E Med exam 3 - Stroke TIA ICH

abrupt onset of a neurologic deficit that is attributable to a focal vascualr cause

stroke

reduction in blood flow that lasts longer than several secs. neuro sx manifest within secs

stroke

if cessation of flow lasts for more than a few mins, what occurs

infarction or death to brain tissue

when blood flow is quickly restored what can occur to the brain

brain tissue can recover fully and pts sx are only transient AKA TIA

all neuro signs and sx resolve within 24 hrs without evidence of brain infarction on imaging

TIA

if neuro signs and sx last for >24 hrs or brain infarction is seen on imaging what is this dz

stroke

when blood flow is interrupted to part of the brain this occurs

stroke

what happens when there is no blood supplying a part of the brain

oxygen and nutrients cannot be supplied and waste products can’t be removed. brain cells begin to quickly die.

depending on the region of the brain affected a stroke can cause

paralysis, speech impairment, loss of memory and reasoning ability, coma, or death

strokes occur more in what gender

males until age 55, then the risk is the same

what ethnicity is most at risk for strokes

AA, hispanic, and API pop

does fhx matter

yeah if your immediate fam had a stroke or TIA your risk goes up

pts with this other condition are at a greater risk of a stroke

DM

how to prevent strokes

lower BP, cholesterol, stop smoking

Leading cause of a stroke is

HTN

pathogenesis of HTN causing strokes

blood vessels damaged by high intraluminal pressure causing a narrowing, rupture, or leak. also causes blood clots to form in arteries

how can DM cause a stroke

free sugars get into blood vessel walls causing damage and accelerating atherosclerotic plaques

what is a hypertensive urgency

severe elevation in BP (>180/>120), NO evidence of acute target organ damage. pts are usually asx, or have HA, dizziness, mild SOB, nausea

mcc of hypertensive urgency

missing blood pressure meds. also can be from pain, anxiety, drug use (cocaine/amphetamines), meds like NSAIDs, steroids, decongestants, underlying kidney dz or undx HTN

how to tx a hypertensive urgency

adjust or restart PO meds (captopril, labetalol, amlodipine) to slowly lower BP over hours-days. rapid lowering is bad bc can cause ischemia

prognosis of HTN urgency

good, no immediate threat to organ fxn, though indicates a need for better long term BP management

what is a hypertensive emergency

severe BP elevation (>180/>120) WITH acute target organ damage.

what are target organ damage example sin a hypertensive emergency

encephalopathy, ICH/stroke, ACS, acute HF/pulm edema, AKI, aortic dissection, hypertensive retinopathy, seizures

how to tx hypertensive emergency

ICU admit and continue BP monitoring. use IV antihypertensives.

goal of hypertensive emergency treatment

dec MAP by 10-20% in the first hr. then dec another 5-15% over the next 23 hrs

what is the significance of MAP

provides a more accurate reflection of blood Q to tissues and organs.

nl range of MAP

70-100, 110 mmHg

abnl MAP levels

<60-65 suggests bad perfusion (HoTN), risking organ damage. if MAP >110 then = excessive P, risking CV damage

uses for MAP

used in intensive care to monitor pts with sepsis, stroke, or severe trauma

how to calculate MAP

(SBP+2(DBP))/ 3

IV first line drug tx for hypertensive emergency

nicardipine, labetalol, nitroprusside, nitroglycerin, esmolol

when is nicardipine indicated to tx HTN emergency

first line in many cases like stroke and general use

when is labetalol used to tx HTN emergency

good for most situations, including pregnancy

when is nitroprusside used in HTN emergency

rapid and potent. use w caution bc can cause cyanide tox

when is nitroglycerin used in HTN emergency

pref in ACS or pulm edema

when is esmolol used in HTN emergency

short acting, ideal for aortic dissection

tx route for HTN emergency

IV

first line meds for HTN urgency

lisinopril, amlodipine, labetalol, clonidine

how does hyperlipidemia contribute to a stroke

progression of atherosclerosis is directly related to cholesterol and LDL levels, and inversely to HDL. hi lipoprotein A is directly assoc with inc stroke risk and is used as a screening tool

how does cig smoking contribute to stroke risk

inc risk 2x. leads to hypercoagulable state and vascular damage

mini stroke/warning stroke

TIA

transient disruption of blood Q that results in focal neuro sx. stenosis or small emboli blocks vessels and tissue deprived of blood and oxygen and become symptomatic. body auto regulates and vasodilates or breaks up clots with endogenous tpa and blood Q returns and sx resolve

TIA

half of all strokes occur within how much time after a TIA

first 2 days after

how to eval stroke risk in 7 days after TIA

ABCD2 score

how to prevent stroke after TIA

aspirin and clopidogrel

what is the ABCD2 score

Age >60 (1)

BP > 140/90 (1)

Clinical features - u/l weakness (2), speech disturbance w/o weakness (1)

Duration of sx - > 10 min but < 59 min (1), >60 min (2)

Diabetes (1)

score <5 = 4%, 5 = 16%, 6 or more = 35%

why do we hospitalize TIA pts

facilitate early therapy and secondary prevention

what lab testing do we do on TIA pts

see full blood count, serum electrolytes and Cr, fasting blood glucose and lipids.

when is an EKG ordered for a stroke pt

within 48 hrs

what brain imaging study is indicated for TIA pts

CT or MRI in 48 hrs

what vascular imaging is used for TIA pts

carotid imaging, CT or MR angiography, or transcranial doppler w/i 48 hrs

how are strokes divided into

ischemic or hemorrhagic

what are the types of ischemic strokes

thrombotic or embolic

what is a thrombotic stroke

atherosclerotic clot forms within cerebral circulation.

what is an embolic stroke

clot forms elsewhere and travels to brain’s circulation

which type of strokes are more common

ischemic

what type of stroke poses higher mortality

hemorrhagic

the result of the deficit in a stroke depends on

size of occlusion and the amount of collateral circulation the pt has to compensate for loss of blood Q

how does a cerebral ischemia lead to cell death and worsen the deficit

releases excitatory and other neuropeptides that may augment the flow of calcium ions in neuronal channels

mcc of cerebral embolism is

a fib

how does a fib cause cerebral embolism

atria of the heart beat weakly and fast, blood w/i the atria is not completely emptied. the stagnant blood forms clots in the atria which break off and enter circulation

how to reduce risk of stroke from a fib

daily use of anticoagulant meds like coumadin, pradaxa, xarelto, eliquis

cardiac sources of emboli in cardioembolic stroke

m/c, typically from left sided chambers/valves that form in myopathy or arrhythmia

artery to artery sources of emboli in cardioembolic stroke

from ruptured plaque in internal carotid arteries

paradoxical embolism source of emboli in cardioembolic stroke

vein to artery, usually occurs when venous thrombus from periphery enters the right side of the heart and is shunted via ASD/PFO or VSD to left circulation

other causes of cardioembolic stroke

a flutter, dilated cardiomyopathy or CHF with EF <30%, dec output = stasis and clot formation, MI, ETOH, genetic, infectious endocarditis, mitral valve stenosis or disease, atrial myxoma

persistent connection b/w the right and left atrium. embolus bypasses lungs via hole and enters left side of heart into circulation.

PFO

how to screen for PFO

echo (TEE is best)

high freq of PFO is found in what pop

YA with cryptogenic ischemic stroke

mcc fo stroke in young pop

cryptogenic ischemic stroke from PFO

how to tx PFO

ASA/ plavix, NOT closure unless the hole is very large or pt has recurrent embolic events

locations for ischemic strokes

lacunar infarct, anterior cerebral artery infarct (ACA), middle cerebral artery infarct (MCA), posterior cerebral artery infarct (PCA), vertebro-basilar arteries infarct

this infarct is a small lesion less than 5mm in diameter. found in short penetrating arterioles of basal ganglia, pons, cerebellum, internal capsule/ assoc with uncontrolled HTN, DM.

lacunar infarct

pt has pure contralateral motor deficits, pure c/l sensory deficits, ipsilateral ataxia, dysarthria with hand clumsiness.

lacunar infarct

prognosis of lacunar infarct

deficits stabilize withing 24-36 hrs and generally have good prognosis at small size

obstruction of carotid circulation causes what infarcts

ACA, MCA, ophthalmic artery or central retinal

pt has contralateral hemiparesis and hemisensory loss of the lower extremity. may be a contralateral grasp reflex, marked confusion, apraxia. urinary incontinence

anterior cerebral artery infarct

b/l ACA occlusions tend to lead to what sx

marked behavioral changes and memory loss

pt has contralateral hemiplegia, hemisensory loss, and homonymous hemianopia (b/l symmetric loss of vision in half the visual fields) w eyes deviated to side of lesion

MCA infarct

MCA infarct leads to a large risk for

hemispheric swelling, stupor, coma, confusion

anterior division of MCA infarct produces what sx

expressive aphasia (Broca’s), c/l paralysis and sensory loss to face and arm, lesser so the leg. these pts understand you but can’t communicate

posterior division of MCA infarct produces what sx

receptive aphasia (wernicke’s) and homonymous visual field defect. these pts can’t comprehend what you’re saying

inability to formulate or comprehend language

aphasia

lesions fo left frontal lobe, inability to express language, motor problem and not fluent, stutter and can’t formulate words

Broca’s aphasia

lesions of left superior temporal lobe, inability to understand language, fluent, “word salad”, use real words but continuous flow of nonsensical sentences

wernicke’s aphasia

this infarct leads to sudden painless visual loss with retinal pallor and a macular cherry red spot on fundoscopic exam. pts get sudden transient vision loss in one eye (amaurosis fugax) is a TIA in this arterial territory

ophthalmic artery infarct

obstruction of the vertebrobasilar circulation causes these arteries to infarct

posterior cerebral artery, vertebral artery, basilar artery, cerebellar artery

this infarct leads to thalamic syn leading to c/l hemisensory disturbances followed by the development of spontaneous pain and hyperpathia (exaggerated levels of pain). pts usually have macular sparing homonymous hemianopia

PCA infarct

this infarct may be clinically silent bc circulation is maintained by the other vertebral artery

vertebral artery infarct, distally below level of anterior spinal and posterior inferior cerebellar arteries

when one of these arteries is occluded it causes sx like ipsilateral sensory loss of the face, limb ataxia and numbness, vertigo, nystagmus, and Horner’s syn (ptosis miosis anhidrosis)

posterior inferior cerebellar artery or vertebral artery

occlusion of this artery leads to coma with pinpoint pupils, flaccid quadriplegia, and sensory loss, and variable CN abnormalities

basilar artery infarct

occlusion of these arteries leads to vertigo, n/v, nystagmus, ipsilateral limb ataxia, and contralateral spinothalamic sensory loss of the limb. if massive infarction occurs then this can lead to coma, tonsillar herniation and death

cerebellar artery infarct

13 item scoring system that integrates neuro exam, language, and levels of consciousness that indicates severity of neuro dysfxn. score of 1-4 of minor stroke, 5-15 = moderate, 15-20 = moderately severe, >20 = severe

NIH stroke scale

what imaging should be preformed immediately before giving ASA or other antithrombotic agent to exclude cerebral hemorrhge

non contrast head CT

bc a CT is insensitive to acute ischemic strokes in the first 6-12 hours this imaging is then indicated

MRI with diffusion weighted sequences

what is the usefulness of an MRI in a stroke pt

defines the distribution and extent of infarction as well as exclude tumor or other differential considerations.

if pts present within 6 hrs of stroke onset what imaging is used and why

CTa of head and neck. identify large vessel occlusions amenable to endovascular therapy

regardless of timing of presentation imaging of the cervical vasculature needs to be done to identify the source of stroke using what imaging

CTa, MRa, carotid duplex US, conventional catheter angiography

what labs do you order in a stroke pt

CBC, ESR, CMP, coagulation profile, lipid profile, HgA1c, protein C/S; antithrombin abnl (inc risk of clot), homocysteine level, APLS labs - anticardiolipin, lupus anticoagulant (recurrent clot formation)

how to tx stroke

main goal is to dissolve the clot. give IV TPA within 3 hours of onset of stroke sx. can give in 4.5 hrs if meets criteria and not over 80, diabetic with previous stroke, or severe disability. improves recovery and dec long term disability