ischemic stroke Flashcards
Incidence and mortality rates for cerebrovascular disease
declining due to lessening stroke severity and better treatment of stroke risk factors
Define stroke or cerebrovascular disease
general term that refers to any vascular injury to the brain
Define ischemic stroke
ischemic injury to the brain causing a persistent clinical deficit at 24 hours. Even mild residual deficits are classified as strokes. The severity of the deficit is not the determinant, only that the deficit is present at 24 hours.
define transient ischemic attacks
ischemic neurological deficits that have completely resolved by 24 hours, regardless of their severity or relative duration (seconds or hours). Some recommend shortening this time period to 1-2hrs, since only short TIAs do not impart any damage to CNS
ischemic Stroke time course of presentation
come on rapidly with no warning, headache, or change in consciousness. Deficit most severe at onset, with progressive improvement over seconds, minutes, hours, days and weeks
Large vessel ischemia
causes deficits in multiple systems. For example, a typical patient with a large vessel ischemic stroke in the middle cerebral artery territory will have a hemiparesis, a hemi-sensory loss, and a homonymous hemi-anopsia contralateral to the ischemic side of the brain
Small vessel ischemia
isolated motor (or isolated sensory) deficit on one side of the body. Caused by occlusion of small penetrating vessels that branch from large arteries and produce lacunar infarctions
Multi infarct dementia
Accumulation of multiple lacunar strokes over many years
What causes multiple areas of ischemia at one time
hypoperfusion: causes multiple areas of mixed small and/or large vessel infarction. Caused by systemic hypotension, , inadequate perfusion during cardiopulmonary bypass, and isolated major vessel stenosis, multiple emboli showers, vasospasm, hypercoagulation or inflammatory processes
Virchows triad
Endothelial disruption, stasis, hypercoagultion
risk factors for stroke
Age, men, race, HTN (increases with any increase in BP), lipid disorders, homocysteine elevation, smoking, obesity, physical inactivity, diabetes, alcohol abuse
Structural risks for stroke
Atrial fibrillation, CHF, valvular disorders, atrial septal defect (embolus can bypass lung and go to brain), arterial stenosis, dissection or occlusion, infectious endocarditis (infectious embolic stroke or mycotic aneurysm), tumors (atrial myxoma)
Causes of Young stroke
vasculopathies, hematological disorders, inflammatory mechanisms, vasospasm
What are vasculopathies
Non-inflammatory, non-atherosclerotic hyperplasia of arteries
Fibromuscular dysplasia population, what is it, treatment, cause, associations
Women in 30’s-40’s. Hypertrophy of arterial media causing multiple areas of segmental occlusion or stenosis. Renal artery, carotid artery and vertebral artery common. Treated with arterial dilation. No known cause, possibly estrogen or viral? Associated with arterial dissection and intracranial saccular aneurysms
Moya Moya- what is it, who gts it, pathology, associations
Non atherosclerotic Focal occlusion of middle cerebral artery. Occurs in children and women in 30-40’s. Pathology is intimal hyperplasia. associated with secular aneurysms and dissection
Arterial dissection- what is it, therapy
Results from a tear in the endothelial lining of the artery that allows blood to dissect between the endothelium and the adventitia, in the media of the artery. The occlusion or stenosis of the artery is typically well tolerated, however, emboli from the injured artery can move into the distal artery territory and cause significant strokes. Therapy is with anticoagulation until the dissection heals, although intra-arterial stenting or surgery can have a role.
Two types of arterial dissection
Traumatic dissection: Major traumatic injury and direct force to artery. Can happen to anyone. Spontaneous dissection: occurs from normal activities such as swinging golf club. Arteries may be unstable due to other vasculopathies (ie. FMD, marfans, coarctation),
Types of hematological disorders that can cause stroke and how are they treated
Familial deficiencies of blood components that help to prevent thrombosis such as deficiencies of Protein C, Protein S, or Antithrombin, or the presence of Factor V Leiden, or Prothrombin Gene, are associated with venous thrombosis, including CNS. Treatment with anticoagulation
Malignancies and stroke
can cause a poorly understood hypercoagulable state. Peripheral venous events more common than arterial
Sickle cell anemia and stroke
SSA responds to transfusion. The Sickle Cell Trait cells can on occasion ‘sickle’ with dehydration or altitude, but this doesn’t seem to impart any additional risk of stroke or CNS hemorrhage
hyperviscosity states and stroke
Protein, elevated hematocrit (60%), thrombocytosis (1,000,000), etc. can generate slowness of flow beyond the pump & pipes ability to compensate.
Oral contraceptives and stroke
Causes stroke or venous thrombosis. Migraine/Smokers/OCP increase risk by 25 times
Antiphospholipid antibodies and stroke
cause a triad of spontaneous miscarriage, thrombocytopenia, and recurrent large vessel thrombosis, arterial or venous. The mechanism appears to be an attack of the phospholipid membranes in the chorion, platelet, and endothelium, respectively. Treatment involves antithrombotics, anticoag or no treatment
Vasculitis and stroke
Can have systemic vasculitis that secondarily affects CNS or isolated CNS vasculitis. Vasculitis has traditionally been considered a manifestation of immunological disorders, but over time, infectious causes are emerging. Varicella-Zoster Virus is increasingly being found in CNS vasculitis.
Migraine and stroke
The mechanism of migraine stroke is either vasospasm (sterile serotonin mediated intramural inflammation perhaps mediated through the autonomic nervous system), or increased platelet aggregation that clogs the microcirculation leading to permanent cellular injury. Antiplatelet therapy is usually effective
Venous infarctions- causes
The most common cause is major head trauma. Most non-traumatic venous infarction occurs from dehydration, CNS infections, and hypercoagulable states (transient or genetic). Post-partum Sagittal Sinus Thrombosis around days 3-5 is a popular board question
Vasospasms causing stroke- causes
sympathometic drugs, severe hypertension, primary vessel irritation (intrathecal drug, catheter contrast, SAH blood) trigger vasospasm that can cause permanent injury.
Therapy to prevent recurrent stroke
Treat risk factors (ie. Eat healthy, low stress, etc), aspirin, thienopyridines (Clopidogrel, Prasurgrel, Ticlopidine) and Anticoagulants
Anti-platelet therapies
Aspirin: (81mg or 325mg/day). May require H2 blocker or proton pump inhibitor if GI problems. Combo therapy: Clopidogrel plus aspirin is useful after catheter based cardiac re-vascularization, after CNS ischemic event, and long term for arteriopaths. Dipyridamole: available with aspirin combo
Anticoagulants
Warfarin: used for atrial fibrillation and patients with mechanical heart valves or CHF. Direct thrombin inhibitors (Dabigatran, Rivaroxiban, and Apixaban): same benefits as warfarin but may be better for lower risk populations and dont work as well for mechanical valves. Injected/IV anticoag: Heparin (AT III, Thrombin), the low molecular weight heparins Enoxaparin & Daltaperin (AT III, Thrombin, Xa), and Argatroban (Thrombin)
Geriatric population and anticoags
there is concern that patients over the age of 75 have a higher risk of hemorrhage, so warfarin may not be preferred. Alternatives include aspirin, DTIs, low intensity warfarin. Grading Scales for Atrial Fibrillation like CHADS (points for age, HTN, CHF, DM, Stroke) estimate the benefit/risk ratio.
Anticoag vs antiplatelets
Anticoagulation is considered in the patients with a high risk of embolization and large vessel occlusion. For patients with small vessel infarctions, or with low risk of embolization and large vessel occlusion, antiplatelet agents are as useful as anticoagulation, but without the risk.
Carotid endarterectomy
Highly beneficial in symptomatic patients with high grade (70-90%) stenosis. Only minimal efficacy in 50-69% stensosis, however asymptomatic patients who undergo carotid endarterectomy plus aspirin and risk factor reduction (with 60% or greater stenosis) benefit.
Catheter options for stroke
angioplasty, stent, coil/balloon, embolize, embolectomy
BP management after stroke
Most patients have relative hypertension after a stroke that slowly improves over the next 7-10 days. There is little reason to initiate treatment unless the blood pressure is elevated to very high levels.
Steps for management of stroke
Fluids (normal saline if not worried about CHF, or dextrose/5% water if not worried about cerebral edema) > tissue plasminogen activator > glucose or glucose (if unstable glucose only )
Contraindications of TPA
TPA is contraindicated in patients with abnormal CT scans (indicating stroke has progressed beyond recovery), severe hypertension, coagulation difficulties, or with coma (indicating another diagnosis).
Time frame of TPA use following stroke
Within 4.5hrs of incident (IV) or up to 12 hrs (intra-arterial TPA infused into thrombus, used when IV TPA is contraindicated)
