spontaneous subarachnoid hemorrhage
Introduction
Introduction to spontaneous subarachnoid hemorrhage Spontaneous subarachnoid hemorrhage is a syndrome caused by sudden rupture of the cerebral blood vessels caused by various reasons, causing blood to enter the subarachnoid space of the brain or spinal canal. It is not a disease but some The clinical manifestations of the disease, 70% to 80% of which belong to the surgical category, clinically divided subarachnoid hemorrhage into two categories: spontaneous and traumatic. Described here is spontaneous subarachnoid hemorrhage, accounting for about 15% of acute cerebrovascular accidents. There are many causes of spontaneous subarachnoid hemorrhage, the most common is intracranial aneurysm and arteriovenous malformation rupture, accounting for 57%, followed by hypertensive cerebral hemorrhage, but some patients still can not find the cause during autopsy, may be aneurysm Or after a small arteriovenous malformation (AVM) rupture, blood clots form without leaving traces. In addition, most autopsy does not examine the venous system or the subarachnoid space of the spinal cord, both of which may be the cause of bleeding. basic knowledge The proportion of the disease: the probability of the population is 0.24% Susceptible people: no specific population Mode of infection: non-infectious Complications: arrhythmia pulmonary edema thrombosis disturbance of consciousness
Cause
Causes of spontaneous subarachnoid hemorrhage
Causes:
Aneurysm (52%):
Aneurysms are the most common cause of bleeding, and large-scale literature shows that aneurysm bleeding accounts for 52% of patients with subarachnoid hemorrhage. In addition, there are still some people who can't find the cause of death, and their proportion is affected by the diagnostic conditions, which was as high as 46.3% in the past. With the advancement of examination methods, the detection rate of the cause of subarachnoid hemorrhage increased, and the proportion of unexplained causes decreased by 9% to 20%. Blood diseases, intracranial infections, drug poisoning, etc. caused by subarachnoid hemorrhage are also occasionally seen.
Smoking (15%):
Smoking is an important factor in spontaneous subarachnoid hemorrhage. About half of cases of subarachnoid hemorrhage are related to smoking and are dose-dependent. The risk factor for subarachnoid hemorrhage in regular smokers is 11.1 times that of non-smokers, and male smokers are more likely to develop the disease. Within 3 hours after smoking, it is the most prone to subarachnoid hemorrhage.
Alcohol abuse (15%):
Alcoholism is also a good cause of subarachnoid hemorrhage, and it is also dose-dependent. The incidence of rebleeding and vasospasm is significantly increased, and the prognosis of subarachnoid hemorrhage is affected.
(two) pathogenesis
Pathology
(1) Meninges and brain reaction: blood flows into the subarachnoid space, so that the cerebrospinal fluid is red-stained, the surface of the brain is purple-red, the blood is in the cerebral cistern, and the cerebral sulcus is deposited. The closer the hemorrhage is, the more blood is accumulated, such as the lateral fissure. The pool, the optician pool, the longitudinal fissure pool, the bridge cerebellum pool and the occipital pool, etc., the blood can flow into the subarachnoid space of the spinal cord, and even flow back into the ventricular system. The position of the head can also affect the accumulation of blood, and the supine position is affected by gravity. Blood tends to accumulate in the posterior fossa. Blood clots, such as in the brain parenchyma, lateral fissures and longitudinal fissures, can compress brain tissue. In a few cases, the blood breaks out of the subarachnoid space and forms a subdural hematoma. Over time, red blood cells dissolve. Releases hemosiderin, yellowing the cerebral cortex, part of the red blood cells along with the cerebrospinal fluid, entering the arachnoid granules, causing the latter to clog, producing traffic hydrocephalus, multinucleated white blood cells, lymphocytes can appear in the hours after bleeding In the subarachnoid space, macrophages also participated in the reaction after 3 days. After 10 days, fibrosis occurred in the subarachnoid space. In patients with severe subarachnoid hemorrhage, the hypothalamus could be hemorrhagic or ischemic.
(2) changes in arterial wall: pathological changes in the arterial wall after hemorrhage include: typical vasoconstriction changes (thickening of the wall, folding of the inner elastic layer, vacuolation of endothelial cells, shortening and folding of smooth muscle cells) and disappearance of endothelial cells, Platelet adhesion, smooth muscle cell necrosis, vacuolization, fibrosis, adventitial fibrosis, inflammatory reaction, etc. cause arterial lumen stenosis. Although there are differences in pathological changes of cerebral vasospasm, cerebral vasospasm is simple vascular smooth muscle contraction. Or the blood vessel wall has the above pathological changes, leading to stenosis of the lumen, but the consensus is that 3 to 7 days after the bleeding (in the early stage of vasospasm) may be caused by abnormal smooth muscle contraction, and the structure of the artery wall with time Changes play a major role in luminal stenosis.
(3) Others: In addition to myocardial infarction or endocardial hemorrhage, there may be pulmonary edema, gastrointestinal bleeding, fundus hemorrhage, etc. The intracranial pathological changes after subarachnoid hemorrhage are shown in Table 2.
2. Pathophysiology
(1) intracranial pressure: subarachnoid hemorrhage caused by rupture of aneurysm during intracranial pressure will increase sharply, when the amount of bleeding is large, diastolic blood pressure level can be reached, causing a brief interruption of intracranial blood circulation, at this time clinically There are often disturbances of consciousness, and the effect of high intracranial pressure on subarachnoid hemorrhage is both beneficial and disadvantageous: on the one hand, high intracranial pressure can prevent further bleeding, which is conducive to hemostasis and prevent rebleeding; on the other hand, it can cause severe whole brain. Temporary ischemia and cerebral metabolic disorders, studies have shown that when the condition worsens, intracranial pressure increases; intracranial pressure in patients with vasospasm is higher than those without vasospasm; patients with intracranial pressure >15mmHg have worse prognosis than intracranial pressure <15mmHg Patients with mild clinical symptoms, after a brief increase in intracranial pressure, can quickly return to normal <15mmHg; patients with severe clinical symptoms, intracranial pressure continue to increase >20mmHg, and B wave can appear, indicating brain compliance Decreased, the exact mechanism of intracranial pressure rise after subarachnoid hemorrhage is unknown, may be related to the subarachnoid blood clot, cerebrospinal fluid circulation obstruction, diffuse vasoparalysis and small blood vessel expansion in the brain.
(2) cerebral blood flow, brain metabolism and brain autoregulation function: due to factors such as cerebral vasospasm, intracranial pressure and cerebral edema, the supply of cerebral blood flow (CBF) decreased after subarachnoid hemorrhage, which is 30 %40%, the cerebral oxygen metabolism rate (CMRO2) is reduced, about 75% of the normal value, and the regional cerebral blood volume (rCBV) is increased due to cerebral blood vessels, especially small blood vessels, accompanied by cerebral vasospasm and loss of nerve function. The above changes are particularly significant. Studies have shown that a simple increase in intracranial pressure of 60 mmHg leads to a decrease in CBF and rCMRO2, but subarachnoid hemorrhage has been observed before the increase in intracranial pressure, which is exacerbated by increased intracranial pressure. Changes, the World Congress of Neurosurgical Union grade I ~ II non-cerebral vasospasm CBF is 42ml / (100g · min) [normal 54ml / (100g · min)], if there is cerebral vasospasm, 36ml / (100g · min The CBF of grade III-IV without cerebral vasospasm is 35ml/(100g·min), and the cerebral vasospasm is 33ml/(100g·min), and the cerebral blood flow drops to the lowest point after 10-14 days after hemorrhage. After that, it will slowly return to normal. This process is longer in critically ill patients, and the intracranial pressure is elevated. Drop, can cause cerebral perfusion pressure (CPP) drop, caused by cerebral ischemia, especially for CBF has been at the critical level of ischemic brain tissue more vulnerable to ischemic damage.
The brain autoregulation function is impaired after subarachnoid hemorrhage, and cerebral blood flow fluctuates with systemic blood pressure, which can cause brain edema, hemorrhage or cerebral ischemia.
(3) Biochemical changes: biochemical changes in the brain include: lactic acidosis, generation of oxygen free radicals, activation of apoptotic pathways, changes in glial function, imbalance of ion balance, intracellular energy production and transport disorders, etc. Cerebral ischemia and energy metabolism disorders after subarachnoid hemorrhage, due to bed rest, fasting, vomiting and application of dehydrating agents, as well as hypothalamic dysfunction, increased blood urinary hormones in patients, etc., can cause systemic electrolyte abnormalities, among which the most Common are:
1 hyponatremia: seen in 35% of patients, often occurs in the second to 10 days of onset, hyponatremia can aggravate disturbance of consciousness, epilepsy, cerebral edema, causing hyponatremia mainly due to cerebral salt loss syndrome and ADH secretion Abnormalities, it is very important to distinguish them, because the former due to excessive urinary sodium excretion leads to hyponatremia and hypovolemia, the treatment should be input with physiological saline and colloidal solution; the latter is caused by increased secretion of ADH, dilute hyponatremia and water load Increased, treatment should limit water and the application of drugs that inhibit ADH such as phenytoin injection.
2 high blood sugar: subarachnoid hemorrhage can cause hyperglycemia, especially in the original diabetic patients, the application of steroids can aggravate hyperglycemia, severe hyperglycemia can be complicated by epilepsy and disturbance of consciousness, aggravating ischemia and hypoxia and nerve Meta damage.
(4) cerebral vasospasm: the most common subarachnoid hemorrhage caused by aneurysm rupture, can also be seen in other lesions such as brain movement, venous malformation, tumor hemorrhage caused by subarachnoid hemorrhage, the exact pathological mechanism of vasospasm It is not clear, but the degradation process of red blood cells in the subarachnoid space is consistent with the occurrence time of clinical vasospasm, suggesting that the degradation products of red blood cells are cariogenic substances. It is currently believed that the hemoglobin degradation product oxidized hemoglobin plays a major role in vasospasm, except It can directly cause cerebral vasoconstriction, and can also stimulate the production of vasoconstrictors such as endothelin-1 (ET-1), and inhibit the formation of endogenous vasodilators such as nitric oxide, and further degradation products such as superoxide anion residues. Oxygen free radicals such as hydrogen peroxide can cause lipid peroxidation, stimulate smooth muscle contraction, induce inflammation (prostaglandins, leukotrienes, etc.), activate immune responses (immunoglobulin, complement system) and cytokines (white blood cells) Interleukin-1) thus aggravates vasospasm.
(5) Other:
1 blood pressure: elevated blood pressure in subarachnoid hemorrhage may be a compensatory response of the body, in order to increase cerebral perfusion pressure, pain, irritability and hypoxia and other factors can also promote systemic blood pressure, due to elevated blood pressure can induce Rebleeding, so try to control your blood pressure to keep it within the normal range.
2 heart: 91% of subarachnoid hemorrhage patients have abnormal heart rhythm, a few of which can cause ventricular tachycardia, ventricular fibrillation and other life-threatening patients, especially in the elderly, low potassium and electrocardiogram on the QT interval prolongation, heart rhythm and Abnormal heart function can aggravate cerebral ischemia and hypoxia, which should be paid attention to.
3 Gastrointestinal tract: About 4% of patients with subarachnoid hemorrhage have gastrointestinal bleeding. Among the deaths of anterior communicating aneurysms, 83% have gastrointestinal bleeding and stress ulcers.
Prevention
Spontaneous subarachnoid hemorrhage prevention
Prevention of risk factors, attention to smoking cessation, restriction of drinking, control of blood pressure, active treatment of diabetes, hyperlipidemia are all conducive to the prevention of spontaneous subarachnoid hemorrhage.
Complication
Spontaneous subarachnoid hemorrhage complications Complications, arrhythmia, pulmonary edema, thrombosis, consciousness
1. Nervous system complications:
(1) Delayed ischemic disorder: also known as symptomatic cerebral vasospasm. Because cerebral angiography or TCD suggests cerebral vasospasm, clinical symptoms are not necessarily present, only in the case of cerebral collateral circulation When rCBF<1820ml/(100g·min), it causes delayed ischemic disorder. Therefore, the incidence of cerebral vasospasm after cerebral angiography and TCD diagnosis of subarachnoid hemorrhage can reach 67%, but it is delayed. The incidence of ischemic disorders is 35%, and the mortality rate is 10% to 15%. Angiography shows vasospasm often occurs 2 to 3 days after subarachnoid hemorrhage, 7 to 10 days is the peak, 2 to 4 Weekly easing, the occurrence of cerebral vasospasm has a certain relationship with the amount of blood in the cerebral cistern on the head CT, the clinical manifestations of delayed ischemic disorders:
1 prodromal symptoms, the symptoms of subarachnoid hemorrhage after treatment or rest and improved or appear or progressive aggravation, blood white blood cells continue to increase, continue to fever.
2 Consciousness from waking to sleepiness or coma.
3 focal signs, depending on the location of cerebral ischemia.
For example, in the distribution of the internal carotid artery and middle cerebral artery, hemiplegia may or may not be accompanied by hypoesthesia or hemianopia. The anterior cerebral artery involvement may result in decreased recognition and judgment ability, lower limb paralysis, varying degrees of consciousness disorder, and no motion silence. Vertebral-based arteries cause pyramidal tract signs, cranial nerve signs, cerebellar signs, autonomic dysfunction, hemianopia or cortical blindness. These symptoms develop slowly and reach peaks in a few hours or days, after 1 to 2 weeks. Gradually relieved, a small number of rapid development, poor prognosis, once the above clinical manifestations, should be done head CT, exclude rebleeding, hematoma, hydrocephalus, etc., and do TCD and cerebral angiography for diagnosis, CT shows that cerebral infarction helps Diagnosis, in addition, water and electrolyte disorders, liver and kidney dysfunction, pneumonia and diabetes and other systemic diseases should also be excluded.
(2) Rebleeding: It is the main cause of death and disability in patients with subarachnoid hemorrhage. The mortality rate can be as high as 70% to 90%. The peak of rebleeding is 48h after the first hemorrhage, and the bleeding rate is 20% to 30% within 2 weeks. Later, it gradually decreased, and the bleeding rate was 3% after half a year.
(3) hydrocephalus: the incidence of hydrocephalus in the acute phase of bleeding is about 20%, often accompanied by ventricular hemorrhage, and hydrocephalus in the late hemorrhage is associated with cerebrospinal fluid malabsorption. The incidence of chronic hydrocephalus has been reported. The difference is large, ranging from 6% to 67%, mainly related to the criteria for hydrocephalus and the evaluation time. Patients with a history of rebleeding and ventricular hemorrhage have more chances of hydrocephalus.
2. Systemic system complications:
Severe systemic complications are the cause of death in 23% of subarachnoid hemorrhage, which occurs in critically ill patients and high-grade patients. Therefore, the importance of systemic complications after prevention and treatment of subarachnoid hemorrhage and delayed onset of prevention and treatment Blood disorders are as important as rebleeding and should be taken seriously.
(1) water, electrolyte disorder: common hyponatremia, seen in 35% of patients, occurs in the second to 10 days after bleeding, can aggravate disturbance of consciousness, epilepsy, cerebral edema, cause hyponatremia: brain salt loss synthesis Syndrome and urinary hormone secretion abnormal syndrome (SIADH), should pay attention to the identification of the above two syndromes, because the two principles of treatment are completely different.
Low blood volume is also a common complication after subarachnoid hemorrhage. In more than 50% of patients, the blood volume can be reduced by more than 10% in the first 6 days after subarachnoid hemorrhage, and the blood volume is reduced, which can increase the viscosity of red blood cells. The stagnation affects the brain microcirculation, increases the susceptibility to vasospasm, and expands the blood pressure to prevent delayed ischemic disorders caused by vasospasm.
(2) Hyperglycemia: Subarachnoid hemorrhage can cause high blood sugar, especially in elderly patients with recessive diabetes. The use of steroids can aggravate hyperglycemia, and severe hyperglycemia can cause disturbance of consciousness, epilepsy, and worsening the brain. Vasospasm and cerebral ischemia.
(3) Hypertension: Most patients with subarachnoid hemorrhage have a compensatory blood pressure (Cushing reaction), which reduces the cerebral perfusion pressure after responding to hemorrhage, but the blood pressure is too high (the systolic blood pressure is maintained above 180-200mmHg). ) can induce rebleeding, especially inappropriately reduce intracranial pressure, while not controlling blood pressure, excitement, irritability, pain and hypoxia can promote blood pressure.
3. Other organ complications in the body:
(1) Heart: Arrhythmia is common in 91% of patients, advanced age, hypokalemia, electrocardiogram with prolonged QT interval is prone to arrhythmia, common ventricular, supraventricular tachycardia, migratory rhythm, bundle branch resistance Hysteresis, mostly benign processes, but a small number of patients are life-threatening due to ventricular tachycardia, ventricular fibrillation, and room flutter. Previously, the clinical significance of arrhythmia was not significant, but it is currently considered that the above arrhythmia suggests subarachnoid hemorrhage. Induced myocardial damage, about 50% of patients may have ECG abnormalities, such as T wave inversion, ST segment depression, QT interval prolongation, U wave appears.
(2) Deep vein thrombosis: About 2% of patients with subarachnoid hemorrhage, about half of them can have pulmonary embolism.
(3) Gastrointestinal bleeding: About 4% of patients with subarachnoid hemorrhage have gastrointestinal bleeding, and 83% of patients who died of anterior communicating aneurysm bleeding have gastrointestinal bleeding and gastroduodenal ulcer.
(4) Pulmonary: The most common pulmonary complications are pneumonia and pulmonary edema. Neuropathic pulmonary edema is characterized by irregular breathing, pink foamy secretions in the respiratory tract, and high protein content (>45g/L). 2% of patients with subarachnoid hemorrhage, the most common in the first week after subarachnoid hemorrhage, the exact cause is unclear, and the capillary contraction of the lungs after subarachnoid hemorrhage, vascular endothelium damage, permeability Increase related.
Symptom
Symptoms of spontaneous subarachnoid hemorrhage Common symptoms Cold and cold back pain Arachnoid cysts Sensory disorder Single nausea and vomiting Ocular nerve palsy Dead coma
Subarachnoid hemorrhage is the most common cause of sudden death caused by stroke. Many patients died on the way to hospital. The mortality rate before admission was 3% to 26%. The causes of death were intraventricular hemorrhage, pulmonary edema and rupture of vertebral-basal artery aneurysm. Etc. Even if sent to the hospital, some patients died before definitive diagnosis and specialist treatment. In the 1985 literature, only 35% of patients after aneurysm rupture received neurosurgery within 48 hours after symptoms and signs of subarachnoid hemorrhage. Corresponding treatment.
1. Inducing factors: About 1/3 of aneurysm rupture occurs in strenuous exercise, such as: weightlifting, emotional agitation, cough, bowel movements, sexual intercourse, etc. As mentioned above, smoking, drinking is also subarachnoid hemorrhage Risk factors.
2. Aura: unilateral eyelid or post-balloon pain with oculomotor nerve palsy is a common aura, headache frequency, duration or intensity change is often a precursor to aneurysm rupture, seen in 20% of patients, sometimes accompanied by nausea, vomiting and dizziness, However, meningeal irritation and photophobia are rare, usually caused by a small amount of subarachnoid oozing, or due to blood breaking into the aneurysm dissection, the tumor wall is acutely dilated or ischemic, occurs 2 hours before the true subarachnoid hemorrhage ~ Within 8 weeks.
3. Typical performance:
More sudden or sudden, mainly have the following symptoms and signs:
(1) headache: seen in 80% to 95% of patients, sudden, cleft palate-like pain, throughout the head or forehead, occipital, and then extend the neck, shoulder and back and lower limbs, etc., Willis ring anterior aneurysm The headache caused by rupture can be confined to the ipsilateral frontal and eyelids, flexion of the neck, active head and Valsalva test, as well as sound and light can aggravate pain. Resting in bed can relieve pain. There are often incentives before the onset of headache: strenuous exercise, breath holding Action or sexual life, accounting for about 20% of the number of cases.
(2) nausea and vomiting, pale, cold sweat, about 3/4 of the patients developed headache, nausea and vomiting after the onset.
(3) Disorder of consciousness: When seen in more than half of the patients, there may be a transient ambiguity to coma, 17% of patients are in a coma at the time of presentation, and a few patients may change unconsciously, but there are signs of fear, indifference, fear of noise and vibration. .
(4) Psychiatric symptoms: manifested as convulsions, stupor, disorientation, fiction and dementia.
(5) Epilepsy: seen in 20% of patients.
(6) Signs: 1 Meningeal irritation, about 1/4 of patients may have neck pain and neck stiffness, appear in the hours of the disease to 6 days, but most often in 1 to 2 days, Kernig sign is more common than neck. 2 unilateral or bilateral pyramidal tract disease. 3 fundus hemorrhage: manifested as subglacial flaky hemorrhage, more common in anterior communicating aneurysm rupture, due to increased ICP and clot oppression of the optic nerve sheath, causing central retinal vein hemorrhage, this sign has special significance, because after the cerebrospinal fluid returns to normal, it still Existence is one of the important basis for the diagnosis of subarachnoid hemorrhage. Optic disc edema is rare. Once it appears, it indicates intracranial space-occupying lesions. Because of intraocular hemorrhage, the patient's visual acuity often decreases. 4 focal signs, usually lacking, may have one side of oculomotor nerve paralysis, single or partial hemiplegia, aphasia, sensory disturbances, visual field defects, etc., they may indicate the primary disease and location or due to hematoma, cerebral vasospasm.
4. Atypical performance:
(1) A small number of patients have no headache at the onset, showing nausea, vomiting, fever and general malaise or pain. Others show chest and back pain, leg pain, sudden loss of vision and hearing.
(2) Characteristics of subarachnoid hemorrhage in the elderly: 1 less headache (<50%) and not obvious; 2 more disturbance of consciousness (>70%) and weight; 3 neck toughness is more common than Kernig.
(3) characteristics of children with subarachnoid hemorrhage: 1 less headache, but should be paid attention to once; 2 often with systemic lesions, such as aortic arch stenosis, polycystic kidney disease.
Examine
Spontaneous subarachnoid hemorrhage
Lumbar puncture cerebrospinal fluid examination is also a common method for diagnosing subarachnoid hemorrhage, especially those with negative head CT examination, but the timing of lumbar puncture should be grasped. The cerebrospinal fluid obtained after lumbar puncture for several hours after subarachnoid hemorrhage may still be clear, so it should be Lumbar puncture examination was performed 2 hours after subarachnoid hemorrhage. The bleeding caused by operation injury was different from subarachnoid hemorrhage:
1. Continuous drainage, the red blood cell count in each tube is gradually reduced.
2. If the red blood cells are >25×1010/L, blood coagulation will occur.
3. No cerebrospinal fluid yellowing.
4. The RBC/WBC ratio is normal, and for every 1000 red blood cells added, the protein content is increased by 1.5 mg/100 ml.
5. There are no macrophages that phagocytose red blood cells or hemosiderin.
Cerebrospinal fluid yellowing is due to high protein content in the cerebrospinal fluid or erythrocyte degradation products, usually appear 12h after subarachnoid hemorrhage, spectrophotometer detection can avoid omission, generally the detection rate of cerebrospinal fluid yellowing 12h ~ 2 weeks after hemorrhage 100%, 70% after 3 weeks, 40% after 4 weeks, lumbar puncture is an invasive examination, which can induce rebleeding or aggravating symptoms. The pros and cons should be measured before operation, and the family members agree.
6. CT scan:
Head CT scan (Figure 1A) is currently the first choice for the diagnosis of subarachnoid hemorrhage, its role is:
(1) to determine the existence and extent of subarachnoid hemorrhage, to provide clues to the bleeding site.
(2) Enhanced CT examination, sometimes can determine the cause of subarachnoid hemorrhage, such as showing the effect of augmentation of AVM or aneurysm.
(3) can understand the accompanying brain, intraventricular hemorrhage or obstructive hydrocephalus.
(4) follow-up treatment effect and understanding of complications, the sensitivity of CT examination depends on the time and clinical grade after bleeding, 1h, more than 90% of cases can find hemorrhage in subarachnoid hemorrhage, 85% after 5 days The subarachnoid hemorrhage can still be detected from the CT slice, 50% after 1 week, 30% after 2 weeks, and the amount and location of subarachnoid hemorrhage on the CT slice are well correlated with the occurrence of vasospasm. The worse the classification, the more severe the bleeding on CT and the worse the prognosis.
Diagnosis
Diagnosis and diagnosis of spontaneous subarachnoid hemorrhage
diagnosis
First of all, it should be clear whether there is subarachnoid hemorrhage, sudden onset of headache, disturbance of consciousness and meningeal irritation and corresponding neurological damage symptoms, should be highly suspected subarachnoid hemorrhage, sudden headache should be caused by sudden headache, timely head CT examination, if necessary, lumbar puncture to clear bleeding.
Differential diagnosis
Symptoms such as auratic headache before subarachnoid hemorrhage should be noted and differentiated from migraine, hypertensive encephalopathy and other systemic diseases.
1. Sudden and severe headache caused by subarachnoid hemorrhage must be differentiated from the headache caused by the following diseases:
(1) Intracranial disease:
1 vascular: subarachnoid hemorrhage; pituitary apoplexy; venous sinus embolization; intracerebral hemorrhage; cerebral embolism.
2 infection: meningitis; encephalitis.
3 increased intracranial pressure caused by new organisms, intracranial hemorrhage or brain abscess.
(2) Benign headache:
1 migraine.
2 nervous.
3 infectious headaches.
4 benign fatigue headache.
5 headaches related to excitement.
(3) Headache from the cranial nerve:
1 due to tumors, aneurysms, Tolosa-Hunt sign, Raeder trigeminal neuralgia, Gradenigo sign causes brain nerve compression or inflammation.
2 neuralgia: trigeminal nerve; glossopharyngeal nerve.
(4) Intracranial involvement pain: 1 eyeball: post-ball neuritis; glaucoma, 2 paranasal sinusitis, 3 periodontal abscess, temporomandibular arthritis.
Systemic diseases: 1 malignant hypertension; 2 viral diseases; 3 cervical spinal cord AVF, can cause subarachnoid hemorrhage, for DSA intracranial examination, spinal angiography should be done.
2. Identification of subarachnoid hemorrhage and intracranial hemorrhage or ischemic stroke from clinical manifestations is sometimes difficult, generally with meningeal irritation, lack of focal neurological symptoms and relatively young age (<60 years), subarachnoid Cavitation bleeding is more likely, sudden headache and vomiting are not unique symptoms of subarachnoid hemorrhage, often can not be used as a basis for differential diagnosis of intracranial hemorrhage or ischemic stroke, epilepsy in patients with subarachnoid hemorrhage The incidence is similar to that of patients with intracranial hemorrhage, but epilepsy is less common in patients with ischemic stroke.
3. After the diagnosis of spontaneous subarachnoid hemorrhage, the cause of subarachnoid hemorrhage should be diagnosed mainly by cerebral angiography or 3D-CTA, but the first cerebral angiography can be 15% to 20% of patients can not A positive result was found, called "angiographically negative subarachnoid hemorrhage", in which 21% to 68% of patients showed only blood in front of the brain stem during CT scan, called "subarachnoid subarachnoid Cavity bleeding, which is a special, prognosis of spontaneous subarachnoid hemorrhage, accounting for about 10% of spontaneous subarachnoid hemorrhage, compared with patients with positive angiography, younger, male More, the clinical classification is better, the bleeding on CT is only in front of the brain stem, does not involve the sulci and ventricle, less vasospasm after rebleeding and hemorrhage, the prognosis is good, the cause of the disease is currently unknown, may be caused by venous hemorrhage, but the vertebra - Basilar artery aneurysm rupture and bleeding can also have similar CT findings, so it can not be easily diagnosed as "subarachnoid hemorrhage around the midbrain."
Cerebral angiography should be repeated in about 2 weeks for cerebral angiography-negative subarachnoid hemorrhage. The detection rate of etiology in the literature ranges from 2% to 22%.
4. When the cause of diagnosis of subarachnoid hemorrhage is multiple rupture of aneurysm, the ruptured tumor should be further identified. The following points are available for reference:
(1) Excluding epidural aneurysms.
(2) CT showed local subarachnoid hemorrhage.
(3) There is a vasospasm or mass effect near the aneurysm that ruptures in angiography.
(4) Large irregular irregular aneurysms are small and regular ones are prone to rupture.
(5) Positioning signs can help diagnose.
(6) Repeat angiography, see aneurysm enlargement and local vascular morphological changes.
(7) Select the most likely ruptured aneurysm, such as a anterior communicating aneurysm.
(8) The largest, the most proximal aneurysm is most likely to rupture.
