Keywords: cerebral infarction treatment
Brain cells can tolerate ischemic damage limited time. Should be made public and medical personnel are aware of the urgency of cerebral infarction treatment organization efficient rescue system. The patient stroke signs via ambulance brigade immediately to community stroke to the nearest medical institution. Establishment of stroke units in order to continuously improve the quality of medical care.
(A) to prevent and treat a variety of complications prevent complications is extremely important to reduce the mortality rate of stroke, to avoid ischemia brain cells to further damage and recovery and create favorable conditions for the defects of the brain function better.
To maintain a good heart and lung function, to keep the airway open and not allow oxygen content decreased. Should be alert to the occurrence of arrhythmias, myocardial infarction, heart failure, preferably 24 to 48-hour ECG monitoring. Water, electrolyte and nutritional intake, record and out of fluid volume, and promptly correct hypovolemia, improve cardiac output. The glucose infusion avoid, because high blood sugar will aggravate cerebral infarction damage. Disturbance of consciousness or swallowing dysfunction not eat by mouth, to avoid aspiration pneumonia, nutritional supplements nasogastric tube. Paralysis can not afford the patient should adopt inflatable bedding, changing position regularly, pay attention to skin care and paralyzed limbs remain active, mandatory the hyperventilation or cough to prevent bed sores, joint contractures, atelectasis, deep vein thrombosis and pulmonary embolism occurred . Keep urine clear. To patients spiritual support and encouragement. Occur secondary to give full play to the normal part of the patient’s body and function part of the role is not completely lost.
1. Blood pressure in the acute phase of stroke patient’s blood pressure is essential. Decided because of cerebral blood flow in cerebral perfusion pressure (the cerebral perfusionpressure CPP) CPP and mean arterial pressure (MAP) and intracranial pressure (ICP) the difference between the positive correlation. Must maintain in order to avoid the aggravation of cerebral ischemia, CPP between 6.67 ~ 20.0kPa (50 to 150mmHg). Stroke and other brain damage, cerebral vascular automatically adjust incapacity passive cerebral blood flow and increase or decrease with MAP. Therefore, should be very careful about the treatment of hypertension in patients with acute cerebral infarction. MAP increased sometimes cerebral hernia harbinger reduce intracranial pressure, blood pressure can be improved. However, the mean arterial blood pressure is too high can increase brain swelling and intracranial pressure. 20.3kPa (220mmHg) or diastolic blood pressure more than 16.0kPa (120mmHg) systolic blood pressure over 15 minutes every 3 consecutive case retest oral captopril (captopril) or nicardipine ( nicardipine) to slowly lower the blood pressure of about 15%. Intravenous labetalol (labetalol) 10mg, necessary to closely monitor the blood pressure cases injected once every 20 to 30 minutes.
MAP or CPP than premorbid reduced by 1/3 or MAP <9.33kPa (70mmHg) or CPP <6.67kPa (50mmHg) while no hypovolemia should be given to the dopamine or other vasopressors rises slightly lower than the disease before the blood pressure levels. While research hypotension reasons.
2. The majority of intracranial pressure and cerebral infarction cerebral edema, but usually does not become a problem, especially in elderly patients have different degrees of brain atrophy can adapt to the severe brain swelling. Young patients or brain, large areas of the cerebellar hemisphere infarction, the most the severity in the 2 to 5 days after the onset of brain swelling, increased intracranial pressure due to brain herniation and death. Intracranial pressure higher than 2.67kPa (20mmHg or 270mmH2O) or drowsiness, patients from sober to the side of the pupillary light reaction dull rapid intravenous infusion of mannitol, 20 to 100 g every 2-6 hours to increase the plasma penetration pressure to be higher than 300mosmol / L, the moisture from the brain to the intravascular reduce intracranial pressure by reducing brain volume. Record and out of the fluid volume, diuresis, dehydration treatment 10-14 days until the brain capacity of resistance (compliance) to return to normal. The treatment should be adjusted according to the clinical situation, intracranial pressure, plasma osmolality changes. Mannitol infusion in 10 to 20 since the beginning, you can reduce intracranial pressure, should be fast drops, but the speed is too fast can cause hemolytic reaction.
Furosemide (furosemide) and acetazolamide (acetazolamide) can be used either individually or combined to reduce cerebral edema.
Hyperventilation for the effective treatment of increased intracranial pressure. PaCO2 from 5.33kPa (40mmHg) dropped 3.33kPa (25mmHg) reduces cerebral blood flow of 25%. By reducing cerebral blood flow and cerebral blood volume in order to reduce the intracranial pressure. But some cranial hypertension patients may have relatively lower cerebral blood flow exists, hyperventilation caused by ischemic damage.
3. Blood sugar low blood sugar or high blood sugar will aggravate ischemic brain damage, should be discovered and corrected in a timely manner. Glucose above 150mg/dl should be given insulin.
4. The body temperature lower the body temperature can be reduced the experimental infarct volume, increased body temperature, increase the scope of damage. A considerable part of the stroke patients with a history of infection before the onset of stroke and then often complicated by lung infections. Therefore, close monitoring of body temperature, active control infection and fever, and hypothermia.
(B) of the ischemic damage prevention mechanism based on the occurrence of cerebral ischemic damage some treatment, their efficacy, safety, and adapt to the object, dose, method of administration, have yet to be determined.
1. Fibrinolytic fibrinolytic treatment of acute stroke four international multi-center study enrolled 328 to 622 patients in the phase of analysis, due to cerebral hemorrhage treatment group was significantly higher conversion rate (about 3-4 times) and suspended in 1995. MAST-1 study group found that severe neurologic deficits, and lacunar infarction were the risk factors for cerebral hemorrhage. The ASK Study Group stop accepted the onset three hours or longer patient. Moreover, there again thrombus after thrombolysis.
2. The anticoagulant heparin prevents blood clots expansion inhibit vascular smooth muscle cell proliferation and platelet aggregation. VA can be used for the acute blockage to prevent the extension to the BA, also can be used for heart bolt cerebral infarction. Large cerebral infarction of the internal carotid artery system should not be used, is likely complicated by the infarct risk of bleeding, and there was no problem to prevent further thrombus extension. In order to avoid excessive anticoagulation, usually a rate of 800 per hour to 1200 units of heparin intravenous titration, prolong the activated partial thromboplastin time, PTT, 1 to 1.5 times. Change warfarin oral maintenance.
The heart bolt cerebral infarction often bleeding, anticoagulation will increase the bleeding should be over 2 to 4 days after stroke warfarin therapy, the prothrombin time (PT) 1.2 to 1.5 times longer than the control.
Exclude hemorrhage before treatment imaging studies, patients had no bleeding tendency during treatment follow-up imaging studies.
The recent advent of low-molecular-weight heparin only daily subcutaneous injections of 1 or 2 times, does not increase the risk of bleeding and simplifies laboratory monitoring. A set of random, double-blind, controlled study, the treatment group within 48 hours after the onset of 6 months when the prognosis is better than the control group.
3. The experimental study of the anti-platelet, platelet activation and peanut arachidonic acid metabolites may exacerbate ischemic damage. Low-dose aspirin inhibition of platelet production can promote platelet aggregation and vasoconstriction of thromboxane A2 (thromboxane A2). Ticlopidine (ticlopidine) inhibition of platelet and fibrin $ binding. The ongoing multi-center study of aspirin treatment of acute cerebral infarction.
4. Hemodilution therapy the Greek can reduce blood viscosity to increase cerebral blood flow. Applicable to patients with high blood viscosity, caused due to hemodynamic factors of cerebral infarction, lacunar infarction. Large artery atherosclerotic artery infarction NA. Isovolumic dilution (intravenous dextran and phlebotomy phlebotomy) has proved to be 12 to 24 hours after the onset of the patient is not valid. Does not apply to patients with increased intracranial pressure, acute myocardial infarction, congestive heart failure, arrhythmias, severe hypertension and hematocrit hematocrit (Hct) is not high (<36%). If Hct is higher than 46%, confirmed that dehydration should complement the crystal. Hypovolemia should be to add volume. Individual very early patients, Hct increased rather than caused by dehydration nor contraindications careful intravenous dextran. The Swan-Ganz catheter is inserted to maintain pulmonary capillary wedge pressure 1.60kPa (12mmHg) to prevent pulmonary edema, congestive heart failure, dextran can still provoke allergic reactions, kidney failure.
5. Nimodipine given nimodipine artery occlusion animal brain infarct volume is less than the control group. The oral drugs on the onset of 12 to 24 hours after the patient is invalid. Can onset early trial, 30mg, once every 6 hours. Or intravenous infusion, first 3 days later converted to oral. The need for timely detection and lower blood pressure and to the correction of.
6. Pentoxifylline (pentoxifylline, PTX) can improve the ability of red blood cell deformability, reducing whole blood and plasma viscosity, inhibit the aggregation of red blood cells and platelets, increasing tissue oxygenation. Group treated within 12 hours after the onset of a randomized, double-blind, controlled study, intravenous infusion PTX72 hour during the progress of neurological symptoms was significantly better than the control group, 2-group difference that is not converted after oral administration.
The brain defect function (c) the treatment of stroke treatment goal is to avoid individual or brain cell death and promote the recovery of the defects of the brain function. The former is the key of the acute phase, short therapeutic window. The latter should also be the acute phase, the therapeutic window may be quite long. The limb should begin as soon as possible passive activities, active sports and various functional activities, carry out targeted rehabilitation of movement, speech, cognitive impairment of brain function. Mobilize patient initiative, the enthusiasm of the family and society, adhere to long-term, and gradually increase the difficulty of the functional exercise. Acupuncture, massage, physical therapy, physical therapy, qigong, neuropsychological therapy, occupational medicine and speech therapy according to the disease and objective conditions. We had eight cases of cerebrovascular disease hemianopia have been more than six months (mean 40 months) patients the directional dynamic color light stimulation to six weeks, seven cases of visibility and significantly expanded significantly improved visual function. 99mTc-HMPAO brain SPECT rCBF examination findings the lesion side occipital lobe and midbrain radioactive defect, rCBF was significantly increased the visual progress after treatment, 7 cases. The clinical progress no change. There is a considerable time after stroke brain function defects, there is still the prospect of improvement.
(D) preventive treatment during some very cerebral ischemic damage may contribute to the diagnosis and treatment measures (carotid surgery or intubation, etc.) before the short-range applications nimodipine equality cerebral protective agent through the dangerous phase, more and similar to the experimental cerebral ischemia, the effect should be better than ischemia after the start of the administration. Patients with cerebrovascular disease risk factors in climate unfavorable season could be considered a long time to take brain protection agents.