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
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
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
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)
5
Q
ICH
A
- Intracerebral hemorrhage
- Uncontrolled HTN is common etiology
- Antithrombotic therapy is associated with ICH
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
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
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
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
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
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
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
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
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
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
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
