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850 > Stroke > Flashcards

Stroke Flashcards

1
Q

Stroke Background

A
  • Abrupt onset of focal neurologic damage that is presumed to be vascular in origin
  • Stroke is leading cause of disability and fifth in mortality
  • CVA: defined as decreased blood flow to brain as a result of obstructed ruptured blood vessels
  • Overall, on a downward trend
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2
Q

Ischemic Stroke

A
  • 83% of stroke incidences
  • Caused by occlusion with a cerebral artery or emboli from a proximal source resulting in cerebral artery occlusion
  • Emboli may be cardiac or non-cardiac sources
  • Vascular changes can lead to occlusion
  • Blood vessels ability to dilate/constrict can be impaired in chronic HTN, acute injury, or atherosclerosis
  • Tissue surrounding core area of infarct is ischemic but maintain tissue integrity, aka ischemic penumbra
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3
Q

Hemorrhagic Strokes

A
  • 13% of stroke incidences
  • Occurs when blood enters either subarachnoid space or within intracerebrum forming a hematoma in brain
  • Significantly higher mortality compared to ischemic stroke
  • Types: SAH or ICH
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4
Q

SAH

A
  • Subarachnoid Hemorrhage
  • Occurs when blood enters subarachnoid space
  • Can occur following trauma, rupture of intracerebral aneurysm, or rupture of an arteriovenous malformation (AVM)
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5
Q

ICH

A
  • Intracerebral hemorrhage
  • Uncontrolled HTN is common etiology
  • Antithrombotic therapy is associated with ICH
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6
Q

TIA

A
  • Transient Ischemic Attack
  • Transient episode of neuological dysfxn caused by focal brain, spinal cord, or retinal ischemia without acute infarction
  • TIA thought to be benign but should be considered similar in spectrum to stroke
  • Require urgent intervention to reduce risk of stroke
  • TIA patients have a 10-15% chance of a subsequent stroke especially the first few days following TIA
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7
Q

Comorbidities

A
  • Atherosclerosis of large arteries can increase ischemic stroke risk
  • Afib, valvular heart disease, or other prothrombogenic heart problems can increase risk of emboli
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8
Q

Pathophysiologies

A
  • Ischemic: manifested occlusion of cerebral artery reduces cerebral blood flow causing neurologic deficits
  • Hemorrhagic stroke: neuronal damage by mechanical compression of the brain parenchyma itself
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9
Q

Clinical Presentation

A
  • Specific areas of neurologic deficit are determined by the area of brain that is not involved
  • Posterior circulation: vertigo and double vision
  • Anterior circulation: asphasia
  • Ischemic strokes are not painful but may include headache
  • Hemorrhagic strokes are more severely painful and have headaches
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10
Q

BEFAST

A
  • B: balance, loss of balance, HA, or dizziness
  • E: Eyes, blurred vision
  • F: Face, drooping on one side of face
  • A: Arms, arm or leg weakness
  • S: Speech: speech difficulty
  • T: Time to call for ambulance immediately
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11
Q

Diagnosis

A
  • Lab: blood glucose, platelet count, coagulation parameters
  • Imaging: CT scan (immediately on arrival to rule out hemorrhagic), if used IV contrast may be able to reveal ischemic stroke
  • MRI: longer duration, visualizes small, deep infarcts, can help distinguish between acute and chronic ischemic
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12
Q

CPSS

A
  • Tests for 3 signs of abnormal findings: facial droop, arm drift, or changes in speech
  • If one of the findings is new there is a high chance its ischemic stroke
  • If all three are abnormal, there is a higher chance of acute stroke
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13
Q

NIHSS

A
  • Evaluation to qualify severity of stroke
  • Scoring tool ranges from 0-42
  • 0: no stroke, 0-4: minor, 5-15: moderate, 16-20: moderate to severe, 21-42: severe
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14
Q

Fibrinolytic Therapy

A
  • Beneficial for patients presenting <4.5 hours with an acute ischemic stroke sxs
  • Alteplase of tenecteplase are utilized, others aren’t recommended
  • Binds to fibrin and initiates fibrinolysis by converting plasminogen to plasmin
  • Don’t delay initiation; only blood glucose levels are needed before starting alteplase
  • Baseline ECG and troponins are recommended but not necessary before initiation
  • Alteplase is standard therapy, make sure they have NO CI to tPA
  • Tenecteplase considered as an alternative for patients who can undergo mechanical thromboectomy
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15
Q

Absolute tPA CI

A
  • Head trauma or stroke in last 3 months
  • History of ICH, AVM, or aneurysm
  • Signs/sxs suggesting SAH
  • Recent intracranial or intraspinal surgery in past 3 months
  • Elevated BP (>185/110)
  • Known bleeding disorder or low platelets
  • Blood glucose <50
  • Aortic arch dissection or infective endocarditis
  • Anticoagulant use
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16
Q

Anticoagulant Use

A
  • Warfarin: INR > 1.7
  • Therapeutic heparin: aPTT>40
  • Therapeutic enoxaparin: last dose =< 24 hor or anti-Xa >= 0.3
  • DOAC: last dose =< 48 hours or abnormal renal fxn (CrCl < 30)
17
Q

Blood Pressure Management

A
  • Not a candidate for fibrinolytic therapy: don’t treat in acute period of stroke
  • Lower blood pressure if >220/120 or evidence of aortic dissection, acute MI, pulmonary edema, or hypertensive encephalopathy
  • Candidates for alteplase: correct blood pressure if >185/110 with CCB or BB before initiating
  • During/following tPA: strict BP control should be continued with <180/105 as the foal for at least 24 hours after infusion
18
Q

Managing Hemorrhagic Strokes

A
  • No standard management
  • Obtain history to determine if patient is on antiplatelet for anticoag therapy
  • If so, determine when last dose was taken
  • Usually reversed in an attempt to prevent further bleed expansion
19
Q

Hemorrhagic BP Control

A
  • Greatly elevated BP can expand bleeding or can re-bleed, but too low can cause cerebral ischemia
  • Optimal BP isn’t determined, but aggressive reduction if SBP >= 220 and modest if SBP >= 180
  • General goal: 140-160
20
Q

Vasospasms

A
  • Thought to cause delayed ischemia and can occur 4-21 days after hemorrhagic stroke
  • Nimodipine should be administered to patients with aneurysmal SAH
  • Start with 96 hours of onset
  • Greater effect on cerebral arteries, believed to be due to lipophilicity
21
Q

Seizures

A
  • Patients with change in mental status found to have electrographic seizures on ECG should be given anti-seizure drugs
  • Guidelines: recommend against prophylactic use of anti-seizure
22
Q

Large Vessel Occlusion

A
  • Non-pharm
  • LVO: catheter guided to femoral artery, aorta, and carotid to remove clot
  • Eligible up to 24 hours of last known normal
  • Depending on location, timing, and severity, could use along or with tPA
23
Q

CEA

A
  • Non-pharm
  • Carotid Endarterectomy: carotid cut open to remove plaque to improve vessel blood flow
  • Usually done in patients with 70-99% stenosis
  • Use ASA and clopidogrel after procedure for at least 3-6 months after, maybe life lof
24
Q

Other Non-pharm

A
  • Surgical clipping or endovascular coiling

- Mechanical treatment for prevention of rebleeding or aneurysmal SAHs

25
Q

Primary Stroke Prevention

A
  • Identify modifiable and non-modifiable risk factors
  • Physical activity
  • Statin therapy if high 10-year risk for CV events
  • Maintaining regular blood pressure or treating HTN
  • Smoking cessation/abstinence
  • Afib patients at increased risk, give anticoagulation therapy
  • Aspirin 81-100 mg a day can be useful for CV prophylaxis and in women (diabetes)
  • Cilostazol may be reasonable to prevent first stoke in peripheral arterial disease patients
26
Q

Secondary Ischemic Stroke/TIA Prevention

A
  • Antiplatelet therapy: ASA 160-325 mg daily
  • Delay ASA if treated with IV alteplase for 24 hours after infusion
  • Clopidogrel and Ticagrelor can also be recommended (latter not over aspirin for ischemic stroke patients)
  • Minor ischemic strokes can be treated with DAPT (ASA/clopidogrel) indefinitely
  • Anticoag therapy may be indicated for cardioembolic stroke patients
  • High intensity statin for those with atherosclerosis
  • Venous thromboembolism prophylaxis: compresion device, chemical prophylaxis after 24 hours of tPA infusion, no clear recommendation on restarting after hemorrhagic stroke

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