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Stroke, 8. go through case study at the end of the lecture - Coggle Diagram
Stroke
7. Special Populations and Evolving Care
restarting antithrombotics post-ICH: case-by-case
emerging therapies
factor 11a inhibitors
colchicine (CADENCE, OCEANIC)
ICH management (Intracerebral Hemorrhage)
subclasses that fall under ICH are IPH and SAH
same sx of a stroke; requires neuroimaging to identify which class of ICH it is
❌ do NOT take ASA at the first signs of a stroke bc it might be an ICH, not an ischemic stroke
tx: compression stockings in first 24hrs, target systolic BP <160 right now, and then long term <130/80; surgery potentially
treated more aggressively than ischemic strokes
cerebral venous sinus thrombosis
clot happens in veins in the brain, leading to infarction and/or bleeding
frequent in women, children, young adults
headache, seizure, typical stroke sx
most pts recover
tx: DOAC
risk factors: estrogen meds, pregnancy, infections, thrombophilias, smoking, dehydration
cervical artery dissection
most frequent cause of stroke in pts under 45y
risk factors: trauma, HTN, oral contraceptives, genetic disorders, migraine
trauma that causes it: car accident, coughing, sneezing, cracking neck bones, sports, cervix manipulation
tx: ASA or DOAC
cryptogenic/ESUS
RESPECT
ARCADIA
NAVIGATE
trials show that for cryptogenic causes of stroke, ASA is better for secondary prevention than a DOAC
6. Secondary Prevention
statins: target LDL <1.8
atorvastatin 80mg
PCSK9i (eg.
evolocumab
) added to a statin +/- ezitimibe greatly decreases LDL as well, and is very beneficial
BP target: <130/80
tx of choice:
perindopril + indapamide
antiplatelet vs anticoagulant (based on cause)
antiplatelets indicated for:
most other causes than the above like DM, HTN, lipids
eg. if a pt with HTN, lipids, DM has a stroke but they were already on ASA before the stroke, keep them on ASA post-stroke and optimize lifestyle changes
KNOW THIS! ⭐️
if ASA fails, consider antithrombotics
anticoagulants indicated for:
antiphospholipid antibody syndrome, cerebral venous sinus thrombosis, cancer clot, A-fib, mechanical heart valve, LV thrombus, rheumatic stenosis
no DOAC is superior to another, but note that river and dabiga have lower ICH which is good for stroke prevention. also no need for INR monitoring!
watch out for d/I with DOAC + phenytoin/carbamazepine, antivirals, antifungals, antibiotics :red_cross:
warfarin + ASA is ok. DOAC + ASA is NOT ok
initiate DOAC 3-14 days after stroke
when to consider DOAC + ASA
ACS + stroke pt; mechanical heart valve pt; needs a DOAC + has a stent
if a pt is on ASA already, and they start a DOAC for another reason (like DVT) then stop the ASA until the DOAC course is complete, and restart ASA after
DM/lifestyle/smoking changes (try to cut down, if fully unable to quit)
determine stroke cause
large/small vessel
cryptogenic
cardioembolic (Afib, LVT)
surgical options
CEA for carotid artery stenosis; pt has to be on ASA prior to procedure
stenting (symptomatic stenosis); pt has to be loaded with ASA and clopidogrel, then left on them for
6-12 weeks
(extra cranial) or
3-6 months
(intracranial)
1. Stroke Basics
hemorrhagic transformation
bleeding into the area of cerebral infarction
stroke in evolution
worsening neuro deficits over minutes or hours suggesting the area of blood flow blockage is widening in the brain
TIA vs stroke
a TIA is a
BRIEF
episode of neuro dysfunction caused by brain, spinal cord, or retinal blood flow blockage, with sx lasting
less than 24hrs
and without imaging evidence of acute infarction
stroke classification
hemorrhagic
,
atherosclerotic cerebrovascular disease, small vessel disease, cardiac embolism, cryptogenic
(
all in italics are ischemic
)
KNOW THIS! ⭐️
hemorrhagic stroke: caused by blood leaking into brain tissue
(higher death rate than ischemic)
ischemic stroke: caused by a clot in the brain which stops blood supply to areas of the brain
definition
brain, spinal cord, or retinal cell death due to blood flow blockage, based on evidence of permanent injury using neuroimaging or pathology. includes intracerebral hemorrhage (ICH), and subarachnoid hemorrhage
5. Acute Stroke Management
EVT (endovascular therapy):
large
vessel occlusion
mechanically going in and dissolving a clot in a large vessel
pt has to present within 6h of stroke sx (24h window in select pts only)
can be performed after tPA
antiplatelet use
(rapid admin of thrombolytics or EVT
is more important than anti platelets)
ASA/clopidogrel/ticagrelor post-imaging
if no tPA/TNK or EVT are planned on being given, give anti platelets right away
delay if thrombolytics used
administer 24h after tPA/TNK and after repeat CT scan rules out hemorrhagic transformation
if you go with DAPT (ASA + clopidogrel ) make sure it's only for
21-30 days (for TIA/stroke)
, and then just do ASA monotherapy/ clopidogrel mono therapy (either of these 2) to avoid major risk of future bleeding
thrombolytics (tPA aka alteplase, TNK aka tenecteplase)
eligibility
suspicion of ischemic stroke
pt presents with ischemic stroke within 4.5h of onset
pt has no c/i
pt has a mobile disability
timing
4.5h max to receive thrombolytics, after that it isn't recommended
supportive care
BP, glucose control, DVT prophylaxis, hydration, infection, intracranial pressure, vomiting, IV fluids, electrolytes
ischemic vs hemorrhagic stroke workflow (after CT scan is done)
ischemic
evaluate for thrombolysis (drugs that break down clots), then decide to give a tPA or not or if endovascular intervention is chosen
hemorrhagic
surgery
4. Primary Prevention
(90% of strokes are caused by modifiable risk factors. if we can change our lifestyle, stroke rates go down by a lot!)
lifestyle modifications
diet (Mediterranean), exercise (150min/wk moderate-intense), smoking cessation 🚭
pharm
HTN management
ACEi/ARB, thiazides, CCB with target of <130/80
diabetes control
metformin, SGLT2i (not really stroke prevention, but still good drug), GLP1(good drug if A1c >7, and high risk of CVD)
tight glycemic control hasn't been shown to reduce risk of stroke
lipid management
statins, PCSK9i
risk assessment tools
Framingham, ASCVD, CHADS-65 (if pt has A-Fib --> 0 points + CAD =
ASA
, 1+ point =
anticoagulation
)
role of ASA (not recommended for
primary
prevention of a stroke).
rmr ASA is used in secondary prevention, bc if it's used in primary prevention, it just puts the pt at high risk of bleeding if anything
3. Clinical Presentation and Work-Up
stroke mimics
seizure, migraine, Bell's palsy, vertigo, sepsis, syncope, tumours, metabolic conditions
sequelae (following stroke)
hemiplegia, aphasia, dysphagia, depression, confusion, n+v, loss of driving privileges, cannot return to work, seizures, increased risk of infection
cardinal signs (FAST)
headache, weakness/paralysis bilateral/unilateral, speech, vision, dizziness
F - face drooping, A- arms can't raise, S - slurred speech, T - time to call 911 right away
work up
imaging; CT, MRI, MRA, carotid US (preferred over MRI)
Labs: CBC, INR, lipids, A1c, troponin, CRP, CK
note: thrombin time is used if you RAPIDLY need to assess for prescence of dabigatran
NIHSS (0-42 scale, higher number is worse)
cardiac workup: ECG, 24h Holter, TTE/TEE
vitals: BP, HR, O2 sat, temp
2. Risk Factors
modifiable risk factors
HTN, DM, lipids, smoking, A-Fib, sleep apnea, lifestyle, stress, alcohol, waist-hip ratio, cardiac issues, illicit drug use, oral estrogen
non-modifiable risk factors
age, sex, ethnicity, FHx, prior TIA/stroke hx
outcomes and impact
if 100 people had a stroke, only 10 would recover completely, and 15 of the 100 would die right away. the other 75 would recover but with lifelong disabilities
8. go through case study at the end of the lecture