, and is rarely used now. At present, the minimally invasive small bone window method or “Keyhole” surgery is used, which usually involves a straight incision 1 cm in front of the temporal ear, a layer-by-layer incision to reach the bone surface, and a 3-cm diameter bone window is formed with a milling knife after drilling with a grinding drill to enter the cranium. The advantage is that the hematoma is completely removed and hemostasis is stopped under the operating microscope to achieve immediate decompression, and after the operation, the bone flap is reset and sutured layer by layer. If the preoperative condition is serious, the cerebral edema is obvious, and the cranial pressure does not drop significantly at the end of surgery, the bone window can be enlarged for decompression and the drainage tube can be left in the hematoma cavity if necessary to facilitate the postoperative reaction period. For those with bleeding into the ventricle, preoperative ventriculoperitoneal puncture is feasible to release fluid to reduce cranial pressure. After the intracerebral hematoma is cleared, saline can also be slowly injected through the drainage tube to flush out the blood accumulated in the ventricles through the hematoma cavity and continue drainage for several days after surgery.
Since the minimally invasive small bone window method is less invasive and can quickly remove the hematoma and stop bleeding satisfactorily, it is especially suitable for those who have shell nuclei or bleeding sites that are not deep and whose preoperative condition is graded at grade II or III. In addition, cerebellar hemisphere hemorrhage can also be used in order to achieve rapid decompression.
(2) Aspiration of hematoma by puncture: Before the introduction of CT, it was not effective because accurate judgment could not be made on the site of hematoma and the amount of hemorrhage, and it was not possible to compare the ratio of the aspirated amount to the total amount of hemorrhage before and after puncture. Some people even believed that simple puncture could not stop the bleeding, but could instead increase the chance of rebleeding. With the continuous clinical and experimental research and the improvement of diagnosis and treatment methods, puncture aspiration of hematoma has become increasingly popular and widely used because of its small trauma and easy operation.
①The basis of puncture aspiration of hematoma.
A. The puncture needle or suction tube is accurately placed in the center of the hematoma by using CT guidance or stereotactic technology, which can prevent damage to the surrounding tissues when aspirating the hematoma.
B. Clinical practice proves that even with open surgery, it is not necessary to remove the entire bleeding. Therefore, when the bleeding is not excessive, the first puncture, if it can aspirate 60% to 70% of the total bleeding, the intracranial pressure and cerebral pressure can be relieved to a certain extent, and the remaining part can be resolved in stages to avoid accidents with excessive fluctuations in cranial pressure and too rapid midline repositioning.
C. Several hours after bleeding, the liquid bleeding only accounts for 1/5 of the hematoma volume, and the rest have formed jelly-like blood clots, which are not easily solved by simple extraction. For this reason, CUSA, Archimedes drill, rotary stranded wire, etc. can be used to break up the hematoma and then aspirate it.
D. Intraoperative aspiration pressure can be mastered according to the nature of the hematoma, and some experiments have been calculated using the negative pressure range (<31, 7kPa or 0, 2atm) to ensure safety.
E. Calculate the total amount of aspiration, and inject fibrinolytic agents, such as urokinase and recombinant streptokinase, into the residual hematoma, and clamp the drainage tube for 4h for dissolution to facilitate drainage and discharge.
F. Postoperative CT can be used to review whether there is rebleeding and take corresponding measures in time.
②Puncture aspiration to remove the hematoma Method.
A. According to CT positioning, the puncture point is determined by using the stereotactic principle with the center of the hematoma as the target point. The puncture point should be chosen at the point where the hematoma is closest to the scalp, without large blood vessels or important functional areas. The puncture point for cerebral bridge hemorrhage is mostly chosen 1 cm below the transverse sinus and 4 cm next to the midline, and the puncture direction is 60° to the sagittal plane.
B. Cranial drilling: conventional scalp incision, mastoid pull hook retraction, drilling with cranial drill; or drilling with a special fine head electric drill after making a small incision in the scalp.
C. After successful hematoma puncture, direct aspiration of the hematoma, fragmentation and aspiration of the hematoma, and lysis and drainage of the hematoma cavity with fibrinolytic solution are performed according to the preoperative plan. If the brain parenchymal hemorrhage is less than 40 ml, it can be removed at one time; if the hemorrhage is large and the midline shift is serious, it is appropriate to aspirate it in several times. In cases where the hematoma has broken into the ventricle, the bleeding in the brain parenchyma can be aspirated first, and then one or both sides of the ventricle can be drained according to the extent of bleeding, with the application of fibrinolytic agents and/or regular flushing.
The puncture aspiration method is suitable for hemorrhage in all parts, especially deep hemorrhage, such as thalamic hemorrhage, parenchymal hemorrhage with ventricular hemorrhage, and slow progressing brainstem hemorrhage. Since this method cannot stop bleeding, it should be performed only when there is no active bleeding. It has been suggested that 3 days after bleeding is appropriate, especially when combined with the application of fibrinolytic agents, to reduce the chance of rebleeding. However, there are different views in the literature. In a group of 505 cases of cerebral hemorrhage treated by puncture, 84% (424 cases) of the hematomas were aspirated 1 to 3 days after hemorrhage, of which 14,3% (72 cases) were from 1 to 7 h, 39,2% (198 cases) were from 8 to 24 h, and 30,5% (154 cases) were from 25 to 72 h. Only 2 cases of rebleeding were found in the whole group. In another group of 1041 cases, the rebleeding rate after puncture was 3.2%, pointing out that rebleeding was related to early, especially ultra-early surgery, excessive suction, and high intraoperative blood pressure (>27kPa), and suggesting that a hematoma clearance rate of 65% to 75% is safe. If intraoperative bleeding is encountered, 10,000 U of bactrim (lithotripsin) can be injected into the hematoma cavity and kept for several minutes, and bleeding can mostly be stopped. In order to reduce postoperative rebleeding, a balloon has been left in the hematoma cavity and used to stop bleeding by compression. It is worth suggesting that since this method cannot be used to draw out the bleeding at one time, prompt measures should be taken in patients with heavy bleeding when the puncture effect is not significant. In addition, it is recommended to be used with caution in patients with cerebellar hemorrhage, especially when the amount of bleeding is high. In summary, puncture aspiration of hematoma has its unique advantages, but some people have reservations because the toxic hematoma cannot be emptied at once and continues to damage the surrounding tissues, so experience should be accumulated continuously to improve the deficiencies.
(3) Neuroendoscopic removal of hematoma: Although the history of endoscopic application is long, the high technological content of neuroexternal
Prognosis
The prognosis of hypertensive cerebral hemorrhage is poor, with an overall mortality rate of more than 50%. Death is most common within 2 days of onset. The rate of death at first onset increases with age, and is about 40% in the 40-60 year old group, 50% in the 60-70 year old group, and 80% in those over 71 years of age. The primary cause of death within 2 to 3 days of onset is brain herniation due to high cranial pressure, followed by brainstem compression and secondary hemorrhage; death after 5 to 7 days of onset is mostly due to complications such as pulmonary infection. Most patients who survive often have permanent sequelae, such as hemiparesis and incomplete aphasia.
Prevention
Hypertension is the cause and main risk factor of cerebral hemorrhage. On the basis of persistent hypertension, excessive exertion, agitation and other triggers can cause a sudden rise in blood pressure and lead to cerebrovascular rupture and bleeding. Therefore, the prevention of cerebral hemorrhage requires the removal or control of these factors that cause a sudden rise in blood pressure. For patients with persistent hypertension, antihypertensive drugs such as captopril and nifedipine should be used; it is appropriate to control blood pressure below 120/90 mmHg without increasing blood lipids, blood glucose and blood viscosity, and without affecting cardiac and renal functions. For patients with initial hypertension, sedative and diuretic drugs can be used, low salt diet observation; if ineffective available nifedipine or captopril and other drugs to lower blood pressure. Intensive education on prevention and treatment of hypertension and stroke should be provided to people over 35 years of age and people with a family history of hypertension to improve their self-care ability and to implement interventions such as regular follow-up examinations and supervision of treatment for hypertensive patients. The seven-city Chinese cerebrovascular disease risk factor intervention trial demonstrated that the use of hypertension interventions not only intervened in the blood pressure levels of the population, but also reduced the incidence of hypertension and stroke. To prevent intracerebral hemorrhage, in addition to active treatment of hypertension, one should lead a regular life, combine work and rest, have a calm mind, and stop smoking and limit alcohol to prevent triggering hypertensive cerebral hemorrhage.