Subarachnoid hemorrhage refers to the rupture of blood vessels at the bottom of the brain or the superficial part of the brain, and blood directly enters the subarachnoid space. Arachnoid is a kind of meninges covering the brain surface, soaked in cerebrospinal fluid. Although the bleeding here is brain bleeding, it sometimes bleeds from this part. Because brain trauma can lead to subarachnoid hemorrhage. Spontaneous (primary) subarachnoid hemorrhage is usually caused by rupture of congenital intracranial aneurysm. It is rare, but as the primary disease, there are also bleeding caused by rupture of cerebral aneurysm and cerebral arteriovenous malformation. In youth, spider webs bleed under wax, and the latter is more common. It can also be caused by fungal (bacterial) aneurysms, atherosclerotic aneurysms, arteriovenous malformations or hemorrhagic diseases. Subarachnoid hemorrhage caused by ruptured aneurysm can occur at any age, but it is most common in the period of 40-65 years old. Primary subarachnoid hemorrhage is mostly congenital and almost impossible to predict in advance. Most of them were accompanied by severe headache and disturbance of consciousness before onset, and some of them died suddenly within five minutes. Some people survived by removing the cerebral hemisphere. It is still unclear why only part of the bleeding showed such a violent reaction. If there is blood in the concrete in cerebrospinal fluid, I'm afraid it will bring bad consequences. Before rupture, the aneurysm may not cause any symptoms, but early warning of leakage and bleeding is often accompanied by mild headache. Sudden severe headache, if CT scan or magnetic resonance imaging and cerebrospinal fluid examination are normal, there is generally no secondary subarachnoid hemorrhage; Tension headaches or migraines are more common. However, for any new headache, or headache whose primary headache has changed the nature of headache, further examination must be made to rule out subarachnoid hemorrhage caused by aneurysm rupture or aneurysm expansion. A few aneurysms can produce symptoms by compressing adjacent structures. Paralysis of the external eye muscle, diplopia, strabismus and facial pain indicate that the third, fourth, fifth and sixth cranial nerves are compressed. The decreased vision and bilateral temporal visual field defects suggest that the optic chiasma is compressed, and the compression of the optic bundle can cause bilateral inconsistent homonymous hemianopia. Once an aneurysm ruptures, there is usually a severe headache. Patients may have a headache as the only symptom, or they may show different degrees of nervous system disorder, or they may have a change of consciousness. Blood mixed with cerebrospinal fluid stimulates the meninges, leading to increased intracranial pressure, headache, vomiting, dizziness and changes in pulse and respiratory rate. Occasional seizures. There is usually no neck stiffness at the beginning of the disease, unless there is a case of cerebellar tonsil hernia into the foramen magnum. However, within 24 hours, moderate to severe neck stiffness, Kernig sign and bilateral babinski sign may occur. In the first 5- 10 days, the body temperature may increase; Patients often have persistent headaches and insanity. Because bleeding may also enter the brain parenchyma, or accompanied by vasospasm and ischemia, about 25% cases may have focal signs (generally including hemiplegia). Re-bleeding is very common in patients with untreated aneurysms.

Etiology, pathology and pathogenesis

Any cause that can cause cerebral hemorrhage can also cause this disease, but intracranial aneurysm, arteriovenous malformation, hypertensive arteriosclerosis, abnormal vascular network at the bottom of the brain (Moya-Moya disease) and hematological diseases are the most common. After subarachnoid hemorrhage, secondary intracranial pressure often increases, which can last for several days or weeks. Communicative hydrocephalus often occurs, which can cause headache or unresponsiveness or dementia after bleeding. It often happens when you are emotional or overexert. Aneurysms often occur in the branches of the great arteries in the basilar artery ring, especially in the first half of the ring. Arteriovenous malformations are mostly located in the distribution area of middle cerebral artery in the cerebral hemisphere. When blood from ruptured blood vessels flows into subarachnoid space of brain, the contents of cranial cavity increase, the pressure increases, and then cerebral vasospasm occurs. The latter is caused by extensive ischemic injury and edema of neuromuscular junctions formed between smooth muscle cells in the blood vessel wall due to the traction of blood clots and fibrous cords around the blood vessel wall after bleeding (mechanical factors). In addition, a large number of hematocele or blood clots are deposited on the skull base, and some agglutinated red blood cells can also block the small sulcus between arachnoid villi, which hinders the reabsorption of cerebrospinal fluid, thus causing acute communicating hydrocephalus, sharply increasing intracranial pressure, further reducing cerebral blood flow, aggravating brain edema, and even leading to the formation of cerebral hernia. All of the above can make the patient's condition improve steadily, and then there will be disturbance of consciousness or local neurological symptoms again. Most aneurysms are located on the Willis arterial ring at the base of skull, along the middle cerebral artery, anterior cerebral artery or anterior and posterior communicating artery. They usually occur at the bifurcation of arteries, where the muscular layer of arterial wall is underdeveloped, and arteriosclerosis and hypertension may also play a role in promoting them.

pathology

After blood enters subarachnoid space, cerebrospinal fluid stained with blood can stimulate brain tissues such as blood vessels, meninges and nerve roots, causing aseptic meningitis reaction. The surface of the brain is often covered with thin clots, and sometimes ruptured aneurysms or blood vessels can be found. With the passage of time, a large number of red blood cells began to dissolve, releasing hemosiderin, which made the pia mater rust, which was related to different degrees of adhesion. If the red blood cells in the sulcus dissolve and the sulcus between the arachnoid villi cells reopen, the absorption of cerebrospinal fluid can be restored.

Laboratory examination: Intracranial pressure increased after lumbar puncture, cerebrospinal fluid was bloody in the early stage, and began to yellow after 3 ~ 4 days. At the early stage of the disease, some patients' peripheral white blood cells can increase, and most of them are accompanied by nuclear left shift. Electrocardiogram may have arrhythmia, especially tachycardia and conduction block. Within 4 days, the positive rate of skull CT scan was 75-85%, which showed that the density of cistern, longitudinal fissure and sulcus of skull base increased, and the thicker hematocele suggested that it might be at or near the location of arterial rupture. Examination and diagnosis, CT scanning can often provide diagnostic basis, without lumbar puncture. However, if the bleeding is not extensive, subarachnoid hemorrhage may not be seen on CT scan. The diagnosis depends on lumbar puncture, and blood can be found in cerebrospinal fluid and the pressure is increased. Jaundice appeared in the supernatant of cerebrospinal fluid after centrifugation 6 hours or more after bleeding. Cerebrospinal fluid will gradually become clear unless it bleeds again; Moreover, unless hydrocephalus occurs, the cerebrospinal fluid pressure generally returns to normal in about 3 weeks. Acute subarachnoid hemorrhage is sometimes similar to myocardial infarction because it can be accompanied by syncope and abnormal ECG. Subarachnoid hemorrhage must be distinguished from cerebral hemorrhage (subarachnoid hemorrhage can often be accompanied by cerebral hemorrhage), arteriovenous malformation hemorrhage, brain contusion and laceration, subdural hematoma and sometimes brain tumor hemorrhage. In addition to CT scanning, cerebral arteriography is often needed to assist in differential diagnosis. Arteriography should be done as soon as possible after the first aneurysm rupture and bleeding. A whole cerebral angiography should be performed to show all four main cerebral arteries, because sometimes there are multiple cerebral aneurysms.

Diagnostic examination:

Cerebrospinal fluid: abnormal

Decreased serum osmotic pressure

Elevated antidiuretic hormone

Cerebrospinal fluid: LDH is elevated.

Cerebrospinal fluid: protein elevation.

Cerebrospinal fluid: erythrocytosis

Cerebrospinal fluid: yellowing

Cerebrospinal fluid: glucose decreased

Cerebrospinal fluid: aspartate aminotransferase increased.

Elevated blood sugar

differential diagnosis

Bacterial meningitis

tetanus

epidural hematoma

brain abscess

meningitis

Acute subdural hematoma/hemorrhage

It can happen at all ages, especially in young adults. Most patients have acute attacks under emotional excitement or exertion, and some patients may have a history of recurrent headaches. Headache and vomiting: sudden and severe headache, vomiting, pale face and cold sweat all over. If the headache is confined to a certain place, for example, the anterior headache indicates supratentorial cerebellum and cerebral hemisphere (unilateral pain), and the posterior headache indicates posterior cranial fossa lesions. Clinical manifestations, disturbance of consciousness and mental symptoms: Most patients are unconscious, but they may be agitated. Critically ill patients may have delirium, different degrees of unconsciousness or even coma, and a few may have seizures and mental symptoms. Meningeal irritation sign: it is common and obvious in young and middle-aged patients, accompanied by neck and back pain. Elderly patients, people with early bleeding or deep coma may not have meningeal irritation.

Other clinical symptoms: low fever, low back pain, etc. Mild hemiplegia, visual impairment, third, ⅴ, ⅵ, ⅶ cranial nerve paralysis, retinal hemorrhage and papilla edema can also be seen. In addition, it can also be complicated with upper gastrointestinal bleeding and respiratory infection.

Other complications:

Sinus arrest

high heat

Bradycardia arrhythmia

"grand mal

Acute acquired brain edema

Noncardiogenic pulmonary edema

Cushing's/gastric stress ulcer

Hyperglycemia

insensitive

sinus brady-cardia

more

Treatment:

Intensive care

Neurosurgical treatment

more

The mortality rate of first ruptured aneurysm is about 35%. Within a few weeks after rebleeding, 15% cases died. If there is no rebleeding 6 months after the first bleeding, the chance of the second bleeding every year is about 3%. Generally speaking, the prognosis of ruptured cerebral aneurysm bleeding is more serious, and the prognosis of arteriovenous malformation bleeding is better. The best prognosis is the cases with no lesions found by whole cerebral angiography, which may have few bleeding sources and may have healed on their own.

Some basic diseases, such as vascular diseases, hematological diseases, heart diseases and syphilis, should also be treated accordingly. Physical exertion should be avoided; You must stay in bed. Body fluid balance and nutrition should be maintained, and parenteral route should be adopted if necessary. If you have irritability, you can give benzodiazepines, but it should be noted that the irritability of elevated blood pressure may be caused by increased intracranial pressure. Severe headaches may require injection of narcotic analgesics to relieve them. Constipation can easily lead to exertion when defecating, so preventive measures should be taken. Anticoagulants and antiplatelet drugs are prohibited.

Reactive vasospasm can lead to ischemic diseases. Early application of nimodipine, a calcium channel blocker, 60mg orally, every 4 hours 1 time (under the condition of stable blood pressure) for 2 1 day may relieve vasospasm.

It is rarely used to release cerebrospinal fluid through lumbar puncture to reduce intracranial pressure because the effect is short-lived. If there are clinical signs of acute hydrocephalus, ventricular drainage (including shunt of ventricular system) should be considered quickly. ε-aminocaproic acid and its related preparations can not reduce the overall mortality, because their application leads to an increase in the incidence of vasospasm (ischemia).

Surgical ligation or closure of aneurysms can reduce the risk of rebleeding and death. Silver clips are recommended as aneurysm clips, but occasionally other surgical methods can be used, such as ligating the proximal carotid artery to induce thrombosis in the aneurysm, or covering the aneurysm sac with plastic, gauze or muscle. If the patient is in a stupor or coma, the mortality rate of surgical treatment is very high, unless the disturbance of consciousness is caused by resectable hematoma or acute hydrocephalus. For cases of mild nerve injury, most neurosurgeons now advocate operating within 72 hours after onset, although opinions on the best time are still not uniform. Early operation can minimize the risk of rebleeding, and also reduce the risk of vasospasm and secondary systemic complications after cerebral infarction. Delaying operation 10 days or more can reduce the risk of operation, but the incidence of rebleeding increases, and the total case mortality also increases.

Even through surgical treatment, many patients have sequelae of neurological disorders. In a few cases, after subarachnoid hemorrhage, the reaction is slow, the mental disorder and the recovery of motor function are slow, which can last for several weeks, which is caused by secondary communicating hydrocephalus. If this situation is not improved for a long time, ventricular shunt surgery is sometimes performed.