Subarachnoid hemorrhage

Subarachnoid hemorrhage clinical manifestations:

(1) before unruptured saccular aneurysms are usually asymptomatic, but larger aneurysms can cause headaches or focal signs: partial paralysis of eye movements associated with dilated pupils often posterior communicating artery and carotid artery junction aneurysm in cavernous also oppressed section ⅲ, ⅳ, ⅵ cranial nerve V or the eye pieces.

(2) The vast majority (over 90%) sudden onset, slow onset minority. The disease mainly headache is common and first symptom, manifested as sudden severe headache whole, or headache is located in the first part, and soon spread to the whole head, often accompanied by nausea, vomiting; headache on one side who ruptured blood vessels in the side. However, due to different circumstances age, lesions, ruptured blood vessel size, the number of times the incidence, clinical manifestations vary greatly; light can no obvious symptoms and signs, severe sudden coma and stillbirths in the short term, 20% of have seizures. Older, less bleeding, pain tolerance strong or severe coma can no obvious meningeal irritation. Sometimes lower back pain more prominent position than the headache. Approximately 25% of patients may appear before the retina or vitreous hemorrhage, which is clinically useful characteristic signs. Most young age of onset, but also children and elderly onset. Most before the onset of obvious incentives, such as strenuous exercise, fatigue, cough or defecation, drinking, emotional and other dynamic at onset, a small number of patients in a quiet disease, including sleep. More than a third of patients, the disease a few days before the headache, stiff neck, nausea, vomiting, fainting or vision impairment, often due to the small amount of bleeding caused by an aneurysm. Subarachnoid hemorrhage in the early stages up to 25% misdiagnosis can lead to delays in treatment, and increased mortality.

(3) small number of patients side hemiparesis, sensory disturbances, aphasia, etc., were mostly due to the early stage of hemorrhage broken into the brain parenchyma and cerebral edema, often late Department of delayed vasospasm. Fundus examination shows 25% of vitreous film showings massive bleeding, such bleeding can occur within hours of the onset of l. This is the basis for diagnosis of SAH is quite strong, excessive bleeding, blood can invade the body cause glass visual impairment. 10% to 20% visible papilledema.

Clinical features (4) of the disease in old age is not typical, familiar with the characteristics of the elderly subarachnoid hemorrhage, timely and correct diagnosis and treatment is the key to reducing mortality. 40 to 70 years more. Sudden onset, may have emotional force, defecation, coughing and other incentives. The most common symptoms are sudden severe headache, nausea, vomiting, paleness, cold sweat. Half of the patients may have varying degrees of consciousness, to a transient unconsciousness as much, severe coma. 20% may have a seizure. Psychiatric symptoms or even the only symptom of some elderly patients. Delirium, agitation, hallucinations and delusions, disorientation, personality changes.

(6) children subarachnoid hemorrhage

① minor bleeding: can be asymptomatic and signs, or only mild irritability, muscle tension slightly under BCSF often recover within a week, more common in premature children, accounting for 75% of SAH in newborns;.

② bleeding more: full-term children more common, often convulsions within 48 hours after birth, but generally in good condition;

③ heavy bleeding: acute progressive disease, rapid death. The first two cases the prognosis is good, but can cause hemorrhagic hydrocephalus.

(7) complications

1) re-bleeding: the emergence of projections severe headache, vomiting, disturbance of consciousness, meningeal irritation, retinal fresh hemorrhage and other relevant neurological symptoms and signs his condition stabilized or improved once again, re-bleeding occurred in one after the first bleeding for the month, especially two weeks, its mechanism for the first 7 to 14 days after the bleeding plasmin activity increased, prompting clot primary vessel rupture due to dissolution; the causes for the patient irritability, excitement will Fen, defecation and high blood pressure.

2) cerebral vasospasm: clinically seen mainly delayed spasm, manifested as a gradual emergence of a stable or improving condition after disturbance of consciousness, paralysis or partial absence of neurological signs, but no sign of bleeding Ran said. Delayed cerebral vasospasm usually occurs in 4 to 14 days after the hemorrhage, the mechanism may be related to the cerebrospinal fluid oxyhemoglobin, 5-HT, TXA2 levels increased about.

3) hydrocephalus: non-traffic and normal pressure hydrocephalus.

Non-communicating hydrocephalus: clinical manifestations of the gradual emergence of increased intracranial pressure symptoms, such as apathy, unresponsive, headache intensified, deepened consciousness, neck stiffness worse. According to the time of onset can be divided into acute and chronic: Acute means the disease within seven days of hydrocephalus caused by ventricular dilatation, more than this time are known as chronic hydrocephalus acute hydrocephalus and more as the third ventricle, cerebral aqueduct, fourth ventricle or basal accumulation of blood pool. Cerebrospinal fluid circulation obstruction caused by chronic preserved more due to the aqueduct and basal cell adhesions.

Normal pressure hydrocephalus: ① The main symptoms of mental disorders, the light show is forgetful, unresponsive, severe dementia. ② abnormal gait, initially only walk weak legs, dragging step, after the development of spastic gait. ③ urinary incontinence: more mental disorders and abnormal gait appear after, occurred in 4 to 6 weeks after subarachnoid hemorrhage. ④ Other signs include: horizontal nystagmus, extrapyramidal signs.

4) Water and electrolyte imbalance: after SAH 5% ~ 30% of patients with hyponatremia can occur within blood vessels and reduce blood volume, may aggravate cerebral edema, mainly caused by inappropriate secretion of antidiuretic hormone.

5) neurogenic cardiopulmonary disorders: severe SAH with fluctuations in the level of catecholamines and sympathetic tone, which in turn causes neurogenic cardiac dysfunction, neurogenic pulmonary edema, or both simultaneously.