Hypertensive cerebral hemorrhage (commonly known as cerebral hemorrhage, also known as stroke) is a primary non-traumatic hemorrhage in the brain parenchyma, which belongs to cerebrovascular disease and is a disease with high morbidity, disability and mortality rates. With the progress of society, urbanization and the accelerated pace of life, there is a trend of increasing year by year. According to statistics, the incidence rate of hypertensive cerebral hemorrhage in China is 110/100,000, and the mortality rate varies with the different sites of hemorrhage (about 50%), and the disability rate is almost 90% or more, which seriously affects the health of the people. However, there are still so many people who have certain blind spots and misunderstandings about its clinical treatment. Long-term hypertension is the most common cause of hypertensive cerebral hemorrhage, especially when hypertension and atherosclerosis coexist. Studies have found that long-term hypertension and atherosclerosis can cause hypoxia in the walls of small arteries or deep penetrating branches in the brain, resulting in fibrinoid necrosis or lipid hyaline degeneration and the formation of microaneurysms, which tend to occur in the basal ganglia area because of their thin vessel walls, which is also an important cause of hemorrhage. Hypertensive cerebral hemorrhage mostly occurs in patients over 50 years old with hypertension, especially more common in the age group of 60 to 70 years old. However, in recent years, there is an increasing trend of younger patients under 50 years of age, and the difference between genders is not significant; the hemorrhage can occur throughout the year, but it occurs more often during cold winter or sudden changes in temperature, when blood pressure is easy to rise and fluctuate; the onset of the hemorrhage is usually triggered by emotional excitement, nervousness, strenuous activity, violent coughing or straining to defecate, etc., which causes the blood pressure to rise. The onset of hemorrhage is often sudden, and most of them have no prodromal symptoms before hemorrhage. The severity of clinical manifestations after hemorrhage is greatly related to the site of hemorrhage, the amount of hemorrhage, the speed of hemorrhage and compensatory ability. A few patients may have headache, dizziness, transient confusion, drowsiness, psychiatric symptoms, transient limb movement, abnormal sensation or slurred speech and other cerebral symptoms a few hours or days before the hemorrhage, which are not the unique prodromal symptoms of cerebral hemorrhage. Most patients have a rapid onset, often developing to a peak within minutes or hours, or falling into a coma within minutes, and generally have the following different manifestations during the course of the disease: 1. Headache: It is often the first symptom, manifested as a sudden and severe headache, first located in the temporal region of the affected side, and then throughout the head or the posterior occipital region, caused by blood stimulation of pain-sensitive structures in the skull and increased intracranial pressure; a small number of supratentorial cerebral hemorrhage and some elderly patients have only mild headache or no headache. Patients have only mild headache or no headache. 2.Dizziness: It can be accompanied by headache or be the main manifestation, mostly occurring in the posterior cranial recess when there is subcurtain hemorrhage. Nausea and vomiting: It is one of the early symptoms and is more obvious when the headache is severe, but in the case of subcranial hematoma, the headache is not severe and vomiting can still be very frequent; if vomiting coffee-colored material, it indicates damage to the subthalamic area. 4.Disorders of consciousness: the lighter ones are confused and drowsy, the heavier ones are comatose and de-cerebral tonic, a very small amount of hemorrhage can be without obvious disorders of consciousness. 5. Increased blood pressure: The majority of cases are between 22.7-33.3/13.3-20 Kpa (170-250/100-150
mmHg), which is due to pre-existing hypertension or compensatory increase in blood pressure due to increased intracranial pressure. 6. Pupillary changes: Generally, when the hemispheric hemorrhage is not large, the pupil size is normal and the light response is good, sometimes the pupil on the sick side is smaller than the opposite side. If brain herniation occurs and the arteriolar nerve is compressed, the ipsilateral pupil becomes dilated, the light response is blunted or disappears, the margins are not aligned, and if the condition continues to worsen, the contralateral pupil also becomes dilated. If the brainstem and bridge hemorrhage or ventricular hemorrhage enters the subarachnoid space, the pupil is often pinpoint narrowed. 7. Other: fundus examination shows arteriosclerosis, retinal hemorrhage and optic papillary edema; meningeal irritation sign due to hemorrhage into the subarachnoid space; hemorrhage occupancy and destruction of brain tissue leading to hemiplegia, aphasia and change of eye position. In conclusion, a more typical intracerebral hemorrhage first presents with headache, nausea, vomiting, and after a few minutes to hours, signs of impaired consciousness and focal neurological deficits, flushing, incontinence, elevated blood pressure, and even convulsions, deepening coma, and snoring whistling. Cranial CT scan provides an accurate and reliable tool for the diagnosis and differential diagnosis of cerebral hemorrhage, and the diagnosis of cerebral hemorrhage can be almost 100%. It not only provides a reliable basis for the qualitative, localization and quantitative diagnosis of cerebral hemorrhage, but also can visually reflect the morphology of the hematoma, the direction of expansion, the degree of penetration into the ventricles and its resulting cerebral edema, and the displacement of brain structures. Therefore, CT examination is not only an effective diagnostic method, but also an important basis for formulating treatment plans, observing the efficacy and judging the prognosis. For patients suspected of having cerebral hemorrhage, CT scan examination should be preferred and should be performed early and, if necessary, several times to observe the dynamic changes of the hematoma. First aid in case of cerebral hemorrhage: 1. Keep quiet, avoid unnecessary moving, especially avoid head shaking. 2, absolute bed rest, the head of the bed can be raised 30 ° angle, in order to facilitate intracranial venous reflux, thereby reducing cerebral edema. 3, to ensure a clear airway, the patient’s head to the side, so as to avoid secretions, vomit inhalation of the airway or posterior tongue drop and cause asphyxia. Once there is secretion or vomit in the mouth, it should be removed immediately. 4.Keep intravenous access open, oxygen, and cardiac monitoring. 5. It is best to quickly transport to a hospital with CT examination equipment and a neurosurgery department. The traditional treatment for hypertensive cerebral hemorrhage is internal conservative therapy, but with the progressive development of science, people’s innovation in surgical techniques and the development of equipment technology, surgical treatment has been commonly used, but the two treatments are still controversial, so now when the doctor takes the treatment plan still have to consult the patient’s family. Minimally invasive surgery for hypertensive cerebral hemorrhage is of course the more popular treatment method nowadays. It has the advantages of less trauma, lower cost and better surgical effect, which can significantly reduce the disability and death rate of patients after surgery; surgical treatment can quickly remove the hematoma, relieve the pressure on the brain tissue, lower the intracranial pressure, improve the brain crest fluid circulation and reduce the damage to the brain tissue. However, the technical requirements for surgeons are also high, and they must be skilled in microsurgical operations and cranial microanatomy. The timing of surgery for hypertensive cerebral hemorrhage is divided into ultra-early (within 6 hours of hemorrhage), early (1 to 2 days after hemorrhage) and postponed (3 days after hemorrhage) surgery. In recent years, the number of scholars advocating early or ultra-early (within 6 hours after bleeding) surgery has been increasing. This reduces the pressure of the hematoma on the brain tissue and breaks the malignant pathophysiological cycle, which is conducive to improving the therapeutic effect and the patient’s postoperative survival quality, thus improving the prognosis. The traditional surgical method is large bone flap decompression hematoma removal, which is relatively more traumatic, with long operation time, more bleeding, heavier postoperative patient reaction, heavier edema reaction after brain tissue injury, and longer postoperative recovery period. Minimally invasive small bone window craniotomy hematoma removal is less traumatic, easy to operate, short cranial entry time, light brain injury, more complete hematoma removal, reliable hemostasis, and can quickly relieve the pressure on brain tissue. It has gradually appeared to replace the traditional large bone flap decompression hematoma removal trend. Of course, surgery is not a panacea. Patients in deep coma, near-death state, whistling arrest, and bilateral pupil dilatation should be considered for deferring surgery if they have one of these conditions. The principle of individualization also applies to cerebral hemorrhage, and each patient should be analyzed specifically and considered comprehensively to make scientific decisions. The Department of Neurosurgery of Tongji Hospital of Tongji University was early to carry out minimally invasive surgery for hypertensive cerebral hemorrhage in China, and after continuous exploration, a set of safe and reliable techniques for minimally invasive treatment of hypertensive cerebral hemorrhage has been formed, with good surgical results and significantly lower postoperative lethality and disability rates.