Stroke, TIA, SAH Flashcards

1
Q

Ischemic v. Hemorrhagic
where does a TIA, SAH, ICH fall

A

Ischemic: ishemic = ischemia (decrease flow) which can LEAD to infarction (tissue death)
- ischmic stroke is a result of a blood clot or narrowing of vessels which creates a decrease in neurological functioning
- ishemic: can be spinal, cerebral or retinal infarction = seeing death of tissue on brain imaging

TIA = a transient episode of neurologc dysfunction, due to brain ischmeia BUT NO EVIDENCE OF ACUTE INFARCTION on imaging

Hemorrhagic: weakened vessels which rupture and BLEED into surrounding tissue causing brain damage

SAH: subarachnoid hemorrhage (below arachnoid)
ICH: intracerebral hemorrhage (within the brain tissue itself)

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2
Q

Ischemic Stroke
thrombotic v embolic

A

Thrombolic: a narrowing of vascularture within the brain as a result of something INSIDE the brain vessle; usually a clot that FORMED THERE - in the brain
Reasons for a thrombus in the brain
- atherosclerosis
- vasculitis disorders
- hypercoaguable states
- infection

Embolic: obstruction of a normal vascular lumen in the brain; a result of material which came from somewhere else in the body and traveled there
- A fib (clot thrown from the atria)
- valvular vegitation (IVDU)
- cardiac tumor piece
- fat emoli

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3
Q

Vascular Anatomy

anterior circulation
posterior circulation

A

Anterior circulation
- the Left and Right interal Carotid arteries give rise to the right and left middle cerebral arteries (MCA) as well as the left and right anterior cerebral arteries
- the MCA supplies the lateral aspects (affecting face and hands > legs) and the ACA supplies the medial aspects (affecting legs and trunk > hands and face)

Anterior Circulation Supplies
- cerebral cortex
- Subcortical White Matter
- Basal ganglia, thalmus and hypothalmus (in combo with the PCA)
- the internal capsule

Posterior Circulation
- the left and right vertebral arteries enter and combine to form the basilar artery
- the basilar artery branches to form the left and right PCA: posterior cerebral arteries
- other branches include: PICA, posterior/anterior spinal, anterior inferior cerebellar and superior cerebellar

Posterior Circulation Supplies..
- cerebellum
- Brain Stem
- Spinal Cord
- parts of thalmus, hypothalmus, occipital and temporal lobes (in combo with the MCA)

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4
Q

Deficts in the Anterior Circualtion result in ….

Left sided defict
Right sided defict

A

Anterior circualtion = ACA and MCA
need to thing about which hemisphere is affected

if the LEFT hemisphere is affecting: detriments to the right side will include
- hemiparesis: motor deficts of facial weakness & horizontal gaze palsy TOWARD the side of the lesion (to the left)
- hemisensory deficts: of pain and temperature
- left sided deficts will also have significant speech issues since this is the dominant speech area for those right-handed (80%) : aphasia, apraxia and agnosia

if the RIGHT hemisphere is affected: detriments to the left side will include
- hemiparesis: facial weakness, horizontal gaze palsay toward the RIGHT
- hemisensory deficts: temperature and pain
- right sided deficts will also result in inattention/neglect of the left side, extinction and dysarthria without aphasia since language usually is on the left, the issue is just weakness of motor muslces not the speech centers!!!

both sides of an anterior circualtion defict can result in homonymous hemianopsia

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5
Q

results of a lacunar infarct

A

MCA (from anterior circulation) also help to supply the perforating vessels which supply the deeper structures of the brain ( basal ganglia, thalmus, hypothalmus)

  • an occlusion of these smaller vessels can cause huge deficts out of proportion to the size of infarct, as these structures play a role in the relay process of signals
  • can have pure motor or pure sensory deficts: ex. damange of the somatosensory projections from the thalmus can result in similar sensory issues as a larger vessel occlusion
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6
Q

Posterior Circulation Deficts result in….

specific to the PCA
cerebellum
vertebrobasilar
basilar

A

(left or right doesnt really matter here as they supply same structures)

brainstem or cerebellar dysfunction = difficult to pick up, espeically since NIHSS tests more of the motor and sensory deficts seen with an anterior stroke

Common symptoms (regardless of the exact artery include)
- vertigo & dizzy
- N/V
- same sided facial deficts
- opposite sided limb deficts
- swallowing difficulties

PCA: opposite sided homoynous hemianopsia, unliateral HA, sensory deficts, inability to read, inability to name colors, unilateral CNIII palsy

Cerebellum: HA, N/V, vertigo, gait instability, limb ataxia, dysarthria

Vertebrobasilar: vertigo, occular palsies, visual issues, swallowing issues, ataxia, dipolpia, horners

Basilar: quadriplegia, coma “locked- in” syndrome, vertical upward gaze

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7
Q

TIA: transient ischemic attack
what is it
what does it imply

Risk Factors

A

TIA: a transiet (short-lived) episode of neurologic dysfunction: due to brain ischemic but NO EVIDENCE OF ACUTE INFARCTION on brain IMAGING

  • this is an EARLY warning sign: that a stroke is coming; high risk for a stroke in the following days, weeks, months etc.

RISK FACTORS
- high cholesterol
- DM
- HTN
- current smoker
- OSA, obestiy, metabolic syndrome, poor diet, etc.
- stressors in life
- alcohol consumption
- cocaine use
- A fib: throwing a clot to the brain from the heart
- valvular heart disease; PFO, vasculitis
- hx. of TIA stroke (or family hx.)
- giant cell arteritis

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8
Q

TIA
Symptoms

Reasons for a TIA

A

Symptoms
- sudden onset with quick resolution of symptoms (usually less than 24 hours)
- focal or unilateral neurological defects of motor or sensory symptoms
- these symptoms or stroke like things will go away after the TIA is over (although lasting effects are possible)

other symptoms
- increase HR, BP, carotid bruits, etc.

Reasons
- tumor
- CNS infection
- syncope/fall/trauma
- hypoglycemic/metablic disturbance
- MS
- SAH (with addition symptom of HA)

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9
Q

Symptoms of TIA v a mimicking event (seizure, etc.)

A

TIA
- will have unilateral paresis
- will not have memory loss
- will have dysarthria
- may have double vision or monocular blindness transiently
-

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10
Q

Workup of a TIA

labs
imaging
differentiate between what and waht types
score calcultor for stroke risk? for a fib clot induced stroke risk

A

evaluation must occur within 12 hours completed by 48 hours
- CT or MRI (within first 24-48 hours)
- brain vasculature imaging (carotid imaging, doppler or MRA needed)
- EKG & echo
- labs: CB, a1c, lipids, CMP

need to find underlying source, is it embolic (from a fib clot) or thrombotic from atherosclerotic origins

Scores
ABCD2 Score: determines the short-term risk of pt. having a stroke within 2-90 days of the TIA event
score > 4 = probably should hospitalize to watch for stroke risk in next 2 days
score > 6 = definately neeed to hospitalize

CHA2DS2-VASc Score: determines the risk of a clot being thrown from A fib (to see if anticoag. is needed)

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11
Q

TIA
Management
Medications
antiplatelet v anticoag.

A

TIA: need to assess and address other factors which increase likelihood of a TIA & stroke
- HTN management
- lipid management
- DM control

Antiplatelet Thearpy: if the cause is atherosclerotic in origin; daily long-term antiplatelet
- asprin as monothearpy
- asprin allergy –> clopidogrel (get labs to see if responsive to clopidogrel)
- clopidogrel resistant –> ticagrelor

HIGH RISK PTS: need dual therapy with aspring + clopidogrel or asprin + ticagrelor (unless GI bleed risk)

Anticoagulation Therapy: if the cause is A. Fib throwing clot in origin (to prevent that) long term anticoag. needed

DOACS are first line for anticoagulation
- apixiban > dabigatran or rivoroxaban
- warfarin can be used but D-D interactions and needs monitoring of INR
- unable to anticoag. –> need watchmans device or surgical ligation

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12
Q

HTN and Lipid goasl for our TIA pts.

A

HTN: want BP < 130/90
- ACE +/- diuretic, or an ARB

Lipids
- statin thearpy
- LDL< 100 (if atherosclerotic pt. want < 70)
- 50% reduction desired

smoking cessaion, exercise, reduce alchol and hange diet can all help

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13
Q

Ischemic Strokes
- causes
- pathogenesis

A

Ischemic Stroke: ischemic tissue leads to infarction (due to blockage)
Causes
- A fib: a clot is thrown and gets stuck (blocks flow)
- atheroscelrosis: narrowing of the vessels
- lacunar (small vessel) infarctions
- systemic hypoperfuction (cardiac arrest, overdose, etc.)

majority of the strokes which occur are in the large arteries in the anterior or posterior circulation

Pathogenesis
- occulded blood flow = no oxygen
- ischemia develops when there is less than 20% blood flow to the area than normal (at 80% flow its ischemic)
- this border of ischemic tissue is called the penumbra – this is the area that if help is gotten, could be restored and not dead “the at risk of dying if not helped area”

ischemic strokes can evolve to become…
1. Vasogenic: inflammation continues after the stroke
- leading to hernation, or death if infarction is large enough
- symptoms will worsen after stroke

  1. Hemorrhagic transofrmation: begin to bleed
    - result of BBB disrupted, capillaries disrupted, HTN or reperfusion goes wrong
    - dramatic decline in symptoms
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14
Q

Ischemic Stroke
Symptoms

A

symptoms depend on the area in which the stroke is occuring: infarcted tissue in different areas will ahve different presentations

Thrombotic: ususally a step-wise or gradual progression to their worst

Embolic: will be abrupt and max insult will be immediate

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15
Q

Anterior Cerebral Artery Occulsion: ACA Stroke

symptoms

A

ACA: supplies the medial frontal lobe: specifically in the motor and sensory hommunculs (the LE&raquo_space; UE and face)

Symptoms
- Lower extremity weakness and lost sensation more than upper extremity and facial symptoms on the contralateral side (since we know that they cross at the medulla)
- paracentral lobule: urinary urgency/incontinence
- limbic/prefrontal cortex supply: AMS, disinhibition, impaired judgement
- (speech of prefrontal cortex): speech peserveration (repeating), nonfluent speech but comprehension is ok

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16
Q

Middle Cerebral Artey Occlusion: Symptoms

A

MCA: supplies the lateral sides of the frontal, parietal and temporal lobes

most common type of stroke M1 occulsion v M3/M4 can differntiate symtpoms

Symptoms
- hitting the lateral hommunculus: so youll see issues with facial and upper extremitiy motor and sensory abilities on the contralateral side of the stroke
- speech: aphasia if left MCA
- hemineglect: if right MCA
- gaze preference to the side of the lesion (side the opposite side controls the opposite eye: therefore if there is a R sided stroke, controlling left eye field, cant look that way, looks right)

homonymous hemianopia

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17
Q

Internal carotid artery Occlusion
symptoms

A

** can be asymptomatic if there is collateral circulation which is adequate**

  • preceeding amarousis fuax (transient monoccular blindness) possible
  • dizzy, sudden and severe HA possible
  • contralateral sesnsory and motor deficts
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18
Q

Subcortical/Lacunar Infarct
risks
syndromes

A

those branches off the MCA which travel to the deeper parts of the brain: supplying internal capsule, basal ganglia, thalmus or brainstem

Risks: HTN, smoking, DM, lipids

Symptoms (5 classic syndromes)
- pure motor stroke: only motor weakness
- pure sensory stroke: only sensory loss
- mixed sensorimotor
- ataxic hemiparesis
- clumsy-hand & dysarthria (speech) : brainstem stroke

other Lacunar Infarcts: can be asymptomatic (clincally silent)
- can present with acute or subacute symptoms (those above)
- okay prognosis but can worsen

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19
Q

Watershed Infarct: Bilateral
what is it
symptoms

A

Watershed Infarct
- the junction between the two arterial areas of the ACA and the MCA
- usually a result of poor perfusion: lacking blood flow to both these arteries results in a “no mans land” of no oxygen getting to these sites

the resulting zone: is
- proximal UE motor and sensory loss of the contralateral side (usually abilaterally occurence)
- the extremities (face, hands, legs and feet) are ok
- “man in barrel syndrome” as the trunk is effected

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20
Q

Posterior Circulation Strokes: Posterior Communicating Arterty Occulsion

Symptoms

A

PCA Stroke: most commonly due to an embolsim: from the heart

Symptoms
key one: contralateral homonymous hemianopsia = most common due to infarct occuring in the occipital lobe regions impacting the contralateral side of vision

  • headaches (common)
  • limb weakness
  • dizzy, nausea
  • memory loss

Thalmaic Syndrome
- contralateral hemisensory disturbance: paresthisias of face, limbs and trunk (becuase thalmus is relay)
- spontaneous pain

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21
Q

Vertebrobasilar Occulsions
symptoms

A

Vertibrobasilar Occulsions
- the verterbal artery - basilar artery junction = site of occlusion (just before the PICA) is the most common location
- this impacts the cerebellum and the brainstem

Symptoms
- asymptomatic (if good collateral flow)
- TIAs or Horner’s Syndrome possible

Locations or types of this inarct
- lateral meduallary infarct = wallenburg
- medial meduallary infarct
- cerebellar infarcts of PICA
- basilar infarct via embolsim or thrombosis

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22
Q

Basilar Artery Occlusion
symptoms

A

Basilar Artery: the combo of the two vertebral arteries which is formed right at the pons & impact cranial nerves!!
(supplies cerebellum and pons)

Symptoms
- dysphagia & dysarthia (motor and comprehension issues)
- tongue/palate deviation
- EOM deficts
- ataxia (cerebellar dysfunction)
- crossed sensory/motor deficts: same side of face but opposite side of body

think basilar arteries: supplying pons & inside the pons is…
- in the pons, the contralateral sensation has already crossed over (in medulla) so lack of sensation on the contralateral side
- in the pons, the same side of the cranial nerves for sensation and motor of the face via the trigeminal nerve

locked-in syndrome : in tact consciousness but in ability to speak and move because the pons is damanged (conscious becuase the reticualr formation is perserved)

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23
Q

PICA occulsion
symptoms

A

PICA: posterior inferior cerebellar artery
supplies the posterior and inferior cerebellum

results in
- cerebellar infarct
- vertigo and nystagmus
- n/v
- ipslateral limb ataxia and numbness and headache

high risk of hernation of the brain and coma progression

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24
Q

Wallenberg Syndrome
(lateral meduallary syndrome)

A

occlusion in…
- PICA or vertebral artery

Symptoms
- contralateral pain and temperature sensation issues of upper and lower extremities (as a result of the spinothalamic tract)
- contralateral motor fuction is ok, since motor travels through the corticospinal fibers & these are more ventral (below) where this is occuring

  • vertigo and nystamgus (to the affected side)
  • N/V & hiccups (uncontrolled)
  • CN IX, X issues will speaking, and gag reflex
  • horners syndrome (sympatheitc fibers injured)
  • ataxia towards same side of lesion
  • imparied facial sensation on the same side as lesion (but not motor since these arent near medulla and already have left)
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25
Q

Vertical Gaze Palsies & Horner’s Syndrome

A

Horner’s Syndrome
- slight ptosis
- miosis (constriction)
- anhidrosis (lack of sweating)
DUE TO
- carotid or vertebral artery occulsion, injury or dissection (brainstem lesions or blood to BS lesions)
- sympathetic fibers running along the arteries
- connective tissue disorders (Erhler’s Danlos)

Vertical Gaze Palsies
- junction of the thalamus and mid-brain is the last area of the vertical gaze pathway
- symptoms: blurred vision, “bounding images”, nystagmus, dizzy, vertigo, postural changes, gait ataxia

DUE TO
- mid-brain/thalamic stroke, hemorrhage, etc.
- hydrocephalus (3rd ventricle)
- encephalitis, neurosyphilisis, TBI, metabolic issues, Pineal tumor
- drug induced: barbituates, carbmazepines

26
Q

what is the Cincinnati Prehospital Stroke Screen

A

FAST
F: Facial Droop (ask to smile)
- normal = both side will go up
- abnormal = one side of the face does not move

A: Arm Drift (ask to raise both arms in front)
- normal = both arms will move equally or not at all (together)
- abnormal = one arm will drift compared to the other one

S: Speech (ask them to repeat “you can’t teach an old dog new tricks”)
- Normal = correct words without slurr
- abnormal = slurred or inapporpriate words

T: (Time) get them ASAP to help

27
Q

what is the Rapid Evaulation for an Ischemic Stroke
5 key components when the pt. walks in

A
  1. Obtain History THE PATIENTS LAST KNOWN WELL TIME IS CRITICAL : helps assess what therapy can be done or not (window for ablility to give TPA)
  2. FS blodsugar: if too high results can cause simialr symptoms to the stroke presenation
  3. Blood Pressure: if too high can impact ability to give TPA
  4. NIHSS: not a full neuro, need the stroke scale first
  5. STAT NONCONTRAST HEAD CT: quicker than if contrast was obtained
  • often times if caught early: the head CT will appear normal (within 6hours) but will develop
  • MRI is technially more sensitve for acute strokes but not as avalible as a CT
28
Q

After the first 5 components of the ischemic stroke assessment are complete: waht labs and orders do you need to do

A

LABS
- PT/INR, PTT (determine bleeding)
- CBC & platelets
- Troponin
- EKG (look or afib or aflutter)

Other Labs to obtain
- BMP, LFTs
- tox screen, alcohol
- pregnancy test
- chest xray
- EEG (seizure suspected)

29
Q

What is the NIHSS

score categories indicate what severity of stroke

whhy does the score matter & relate to pt outcomes

negatives of the NIHSS

A

NIHSS: NIH Stroke Scale = ability to determine the extent of damage from a CVA
- a score baased on neuro assessment, picutres, images, questions, etc.

0 = NO stroke symptoms
1-4 = Minor Stroke
5-15 = moderate stroke
16-20 = moderate to severe stroke
21-42 = severete stroke

NIHSS can be found on MD calc

NIHSS score severity is DIRECTLY related to pt. outcomes of the stroke

  • negatives = it is skewed to pick up a left MCA stroke (Assessing langugae and UE more) than right MCA (but in R MCA you will see neglect of the left side)
  • neagtive: not great for assessing posterior circulation strokes
30
Q

Acute Ischemic Stroke: Management
Overview: what are you to do regardless of emobloic or thrombic

A
  1. assess if they can & adminster if able: TPA (IV Thrmobolysis) the clot buster (but their are contraindications to be aware of)
  2. Endovascualr Revascularization: assess if they area appropriate pt. for this procedure to remove clot
  3. Inpatient Care (ICU) : figure out underlying ause of stroke, risk factors & treat via antitcoagulation or antiplatelet treatment (depending on cause of stroke)
  4. Long-Term Care: manage risk factors and prevention of future strokes
31
Q

IV Thrombolysis (TPA)
- what is it & how does it work
- what type of pt. to recieve TPA (based on NIHSS)
- Indications for administration of TPA

A

TPA: alteplase = an IV recombinant tissue plasminogen activator
MOA: plasminogen helps to BREAKDOWN the thrombus by degrading fibrin: therefore the plasminogen turns into the active plasmin to do this

early adminsitration of TPA relative to their time of last known well treatment is assocaited with improved stroke outcomes!!!

NIHSS: those who have “debilitating” symptoms according to the scale should be given TPA

TPA administered regardless of the TYPE of clot: we just know there is a clot: and we need to break it apart asap since its blocking blood flow

Administeration
- IV access with 2 peripheral IVcs
- 0.9mg/kg (10% as bolus then 90% over an hour)

32
Q

Specific Indication for when TPA should be used in AIS (acute ischemic stroke)

A

WHEN CAN YOU USE TPA????

  • there is a clinical dx. of a stroke with debillitating symptoms
  • anyone with symptoms of the stroke lasting for less than 4.5 hours (if longer we cant use) EXCEPT FOR…
    1. those > 80 (cant use TPA even if their symptoms < 4.5 hours)
    2. those with NIHSS > 25
    3. those on anticoags.
    4. those with history of stroke + DM
  • CT scan showing no hemorrhage, showing an established infarct or those with no other explination for the focal deficts they’re presenting with

TPA IS THE STANDARD OF CARE: CAN BE GIVEN WITHIN CONSENT IF NO ONE IS ABLE TO CONSENT

33
Q

TPA Contraindications

ABSLOUTE

A
  • evidence of a intercerebral hemorrhage on CT (they’re bleeding, dont give them clot buster to bleed more)
  • major signs of early infaract (> 1/3 of the MCA terriotory injured)
  • patients with a BP than you cant get below 185>110 (they’re at a high risk of bleeding)
  • those with glucose FS < 50 or > 400 (this coul be reason for symptoms instead)
  • history of coagulopathy or bleeding
  • platlets < 100k
  • **PTT < 40
  • INR > 1.7**
  • use of LMWH or Enoxoparin within 24 hours
  • use of DOAC within 48 hours
  • severe head trauma within past 3 months
  • symptoms as a result of infective endocarditis
  • structursal GU/GI malignancy or bleed within 21 days
  • symptoms of subarrachnoid hemorrhage
  • aortic arch dissection
34
Q

TPA relative exclusions/warnings for use

A
  • seizure during stroke
  • stroke + sickle cell dz.
  • history of bleeding tendency
  • head trauma within 14 days
  • stroke within 3 months
  • LP within 7 days
  • pregnancy or early post-partum
  • extra axial neoplasm
  • cerebral microbleed
  • hx. of hemorrhage intracerebrally
  • recent MI with stroke in 3 months
  • pericarditis
  • major surgery within 14 days
35
Q

what are some risks associated with giving TPA

A
  • bleeding!!!
  • a minor nose or gum bleed is common: evaluate how severe
  • risk of ratal internal or external bleed (at arterial or venous puncture sites)
  • fatal cases of hemorrhage associated with tramatic intubation
  • low risk of intracranial hemorrage (6%)

always delay anticoagulation/antiplatlet meds for at least 24 hours after giving a TPA

36
Q

order of events for stroke

A
  • adminsiter TPA if able
  • get imaging: esspecially of the vessels: CT-angiography or CT-perfusion study (assess if you can use contrast or not)
  • thrombectomy (if able)
  • post tpa care
  • admin meds (platlet or coag)
37
Q

Endovascular Treatment : Thrombectomy
what is it
eligibility for surgery

A
  • get CT-A or CT-Perfusion to see vessels

Thrombectomy = the mechanical removal or a stroke causing clot via asiration or stent retrever

  • this can be done after TPA or instead of TPA (if they are outside the TPA window (4.5 hours)

Eligibility
- Modified Rankin Score (0-1) : amount of disability prior to stroke
- if large vessel occlusion (MCA (M1 segment), ICA)
- can consider for smaller: basilar artey, vertebral, PCA, or M2 and M3 of MCA
- older than 18 years
- NIHSS > 6
- ASPECTS < 6 (any more than 6 is poor outcomes anywya)
- treatment within 6hours of symptom onset – up to 24 hours

38
Q

what is a Ct perfusion

A
  • looks at flow thorugh the brain through contrast (need to ensure pt. can have contrast)
  • CORE : (pink) = infarcted tissue
  • Penumbra (green) = aread of reduced perfusion ut not yet infarcted
  • magic ratio: 2:1 want the penumbra bigger than infarct to show it sowrth saving
  • flow is low and volume high = potential ability to save brain tissue
39
Q

Post- TPA care (ICU)
post-thrombectomy care

A
  • BP and neuro checks Q15 mins then Q30 after 6 hours then hourly for 24
  • BP: can be as high as 180 (can stay high to ensure perfusion)
  • if SBP > 180 or DBP > 104 = need to monitor more frequently
  • any development of severe HA, acute HTN, N/V or declined MS = stop infusions and obtain STAT CT (bleed risk)
  • delay NG tube, catheters and other invasive tubing (bleed risk)
  • obtina CT or MRI 24 hours after before starting anticoags/antiplatlets

Post Thrombectomy Care
- pt. stays flat with knee immobilzer (went through the groin usually)
- monior peripheral pulses and signs of bleeding
- if bleed: PRESSURE!!!!

40
Q

Post AIS Care
- other tests to preform

A
  • fundoscopic exam: papilledema or retinal emobli
  • CV: for bruits, cardiac abnormalities
  • FULL neuro exam now
  • echocardiogram: r/o emobli cause from a fib or heart, evalute structural disease or get TEE for other cardiac conditions
  • Vascualr Imaging: carotid US, MR-A or CT-A or repeat angiogram to see
  • lipids, A1C, coag. labs if you think thats the cause
41
Q

Post AIS Care: Neuroprotection

A

Control BP Acutely!!
- typically systolic: 161-180 is ok
- if givng TPA: carefully reduce to < 185/110
- if severe HTN (> 220/115) need to reduce within the first 24 hours via nicardipine or clevidine
- restart at home anti-HTN 24 hours after stroke

Control Oxygenation
- hypoxia and increase metabolic demand can extend the infarct spread
- get SpO2 > 94%

Glucose Managment
- if > 140 = poor outcomes
- if they’re 140-185 = consider insulin!!
- avoid hypogly.

Maintain normothermia
- avoid hyperthermia
- use antipyretics for fever

42
Q

AIS Management: Risk of Cerebral Edema

A

Cerebral edema = post stroke swelling after a large infarct can happen (up to 3-5 days post stroke)

an infarct > 1/3MCA teritory on MRI within 6 hours is risk factor
large cerebellar infarct is risk factor

-swelling more in younger pt. = less room for the brain to expand

Sympotoms
- lethragy
- decrease alterness
- CN deficts (dilated ipslateral pupil)
- worsening motor weakness

treatment
- try isotonic fluids
- avoid dextrose fluids
- hemicraniotomy can be done to remove skull and let it swell

43
Q

AIS Managment: Hemorrohargic Conversion

A

when the stroke turns into a hemorrhagic stroke

what to do
- bleeding occuring within 24 hours of TPA adminsiterion = give cryoprecipitate
- obtain STAT CT of head and labs (CBC, PTT/INR/PT,fibrongen, type and screen)

whos more at risk
- older age
- larger NIHSS and ASPECTS score (because more injury)
- cardiac and renal comorbidites
- pt. has baseline use of antiplatelets

44
Q

AIS Management: Dysphagia

A

all pt. coming into hospital with facial weakness should be NPO until SLP evaluates
- if need ASA : give rectally
- if TPA given (dont put NG for 24 hours)
- pt. may need modified barium swallow test
- if fail: need PEG tube
- worse dysphagia = worse outcomes

45
Q

AIS Mangement: DVT Prophylaxis

A
  • all pts. nonabulatory post ischmeic or hemorrhagic stroke should get DVT prophalyxis

Treatment
- early mobilization
- compression stockings
- subcutaneous unfrationated heparin, LMW heparin, direct thrombin inhibitors

46
Q

AIS Management: Anticoags v antiplatlets

A

Antiplatlets: to prevent clot from forming
- asprin: give rectally if cant get swallow study
- if gotten TPA prior: wait 24 hours then give

Treatment = dual antiplatlet treatment
- asprin + clopidogrel (plavix) for 21-90 days

if thye conver to hemorrhagic: consult attending to see when to start

Anticoagulation: for those who have a clot from A fib (emoboli: traveled to the heart)
- if stroke from a fib/prosthetic heart = wating 24 hours after TPA to give
- smaller stroke: can start earlier;, larger might need to wait
- if TIA from a fib: do NOT wait to give

Treatment = Apixaban (Eliqus)

47
Q

AIS Management: Lipids

A
  • initiate daily statin post-stroke
  • LDL : < 70-100
  • want 50% reducing
48
Q

Strokes post seizure? what do you do

A

they can happen: but not enough to put them on prophylaztic meds post-stroke

49
Q

AIS management: Sholder Sublux

A
  • arm weakness = likely to have subluxation
  • get pillows and avoid use of that arm
50
Q

Discahrge List for AIS

A
  • thrombotic stroke = antiplatlet
  • *DAPT with asprin and clopidogrel for 21-90 days
  • if they have aspring alelrgey: clopidogrel monothearpy*
  • cardioembolic = anticoagulation
  • *lifelong anticoags. DOAC preferred or warfrin (2-3 INR range)
  • aspring can be used if contraindication to DOAC or warfarin*
  • if have mechanical valve = warfarin
  • statin (for lipids)
  • stop smoking
  • HTN, DM, alcohol, drugs and obesity risk factor reduction
  • acute, subacute rehab and home PT.OT
  • education
51
Q

Maniging carotid artery disease in your post stroke pt.

maninging intracranial arterial stenosis

A
  • via imaging (CT-a or MR-A, dopplet or catheter) to see if stenosis is present
  • if a TIA/CVA happened : should get vascualr intervention within 2 weeks if that is likely a cause/confounder

Treatment/Control
- antiplatelet, statin, Bp control lifestlye
- CEA: caroitdi endarterectomy recommened if >70% stenosis and have symptoms

Intracranial arterial stenosis
- vertebral arteries likely to stenosis
- treat: DAPT, statin, BP, lifestlye, etc. can intervere if fail medical
- can do an endovasualr angio or by-pass (risks!)

52
Q

Hemorrhagic Stroke
what is it

A

Hemorrhagic Stroke: bleeding within the brain parynchma caused by a weakened vessel; ruputred anyureusm, small vessel or an AV malformation
- can be intracerebral or subarachnoid
- higher mortality than ischemic (because increase ICP)

53
Q

Hemorrhagic Stroke: Risk Factors

A
  • uncontrolled HTN is most common
  • medication use; either anticoag. or DAPT
  • durgs (cocaine and ampethamines)
  • DM
  • smokers
  • chronic liver, alchol abuse = coagulopathy
  • older age and men
54
Q

Hemorrhagic Stroke: Etologies and Common locations for it to occur

A
  • amyloid buildup in cortex (cerebral amyloid anigopahty: think of this in dementia pts. : beta-peptids)
  • transformation from ischemic
  • AV malformation (common: kids)
  • Brain tumor (primary or metsmelanoma)
  • dural AV fistula, capillary telangietascias

Common Locations
- Basal ganglia= 50%
- thalamus
- pons
- cerebellum

- ^^ all the above because of HTN rupturing the small arterioles
- intercerebral/cortical bleed: AV malformations but this category is less likely: due to the destuction or compression of the parynchma

55
Q

Hemorrhagic Stroke: Clinical Presentation & Mechanism

A

HA, nausea, vomiting often preceeed the neurologic deficts
- sudden onset of focal neurologica deficts (depend on the location of the bleed)
- less predictable pattern of focal involvement due to cerebral edema around bleed & compression of the tissue due to bleed
- acute, severe HTN
- decrease consciousness
- seizures (More common in cortical > SAH)

Mechanism of Injury

Initial Hemorrhage
- direct injury to those neurons
- compression of the neurons = dysfunction
- clincal and rapid deterioriation = decrease GCS score fast

Peri-Hematomal Edema (due to asogenic or cytotoxic things)
- pressure on the tissue leads to regional perfusion deficts and ischmeia
- hemotoxicity: blood is toxic to tissue!!!

56
Q

Hemorrhagic Stroke: Diagnosis

A

non-contrast CT shows it
MRI can be done but not helpful in acute setting
cerebral angiography: helpful if there no obvious lesion
tox scree/pregnancy check

57
Q

Hemorrhagic Stroke: Treatment, Management

A

Management
- Airway: intubated (GCS so low)
- BP: control SBP 140-180: to prevent bleeding from continueing (give nicardipine or clevidipine)
- reversal coagulopathy if can
- Prophlaic seizure meds: for cortical and SAH only
- continue to image to watch bleed
- identify & correct underlying (glucose check)
- DVT prophylaixs (once stable)

Treatment
- get Platelets > 100k & INR > 1.3
- give the reversals!!!!
- Coumadin: given 4F PCC/K-centra (quick) or Vitamin K
- DOACS: give andexxa
- Dabigatran: give praxbind (idrucizumab)
- Heparin: protamine
- antiplatelts (aspring or clopidagrel): give platelets

58
Q

Hemorrhagic Stroke: Prognosis

A

ICH Score: 30 day mortality risk assessment

  • lots experience hematoma growth after initial presentaion and this is associated with worse outcomes
  • spot sign on CT: shows extravasation in the hematoma showing growth (bad)
59
Q

Hemorrhagic Stroke: Management with ICP

surgery???

A
  • for suspected elevated ICP treat via
    • hypertonic saling & mannitol
  • sedation to decrease metaboilc rate
  • EVD (drain) or ICP monitor can be placed

surgery?
- supratentoral hematomas can be surgically delt with if all other measure fail (life-saving treatment)
- those with cerebellar hemorrage + poor status can do surgery to remove hemorrage

studies show surgery doesnt really help compared to managemnet

60
Q

Subarachnoid Hemorrhage
what is it
risk factors
symptoms on presentations

A

What
- a leakage of blood from the subarachnoid space: an area of arteries; due to aynurysum rupture
- typically at branching points of larger arteries
- 90% in the anterior circualtion: ACA/AcarotidA, MCA, etc.
- 10% posterior circulation

Risk Factors: smoking, uncontrolled HTN, alcohol, PCKD, connective tissue d/o , coarchtation of aorta

Symptoms
thunderclap headache: worst HA of life: within minutes it comes on to worst pain
LOC, seizure, diplopia, photophobia
elevated ICP signs: HA, N/V, AMS, GCS low
can happened during activity

61
Q

Subarachnoid hemorrhage
Diagnosis

A

Diagnosisi
- non-contrast CT
- if stil sus but CT shows nothing; can do LP for CSF eval of RBC products
- vessel imaging: CT-a or MR-A
- vessel imaging: DSA or catheter IR anigo is GS
- serial CT should be done to monitor

62
Q

SAH: management and Treatment

A

Management
- securing of the anyuresum: within 24 hours via clipping surgicall or endovascualr coling
- if obstructive hhydrocephalus occurs: EVD (drain) can be placed
- electrolyte imbalances is high risk: hyponatremia, SIADH can occur
- caridopulm. risks: monitor for MI or QT prolongation
- acute lung injury or ARDS possible

Treatment
- Anyurysm Treatment
- 1. via clipping in craniomty or vascualr bypass: no antiplateley needed
- 2. endovascualr options: antiplatelets may be needed (coil or flow diversion)

  • risk of rebleeding highest in 24 hours after
  • correct any coagulopathy
  • conrol BP SBP < 160 or MAP < 110
  • ICP control: keep HOB > 30 degrees
  • normothermia
  • seiure management: prophylatic seizure managemnet
  • prevent and monitor cerebral vasospams with nimodipine (a CCB dihydro.) to dilate (FDA approved)
  • keep Hgb 8-10, ensure euvolemia and check doppler