Cerebral infarction (CI), also known as ischemic stroke (CIS), refers to localized cerebral tissue that is impaired by blood circulation, resulting in ischemic and hypoxic necrosis and corresponding neurological deficits. Cerebral infarction is the most common type of cerebrovascular disease, accounting for about 70% of all strokes. According to the pathogenesis and clinical manifestations of cerebral infarction, it is usually classified as cerebral thrombosis, cerebral embolism, and lacunar cerebral infarction. Common causes: cerebral thrombosis as atherosclerosis and arteritis; cerebral embolism as cardiogenic and non-cardiogenic emboli; lacunar cerebral infarction as hypertension, atherosclerosis and microemboli, etc.
I. Symptoms and signs.
Cerebral infarction is good for people aged 50 to 60 years or older, often with atherosclerosis, hypertension, wind heart disease, coronary heart disease or diabetes, as well as patients with bad habits such as smoking and alcohol consumption. About 25% of the patients have a history of transient ischemic attack before the disease. Most patients have prodromal symptoms before the onset of the disease, which are headache, dizziness, vertigo, transient limb numbness and weakness. The onset of the disease is usually slow, and patients tend to start in quietness and during sleep. Most of the patients’ symptoms reach their peak after a few hours or even 1 to 3 days.
1.Main clinical symptoms.
(1) Subjective symptoms: headache, dizziness, lightheadedness, vertigo, nausea and vomiting, motor and/or sensory aphasia, and even coma.
(2) Cerebral neurological symptoms: bilateral eye gaze to the side of the lesion, central facial and tongue palsy, pseudomyelinating palsy such as choking on water and dysphagia.
(3) Somatic symptoms: limb hemiparesis or mild hemiparesis, hemianesthesia, unsteady gait, limb weakness, incontinence, etc.
2.Types of clinical manifestations.
According to the speed and degree of occurrence of cerebral infarction, whether the condition is stable or not and the severity, cerebral infarction is divided into the following five types.
(1) Complete cerebral infarction: the condition reaches its peak within 6h of cerebral ischemia, often with complete hemiparesis, and the condition is generally severe.
(2) Progressive cerebral infarction: the condition is still progressively aggravated after 6h of ischemic attack, and such patients account for more than 40%. There are many reasons for progression, such as the expansion of thrombus, obstruction of other vessels or collateral vessels, cerebral edema, hyperglycemia, high temperature, infection, cardiopulmonary insufficiency and electrolyte disorders, most of which are caused by the first two reasons.
(3) Slowly progressive cerebral infarction: symptoms are still progressing within 2 weeks of onset.
(4) Stable cerebral infarction: Those whose condition does not change significantly after onset tend to have stable stroke. It is generally considered that those with ischemic attack in the internal carotid artery system for more than 24h and those with ischemic attack in the vertebrobasilar artery system for more than 72h have stable condition and can be considered as stable stroke. In this type of stroke, there is a high chance of infarct foci consistent with clinical manifestations seen on brain CT scan, suggesting that there has been irreversible lesion of brain tissue.
(5) Reversible ischemic neurological deficit (RIND): It refers to ischemic focal neurokinetic deficits that recover only in 24-72h, or completely recover within 4 weeks at the latest, without sequelae, and there is no infarct lesion in the corresponding area on brain CT scan.
Second, auxiliary examinations.
1.Blood examination: including blood routine, blood rheology, blood biochemistry, etc., mainly related to cerebrovascular disease risk factors such as hypertension, diabetes mellitus, hyperlipidemia, heart disease, atherosclerosis, etc.
2.Neuroimaging examinations.
(1) Brain CT: The main manifestations are: ① Hypodensity of the lesion: it is an important characteristic manifestation of cerebral infarction, and this sign may be due to ischemic edema of brain tissue. (2) Localized brain tissue swelling: it shows the disappearance of the cerebral sulcus, the deformation of the brain pool and ventricles by compression, and the displacement of the midline structures to the opposite side, i.e. the brain CT scan shows the occupying effect. This sign can be observed 4-6 h after the onset of the disease. (iii) Dense arterial shadow: It is an increased density shadow of the major cerebral arteries, commonly in the middle cerebral artery. The mechanism of occurrence is set off by the high density of thrombus or emboli compared to the contralateral or surrounding brain tissue. It can appear within 24h of ischemia in some patients.
(2) Brain MRI: It can detect cerebral infarction at an earlier stage, especially lesions in the brainstem and cerebellum. t1 and t2 chorography time is prolonged, t1 is low signal in the lesion area on weighted images, t2 is high signal, brain MRI examination can detect smaller infarct lesions, brain MRI diffusion imaging can reflect new infarct lesions. mri is dominant in the evaluation of early diagnosis and differential diagnosis of ischemic cerebral infarction, mri diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) are used for better early diagnosis of cerebral infarction.
(3) DSA, MRA and transcranial Doppler ultrasound: the main purpose of these 3 examinations is to find the etiology of the vascular aspects of cerebrovascular disease.
(3) Cerebrospinal fluid examination: it is generally not used as a routine examination for ischemic cerebrovascular disease. Most patients with cerebral infarction have normal cerebrospinal fluid, but the pressure may be increased if the infarct area is large and cerebral edema is obvious. A few patients with hemorrhagic infarction may have increased red blood cells, and there may be white blood cells and cell phagocytosis in the later stage.
III. Treatment options
1. The treatment principles of acute cerebral infarction are: ① Comprehensive treatment and individualized treatment: at different times of disease development, targeted comprehensive treatment and individualized treatment measures are taken for different conditions and etiologies. ② Actively improve and restore the blood supply to the ischemic area, promote cerebral microcirculation, and block and terminate the pathological process of cerebral infarction. ③Prevent and treat ischemic cerebral edema. ④Early treatment with cerebral cytoprotection should be used in the acute stage, and comprehensive measures can be taken to protect the brain tissue in the ischemic peripheral semidark zone to avoid aggravation of the disease. ⑤ Strengthen care and prevention of complications, eliminate pathogenic factors and prevent recurrence of cerebral infarction. ⑥Actively carry out early standardized rehabilitation treatment to reduce the rate of disability. ⑦Other: It is better not to use glucose liquid within 12h after the onset of the disease, but use hydroxyethyl starch (706 plasma substitute) or Ringer’s liquid with triphosphate adenosine (ATP), coenzyme A and vitamin C. Avoid aggravating acidosis and brain damage with high sugar liquid in the acute stage.
2. General treatment: including maintenance of vital signs and management of complications.
(1) Blood pressure: Elevated blood pressure in the acute phase of ischemic stroke usually does not require special treatment (except for hypertensive encephalopathy, subarachnoid hemorrhage, aortic dissection, heart failure, renal failure), unless systolic blood pressure is >220 mmHg or diastolic blood pressure is >120 mmHg and mean arterial pressure is >130 mmHg.
(2) Oxygenation and ventilation support: Airway support and assisted ventilation are required in critically ill patients with brainstem stroke and large infarcts or those with play involvement.
(3) Blood glucose: Blood glucose should be routinely checked, and when it exceeds 11.1 mmol/L, insulin therapy should be given immediately to control blood glucose below 8.3 mmol/L.
(4) Cerebral edema: It is mostly seen in large infarcts, and cerebral edema peaks 3-5 days after the onset. The therapeutic goals are to reduce intracranial pressure, maintain sufficient able in cerebral perfusion and prevent brain herniation from occurring. Can apply 20% mannitol 125-250ml / time static point, 6-8 hours once; for patients with cardiac and renal insufficiency can be replaced with furosemide 20-40mg intravenous, 6-8 hours once; can be applied at the same time as appropriate glycerol fructose 250-500ml / time static point, 1-2 times / day; can also be used for injectable heptaosaponin sodium and albumin adjuvant therapy.
(5) Infection: the acute phase is prone to respiratory and urinary tract infections, etc., which are important causes of exacerbation of the disease.
(6) Upper gastrointestinal bleeding: Stress ulcers are likely to occur in the acute phase in elderly and seriously affected stroke patients, routine application of intravenous anti-ulcer drugs (H2 receptor antagonists) is recommended; in patients prone to gastrointestinal bleeding, ice-saline gastric lavage, local application of hemostatic drugs (such as oral or nasal Yunnan Baiyao, thrombin, etc.) should be performed; in cases where the amount of bleeding causes shock, transfusion of fresh whole blood or red blood cell component transfusion is required if necessary .
(7) Fever: For patients with central fever, physical cooling (ice cap, ice blanket or alcohol bath) should be the mainstay, and artificial subhypothermia should be given if necessary.
(8) Deep vein thrombosis: Patients at risk of DVT and PE can be treated with prophylactic medication, preferably low molecular heparin 4000 IU subcutaneously 1-2 times/day; those with proximal DTV and no relief from anticoagulation should be given thrombolytic therapy.
(9) Water-electrolyte balance disorder: perform water-electrolyte test and correct it in time.
(10) Cardiac injury: The heart should be closely observed during the acute phase of stroke, and dynamic ECG monitoring and myocardial enzyme profile should be performed if necessary.
(11) Epilepsy: Prophylactic antiepileptic treatment is not usually used, but may be given in case of seizures or persistent status. If epilepsy occurs 2 weeks after stroke, long-term antiepileptic therapy should be administered to prevent recurrence.
3. Special treatment: including ultra-early thrombolysis, anti-platelet aggregation therapy, anticoagulation, endovascular therapy, cytoprotective therapy and surgical treatment.
(1) Intravenous thrombolytic therapy.
Indications: ① Early initiation of thrombolytic therapy can prevent massive cerebral infarction and save ischemic hemithorax and hypoperfusion state at least within 4-6h of symptom onset. ② Age <75 years. ③No impairment of consciousness, but for basilar artery thrombosis, even coma is not contraindicated due to poor prognosis. ④Brain CT scan excludes cerebral hemorrhage and there is no hypointense area corresponding to neurological deficit. ⑤ Thrombolytic therapy can be performed within 6 hours after onset, or within 12 hours in case of progressive stroke. (6) The patient's family should sign the consent.
Contraindications: ① Simple ataxia or sensory impairment. (2) Rapid recovery of clinical neurological deficit. ③Active internal bleeding, or bleeding quality and bleeding disorders, coagulation disorders, hypocoagulable state. ④Oral anticoagulants and those with prothrombin time >15s, or those who have used heparin within 48h and have prolonged partial thromboplastin time, hypoproteinemia. ⑤ Intracranial aneurysm, arteriovenous malformation, intracranial tumor, subarachnoid space hemorrhage, cerebral hemorrhage. ⑥History of cerebrovascular disease within 6 months, but lacunar infarction without significant limb paralysis is not affected. major surgery or severe trauma within 6 weeks. (⑦) Significantly increased blood pressure before treatment, systolic blood pressure > 24 kPa (180 mmHg), or diastolic blood pressure > 14.66 kPa (110 mmHg). (8) Others: those who have had cerebral hemorrhage or hemorrhagic cerebral infarction; those with gastrointestinal and urinary bleeding or active tuberculosis within 3 weeks; those who are menstruating, pregnant or within 10 days after delivery; those with severe liver and kidney dysfunction; those with platelet count <100,000; those with allergy to thrombolytic drugs; those with acute or subacute bacterial endocarditis.
Commonly used drugs for thrombolysis: ①Urokinase (UK): 1 million to 1.5 million IU plus 100-200 ml of saline, continuous sedation for 30 minutes. ②Recombinant tissue-type fibrinogen activator: a single dose of 0.9 mg/kg, maximum dose <90 mg, 10% of the dose is pushed intravenously, and the rest of the dose is continuously administered intravenously over about 60 minutes.
Complications of thrombolysis: (1) secondary bleeding from the infarct site or bleeding from other parts of the body; (2) fatal reperfusion injury and cerebral edema; (3) re-occlusion after thrombolysis.
(2) Arterial thrombolysis: for patients with severe stroke caused by occlusion of large arteries such as middle cerebral artery, arterial thrombolysis is feasible within 6 hours of onset.
(3) Anti-platelet aggregation: commonly used anti-platelet aggregation agents include aspirin and clopidogrel. Patients with acute cerebral infarction for thrombolysis should take aspirin within 48 hours, 100-325 mg/d, but aspirin is generally not applied within 24 hours after thrombolysis to avoid increasing the risk of bleeding. The antiplatelet aggregation efficacy of clopidogrel is generally considered superior to that of aspirin and can be given orally at 75 mg/d. Combining clopidogrel with aspirin for acute ischemic stroke is not recommended.
(4) Anticoagulation therapy: mainly includes heparin, low molecular heparin and warfarin.
(5) Cerebroprotective therapy: Cerebroprotective agents include free radical scavengers, opioid receptor blockers, voltage-controlled calcium channel blockers, excitatory amino acid receptor blockers and magnesium ions, which can reduce ischemic brain injury by reducing brain metabolism and interfering with ischemia-induced cytotoxic mechanisms. However, most cerebroprotective agents have been shown to be effective in animal experiments, on the lack of evidence from multicenter, randomized, double-blind clinical trial studies.
(6) Endovascular treatment: Endovascular treatment includes percutaneous transluminal angioplasty and endovascular stenting. For carotid stenosis >70% and neurological deficits associated with it, endovascular treatment can be considered according to the patient’s specific situation. Endovascular treatment is a newly introduced technique, and there are no large-scale clinical studies with long-term follow-up, so it should be chosen carefully.
(7) Surgical treatment: Interventional therapy for cerebral infarction and internal carotid artery stenosis, which is performed with the help of a digital subtraction angiography (DSA) machine with high definition and high resolution, and a small catheter is sent to the lesion in the brain under television guidance for examination, diagnosis and treatment.
(8) Rehabilitation treatment: It is advisable to start early, and after the condition is stabilized, education on rehabilitation knowledge and general training methods should be actively carried out, and attention should be paid to the position of the affected limbs.
(1) Reclining position: The upper limb should be in light external booth, elbow lightly flexed, scapula, forearm and hand supported by pillow, palm up, so that the forearm is kept in rotated posterior position to prevent the scapula from retracting. The pelvis and arms of the lower limbs are supported with pillows to prevent external rotation of the lower limbs and posterior fall of the pelvis. Patients with high extensor muscle tone of the lower limbs should be placed in the lateral position.
②When lying on the affected side: the shoulder on the affected side is extended forward, the elbow is extended, and the palm is upward. If the fingers are flexed and the muscle tone is high, the thumb is separated from the other four fingers by a roll of cloth or paper. The lower extremity is slightly flexed, and the foot is kept as vertical as possible to the lower leg.
③In the healthy side lying position: put a pillow under the upper limb of the affected side, straighten the upper limb, palm down, and raise the wrist slightly.
Encourage the patient to establish confidence in restoring self-care and cooperate with medical treatment and rehabilitation for early recovery, while supplementing with acupuncture, massage and physical therapy to reduce the disability rate and improve the quality of survival. Regarding the implementation of rehabilitation exercises, rehabilitation exercises for paralyzed limbs and other neurological deficits can be carried out moderately as early as possible under the guidance of a doctor, i.e., massage of the proximal and distal ends of the affected limbs and helping the joints of the affected limbs to do passive joint movement training. The patient is encouraged to use the affected limb more often according to the condition, and encouraged to use the healthy hand to help the affected hand to exercise. Gradually carry out turning training, sitting training, standing training and walking training. The functional training of the hand is repeated with the help of exercise equipment.
The study showed that rehabilitation exercise patients were significantly better than those who did not undergo rehabilitation exercise. It indicates that early rehabilitation treatment for cerebrovascular patients can significantly improve the cure and improvement rate, and the efficacy is significant for light and medium-sized patients, and heavy patients also have significant progress compared with those before rehabilitation.