Stroke 2 Flashcards
(36 cards)
ACUTE ISSUES
• Supportive
- prevent comp
Supportive • Vomiting • Airway • Oxygenation • IV fluid
Prevent Complications • Dehydration • DVT • Electrolyte imbalances • Fever • Hypertension • Hyperglycemia • Hem transformation • Infection • Intracranial pressure • Seizures
DEHYDRATION
• Manage with IV fluid (NaCl 0.9% - normal saline) or enterally (PO/NG PRN) • AVOID using: • Dextrose solutions • Hypertonic solutions • Hypotonic solutions
DVT PROPHYLAXIS
• Common due to immobility (hemiplegia)
• Prophylaxis options:
• First line: UFH/LMWH +/- Sequential compression device
• Heparin 5000 units SC BID (TID dosing in morbidly
obese)
• Dalteparin 5000 units SC Daily (7500 units in morbidly
obese)
• Tinzaparin 4500 units SC Daily (8000 units in morbidly
obese)
• Wait 24 hours post tPA
• ASA
• Give until ambulatory
ELECTROLYTE IMBALANCES
- SIADH occurs in 10-14% of patients
- Monitor daily lytes
- Correct imbalances prn
FEVER
• 1/3 of patients febrile within hours after stroke onset
• Causes include CNS deregulation, DVT, or infection
• Fever associated with poorer outcomes, increased
mortality
• Acetaminophen treatment of choice
• Impact of therapy on outcomes not established
HYPERTENSION
• Common due to loss of cerebral autoregulation (or pain or increased ICP)
• Only treat in first 24 hours if BP > 220/120mmHg (if no IV tPA/EVT given)
or concomitant conditions requiring antihypertensive agents
• Rapid decrease avoided first 7-10 days
• Theory to avoid decreased perfusion to ischemic area
• More aggressive BP monitoring and lowering if received IV tPA/EVT
(target SBP < 185, DBP < 110)
• Bottom line: treat “cautiously” (decrease ~15% of SBP/day)
• Can use PO/SL captopril, or IV labetalol/hydralazine/enalaprilat acutely
• How to manage anti-hypertensive meds from pre-admission?
• Recent studies (SCAST, COSSACS, CATIS) have not clarified issue
• No benefit, but not harmful? Serious flaws with studies
HYPERGLYCEMIA
• Associated with larger infarcts and worsened
prognosis
• Target BG of 8-10 mmol/L (GIST-UK)
• BBIT or insulin infusion to keep BG < 10
• Avoid hypoglycemia
• Difficult to control BG with tube feeds in NG patients
HEMORRHAGIC TRANSFORMATION
• 5-30% incidence
• Hemorrhagic infarction
• Bleeding into ischemic/dead brain tissue
• Not usually associated with symptoms
• Parenchymal hemorrhage
• Hematoma formation in viable brain tissue
• May have severe clinical consequences
• Risk appears directly correlated with time to reperfusion of
ischemic region
• Antiplatelet therapy may or may not be held depending on size
of hemorrhage; clinical judgment required on case by case basis
INTRACRANIAL PRESSURE (ICP)
• Common cause of early death (24-96 hours post
stroke)
• 10-20% develop edema requiring clinical intervention
• Manifested by decreased LOC, worsening neurologic
deficits
• Therapeutic options:
• Mild fluid restriction
• Mannitol 0.25-1 g/kg IV q6h PRN until serum osmolality ~
300 or increased ICP resolves (no data)
• Hypertonic saline (3% Na)
• Surgery (hemicraniectomy)
• Steroids provide NO bene
INFECTION
increased risk for
• Increased risk for: • Aspiration pneumonia • UTI (catheters) • Secondary septicemia • Monitor and treat prn • Pneumonia should be treated early as major cause of death after stroke
SEIZURES
• Most common cause of new-onset seizures in the elderly
• No data regarding using prophylactic anticonvulsants
• Treat only if seizures occur
• “Provoked” seizure and thus typically short duration of
therapy (months)
• Duration of therapy also affected by how close seizure
occurs to acute event
• Many drug interactions with anticonvulsants!
Ischemic Stroke
ì What was the cause?
ì Cardioembolic (Afib, CM, LVT, valvular disease, etc) ì Large vessel atherosclerosis ì Small vessel disease ì Cryptogenic ì Other
RISK FACTOR MANAGEMENT
secondary stroke prevention
- HYPERTENSION
- 28% RRR in recurrent stroke if treat hypertension (PROGRESS)
- Perindopril +/- indapamide treatment of choice
- Many agents studied – “Bottom line” decrease BP
- Benefit for normotensive patients as well
• DYSLIPIDEMIA
• 2.2% 5 year ARR in recurrent stroke (SPARCL)
• Atorvastatin 80mg PO daily treatment of choice
• Small increase in ICH in treatment group but found to be hypothesis
generating
• Start statin in patients regardless of LDL if stroke thought to be of
atherosclerotic origin
• PCSK9 Inhibitors (evolocumab, alirocumab
Major trials: FOURIER (evolocumab) ODYSSEY-OUTCOMES
(alirocumab)
- At 48 weeks, decreased LDL ~59%, ischemic stroke RRR 25%, no major adverse effects, ~$8400/year, NNT ~74 over 2.2 years
- GLAGOV – Evolocumab showed coronary plaque regression (statin + evolocumab/placebo) over ~1.6 years
- DIABETES
- SMOKING
SURGICAL INTERVENTION
secondary stroke prevention
- Carotid artery stenosis
- Symptomatic high-grade stenosis (50-99% on vascular imaging)
- ?Asymptomatic stenosis
- Intervention:
- Carotid endarterectomy (CEA)
- Carotid stenting
• CEA
• Patient must be on just ASA prior to procedure (bleed risk of DAPT too
high)
• Stent
• Patient loaded with ASA (325-650mg) and clopidogrel (300-600mg)
prior to stenting and kept on DAPT for 6-12 weeks (data lacking)
ANTIPLATELET VS. ANTICOAGULATION
• Depends on source of ischemic stroke
• Antiphospholipid antibody syndrome =
anticoagulation
• Cerebral venous sinus thrombosis = anticoagulation
• Cancer associated thrombosis = anticoagulation
- Cardioembolic = anticoagulation
- A-fib
- Mechanical heart valve
- Poor LV function (EF<35%)
- LV thrombus
- Rheumatic stenosis
• Most other causes = antiplatelet
RISK STRATIFICATION FOR A-FIB (CHADS2)
CHADS2 pof 2 at least with stroke
• 0 points and <65 = no antithrombotic
• 0 points + CAD or PAD = ASA 81mg daily
• >1 point OR >65 years of age = anticoagulation
Which DOAC is clearly superior to other
DOACs in terms of preventing ischemic stroke
from non-valvular atrial fibrillation?
- Dabigatran
- Apixaban
- Rivaroxaban
- Edoxaban
- It’s a trap! There is no clearly superior DOAC
- It’s a trap! There is no clearly superior DOAC
DOACs – a PANACEA?
• Advantage is no INR monitoring
• Reduced ICH but more GI bleeds with dabigatran and
rivaroxaban
• Guidelines favour their use however…
• Are still anticoagulants
• Require careful selection in renal dysfunction
• No real guidelines on weight extremes (<50kg, >120kg)
• Alberta Blue Cross coverage
• Drug interactions – p-glycoprotein/CYP3A4 pathways
• Phenytoin, Carbamazepine, AVRs, Antifungals, Abx…
-> many on pheny and carba
• Danger of “fire and forget”
• Monitoring tool – thrombosiscanada.ca
DOACs – Antidotes
• DOACs not easily reversible – dialysis, activated charcoal, PCC
(Octaplex) are not very effective if bleeding occurs
• Idarucizumab (Praxbind) – first approved reversal agent for any DOAC in Canada; reverses dabigatran (RE-VERSE AD)
• Monoclonal antibody fragment that binds dabigatran with an affinity
350 times greater than thrombin
• Binds free and thrombin bound dabigatran
• Andexanet-alfa – in development for Xa inhibitors
• Aripazine – in development as universal DOAC antidote
WARFARIN VS ASA FOR NON A-FIB
• WARSS
• Compared warfarin vs. ASA in non-cardioembolic
ischemic strokes
• No significant difference found in primary end point of death or recurrent stroke. No sig diff in rates of majornhemorrhage
• WASID
• Compared warfarin vs. ASA in intracranial arterial
stenosis strokes or TIAs
• Trial stopped early due to significantly higher rates of
adverse events in the warfarin group
INITIATING ANTICOAGULATION
secondary prevention
• How long should you wait post stroke if initiating AC for Afib?
• Within 3-14 days is reasonable per CSBPR 2020
• “The larger the infarct the longer you wait”; hem transformation
- wait 6 days for moderate stroke
- the sooner you start the greater the chance of staring hemorrhage
• Stroke neurologists/pharmacist will decide based on clinical experience
• “Bridge” with ASA(14 days) (i.e. patient will be on ASA 81mg daily until it is time to start anticoag. If starting warfarin, usually “bridge” with ASA nstead of therapeutic LMWH/IV UFH)
• If active clot or mechanical valve will initiate AC sooner
• Warfarin – wait until INR therapeutic for 48 hours then stop ASA/DVT prophylaxis
• DOAC – stop ASA/DVT prophylaxis upon initiation of AC
which antiplatemet
secondary prevention
we tipically go with aspirin
- ASA
- Decreases recurrent stroke/TIA risk by ~15% (RRR) vs placebo
- “ASA Failure”- remains a mystery on how to best manage
- Clopidogrel
- No significant benefit over ASA (CAPRIE)
- Ticagrelor
- Failed to show superiority of ticagrelor over ASA (SOCRATES)
- ASA + Clopidogrel (dual)
- Increased benefit (CHANCE, POINT)
- 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 (only this long but longer -> bleed)
• ASA + Ticagrelor
• Increased benefit of ASA + Ticagrelor x 30 days (THALES)
• No reduction in disability. Increased bleed. NIHSS <=5
(though ~60% <=3). Much more expensive than clopidogrel
Are more antiplatelets better?
secondary
adding 3 (asa +clopid + dipyridamole)
Results
• No difference in the incidence or severity of
recurrent ischemic stroke
• Statistically significant increase in frequency and
severity of bleeding
Typical Duration of DAPT (before step-down
to monotherapy) after a stroke
• Minor stroke/TIA
• 21-30 days
- drop to asa everyday
- Stent (i.e. internal carotid artery stent)
- 6-12 weeks – guided by neurosurgery
- Intracranial Atherosclerosis
- 90 days
