Prevention and treatment of cerebral infarction
I. Overview
Acute cerebrovascular disease, also known as stroke, is an acute localized brain dysfunction caused by impaired cerebral blood circulation, with clinical manifestations of signs and symptoms such as aphasia, limb paralysis, and sensory disturbances. The clinical picture usually includes cerebral infarction, transient ischemic attack (TIA), cerebral hemorrhage, and subarachnoid hemorrhage. Sometimes stroke refers specifically to cerebral infarction.
The incidence of stroke in China is the second highest in the world. The annual incidence rate is about 250 per 100,000 people. There are about 3.5 million new cases each year and the death rate is about 120/100,000. The incidence of ischemic stroke is increasing, while the incidence of hemorrhagic stroke is decreasing. The age of onset of stroke tends to be younger.
Cerebral infarction is irreversible damage to brain tissue caused by focal cerebral ischemia, which manifests clinically as focal neurological deficit manifestations, such as hemiplegia, hemianopia, aphasia, hemianopia, dizziness, ataxia, etc. Cerebral infarction detected by CT or MRI scan of the brain during physical examination without obvious symptoms is called asymptomatic cerebral infarction.
Classification of ischemic cerebrovascular disease
1.Insufficient blood supply to the brain
2.Transient ischemic attack (TIA): see mini-stroke. The symptoms and signs of focal neurological deficit disappear completely within 24 h. Cerebral infarction occurs in 5% of patients within two days and 10% within 90 days after the TIA attack. The risk of cerebral infarction in the near future is further increased when the patient with TIA is >60 years old, has diabetes mellitus, and the attack presents with hemiparesis, aphasia, and/or an attack duration >10 minutes.
3. Cerebral infarction
(1) Cerebral thrombosis (atherosclerotic thrombotic cerebral infarction): cerebral infarction caused by severe narrowing or occlusion of arteries due to lesions in the inner wall of cerebral arteries (such as atherosclerosis, arteritis, etc.). It starts in the quiet state and progresses gradually after the onset, reaching a peak in a few hours to a few days.
(2) Cerebral embolism (embolic cerebral infarction): cerebral infarction caused by various kinds of emboli (blood clots, atheromatous plaques, fat, etc.) entering the blood vessels of the brain with the blood flow and blocking the cerebral arteries. The onset is sudden and rapid, peaking instantaneously (within seconds to minutes).
(3) Lacunar cerebral infarction: occlusion of the lumen due to lipid vitreous degeneration of small penetrating arteries is the main cause of the formation of lacunar cerebral infarction; atherosclerotic lesions at the exit of penetrating branch arteries can also block the exit of penetrating arteries, thus causing lacunar cerebral infarction. Small emboli entering the small blood vessels in the brain causing embolism of small blood vessels in the brain is also an important cause of lacunar cerebral infarction. The symptoms are mild and can be slightly progressive or non-progressive, and mostly develop after morning activities.
(4) Asymptomatic cerebral infarction: cerebral infarction detected by CT or MRI scan of the brain during physical examination without obvious symptoms is called asymptomatic cerebral infarction.
III. Risk factors of cerebral infarction
The risk factors of cerebral infarction are a series of genetic traits, lifestyles and some diseases. Prevention of cerebral infarction can be achieved through intervention of risk factors. Therefore, understanding these risk factors and taking targeted preventive measures can minimize the occurrence of cerebrovascular disease, which is of great importance to reduce patient suffering and the burden on families and society.
Common risk factors for stroke.
Controllable risk factors: wind heart disease, coronary artery disease, atrial fibrillation, carotid artery stenosis, hypertension, diabetes, abnormal lipid metabolism [high cholesterol, low high density lipoprotein (HDL)], smoking, excessive sodium intake (eating salt), obesity, lack of exercise, moderate and heavy alcohol consumption, hyperhomocysteinemia, periodontal disease, severe dehydration, acute blood loss, improper use of antihypertensive drugs, etc. Blood pressure sudden drop, blood component abnormalities such as true erythrocytosis, increased blood coagulation (antiphospholipid antibody syndrome, S protein, C protein or antithrombin III), etc.
Uncontrollable risk factors: genetic factors, age factors, gender factors, etc.
IV. Performance and diagnosis
1.Diagnosis of TIA
It is generally believed that the cause of TIA is atherosclerosis. On the basis of this, arterial appendage thrombus or atheromatous plaque dislodged, emboli cause transient occlusion of the distal artery; or on the basis of severe arterial stenosis blood volume, blood pressure abruptly reduced the distal blood flow of the artery can be caused.
The main basis for diagnosis is as follows.
(1) Atherosclerotic risk factors and associated diseases.
(2) Transient: episodes lasting from a few minutes to more than 10 minutes and not more than 24 hours (usually <1 hour);
(4) No evidence of acute cerebral infarction on brain CT and MRI scans.
2.Cerebral thrombosis (atherosclerotic thrombogenic cerebral infarction)
It can be divided into cerebral arterial thrombosis cerebral infarction, arterial to arterial embolism, junctional area or watershed cerebral infarction.
The main features of atherosclerotic thrombotic cerebral infarction are as follows.
(1) Risk factors for atherosclerosis: hypertensive disease, diabetes mellitus, hyperlipidemia, etc.
(2) Extracerebral atherosclerotic diseases: coronary artery disease, limb artery occlusive disease, narrow carotid atherosclerosis, etc.
(3) Antecedent TIA manifestations.
(4) Mostly static onset, a few dynamic onset, progression peaking in hours to days, very few exacerbation periods of half a month to a month.
(5) No or only mild headache or impaired consciousness.
(6) Syndromes of main cerebral artery occlusion: hemiparesis, hemianesthesia, aphasia, hemianopsia, dizziness, ataxia, etc.
(7) Imaging manifestations of cerebral artery occlusion (ultra early brain CT cannot detect lesions but can exclude hemorrhage, brain MRI may detect lesions, DMI can see obvious lesions, and brain MRA can show real relevant regional cerebrovascular occlusion).
3.Watershed cerebral infarction
Abrupt drop in cerebral perfusion pressure: swift hypotensive treatment, acute blood and salt loss, cardiogenic shock, etc.
Imaging manifestations of cerebral infarction with crossborder distribution.
Other as cerebral thrombosis.
4.Cardiogenic cerebral embolism
When the heart disease, the thrombus in the heart as the source of embolus, etc., can be dislodged to cause cardiogenic cerebral embolism. The diagnosis of cardiogenic cerebral embolism requires the heart disease from which the embolus originates and the sudden characteristics of cerebral embolism.
(1) Cardiac disorders providing emboli: atrial fibrillation, acute myocardial infarction, bacterial endocarditis, cardiac mucinous tumor, etc.
(2) Sudden onset of neurological deficits with transient (within seconds) peaks.
Other as cerebral thrombosis.
5.Lacunar cerebral infarction
Lacunar cerebral infarction occurs in patients with hypertensive disease and diabetes mellitus.
The diagnosis of cerebral infarction is mainly based on the following points.
(1) History of hypertension and/or diabetes mellitus.
(2) Acute onset, many after morning activity, peaking within minutes to hours, with limited exacerbation; sometimes a prodromal manifestation of a large cerebral infarction.
(3) manifestations of various lacunar syndromes: common lacunar syndromes include simple motor light hemiparesis, simple sensory stroke, dysarthria hand clumsiness syndrome, ataxia light hemiparesis, etc. The symptoms are generally mild and easily ignored by the patient and family.
(4) Imaging: deep small punctate lesions.
V. Auxiliary examinations
1.Laboratory examination
Laboratory tests for acute cerebral infarction include routine blood, blood glucose, blood lipids, renal function, blood electrolytes, blood gas analysis, cardiac enzymology, coagulation series, C-reactive protein, etc. Sometimes it is also necessary to check syphilis serology, anti-cardiolipin antibody, autoantibodies and other indicators.
2.Imaging diagnosis
Head CT, brain MRI and DWI, brain and neck MRA, carotid ultrasound, transcranial Doppler cerebrovascular ultrasound (TCD), brain digital subtraction angiography (DSA), etc.
VI. Treatment of cerebral infarction
Treatment of acute phase
The treatment principles of acute cerebral infarction include the reconstruction of cerebral blood flow as soon as possible, cerebral protection treatment, treatment of cerebral edema and high cranial pressure crisis, management of comorbidities, and early rehabilitation treatment.
1.Pre-hospital treatment: Sending to the nearest hospital with examination and treatment conditions as soon as possible is the first task of pre-hospital treatment. In the process of transportation, the patient should generally be placed in a flat or lateral position to prevent the inhalation of vomitus and other airways. Oxygen inhalation has no practical significance. When blood pressure is below 170 mmHg, antihypertensive drugs are generally unnecessary and sublingual nifedipine is prohibited. However, if the patient has agitation or onset during exercise, headache, vomiting, neck resistance and other manifestations, appropriate antihypertensive measures should be taken when cerebral hemorrhage is suspected to be more likely.
2. General treatment: The limbs should be kept in a functional position. Those with vomiting, swallowing disorder or unconsciousness in the acute stage should be controlled to eat and drink to prevent vomiting and accidental aspiration. Pay attention to the protection of the respiratory tract, and inhale oxygen if necessary.
3. Thrombolytic therapy.
rtPA (recombinant tissue fibrinogen activator) is the only drug approved by FDA for cerebral infarction treatment. It can be used rtPA 0, 9mg/kgBW, 10% of the full amount is pushed intravenously within 1 minute, and the remaining amount is dripped intravenously within 1 hour. However, the risk of symptomatic cerebral hemorrhage does increase to 6,4%, which is higher than 0,6% without thrombolytic therapy.
The indications for tPA are as follows.
Ischemic stroke with onset ≤ 3 hours.
No history of trauma or major surgery within the last 2 weeks, no gastrointestinal or urinary tract bleeding within 3 weeks, no history of severe cranial trauma, surgery, or stroke within 3 months, and no previous history of intracranial hemorrhage.
No rapid and marked improvement in symptoms after onset.
Bp: <185/110 mmHg.
CT of the brain: no intracranial hemorrhage, early signs of cerebral ischemia not extending beyond 1/2 of the middle cerebral artery region.
PT < 15 and platelets > 100,000/mm3.
Optional urokinase, 1-1,500,000 units, 10% IV push for the full dose and the remaining dose intravenously over 1 hour. Indications and contraindications as above.
4.Anticoagulation therapy
Low molecular heparin: the effect is not certain, non-essential.
Warfarin: progressive stroke, monitor PT (INR) at the same time.
5.Anti-platelet therapy
Aspirin: Routine use.
Clopidogrel: second-line drug. Better effect on posterior circulation than aspirin.
6. Hemodilution: Low molecular dextrose or 706 plasma substitute may be used if low perfusion causes are considered.
7.Cerebral protection therapy
Subcritical therapy.
Edaravone: free radical scavenger, used within 24 hours of onset has a protective effect, generally use 30mg, IV, twice a day, 14 days / course.
8, blood pressure management: systolic blood pressure within 220 and diastolic blood pressure below 120 mmHg during the acute period (European and American standards), our standard when 180/100 mmHg or less in principle without antihypertensive drugs. Reducing various discomfort symptoms of patients helps stabilize blood pressure, but for patients treated with thrombolysis, blood pressure should be maintained below 170/100 mmHg to reduce hemorrhagic transformation of infarction.
9. Treatment of cerebral edema and high cranial pressure
Mannitol: 250ml or 125mlbid or q8h at intervals depending on the degree of increased intracranial pressure. Pay attention to its renal damage.
Mannofructose: less renal damage, can provide partial heat, but with intravascular hemolysis, elevated blood glucose, and non-ketotic hyperosmolar coma.
Tachyphylaxis: indicated in the presence or concern of left heart insufficiency and renal impairment when mannitol can be appropriately reduced.
Human albumin: the effect of general dose use on the treatment of cerebral infarction and cerebral edema has not been clarified and is not used as a routine drug.
Hypothermia therapy: It can significantly reduce cerebral edema in animal tests, and clinical use is still being explored.
Craniotomy decompression: For large cerebral infarcts (so-called “malignant cerebral infarcts”) and cerebellar infarcts, it can reduce mortality.
Ventricular puncture and drainage: can be used when obstructive hydrocephalus occurs, resulting in a rapid increase in intracranial pressure.
10.Management of comorbidities
Pulmonary infection: control diabetes mellitus, reduce bed rest, avoid choking as much as possible, turn and pat the back, and encourage coughing up sputum.
Urinary tract infection: reduce bed rest and catheter time as much as possible.
stressful upper gastrointestinal bleeding: antacids may be used prophylactically
Decubitus ulcers: turning regularly, sitting rather than lying, standing rather than sitting.
Deep vein thrombosis and pulmonary embolism of the lower extremities: turn over regularly, sit rather than lie, stand rather than sit, and perform more limb activities and massage and extrusion.
VII. Prevention of cerebral infarction
1. systemic atherosclerotic lesions: including coronary heart disease, cardiac insufficiency, symptomatic peripheral arterial lesions, etc. Treatment for these diseases can reduce the incidence of stroke.
2. Hypertensive disease: lowering blood pressure (especially systolic blood pressure) can reduce the incidence of cerebral infarction and cerebral hemorrhage. Blood pressure should generally be controlled to below 140/90 mmHg (below 130/80 mmHg in diabetic patients). For patients with long-term hypertension, long-term diabetes and cerebral artery stenosis, it is more prudent to adopt a phased and gradual blood pressure lowering program to reduce the risk of causing hypoperfusion cerebral infarction.
3.Diabetes: In diabetic patients, blood pressure should be lower than 130/80 mmHg, with the addition of statin lipid-lowering drugs.
4, atrial fibrillation: In principle, patients with atrial fibrillation should receive anticoagulation therapy. When considering the indications for anticoagulation need to be graded classification of stroke risk.
5.Lifestyle.
(1) Diet should generally include more vegetables and fruits and reduce sodium intake (no more than 2 or 3 grams per day). Low-fat dairy products and reduced intake of animal and vegetable fats can help prevent stroke.
(2) Exercise and leisure can reduce the risk of stroke. 30 minutes or more of moderate intensity exercise daily is a healthy lifestyle.
(3) Weight control contributes to stroke prevention.
6.Drinking alcohol: A small amount of moderate alcohol can reduce the incidence of stroke, while a large amount of alcohol increases the chances of incidence. It is generally believed that: 50ml of white wine, 1 small glass of red wine (2~3ml) and 1 bottle of beer per day is more appropriate.
7, oral contraceptive drugs: there is an increased risk of blood clots in the venous system, it is recommended that women with hypertension, diabetes, smoking, a history of migraine headaches and thromboembolic disease to avoid using oral contraceptives.
8, sleep apnea syndrome: can increase the risk of hypertension, cardiovascular and cerebrovascular disease. Treatment is recommended.
9, hyperhomocysteinemia: taking folic acid and B vitamins may help in stroke prevention.
The treatment of each disease should follow the principle of individualization. The above mentioned are only directions or principles for reference only, and the specific program gram depends on the specific situation of the patient. Herewith a note!