Acidente vascular encefalica Flashcards
Quais os principais diagnósticos diferenciais de síndrome neurovascular aguda?
There are several common causes of sudden-onset neurologic symptoms that may mimic stroke, including seizure, intracranial tumor, migraine, and metabolic encephalopathy
Quando um familiar deve ligar para a ambulancia na suspeita de AVC?
Patients and their family members should be counseled to call emergency medical services immediately if they experience or witness the sudden onset of any of the following: loss of sensory and/or motor function on one side of the body (nearly 85% of ischemic stroke patients have hemiparesis); change in vision, gait, or ability to speak or understand;
Quais as etapas fundamentais do manejo da síndrome neurovascular aguda?
(1) The first goal is to prevent or reverse brain injury. Attend to the patient’s airway, breathing, and circulation (ABC’s), and treat hypoglycemia or hyperglycemia if identified.
(2) Perform an emergency noncontrast head CT scan to differentiate between ischemic stroke and hemorrhagic stroke; there are no reliable clinical findings that conclusively separate ischemia from hemorrhage, although a more depressed level of consciousness, higher initial blood pressure, or worsening of symptoms after onset favor hemorrhage, and a deficit that is maximal at onset, or remits, suggests ischemia.
Quais os pilares do tratamento do AVCi agudo?
. Treatments designed to reverse or lessen the amount of tissue infarction and improve clinical outcome fall within six categories: (1) medical support, (2) IV thrombolysis, (3) endovascular techniques, (4) antithrombotic treatment, (5) neuroprotection, and (6) stroke centers and rehabilitation.
Qual deve ser o suporte medico no AVCi agudo?
(1) Many physicians use pneumatic compression stockings to prevent DVT; subcutaneous heparin (unfractionated and low-molecular weight) is safe and more effective and can be used concomitantly
(2) Blood pressure should be lowered if there is malignant hypertension or concomitant myocardial schemia or if blood pressure is >185/110 mmHg and thrombolytic therapy is anticipated. When faced with the competing demands of myocardium and brain, lowering the heart rate with a β1-adrenergic blocker (such as esmolol) can be a first step to decrease cardiac work and maintain blood pressure.
(3) Fever is detrimental and should be treated with antipyretics and surface cooling.
(4) Serum glucose should be monitored and kept at <6.1 mmol/L (110 mg/dL) using an insulin infusion if necessary.
(5) Between 5 and 10% of patients develop enough cerebral edema to cause obtundation or brain herniation. Edema peaks on the second or third day but can cause mass effect for ∼10 days. The larger the infarct, the greater the likelihood that clinically significant edema will develop. Water restriction and IV mannitol may be used to raise the serum osmolarity, but hypovolemia should be avoided as this may contribute to hypotension and worsening infarction. Combined analysis of three randomized European trials of hemicraniectomy (craniotomy and temporary removal of part of the skull) shows that hemicraniectomy markedly reduces mortality, and the clinical outcomes of survivors are acceptable.
Quais as evidencias para o tratamento trombolítico endovenoso?
(1) The NINDS study used IV rtPA (0.9 mg/kg to a 90-mg max; 10% as a bolus, then the remainder over 60 min) versus placebo in patients with ischemic stroke within 3 h of onset. One-half of the patients were treated within 90 min. Symptomatic intracerebral hemorrhage occurred in 6.4% of patients on rtPA and 0.6% on placebo. There was a nonsignificant 4% reduction in mortality in patients on rtPA (21% on placebo and 17% on rtPA); there was a significant 12% absolute increase in the number of patients with only minimal disability (32% on placebo and 44% on rtPA). Based on these combined results, the European Cooperative Acute Stroke Study (ECASS) III study explored the safety and efficacy of rtPA in the 3- to 4.5-h time window. Unlike the NINDS study, patients older than 85 years of age and diabetic patients were excluded.
Quais os cuidados com o trombolítico endovenoso?
(1) Intravenous access with two peripheral IV lines (avoid arterial or central line placement)
(2) Review eligibility for rtPA
(3) Administer 0.9 mg/kg IV (maximum 90 mg) IV as 10% of total dose by bolus, followed by remainder of total dose over 1 h
(3) Frequent cuff blood pressure monitoring
(4) No other antithrombotic treatment for 24 h
(5) For decline in neurologic status or uncontrolled blood pressure, stop infusion, give cryoprecipitate, and reimage brain emergently
(6) Avoid urethral catheterization for v2 h
Quais as contraindicações a terapia trombolítica endovenosa?
(1) Sustained BP >185/110 mmHg despite treatment
(2) Platelets <100,000;
(3) HCT <25%;
(3) glucose <50 or >400 mg/dL
(4) Use of heparin within 48 h and prolonged PTT, or elevated INR
(5) Rapidly improving symptoms
(6) Prior stroke or head injury within 3 months;
(7) Prior intracranial hemorrhage
(8) Major surgery in preceding 14 days
(9) Minor stroke symptoms
(10) Gastrointestinal bleeding in preceding 21 days
(11) Recent myocardial infarction
(12) Coma or stupor
Quando indicar o tratamento endovascular para o AVE?
Occlusions in such large vessels (middle cerebral artery [MCA], internal carotid artery, and the basilar artery) generally involve a large clot volume and often fail to open with IV rtPA alone. (1) The Prolyse in Acute Cerebral Thromboembolism (PROACT) II trial found benefit for intraarterial pro urokinase for acute MCA occlusions up to the sixth hour following onset of stroke. (2) The Mechanical Embolus Removal in Cere bral Ischemia (MERCI) and multi-MERCI single-arm trials investigated the ability of a novel endovascular thrombectomy device to restore patency of occluded intracranial vessels within 8 h of ischemic stroke symptoms. Recanalization of the target vessel occurred in 48–58% of treated patients and in 60–69% following use of adjuvant endovascular methods, and successful recanalization at 90 days correlated well with favorable outcomes
Qual o tratamento antitrombótico para o AVCi agudo?
Two large trials, the International Stroke Trial (IST) and the Chinese Acute Stroke Trial (CAST), found that the use of aspirin within 48 h of stroke onset reduced both stroke recurrence risk and mortality minimally. Among 19,435 patients in IST, those allocated to aspirin, 300 mg/d, had slightly fewer deaths within 14 days (9.0 versus 9.4%), significantly fewer recurrent ischemic strokes (2.8 versus 3.9%), no excess of hemorrhagic strokes (0.9 versus 0.8%), and a trend toward a reduction in death or dependence at 6 months (61.2 versus 63.5%). In CAST, 21,106 patients with ischemic stroke received 160 mg/d of aspirin or a placebo for up to 4 weeks. There were very small reductions in the aspirin group in early mortality (3.3 versus 3.9%), recurrent ischemic strokes (1.6 versus 2.1%), and dependency at discharge or death (30.5 versus 31.6%). Numerous clinical trials have failed to demonstrate any benefit of anticoagulation in the primary treatment of atherothrombotic cerebral ischemia.
Qual o tratamento neuroprotetor para o AVEi agudo?
Neuroprotection is the concept of providing a treatment that prolongs the brain’s tolerance to ischemia. Drugs that block the excitatory amino acid pathways have been shown to protect neurons and glia in animals, but despite multiple human trials, they have not yet been proven to be beneficial.
Como deve ser a reabilitação dentro das Stroke Units?
Proper rehabilitation of the stroke patient includes early physical, occupational, and speech therapy. It is directed toward educating the patient and family about the patient’s neurologic deficit, preventing the complications of immobility (e.g., pneumonia, DVT and pulmonary embolism, pressure sores of the skin, and muscle contractures), and providing encouragement and instruction in overcoming the deficit. The goal of rehabilitation is to return the patient to home and to maximize recovery by providing a safe, progressive regimen suited to the individual patient. Additionally, the use of restraint therapy (immobilizing the unaffected side) has been shown to improve hemiparesis following stroke, even years following the stroke, suggesting that physical therapy can recruit unused neural pathways.
O que deve ser feito para investigação de mecanismo do AVE?
(A) Clinical examination should focus on the peripheral and cervical vascular system (carotid auscultation for bruits, blood pressure, and pressure comparison between arms), the heart (dysrhythmia, murmurs), extremities (peripheral emboli), and retina (effects of hypertension and cholesterol emboli [Hollenhorst plaques]).
(B) Neurological exam may suggest lacunar syndrome: (1) pure motor hemiparesis from an infarct in the posterior limb of the internal capsule or basis pontis; the face, arm, and leg are almost always involved; (2) pure sensory stroke from an infarct in the ventral thalamus; (3) ataxic hemiparesis from an infarct in the ventral pons or internal capsule; and (4) dysarthria and a clumsy hand or arm due to infarction in the ventral pons or in the genu of the internal capsule.
(C) An imaging study of the brain is nearly always indicated and is required for patients being considered for thrombolysis; it may be combined with CT- or MRI-based angiography to interrogate the neck and intracranial vessels.
(D) A chest x-ray, electrocardiogram (ECG), ecocardiogram, urinalysis, complete blood count, erythrocyte sedimentation rate (ESR), serum electrolytes, blood urea nitrogen (BUN), creatinine, blood sugar, serologic test for syphilis, serum lipid profile, prothrombin time (PT), and partial thromboplastin time (PTT) are often useful and should be considered in all patients.
(E) Since this risk factor is so important, many clinicians are performing extended ambulatory monitoring to detect intermittent atrial fibrillation in otherwise cryptogenic stroke since its detection would shift toward prescription of oral anticoagulation long term.
Quais os possíveis tratamentos para os fatores de risco?
(1) Oral contraceptives and hormone replacement therapy increase stroke risk, and certain inherited and acquired hypercoagulable states predispose to stroke.
(2) The Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) trial showed benefit in secondary stroke reduction for patients with recent stroke or TIA, who were prescribed atorvastatin, 80 mg/d. The primary prevention trial, Justification for the Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER), found that patients with low LDL (<130 mg/dL) caused by elevated C-reactive protein benefitted by daily use of this statin. Primary stroke occurrence was reduced by 51% (hazard ratio 0.49, p = 0.004) and there was no increase in the rates of intracranial hemorrhage. Therefore, a statin should be considered in all patients with prior ischemic stroke.
(3) Tobacco smoking should be discouraged in all patients.
(4) Tight control of blood sugar in patients with type 2 diabetes lowers stroke risk MI and death of any cause, but no trial sufficiently powered to detect a significant reduction in stroke has yet been performed.
(5) Lowering blood pressure to levels below those traditionally defining hypertension appears to reduce the risk of stroke even further. Data are particularly strong in support of thiazide diuretics and angiotensin-converting enzyme inhibitors.
(6) Symptomatic carotid stenosis was studied in the North American Symptomatic Carotid Endarterectomy Trial (NASCET) and the European Carotid Surgery Trial (ECST). Both showed a substantial benefit for surgery in patients with a stenosis of ≥70%. In NASCET, the average cumulative ipsilateral stroke risk at 2 years was 26% for patients treated medically and 9% for those receiving the same medical treatment plus a carotid endarterectomy. This 17% absolute reduction in the surgical group is a 65% relative risk reduction favoring surgery. recent meta-analysis of the NASCET and ECST trials demonstrated that endarterectomy is most beneficial when performed within 2 weeks of symptom onset. In addition, benefit is more pronounced in patients >75 years, and men appear to benefit more than women. In summary, a patient with recent symptomatic hemispheric ischemia, high-grade stenosis in the appropriate internal carotid artery, and an institutional perioperative morbidity and mortality rate of ≤6% generally should undergo carotid endarterectomy. The Carotid Revascularization Endarterectomy versus Stenting Trial (CREST) enrolled 2502 patients with either asymptomatic or symptomatic stenosis. The 30-day risk of stroke was 4.1% in the stent group and 2.3% in the surgical group, but the 30-day risk of MI was 1.1% in the stent group and 2.3% in the surgery group, suggesting relative equivalence of risk between the procedures. At median follow-up of 2.5 years, the combined endpoint of stroke, MI, and death was the same (7.2% stent versus 6.8% surgery).
(7) Aspirin is inexpensive, can be given in low doses, and could be recommended for all adults to prevent both stroke and MI. However, it causes epigastric discomfort, gastric ulceration, and gastrointestinal hemorrhage, which may be asymptomatic or life threatening.
(8) Several trials have shown that anticoagulation (INR range, 2–3) in patients with chronic nonvalvular (nonrheumatic) atrial fibrillation prevents cerebral embolism and is safe. For primary prevention and for patients who have experienced stroke or TIA, anticoagulation with a VKA reduces the risk by about 67%, which clearly outweighs the 1–3% risk per year of a major bleeding complication. A recent randomized trial compared the new oral thrombin inhibitor dabigatran to VKAs in a noninferiority trial to prevent stroke or systemic embolization in nonvalvular atrial fibrillation. Anticoagulation also reduces the risk of embolism in acute MI. Most clinicians recommend a 3-month course of anticoagulation when there is anterior Q-wave infarction, substantial left ventricular dysfunction, congestive heart failure, mural thrombosis, or atrial fibrillation.Stroke secondary to thromboembolism is one of the most serious complications of prosthetic heart valve implantation. The intensity of anticoagulation and/or antiplatelet therapy is dictated by the type of prosthetic valve and its location. Many neurologists recommend combining antiplatelet agents with anticoagulants for patients who “fail” anticoagulation (i.e., have another stroke or TIA).
Quais os pilares do manejo de hemorragia intraparenquimatosa?
(1) Nearly 50% of patients with a hypertensive ICH die, but others have a good to complete recovery if they survive the initial hemorrhage. The ICH scoring system is a validated metric that is useful for prediction of mortality and clinical outcomes. Tissue surrounding hematomas is displaced and compressed but not necessarily infarcted. Hence, in survivors, major improvement commonly occurs as the hematoma is reabsorbed and the adjacent tissue regains its function.
(2) Any identified coagulopathy should be reversed as soon as possible. For patients taking VKAs, rapid reversal of coagulopathy can be achieved by infusing prothrombin complex concentrates which can be administered quickly, followed by fresh-frozen plasma and vitamin K. When ICH is associated with thrombocytopenia (platelet count <50,000/μL), transfusion of fresh platelets is indicated
(3) Evacuation of supratentorial hematomas does not appear to improve outcome. The International Surgical Trial in Intracerebral Haemorrhage (STICH) randomized 1033 patients with supratentorial ICH to either early surgical evacuation or initial medical management. No benefit was found in the early surgery arm. For cerebellar hemorrhages, a neurosurgeon should be consulted immediately to assist with the evaluation; most cerebellar hematomas >3 cm in diameter will require surgical evacuation. If the patient is alert without focal brainstem signs and if the hematoma is <1 cm in diameter, surgical removal is usually unnecessary. Patients with hematomas between 1 and 3 cm require careful observation for signs of impaired consciousness and precipitous respiratory failure.
Glucocorticoids are not helpful for the edema from intracerebral hematoma. Once ICP is recorded, further hyperventilation and osmotic therapy can be tailored to the individual patient to keep cerebral perfusion pressure (MAP-ICP) above 60 mmHg. For example, if ICP is found to be high, CSF can be drained from the ventricular space and osmotic therapy continued; persistent or progressive elevation in ICP may prompt surgical evacuation of the clot or withdrawal of support
