Cerebral hemorrhage, also known as cerebral hemorrhage, refers to bleeding within the brain parenchyma and is directly related to hypertension, which is a common acute cerebrovascular disease in middle-aged and elderly people, with high rates of death and disability. Cerebral hemorrhage accounts for 10% to 20% of all stroke patients. The close relationship between cerebral hemorrhage and hypertension lies in the fact that about 1/3 of hypertensive patients have a chance of having a cerebral hemorrhage, and about 95% of patients with cerebral hemorrhage have hypertension.
There are many theories about the mechanism of cerebral hemorrhage formed by hypertension, and the more recognized one is the microaneurysm theory. As a result of long-term hypertension, resulting in cerebral artery lining damage and atherosclerosis, the penetrating arteries in the brain can form microaneurysms. This aneurysm is a sac that forms in a weak part of the blood vessel wall, and when blood pressure suddenly rises, this sac ruptures causing cerebral hemorrhage.
Causes of cerebral hemorrhage include malformations of the cerebral blood vessels (the main cause of cerebral hemorrhage in young people), traumatic brain injuries, brain tumors, and blood disorders, in addition to high blood pressure.
(I) Factors predisposing to cerebral hemorrhage:
(1) hypertension, with elevated systolic blood pressure being particularly important;
(2) short temper or emotional tension, commonly seen after anger and quarrels with others;
(3) smoking, alcoholism, too much salt, and excess weight;
(4) over-fatigue, over-exertion of physical and mental labor, defecation exertion, exercise.
(2) The parts of the brain prone to hemorrhage:
(1) basal ganglia of the brain, accounting for 70%, including the external capsule and the thalamus;
(2) pontine hemorrhage, accounting for 10%;
(3) lobar hemorrhage, accounting for 10%, frontal, temporal, occipital lobe can occur, with parieto-temporal more frequent;
(4) cerebellar hemorrhage;
(5) ventricular hemorrhage, a brain hemorrhage close to a ventricle that breaks into the ventricle is called a secondary ventricular hemorrhage.
After brain CT was applied to the clinic, cerebral hemorrhage was meticulously diagnosed and staged, and was divided for the purpose of selecting indications for surgery and estimating prognosis.
(C) Clinical manifestations of cerebral hemorrhage:
Cerebral hemorrhage is usually easy to develop during physical and cerebral stressful activities or emotional excitement. The onset of the disease is rapid, rapid development, tens of minutes to hours to reach the peak. It is common to see patients with cerebral hemorrhage collapsing on the side of the road, in the toilet, on the ground next to the bed, unconscious, snoring loudly, vomiting stomach contents, sometimes coffee-colored, incontinence, hemiplegia. Patients with smaller amounts of cerebral hemorrhage describe more severe headaches. There is hemorrhage in the fundus of the eye and the vision is not clear. There is a high density hemorrhagic shadow on CT examination.
The degree of cerebral hemorrhage has a great deal to do with the site of bleeding and the amount of bleeding. From the onset of the disease, there is confusion, gradually aggravated, indicating that the bleeding site is bad and the amount of bleeding is large.
The following is a description of the manifestations of cerebral hemorrhage in common sites.
1?The shell nucleus? Hemorrhage in the internal capsule There is typical distortion of the mouth and eyes, hemiparesis, hemisensory loss, hemianopsia, aphasia.
2?Temporal lobe hemorrhage The headache is more severe on the bleeding side, and the neck is toned. Hemiparesis, aphasia may also occur.
3?Ventricular hemorrhage If the hemorrhage is large, it can cause rapid coma, high muscle tone of the limbs, high fever (over 40℃), excessive sweating, gastrointestinal bleeding (vomiting coffee-colored substances, tarry stools), and high mortality.
4?Pontine hemorrhage Deep coma at the beginning. The pontine brain is the center of life, and bleeding of less than 5 milliliters causes serious consequences. Pupils are extremely narrowed, such as "pinpoint", high fever of more than 40 ℃, respiratory failure, followed by respiratory arrest, mostly within 24 hours of death.
5?Cerebellar hemorrhage with acute dizziness, severe headache, with frequent vomiting as the first symptom, early consciousness, soon into a coma. Cerebellar hemorrhage does not appear hemiplegia.
In the past, the diagnosis of cerebral hemorrhage relied on lumbar puncture to obtain cerebrospinal fluid, but now it is rarely done except in remote areas and grassroots hospitals. Currently, the most commonly used is CT scanning of the brain, which can accurately display hematomas larger than 1.5 centimeters in diameter. The location of the hemorrhage, the size of the hematoma, whether it breaks into the ventricle, whether there is cerebral edema and brain hernia formation, can be determined, and almost nothing is missed.
(4) First aid principles of cerebral hemorrhage:
(1) Quiet bed, minimize moving. Call the ambulance doctor out, to be more stable condition, immediately sent to the hospital emergency.
(2) The first 5 minutes of cerebral hemorrhage is crucial for life. As the patient's tongue falls back, it is easy to block the airway and cause asphyxia. Before the arrival of the ambulance, take measures to ensure that the respiratory tract is open: loosen the collar, remove the denture, lateral position, head tilted back to facilitate the flow of oral secretions, and timely removal of oral vomitus, once asphyxia, as soon as possible, pull out the mouth, artificial respiration.
(3) adjust the blood pressure, the higher blood pressure of cerebral hemorrhage, the available small amount of lipiodol treatment or magnesium sulfate 10 ml deep intramuscular injection; clear mind to give oral cardiac pain in the.
(4) If the patient collapsed in the toilet, bath and other small places, we should try to move to a spacious place as soon as possible. Specific practices according to local conditions, the principle is to try not to vibrate the head, keep the head horizontal position handling, so as not to block the airway.
(5) with hemostatic drugs, commonly used hemostatic minerals, anti-fibrinolytic aromatic acid, vitamin K. The dosage of hemostatic drugs should not be too large, the type should not be more.
(6) Prevention and treatment of lung infections and bedsores. Especially in patients with brain hemorrhage coma, early antibiotics to prevent lung infections, turn over regularly to prevent bedsores, and move the limbs to prevent joint stiffness.
(7) Surgical treatment, can do hematoma puncture aspiration or craniotomy to remove hematoma. The aim is to increase the survival rate and reduce the rate of disability.
The acute stage of cerebral hemorrhage often has cerebral edema, increased intracranial pressure, and even leads to the formation of cerebral hernia, therefore, dehydrating agents should be applied in time to reduce intracranial pressure and control cerebral edema.
The principles of application of dehydrating agents are:
(1) Decide the dosage and usage of dehydrating agents according to the patient's clinical symptoms and actual needs. And closely observe the dynamic changes of intracranial pressure, adjust the treatment program, so as to achieve effective control and rational use of drugs.
(2) For those who have consciousness disorder, suggesting that the scope of the lesion is large and the midline structure has been affected, 20% mannitol 250 ml can be given intravenously, once every 6 hours, and observe the dynamic changes of the condition and consciousness disorder, and pay attention to whether the symptom is relieved after using the medicine, so as to adjust the dosage and the interval between the medication.
(3) If the patient's coma deepens, tendon reflexes and muscle tone gradually decreases, and contralateral pyramidal sign or de-cerebralized tonic-like reaction occurs, it is a sign that the lesion is enlarged or the midline structure is shifted and aggravated. In addition to 20% mannitol 250 ml intravenous drip should be given for active dehydration therapy, and should be added dexamethasone 10-20 mg intravenous drip, 1 to 2 times a day, the above two drugs can be applied at the same time or alternately.
(4) If the clinical symptoms are mild, the patient is clear, there is no severe headache or vomiting, and the funduscopic examination does not show any optic papillary edema, the dehydrating agent may not be used for the time being. On the contrary, if there is severe headache or vomiting, try to give 50% dextrose 60 ml intravenous injection, and closely observe the effect of medication. If symptoms improve, say there is clearly increased intracranial pressure. If headache, vomiting and other symptoms are not reduced, may be due to subarachnoid hemorrhage stimulation, it is appropriate to use analgesic or sedative. For such patients, generally advocate the temporary use of mannitol, so as not to interfere with the stability of intracranial hypertension.
(5) Dehydration agents are generally applied for 5 to 7 days. However, if the combination of pulmonary infection or frequent seizures, often due to infection, toxicity, hypoxia and other factors, which aggravate cerebral edema, the application of dehydrating agents can be appropriately prolonged.
(6) In the process of applying dehydrating agent, it is necessary to pay attention to whether the purpose of dehydration has been achieved, but also to prevent the adverse reactions caused by excessive dehydration, such as blood volume insufficiency, hypotension, electrolyte disorders and renal function damage.
Gastrointestinal bleeding caused by cerebral hemorrhage complicating stress ulcers is one of the most common serious complications of cerebral hemorrhage. It is reported to account for about 19% of patients with cerebral hemorrhage, with a high mortality rate, and often life-threatening if not rescued in time. Its pathogenesis is currently believed to be related to subthalamic injury. Some scholars point out that, due to the subthalamic injurious stimulation, the sympathetic vasoconstrictor fibers become paralyzed, vasodilatation, blood flow is slow and stagnant, resulting in gastrointestinal mucosal erosion, necrosis and bleeding or perforation. However, some scholars believe that, due to the thalamus injury, make the vagus nerve excitation, tension, gastrointestinal hyperfunction and spasmodic contraction, which leads to local ischemia, embolism, and cause ulcers and hemorrhage.
References:
What is a brain hemorrhage?
The term cerebral hemorrhage refers to the rupture and bleeding of blood vessels in the brain parenchyma. Its common cause is high due pressure. Some data show that more than 80% of patients with cerebral hemorrhage have a history of high blood pressure, so, in the past, it was often called hypertensive cerebral hemorrhage.
Cerebral hemorrhage can occur in any part of the brain parenchyma and can be single or multiple. However, most hypertensive cerebral atherosclerotic cerebral hemorrhages tend to be single. The preferred site is the internal capsule, so it is called internal capsule hemorrhage, and the hemorrhage occurs mostly in the bean stripe artery, so some people call the bean stripe artery "hemorrhagic artery", followed by the basal ganglia, and the hemorrhage in the external capsule, pontine, lobe, and cerebellum is relatively rare.
The onset of cerebral hemorrhage is often sudden, and the condition progresses rapidly, deteriorating within minutes or hours in severe cases, with the patient experiencing impaired consciousness, hemiparesis, vomiting, and incontinence, as well as headache and elevated blood pressure.
The clinical manifestations of cerebral hemorrhage are roughly divided into two kinds: (1) whole brain symptoms, mostly caused by cerebral hemorrhage, edema and increased intracranial pressure. The manifestations are headache, vomiting , drowsiness, coma and so on. (2) Focal symptoms, localized symptoms caused by blood breaking into the brain parenchyma, such as central hemiparesis, facial paralysis, aphasia and hemiplegia.
The three routine examinations of blood, urine and stool in patients with cerebral hemorrhage after the onset of the disease are not specifically helpful. Electroencephalogram and cerebral hemogram also have no diagnostic value. Lumbar puncture examination of cerebrospinal fluid, brain CT, nuclear magnetic **** vibration examination can help clarify the diagnosis. In particular, brain CT scanning examination can accurately display hematomas larger than 1 5 centimeters or more in diameter, and can determine the location of the bleeding, the size and shape of the hematoma, the presence of ventricular compression, displacement of midline structures, and the presence of cerebral edema or hydrocephalus.
The onset of cerebral hemorrhage occurs between the ages of 40 and 60, and is more common in men than in women. Any factor that can cause a sudden rise in blood pressure can be the direct cause of cerebral hemorrhage, such as strenuous activity, emotional excitement, and straining to defecate. Cerebral hemorrhage can also cause secondary ventricular hemorrhage, cerebral hernia, high fever and other serious consequences, if the above situation, its mortality rate is very high, so the purpose of clinical work in the treatment of cerebral hemorrhage, first of all, is to save the patient's life, and secondly, is to reduce the incapacity rate.
What is cerebral hemorrhage?
The rupture of a blood vessel in the brain parenchyma is called cerebral hemorrhage, or cerebral hemorrhage. It does not include traumatic brain hemorrhage and occurs more often in middle-aged and older people, and more often in men than in women.
The common cause of cerebral hemorrhage is high blood pressure. Some data show that more than 80% of patients with cerebral hemorrhage have a history of high blood pressure. Due to long-term high blood pressure, small arteries in the brain form corn-like size aneurysm expansion, under the action of certain factors, when the blood pressure suddenly rises, it will make the tiny aneurysm rupture and cerebral hemorrhage occurs. Long-term high blood pressure, but also can make the brain small artery endothelium damage, lipid deposition, hyaline-like change, wall brittleness enhancement, more likely to rupture bleeding. In addition, cerebral arteriosclerosis, cerebrovascular malformation is also a common cause of cerebral hemorrhage. All the factors that can make the blood pressure rise suddenly, such as emotional excitement, strenuous activities, drinking too much alcohol, stool force, etc., are the triggering factors of cerebral hemorrhage.
Cerebral hemorrhage can occur in any part of the brain parenchyma, and can be single or multiple. However, most of the hypertensive and cerebral arteriosclerotic cerebral hemorrhage is single. The most common sites are the internal capsule and basal ganglia, followed by the external capsule and frontal lobe. The brainstem and cerebellum are less common.
The onset of cerebral hemorrhage is often sudden, the course of the disease progresses rapidly, and in severe cases, deteriorates within minutes or hours. The patient presents with impaired consciousness, hemiparesis, vomiting and incontinence. There may also be headache and elevated blood pressure.
The clinical manifestations of cerebral hemorrhage are broadly classified into two kinds: (1) Whole-brain symptoms, which are mostly caused by cerebral hemorrhage, edema and increased intracranial pressure. Performance headache, vomiting, drowsiness, coma and so on. (2) Focal symptoms, which are localized symptoms caused by blood breaking into the brain parenchyma, such as central hemiparesis, facial paralysis, aphasia and hemiplegia.
The clinical prognosis is different due to different hemorrhage volume and hemorrhage site. If the hemorrhage is large, the hemorrhage spreads to the ventricle and forms cerebral hernia, or when it is complicated by central hyperpyrexia or stress gastrointestinal hemorrhage, the consequences are serious and the mortality rate is high. Therefore, we should pay great attention to the above situations and actively carry out rescue treatment in order to reduce the death rate and disability rate.
Does cerebral hemorrhage cause headache
Cerebral hemorrhage refers to hemorrhage within the brain parenchyma caused by non-traumatic factors, and it is a disease with extremely high morbidity and mortality. Hypertension and atherosclerosis coexisting at the same time is the most common cause of cerebral hemorrhage, other rare causes are: hemorrhage secondary to cerebral infarction, congenital cerebral vascular malformations forming aneurysms, blood disorders, cerebral arteritis, amyloid angiopathy, tumors, etc., the age of onset is often in the age of 50-70 years old, the onset of the cold season is more, the onset of the onset of the disease is often sudden and without foreboding, and a small number of patients with dizziness, headache and other prodromal symptoms, which may be related to the blood pressure A few patients have precursor symptoms such as dizziness and headache, which may be related to increased blood pressure. Headache is the main manifestation of cerebral hemorrhage patients in the acute stage, often accompanied by dizziness, vomiting, impaired consciousness, limb paralysis, aphasia, incontinence, etc. The nature of headache sometimes helps to determine the nature of cerebral hemorrhage. The nature of headache sometimes helps to determine the location of cerebral hemorrhage, such as posterior occipital headache is mostly a symptom of cerebellar hemorrhage, but most of the time the headache is a non-specific symptom, and the determination of the location of cerebral hemorrhage and the volume of hemorrhage is dependent on other symptoms and other examinations. Current imaging tests such as CT scanning or magnetic **** vibration imaging can correctly determine the presence or absence of bleeding in the patient's brain 2 hours after the onset of the disease. Headache is a manifestation of increased intracranial pressure in patients with cerebral hemorrhage, when the patient's condition is stabilized and the intracranial pressure returns to normal, the patient's headache will disappear. Of course, if the vegetative nervous system dysfunction remains, the patient will still have sequelae such as headache, dizziness, red face, sweat disorder and so on. Cerebral hemorrhage has a high mortality rate and disability rate, so it should be actively prevented. Prevention should start from actively controlling high blood pressure, in addition to regular use of antihypertensive drugs, should establish a reasonable system of life and work, work and rest, to avoid prolonged overstress, smoking cessation, a small amount of alcohol, to avoid heavy physical labor and intense emotional fluctuations.
Why are hypertensive patients prone to cerebral hemorrhage?
Cerebral hemorrhage is the most serious type of acute cerebrovascular disease. It is reported that cerebral hemorrhage patients with a long-term history of hypertension accounted for 89%, with an average of 13 years, and these patients generally have systolic blood pressure between 21.3 and 31.0kPa (160-240mmHg), and diastolic blood pressure between 12.0 and 21.3kPa (90-160mmHg), which is the most serious complication of hypertension in the elderly.
The reasons why hypertensive patients are prone to cerebral hemorrhage: (1) Hypertension promotes atherosclerosis and the formation of microaneurysms. When blood pressure rises, the long-term pressurization of small arteries, so that the arterial lining thickening, vitreous degeneration, fibrosis proliferation, so that the formation of small arteriosclerosis. Such small penetrating arteries within the brain parenchyma often have microaneurysm formation under the action of long-term hypertension. They are mainly distributed in the basal ganglia and pontine brain. The wall of the miniature aneurysm is weak, and when the blood pressure rises suddenly, the aneurysm is prone to rupture and produce cerebral hemorrhage. (2)Due to the role of long-term high blood pressure, so that has been hardened arterial vascular endothelial integrity damage, promote the plasma lipids easy to enter the endothelial membrane through the breach, so that the arterial wall fat vitreous change or cellulose-like necrosis, increasing the brittleness of the vessel wall, when emotional excitement, tiredness, or use force to defecate and other reasons, resulting in a further increase in blood pressure, it is easy to cause rupture of the blood vessels, the occurrence of cerebral hemorrhage.
Cerebral hemorrhage can be caused by a variety of factors, but long-term high blood pressure is the most important factor leading to cerebral hemorrhage, therefore, effective control of high blood pressure is very important to prevent cerebral hemorrhage.
How to distinguish between cerebral hemorrhage and cerebral infarction?
Cerebral hemorrhage and cerebral infarction are different in nature and different in treatment, therefore, early diagnosis is needed. In the absence of conditions for CT or nuclear magnetic **** vibration examination, can be identified according to the following: (1) cerebral hemorrhage patients have hypertension and cerebral atherosclerosis history, while cerebral infarction patients have transient ischemic attack or history of heart disease. (2) Cerebral hemorrhage mostly develops under emotional excitement or exertion, while cerebral infarction mostly develops during quiet rest. (3) The onset of cerebral hemorrhage is acute and rapid, often reaching its peak within a few hours, and there is no aura before the onset of cerebral hemorrhage. On the other hand, cerebral infarction progresses slowly, and is often aggravated gradually after 1 to 2 days, and there is often a history of transient ischemic attack before the onset of the disease. (4) After the onset of cerebral hemorrhage, patients often have symptoms of increased intracranial pressure such as headache, vomiting, neck stiffness, etc., and high blood pressure, and heavy consciousness disorder. At the onset of cerebral infarction, the blood pressure is more normal, and there are no symptoms such as headache, vomiting and so on, and the consciousness is clear. (5) Cerebral hemorrhage patient lumbar puncture cerebrospinal fluid pressure is high, mostly bloody, while cerebral infarction patient cerebrospinal fluid pressure is not high, clear and bloodless. (6) Central respiratory disorder is common in patients with cerebral hemorrhage, and the pupils are often asymmetric, or both pupils are narrowed, and the eyeballs are in the same direction of hemianopsia and floaters. Cerebral infarction patients with central respiratory disorders are rare, the pupils are symmetrical on both sides, and the eyeballs are rarely polarized and floating.
Of course, individual patients with mild cerebral hemorrhage have mild clinical symptoms similar to those of cerebral infarction, and it is difficult to distinguish the two. And large cerebral infarction patients, the appearance of increased intracranial pressure, consciousness disorder, also resembles cerebral hemorrhage, clinical distinction is not good. CT scan should be done as early as possible. Cerebral hemorrhage CT manifestation of high-density shadow, while cerebral infarction manifested as low-density shadow, the two are very different.
What is the difference between cerebral hemorrhage and subarachnoid hemorrhage?
Cerebral hemorrhage: common in middle-aged and elderly people
Causes: hypertension, cerebral atherosclerosis, craniocerebral trauma
CT: mass hyperdense shadow surrounded by edema
Cerebral angiography: vascular compression can be seen to be shifted, and the small blood vessels can be seen to be destroyed by hemorrhage or compression of the non-visible
Mortality rate: high
Subarachnoid hemorrhage: young and middle-aged people are often affected by cerebral hemorrhage, but the difference between the two is not obvious. Hemorrhage: common in young adults
Aetiology: congenital aneurysm, arteriovenous malformation, hematologic disease
CT manifestations: usually no mass hyperintensity
Cerebral angiography: cerebral angiography can be seen aneurysm, arteriovenous malformation, etc.
Mortality rate: rebleed mortality rate is high
Why is hypertension prone to cerebral hemorrhage?
The incidence of cerebral hemorrhage in hypertensive patients is still lacking in domestic statistics. However, there is information that 70% of cerebrovascular patients have a history of hypertension. And the vast majority of cerebral hemorrhage is caused by hypertension. This indicates that hypertension has a very close relationship with cerebrovascular disease, and it is the primary risk factor for cerebral hemorrhage. Therefore, the cerebral hemorrhage is called hypertensive cerebral hemorrhage.
So, why is hypertension prone to cerebral hemorrhage?
(1) Hypertension promotes cerebral arteriosclerosis and the formation of tiny aneurysms.
When blood pressure rises, the long-term pressurization of small arteries, so that the arterial intima-media thickening, vitreous degeneration, fibrosis and hyperplasia to the formation of small arteriosclerosis. This small penetrating arteries within the brain parenchyma often have tiny aneurysm formation under the effect of long-term hypertension, mainly distributed in the basal ganglia and pontine brain. The walls of the tiny aneurysms are weak, and when blood pressure rises suddenly, the aneurysm ruptures and produces a cerebral hemorrhage.
(2) Due to the role of long-term hypertension, the integrity of the endothelium of the arterial vessels that have been hardened is destroyed, promoting the lipids in the plasma to easily enter the endothelium through the rupture, so that the arterial wall undergoes lipoglass-like or fibrinoid-like necrosis, which increases the brittleness of the vascular wall. When emotional excitement, exertion or straining to defecate and other reasons, resulting in a further increase in blood pressure, it is easy to trigger cerebral hemorrhage.
Cerebral hemorrhage can be caused by a variety of factors, but long-term high blood pressure is the most important factor leading to cerebral hemorrhage, therefore, effective control of high blood pressure is very important to prevent cerebral hemorrhage.
How is cerebral hemorrhage diagnosed?
Cerebral hemorrhage is one of the more common and serious diseases of acute cerebrovascular disease. It has a higher mortality and disability rate than other acute cerebrovascular diseases. Therefore, in diagnosis, it is necessary to ask a detailed medical history, comprehensive physical examination, meticulous and thoughtful analysis, and strive to make a clear diagnosis as early as possible, and actively and effectively carry out treatment.
First of all, it is necessary to grasp the general features of acute cerebrovascular disease that cerebral hemorrhage has. Secondly, it is also necessary to grasp the characteristics of cerebral hemorrhage itself. Acute cerebrovascular disease general characteristics, acute onset, rapid progression of the disease, often within minutes, hours or days to reach the peak. At the same time, there are clear localization signs. Focal localization signs due to brain function damage often appear within a short period of time after the onset of the disease. Thirdly, there is significant acute cerebral circulatory impairment. Diffuse, brain-wide symptoms such as impaired consciousness, intracranial hypertension, and impaired visceral function occur dramatically after the onset of the disease.
Based on these general features, acute cerebrovascular disease can be initially considered. Then, the diagnosis can be confirmed according to the specific features of hypertensive cerebral hemorrhage.
The diagnostic criteria for cerebral hemorrhage, as revised by the Second National Cerebrovascular Disease Conference of the Chinese Medical Association, are as follows: ① The hemorrhage often occurs during physical activity or emotional excitement. ②The onset of repeated vomiting, headache and elevated blood pressure. ③ The disease progresses rapidly, often with impaired consciousness, hemiparesis and other neurological focal symptoms. ④ There is mostly a history of hypertension. ⑤ Lumbar puncture cerebrospinal fluid mostly contains blood and increased pressure (about 20% of it may not contain blood). (6) Ultrasonography of the brain is often associated with a shift of the midline wave. If the differential diagnosis is difficult, CT examination can be done if available.
What are the clinical manifestations of primary pontine hemorrhage?
Primary pontine hemorrhage accounts for about 2% to 10% of cerebral hemorrhages, and is mainly caused by rupture of the paracentral artery, a branch of the basilar artery. The common causes are hypertension and atherosclerosis. A few patients can be caused by vascular malformations, blood diseases or tumors in the pontine brain. It is common in middle-aged and elderly people and is induced by emotional excitement and exertion.
The clinical manifestations of this disease are varied. Generally start suddenly, quickly into a deep coma, die soon, failed to fully expose the neurological localization of physical evidence, and difficult to diagnose. However, there are some patients show sudden headache (to the occipital part of the obvious), dizziness, vomiting, blurred vision, diplopia, dysarthria, dysphagia, one side of the face numbness and paralysis of the contralateral limbs, etc., the two eyeballs to the side of the paralyzed limb staring, or spontaneous vertical eye floaters, the eyeballs to both sides of the movement can not. When the hemorrhage spreads to both sides, facial paralysis and flaccid paralysis of the limbs appear on both sides. A few were spastic paralysis or showed deafferentation with positive bilateral pyramidal tract signs. In about 1/3 of the patients, due to the involvement of sympathetic nerves in the brain, there is bilateral pupil narrowing and pinpoint pupils, which is a characteristic symptom of pontine hemorrhage. Most patients have a markedly elevated body temperature, often above 40 degrees Celsius, which is caused by the involvement of the downstream thermoregulatory fibers in the lateral part of the pontine brain. Since the respiratory center in the pontine brain is damaged, more than 80% of patients have central respiratory disorder, showing increased respiration, slowed respiration, irregular respiration, Chen-Schiff's respiration or wheezing, and so on. Most patients have increased heart rate, often above 120 beats/minute. In a few patients, the heart rate slows down to less than 60 beats/minute. If the body temperature drops suddenly and the pupils are dilated, it suggests that the life is in danger. When the lesion is located in the ventral side and extensive, the patient may appear quadriplegia, conscious, expressionless, silent, with the eyeballs up and down movements and eyelid opening and closing to convey the meaning of atresia syndrome manifestations.
The diagnosis of pontine hemorrhage is often difficult, but it is easier to diagnose if there are typical features of pontine localization such as pupillary constriction, cross paralysis or quadriplegia.
The prognosis for pontine hemorrhage is poor, with most patients dying within 24 or 12 hours of onset and a few surviving for several days.
What are the characteristics of thalamic hemorrhage?
The thalamus is located on the dorsal side of the mesencephalon and is a pair of ovoid gray matter masses. The thalamus is a pair of ovoid gray matter blocks from which various sensory conduction bundles of the body pass, so it is the subcortical sensory "headquarters". When one side of the thalamus is stimulated, the opposite half of the body becomes hypersensitive or painful. If one side of the thalamus is destroyed, the opposite half of the body is impaired in superficial and deep sensations.
Thalamic hemorrhage is mainly caused by rupture of the geniculate artery or a perforating branch. If the hemorrhage is small, the patient is often alert or only mildly unconscious. There is abnormal sensation, pain or loss of sensation on the side opposite the lesion, but no hemiparesis. If the hemorrhage directly invades the internal capsule, hemiparesis often occurs. In massive thalamic hemorrhage, intracranial pressure is elevated, and the patient often has headache, vomiting, and coma. After the hematoma breaks into the ventricles, the lumbar puncture cerebrospinal fluid is bloody.
Thalamic hemorrhage is characterized by ocular motor disorders. Mainly for the upper vision disorder, the patient's bilateral eyeballs to inward and downward gaze, seems to be looking at the tip of his nose, as if the "sunset". The pupils are often narrowed, and the light reflex is weakened or absent. After the blood breaks into the third ventricle, the patient stares at the hemiplegic side with both eyes, and this abnormal eye position and dyskinesia is a reliable basis for the diagnosis of thalamic hemorrhage. A few patients may have involuntary movements on the opposite side of the lesion because the pyramidal system is affected.
The prognosis of thalamic hemorrhage is related to the size of the hemorrhagic focus. The prognosis is poor if the hemorrhagic foci are large and the blood penetrates into the ventricles, causing brainstem damage, increased intracranial pressure, and cerebral herniation. The mortality rate for thalamic hemorrhage is about 50%.
Thalamic hemorrhage is more difficult to diagnose by relying solely on clinical manifestations. Cranial CT scan, the diagnostic accuracy is higher.
What are the characteristics of lobar hemorrhage?
Lobar hemorrhage is an intracerebral hemorrhage in the subcortical white matter of the brain, which is mostly caused by rupture of arteriovenous malformation. More than half of the cases have a history of hypertension. The hemorrhage can occur in any part of the frontal, parietal, temporal, occipital, and insula lobes, but the parietal and temporal lobes are more common.
After lobe hemorrhage, the main manifestations are headache, vomiting, convulsions, aphasia, visual field loss, and deflective sensory and motor deficits. However, since each lobe has its own special neurological function, the clinical manifestations and their extent depend mainly on the location of the hemorrhage.
Frontal lobe hemorrhage is dominated by mental disorders and is often accompanied by signs and symptoms of mild pyramidal tract damage. Motor aphasia may be present with damage to the dominant hemisphere. Temporal lobe hemorrhage starts with severe headache, nausea, and vomiting mainly on the side of the lesion. After the hemorrhage breaks into the subarachnoid space, there may be a full headache, neck stiffness, and a positive Koenig's sign, which clinically resembles a subarachnoid hemorrhage. Parietal lobe hemorrhage is mainly characterized by unequal hemiparesis, mostly lower limbs heavier than upper limbs and face, or upper and lower limbs palsy heavier than face, hemiplegia, as well as somatoform disorders and dysmetria. Occipital lobe hemorrhage is dominated by visual field changes. It is mainly isotropic hemianopsia. When the hematoma is large, the hippocampal gyrus can be herniated, showing signs and symptoms of brainstem damage such as impaired consciousness, de-cerebral tonus, binocular downgaze, pupil dilation, and loss of light reflex.
In conclusion, compared to lobular hemorrhage, it has the following characteristics:
(1) Because lobular hemorrhage does not easily involve motor conduction tracts like internal capsule hemorrhage, the incidence of hemiparesis is low.
(2) The hematoma site is farther away from the ventricles, resulting in less chance of intracranial hypertension and brainstem compression, and low incidence of coma.
(3) Lobar hemorrhage is prone to break into the subarachnoid space at an early stage, with many signs of meningeal irritation.
(4) Lobar hemorrhage has a better prognosis after timely treatment.
How to diagnose small cerebral hemorrhage?
Small cerebral hemorrhage refers to hemispheric hemorrhage with a bleeding volume of less than 10 milliliters, which is also more common in clinical practice. It is reported to account for about 24% of the patients hospitalized with cerebral hemorrhage during the same period, but due to the small amount of bleeding, clinical symptoms are light and atypical, so it is very easy to misdiagnose.
There is no uniform diagnostic standard for small amount of cerebral hemorrhage, the following points can be used as a reference basis: ① middle-aged and old people, headache suddenly occurs during strenuous activities or emotional excitement. ② Hypertensive patients, a sudden rise in blood pressure, accompanied by headache; after the condition improves, the blood pressure quickly returned to normal. ③No previous history of stroke, often for the first time. Sudden onset of focal neurologic symptoms such as mild facial paralysis, hemiparesis, and sensory disturbances. (iv) No consciousness disorder, vomiting, cervical rigidity and positive bilateral baroreflex signs.
Lumbar puncture for cerebrospinal fluid examination will be helpful in the diagnosis of small cerebral hemorrhage. However, a normal lumbar puncture cannot be completely excluded. Because more than 10% of patients, because the blood did not break into the ventricles and subarachnoid space, lumbar puncture cerebrospinal fluid examination is negative.
CT examination is a safe and reliable method to confirm the diagnosis of small amount of cerebral hemorrhage. It can not only show the location of the bleeding, the amount of bleeding and whether it breaks into the ventricle or subarachnoid space, but also can show whether the midline is displaced, ventricular compression and so on.
Small cerebral hemorrhage generally has a better prognosis. However, if the hemorrhage site is close to the midline structure of the brain, or if the hemorrhage occurs again during the course of the disease, it can also be life-threatening. Therefore, the condition should be closely monitored and treatment should be actively pursued to prevent further bleeding or rebleeding.
What is the principle of applying dehydration in cerebral hemorrhage?
The acute stage of cerebral hemorrhage often has cerebral edema, increased intracranial pressure, and even leads to the formation of cerebral hernia, therefore, dehydrating agents should be applied in time to reduce intracranial pressure and control cerebral edema. The application principles of the dehydrating agent are:
(1) Decide the dosage and usage of the dehydrating agent according to the patient's clinical symptoms and actual needs. And closely observe the dynamic changes of intracranial pressure, adjust the treatment program to achieve effective control and rational use of drugs.
(2) For those who have consciousness disorder, suggesting that the scope of the lesion is large and the midline structure has been affected, 20% mannitol 250 ml can be given intravenously, once every 6 hours, and observe the dynamic changes of the condition and consciousness disorder, and pay attention to whether the symptom is relieved after using the medicine, so as to adjust the dosage and the interval between the medication.
(3) If the patient's coma deepens, tendon reflexes and muscle tone gradually decreases, and contralateral pyramidal sign or de-cerebralized tonic-like reaction occurs, it is a sign that the lesion is enlarged or the midline structure is shifted and aggravated. In addition to 20% mannitol 250 ml intravenous drip should be given for active dehydration therapy, and should be added dexamethasone 10-20 mg intravenous drip, 1 to 2 times a day, the above two drugs can be applied at the same time or alternately.
(4) If the clinical symptoms are mild, the patient is clear, there is no severe headache or vomiting, and the funduscopic examination does not show any optic papillary edema, the dehydrating agent may not be used for the time being. On the contrary, if there is severe headache or vomiting, try to give 50% dextrose 60 ml intravenously, and closely observe the effect of medication. If symptoms improve, say there is clearly increased intracranial pressure. If headache, vomiting and other symptoms are not reduced, may be due to subarachnoid hemorrhage stimulation, it is appropriate to use analgesic or sedative. For such patients, generally advocate the temporary use of mannitol, so as not to interfere with the stability of intracranial hypertension.
(5) Dehydration agents are generally applied for 5 to 7 days. However, if the combination of pulmonary infection or frequent seizures, often due to infection, toxicity, hypoxia and other factors, which aggravate cerebral edema, the application of dehydrating agents can be appropriately prolonged.
(6) In the process of applying dehydrating agent, it is necessary to pay attention to whether the purpose of dehydration has been achieved, but also to prevent the adverse reactions caused by excessive dehydration, such as blood volume insufficiency, hypotension, electrolyte disorders and renal function damage.
What are the commonly used dehydrating agents?
Cerebrovascular patients are often accompanied by cerebral edema, especially cerebral hemorrhage is more obvious, if not treated in time can make the condition worse, and even the occurrence of cerebral hernia, and life-threatening. Therefore, in order to eliminate cerebral edema, according to the condition of the choice of dehydrating agent. Dehydration agents are clinically divided into three major categories according to their pharmacological effects.
(1)Hypertonic dehydrating agentsThis type of drug input