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Atherosclerotic Cerebral Infarction

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What is Atherosclerotic Cerebral Infarction

Atherosclerotic cerebral infarction cerebral infarction is the most common type, in atherosclerosis appear on the basis of the vascular wall lesions caused by stenosis, occlusion or thrombosis, resulting in cerebral blood flow interruption of blood supply to the area occurrence of brain tissue ischemia, to hypoxia and softening necrosis, caused the signs and symptoms of the nervous system. Acute cerebral lesions by ischemic core and surrounding ischemic penumbra, the central area due to serious complete ischemia caused by the death of brain cells and brain tissue irreversible damage; ischemic penumbra local brain tissue exist the great arteries residual blood and collateral circulation, the degree of cerebral ischemia light only functional deficits are reversible.

Symptoms of Atherosclerotic Cerebral Infarction

The disease often quiet rest onset, generally a clear consciousness; but the occurrence of basilar artery occlusion or Omo Peru cerebral infarction, serious illness, often a disturbance of consciousness, or even death. The clinical manifestations are due to occlusion of blood vessels occurs varies carotid system cerebral infarction usually presents the central contralateral hemiplegia, hemisensory barriers, such as can occur in the dominant hemisphere aphasia; vertebral - basilar artery cerebral infarction is manifested involvement of the brain stem and cerebellar symptoms and signs, cross paralysis cross sensory disturbances, cranial nerve palsy and ataxia.

What Causes Atherosclerotic Cerebral Infarction

Tests and Diagnosis for Atherosclerotic Cerebral Infarction

CT scan in 24-48 hours after the onset of visible low-density lesions, MRI in a few hours after the onset low T1 signal, high T2 signal lesions on the brain stem, cerebellar infarction and infarction than CT show more clearly. Functional MRI, such as Ephesians San weighted imaging (DWI) and perfusion-weighted imaging (PWI), can be detected within a few minutes after the onset of ischemic changes. The disease should pay attention to the identification of cerebral hemorrhage and intracranial space-occupying lesions.

Treatments of Atherosclerotic Cerebral Infarction

Treatment

(A) the acute phase of treatment

Super early (within 6 hours) and the acute phase of treatment, attention should be paid attention to the combination of the overall comprehensive treatment and individual treatment. Take targeted treatment for different conditions, different time of onset and etiology.

l thrombolytic therapy

The purpose of thrombolytic therapy of acute cerebral infarction to save ischemic penumbra, occlusion of the cerebral artery recanalization by dissolving blood clots, hungry complex blood supply of the infarcted area, to prevent the ischemic brain tissue irreversible damage occurs.

The thrombolytic therapy commonly used drugs, including tissue-type plasminogen activator (rt-PA) and urokinase (UK). The timing of thrombolytic therapy is the key to influencing efficacy results of controlled clinical trials, the incidence of 3 to 4.5 hours of rt-PA therapy can reduce the degree of neurological deficit and reduce stroke mortality. rt-PA is a selective fibrin dissolving agent, can be selectively combined with the fibrin of the thrombus surface, forming rt-PA fibrin complexes thrombus site to activate plasminogen into plasmin, a thrombolytic . Therapeutic dose of 0.9mg/kg, maximum dose of 90mg, 10% within 1 minute intravenous injection, and the remaining 90% of the dose intravenous infusion within 60 minutes, general use within 4.5 hours of onset; UK in the old application more, the usual dose of 1 million to 1.5 million U, dissolved in saline 100 ~ 200 ml continuous 30-minute intravenous infusion, also under the surveillance of the DSA the selective intervention dissolving Gui.

Indications of thrombolytic therapy is currently no consensus on the following points of reference: ① 18-75 years of age; ② 4.5 hours of the onset of (rt-PA) or 6 hours of (urokinase); ③ brain function, signs of damage sustained presence of more than one hours, and more serious; ④ head CT to exclude cerebral hemorrhage, and early massive cerebral infarction imaging changes; the ⑤ patients or their families signed informed consent.

Contraindications for thrombolytic therapy include: ① bleeding tendency or bleeding diathesis. ② a history of intracranial hemorrhage, including subarachnoid hemorrhage; history of head trauma in the past three months; nearly three weeks, gastrointestinal bleeding or urinary system; nearly 2 weeks before major surgery; recent l week Do not oppress the site of arterial puncture. ③ nearly 3-month history of stroke or myocardial infarction, but old lacunar infarction is not left behind signs of neurological function except. ④ serious heart, kidney, liver dysfunction or severe diabetes. ⑤ On examination, there is active bleeding or trauma (such as fractures) evidence. ⑥ blood pressure greater than 180/110mmHg, platelet count <100 x 109 / L, blood glucose <2.7 mmol / L ⑦ oral anticoagulation and INR> l.5 48 hours received heparin therapy (APTT outside the normal range). ⑧ pregnancy. The ⑨ uncooperative.

Hemorrhage, or other body parts hemorrhagic complications of thrombolytic therapy for cerebral lesions.

Of thrombolytic therapy Note: ① periodic assessment of neurological function, intravenous infusion of thrombolytic agents process evaluated once every 15 minutes, the next six hours once every 30 minutes thereafter once per hour for up to 24 hours. ② suffered from severe headaches, dramatically increased blood pressure, nausea or vomiting should immediately stop using thrombolytic drugs, emergency head CT. (3) attention to monitoring blood pressure, thrombolysis within the first two hours once per minute, the next six hours once every 30 minutes thereafter once per hour for up to 24 hours. If the blood pressure is higher than 185/105mmHg, several monitoring blood pressure, can be selected as appropriate β receptor blockers, such as labetalol, urapidil hydrochloride injection (clonidine), blood rub is higher than 230 / 140mmHg, intravenous infusion of sodium nitroprusside. ④ thrombolytic therapy is not used within 24 hours of anticoagulation, antiplatelet drugs, available 24 hours after the contraindications to aspirin 300 mg / d, later changed to maintain the amount of 50 to 150 mg / d. ⑤ can not be too early to place a gastric tube, catheter, or arterial Neice pressure tube.

Defibrase treatment

The degradation of fibrinogen in the blood, increasing the activity of the fibrinolytic system, to inhibit thrombus formation. The cerebral infarction early (especially 12 hours) optional Defibrase treatment, high fiber egg apply to hyperlipidemia patients more actively Defibrase treatment.

(1) batroxobin: significantly reduce the level of fibrinogen, symptoms improve faster and more pronounced, adverse reactions, but should also pay attention to the bleeding tendency. The first dose the 10u, after every other day the 5u, intravenous, shared three times before each dose required to detect serum fibrinogen levels.

The (2) defibrase: effectively reduce belly infarction patients with blood fibrinogen levels, improve nerve function, reduce the rate of recurrence of stroke. Onset within 6 hours with better results. Is worth noting that fibrinogen fell below l.3g / L increased bleeding tendency.

(3) preparations of Defibrinogen: the lumbrokinase the Agkistrodon enzymes clinical but also can be applied.

3 anticoagulant therapy

The main purpose is to prevent early recurrence of ischemic stroke to prevent extension of thrombosis and distal vascular thrombosis secondary to promote collateral circulation. The acute phase of anticoagulant therapy Although widely used for many years, but has been controversial, acute pulmonary infarction patients generally do not recommend the routine use of anticoagulants, patients for thrombolysis, anticoagulants is not recommended to be used within 24 hours after thrombolysis. If no bleeding tendency, severe liver and kidney disease, blood pressure> 180/100mmHg, contraindications, the following situations may consider applications anticoagulant therapy: ① progressing stroke; (2) of deep vein thrombosis and pulmonary embolism; ③ hypercoagulable syndrome patients ; ④ cardioembolic infarction (such as artificial valves, atrial fibrillation, myocardial infarction with mural thrombus, left atrial thrombosis); ⑤ intracranial arterial stenosis artery atherosclerosis stroke or frequent emboli caused by stroke.

Commonly used anticoagulants heparin and warfarin. Low molecular weight heparin clinical applications safer, 4000U subcutaneous injection, 2 times a day, 10 days for a course of treatment. Anticoagulant therapy, clotting function should be closely monitored.

4 anti-platelet aggregation therapy

Can reduce the recurrence rate of stroke and improve patient outcomes.

(1) patients who did not receive thrombolytic therapy, the absence of contraindications after stroke as soon as possible (preferably within 48 hours) use of aspirin.

(2) thrombolysis patients after thrombolysis 24 hours, use of aspirin or aspirin and dipyridamole complex preparation of the release agent.

(3) Aspirin recommended dose is 100 to 300 mg / d, preventive dose 4 weeks later changed.

5. Expansion treatment

Acute cerebral infarction due to hypoperfusion of cerebral blood flow, such as watershed cerebral infarction may, at their discretion, consider the expansion of the treatment, it should be noted that may aggravate cerebral edema, heart failure and other complications.

6 Chinese medicine treatment

The principle of treatment for promoting blood circulation, through the meridians. Animal experiments have shown that single component of Chinese medicine, or a variety of drug combinations can reduce platelet aggregation, anticoagulant, improve cerebral blood flow, reduce blood viscosity, as well as a neuroprotective effect. Drugs, including notoginseng, Salvia, Chuanxiong, puerarin, leeches and Ginkgo biloba preparations.

7. Brain protection treatment

(1) The neuroprotective agent: You have conducted many trials and clinical research, effective of many neuroprotective agent in animal experiments, but the lack of convincing clinical observation of the large sample data. Commonly used prior citicoline edaravone.

(2) treatment of mild hypothermia: hypothermia (32 ~ 34 ℃) can reduce the metabolic rate of brain tissue oxygen inhibition of excitatory amino acid release and intracellular calcium overload, reduce the formation of free radicals. Local mild hypothermia may be more promising treatments.

B. resistance to the treatment of cerebral edema

Peak of cerebral edema after the onset of the first 3 to 5 days, based on clinical symptoms or intracranial pressure monitoring, given 20% mannitol 125-250ml, 6 to 8 hours; may also use furosemide 40mg or 20% white protein 50ml, intravenous; massive cerebral infarction cerebral hemisphere, which may be imposed by the cranial decompression or resection of part of the brain tissue; the larger cerebellar infarction, especially affecting brainstem function or cause obstruction of cerebrospinal fluid circulation, posterior cranial feasible fossa craniotomy or direct excision partial infarction of the cerebellum.

9. Comprehensive medical treatment

(1) bed rest, pay attention to the care of the skin, mouth, urethra, turning over on time, to avoid pressure sores and urinary tract infection. The proper elevation head bit, generally in the 15. ~ 30. Around the coma patient should head twisted to one side, in order to facilitate oral secretions and vomiting logistics out, to keep the airway open airway disturbance of consciousness, patients should be given support and assisted ventilation, oxygen saturation remained at 95% or more. Close attention to the patient's altered consciousness, pupil size, blood pressure, respiration, conditions should be conducted guardianship. Dysphagia risk of aspiration, eating should sit up and generally soft diet, pasty or sticky foods sitting for more than 0.5-1 hours after eating should remain indwelling stomach tube nasogastric necessary. Increase the activities of the paralyzed limb as much as possible, to avoid the occurrence of deep vein thrombosis and pulmonary embolism. Prevention and control of aspiration pneumonia, upper gastrointestinal bleeding, water and electrolyte disorders, heart failure and other complications.

(2) the regulation of blood pressure: cerebral infarction hypertension treatment depends on the degree of blood pressure and the patient's overall situation. Systolic blood pressure <180mmHg or diastolic blood pressure <110mmHg, no blood pressure lowering therapy, such as systolic blood pressure of 185-210mmHg or diastolic blood pressure between 115 ~ 120mmHg do not have to rush to the buck, but should be closely observed changes in blood pressure; blood pressure> 220/120mmHg, should be given to slow down blood pressure treatment and close observation of changes in blood pressure, to avoid the blood pressure to drop too low; before and after thrombolytic therapy if blood pressure 180/105mmHg, should be timely blood pressure lowering treatment to prevent secondary bleeding occurs, it is best to use a micro-infusion pump intravenous sodium nitroprusside.

(3) control of blood glucose: hyperglycemia in patients with acute stroke may be the performance of the original diabetes or stress response. High blood sugar and low blood sugar can aggravate ischemic brain damage, leading to poor prognosis in patients. Patient hyperglycemia than 11.1mmol / L, should be immediately given insulin therapy to control blood glucose below 8.0mmol / L (fasting blood sugar) and 11.0mmol / L (the randomized blood sugar). Initial monitoring of glucose using insulin should l two hours. , Usually need to be given insulin to maintain glycemic control. The Acute Stroke few hypoglycemia, a low blood sugar should be promptly corrected.

10. Interventional treatment

Carotid endarterectomy for carotid stenosis of more than 70% of patients. Interventional treatments such as angioplasty of intracranial vascular, endovascular stent implantation has been more and more attention.

11 stroke unit

The stroke unit is a brain disease management model, referring to the stroke ward by neurologists, physical therapists, and speech rehabilitation teacher, psychotherapist and professional caregivers, patient drug treatment, physical rehabilitation, language training, comprehensive treatment of psychological rehabilitation and health education, stroke first aid, treatment, care and rehabilitation organically integrated to reduce the mortality and morbidity, and to improve the prognosis of patients.

(B) convalescent treatment

1. Rehabilitation

Should be carried out as soon as possible, as long as the patient's consciousness is clearly vital signs were stable, the condition is no longer progress, can be carried out after 48 hours should also be noted that, in addition to sports rehabilitation, language, cognitive, psychological, vocational and social rehabilitation.

Secondary prevention of cerebrovascular disease

Active treatment intervention stroke risk factors, the application of anti-platelet aggregation drugs, reduce the risk of stroke recurrence.

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active 7 March 2013 at 16:32

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