subarachnoid hemorrhage
Introduction
Introduction to subarachnoid hemorrhage Subarachnoid hemorrhage (SAH) is a type of hemorrhagic cerebrovascular disease, divided into primary and secondary. Primary subarachnoid hemorrhage is caused by rupture of blood vessels on the surface of the brain and the bottom of the brain, and blood directly flows into the subarachnoid space, also known as spontaneous SAH. Brain parenchyma or intraventricular hemorrhage, traumatic subdural or epidural hemorrhage into the subarachnoid space is secondary SAH. Subarachnoid hemorrhage is one of the most common emergencies in neurology, and the incidence rate accounts for 6% to 10% of acute cerebrovascular diseases. basic knowledge Proportion of disease: 6% to 10% of acute cerebrovascular disease Susceptible people: no specific population Mode of infection: non-infectious Complications: coma
Cause
Causes of subarachnoid hemorrhage
Aneurysm (45%):
The miliary aneurysm accounts for about 75% of the cause, and the annual incidence rate is 6/100,000. Arteriovenous malformation accounts for about 10%, more common in young people, more than 90% are on the screen, abnormal vascular network (Moyamoya disease) accounts for 20% of children's SAH, accounting for 10%.
Vascular malformation (20%):
It is generally believed that most of the patients before the age of 30 are vascular malformations. Most of the patients after the age of 40 are ruptured intracranial aneurysms. Those over 50 years old are often caused by hypertensive cerebral arteriosclerosis and brain tumors.
Smoking, drinking (15%):
Smoking and drinking are closely related to subarachnoid hemorrhage. Foreign animal experiments have shown that there are three factors in the formation of aneurysms: Willis ring pressure, increased blood pressure and vascular fragility, smoking can affect these three factors, causing acute rise in blood pressure, After 3 hours, it gradually fell back. The incidence of subarachnoid hemorrhage in clinical practice was the highest within 3 hours after smoking. Smoking also activates pulmonary macrophage activity, promotes the release of hydrolase, and can cause lung damage and increased cerebrovascular fragility. , thereby increasing the risk of subarachnoid hemorrhage, heavy drinking may cause high blood pressure or other changes including hemagglutination mechanism and cerebral blood flow, can accelerate the subarachnoid hemorrhage, it has been reported that excessive drinking under the subarachnoid The incidence of luminal bleeding is twice as high as that of non-drinkers.
Pathogenesis
Miliary aneurysms may be associated with genetic and congenital developmental defects. Autopsy found that approximately 80% of patients with Willis ring arterial wall elastic layer and medial membrane dysplasia or impaired, with age due to arterial wall atherosclerosis, hypertension and Influence of blood vortex impact and other factors, the elasticity of the arterial wall is weakened, and the weakened wall gradually expands outward to form a saccular aneurysm; the larger the aneurysm, the more easily it ruptures, the diameter is less than 3mm, and the bleeding is 5-7mm.
Cerebral arteriovenous malformation is a malformed vascular group formed by abnormal development of the embryonic stage. The weakened blood vessel wall is in a critical state of rupture. The stimulating or inconspicuous cause can cause rupture, arteritis or intracranial inflammation causes vascular wall lesions, and tumor or metastatic cancer directly erodes blood vessels. Can cause bleeding.
1, the main lesion
85% to 90% of congenital miliary aneurysms are located in the anterior circulation, which is characterized by weak development of the vascular wall bifurcation, mostly single; about 20% of cases are multiple, mostly located on the same side of the same blood vessels (mirrible aneurysm ).
The frequency of aneurysm rupture is: internal carotid artery and bifurcation 40%, anterior cerebral artery and anterior communicating artery 30%, middle cerebral artery and branch 20%, vertebral-basal artery and branch 10%, posterior circulation is common in basilar artery tip And the inferior cerebellar artery.
The ruptured aneurysm is irregular or polycystic, often ruptured in the aneurysm, other congenital abnormalities such as polycystic kidney disease and aortic coarctation often associated with miliary aneurysm, infective endocarditis spread to The cerebral arteries can cause "mycotic" aneurysms, which account for 2% to 3% of ruptured aneurysms. They are more common in the distal part of the cerebral artery. Arteriovenous malformations are formed by abnormal vascular communication, and arterial blood does not enter directly through the capillary bed. The venous system is common in the distribution of the middle cerebral artery.
2, gross and microscopic pathological changes
The blood enters the subarachnoid space, so that the cerebrospinal fluid is stained with blood. Some or the whole brain surface is purple-red. The red blood cells are deposited in the brain pool and the sulci, so the staining is deeper, the blood volume is large, and the brain surface can be covered with a thin layer of blood clots. Blood clots and blood accumulation can be seen at the bottom, brain pool, cerebral sulcus, etc., with the most obvious at the bottom of the brain, even burying blood vessels and nerves. As the disease progresses, red blood cells dissolve and release hemosiderin, which makes the meninges and cerebral cortex appear. Different degrees of rust color, but also different local adhesions.
Early microscopically, the cells reacted and phagocytized, and fibroblasts gradually entered the blood clot, and finally formed a scar that blocked the subarachnoid space.
Microscopic examination, meningeal reaction can occur 1 to 4 hours after hemorrhage, a small amount of polymorphonuclear leukocyte aggregation can be seen around the pia mater, 4~6h polymorphonuclear cell reaction is strong, 16~32h there are a lot of white blood cells and lymphocytes. It can be seen that the destruction of white blood cells is partly in the subarachnoid space, and some in the cytoplasm of phagocytic cells and leukocytes. After 3 days of hemorrhage, all kinds of inflammatory cells participate in the reaction, and the polymorphonuclear leukocyte reaction reaches the peak, lymphatic. The cells and phagocytic cells increased rapidly. In the phagocytic cells, intact red blood cells, hemosiderin particles and denatured white blood cells were observed. After 7 days, polymorphonuclear leukocytes disappeared, lymphocytes infiltrated, and phagocytic cells phagocytized actively, although there were some complete The red blood cells, but mostly the decomposition products of heme, after 10 days, different degrees of fibrous tissue gradually immersed in the blood clot, forming a layer of scar tissue.
3. Pathogenesis of cerebral vasospasm after subarachnoid hemorrhage
Regarding the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage, mechanical factors, neurological factors and chemical factors are currently considered.
(1) Mechanical factors: Stimulation of the internal carotid artery of the dog, vertebral-basal artery can cause vasospasm, presumably when the subarachnoid hemorrhage, due to the impact of bleeding, clot compression, cerebral edema, ventricular dilatation Pulling, etc., may be a common mechanical stimulus, and this mechanical stimulus often only causes transient local cerebral vasospasm.
(2) Neurological factors: Animal experiments confirmed that sympathetic hyperfunction was observed in subarachnoid hemorrhage, and the incidence of myocardial ischemia or infarction and hypertension was significantly increased. It is believed to be due to sympathetic nerve after subarachnoid hemorrhage. Hyperthyroidism leads to increased levels of norepinephrine, which simultaneously causes changes in hypertension and myocardial ischemia, while sympathetic hyperactivity can cause cerebral vasospasm. In addition, there are some arachnoid filaments in the blood vessels of the subarachnoid space. Membrane nerve fiber knots, when the mechanical action of bleeding causes the blood vessels to shift or expand the subarachnoid space, or when the broken blood flows into the subarachnoid space, these nerve fiber knots can cause vasoconstriction and cause vasospasm.
(3) Chemical factors:
1 vasospasm of the nervous media: Most scholars believe that the destruction of platelet cells is the main cause of vasospasm, due to subarachnoid hemorrhage, platelet lysis in the subarachnoid space, release of vasoconstrictor neurotransmitter catecholamines and 5 - caused by serotonin.
2 Endothelin (ET): In recent years, studies have shown that patients with cerebrospinal fluid (CSF) and plasma ET levels increase after subarachnoid hemorrhage, speculation that vasospasm and delayed cerebral ischemia may be ET to make the cerebral artery continue to shrink Caused.
3 Other factors: The factors involved in the formation of delayed vasospasm are more complicated. Through clinical and animal experiments, it has been reported that various substances include oxygen free radicals, lipid peroxides, bilirubin metabolites, and arachidonic acid. And acetylcholine can cause sustained contraction and degeneration of vascular smooth muscle, and the abnormal release of these substances is mainly because red blood cells release a large amount of oxyhemoglobin after entering the subarachnoid space, so it is suggested that acute sputum is released by platelets 5- Caused by serotonin, chronic sputum is caused by oxyhemoglobin, and these are closely related to blood entering the subarachnoid space.
Prevention
Prevention of subarachnoid hemorrhage
Young and middle-aged people should improve their awareness of disease prevention, develop good habits such as quitting smoking, avoiding alcohol, eating a balanced diet, regular living, and smooth stools. Usually, they should work and rest, exercise moderately, maintain a peace of mind, and actively treat diseases such as high blood pressure. . For patients with suspected subarachnoid hemorrhage, those with conditions can choose CT scan of the brain. CT scan can not confirm the lumbar puncture and cerebrospinal fluid examination. In the event of discomfort, patients should try to avoid emotional or mental stress and go to a regular hospital for medical treatment.
Complication
Subarachnoid hemorrhage complications Complications
1, acute obstructive hydrocephalus
It is an important and serious complication of subarachnoid hemorrhage. It refers to hydrocephalus caused by acute or subacute ventricle enlargement within a few hours to 7 days after subarachnoid hemorrhage. The ventricle system is filled with blood and is an acute ventricle. Prerequisites for expansion, causing cerebrospinal fluid circulation pathway to lead to sudden increase in intracranial pressure, is one of the main causes of death after subarachnoid hemorrhage, acute obstructive hydrocephalus, suggesting a poor prognosis, such as early detection of double Lateral ventricle dilatation, lumbar puncture pressure can not be high, suggesting acute obstructive hydrocephalus, should immediately drain the ventricles, and sometimes can turn to safety.
In addition to severe headache, frequent vomiting, and meningeal irritation, acute hydrocephalus often has increased intracranial hypertension, such as aggravation of consciousness, especially in 3 days after subarachnoid hemorrhage, coma gradually disappears, pupils shrink, and light reflexes disappear or disappear. The condition deteriorated.
2, normal intracranial pressure hydrocephalus
It refers to the enlargement of the ventricles after a few weeks or years after the subarachnoid hemorrhage. It is a clinical syndrome caused by various reasons, also known as occult hydrocephalus, low-stress hydrocephalus, and traffic-induced brain accumulation. Water or brain water dementia.
The pathogenesis of normal intracranial pressure hydrocephalus is that the normal intracranial pressure can be caused by normal intracranial pressure, which can cause normal cranial pressure hydrocephalus outside the ventricular system, that is, in the brain basement pool or the convex surface of the brain. The three main signs of hydrocephalus are mental disorders, gait abnormalities and urinary incontinence, and personality changes, epilepsy, extrapyramidal symptoms, strong grip reflexes, sucking reflexes, etc., and central paralysis in the late lower extremities.
Symptom
Symptoms of subarachnoid hemorrhage Common symptoms Irritability, irritability, nausea, phobia, intestinal peristalsis, reduction of back pain, dizziness, arachnoid, thickening, fundus, sensory disturbance
(A) headache and vomiting: sudden severe headache, vomiting, pale face, body cold sweat. Such as headache limitations have a certain meaning in somewhere, such as the former headache prompts the cerebellum and cerebral hemisphere (unilateral pain), the posterior headache indicates posterior cranial fossa lesions.
(2) Disorders of consciousness and mental symptoms: Most patients have unconsciousness, but they may have irritability. Critically ill people may have embarrassment, varying degrees of confusion and coma, and a small number of seizures and psychiatric symptoms may occur.
(3) Meningeal irritation sign: Young and middle-aged patients are more common and obvious, accompanied by neck and back pain. Older patients, early bleeding or deep coma may have no meningeal irritation.
(4) Other clinical symptoms: such as low fever, low back pain and so on. It can also be seen with hemiparesis, visual impairment, cranial nerve palsy of III, V, VI, VII, retinal flaky hemorrhage and papilledema. In addition, gastrointestinal bleeding and respiratory infections can be complicated.
(5) Laboratory examination: the intracranial pressure of the lumbar puncture is increased, the early stage of the cerebrospinal fluid is bloody, and the yellowing begins after 3 to 4 days. In the early stage of the disease, the white blood cells in the peripheral blood of some patients may be increased, and more often accompanied by nuclear left shift. Electrocardiogram can have arrhythmia, and tachycardia and conduction block are more common. The CT scan of the skull within 4 days, the positive rate was 75-85%, which showed that the pool of the skull base, the longitudinal fissure of the brain and the density of the sulcus increased. The thicker part of the blood may indicate that the ruptured artery is located at or near the ruptured artery.
Examine
Examination of subarachnoid hemorrhage
Laboratory inspection
1, blood routine, urine routine and blood sugar
In patients with severe subarachnoid hemorrhage, white blood cells can be seen in the blood routine examination, and urine sugar and urine protein can be positive. The acute blood sugar level is caused by stress reaction. The blood sugar elevation not only directly reflects the metabolic state of the body, but also Reflecting the severity of the disease, the higher the blood sugar, the higher the incidence of complications such as stress ulcer, metabolic acidosis, and azotemia, the worse the prognosis.
2, cerebrospinal fluid
Uniform blood cerebrospinal fluid is the main indicator for the diagnosis of subarachnoid hemorrhage. Pay attention to the lumbar puncture immediately after onset. Since the blood has not entered the subarachnoid space, the cerebrospinal fluid is often negative. After the patient has obvious meningeal irritation, or the patient After a few hours, the positive rate of lumbar puncture will be significantly improved, and the cerebrospinal fluid will be homogeneous and bloody without clots.
The vast majority of subarachnoid hemorrhage cerebrospinal fluid pressure increased, mostly 200 ~ 300mmH2O, individual patients with low cerebrospinal fluid pressure, may be blocked by the blood clot subarachnoid space.
The protein content in cerebrospinal fluid can be increased to 1.0g/dl. The protein increases most in 8-10 days after hemorrhage, and then gradually decreases. The content of sugar and chloride in cerebrospinal fluid is mostly within the normal range.
There are three characteristic evolutions of white blood cells in cerebrospinal fluid after subarachnoid hemorrhage in different periods:
The neutrophil-based blood cell reaction in cerebrospinal fluid from 16 to 72 hours was significantly reduced after 72 hours, and gradually disappeared after 1 week.
Lymphocyte-mononuclear phagocytic response occurred in 23 to 7 days, and immune activated cells were significantly increased, and red blood cell phagocytic cells appeared.
The hemosiderin phagocytic cells began to appear in the cerebrospinal fluid for 33 to 7 days, and gradually reached a peak in 14 to 28 days.
Film degree exam
Brain CT scan or MRI examination: clinically suspected SAH is the first choice for CT examination, safe, sensitive, and early diagnosis. The sensitivity of the day of bleeding is high. More than 90% of SAH can be detected, showing the lateral cerebral cistern, anterior longitudinal fissure pool. High-density hemorrhage signs in the upper saddle pool, bridge cerebral angle pool, ring pool and posterior longitudinal fissure pool, and can determine intracerebral hemorrhage or ventricular hemorrhage, with hydrocephalus or cerebral infarction, can dynamically observe the condition, CT enhancement can be found large Most arteriovenous malformations and large aneurysms, MRI can detect small arteriovenous malformations of the brainstem, but it should be noted that the acute phase MRI of SAH may induce rebleeding. CT can show that about 15% of patients have only a small amount of bleeding in the middle brain ring pool. Non-aneurysmal SAH (non aneurysmal SAH, nA-SAH).
A CT scan or MRI may be performed in one of the following cases to prompt or exclude the disease:
1 clinical manifestations suspected of intracranial hemorrhage.
2 Patients with partial seizures or a history of generalized seizures.
3 have a history of chronic episodes or progressive neurological dysfunction, such as partial movement or sensory disturbance.
4 have a history of chronic headache, other reasons are not well explained.
Diagnosis
Diagnosis and diagnosis of subarachnoid hemorrhage
The diagnosis of this disease is relatively easy, such as sudden severe headache and vomiting, pale, cold sweat, meningeal stimulation positive and blood cerebrospinal fluid or head CT see the skull base pool, cerebral longitudinal fissure and blood in the sulci. A few patients, especially the elderly, headache and other clinical symptoms are not obvious, should pay attention to avoid missed diagnosis, timely lumbar puncture or CT scan can confirm the diagnosis.
Through medical history, neurological examination, cerebral angiography and CT scan, it can assist in the diagnosis and differential diagnosis. In addition to identification with other cerebrovascular diseases, it should be identified with the following diseases:
1 Meningitis: There are symptoms of systemic poisoning, there is a certain process of onset, and cerebrospinal fluid is inflammatory.
2 cerebral venous sinus thrombosis: more in the postpartum onset or pre-existing infection history, facial and scalp visible vein dilatation, meningeal stimulation sign negative, cerebrospinal fluid generally no blood changes.
