I. Definition of hypertensive cerebral hemorrhage.
Hypertensive cerebral hemorrhage is one of the most serious complications of hypertensive disease, often occurring between the ages of 50 and 70, slightly more in men, and more likely to occur in winter and spring. Hypertensive disease often leads to pathological changes in the small arteries at the base of the brain, highlighted by glassy or fibrous degeneration and focal hemorrhage, ischemia and necrosis in the walls of these small arteries, weakening the strength of the vessel walls, appearing as limited dilatation, and tiny aneurysms can be formed. The rupture and bleeding of an already diseased cerebral vessel is caused by a violent increase in blood pressure due to emotional excitement, excessive mental and physical labor, or other factors. Among them, rupture of the doublestripe artery is the most common, and the others are thalamic penetrating artery, thalamic geniculate artery and posterior internal choroid plexus artery, in that order.
II. Etiology.
Increased blood pressure is the underlying cause and usually develops during activity and emotional stress.
The vast majority of scholars believe that long-term hypertension can cause vitreous degeneration of cerebral arteries, which first causes swelling of the subendothelial matrix, lipid deposits under the endothelium, formation of structureless material between the endothelium and the internal elastic layer, reduced elasticity and increased brittleness. The loss of vessel wall tension and fibrinoid necrosis produce local arterial fusiform or spherical projections under blood pressure shock, i.e., cornual aneurysms, and blood may also invade the vessel wall and form a coarctation aneurysm. When the blood pressure rises suddenly, the aneurysm ruptures and causes bleeding.
Clinical manifestations: Hypertensive cerebral hemorrhage often develops during activity, excitement, and forceful defecation, etc. The onset of the disease is rapid, and it often develops to a peak within minutes or hours. Clinical manifestations vary depending on the site of bleeding, the amount of bleeding, and the general condition. The onset is usually a sudden onset of severe headache, nausea, vomiting, and is often accompanied by restlessness, drowsiness or coma. When the hematoma expands and the cerebral edema increases, the intracranial pressure increases, causing brain herniation crisis such as dilated pupils on the side of the hematoma, respiratory impairment, slowed pulse rate and increased blood pressure. Subsequently, it turns into central failure.
Treatment: Active and reasonable treatment can save the patient’s life, reduce the degree of neurological disability and lower the recurrence rate.
1.Medical treatment
Keep the patient in bed and quiet. In severe cases, closely observe body temperature, pulse, respiration, blood pressure and other vital signs, and pay attention to pupil and consciousness changes. Keep the respiratory tract unobstructed, clear the respiratory secretions in time, administer oxygen if necessary, and maintain the arterial oxygen protection above 90%. Enhance care and maintain the functional position of the limbs. Fasting for 24-48 hours is recommended for those with impaired consciousness and gastrointestinal bleeding, after which a gastric tube should be placed.
(1) Control hypertension For hypertensive cerebral hemorrhage, appropriate antihypertensive drugs should be applied promptly to control the excessive blood pressure. However, the blood pressure should not be lowered too fast or too low. Elevated blood pressure in acute cerebral hemorrhage is a cerebrovascular auto-regulatory mechanism to maintain normal cerebral blood flow under the condition of increased intracranial pressure, and lowering blood pressure can affect cerebral blood flow and lead to hypoperfusion or cerebral infarction, but continuous high blood pressure can worsen cerebral edema. It is reasonable to lower diastolic blood pressure to a level of about 100 mmHg, and individuals are unusually sensitive to antihypertensive drugs. Blood pressure can be controlled with drugs routinely after the acute phase.
(2) Control cerebral edema and lower intracranial pressure The edema peaks 48 hours after cerebral hemorrhage and gradually subsides after maintaining for 3 to 5 days or longer. Cerebral edema can increase intracranial pressure and lead to brain herniation, which is the main cause of death in cerebral hemorrhage. Therefore, reducing the intracranial pressure is an important part of the acute treatment of cerebral hemorrhage. Commonly used 20% mannitol, 50% glycerol saline and diuretics such as tachyphylaxis; or 10% plasma albumin. The application of mannitol has a rapid dehydrating effect, but the renal function should be monitored to prevent renal impairment.
(3) Hemostatic and coagulant drugs It is generally believed that intracerebral arterial hemorrhage is difficult to be stopped by drugs, and rebleeding at the site of hemorrhage is not common, so antifibrinolytic drugs are usually unnecessary. Antifibrinolytic drugs such as 6-aminocaproic acid and haemostatic cyclic acid can be given early (<3< span="">hours) if they are needed. Lidostat is also recommended. Coagulation assessment after cerebral hemorrhage is necessary to monitor hemostatic therapy.
(4) Maintain nutrition and water-electrolyte balance Daily fluid intake is calculated as urine volume + 500 ml. Patients with high fever, excessive sweating, vomiting or diarrhea also need to increase the amount of fluid intake appropriately. Pay attention to prevent hyponatremia, which may aggravate cerebral edema.
(5) Complication control
①Infection
(i) Elderly patients with combined impaired consciousness are prone to complications of pulmonary infection, and urinary retention or catheterization are prone to combined urinary tract infections, which can be treated with antibiotics selected based on experience, sputum and urine cultures, and drug sensitivity tests.
②Stress ulcer
can cause gastrointestinal bleeding, can be prevented by H2 receptor blockers, such as methocarbamol intravenous, ranitidine oral, loxacillin; if upper gastrointestinal bleeding occurs, norepinephrine with ice saline oral, Yunnan Baiyao oral, conservative treatment is ineffective in the gastroscopy under direct vision to stop bleeding.
(iii) Dilutional hyponatremia
It can occur in 10% of patients with cerebral hemorrhage and should be corrected slowly so as not to lead to central pontine myelinolysis; ④ Deep vein thrombosis of the lower limbs Progressive edema and stiffness of the affected limbs are common, which can be prevented by regular turning, passive activity or elevation of paralyzed limbs.
2.Surgical treatment
The prognosis is directly related to the preoperative level of consciousness, and the surgical effect is usually poor in comatose patients.
(1) Indications for surgery
(1) Patients with cerebral hemorrhage have increased intracranial pressure with signs of brainstem compression, such as slow pulse, elevated blood pressure, slowed respiratory rhythm, and decreased level of consciousness.
② cerebellar hemisphere hematoma volume ≥ 10 ml or earth > 6 ml, hematoma broken into the fourth ventricle or brain pool pressure disappears, and brainstem pressure symptoms or signs of acute obstructive hydrocephalus appear.
(iii) Severe ventricular hemorrhage leading to obstructive hydrocephalus.
(4) Lobar hemorrhage, especially due to cerebral arteriovenous malformation and obvious occupational effect.
(2) Contraindications to surgery
Brain stem hemorrhage, deep cerebral hemorrhage and amyloid angiopathy leading to lobar hemorrhage should not be treated surgically. Most cases of deep cerebral hemorrhage may break into the ventricles and decompress spontaneously, and surgery may cause destruction of normal brain tissue.
(3) Commonly used surgical methods are
(1) Cerebellar decompression
is the most important surgical treatment for hypertensive cerebellar hemorrhage, which can save lives and reverse neurological deficits, and is effective when the patient is awake in the early stage of the disease.
②Craniotomy for hematoma removal
surgical treatment may be effective in cases of displacement of midline structures and initial brain herniation caused by occupancy effects.
(iii) borehole enlargement for bone passing hematoma removal.
④drilling for minimally invasive intracranial hematoma removal
⑤ ventricular drainage for ventricular hemorrhage.
3. Rehabilitation treatment
It is advisable to carry out rehabilitation treatment as early as possible after the condition of brain hemorrhage patients is stabilized, which is beneficial to the recovery of neurological function and improvement of quality of life. If the patient appears depressed, drug (such as cloxetine) treatment and psychological support can be given in time.
4.Diet and contraindications
Patients in the recovery period are weak and should pay attention to diet.
(1) The diet should be light, easy to digest and high in vitamins.
(2) Eat more cabbage, radish and other coarse fiber foods to keep the bowels open.
(3) Avoid fatty and sweet foods, quit smoking and alcohol.