Lecture 29+30 Stroke Flashcards
(22 cards)
What is a stroke?
CNS infarction, defined as brain, spinal cord, or retinal cell death attributable to ischemia, based on neuropathological, neuroimaging, and/or clinical evidence of permanent injury
also broadly includes intracerebral hemorrhage and subarachnoid hemorrhage
What is a transient ischemic attack (TIA)?
brief episode of neurological dysfxn caused by focal brain, spinal cord or retinal ischemia, with clinical sx lasting <24 hours and without imaging evidence of acute infarction
What are risk fx for stroke?
Modifiable: HTN, dyslipidemia, DM, smoking, homocysteine, waist-hip ratio, diet, exercise, alcohol, stress, depression, cardiac issues (valvular heart disease, cardiomyopathy, AF, PFO, etc), sleep apnea, illicit drug use, oral estrogen tx
Non-Modifiable: age, sex, ethnicity, FHx, previous episode
What are the S&S of stroke and what other diseases/conditions can cause these symptoms?
FAST ⇒ Face (is it drooping?), Arms (can you raise both?), Speech (is it slurred or jumbled?), Time (to call 911)
Cardinal Signs: pt may have 1 or more present ⇒ severe H/A, sudden weakness, sudden changes in speech, sudden changes in vision, sudden dizziness
Mimics: seizure, syncope, sepsis, migraine, space occupying lesions, fxn disorders, metabolic conditions, vertigo, Bell’s Palsy
What are consequences of stroke, what can happen as a result of it?
hemiparesis/hemiplegia, aphasia/dysphasia, altered LOC, N/V, dizziness, disorientation/confusion, vision changes, dysphagia, loss of driving privileges, inability to return to work, depression, neuropsychiatric dysfxn, seizures, increased susceptibility to infection
What are risk assessments that can be done for stroke?
FRS: estimated 10 year risk of manifesting clinical CVD
ACC AHA ASCVD Risk Estimator: 10 year and lifetime estimated risk for ASCVD
CHADS-65: if AF is present
can also check patient’s lifestyle - smoking, diet, activity
metabolic - HTN, dyslipidemia, DM
environmental - air pollution, lead exposure
What are components involved in primary prevention of stroke?
HTN: in pt with stage 2 HTN or stage 1 with risk factor recommended <130/80 target
Dyslipidemia: in adults who qualify for statin tx it should be started to reduce risk
DM: increases risk by 1.5-2 fold, if A1c >7% and high risk of CVD recommended to start a GLP-1RA
Diet: adults without prior CVD and who are at high or intermediate CVD risk should start a Mediterranean diet
Exercise: moderate 150 min per week OR vigorous 75 min per week OR combo, avoid excessive time in sedentary
Smoking: stop it
Antiplatelets: balance potential benefit vs risk of GI bleed, can also use risk scores like CHADS-65 or HAS-BLED to assess appropriateness
When is t-PA (alteplase) or TNK (tenecteplase) eligible for thrombolysis in stroke?
suspicion of an ischemic stroke
presentation within 4.5 hours
no absolute contraindications
debilitating disability
When might endovascular intervention be used in stroke, and what is actually performed?
mechanical thrombectomy in pt with large artery occlusions presenting within 6 hours (majority of pt) of onset of stroke - often called endovascular therapy (EVT)
can be done up to 24 hours from onset in certain pt
may be performed post-tPA (alteplase)
NNT can be as low as 2
What is the general principle for antithrombotics in acute stroke, when are they used?
rapid admin of TPA/TNK or performing EVT is more important than rapid admin of antiplatelet
antiplatelet(s) given as soon as possible once hemorrhage is ruled out on initial CT (if no thrombolytics given and no plans of EVT)
delayed for 24 hours post tPA/TNK until repeat CT scan rules out hemorrhagic transformation
anticoagulation is typically avoided in acute setting as newly infarcted brain tissue is at high risk of hemorrhagic transformation
What are antithrombotic options for acute stroke?
ASA Monotherapy: given as 325 mg PO/PR initial loading dose then continued at 81/80 mg PO/NG QD (or 325 mg PR if no gastric access), decreases recurrent ischemic stroke risk, decreases pt dead or dependent
Clopidogrel Monotherapy: given as 300 mg PO loading dose then 75 mg PO/NG QD, lack of literature in acute setting, some clinicians prefer this in ‘ASA failure’
Ticagrelor Monotherapy: NOT FOUND TO BE SUPERIOR TO ASA (SOCRATES)
Dual Antiplatelets: ASA + dipyridamole - showed no increased benefit (EARLY)
ASA + clopidogrel - increased benefit (CHANCE, POINT), only used in TIA/minor stroke due to risk of hemorrhagic transformation, 21-30 days then step down to single antiplatelet
ASA + ticagrelor - increased benefit (THALES), lowered composite risk of stroke/death within 30 days but no reduction in disability, increased bleeding
What is hemorrhagic transformation in stroke?
5-30% incidence
hemorrhagic infarction: bleeding into ischemic/dead brain tissue, not usually associated with sx
parenchymal hemorrhage: hematoma formation in viable brain tissue, may have several clinical consequences
risk appears directly correlated with time to reperfusion of ischemic region
antiplatelet tx may or may not be held depending on size of hemorrhage, clinical judgement required on case by case basis
What are sources of ischemic stroke which favour anticoagulation rather than antiplatelet?
Antiphospholipid antibody syndrome
cerebral venous sinus thrombosis
cancer associated thrombosis
cardio embolic - AF, mechanical heart valve, LV thrombus, rheumatic stenosis
How long should you wait to initiate anticoagulation post stroke for AF?
within 3-14 days is reasonable per CSBPR 2020
the larger the infarct the longer you wait
often starts with ASA monotherapy then discontinue it when changing to DOAC
if there is an active clot or mechanical valve will initiate DOAC sooner
warfarin can either overlap with ASA or therapeutic LMWH depending on indication and stroke size
Which antiplatelets are used for secondary stroke prevention?
ASA: decreases recurrent stroke/TIA risk by 15% (RRR)
Clopidogrel: no sig benefit over ASA, has drug intx
Ticagrelor: failed to show superiority over ASA
ASA + Clopidogrel: increased benefit vs monotherapy, only used in TIA/minor stroke (NIHSS 3 or less) due to risk of hemorrhagic transformation, 21-30 days only then step down to single antiplatelet
ASA + Ticagrelor: increased benefit of ASA + ticagrelor vs monotherapy x 30 days, increased bleed though
What is the typical duration of DAPT for stroke before step-down to monotherapy?
Minor stroke/TIA ⇒ 21-30 days
Stent ⇒ if extracranial 6-12 weeks guided by neurosurgery/interventional radiology, if intracranial 3-6 months guided by neurosurgery/interventional radiology
Severe intracranial atherosclerosis ⇒ 90 days
What is the tx of choice after a cryptogenic/ESUS, regarding secondary prevention?
antiplatelets
shows similar rate of recurrence to anticoagulants but lower bleeding
Cervical artery dissection (risk fx, causes, tx)
most frequent cause of stroke in young people,, accounts for 2% of all ischemic strokes but accounts for 8-25% of strokes in pt under 45, can be spontaneous or traumatic
Risk Fx: trauma, HTN, oral contraceptives, genetic disorders affecting connective tissues, migraine
Causes: common traumas - MVC, coughing, sneezing, cracking neck, sports like heavy lifting, golf, tennis, yoga, contact sports
cervical manipulative tx
Treatment: antiplatelet OR anticoagulation
Cerebral venous sinus thrombosis (CVST) (S&S, risk fx, Tx)
thrombosis occurring in venous circulation leading to infarction +/- bleeding, around 1.32/100000 persons/year
more frequent in women and more frequent in children and young adults
S&S: H/A +/- seizure +/- typical stroke sx,, <5% mortality and 80% pt fully recover
Risk Fx: pro-thrombotic meds (ex. estrogen), pregnancy and purperium, infections, thrombophillias (APLAS, F5L, etc), myeloproliferative disorders/malignancies, smoking, dehydration, in 13% of cases there aren’t any risk fx
Treatment: LMWH/IV UFH ⇒ oral anticoagulant
How is TIA risk assessment done, what is looked at to classify, and what is the tx started?
High Risk: sx onset within 48 hours, need urgent brain/vessel imaging, ECG
Increased Risk: sx 48 hours to 2 weeks, fluctuating/persistent sx should be seen by neurologist within 24 hours, with no neurologic deficits should be seen within 2 weeks
Lower Risk: >2 weeks from sx onset, should see neurologist within 1 month
Tx: antithrombotic (CHANCE/POINT) (ASA + clopidogrel for 21-30 days), risk fx management
How is intracerebral hemorrhage managed (ICH)?
accounts for 10-15% of all strokes
mortality much higher than seen in ischemic strokes (40% vs 15%)
DVT Prophylaxis - pneumatic compression stockings start in first 24 hours, LMWH or UFH after 2-3 days if bleed stable
BP Management: current standard to acutely target SBP <160, long term <130/80
surgical intervention in select pt
How is subarachnoid hemorrhage managed (SAH)?
determine the cause - possible aneurysm, CVST
surgical intervention
If aneurysmal: nimodipine 60 mg PO Q4H for 21 days - vasospasm and possibly neuroprotective, improved outcomes, very expensive (alternate CCB reasonable as outpatient)
usually traumatic causes but could occur from intracranial hypotension, coagulopathy or in association with antithrombotics
could be acute or chronic
requires neurosurgical consultation/intervention
