Ischemic strokes + TIAs Flashcards

1
Q

Stroke vs TIA

A

Stroke:
- neurological sx lasting longer than 24 hrs
- demonstrated infarction on imaging

Transient Ischemic Attack (TIA) :
- temporary period of neurological dysfunction: brief interrruption of blood flow
- sx resolves completely and spontaneously within 24 hrs (often only minutes)
- can have infarction but will be no infarction if brain flow is rapidly restores

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2
Q

Cerebrovascular disease risk factors:

A

BLACK (2x more likely) > white*
Age >55 years *
HTN *
Smoking *
Atrial fibrillation (afib) *
Male *
Previous strokes*

anything that causes vascular pathology:
- Obesity/DM/Hyperlipidemia
- Cerebral amyloid angiopathy
- Neoplasm
- Cerebral aneurysms
- Carotid bruits
- Drug use (e.g., cocaine, oral contraceptives)
- Migraines with aura
- Hematologic disorders: multiple myeloma, sickle cell disease, polycythemia vera

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3
Q

types of strokes

A

Ischemic: 87%
- 2/3 are thrombotic: due to a clot forming at the site of atherosclerotic plaque
- 1/3 embolic: clot forms elsewhere and travels to the brain)

Hemorrhagic: 13%
- intracerebral hemorrhage: HTN, AVM
- SAH: due to aneurysms

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4
Q

Stroke definition: A stroke refers to the (abrupt/insidious) onset of a __________ that is caused by a __________, meaning a localized problem in the blood vessels.

A

General term:
A stroke refers to the ABRUPT onset of a NEUROLOGICAL DEFICIT that is caused by a FOCAL VASCULAR ISSUE (meaning a localized problem in the blood vessels)

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5
Q

thrombotic strokes: MCC, risk factors, types of occlusion

A

MCC: Atherosclerotic plaque rupture

Risk factors:
- HTN
- High cholesterol/DM
- Blood clotting disorders
- Smoking
- Recreational drug use
- Vessel trauma: ex cervical artery dissection
- dehydration

types of occlusion:
- Large vessel occlusion *: internal carotid, MCA, ACA
- small vessel occlusion: lacunar strokes

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6
Q

thrombotic strokes: definition and common causes

A

Definition: formation of a blood clot (thrombus) inside a blood vessel in the BRAIN

common causes:
- MCC: atherosclerotic plaque rupture
- LVO
- SVO: lacunar stroke - small penetrating arteries (basilar, distal vertebral)
- dehydration: increases viscosity of blood -> clots

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7
Q

embolic strokes: two types

A

Cardioembolic: 20% of all ischemic strokes
- MCC: Afib
- paradoxical embolism: venous clot from DVT -> patent foramen ovale
- bacterial endocarditis: septic emboli with multiple strokes in different areas
- others: : MI, prosthetic valves, rheumatic heart disease, ischemic cardiomyopathy

Artery-to-artery embolic stroke:
- MCC of LVO
- Aortic arch
- Common carotid bifurcation
- Internal carotid
- Vertebral artery
- Basilar artery

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8
Q

Cardioembolic strokes: causes, sx

A

Cardioembolic: 20% of all ischemic strokes
- MCC: Afib
- paradoxical embolism: venous clot from DVT -> patent foramen ovale
- bacterial endocarditis: septic emboli with multiple strokes in different areas
- others: : MI, prosthetic valves, rheumatic heart disease, ischemic cardiomyopathy

Sx: SUDDEN MAXIMUM NEUROLOGIC DEFICIENT AT ONSET

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9
Q

paradoxical embolization: how does it happen what imaging

A

Rare: VENOUS thrombi migrate to the arterial circulation
- Patent foramen ovale (PFO)
- Atrial septal defect

Imaging: bubble-contrast echocardiography
- shows Right-to-left shunting

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10
Q

cervical artery dissection (2% of all ischemic strokes): location, types, sx, risk factors, causes

A

Location:internal carotid or vertebral arteries (most heal spontaneously and don’t turn into strokes)

Type:
-Artery to artery embolus: Common in youngpts (<60 yrs)
- Complete thrombotic occlusion

Sx:
- Painful dissection preceding stroke by hours/days

Risk factors:
- Ehlers-Danlos, Marfans disease
- cystic medial necrosis
- fibromuscular dysplasia
- polycystic kidney ds

Causes:
- Trauma: MVA, sports
- Spinal manipulative therapy = vertebral artery dissection

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11
Q

internal carotid artery dissections vs vertebral artery dissection sx

A

internal carotid:
- unilateral anterior neck pain or headache around the area or frontal area w/ TIA/stroke sxs
- think this with younger person with ipsilateral pain + neurological deficits
- horners sx
- monocular blindness
- CN palsies

Vertebral artery:
- sx: occipital or posterior neck pain with TIA/stroke sxs
- cause: spinal manipulative therapy

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12
Q

what are some complications of strokes

A
  • hemorrhagic transformation: ischemic damage -> increased permeability -> hemorrhagic tissue
  • cerebral edema: defective ATP + increased permeability of BBB
  • liquefactive necrosis: within 3-21 days
  • DVT: immobile
  • seizures
  • pneumonia/dysphagia: intubation
  • dementia
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13
Q

Anosognosia: def + what type of stroke would this be found in

A

Def: lack of awareness of illness

Found in:
- Right/non-dominant hemisphere strokes (parietal lobe): MCA

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14
Q

Ataxia: definition + what artery location for this sx

A

Ataxia: Loss of full control of bodily movements

location: Posterior circulation
- PCA
- basilar, vertebral -> lacunar strokes

Wallenberg syndrome: ipsilateral gait ataxia

stroke in Internal capsule posterior limb: Ataxic hemiparesis -> same side motor weakness + ataxia

PCA:
- Vertigo, ataxia, nausea

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15
Q

Ischemic penumbra: definition

A

Tissue surrounding the core region of infarction which is ischemic but REVERSIBLY dysfunctional:
- Maintained by collaterals
- Can be salvaged if re-perfused in time!

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16
Q

common signs and sx of stroke

A

MC: Weakness or numbness to the face, arm, leg*

Common:
- Trouble speaking or understanding
- Sudden trouble seeing in one or both eyes
- Sudden trouble walking
- Dizziness or loss of balance or coordination
- Sudden severe headache with no known cause
- Sudden confusion

The symptoms and signs inischemicattack are‘negative’in nature (i.e. loss of normal brain function) hence called “Neurologic Deficit

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17
Q

anterior circulation strokes vs posterior circulation strokes: incidence, which arteries, common sx

A

Anterior (70%): ACA, MCA, internal carotid artery
- common stroke sx: contralateral hemiparesis or speech issues
- ICA = same sx as others + amaurosis fugax

Posterior (30%): PCA, basilar, vertebral artery, PICA branch
- more subtle and tend to be missed
- Vertigo, ATAXIA, nausea, CN palsies
- Dreaded D’s: dysarthria, dysphagia, diplopia, DIZZINESS, drowsiness and DROP attacks

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18
Q

ACA syndrome: what areas does it supply and incidence

A

Areas supplied:
- Medial and superior FRONTAL and PARIETAL lobes
- Corpus callosum (partial)
- Basal ganglia (partial)

incidence: <3% of all strokes

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19
Q

ACA stroke syndrome: what sx

A

CONTRALATERAL HEMIPLEGIA: worse in LEGS > arms/hands/face*

Contralateral sensory loss (usually minimal)*

Frontal lobe dysfunction:
- Abuilia*: Absence of willpower or the ability to act decisively, may have a delay in verbal and motor responses
- urinary incontinence
- gait apraxia**: motor planning deficit that affects walking ability despite intact basic motor function of the legs

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20
Q

MCA syndromes: incidence and divisions

A

Most common occurence (70%)

M1: proximal MCA
M3 superior: lateral frontal lobe; superior parietal lobe
M3 inferior: lateral temporal lobe and inferior parietal lobe

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21
Q

MCA stroke syndrome: general sx

A

Contralateral hemiplegia: FACE/ARMS > leg**

Contralateral hemisensory loss

Contralateral homonymous hemianopia: Loss of vision in the same half of the visual field in both eyes

Ipsilateral Gaze preference: The eyes may deviate toward the side of the stroke

Dysarthria: Slurred speech due to facial muscle weakness.

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22
Q

MCA stroke: left/dominant vs right/non-dominant sx

A

Dominant/LEFT: aphasia
- superior M3 = expressive aphasia/”Broca’s”:Difficulty speaking, but good comprehensio
- inferior M3 = receptive aphasia/”wernicke’s”: Fluent but nonsensical speech, and poor comprehension; contralateral homonymous hemianopia
- M1 = global aphasia

non-dominant/RIGHT:
- Anosognosia
- Contralateral neglect
- Constructional apraxia: Difficulty in motor planning, inability to execute tasks despite understanding the instructions and having the physical capability to perform them
(ex: drawing or assembling objects)

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23
Q

dominant vs nondominant hemispheres (work in progress)

A

Left/Dominant:
- receptive aphasia: wernickes area
-

Right/Non-dominant

Right handed (90%): left hemisphere dominant

Left handed (10%): right hemisphere dominant

Typically:
- dominant = left
- non-dominant = right

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24
Q

ICA syndrome

A
  • Internal carotid artery occlusion may be ASYMPTOMATIC
  • Symptomatic occlusion similar to mainstem MCA stroke + preceded by amaurosis fugax*
  • Often preceded by TIAs or transient monocular blindness due to ophthalmic artery branch
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25
Q

lacunar stroke defintion

A

Definition:
- small NON-cortical infarcts of a single penetrating branch of a larger cerebral artery (think internal capsule, thalamus, and brainstem)

Sx: mostly contralateral motor/sensory defects without higher cortical function

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26
Q

match stroke to leasion site:
- pure motor stroke
- pure sensory stroke:
- ataxic hemiparesis
- Dysarthria-Clumsy Hand Syndrome:

A

Pure motor stroke: internal capsule lesion

Pure sensory stroke: thalamus

Ataxic hemiparesis: internal capsule posterior limb; contralateral limb ataxia

Dysarthria-clumsy hand syndrome: pons/internal capsule; slurred speech, contralateral hand weakness, clumsiness

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27
Q

non-cortical regions of the brain

A

non-cortical: beneath the cerebral cortex

Internal Capsule: A major pathway for motor and sensory information, connecting the cortex to other parts of the brain and spinal cord (explained further below).
Thalamus: Relay station for sensory and motor signals.
Basal Ganglia: Involved in movement regulation.
Brainstem: Controls basic functions like breathing, heart rate, and arousal.

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28
Q

PCA stroke syndromes: what does the PCA supply

A

PCA: occipital lobes, inferior temporal lobes, parts of the thalamus, and midbrain

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29
Q

PCA stroke: sx

A

General:
- Contralateral Homonymous Hemianopia with MACULAR Sparing** (b/l blood supply w MCA): (lateral geniculate nucleus)
- Contralateral Sensory Loss

Dominant/Left:
- Alexia without agraphia: can’t read, can write **
- Anomia: difficulty naming objects and colors
- Visual agnosia: inability to describe what an object is used for

Non-dominant/Right: Prosopagnosia- inability to recognize faces

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30
Q

Gerstmann syndrome: what is it, causes, main sx

A

AFFECTS: Parietal lobe of the dominant side (usually left) in ANGULAR GYRUS = READING CENTER

Causes: MCA Stroke (MC), TBI, Tumor

Sx:
- Left-right disorientation
- Agraphia: Inability to write when you could previously
- Acalculia: Inability to calculate numbers
- Alexia: Inability to read/recognize words you once could read
- Finger agnosia: Impairment in recognizing and naming their own fingers

31
Q

Anton syndrome: definition, causes

A

Anton syndrome (cortical blindness)
- RARE
- are often unaware they are unable to see

Cause: b/l occipital lobes affected
- distal basilar artery
- bilateral PCA stroke
Cortical blindness,

32
Q

BASILAR artery occlusion: overview and where does it supply

A

Overview:
- super rare <1%
- incompatible with life: SUDDEN COLLAPSE AND COMATOSE SX
- consider it when there is DIZZINESS + neuro deficits

basilar artery supplies: midbrain, medial and lateral pons, part of the cerebellum, medial temporal and the occipital lobes

33
Q

Mid-basilar occlusion

A
  • affects the ventral pons
  • can lead to LOCKED IN SYNDROME: complete paralysis (quadraplegia) + preserved consciousness/vertical eye movement

Mid basilar occlusion:
- ipsilateral CN VII palsy
- contralateral hemiparesis

34
Q

Top of the Basilar Syndrome

A

Coma (due to ARAS involvement)*

can also have:
- Oculomotor disturbances (roving eye movements or downward/inward gaze)
- Hemianopia (loss of half the visual field)
- Bilateral ptosis (drooping of both eyelids)
- CN III palsy (pupillary enlargement with light reaction preserved)

35
Q

Vertebral artery syndrome

A

Symptoms of occlusion are variable
Have plenty of collateral supply
Dissection denoted by pain
- wallenberg syndrome: PICA infarct off vertebral

36
Q

Wallenberg syndrome

A

location:
- lateral medulla: occlusion of the posterior inferior cerebellar artery (PICA) -> branch of the vertebral artery

Sx:
- Dizziness, nystagmus, N/V, dysarthria, dysphagia, diplopia, HICCOUGHS*

Mixed: ipsilateral:
- CN V facial numbness
- horners syndrome
- gait ataxia

Mixed: Contralateral
- spinothalamic: loss of pain + temp sensation

37
Q

horner’s syndrome: causes and 3 order neuron pathway (not too important on test)

A

Cause: damage to sympathetic nerve supply
- oculosympathetic pathway: 3 orders of neurons -> damage at any point will cause horners
- need huge workup

first order: hypothalmus -> spinal cord; stroke damage

second order: spinal cord -> lung apex -> neck -> cervical ganglion
- carotid dissections
- lung tumor (pancoast)
- trauma

3rd: go up internal carotid -> cavernous sinus -> innervation

Ipsilateral sx: ptosis, miosis, anhidrosis

38
Q

Headache sx: DDx

A

ischemic stroke: rarely associated w headache -> rare in prodromal period before thrombotic stroke

more likely:
- SAH
- Intracerebral hemorrhage
- Cerebral venous thrombosis

39
Q

Neck Pain, fever, vomitting, chest pain sx: what DDx

A

Neck pain:
- Indicative of vertebral or carotid artery DISSECTION -> can cause ischemic stroke

Fever:
- endocarditis
- embolic stroke

Vomitting:
- posterior circulation large artery ischemic stroke
- elevated ICP

Chest pain:
- aortic dissection preceding ischemic stroke
- acute MI + stroke simulataneously from atherosclerosis

40
Q

Stroke PE:

A

NIHSS is a DIRECTED neuro exam
Blood pressure
Comparison of blood pressure and pulse on the two sides can reveal differences related to atherosclerotic disease of the aortic arch or coarctation of the aorta.
Ophthalmoscopic examination : embolization in the anterior circulation
Neck examination : carotid pulses or the presence of carotid bruits.
Cardiac examination : arrhythmias or murmurs related to valvular disease
Palpation of the temporal arteries : giant cell arteritis (tender, nodular, or pulseless)
Distal extremity exam: DVT

41
Q

CincinattiPrehospital StrokeScale (CPSS)

A
  • scoring tool for EMS in pre-hospital setting

test: if there is 1 sx = 72% chance of stroke
- Facial droop: ask pt to smoile
- Arm drift: Ask the patient to close their eyes and extend both arms straight out with palms up
- Abnormal speech

42
Q

Acute management of strokes

A

If hemorrhagic stroke is ruled out, thrombolytic therapy is indicated because it improves outcomes and needs to be urgently prescribed; the window for administration is only 3/4.5 hours from onset of symptoms

43
Q

Stroke/TIA Initial Management Flowchart:

A

ABCD approach:

AIRWAY:Can they clear oral secretions & maintain airway?
BREATHING:Provide supplemental O2 if oxygen saturation is <94%
CIRCULATION:Are they hemodynamically stable?
- hypotensive: mimics stroke -> RESTORE BP
- HTN: could be ischemic vs hemorrhagic -> need IMAGING
- obtain 2 IV lines: ones for tPA, other for other drugs
- initiate labwork: need to check cardiac enzymes, CBC, lipid panel, etc

Disability:
- Perform a focused neurological exam
- obtain POC glucose to rule out hypoglycemia mimic for stroke

44
Q

Stroke/TIA Management Flowchart: what imaging

A

Non-contrast CT head or Brain MRI with DWI (diffusion weighted imaging)

Followed by CTA head/neck if NO hemorrhage shown in CT

45
Q

best initial imaging for suspected stroke: pros and cons

A

NON-contrast CT -> get CTA after if you find no bleeding

Pro’s:
- can r/o bleed: differentiate ischemic vs hemorrhagic BUT Acute ischemic stroke is often not visible in the early hours
- Detect a hyperdense vessel
- Determine if the stroke is completed
- can exclude: Exclude ICH, abscess, tumor, other stroke mimics

Cons:
- Acute ischemic stroke is often not visible in the early hours.
- Fails to detect small cortical or posterior circulation strokes.

46
Q

Early signs of cerebral ischemia on CT:

A

Small and subtle hypodensity
Ventricular compression
Hyperdense MCA sign
Loss of gray-white differentiation
- IV-tPA is not beneficial in areas of extensive regions of obvious hypodensity, as it is consistent with irreversible injury

47
Q

gold standard imaging of suspected stroke: pros and cons

A

Brain MRI with DWI (Diffusion-Weighted Imaging) is the gold standard for detecting acute ischemic infarction
- DWI detects areas of decreased water diffusion, which appear bright or hyperintense on imaging. This indicates early ischemia

Pros:
- Superior to NCCT for detecting early stroke, particularly small or posterior circulation strokes
- Even after resolution of symptoms in TIA, 30% of patients may have an infarct visible on MRI

Cons:
- Time-consuming
- less accessible in hospitals
- CI: metal implants, claustrophobia

48
Q

initial eval stroke: Lab work and other diagnostics

A

Cardiac monitoring:
ECG
Holter
Chest xray
Urinalysis
CBC
ESR
BMP and LFTs
Lipid panel: high cholesterol
Coags (PT/PTT, INR)

Consider:
Blood culture
(if suspicious of endocarditis)
VDRL
HIV
Lyme
ANA
Anti-phospholipid

49
Q

You and the stroke team: what must you determine while you wait for neuroimaging for stroke initial eval

A

Determine the last known well (LKW)
Determine if patient is on anticoagulation
Determine a NIHSS score

50
Q

National Institutes of Health Stroke Scale (NIHSS)

A
  • evaluates patients with suspected acute stroke and to make decisions about acute treatment
  • Correlates with infarct size, clinical severity, and long term outcome
  • ≥6 correlates with cortical stroke BUT A score of 0 does NOT mean there is no stroke!
  • Not all stroke symptoms are captured by the NIHSS
  • Good at identifying ANTERIOR (70%) strokes but its not as reliable for POSTERIOR circulation (30%)
  • Very time-consuming
51
Q

suspected stroke: CTA/MRA head and neck - purpose and who gets one

A

purpose:
- help identify large vessel occlusions -> treatable with endovascular therapy within 24 hrs
- Gives insight into the etiology of stroke: vascular malformations, plaque
- performed after non-contrast CT with no hemorrhage

who gets CTA/MRA:
- Qualify for mechanical thrombectomy
- Last seen well within 4.5 hours
- Last seen well within 24 hours + NIHSS ≥6 or VAN (Visual, Aphasia, Neglect) positive or LVO syndrome

52
Q

GOLD STANDARD for identifying and quantifying atherosclerotic stenosis of cerebral arteries - which imaging and benefits/risks

A

Cerebral angiography
- Can characterize aneurysms, vasospasm, thrombi, arteriovenous (AV) fistulas, vasculitis, and fibromuscular dysplasia

Risk: Risk: arterial damage, hemorrhage, embolic stroke, renal failure from contrast nephropathy

53
Q

suspected stroke: ultrasound

A

Transcranial dopplers (TCD) can assess MCA, ACA, PCA flow
Carotid ultrasounds can identify carotid atherosclerosis as source of emobli

54
Q

suspected stroke: cardiac echo purpose

A
  • check Afib emboli
  • valvular heart ds
  • thrombi in heart chambers
55
Q

1 goal of Acute ischemic stroke:

A

Prevent or reverse brain injury!!!
- salvage Penumbra

56
Q

Acute ischemic stroke: medical management - what are we treating and what tx

A

1) BP: IV labetolol or nicardipine
- Collateral blood flow is blood pressure dependent -> Allow permissive hypertension in the acute phase
- tPA eligible pts: reduce BP if over >185mmHg SBP or >110mmHg DBP*
- non-tPA eligible: reduce BP if >220mmHg systolic or >120mmHg diastolic *

2) Cerebral edema management!!!
- Hyperglycemia is associated with worse clinical outcome -> goal: 60-180 mg/dL*
- Give antipyretics if fever present

3) Protecting airways + prevent aspiration
- HOB elevation 30%*
- NPO until cleared by specialist

57
Q

tPA administration: time goals and administration, dosing

A

Goal:
- door-to-needle time ≤60 minutes
- within ≤ 3 hours from onset of sx (some ≤4.5 hrs)

Administration:
- inclusion criteria: 18+, LKW within 3/4.5h, clinical dx of ischemic stroke
- need TWO peripheral IV lines (one for tPA other for other meds)
- frequent BP monitoring with goal BP under 180/105
- Avoid urethral catheterization ≥2 hours
- No other anti-coagulants/platelet for 24 hours
- dose: 0.9 mg/kg IV (maximum dose 90 mg) and give 10% of the total dose is given as an initial bolus over 1 min -> The remaining 90% is infused over 1 hr

58
Q

tPA acute ischemic stroke complications and tx

A

Bleeding:
- make sure that before any tPA administration: pt is stratified beforehand
- is bleed clinically significant? - small petechial hemorrages have no change in NIHSS..
- sx of a significant bleed: Worsening neuro status, seizure, stuttering lacunar infarct, new headache, nausea, vomiting, ↑ BP
- FIRST STEP = STOP TPA -> next step: there is no single treatment universally accepted
- AHA recommended steps: Administer 6-8 units of platelets + 10 units of cryoprecipitate (rich in fibrinogen, factor VIII, and von Willebrand factor to help reverse the clotting defect) -> reimage brain emergently
- +/- consider: Pro-thrombin complex concentrates, Antifibrinolytics ( ex: TXA, tranexamic acid)

Angioedema:
- stop tPA immediately, check for ACEi use -> IV Methylprednisolone/Diphenhydramine/Famotidine

59
Q

when should you not administer tPA to ischemic stroke pts

A

Do not administer if pt is a bleed risk!!!! or if they have hemorrhagic stroke or reversible injury!!!!

Clinical presentation:
- SBP>185, DBP>110 -> give IV labetolol or nicardipine first
- pt with active internal bleed
- sx of infective endocarditis
- stroke associated with sx of aortic dissection

Hematologic:
- Platelet count <100,000/mm
- Current anticoagulant use with INR >1.7, PT >15 seconds, aPTT >40 seconds, or PT >15 seconds
- Therapeutic doses of LMWH within the last 24 hrs
- Use of direct thrombin inhibitors or factor Xa inhibitors within the last 48 hours with evidence of anticoagulation effects on labs

Surgery:
- Ischemic stroke or severe head trauma in the last 3 months
- Intracranial or intraspinal surgery in the last 3 months.

Hx:
- Intra-axial intracranial neoplasm
- previous intracranial hemorrhage
- GI malignancy or GI hemorrhage within 21 days

simply just not indicated: hemorrhagic strokes or irreversible damage
- sx of SAH (hemorrhagic stroke)
- extensive hypodensity on CT, consistent with irreversible injury
- active internal bleeding on head CT

60
Q

mechanical thrombectomy/endovascular therapy: who are candidates and general criteria

A

Patients who present after 4.5 hours but within 24 hours, AND have a large vessel occlusion (LVO)
- sometimes IV fibrinolytics alone arent enough in anterior circulation or its an alternative to ineligible tPA pts

General criteria for MT:
- within 4.5 - 24h of sx onset/LKW
- CTA imaging shows proximal LVO in anterior circulation
- Persistent disabling neurologic deficit
- A small infarct core (aka limited signs of early ischemic change - penumbra still salvagable) on neuroimaging
- no hemorrhage

61
Q

what is Mechanical thrombectomy (MT)

A

given to ischemic stroke pts with LVO within 24 hrs

Mechanical thrombectomy:
- Minimally invasive and endovascular procedure
- A catheter is guided up from the groin or radial artery, the clot is broken up, pieces are removed
- Performed by neuro-interventionalist radiologist

62
Q

antiplatelet therapy for acute ischemic strokes: dose and time frame

A

All pts get 160-300mg ASA within 24-48hr of onset
- After tPA: Aspirin therapy is delayed for 24-48 hrs to reduce the risk of bleeding complications

Dual antiplatelet therapy:
- for pts with minor non-cardioembolic ischemic stroke (NIHSS score ≤5) who did not receive IV-tPA***
- give within 24hrs of sx onset and continue for 21 days (up to 90 days)

DAPT combos:
- Aspirin (81 mg QD) + Ticagrelor (180 mg load, followed by 90 mg BID) for 30 days
- Aspirin (81mg QD) + clopidogrel (600 mg load, then 75 mg daily) for 30 days
- after 30 days: montherapy 81 mg ASA after or extend DAPT to 3-months if large intracranial atherosclerosis

63
Q

post-ischemic stroke: what meds to give them and complications to prevent in bedridden pts

A

meds:
- start on statin tx: Atorvastatin 80mg QD with LDL goal <70
- seizure prophylaxis: NOT RECOMENDED

Prevent complications of bedridden patients:
- DVT prevention with intermittent pneumatic compression devices or subq heparin (delay 24 hrs if getting tPA)
- UTI prevention – no foleys
- Skin protection – frequent turning prevent bed sores
- Pneumonia

64
Q

post stroke complications

A

Cerebral EDEMA and brain herniation!!!!
- Edema peaks on days 2-3 after stroke
- Can cause mass effect ~10 days
- Larger infarct = greater risk for edema

Management:
- IV mannitol and water restriction
- Do not allow hypotension
- Special vigilance should be held for CEREBELLAR infarcts ->
obstructs CSF flow -> hydrocephalus and compress directly on the brain stem
-> COMA and RESPIRATORY ARREST

65
Q

post acute ischemic stroke: what is secondary prevention and first steps

A

Initial phase of AIS is medical stabilization + reperfusion therapy (tPA and/or MT)

Next stage: determine pathophysiology for secondary prevention

want to do a comprehensive eval:
- Cardiac Monitoring: check for hidden afib
- Echo (TEE/TTE): check for source of cardio-embolism
- vascular studies: US neck; CTA/MRA of neck and head arteries
- Hypercoagulable blood testing: check for underlying disorders

66
Q

pt with ischemic stroke due to Afib causing cardioembolic infarct: what treatment

A

APIXABAN: 5mg BID daily for life to prevent further embolic events
- or Warfarin
- ARISTOTLE trial: showed apixaban has a slight edge over warfarin

67
Q

Carotid stenosis: cause of acute ischemic stroke what treatment

A

Carotid endarterectomy (CEA) or stenting (CAS)
- recommended for patients with 70% stenosis or more
- for 50-70% stenosis: benefit is significant but less robust
- <30% stenosis: harmful -> do medical management

68
Q

Risk factor modification for secondary prevention of ischemic strokes

A

MOST SIGNIFICANT RISK FACTOR: Hypertension!!!!!!**
- Goal <130/80mmHg

High cholesterol levels***:
- SPARCL trial = Atorvastatin 80mg daily
- Goal LDL: < 70 mg/dL

Other great things:
- Tobacco cessation
- Alcohol reduction / abstinence
- Regular exercise x 40 min / week
- Mediterranean diet
- Wt loss

69
Q

post stroke rehab

A
  • Stroke rehab programs
  • Multi-disciplinary approach to recovery: Early PT, OT, and speech therapy

Addressing complications and disabilities:
- Educate patient and family on prevention of complications due to limited mobility: pna, dvt, pe, pressure ulcers, muscle contractures

70
Q

Transient ischemic stroke: definition, workup/why do we care

A

Definition:
- Short lasting neurologic dysfunction due to transient focal ischemia WITHOUT infarction
- duration of neuro sx <24 hr (often minutes to 1 hr)

Work-up:
- same as stroke
- imaging: CT/MRI brain, CTA/MRI neck, Carotid ultrasound

Stats: high risk of stroke after a TIA
- 50% in first 24-28 hours if high risk DM/HTN
- 10-20% in the first 3 months

71
Q

Transient ischemic stroke: risk stratification tool and prevention

A

Risk stratification tool: ABCD2
- Predicts likelihood of subsequent stroke in 2 days
- ABCD2 score <4: ASA alone
- ABCD2 score≥ 4: DAPT x 21 days

Prevent the stroke by targeting the cause/ethiology:
- Non-cardioembolic stroke= DAPT (ASA+clopidrogel or ASA+ticagrelor)
- Afib: anticoagulation - apixaban (DOAC); LMWH; warfarin
- heart thrombus: DOAC
- carotid stenosis: 50-99%= CEA or Stenting + BP control + HLD control

72
Q

amaurosis fugax: description, ddx, prognosis

A

Description:
- Unilateral visual loss, painless, transient (20-30 min) ***
- Spontaneously self resolves **
- Curtain coming down” or “darkening”
- Complete or partial visual field

DDx:
- INTERNAL CAROTID: ipsilateral ICA ophthalmic artery branch occlusion/stenosis
- giant cell arterities
- central retinal artery occlusion/CRVO
- papilledema
- sickle cell anemia
- MS

Prognosis:
- Amaurosis fugax = harbinger of strokes -> particularly involving the carotid circulation
- needs WORKUP

73
Q

amaurosis fugax: causes of occlusion, risk factors, dx

A

Occlusion or stenosis of the ipsilateral internal carotid artery (ICA) ophthalmic artery branch:
- Thromboembolism from carotid plaque
- Hypoperfusion from stenosis or other cause
- Vasospasms
- Increased plasma viscosity (e.g. MM)
- Atherosclerosis

Risk factors:
- >50 years old
- Vascular risk factors : HTN, HLD, DM, Smoking, TIA/CVA hx, PVD, cocaine, afib

Retinoscopy: hollenhorst plaques (arrows: cholesterol emboli) , pale retina

74
Q

amaurosis fugax: workup

A

Complete ophtho exam
Cardiovascular eval: echo, ecg, CTA/MRA/US of the neck
Neuroimaging: CT/MRI brain
Labs including inflammatory markers: ESR/CRP