I. Definition Cerebral infarction, also known as ischemic stroke, refers to ischemic necrosis and cerebral softening of limited brain tissue caused by impaired blood supply to the brain, ischemia and hypoxia. The common clinical types of cerebral infarction are cerebral thrombosis, cerebral embolism, lacunar cerebral infarction and watershed cerebral infarction. Second, the etiology 1, embolic cerebral infarction: cardiogenic including atrial fibrillation, recent myocardial infarction, artificial valve, congenital valve disease, endocarditis, appendage thrombosis, dilated myocarditis; arterial origin refers to thrombotic, cholesterol emboli, developing from the arterial arch and extracranial arteries (such as the internal carotid artery and vertebral artery). 2, thrombogenic cerebral infarction: including endothelial cell injury and loss, revealing subendothelial structures activating platelets, promoting thrombosis, inhibiting the fibrinolytic system, blood clotting, and systemic atherosclerosis in patients can produce atherosclerosis of intracranial arteries. 3.Lacunar cerebral infarction: refers to small softening foci occurring deep in the brain, most lacunae are about 0.5 cm in diameter, and the maximum diameter can be up to 1.8 cm. The etiology includes micro-arterial atherosclerosis, lipid hyaline degeneration, and fibrinoid necrosis caused by secondary hypertension, vasculitis, atherosclerotic vitreous degeneration, and amyloid vascular degeneration; however, most of them are related to hypertension. 4.Watershed cerebral infarction: It refers to local ischemia in the watershed area or marginal zone between adjacent vascular blood supply areas, usually mostly on the basis of internal carotid artery stenosis or occlusion, due to hemodynamic disorders, but also by cardiogenic and arterial-derived microemboli staying in the small arteries at the end, causing ischemic necrosis of brain tissue in the watershed area. 5, other causes: inflammation of the arterial wall such as tuberculosis, syphilis, septic, leptospirosis infection, connective tissue disease, allergic arteritis, etc. It is also seen in congenital vascular malformation, true erythrocytosis, blood hypercoagulable state, etc. 6. Unknown cause: Some cerebrovascular diseases have unknown causes. Diagnosis 1.Define whether it is cerebral infarction: the sudden clinical appearance of focal symptoms and signs should suspect the possibility of cerebral infarction. (2) Diagnosis of different types of cerebral infarction: (1) Embolic cerebral infarction: ① sudden onset, symptoms must reach the peak quickly ② history of rheumatic heart disease or acute myocardial infarction ③ electrocardiogram indicates atrial fibrillation ④ carotid and aortic ultrasound found unstable plaque ⑤ TCD embolism detection found excessive emboli in cerebral blood flow ② thrombogenic cerebral infarction: ① onset age is more advanced ② most have atherosclerosis and ③TIA may be present before the onset of the disease ④The onset of the disease is more frequent at quiet rest, and symptoms often appear after waking up ⑤Symptoms tend to worsen gradually within a few hours or longer ⑥Most patients are conscious, and focal signs of the nervous system such as hemiparesis and aphasia are obvious ⑦The CT examination is mostly normal in the early stage, and hypodense foci appear in 24-48 hours. (3) lacunar cerebral infarction ① Mostly occurs in middle-aged and elderly people aged 40-60 years and above, often accompanied by hypertension ② Acute onset, with less than 20% showing TIA-like onset, mostly during daytime activities ③ Diverse clinical manifestations, mild symptoms, single signs, no headache, intracranial hypertension and impaired consciousness. Common clinical cavernous syndromes include pure motor mild hemiparesis, pure sensory stroke, ataxic mild hemiparesis, dysarthria syndrome, and sensorimotor stroke. (4) Watershed cerebral infarction ① corroboration of systemic blood pressure drop in medical history ② onset in sitting or prone position to upright position ③ recurrent transient black haze in medical history ④ high degree of stenosis found in carotid artery examination ⑤ imaging findings of watershed cerebral infarction 3. ancillary examinations ① CT and MRI of the head ② PWI and DWI: to determine the presence of ischemia with dark bands, which is the basis for thrombolytic therapy ③ looking for evidence of arterial stenosis (4) Risk factor examination must be performed: such as blood glucose, lipid, blood homocysteine examination (5) Patients suspected of cerebral embolism must perform echocardiography and electrocardiography to clarify the source of embolus (4) Differential diagnosis 1. clinical significance, but sometimes the information obtained from the medical history varies greatly, and CT and MRI can provide a definitive diagnosis. 2. Intracranial occupying lesions: certain subdural hematomas, intracranial tumors, brain abscesses, etc. may also present with stroke-like onset and focal neurological deficits such as hemiparesis, which can be confused with cerebral infarction due to signs of cranial hypertension, especially optic papilloedema, which is not obvious. (1) Maintain respiratory function: monitor PO2 and PCO2, maintain oxygen saturation above 95%, and generally administer oxygen via nasal catheter; patients with acute cerebral infarction without hypoxemia do not need oxygen therapy. Patients with impaired consciousness and brainstem infarction are more likely to have respiratory complications due to oropharyngeal motor impairment and loss of protective cough reflex, and endotracheal intubation and assisted ventilation can help in treatment. (2) Adjustment of blood pressure: The increase in blood pressure in the acute phase is a compensatory response to the increase in cranial pressure, which can also be caused by irritability, bladder filling, pain, and the presence of pre-existing hypertension. Therefore, the triggers causing the increase in blood pressure should be removed first, and the cranial pressure should be treated with dehydration. Theoretically, antihypertensive treatment can improve cerebral edema, reduce the risk of infarct hemorrhage, avoid further vascular damage, and (3) control blood sugar: high blood sugar aggravates cerebral infarction, and it is not easy to input high-sugar fluids in the acute stage, and insulin should be given if blood sugar is >300mg/dl. Hypoglycemia rarely occurs in patients with acute cerebral infarction, and if it is found, it should be corrected in time. (4) Temperature control: Increased body temperature after ischemic stroke may be associated with increased metabolic demand, neurotransmitter release, and increased free radical products. A recent meta-analysis suggests that increased body temperature after stroke is associated with significantly increased morbidity and mortality. Reducing the acute elevated body temperature may improve the patient’s prognosis by pharmacological and physical means such as systemic cooling with an ice blanket. (5) Nutritional support: Gastric tube nasal feeding is performed for those with impaired consciousness and bulbar palsy who cannot eat. Patients with nasal feeding should have a process of adaptation, the initial amount should be small and light, and later can be gradually increased, each infusion volume of about 200-300ml, up to 500ml, 6 times a day, with an interval of 3 hours between. The head of the bed should be elevated 30-40c during nasal feeding to avoid gastric and esophageal reflux causing misaspiration and avoid overfeeding and rapid injection, which can easily produce nausea and vomiting and lead to misaspiration. The stomach contents should be aspirated before each nasal feeding, and if there is still food from the last feeding, the amount should be reduced as appropriate to avoid vomiting caused by gastric dilatation. Nasal nutrients should include carbohydrates, fats, proteins, vitamins, minerals, and trace elements. Currently available enteral total nutrition preparations for clinical use include Risu and Nenso. Stress ulcers are a common complication of stroke. For those who have severe brain injury with impaired consciousness and have to be fed nasally, clinical studies have shown that giving enteral nutrition preparations can effectively prevent the occurrence of stress ulcers. 2.Dehydration to lower cranial pressure: When large cerebral infarction has obvious intracranial hypertension, dehydration to lower cranial pressure drugs should be used. Commonly used 20% mannitol (mannitol) 125-250ml, rapid intravenous drip, 1 time / 6-8 hours; tachyon 20-40mg, intravenous injection, 1 time / 6-8 hours; or alternatively, can reduce mannitol-induced renal damage. Mannofructose has weak dehydration effect, 250ml intravenous drip, 1 time/6-8 hours, can be used alone or alternately with mannitol and tachypnea, suitable for those with renal insufficiency with intracranial hypertension. 3, thrombolytic therapy: within 6h, intravenous urokinase 1 million – 1.5 million units, arterial thrombolysis with urokinase if available. Intravenous rt-pA (0.9mg/kg, maximum dose 90mg) is the only FDA approved treatment for patients with acute cerebral infarction within 3 hours. (1) Indications: Within 6 hours of onset, CT confirmed no hemorrhagic foci nor infarct foci, or can be tried if CT remains unchanged at 12 hours of onset, age less than 75 years, blood pressure for 1 minute, and intravenous drip for the rest of half an hour. ②Monitor neurological changes and signs of bleeding. ③Measure blood pressure q15min*2h, followed by q30min*2h, followed by 60min*16h ④Vital signs q1h*12h, followed by 60min*16h ⑤Neurological function score (NIHSS) q1h*6h, followed by q3h*72h ⑥Nervous system examination daily after 24 hours ⑦Bed rest for 24 hours after drug administration, followed by re-evaluation ⑧Maintain blood pressure below 180/105mmhg ⑨ If severe headache, acute hypertension, nausea and vomiting occur, discontinue the use of UK and CT examination immediately ⑩ Repeat CT examination after 24 hours ⑩ No anticoagulant, aspirin or snake venom preparation should be used within 24 hours after treatment ⑩ Anti-platelet and/or anticoagulation therapy is feasible if CT shows no bleeding after 24 hours. (3) Monitoring items: ① Routine check of blood routine, blood glucose, ECG, coagulation function (PT, APTT, INR, FIB) before treatment. ②Monitor blood routine and coagulation function during treatment. ③Revisit CT 24 hours after onset. ④Management of complications: ①Brain hemorrhage or systemic hemorrhage: discontinue UK, immediately recheck CT, check platelets and coagulation image, transfusion of frozen plasma and fresh frozen plasma is possible. ② Treatment of vascular re-occlusion or persistent exacerbation: under the premise of excluding cerebral hemorrhage, give low molecular heparin (tachyphylaxis) 0.3-0.4 ml twice daily for 7-10 days. ③Lower cranial pressure, prevent stress ulcers and anti-infection. 4.Anticoagulation therapy: The therapeutic value of anticoagulation therapy in ischemic stroke has been controversial. Non-intestinal anticoagulant therapy (plain heparin, low-molecular heparin, or sodium heparinoid) is associated with severe intracranial and other body bleeding complications, and the use of anticoagulants is not recommended for all patients with acute ischemic stroke, especially those with moderate to severe ischemic cerebral infarction, because of the high risk of concomitant intracranial hemorrhage. More studies are needed to determine whether certain subgroups (large-vessel atherosclerotic plaques and those at high risk for recurrent embolic sources) might benefit from anticoagulation. intravenous thrombolytic therapy within 24 hours should not be combined with anticoagulation, and ischemic lesions and arterial stenosis of the vertebrobasilar system have not been shown to benefit from anticoagulation. 5. Anti-platelet aggregation drugs: Once the diagnosis of ischemic stroke is established, aspirin should be given within 48 hours if thrombolytic therapy is not available, and aspirin should be added 24 hours after intravenous thrombolytic therapy. See TIA for common drugs and usage of antiplatelet aggregation. 6. Fibrin-lowering therapy: It is recommended to inhibit thrombus formation by degrading fibrinogen in the blood and enhancing the activity of the fibrinolytic system, and is recommended for early onset. Available drugs include Defibrase, Batroxobin, Ancord and other snake venom preparations. 7.Cerebral protection therapy: No clinical studies have been published so far to prove the effectiveness of the recommended agents, but clinical treatment is mostly given to calcium antagonists, US ions, vitamin E and C. 8.Other: In the acute stage of cerebral infarction, the blood vessels in the ischemic area are paralyzed and in transition perfusion, and vasodilators can lead to blood theft in the brain and aggravate cerebral edema, so they should be used with caution or not. Clinical and experimental studies have shown that it is not easy to use drugs affecting energy metabolism in the acute phase of stroke, which can increase oxygen consumption in the brain cells that are already ischemic and hypoxic, aggravating cerebral hypoxia and cerebral edema, and should be used in the subacute phase of stroke (2-4 weeks after the disease). Chinese medicine treatment is promising and is under evaluation. 9. Surgical treatment: such as carotid endarterectomy, intracranial and extracranial arterial anastomosis, craniotomy and decompression are effective for patients with acute cerebral infarction. For large cerebral infarction and cerebellar infarction with signs of cerebral herniation, craniotomy and decompression treatment are appropriate. 10. Stroke unit: It is the most effective treatment for cerebrovascular disease, with evidence-based medical evidence level I (OR=0.79). It is not a new technology, it does not involve new drugs, but a concept, a management model. 11. Rehabilitation: physical and skill training for patients to reduce disability, improve daily living ability, return to family and society. Complications and prevention measures For those with limb paralysis and clear consciousness, appropriate movement of limbs in the hospital bed should be carried out as early as possible after the condition is stabilized. For those with consciousness impairment, they should turn over, pat their backs, move their limbs passively and elevate the head of the bed on time, and master the amount of nasal nutrition and the method of nasal feeding to prevent pulmonary infection, pulmonary embolism, postural hypotension, deep vein thrombosis of lower limbs, decubitus ulcers, joint ankylosis, etc. For urinary tract infections and pulmonary infections, antibiotics should be used reasonably according to the results of bacterial culture plus drug sensitivity to avoid dysbiosis and fungal infections due to improper use of antibiotics. In patients with cerebrovascular disease, stress ulcers are prone to occur. Some clinical studies have shown that the use of H2 receptor antagonists cimetidine and ranitidine does not prevent upper gastrointestinal bleeding, and alkalized gastric juice increases the incidence of pneumonia, and clinical studies have shown that the administration of enteral nutrition preparations can effectively prevent the occurrence of stress ulcers. In recent years, preventive treatment with drugs such as proton pump inhibitor Losec or cytoprotective drug thioglycollate is promoted to be effective. VII. Prognosis and prevention In conclusion, although there are many endless drugs for the treatment of cerebral thrombosis and the development of vascular interventional thrombolytic therapy, the treatment of cerebral infarction is still a difficult problem, and patients with cerebral infarction have a high rate of death, disability and recurrence. Anti-platelet aggregation drugs have a definite preventive effect.