Subarachnoid hemorrhage in the elderly

Introduction

Introduction to subarachnoid hemorrhage in the elderly Subarachnoid haemorrhage (SAH) refers to the general term for bleeding blood into the subarachnoid space for various reasons. It can be divided into two types: spontaneous and traumatic. Spontaneous is divided into primary and secondary. Kind. Caused by various reasons, the blood vessels of the pia mater rupture into the subarachnoid space, called primary subarachnoid hemorrhage; due to intracerebral parenchymal hemorrhage, blood penetrating brain tissue into the subarachnoid space, called secondary subarachnoid hemorrhage Generally, the so-called subarachnoid hemorrhage refers only to primary subarachnoid hemorrhage, accounting for about 15% of acute cerebrovascular disease. The cases described in this section are also limited to this. The incidence of subarachnoid hemorrhage in the elderly is 21.6. % to 39.5%, which is higher than the adult incidence rate of 10.5% to 20%, so it needs to be taken seriously. basic knowledge The proportion of illness: 0.002% Susceptible people: the elderly Mode of infection: non-infectious Complications: myocardial infarction headache consciousness disorder gastrointestinal bleeding acute pulmonary edema coma hydrocephalus diabetes insipidus cerebral infarction epilepsy

Cause

The cause of subarachnoid hemorrhage in the elderly

After the blood cells of the subarachnoid space disintegrate, various inflammatory substances are released, which leads to a chemical inflammatory process, which further causes an increase in cerebrospinal fluid and aggravates high intracranial pressure; induced vasospasm causes cerebral ischemia or infarction. Hemoglobin and hemoglobin are deposited on the arachnoid granules, causing a slow blockage of cerebrospinal fluid reflux. After a long period of time, traffic hydrocephalus gradually appears and the ventricles expand. Blood in the skull base, or into the ventricles, coagulation causes cerebrospinal fluid reflux obstruction, leading to acute obstructive hydrocephalus, increased intracranial pressure, and even cerebral palsy.

Within a few hours after the subarachnoid hemorrhage, the surface of the cerebrospinal surface is bright red or purple, and the cells in the brain pool and sulcus are mostly purple. If the amount of bleeding is high, the surface of the brain is thin. Blood clots are covered, sometimes blood staining can be seen in the epidural, cerebral pool at the bottom of the skull, cerebral cerebral horn, cerebellar medullary pool and terminal pool can be seen with obvious blood clot accumulation, and even buried in the area of neurovascular tissue The blood vessels must be carefully separated before the nerve vessels are found. Sometimes the ruptured aneurysms or blood vessels can be found. After 48 hours of bleeding, the surface of the brain and spinal cord is soft due to the rupture and dissolution of blood cells and the release of a large amount of hemosiderin. The dura mater is rust or brownish yellow. At the same time, different degrees of local adhesion can be seen. Blood or blood clots can be seen in the ventricles. Some brain tissue in the skull base area is worn out, causing secondary cerebral hemorrhage changes. After 4 hours of bleeding, Microscopically, polynuclear leukocytes ooze around the soft meningeal vessels. After 24 hours, a large number of leukocyte infiltration and phagocytic cells phagocytose, and then these cells are self-necrotic. After 72 hours, various inflammatory cell responses peak. In particular, lymphocytes and phagocytic cells increased more significantly, and a large number of phagocytic cells phagocytizing red blood cells and polynuclear white blood cells containing hemosiderin particles appeared. At 1 week, polynuclear white blood cells disappeared, lymphocyte infiltration was obvious, and phagocytic cells were still most active. Most of the red blood cells are lysed, but there are still some intact red blood cells. After 10 days, there is a phenomenon of mechanization, such as fibrosis on the surface of the brain and spinal cord to form a scar film. The time of the above-mentioned microscopic evolution depends mainly on the amount of bleeding. A small amount of bleeding occurred in 72h, the inflammatory process also depends on the cause of bleeding, such as bleeding caused by infectious causes, the inflammatory reaction is more severe, and some form pus, abscess, abscess, etc., some necrosis Vasculitis, leukemia-induced hemorrhage, meningeal, brain tissue and blood vessels around a large number of immature leukocyte infiltration, bleeding caused by malignant tumors, cancer cells found in the blood clot.

After subarachnoid hemorrhage, it can also cause a series of pathological processes of intracranial and extracranial tissues and organs, mainly in the following aspects:

1. Increase in the amount of cranial content: The blood flows from the blood vessel into the subarachnoid space, causing the intracranial volume to increase, causing an increase in intracranial pressure, and severe cerebral palsy.

2. Obstructive hydrocephalus: blood in the skull base, or into the ventricles, coagulation caused by cerebrospinal fluid reflux blocked, leading to acute obstructive hydrocephalus, increased intracranial pressure, and even cerebral palsy.

3. Hypothalamic dysfunction: As a result of acute high intracranial pressure or blood and its products directly stimulate the hypothalamus, causing neuroendocrine disorders, elevated blood sugar, fever and so on.

4. Autonomic dysfunction: Acute high intracranial pressure or blood directly damages the hypothalamus or brain stem, leading to autonomic hyperfunction, causing acute myocardial ischemia or infarction, arrhythmia.

Prevention

Prevention of subarachnoid hemorrhage in the elderly

Subarachnoid hemorrhage is one of the acute cerebrovascular diseases, and cerebrovascular disease, malignant tumors and cardiovascular diseases are the three leading causes of death in middle-aged and elderly patients. Since the 1970s, many in Japan, North America and Western Europe. Through the prevention and treatment of hypertension, a risk factor for cerebrovascular disease, the country has a significant decline in the incidence and mortality of hemorrhagic and ischemic cerebrovascular diseases. Therefore, prevention of cerebrovascular disease improves the quality of life of the elderly. Extending life is very important.

Primary prevention:

Mainly for the prevention of risk factors for subarachnoid hemorrhage, because most SAH is caused by rupture of aneurysm, about 5% to 6% of aneurysms caused by family history of SAH, research on genetic defects In progress, the abnormalities of structural proteins (such as collagen) are related. Other diseases related to aneurysm rupture include aortic coarctation, polycystic kidney disease, Marfan syndrome, EhlerDandos syndrome, muscle fiber dysplasia and other rare Collagen or elastin disease, these are risk factors for non-intervention, and smoking is the most important risk factor for intervention in SAH. Smoking cessation can reduce but not eliminate the risk of SAH. The pathophysiological relationship between smoking and aneurysm formation is not very high. Clearly, possible hypotheses include increased macrophage release of proteases, accelerated arteriosclerosis, and a temporary increase in blood pressure in smoking. Hypertension is an independent risk factor for SAH, but not as dangerous as smoking, and currently Treatment of high blood pressure and smoking cessation are two of the most effective interventions for SHA and cerebral hemorrhage.

Secondary prevention:

Although great progress has been made in the diagnosis and treatment of SAH in recent years, SAH is still the leading cause of death and disability. Early diagnosis and good medical or surgical treatment can reduce SAH mortality, improve functional prognosis, and avoid Serious complications occur to maximize recovery.

Tertiary prevention:

The prognosis of SAH patients is related to many factors. According to international cooperation studies, the results of 6 months after onset are: 58% of patients with good prognosis, 7% of moderate loss of life, and 5% of severe loss of life. Plant status accounts for 2%, and the mortality rate is 26%. The cause of death: cerebral vasospasm accounts for 39%, and direct death from SAH accounts for 2%. According to reports in the literature, 2922 patients undergoing surgery for 6 months turned into a prognosis. 68%, death accounted for 14%, the prognosis and functional prognosis of elderly people were worse than younger ones. After the onset, the prognosis of patients undergoing surgery within 10 days is better. Acute surgery can reduce the risk of rebleeding and prevent vasospasm. Occurred, due to the wide application of modern diagnostic techniques, the fatality rate of SAH decreased by 0.8%, but there are still about 20% of SAH patients with neuropsychological problems, so the psychological treatment of such patients should be strengthened, which is also the future evaluation of SAH function. Top and treatment strategies should raise issues of high priority.

Complication

Elderly subarachnoid hemorrhage complications Complications myocardial infarction headache consciousness disorder gastrointestinal bleeding acute pulmonary edema coma hydrocephalus diabetes insipidus cerebral infarction epilepsy

Due to the severity of the disease, various complications may occur in the acute, subacute and chronic phases after bleeding.

Heart damage

20% of patients with myocardial ischemia or myocardial infarction, especially in middle-aged patients or patients with more bleeding, due to obvious headache or disturbance of consciousness in patients with subarachnoid hemorrhage, patients with myocardial damage generally have no complaints, so mainly through It can only be discovered when doing an electrocardiogram, which is also a common cause of death after SAH.

2. Gastrointestinal bleeding

Patients with more subarachnoid hemorrhage may have acute gastrointestinal bleeding. The patient presents with vomiting bloody stomach contents or coffee-like substances. In severe cases, hemorrhagic shock may occur, and hemorrhagic shock may only be drawn from the stomach tube. The contents are mainly caused by the increase of intracranial pressure after subarachnoid hemorrhage. When the hypothalamus is damaged, it causes acute ulcer of the digestive tract. This is one of the serious complications of SAH and should be actively prevented and treated.

3. Acute pulmonary edema

Seen in a large number of subarachnoid hemorrhage, the patient showed sudden aggravation of the disease, difficulty breathing, blistering sounds at both lungs and coughing up foamy blood.

4. Rebleeding

The time of rebleeding can be after the first hemorrhage, but it is the peak period within 2 weeks after the previous hemorrhage. The risk of rebleeding within 1 month after the first hemorrhage is the greatest, and the rebleeding rate is 3% every year after half a year. The recurrence rate of SAH patients is 11%-18%, and the recurrence rate within 2 weeks accounts for 54% of re-vaccination cases. The recent recurrence within 1 month accounts for 54%-86%, and the long-term after 2 months. Recurrence is 5% to 30%, and the recent recurrence rate is 41% to 46%, which is significantly higher than the SAH mortality rate (25%). The causes of rebleeding are mostly aneurysms, arteriovenous malformations, and abnormal brain base. Patients with vascular network disease, mental stress, mood swings, forced bowel movements, severe cough, sitting up activities, high blood pressure is a common predisposing factor, and its clinical manifestations are: after the first bleeding, the condition is stable or improved, suddenly suddenly appear again Headache, vomiting, convulsions, coma, even brain rigidity and neurological signs, neck strength and Kernig's sign were significantly aggravated, the cerebrospinal fluid was again fresh red, and a large number of fresh red blood cells with neutrophils appeared again in the cerebrospinal fluid.

5. Cerebrovascular spasm (CVS)

The incidence of cerebral vasospasm is 16% to 66%. It is divided into early onset and late onset according to the time of onset. Early onset occurs within a few tenths of hours after hemorrhage, and late onset occurs in the course of 4 to 16 days. 7 to 10 days peak, average 2 weeks, divided into localized and diffuse multi-segmental, involving the anterior cerebral artery, middle cerebral artery, internal carotid artery, can also occur in the vertebral basilar artery system The lesion side is more than the contralateral side of the lesion. The early onset CVS occurs mostly in the artery of the ruptured aneurysm, mostly unilateral localized CVS, so it has the significance of the positioning of the tumor-bearing artery; while the late-onset CVS is mostly diffuse multi-segment Sexuality, which may be unilateral or bilateral, has no localization value for ruptured aneurysm-bearing arteries. Its clinical manifestations are characterized by neurological symptoms and progressive aggravation on the basis of SAH symptoms after treatment or rest. Symptoms mainly include disturbance of consciousness, increased intracranial pressure and focal local signs. Most of them occur 3 to 7 days after onset, and gradually relieve after 2 weeks. Lumbar puncture has no signs of fresh bleeding in cerebrospinal fluid, and arachidonic acid in cerebrospinal fluid. Increase, see Chen Red blood cells and lymphocytes, currently found in more blood loss, the higher the incidence of vasospasm, SAH is an important cause of death, analyze its mechanism may be:

1 Active substances in the cerebrospinal fluid cause persistent paralysis of the arteries.

2 The active substance causes an inflammatory reaction of the blood vessel wall.

3 Subarachnoid hemorrhage obstructs the micropores between the cerebral vascular adventitia and the subarachnoid space, affecting the nutrition and metabolism of the blood vessel wall. Hyponatremia is easy to cause CVS, and attention should be paid.

6. Hydrocephalus

SAH-induced hydrocephalus in the short-term and long-term hydrocephalus, with long-term concurrent normal intracranial pressure hydrocephalus is more common, and the recent concurrent acute hydrocephalus is also a non-negligible complication, acute brain accumulation after SAH Aquatic hydrocephalus (AHC) refers to hydrocephalus that occurs within 1 week after the onset of SAH, and the incidence rate is 9% to 27%. Most scholars believe that the incidence rate is about 20%. Most of the pathogenesis is considered to be AHC after SAH. Occurrence is closely related to intraventricular hemorrhage, and is also related to the total amount of blood in the brain pool. AHC occurs due to increased ventricular hemorrhage and cerebral blood volume, which causes blood to deposit in the basal pool and the fourth ventricle, affecting the normal cerebrospinal fluid. Circulation, while red blood cells can block the arachnoid granules to make the cerebrospinal fluid recovery disorder. In addition, the circulatory obstruction of the cerebrospinal fluid in the basal pool and ventricular system may form a pressure gradient, most obviously in the lateral ventricle, and the cerebrospinal fluid passes through the third, fourth ventricles and brains. Pool, cerebral palpebral gradual reduction, reducing the recovery of cerebrospinal fluid by arachnoid granules, the above factors lead to the enlargement of the ventricles, the formation of AHC, AHC no specific clinical symptoms and signs, usually manifested as severe headache, Sputum, meningeal irritation, and conscious disturbances, the more prominent symptoms are disturbance of consciousness, especially in 1 or 2 days, gradual coma, pupil diminution, disappearance of light reflex, a small number of patients appear Parinaud (both eyes can not see) comprehensive According to statistics, after SAH, 33% of AHC patients have no clinical symptoms and 38% have no consciousness disorder. In short, the clinical symptoms of ACH and SAH are difficult to distinguish. The exact diagnosis depends on brain CT, while the normal intracranial pressure hydrocephalus is SAH. Long-term complications, caused by cerebrospinal fluid circulation caused by arachnoid adhesion in the brain pool and decreased cerebrospinal fluid recovery from arachnoid granules, the incidence rate is about 35%, and its clinical manifestations are progressive intelligent decline, gait instability, pyramidal tract Symptoms or extrapyramidal symptoms, urgency or even urinary incontinence.

7. Ventricular blood

The incidence of SAH complicated with ventricular hemorrhage is about 50%. It can be divided into two types: reflux and penetrating ventricular hemorrhage. The blood in the countercurrent ventricle is due to the subarachnoid pressure higher than the ventricle after SAH. The median ventricle, the lateral hole reversal into the ventricle, blood deposition in the bilateral ventricle triangle and posterior horn; penetrating ventricular hemorrhage multi-line aneurysm directly through or form a hematoma in the brain, the hematoma breaks into the ventricle, blood deposition on the side The ventricle or the third ventricle may even form a ventricle cast. SAH complicated with ventricular hemorrhage may aggravate the condition, may also be secondary to acute hydrocephalus, and may cause a series of midline symptoms due to ventricular pressure and pressure in the hypothalamus. The diagnosis depends mainly on the head CT. See you.

8. Subthalamic damage

Secondary cerebral edema, cerebral vasospasm, rebleeding, and ventricular hemorrhage can cause different degrees of damage in the hypothalamus, leading to autonomic nerves, visceral function and metabolic disorders, clinical vomiting, hematemesis, melena, acute edema. Central respiratory disorder (tidal breathing), ECG changes, arrhythmia, blood pressure changes, high fever or sweating, hyperglycemia, diabetes insipidus, etc., make the clinical symptoms more complicated and the condition is more serious.

9. Intracranial hematoma

SAH complicated with intracranial hematoma can be intracerebral hematoma and subarachnoid hematoma, with intracerebral hematoma more common, according to the course of the disease can be divided into acute, subacute and chronic, acute course within 3 days, subacute course 4 days ~ 3 weeks, chronic disease for more than 3 weeks, the most common cause is vascular rupture of vascular malformation, followed by rupture of the aneurysm to penetrate the brain parenchyma, the former with the most blood supply area of the middle cerebral artery, the latter with more common anterior cerebral aneurysm, symptoms and The signs depend on the location and size of the hematoma.

10. Infarction

SAH complicated with cerebral infarction is seen in late-onset CVS after SAH. The degree of CVS causes local cerebral blood flow to be less than 18-20ml/100g brain tissue. If the duration is too long, it may lead to cerebral infarction, and some may still have blood infarction. For SAH patients with signs or disturbances of hemiparesis and other disturbances, CT examination should be performed as soon as possible.

11. Epilepsy

The incidence of SAH complicated with epilepsy is 10% to 20%. It is more common in large episodes. A few are localized or psychomotor seizures. The causes are related to diffuse cerebral vasospasm after SAH, cerebral blood flow is reduced, cerebral hypoxia, brain Edema and direct stimulation of diseased blood vessels, etc., seizures can be used as the first symptom of SAH, should be noted.

Symptom

Symptoms of subarachnoid hemorrhage in the elderly Common symptoms Dizziness, hearing loss, visual impairment, consciousness, sleepiness, nausea, vomiting, attention, inconvenience, fundus, abnormal eye movement, nerve palsy, coma

Typical manifestations of subarachnoid hemorrhage are sudden onset of severe headache, vomiting, disturbance of consciousness, meningeal irritation, bloody cerebrospinal fluid and brain CT scan showing high density of subarachnoid space, but due to age of onset, lesion, rupture The size of the blood vessels, the number of episodes, etc. are different, and the clinical manifestations are quite different; the light ones can have no obvious symptoms and signs, and the severe ones suddenly coma and die in a short period of time. The age of onset is most common in 40 to 60 years old.

Incentive

Most patients have obvious incentives before the onset, such as strenuous exercise, excessive fatigue, forced bowel movements or coughing, drinking, emotional agitation and other dynamic onset, and a small number of patients in the quiet.

2. Pioneer symptoms

Most patients develop symptoms without prodromal symptoms. A small number of patients have a short-term or long-term history of severe headache before onset, and the incidence rate is 10%. Some patients have dizziness before the onset, blurred vision, eye muscle migraine, etc. .

3. Main symptoms

The frequency of symptoms after onset has the following main symptoms:

(1) Headache: It is mainly caused by high intracranial pressure and blood chemical stimulation of the dura mater, and headache is the most common symptom of this disease. The frequency is different depending on the age and severity of the disease. The incidence rate is above 90%; the elderly and children account for about 50%. When the headache occurs, it is mainly distributed in the forehead, the occiput or the whole head, and then the upper extension and the total head pain, so the early headache can help determine the rupture. In the arterial part, the nature of the headache is mainly severe pain or cleft palate. The duration of the headache depends on the amount of bleeding, which is usually about 2 weeks.

(2) Vomiting: It is caused by high intracranial pressure and direct stimulation of vomiting center. Vomiting is a manifestation of high blood loss, high intracranial pressure, and severe disease. Most of them are jet vomiting, and vomit is stomach contents. Or coffee samples.

(3) disturbance of consciousness: the incidence rate is more than 50%, mainly because the intracranial pressure is too high, which leads to the inhibition of brain function. Generally, the disturbance of consciousness occurs immediately after the onset, and the degree and duration depend on the amount and location of the bleeding. Light is drowsiness, and severe is coma; some patients recover from waking after a short coma. In addition, some patients develop consciousness disorder after 1 week of onset because of cerebral infarction caused by secondary cerebral artery spasm. Or due to bleeding again, some patients have always had unconscious disorders, which is mainly due to less bleeding or obvious brain atrophy in the elderly, and there is no obvious high intracranial pressure.

(4) Meningeal irritation: It is caused by blood stimulation of the dura mater in the subarachnoid space. The main manifestations are neck stiffness, Brudzinski sign and Kernig sign, and sometimes meningeal irritation is the only clinical manifestation of subarachnoid hemorrhage. Other symptoms and signs, this is because if the subarachnoid hemorrhage does not show meningeal irritation, the amount of bleeding is less, the condition is not heavy, so there is no other performance, therefore, suspected subarachnoid hemorrhage, check the meninges Stimuli sign is very important. The intensity and disappearance of meningeal irritation sign depends on the location of bleeding and the amount of bleeding and the age of the patient. Meningeal irritation usually occurs several hours after subarachnoid hemorrhage. Later, after 3 to 4 weeks, the meningeal irritation of most patients disappeared.

Elderly patients with less bleeding, those with strong tolerance to pain or severe coma, may have no meningeal irritation.

(5) Abnormal fundus: On the day of the onset or the next day, due to acute high intracranial pressure, ocular venous return is blocked, and some patients have retinal and vitreous hemorrhage; after the cerebrospinal fluid returns to normal, there are still traces of bleeding, so the retina And vitreous hemorrhage is one of the important bases for subarachnoid hemorrhage. Intraocular hemorrhage can invade aqueous humor and cause vision loss, which is the cause of permanent visual impairment. For example, if accompanied by optic disc edema, it may indicate that the condition is more serious. .

(6) Psychiatric symptoms: Patients may have various psychiatric symptoms in the acute phase, such as euphoria, convulsions, hallucinations, etc., which disappear after 2 to 3 weeks, and some patients may have memory loss, inattention, analysis Judgment obstacles, etc.

(7) Other manifestations: Most patients do not have clear localized symptoms or signs of brain dysfunction, but a small number of patients may have focal lesions, and some have clinical significance, such as in the cranial nerves. The incidence of oculomotor palsy is higher, and the performance is double vision. At this time, the lateral basilar artery, the posterior cerebral artery or the superior cerebellar artery may have an aneurysm. In addition, facial nerve, trigeminal nerve, nerve, and auditory nerve may also appear. Damage to the optic nerve, etc., can be manifested as a skewed mouth, facial dysfunction, restricted eye movement, decreased hearing, blurred vision, tinnitus and deafness, etc. Some patients have speech disorders, limb paralysis or sensory disturbances, suggesting direct bleeding The possibility of entering the brain parenchyma or complicated cerebral arterial spasm, some patients have seizures due to blood stimulation of the cortex.

Examine

Examination of subarachnoid hemorrhage in the elderly

Blood test

In the early stage of subarachnoid hemorrhage, there may be an increase in blood leukocytes, which is mainly multinucleated. After a serious illness and persists for several days, the white blood cells are obviously increased, suggesting the possibility of infection.

2. Waist wear check

Lumbar puncture examination is the most important basis for determining whether there is bleeding in the subarachnoid space. Therefore, lumbar puncture should be performed as soon as possible. However, if the condition is severe, there is a coma or obvious signs of nervous system, lumbar puncture can easily lead to brain. When you are sputum, you should first perform a brain CT scan, the purpose is to be able to confirm the diagnosis in time, and it is easy to rule out secondary subarachnoid hemorrhage. In a conditional hospital, you should first perform a brain CT scan, and then, if necessary, It is advisable to perform a lumbar puncture examination. The lumbar puncture is mainly used to check intracranial pressure, routine and biochemical, and to pay attention to the analysis of the difference in lumbar puncture.

(1) Appearance: When the waist is worn immediately after bleeding, depending on the amount of bleeding, the color of cerebrospinal fluid is slightly sputum, reddish, pink to deep red, and the bleeding time may be orange or yellow.

(2) intracranial pressure: the intracranial pressure of most patients with subarachnoid hemorrhage increased, the higher than the pressure tube used above, the level of intracranial pressure depends on the amount and time of bleeding, the more bleeding, The higher the intracranial pressure; the intracranial pressure may be higher due to chemical inflammation in the 3 to 10 days after hemorrhage; however, sometimes the formation of blood clots, the pressure on the lumbar wear is reduced, which does not represent the true intracranial pressure. Should pay attention to the difference, generally after 2 weeks of onset, intracranial pressure decreased, and gradually returned to normal.

(3) Cell number: routine examination of cerebrospinal fluid in patients with subarachnoid hemorrhage mainly understands the total number of cells and blood cell classification, and the amount of bleeding is small. Even if the brain CT scan is not found, the lumbar puncture examination is performed within a few hours after the onset of the cerebrospinal fluid. The total number of cells can reach thousands, and the amount of bleeding is as large as hundreds of thousands, or even more than one million. When the lumbar puncture is examined after 24 hours of onset, the total number of cells is relatively decreased due to cell destruction, and lumbar puncture is performed. Attention should be paid to distinguish the damage caused by the lumbar puncture process, and the main difference of blood cerebrospinal fluid is as follows: First, keep 3 tubes continuously when the cerebrospinal fluid is released. If the blood of the cerebrospinal fluid is getting weaker, it may be the injury. Cause, otherwise it is subarachnoid hemorrhage; the second is to check whether the red blood cells in the cerebrospinal fluid are shrinking red blood cells, such as fresh non-shrinking red blood cells, it is caused by damage, such as shrinking red blood cells, it is arachnoid Lower chamber bleeding; Third, the amount of severe bleeding is more, the bloody cerebrospinal fluid that flows out after the waist wear will quickly coagulate.

(4) White blood cell condition: The length of the time interval for the lumbar puncture examination affects the count of white blood cells in the cerebrospinal fluid and the ratio of red blood cells. In the case of no blood disease, the ratio of white blood cells to red blood cells in the cerebrospinal fluid shortly after subarachnoid hemorrhage It is 1:700, which is similar to the ratio in blood. If it exceeds this ratio, it may be caused by chemical inflammation or intracranial inflammatory disease caused by excessive bleeding time. This part of white blood cells can be The following formula is calculated:

Cerebrospinal fluid white blood cell count = cerebrospinal fluid white blood cell count - blood white blood cell count × cerebrospinal fluid red blood cell count / blood red blood cell count.

(5) protein content: as long as it is subarachnoid hemorrhage, the protein content of cerebrospinal fluid has increased to varying degrees, many can be as high as 10g / L or more, the amount of bleeding and the amount of time affects the protein content of cerebrospinal fluid, it is generally considered that each increase of 700 The number of cells can increase 1 mg of protein; 7 to 10 days after hemorrhage, due to the chemical inflammatory reaction, the protein content reaches the highest level and then gradually decreases.

(6) Sugar and chloride: In patients with subarachnoid hemorrhage, the sugar and chloride contents of cerebrospinal fluid are in the normal range regardless of the amount of bleeding and the length of bleeding.

3. ECG

Some patients, especially middle-aged and elderly people, may have an ischemic change of electrocardiogram or even a myocardial infarction in the early stage of the disease.

4. Brain CT scan : It is a rapid, relatively safe and positive rate for detecting subarachnoid hemorrhage. Therefore, brain CT scan is the first choice for this disease. For patients with suspected subarachnoid hemorrhage, brain The following results and their significance can be found after CT scan:

1 No abnormalities found, may not be subarachnoid hemorrhage; or a small amount of subarachnoid hemorrhage.

2 The high density of the subarachnoid space in the skull base can be confirmed as subarachnoid hemorrhage.

3 In the high-density area of the subarachnoid space, local ultra-high density shadows may be found, which may be ruptured aneurysms.

4 brain manifestations of local abnormalities in the image of the mass, may be cerebrovascular malformations.

When there is a hematoma in the medial or lateral brain tissue of the frontal lobe, the aneurysm of the anterior cerebral artery or anterior communicating branch may be ruptured.

6 There is a high-density shadow in the ventricle, which may be due to the countercurrent flow of blood in the subarachnoid space.

7 patients with enlarged ventricles and blood clots in the ventricles are acute obstructive hydrocephalus.

8 combined with the appearance of local brain tissue low density shadow, may have complicated cerebral infarction caused by cerebral artery spasm.

9 There is obvious local high-density shadow of brain parenchyma and connected with high-density shadow of the subarachnoid space or high density shadow in the brain, which may be the subarachnoid hemorrhage secondary to cerebral hemorrhage.

When the amount of subarachnoid hemorrhage reaches a certain level, the brain CT scan can show the high density shadow of the subarachnoid space, and the high-density shadow displayed by the brain CT scan after the onset of the disease disappears. So far, there is no large sample statistics. Analysis report, but it is generally believed that subarachnoid hemorrhage caused by the total number of cells in the cerebrospinal fluid examination of the lumbar puncture is more than 2000, brain CT scan can show high density shadow; after 10 days of bleeding, the brain CT scan shows high Density shadow disappears. 3. Once cerebral angiography is diagnosed as subarachnoid hemorrhage, cerebral angiography should be performed as soon as possible to determine whether there is an aneurysm or vascular malformation and its presence, subarachnoid hemorrhage. The positive rate of cerebral angiography in patients is 85%. The most common aneurysms, vascular malformations and moyamoya disease, 80% of aneurysms can be visualized by cerebral angiography and can clearly understand the location, size, quantity, morphology, and The relationship between normal blood vessels and the supply of collaterals cannot be shown as an aneurysm. The reason is that the tumor is pedicled, the tumor is too thin or the aneurysm ruptures. Therefore, if the first cerebral angiography is negative, the angiography should be repeated in a short period of time. In the cerebral angiography, almost 100% of the cerebral vascular malformation is displayed, which is manifested as a group of irregular vascular shadows. To an abnormally thickened artery and one or more dilated tortuous veins, the latter being shown prematurely in the arterial phase or the capillary phase, because the contrast agent rapidly returns rapidly through a deformed vascular short circuit, the distal branch of the artery The development of light or no development, the positive rate of cerebral vascular infection of moyamoya disease is also 100%, manifested as internal carotid artery occlusion or severe stenosis, the anterior cerebral artery and middle cerebral artery are not developed, and the small irregular blood vessels appearing upward at the base of the skull. Shadow, anterior communicating artery thickening or thickening of blood vessels elsewhere, cerebral angiography can also show other abnormal blood vessels such as infectious aneurysms, brain tumors and so on.

5. Brain MRI: generally not used for the acute phase diagnosis of subarachnoid hemorrhage, because in the acute phase, brain magnetic resonance is easy to induce rebleeding, so brain MRI is mainly used for the recovery of subarachnoid hemorrhage. Cerebral angiography or screening examination of cerebral aneurysms and cerebral vascular malformations, aneurysms can be characterized by short T1 and T2 signals appearing in the tumor area, and cerebral vascular malformations mainly manifest as local mixed signals, with The long T1 and T2 signals are dominant, and the brain or subarachnoid hemorrhage area is characterized by long T1 and T2 signals.

6. Brain MRA: It is mainly used for the recovery of subarachnoid hemorrhage, and there are still suspected intracranial vascular abnormalities. Screening examination can directly observe the morphology, location, degree of abnormal blood vessels and the relationship with surrounding tissue vessels. However, the positive rate of cerebrovascular abnormalities in this examination is not as good as that of cerebral angiography, and if abnormalities are found, cerebral angiography must be performed to determine.

Diagnosis

Diagnosis and diagnosis of subarachnoid hemorrhage in the elderly

diagnosis

Sudden onset of severe headache, vomiting and meningeal irritation should be considered as subarachnoid hemorrhage; if the lumbar puncture or brain CT scan found cerebrospinal fluid or subarachnoid blood, you can confirm the diagnosis, but, in atypical When performance, it is easy to miss diagnosis or misdiagnosis. For example, in elderly patients with little or no bleeding, the headache, vomiting and meningeal irritation are not obvious. At this time, it is mainly confirmed by brain CT scan and lumbar puncture examination.

Differential diagnosis

Vascular headache

Patients with migraine and cluster headaches may have sudden headache and vomiting. People with aura migraine are also accompanied by symptoms of focal neurological dysfunction, sometimes difficult to distinguish from subarachnoid hemorrhage, but patients with vascular headache You can ask if there is a history of repeated similar episodes, no meningeal irritation, no abnormal findings in lumbar puncture or brain CT scan, then it can be distinguished.

2. Intracranial infection

Various types of meningitis and encephalitis patients can show obvious headache, vomiting and meningeal irritation, especially in patients with meningitis, bloody cerebrospinal fluid, such as tuberculous meningitis, cryptococcal meningitis and herpes simplex virus brain. Inflammation, however, the incidence of intracranial infection is slow, accompanied by fever, signs of systemic infection, increased peripheral white blood cells, cerebrospinal fluid showed obvious inflammatory changes, and most of the brain CT scans were normal.

3. Some people with mental symptoms as the main performance should be identified for mental illness. Detailed medical history and examination should be asked. If the patient is suspected of having the disease, he or she can check the cerebrospinal fluid or do CT examination to prevent misdiagnosis.

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