Acidente vascular encefalico Flashcards
Define stroke and TIA.
(1) Stroke: acute onset and persistence beyond 24 hours of neurologic signs and symptoms that can be explained by a vascular mechanism.
(2) Transient ischemic attack (TIA): a clinical stroke that lasts less than 24 hours. High-risk patients should know about the symptoms of TIA, since 30% of patients with TIA will develop stroke within 5 years. Because TIAs can be the harbinger of stroke, neurologists now consider it a relative neurological emergency because some strokes are preventable with rapid intervention (internal carotid disease and atrial fibrillation for example).
List the risk factors for stroke and TIA.
Medical evidence for prevention of stroke is strongest for (1) atrial fibrillation (taking oral anticoagulants), (2) cholesterol (lowering with statin drugs), and (3) hypertension (weight loss and medications). Warfarin sodium, dabigatrin (thrombin inhibitor) and oral factor Xa inhibitors are superior for primary and secondary stroke prevention from atrial fibrillation; however they are more risky than aspirin (a less effective drug) because of risk of bleeding. Treatment of hypertension is responsible for a dramatic reduction in stroke incidence, and there exist multiple lines of evidence that lowering blood pressure into the 120-130 mmHg systolic range is beneficial. Furthermore, treatment of hypertension reduces both stroke and heart disease and as such has been shown to be cost effective. Cholesterol lowering also reduces the risk of stroke. Finally, smoking cessation is essential to prevent vascular disease including stroke, heart attack and peripheral vascular disease. For patients with diabetes, tight glucose control does not appear to influence stroke risk, but the health benefits from (4) tight glucose control outside of the brain support attention to this risk factor. (5) Mild alcohol consumption (1-2 drinks per day) is associated with a lower stroke risk than either no alcohol or excessive alcohol intake.
Classify strokes as ischemic or hemorrhagic.
Strokes are either hemorrhagic or ischemic.
(1) Hemorrhagic strokes occur when a vessel breaks causing bleeding into the brain or into surrounding compartments.
(2) Ischemic stroke occurs when a region of brain tissue is deprived of its blood supply. Ischemic stroke can be divided into large vessel and small vessel stroke. Large vessel strokes occur principally from emboli (clot that travels to the brain blood vessel causing sudden occlusion) while small vessel strokes occur from in situ thrombosis of the vessel itself.
Classify hemorrhagic stroke as intracerebral, subarachnoid or other.
About 15% of stroke is hemorrhagic.
(1) Intraparenchymal (or intracerebral) hemorrhage appears on CT scanning of the brain as a dense (white) object. The blood usually forms a hematoma that displaces the brain substance around it. Amyloid angiopathy is an arteriopathy linked with Alzheimer’s disease and predisposes for parenchymal lobar hemorrhages. Typically, these hemorrhages appear within the major brain lobes and not deep like the small vessel hemorrhage, and they are rare under age 60. Two common causes of intraparenchymal hemorrhage in young patients (< 45 years) are drug abuse (typically cocaine or methamphetamine) and rupture of arterial venous malformationsLarge hemorrhages (> 3 cm) in the cerebellum are often fatal if not removed because of brainstem compression from delayed edema. Nonsurgical management involves controlling intracranial pressure, draining CSF by ventriculostomy (catheter placed into the lateral ventricle) and protecting the patient’s airway until the hemorrhage and edema resolves.
(2) Subarachnoid hemorrhage is defined as bleeding within the subarachnoid space. It can occur from rupture of a berry aneurysm (aneurysmal subarachnoid hemorrhage), from blunt head trauma (traumatic subarachnoid hemorrhage), or extension from blood arising within another compartment, usually from the brain parenchyma.The treatment of subarachnoid hemorrhage from a ruptured aneurysm involves rapidly preventing the aneurysm from re-bleeding. This is accomplished by direct surgical “clipping” whereby a metallic clip is placed over the aneurysm neck or by coil embolization whereby soft metallic, thrombogenic coils are placed inside the aneurysm via catheter. Coiling has been shown to be safer with better outcomes than clipping in two major trials but not all aneurysms can be coiled while most aneurysms can be clipped.
Classify ischemic stroke as large vessel or small vessel.
Compare and contrast large and small vessel strokes and list their predisposing conditions.
(1) Small vessel infarcts occur in particular locations and produce a number of clinically reproducible syndromes, called lacunar syndromes. Lacunes appear on brain imaging and pathologically as CSF-filled “lakes” typically less than 1 ml in volume. There are many lacunar syndromes produced by sudden occlusion of certain small vessels.
(2) Large vessel infarcts are usually caused by embolic occlusion (clot that travels to the brain) of major cortical vessels, and less commonly from primary thrombosis of the artery (thrombotic occlusion). Typically, emboli arise from the heart, aorta, carotid bifurcation, or from a diseased intracranial vessel
List the major causes of cardioembolic infarction.
(1) Atrial fibrillation
(2) Acute myocardial infarction
(3) Mechanical heart valve
(4) Bacterial endocarditis
(5) Marantic endocarditis
List the clinical features of middle cerebral artery, anterior cerebral artery, posterior cerebral artery and basilar artery strokes.
(1) Arteria cerebral media: afasia, negligencia, hemiparesia, desvio do olhar ou hemianopsia homonima.
(2) Arteria cerebral anterior: fraqueza de perna e comprometimento cognitivo
(3) Arteria cerebral posterior: hemianopsia homonima.
(4) Arteria basilar: coma, paralisia de nervos cranianos, apneia ou instabilidade cardiovascular
Describe two common small vessel (lacunar) stroke syndromes.
Two common ones worth mentioning are (1) pure motor stroke and (2) pure sensory stroke. In these, the patient experiences sudden onset of either hemibody weakness or hemisensory loss without other signs, respectively. In pure motor stroke, the lesion is usually within the internal capsule contralateral to the weak side. For pure sensory stroke, the lesion is usually within the thalamus, from occlusion of a thalamogeniculate vessel arising from the posterior cerebral artery.
Describe the general treatments that are available for acute stroke.
(1) In December, 1995 an NIH sponsored trial reported that rt-PA given within 3 hours of symptom onset improved 3 month good outcome by 33% without an increase in mortality. This study is a landmark since it reported the first, proven treatment for stroke; before its publication, acute stroke was viewed as untreatable. The FDA approved rt-PA for use in ischemic stroke in July, 1996. The ECASS-III study published in 2008 showed that intravenous t-PA works if given up to 4.5 hours after ischemic stroke.
(2) In 2006, the FDA cleared a mechanical embolectomy device whereby the endovascular surgeon advances a cork-screw like device into the clot then pulls it out of the body restoring flow quickly. This can be coupled with t-PA to chase clot that embolizes beyond the reach of the catheter. More recent techniques utilize a vascular stent that can be deployed and retrieved with the clot attached, and in other circumstances a balloon is used the simply dilate the clot (balloon angioplasty). As the endovascular surgeon gains more experience with these techniques we will be able to treat a wider array of stroke patients more aggressively
(3) Management of the acute stroke victim involves protecting the patient from worse injury (e.g., aspiration pneumonia), allowing the brain to heal, instituting physical therapy and preventing another stroke. The priorities of initial hospitalization are maintaining a normal to elevated blood pressure to help collateral flow to the ischemic penumbra, protecting the patient’s airway, and treating cardiovascular instability.
Describe how to prevent strokes.
(1) Removal of atherosclerotic plaque from the carotid bifurcation (carotid endarterectomy) prevents artery-to-artery emboli. Three independent trials prove that endarterectomy of plaques causing 70% or greater reduction in diameter of the internal carotid artery reduces recurrent stroke risk and mortality.
(2) Treatment with oral anticoagulants (warfarin, dabigatrin and factor Xa inhibitors) for chronic atrial fibrillation reduces stroke risk with a significant but small risk of bleeding. Especially in patients who present with their first stroke, anticoagulation should be instituted for these patients unless strong contraindications exist (peptic ulcer disease, severe ataxia that predisposes for falls, etc.) The drug dabigatran (an oral thrombin inhibitor) and the drugs apixiban and rivaroxaban (oral factor Xa inhibitors) were approved by the FDA.
(3) Aspirin reduces the risk of stroke recurrence in patients who have suffered ischemic stroke and reduces mortality. Clopidogrel or Aggrenox (aspirin plus dipyridamole) may be substituted for aspirin when aspirin is contraindicated or the patient has failed aspirin.
(4) Since hypertension is the most significant risk factor for stroke its treatment is the mainstay for secondary prevention. We now target a blood pressure no greater than 130/80 and like to see blood pressures around 120/70. (Remember though that we like to keep blood pressure elevated during the first few weeks following a stroke to maintain collateral blood flow.). This is best achieved with angiotensin converting enzyme inhibitors (ACE-I) and or diuretics like hydrochlorothiazide. Low salt diet can help patients who are salt sensitive. Regular exercise and weight loss also help reduce blood pressure.
(5) Control of serum cholesterol is also an effective stroke prevention target. There are now several lines of evidence that use of statin drugs reduce second stroke risk. Current recommendations are to achieve a fasting serum LDL level less than 100 mg/dl in someone who has had a stroke. This can be done with dietary modification, but many patients are unable to do this alone without the addition of a statin drug.
