How should cerebral embolism be treated?

  It is known that cerebral infarction is a disease with high disability rate and high mortality rate, and the incidence is getting higher and higher in recent years, and it is developing to younger and younger, patients aged 30-40 can be seen clinically, but most of them are middle-aged and older than 45 years old, which seriously affects the physical and mental health of patients and increases the economic burden to their families. Therefore, people will have questions about whether cerebral infarction can be treated? How should the correct treatment of cerebral infarction be carried out?
  Cerebral infarction is a common brain disease, and this disease is treatable. The treatment of cerebral infarction cannot be generalized, and highly targeted treatment plans should be determined according to different etiologies, pathogenesis, clinical types, onset time, etc., and individualized treatment with typing and staging as the core should be implemented. On the basis of general medical support treatment, measures such as improving cerebral circulation, cerebral protection, anti-cerebral edema and lowering cranial pressure can be used as appropriate. Usually, the disease can be divided into acute phase (1-2 weeks), recovery phase (2 weeks-6 months) and sequelae phase (after 6 months) according to the course of the disease, with 3-6 hours also known as ultra-early phase. The focus is on thrombolytic therapy within the time window of <6 hours and the staging of the acute phase. In lacunar cerebral infarction, dehydration is not recommended, and the main focus is to improve circulation; in large and medium infarction, active anti-cerebral edema should be used to lower cranial pressure and prevent brain herniation formation.
  1.Thrombolytic therapy
  ”Time is brain.” —- In acute cerebral infarction, time is crucial, and the time window of thrombolytic therapy for acute cerebral infarction is very narrow, and the key to salvage is whether correct thrombolytic therapy can be obtained within the first 3-6 hours of onset (within 3-6 hours of onset). Within the first 3-6 hours of onset is called ultra-early thrombolysis), which can save ischemic brain tissue, avoid ischemic brain tissue necrosis, and prevent recurrence and complications.
  Intravenous thrombolytic therapy with recombinant tissue-type fibrinogen activator (rt-PA) within 3 h of onset has been conclusively shown to significantly reduce the risk of death and severe disability, but also to significantly improve the quality of life of survivors. Intravenous thrombolysis with urokinase is safe and effective within 6 h of onset in patients with acute ischemic stroke who have no significant hypointense changes in brain CT and are conscious.
  (1) Urokinase: 1 million IU ~ 1.5 million IU, dissolved in 100~200 ml of saline, 30 min of continuous intravenous drip.
  ② rtPA: 0.9mg/kg (maximum dose 90mg), 10% intravenous push (1min), the rest of the dose is given continuously by IV drip for 60min.
  The efficacy of thrombolytic therapy is obvious, but it is not suitable for all patients, and the following indications should be noted: age 18-75 years old; onset within 6h, signs of brain impairment persist for more than 1 hour and are relatively severe; intracranial hemorrhage has been excluded by brain CT. Intracranial hemorrhage; history of myocardial infarction in the past 3 months; oral anticoagulation with INR >1.5; heparin therapy within 48 hours (aPTT outside the normal range); platelet count <100,000/mm3, blood glucose <2.7 mmol >180 mmHg, or diastolic blood pressure >100 mmHg are contraindicated.
  Anticoagulation and antiplatelet agents are generally not used within 24 hours after thrombolytic therapy. Aspirin 300 mg/d for 10 days is available for those without contraindications after 24 hours. Do not place nasogastric tube, urinary catheter or intra-arterial pressure measuring catheter too early. Clinically, it should be noted that thrombolysis beyond the time window will not increase the therapeutic effect, and will increase reperfusion injury and bleeding complications, so thrombolysis is not recommended.
  2.Fiber-lowering therapy
  A lot of evidence shows that fibrinogen and blood viscosity in plasma are increased in the acute stage of cerebral infarction. Snake venom preparations can significantly reduce plasma fibrinogen levels, and also increase fibrinolytic activity and inhibit thrombosis, which is more suitable for patients with combined hyperfibrinogenemia. Early cerebral infarction (especially within 12 hours) can be treated with fibrin-lowering therapy.
  Bactrim
  Bactrim can significantly reduce the fibrinogen level and improve the symptoms of acute cerebral infarction quickly with mild adverse effects, but attention should also be paid to the bleeding tendency.
  ② Fibrin-lowering enzyme
  Fibrinogen can effectively reduce fibrinogen levels in the blood of cerebral infarction patients, improve neurological function, and reduce the recurrence rate of stroke, especially within 6 hours of the onset of stroke. It is worth noting that the tendency to bleed is increased when fibrinogen is reduced below 130 mg/dl.
  (3) Other fibrin-lowering agents: earthworm kinase, herbimycin, etc.
  3.Anticoagulation therapy
  The purpose of anticoagulation therapy is to prevent early recurrence of ischemic stroke, prolongation of thrombosis, prevention of secondary thrombosis by blocking the distal small vessels, and promotion of collateral circulation. Commonly used are ①unfractionated heparin (UFH) ②low molecular weight heparin (LMWH).
  When anticoagulation is used, the coagulation function should be closely monitored. Routine and immediate use of anticoagulants is not recommended for patients with acute cerebral infarction in general. In patients treated with thrombolysis, anticoagulants are generally not recommended within 24 hours. In patients with cardiogenic infarction (e.g., prosthetic valve, atrial fibrillation, myocardial infarction with appendage thrombosis, left atrial thrombosis, etc.), application of anticoagulation is likely to recur in stroke.
  4.Anti-platelet agents
  Most patients without contraindications to thrombolysis should be started on aspirin or clobigrel as soon as possible after stroke (preferably within 48 hours).
  Early use of aspirin is effective in reducing mortality and disability, with no significant increase in symptomatic cerebral hemorrhage, but concomitant use with thrombolytic drugs may increase the risk of bleeding.
  ②Clobigrel 75 mg,1 time/d.
  5.Volume expansion
  For patients with cerebral infarction in general, there are no sufficient randomized clinical control studies to support that volume expansion and pressure increase can improve the prognosis, but for acute cerebral infarction caused by cerebral blood flow hypoperfusion such as watershed infarction, volume expansion therapy can be considered as appropriate, but attention should be paid to possible aggravation of cerebral edema, cardiac failure and other complications.
  6.Neuroprotective agents: cytidyl phosphorylcholine, olanzapine, ganglioside, cerebral protein hydrolysate, etc.
  7.Chinese herbal medicine treatment
  A large number of studies have proved that Chinese herbal medicine has unique advantages in the treatment of cerebral infarction. Some single components or multiple drug combinations of TCM, such as Danshen, Chuanxiongzin, thromboxane, safflower and Ginkgo biloba preparations, can reduce platelet aggregation, anticoagulation, improve cerebral blood flow and reduce blood viscosity. Acupuncture, physiotherapy, and rehabilitation training of TCM, and more targeted identification and treatment of different patients by TCM play an important role in all stages of treatment for patients with cerebral infarction.