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344 final > Stroke 2 > Flashcards

Stroke 2 Flashcards

1
Q

ACUTE ISSUES
• Supportive
- prevent comp

A 
Supportive
• Vomiting
• Airway
• Oxygenation
• IV fluid
Prevent Complications
• Dehydration
• DVT
• Electrolyte imbalances
• Fever
• Hypertension
• Hyperglycemia
• Hem transformation
• Infection
• Intracranial pressure
• Seizures
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2
Q

DEHYDRATION

A 
• Manage with IV fluid (NaCl 0.9% - normal saline) or
enterally (PO/NG PRN)
• AVOID using:
• Dextrose solutions
• Hypertonic solutions
• Hypotonic solutions
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3
Q

DVT PROPHYLAXIS

A

• 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

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4
Q

ELECTROLYTE IMBALANCES

A
  • SIADH occurs in 10-14% of patients
  • Monitor daily lytes
  • Correct imbalances prn
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5
Q

FEVER

A

• 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

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6
Q

HYPERTENSION

A

• 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

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7
Q

HYPERGLYCEMIA

A

• 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

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8
Q

HEMORRHAGIC TRANSFORMATION

A

• 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

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9
Q

INTRACRANIAL PRESSURE (ICP)

A

• 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

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10
Q

INFECTION

increased risk for

A 
• 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
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11
Q

SEIZURES

A

• 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!

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12
Q

Ischemic Stroke

ì What was the cause?

A 
ì Cardioembolic (Afib, CM, LVT, valvular disease, etc)
ì Large vessel atherosclerosis
ì Small vessel disease
ì Cryptogenic
ì Other
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13
Q

RISK FACTOR MANAGEMENT

secondary stroke prevention

A
  • 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
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14
Q

SURGICAL INTERVENTION

secondary stroke prevention

A
  • 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)

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15
Q

ANTIPLATELET VS. ANTICOAGULATION

A

• 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

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16
Q

RISK STRATIFICATION FOR A-FIB (CHADS2)

A

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

17
Q

Which DOAC is clearly superior to other
DOACs in terms of preventing ischemic stroke
from non-valvular atrial fibrillation?

  1. Dabigatran
  2. Apixaban
  3. Rivaroxaban
  4. Edoxaban
  5. It’s a trap! There is no clearly superior DOAC
A
  1. It’s a trap! There is no clearly superior DOAC
18
Q

DOACs – a PANACEA?

A

• 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

19
Q

DOACs – Antidotes

A

• 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

20
Q

WARFARIN VS ASA FOR NON A-FIB

A

• 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

21
Q

INITIATING ANTICOAGULATION

secondary prevention

A

• 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

22
Q

which antiplatemet

secondary prevention

A

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

23
Q

Are more antiplatelets better?

secondary

A

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

24
Q

Typical Duration of DAPT (before step-down

to monotherapy) after a stroke

A

• 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
25
Q

ANTICOAGULATION + ANTIPLATELET?

A

• Rivaroxaban 2.5mg BID + ASA 100mg daily vs Rivaroxaban 5mg BID vs ASA 100mg daily (COMPASS)
was not a stroke study but found it was good
• Essentially a study in patients with stable CAD with atherosclerosis
• Part of exclusion criteria: Stroke within 1 month, any history of hemorrhagic or lacunar stroke
profound when looking specifically at
the reduction in ischemic stroke: (60 [1%] of 8313 vs 120 [2%] of 8261; hazard ratio [HR] 0·5

• Full dose anticoagulation + antiplatelet?
• Afib + carotid or intracranial stent
• Acute coronary syndrome + stroke
• If patient would normally be on an antiplatelet for stroke prevention, but they are on anticoagulation for a different reason (e.g. DVT/PE), we would typically stop the antiplatelet until anticoagulation is finished, then restart
= the antiplatelet

26
Q

Cryptogenic / ESUS

A

no athero, non smoker, no risk factors
many are cardioembolic that was not catched w instrument

• Antiplatelet or Anticoagulant? Antiplatelet!
• NAVIGATE ESUS
• Rivaroxaban 15mg daily vs ASA 100mg daily
• No difference in rate of recurrent stroke
• Statistically significantly more major bleeding in Rivaroxaban arm
- more of a failed trial

  • RESPECT ESUS
  • Dabigatran 150mg BID (or 110mg BID) vs ASA 100mg daily
  • Non-statistically significant reduction in stroke in Dabigatran arm
  • Increase in clinically relevant non-major bleeding in Dabigatran arm
27
Q

So far it seems like only the elderly or people
with medical conditions have strokes… Do
young, healthy people have strokes?

A

yes

CEREBRAL VENOUS SINUS THROMBOSIS (CVST)
Cervical Artery Dissection (CD)

28
Q

CEREBRAL VENOUS SINUS THROMBOSIS (CVST)

A
  • Thrombosis occurring in the venous circulation leading to infarction +/- bleeding
  • More frequent in women, and more frequent in children and young adults.
  • Symptoms: Headache +/- typical stroke symptoms
  • Mortality <5%, and ~80% of patients recover fully
  • Treatment: LMWH/IV UFH -> oral anticoag
  • Traditional risk factors for thrombosis:
  • Pro-thrombotic medications (e.g. estrogen, birth control)
  • Pregnancy and purperium
  • Infections
  • Thrombophillias (APLAS, F5L, etc)
  • Myeloproliferative disorders/malignancies
  • Smoking
  • Dehydration
  • In ~13% of cases there are no risk factors
29
Q

Cervical Artery Dissection (CD)

A

• Most frequent cause of stroke in young people
• CD accounts for 2% of all ischemic strokes, but accounts for 8% - 25% of strokes in patients
under 45 years old
• Can be spontaneous or traumatic

  • Risk factors associated with CD:
  • Trauma
  • Hypertension
  • Oral contraceptives
  • Genetic disorders affecting connective tissue
  • Migraine
  • Common trauma that can cause CD:
  • Motor vehicle collision
  • Coughing, sneezing
  • SPORTS – heavy lifting, golf, tennis, yoga, contact
  • Cervical manipulative therapy

• Treatment = antiplatelet OR anticoagulation
• Antiplatelet unless patient has indication for anticoag
UFH for 1 week, if not gone will use warfarin?

30
Q

TIA MANAGEMENT

A

ì HIGH RISK – symptom onset within 48 hours
ì need urgent brain/vessel imaging, ECG
ì INCREASED RISK – symptoms 48 hours to 2 weeks
ì fluctuating/persistent symptoms should be seen
within 24 hours
ì with no neurologic deficits should be seen within 2
weeks
ì LOWER RISK - > 2 weeks from symptom onset
ì should see neurologist within 1 month

31
Q

TIA WORK-UP

A

• After risk assessment:
• Same investigations as stroke patients based on specified
timeline (vessel imaging, echo, holter, labs)
• Start antithrombotic (remember CHANCE/POINT)
• CEA or stenting if symptomatic carotid artery stenosis
• Risk factor management
• HTN, lipids, diabetes, smoking cessation

32
Q

INTRACEREBRAL HEMORRHAGE (ICH)
In Canada, ICH accounts for ~10-15% of all strokes
• Mortality is much higher than seen in ischemic strokes (40%
vs 15%)

A
  • Supportive measures
  • DVT prophylaxis
  • Pneumatic compression stockings start in first 24 hours
  • LMWH or UFH after 48-72 hours if bleed stable
  • BP management
  • Current standard of practice acutely target SBP < 180mmHg
  • Targeting < 140mmHg acutely: No harm, yet no benefit seen
  • Bottom line treat far more aggressively than in ischemic strokes
  • Long-term BP target <130/80mmHg

• Surgical intervention in select patients

33
Q

SUBARACHNOID HEMORRHAGE (SAH

A

Supportive measures
• Determine the cause:
Aneurysm? CVST?
As blood passes through the weakened blood vessel, the blood pressure causes a small area to bulge outwards like a balloon.

  • Surgical intervention
  • If aneurysmal:
  • Nimodipine 60mg PO q4h x 21 days
  • Vasospasm and possibly neuroprotective
  • Improved outcomes (mortality, neurologic outcome)
34
Q

SUBDURAL HEMATOMA (SDH)

A

• Supportive measures
• Determine the cause: Usually traumatic. Could, however,
occur from intracranial hypotension, coagulopathy, or in
association with antithrombotic therapy
• Could be acute or chronic
• Require neurosurgical consultation/intervention

35
Q

HEMORRHAGIC STROKE + ANTIRHROMBOTICS

• When to re-start antithrombotic after SAH or ICH?

A

• Depends on etiology of bleed (ex. Amyloid, hypertensive, AVM) and location (deep vs lobar)
• Depends on size of bleed
• Depends on compelling indication for antithrombotic
• Bottom line is to decide on a case by case basis in
consultation with stroke neurologist
• CSBPR 2020: “The optimal timing and strategy regarding antithrombotic therapy following an ICH is uncertain and should be individualized to the patient (Evidence level C)”

36
Q

The big picture

• Take Away

A

• Pharmacist role is important for stroke prevention
• Stroke is often an endpoint of numerous modifiable
risk factors – modify them!
• Afib should almost always be anticoagulated
• Ensure doses/regimens of antithrombotics are
correct for the condition
• On DAPT for stroke? – double check duration
• Drug interactions with antithrombotics – be vigilant

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