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Neuro: Clin Med IIB > Cerebrovascular Disease > Flashcards

Cerebrovascular Disease Flashcards

1
Q

a sudden onset of neurologic deficit resulting from a loss of blood flow to a part of the brain resulting in brain infarction

A

stroke

Cell death and irreparable damage to brain tissue occurs most often with in 5 minutes of loss of blood flow

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2
Q

what are the 3 main arteries that make up the Cerebral Arterial Supply, and what parts of the brain do they supply?

A

Bilateral branches

  1. Anterior Cerebral Artery (ACA) - medial frontal/parietal lobes, anterior basal ganglia
  2. Medial Cerebral Artery (MCA) - lateral frontal/parietal lobe, anterior and lateral temporal lobes, remaining basal ganglia
  3. Posterior Cerebral Artery (PCA) - thalamus, brainstem, posterior/medial temporal lobes and occipital lobe
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3
Q

what other arteries/vessels make up the cerebral arterial supply?

A
  1. Penetrating vessels - small arteries that supply:
    - basal ganglia
    - pons
    - cerebellum
    - thalamus
    - deep cerebral white matter (less common)
  2. Vertebrobasilar
    - brain stem
    - cerebellum
    - occipital lobe
    - parts of thalamus
  3. Internal carotid
    - branches in to middle cerebral
    - connects to anterior & posterior cerebral arteries
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4
Q

Risk of stroke is 2x higher in the months following what type of infection compared to non-infected individuals

A

Covid-19

Risk of stroke is 3-6 times higher within the first week - 1 month after infection

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5
Q

An acute occlusion of an intracranial vessel leading to a reduction of blood flow resulting in cell hypoxia and a loss of neurologic function to the brain region affected

A

ischemic stroke

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6
Q

difference between ischemic core vs penumbra?

A
  1. Ischemic core is the area of complete loss of flow = death of brain tissue within 4–10 min
  2. penumbra is the surrounding tissue which has only a reduction in flow and can remain viable for hours after onset of stroke
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7
Q

2 caues of ischemic stroke

A
  1. Thrombotic - likely related to ruptured atherosclerotic plaques leading to platelet activation
    - Associated with: HTN, DM, hyperlipidemia, carotid artery disease, alcohol consumption, and smoking
  2. Embolic - embolus originating from extracranial source
    - Associated with: Afib (MC), cardiac valve disease, MI, endocarditis and cardiomyopathy
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8
Q

general risk factors for ischemic stroke

9

A
  1. HTN
  2. DM
  3. Tobacco use
  4. High cholesterol
  5. Smoking
  6. Male
  7. Age
  8. Hx CAD, CABG, or Afib
  9. FHx of TIA/Stroke
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9
Q

risk factors for ischemic stroke in younger pts?

A
  • Traumatic Brain Injury (TBI)
  • Coagulopathies
  • Illicit drug use - cocaine
  • Migraines - women, OC, age < 45, migraine with aura
  • Oral contraceptive use
  • Covid-19
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10
Q

a spontaneous rupture of a cerebral artery leads to:

A
  1. cerebral ischemia resulting from loss of microvascular perfusion d/t acute vasoconstriction and microvascular platelet aggregation
  2. increased ICP
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11
Q

2 causes of hemorrhagic stroke

A
  1. Intracerebral hemorrhage (ICH)
    - MC - damage to vasculature from prolonged uncontrolled HTN
    - Other - bleeding diathesis, iatrogenic anticoagulation, cerebral amyloidosis, and cocaine abuse
  2. Subarachnoid hemorrhage (SAH)
    - aneurysm, arteriovenous (AV) malformations, trauma
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12
Q

RF for hemorrhagic stroke

6

A
  1. Advanced age
  2. HTN (up to 60% of cases)
  3. Anticoagulant use
  4. Hx of stroke
  5. Alcohol abuse
  6. illicit drugs (eg, cocaine, other sympathomimetic drugs)
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13
Q

clinical presentation of stroke

A

BEFAST

Balance - ataxia, vertigo (rare), Disequilibrium
Eyes/ears - visual loss, diplopia, hearing changes
Facial droop
Arm - weakness, unilateral, weakness/sensory
Speech - dysarthria, aphasia (Broca, wernickes)
Time is brain!

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14
Q

Additional S/S more likely seen with hemorrhage:

A
  1. sudden onset HA - generalized or local
    - “the worst HA”
    - “thunderclap HA”
  2. N/V
  3. seizure
  4. syncope
  5. AMS: LOC is more depressed than in ischemic injury
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15
Q

why is hx important in stroke?

A

determines if we can provide a clot buster or not

  1. Onset - the most important info
  2. Timeline - course of symptoms - progression vs regression
  3. Med hx: oral hypoglycemic agents or anticoagulants
  4. PMH: epilepsy, drug overdose or abuse, recent trauma
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16
Q

For a potential stroke - if exact onset is unknown, “sx onset” is defined as ?

A

the last time the patient was known to be “normal”

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17
Q

PE findings of stroke

A
  1. ABC’s and VS
  2. Assess LOC and determine need for airway assistance
    - hemorrhagic strokes often deteriorate more rapidly
  3. Skin
    - petechiae, Janeway lesions, Osler’s nodes (infective endocarditis)
    - livedo reticularis/gangrene (cholesterol emboli)
    - purpura, ecchymoses (bleeding diathesis, anticoagulation)
    - recent surgical sites/scars
  4. HEENT
    - signs of trauma
    - fundoscopy - papilledema (ICP), retinopathy, retinal emboli, retinal hemorrhage
    - mouth - tongue laceration (indicative of seizure)
  5. CV
    - Irregular rhythm, M/G, (cardiogenic emboli) = a.fib, endocarditis, other valvular dz, cardiomyopathy, MI
    - Palpate carotid, radial, and femoral pulses - Assessing absence, asymmetry or irregular rate
    - Auscultation for carotid bruit (thrombotic etiology)
  6. Rsp - abnormal breath sounds, bronchospasm, fluid overload or stridor
  7. Neuro
    - CN
    - NIHSS
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18
Q

what is the NIHSS and the scoring?

A

National Institutes of Health Stroke Scale (NIHSS - provides a quantitative measure of stroke-related neurologic deficit)

  1. Mental status & LOC
  2. Vision - visual fields by confrontation
  3. Motor function - arm/leg lift, facial movement
  4. Cerebellar function - F-N, H-S
  5. Sensory function - sharp sensation
  6. Language (expressive and receptive capabilities) ask pt to describe an image or read sentences shown to patient
    - assessing ability to comprehend task and coordinate speech
  7. Neglect - lack of awareness of disability or visual comprehension

0 = no stroke sx
1-4 = minor stroke
5-15 = mod stroke
16-20 = mod-severe stroke
21-42 = severe stroke

> 10 correlates with an 80% likelihood of proximal vessel occlusion

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19
Q

urgent workup for a stroke

A
  1. Finger stick blood glucose (class I)
  2. CT brain w/o contrast (class I)
    - performed once patient is stabilized (ABC’s)
    — “time is tissue” - do not wait on any nonessential testing
    — Goal - w/n 25 minutes of arrival
    - highly sensitive to exclude or confirm hemorrhage
    — acute bleeding appear hyperdense (lighter than brain tissue)
    — r/os other stroke mimics (e.g. tumor or subdural hematoma)
    - easily accessible and requires no preparation
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20
Q

pt with potential stroke has a CT scan showing evidence of a R hemisphere IC bleed, what type of stroke is this?

A

hemorrhagic

ischemic = normal

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21
Q

other immediate diagnostic studies for stroke

A

should not delay (rt-PA)

  1. CBC, BMP, coag studies, cardiac enzymes
    - CBC - look for hematologic etiology (polycythemia, thrombocytosis, thrombocytopenia, leukemia)
    - BMP/CMP - baseline lab and reveals stroke like mimics (hypoglycemia, hyponatremia) - bedside fingerstick glucose immediately
    - PT/PTT/INR - reveals underlying bleeding disorder, anticoagulation therapy with coumadin
    - Direct factor Xa activity assay - if treated with direct factor Xa inhibitor (Xarelto, Eliquis, or Savaysa) AND a candidate for thrombolytic therapy)
    - Troponin - R/O MI - concurrent or recent MI worsens prognosis
  2. EKG and cardiac monitoring
    - assess for cardioembolic etiology
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22
Q

additional imaging for stroke

A

necessary after stabilization and tx is initiated to look for etiology and severity of stroke damage

  • CTA, MRA and/or MRI of the brain
  • Carotid duplex US
  • Echo
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23
Q

Additional labs (as indicated) for stroke

A

Toxicology screen - suspected drug use (eg. cocaine)
Blood alcohol concentration (BAC) - increases risk of bleeding/stroke mimic
LP - indicated if high suspicion for SAH with a normal CT head
ABG - if hypoxic (avoid if considering fibrinolytic therapy)
hCG - women of childbearing age
ESR/CRP - elevated in infective endocarditis
CXR - if suspected or history of lung disease or (+)fever
EEG - suspected seizure
UA/blood cultures - if (+) fever

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24
Q

tx for general stroke

A
  1. Ensure adequate ABC’s
    - keep O2 saturation >94%
    - Intubate with mechanical ventilation if necessary
  2. Keep NPO
    - risk of aspiration d/t dysphagia
    — consult occupational therapy
    — swallowing has to be assessed prior to advancement of diet
  3. Fluids - IV normal saline
  4. Head/Body Position
    - supine with head in neutral alignment with body
    - elevate head 30° IF risk of
    increased ICP (ICH, cerebral edema associated with large infarct)
    - aspiration (dysphagia or decreased LOC)
    - cardiopulmonary decompensation/O2 desaturation (chronic CV or Pulm disease)
  5. Tx Fever
    - acetaminophen - “PR” (rectal), IV (Ofirmev)
    - surface cooling - Evaporative cooling, Ice water immersion, Whole-body or strategic ice packing
    - search for cause
  6. hypothermia - warm blankets, bear hugger, warm IV fluids
  7. Hyper-/Hypoglycemia (via bedside fingerstick)
    - hypoglycemia - tx if BS <60 mg/dL (class 1)
    - hyperglycemia - tx if BS is >180 mg/dL to a goal of between 140-180 mg/dL (class IIa)
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25
Q

common causes for fever in stroke

A

aspiration pneumonia, UTI

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26
Q

what condition involved with temp can worsen cerebral ischemia in all strokes

A

Hypothermia

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27
Q

what tx is indicated specifically in hemorrhagic strokes?

A

anticoag reversal

  1. Warfarin - vitamin K + 4-factor prothrombin complex concentrate (PCC)
  2. Dabigatran (Pradaxa)
    - Options: activated charcoal vs idarucizumab (Praxbind) vs PCC
  3. Factor Xa
    - rivaroxaban (Xarelto), apixaban (Eliquis), fondaparinux (Arixtra), edoxaban (Savaysa)
    - Options: activated charcoal vs andexanet alfa (Andexxa) vs PCC
  4. Heparin/LMWH - Protamine

Antiplatelets usually do not require reversal or intervention

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28
Q

tx specifically for ischemic stroke

A

Determine eligibility for fibrinolytic therapy (rt-PA)

  1. Hypotension - IV fluids - for organ perfusion
  2. BP goal of SBP ≤ 185 and DBP ≤ 110 before rt-PA can be administered (class 1)
    - 1st line antihypertensives (IV) - nicardipine, clevidipine, labetalol
  3. Elevated BP - Not eligible for rt-PA - BP: Do not treat unless SBP >220 or DBP >120
    - BP should not be lowered >15% in first 24 hrs
    - First-line agents same as AIS eligible for rt-PA
29
Q

Additional indications for tx elevated BP in ischemic stroke:

A
  1. malignant HTN (end organ damage)
  2. comorbid or complicating conditions that require lowering of BP
    - Ex: active ischemic coronary disease, heart failure, aortic dissection, hypertensive encephalopathy, acute renal failure, or pre-eclampsia/eclampsia
30
Q

tx for elevated BP in intracerebral hemorrhage

A
  • SBP 150-220 mmHg - careful titration of therapy to allow for smooth reduction of SBP to a goal of 130-140 mmHg (Class 2a)
  • SBP >220 mmHg - there is currently not enough evidence to provide specific recommendations
  • First line antihypertensives same as AIS
31
Q

Risk vs benefit of treatment of elevated BP in intracerebral hemorrhage

A

risk - loss of cerebral perfusion pressure leading to higher level of infarction
benefit - decreased risk of rebleed

32
Q

tx for subarachnoid hemorrhage

A
  1. Elevated BP
    - No optimal target has been defined - a SBP < 160 or MAP < 110 was a “reasonable” recommendation
    — preferred agents: labetalol, nicardipine or enalapril
    - Risk vs Benefit of treatment same as intracranial hemorrhage
  2. Prevent vasospasm in SAH
    - Goal: prevent delayed cerebral ischemia
    - Nimodipine is drug of choice - given PO or via NG tube and continued for 3 weeks
33
Q

First line Interventional tx for Ischemic Stroke

A

Recombinant tissue-type plasminogen activator (rt-PA)

  1. alteplase (Activase) - IV thrombolytic agent
  2. Off-label: tenecteplase (TNKase)
  3. MUST meet inclusion/exclusion criteria (class I)
    - glucose is only lab value that must be assessed prior to initiation of therapy
  4. Informed consent must be obtained
    - risk of hemorrhage, angioedema
34
Q

rTPA inclusion criteria

A
  1. Clinical diagnosis of ischemic stroke causing measurable neurologic deficit
  2. Onset of sx within 4.5 hours before beginning of tx; if the exact time of stroke onset is not known, it is defined as the last time the patient was known to be normal
  3. Age ≥18 years
  4. Unclear time onset: DWI shows ischemic lesion <⅓ of middle cerebral artery & no visible change on FLAIR (IIa)
35
Q

Management: if tPA is administered for stroke

A
  1. Infuse tPA over 60 minutes
  2. Admit or transfer to ICU at a stroke center or specialized stroke unit
  3. Neuro checks q15m for 3 hours, then q30m for 6 hours, then qhr x 15 hours
  4. Keep BP < 180/105 mmHg
  5. Avoid NG tube, indwelling catheters or intra arterial catheters if possible
  6. Obtain CT at 24 hours post-tPA, before starting antiplatelets or anticoagulants
36
Q

pt is experiencing acute bleeding within 24h of tPA, how do you treat this complication?

A
  1. Acute bleeding within 24 hours of tPA
    - cryoprecipitate or tranexamic acid (TXA)
37
Q

Alternative if rt-PA is CI or ineffective in a pt with a persistent potentially disabling neuro deficit (NIHSS ≥6)

A

Reperfusion Therapy Option - Endovascular mechanical thrombectomy

  1. Indication: large artery occlusion in the anterior circulation (dx by CTA or MRA) with small infarct core and no hemorrhage (dx by MRI)
  2. tx must occur within 24 hours of sx onset and performed at a stroke center with surgeons experienced in procedure
  3. Specific eligibility criteria for tx must be met if < 6 hours since onset and if treatment will occur between 6-24 hours since onset
38
Q

Neurologic Complications - ICH

A
  1. Hematoma
    - Evacuation via minimally invasive surgical procedures is recommended moderate to large ICHs (Class 2a) and large intraventricular extension of ICH’s. (class 1)
  2. Large intracranial hemorrhage
    - Craniotomy vs craniectomy
  3. Cerebral edema
  4. Increased ICP
  5. Hydrocephalus
  6. Seizures - occur most frequently in hemorrhagic strokes
39
Q

Invasive ICP monitoring is reserved for who?

A

patients most at risk for increased ICP

This type of monitoring increases the risk of CNS infection and hemorrhage

40
Q

tx for seizure complications from stroke

A
  1. continuous EEG monitoring x 24 hrs in hemorrhagic strokes
  2. Primary prophylaxis - only if impaired consciousness and evidence of seizure activity on EEG or h/o clinical seizures
  3. Secondary prophylaxis - for all pts and continued x 7 d
  4. Active seizure - IV lorazepam
  5. Prevention - fosphenytoin
    - avoid phenytoin - evidence shows worsened mortality
41
Q

tx for increased ICP complication from stroke

A

occurs most often in hemorrhagic strokes

  • elevate head of bed 30°
  • mild sedation to maintain comfort as needed
  • osmotic therapy (i.e. mannitol, hypertonic saline) may be considered
42
Q

tx for hydrocephalus complication from strokes?

A

increased fluid in the ventricles of the brain leading to pressure on the surrounding cerebral structures

  • may occur with SAH
  • watch for worsening HA and progressively impaired neurological testing
  • CT/MRI brain will show enlarged ventricles
  • consult neurosurgery for consideration of shunt placement
43
Q

what medication to avoid in seizure complication from strokes, as evidence shows it actually worsened mortality

A

phenytoin

44
Q

medical complications from strokes? (9)

A
  1. Dysphagia and aspiration - swallowing eval
  2. Venous thromboembolism
    - pneumatic compression stockings or heparin
  3. UTI
  4. Urinary incontinence
  5. GI bleed - preventative PPI
  6. Depression
  7. Nutritional deficiency, dehydration - consult nutrition
  8. Pressure /ulcers sores - move pt q2h if unable to self adjust
  9. Falls and bone fractures - early education, bed alarms, physical therapy consult
45
Q

pulmonary complications from strokes

A
  1. aspiration pneumonia
    - keep NPO until swallowing eval
  2. mechanical vent
    - laryngeal injury, vocal cord dysfunction, swallowing impairment, tracheal stenosis, tracheoesophageal fistula, sinusitis
  3. oxygen desat
    - continuous pulse ox, oxygen supplementation to maintain O2 sat above 94%
  4. neurogenic pulmonary edema
    - unknown pathophysiology; abrupt onset, rapidly progressing pulmonary edema; supportive treatment
  5. abnormal rsp patterns
    - Cheyne-Stoke respiration, periodic breathing, ataxic breathing, apneustic breathing, gasping, apnea
46
Q

cardiac complications from strokes?

A

monitor for sx, ekg changes, cardiac enzymes

  • acute MI
  • HF
  • Ventricular arrhythmias
  • cardiac arrest
47
Q

needs during admission for strokes?

A
  1. Frequent neuro checks for up to 72 h post stroke
  2. Admission consultations - within 2 d of stroke
    - occupational therapy
    - physical therapy
    - speech therapy
  3. Additional consult on a case by case basis
    - Home health care coordinator
    - rehab coordinator
    - Social worker
    - Dietitian
    - Medical specialist (depending on complications) - psych, urology, GI, pulmonary, cardio, ortho
47
Q

prevention for stroke?

A
  1. primary prevention - Screen for and control all modifiable risk factors
  2. secondary prevention
    - Strict BP control - once pt is neurologically stable and risk of worsening ischemia has resolved
    — 2018 guidelines AIS - restart or initiate BP therapy in any patient with BP > 140/90
    — 2022 guidelines for ICH - goal <130/80
    - Statin therapy - for ischemic strokes
    - Smoking cessation - risk of stroke decreases 2-4 yrs after cessation
    - DM control
    - Weight loss/Exercise
    - Low-fat/Low-salt diet
    - Avoid heavy alcohol intake (>4 drinks/d)
48
Q

Additional prevention recommendations for Ischemic Stroke

A
  1. antiplatelet therapy for 21 d
    - (+) tPA - start ASA 24-48 h after tPA
    - (-) tPA - start ASA and Plavix within 24 h
  2. anticoagulant therapy
    - Indicated in patients with a potential cardiac source of embolism
    — MC - Afib
    — other - mechanic heart valve, left ventricular thrombus, dilated cardiomyopathy, rheumatic valve disease
49
Q

a transient episode of neurologic dysfunction caused by cerebral acute ischemia

A

Transient Ischemic Attacks

blood supply to the brain is temporarily blocked leading to lack of oxygen to brain tissue without death of brain cells

most often sx resolve within 1-2 h

50
Q

if TIAs don’t make permanent damage, then why are they important?

A
  • 30% with stroke have a hx of TIAs
  • 10-15% with TIAs will have a stroke within 90 days - MC within 2 days
51
Q

evaluation for TIA

A

Assessing severity of sx - look for signs of persistent neurologic deficits

  1. Complete hemianopia (≥2 on the NIHSS #3)
  2. Severe aphasia (≥2 on NIHSS question)
  3. Visual or sensory extinction (≥1 on NIHSS question 11)
  4. Any weakness limiting sustained effort against gravity (≥2 on NIHSS question 5 or 6)
  5. Any deficits that lead to a total NIHSS >5
  6. Inability to walk
  7. Any remaining deficit considered potentially disabling by the patient, family, or the treating practitioner
52
Q

management for TIA

A
  1. Eval, work-up and initial treatment is the same as stroke
  2. Interventional tx (e.g. rt-PA) is included if there is persistent neurologic deficit that is potentially disabling
53
Q

8 high RF for admission after TIA?

A
  1. ABCD >= 4
  2. subacute stroke on CT
  3. > =50% ipsilateral stenosis
  4. infarct on MRI
  5. recent TIA with past month
  6. other conditions warranting admit
  7. acute cardiac process, arrhythmia
  8. barriers to rapid outpatient f/u/testing
54
Q

management of underlying etiology in TIA

A

Look for underlying etiology

  1. CAD
    - Dx: carotid US
    - Tx: carotid endarterectomy with medical management
  2. cardioembolic etiology
    - Dx: EKG, echo
    - Tx: treat underlying disorder, antithrombotic therapy as indicated
  3. large and/or small vessel disease
    - Dx: MRA/CTA
    - Tx: revascularization with stent placement for large vessels; medical management for both large and small vessel disease
  4. etiology is unknown despite intensive workup - aka “cryptogenic stroke”
    - medical management only
55
Q

medical management for TIA

A

antiplatelet
antihypertensive
statin therapy
address all modifiable risk factors

56
Q

Carotid atherosclerosis is often most severe within how much of the common carotid artery

A

2 cm of the bifurcation

57
Q

sx from carotid artery stenosis result from ?

A

reduced blood flow and/or superimposed thrombus formation

History of CVA or TIA may be present

58
Q

PE for carotid artery stenosis

A

carotid bruit or palpable sclerosis

59
Q

imaging options for carotid artery stenosis

A
  1. Carotid duplex ultrasound (CDUS)
  2. MRA
  3. CTA
  4. carotid angiography
60
Q

what is the gold standard imaging for carotid artery stenosis

A

carotid angiography

61
Q

pros vs cons of CDUS

A

Pro: least invasive, least expensive, readily accessible, less time consuming
Con: operator dependent; may overestimate the degree of stenosis

62
Q

pros vs cons of MRA

A

Pro: produces a 3D image, more accurate for detecting high grade stenosis; less operator-dependent
Con: more expensive, more time consuming, tight enclosure in supine position, CI in pacemaker, ferromagnetic implant¹

63
Q

pros vs cons of CTA

A

Pro: produces a 3D image, more sensitive and specific than US and more specific than MRA
Con: radiation exposure, requires contrast, CI in renal insufficiency

64
Q

pros vs cons of carotid angiography

A

Pro: gold standard, most accurate in determining severity and collateral blood supply
Con: Invasive, costly, higher morbidity/mortality

65
Q

management for carotid artery stenosis

A
  1. Asx (no hx of stroke or TIA symptoms)
    - recommended at any stage of dz - statins, antiplatelet agents, tx of HTN and DM, smoking cessation and healthy lifestyle changes
    - carotid endarterectomy (CEA) if carotid stenosis is 60-99%
  2. Symptomatic (hx TIA or ischemic stroke w/n previous 6 mo)
    - carotid endarterectomy (CEA) and maximize medical management
    - carotid stenting - alt to CEA for select pts
66
Q

indications for carotid stenting instead of CEA for pt?

A
  1. carotid lesion is inaccessible surgically
  2. radiation induced stenosis
  3. restenosis after endarterectomy
  4. comorbid conditions prevent use of anesthesia
67
Q

while infusing tPA for a stroke pt, they start developing HA, N/V, acute HTN, or neurologic deterioration
what is your next step?

A

Stop infusion and obtain CT if pt develops

68
Q

Pt receiving tPA is now experiencing aniogedema, how do you treat this complication?

A
  • IV methylprednisolone, diphenhydramine and famotidine
  • Consider SQ or inhaled EPI
  • prepare to intubate if edema is rapidly progressing

Neuro: Clin Med IIB (13 decks)

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