Cerebral infarction is a cerebrovascular disease caused by a variety of factors that cause local thrombosis or emboli from other parts to enter the cerebral vessels, narrowing or completely occluding the cerebral arteries, resulting in ischemia, hypoxia and necrosis of brain tissue and causing neurological dysfunction. It can be divided into cerebral thrombosis and cerebral embolism.
The main factors of cerebral infarction are: hypertension, coronary heart disease, arrhythmia, heart valve disease, diabetes, overweight, hyperlipidemia, etc. It is mostly seen in middle-aged and elderly people aged 45 to 70.
Clinical manifestations.
(1) Cerebral thrombosis often develops during quiet rest or sleep. Some patients wake up and find that their mouths and eyes are distorted, they are partially paralyzed, they drool, they drop food grains, they cannot lift chopsticks, and this is the occurrence of cerebral infarction, which often catches people off guard. Only some patients have symptoms of transient cerebral ischemia such as numbness of limbs, slurred speech, transient blackness in front of the eyes, dizziness or vertigo, nausea, and fluctuations in blood pressure (mostly elevated or may be low) before the onset. The onset of the disease peaks within a few hours or 1 to 2 days. Cerebral embolism often has a history of prolonged bed rest, atrial fibrillation, heart valve disease, etc. The thrombus is dislodged into the cerebral vasculature during activity, mostly without prodromal symptoms, with a rapid onset, and develops to a peak within minutes.
(2) The site of infarction and infarct area vary. Headache, vertigo, tinnitus, hemiplegia, either single limb or one limb, upper limb heavier than lower limb or lower limb heavier than upper limb, and a variety of conditions such as dysphagia, slurred speech, nausea, vomiting, etc. In severe cases, coma is soon unconscious. Each patient can have several of the above clinical manifestations.
(3) If the embolism is caused by emboli, in addition to brain signs, embolic signs such as skin, mucous membrane, retina, spleen, kidney and heart can also be seen.
Examination.
1.Imaging examination: MRI is preferred and can detect infarct foci within 6 hours, especially for lacunar infarcts more clearly than CT. CT can show ischemic infarct or hemorrhagic infarct changes, combined with hemorrhagic infarcts highly support cerebral embolism, simple infarct foci usually need about 24 hours to appear on CT. CTA or MRA can detect the degree of carotid stenosis or occlusion. DSA is the gold standard for diagnosing cerebrovascular DSA is the gold standard for the diagnosis of cerebrovascular stenosis or occlusion.
2.Lumbar puncture: increased cerebral pressure indicates large cerebral infarction; cerebrospinal fluid of hemorrhagic infarction may show blood or microscopic red blood cells; cerebrospinal fluid of infected cerebral embolism has an increased cell count (early granulocyte-based, late lymphocyte-based); cerebrospinal fluid of fat embolism can be seen as fat globules.
3.Electrocardiogram: routine examination should be made to determine the evidence of myocardial infarction, wind heart disease, arrhythmia, etc. It is not uncommon that cerebral embolism can be the first symptom of myocardial infarction.
4.Echocardiography: Carotid ultrasonography can evaluate the degree of luminal stenosis and atherosclerotic plaque, which is suggestive of confirming carotid-derived embolism. Echocardiography can detect heart valve disease or thrombus.
Treatment.
Principles of treatment for acute cerebral infarction: individualized, typed and staged treatment.
(i) General treatment.
(1) Adjustment of blood pressure, the use of antihypertensive drugs should be used with caution in cerebral infarction, such as blood pressure of 150-160/100 does not require the use of antihypertensive drugs. (1) Adjust blood pressure.
(2) Keep respiration unobstructed, and give oxygen and tracheotomy if necessary for those who have difficulty breathing.
(3) Reduce intracranial pressure and cerebral edema. Cerebral edema can occur in acute, especially large cerebral infarction, and is a common cause of death within 1 week after the onset. Mannitol should be used to lower intracranial pressure, and glycerol fructose and tachyphylaxis are available for abnormal renal function.
(4) Prevention and treatment of respiratory and urinary tract infections and reasonable application of antibiotics.
(5) Prevent pulmonary embolism and deep vein thrombosis of the lower extremities.
(6) Early activity to prevent the formation of decubitus ulcers, turning and patting the back every 2 hours and passive movement of paralyzed limbs. Avoid pressure and decubitus ulcer formation.
(7) Strengthen nutrition. According to the patient’s specific condition, nasal feeding and intravenous high nutrition should be performed to give the patient a chance to recover.
(2) Thrombolytic therapy: within 3 to 6 hours after the onset of the disease. Thrombolysis can be administered intravenously or arterially, and super-selective arterial thrombolysis is more effective and less risky for bleeding when available now. The main risk and side effect of thrombolytic therapy is intracranial hemorrhage, and the chance of cardiogenic embolism brain hemorrhage is higher.
(iii) Anticoagulation therapy: commonly used drugs are heparin and low-molecular heparin, which must be tested for coagulation. The main side effect is bleeding, of which low-molecular heparin is safer than ordinary heparin.
(iv) Anti-platelet drugs.
(1) Aspirin, is the economic, affordable, safe and most conventional anti-platelet prophylaxis, the minimum effective dose is 50mg or 75mg/day. The dose may be increased to 300 mg/day in the acute phase.
(2) Raltegraviride can be used as a therapeutic and prophylactic drug at a dose and usage of 125-250mg/day, taken orally with meals. During the course of medication, the blood picture, liver function and blood clotting should be tested.
(E) Fibrin-lowering therapy: the function is to increase the activity of fibrinolytic system and inhibit thrombus formation, commonly used drugs include fibrin-lowering enzyme, Dongling pure thrombin and pit viper antithrombin. Use within 24 hours of the onset of disease. Fibrinogen should be detected in the process of drug administration.
(vi) Hemodilution therapy: The purpose is to reduce blood viscosity, improve microcirculation and replenish blood volume deficiency, commonly used drugs include low molecular dextrose and 706 plasma substitute.
(vii) The use of cerebral protective agents.
(H) Traditional Chinese medicine treatment
Rehabilitation period treatment: It is the most important method of treatment for cerebrovascular disease abroad, and generally systematic, standardized and individualized rehabilitation treatment is carried out from 3 to 7 days after the onset of the disease. The purpose is to improve symptoms such as dizziness and headache, limb numbness disorder, unfavorable language, etc., so that they can reach the best state; and reduce the high recurrence rate of cerebral infarction. Neurotrophic drugs, Chinese herbal medicine, acupuncture, physiotherapy, functional training and other comprehensive treatments can be applied.