STROKE

M. Salman
FOPAHS, LCWU
 Stroke is an acute episode of focal neurologic deficit that lasts
at least 24 hours and is presumed to be of vascular origin.

 Acute stroke is frequently referred to as a cerebrovascular

accident.
 It is essential to note that a stroke is not an accidental event

 A more accurate and meaningful term to describe it is "brain attack,"

which carries a similar significance to "heart attack.“

 Stroke encompasses a broader range of variations than heart disease

TYPES OF STROKE
 Stroke is categorized into mainly 2 types:
 Ischemic – around 87% of all stroke
 Hemorrhagic – around 13% of all strokes
 Intracerebral hemorrhage (ICH)
 Subarachnoid hemorrhage (SAH)
PATHOPHYSIOLOGY
 Ischemic stroke
 Ischemic strokes are either due to local thrombus formation
or emboli occluding a cerebral artery.

 Cerebral atherosclerosis is a cause in most cases

 Emboli arise either from intra- or extracranial arteries.

 Twenty percent of ischemic strokes arise from the heart.

 Carotid atherosclerotic plaques may rupture, resulting in collagen
exposure, platelet aggregation, and thrombus formation.
 The clot may cause local occlusion or dislodge and travel distally, eventually occluding
a cerebral vessel

 Cardiogenic embolism
 Stasis of blood flow in the atria or ventricles leads to formation of local clots that can
dislodge and travel through the aorta to the cerebral circulation.

 Thrombus formation and embolism result in arterial occlusion,

decreasing cerebral blood flow and causing ischemia and
ultimately infarction distal to the occlusion.
 Hemorrhagic strokes
 Subarachnoid hemorrhage (SAH) and intracerebral hemorrhage.

 SAH may result from trauma or rupture of an intracranial

aneurysm or arteriovenous malformation (AVM).

 Intracerebral hemorrhage occurs when a ruptured blood vessel

within the brain causes a hematoma.

 Blood in the brain parenchyma causes mechanical compression of

vulnerable tissue and subsequent activation of inflammation and
neurotoxins.
“TIME IS BRAIN”
 When it comes to stroke, “Time is Brain”

 Potential for achieving a complete neurological recovery diminishes with

every minute of untreated acute stroke

 Timely evaluation and management is essential

 Early and targeted treatments,, rehabilitation programs, and long-term

lifestyle modifications can significantly enhance clinical outcomes
BE FAST
RISK FACTORS
 Modifiable  Non modifiable
 Obesity  Age
 Hypertension  Sex
 Diabetes mellitus  Genetics
 Hyperlipidemia
 Smoking
 Alcohol consumption
 Sedentary lifestyle
CLINICAL PRESENTATION
 Patients may be unable to provide a reliable history because of
neurologic deficits.

 Family members or other witnesses usually provide this information.

 Symptoms
 Unilateral weakness
 Inability to speak
 Loss of vision
 Vertigo, or falling
 Ischemic stroke is not usually painful
 Severe headache may occur in hemorrhagic stroke
 Neurologic deficits on physical examination depend on the brain
area involved.

 Hemi- or monoparesis and hemisensory deficits are common.

 Patients with posterior circulation involvement may have vertigo

and diplopia.

 Anterior circulation strokes commonly result in aphasia.

 Patients may experience dysarthria, visual field defects, and

altered levels of consciousness
EVALUATION
 All patients suspected of experiencing acute stroke should undergo
emergency brain imaging evaluation upon arrival at the hospital before
initiating any specific therapy to treat AIS.
 Noncontrast CT (NCCT) and MRI head scans
 Appropriate modalities to exclude ICH before administering intravenous (IV) alteplase

Non –contrast CT
 If a patient with AIS presents within 6 hours of symptom onset
and shows a small core infarct on NCCT
 CT angiography (CTA) or MR angiography (MRA) can be used for guiding
mechanical thrombectomy patient selection

 When a patient with AIS presents within the 6- to 24-hour

window following symptom onset and displays a large-vessel
occlusion in the anterior circulation
 it is recommended to use diffusion-weighted MRI (DW-MRI) with or
without MR perfusion or CT perfusion for evaluation
 For patients experiencing a "wake-up" stroke or with an uncertain time of
symptom onset
 An MRI is crucial in identifying diffusion-positive fluid-attenuated inversion recovery
(FLAIR)-negative lesions.
 This technique assists in determining whether the patient would benefit from
thrombolytic therapy.

 In patients diagnosed with ICH, performing a CTA within the first few hours of
symptom onset can help identify individuals at risk of experiencing hematoma
expansion (HE)
 serial head CT scans within the first 24 hours can also assess for any HE

 The diagnosis of SAH is primarily based on NCCT imaging

 Other tests
 CBC
 Blood glucose level
 Troponin assessment
 BUN & SCr
 Coagulation factors
 Electrocardiographic assessment
TREATMENT
NON-PHARMACOLOGICAL TREATMENT
 Acute ischemic stroke
 Endovascular thrombectomy with a stent retriever
 Done within 6 hours of symptom onset and after IV tPA
 Improves outcomes in select patients with proximal large artery occlusion and
salvageable tissue on imaging

 Surgical decompression is sometimes necessary to reduce

intracranial pressure
 Performed within 48 hours of stroke onset in patients less than age 60

 In secondary prevention, carotid endarterectomy and stenting may be

effective in reducing stroke incidence and recurrence in appropriate
patients.
NON-PHARMACOLOGICAL
TREATMENT CONT’D
Hemorrhagic stroke
 In SAH from ruptured intracranial aneurysm or AVM
 Surgical intervention to clip or ablate the vascular abnormality reduces
mortality from re-bleeding

 Surgical evacuation may be beneficial in some situations after

primary intracerebral hemorrhage
 Insertion of an external ventricular drain with monitoring of intracranial
pressure is commonly performed in such patients.
 Recommendation
Acute treatment  tPA (alteplase) 0.9 mg/kg IV (maximum 90 mg) over 1 hour in
selected patients within 3 hours of Onset
PHARMACOTHERAPY

 tPA 0.9 mg/kg IV (maximum 90 mg) over 1 hour between 3 and

4.5 hours of onset (Evidence: IB)

 ASA 160–325 mg daily started within 48 hours of onset

Secondary prevention
Noncardioembolic Antiplatelet therapy
Aspirin 50–325 mg daily
Aspirin 25mg + extended-release dipyridamole 200mg twice daily
Clopidogrel 75mg daily
Cardioembolic Vit. K antagonists (INR = 2.5)
Apixaban 5mg twice daily
Dabigatran 150 mg twice daily
Rivaroxaban 20 mg daily
Atherosclerosis + High intensity statin therapy
LDL > 100 mg/dL
BP > 140/90 BP reduction
mmHg
KEY HIGHLIGHTS FROM THE AHA/ASA
MANAGEMENT GUIDELINES FOR AIS
 Airway, breathing, and oxygenation:
 Supplemental oxygen should be administered to patients to maintain
the oxygen saturation above 94%.
 It is not recommended for nonhypoxic patients.

 Blood pressure (BP):

 Patients with elevated BP should have their BP carefully reduced to a
systolic BP (SBP) below 185 mm Hg and diastolic BP below 110 mm Hg
before initiating IV fibrinolytic therapy.
 Following the treatment, the BP should be maintained below 180/105
mm Hg for at least 24 hours.
  If a mechanical thrombectomy is planned, and the patient has not received IV
fibrinolytic therapy
 It is reasonable to maintain their BP at or below 185/110 mm Hg before the
procedure and at or below 180/105 mm Hg during and for 24 hours after
the procedure

 Short-acting parenteral agents (e.g., labetalol and nicardipine) are preferred

for BP reduction.
 Temperature:
 Hyperthermia (body temperature >38°C or 100.4°F) should be treated by
administering antipyretic medication
 Blood glucose
 Both hypoglycemia (blood glucose level <60 mg/dL) and hyperglycemia
(blood glucose levels: 140 to 180 mg/dL) should be treated.
Alteplase (t-PA, tissue plasminogen activator)
 If initiated within 4.5 hours of symptom onset reduces disability from
ischemic stroke.
 Adherence to a strict protocol is essential to achieving positive outcomes:
I. Activate the stroke team
II. Treat as early as possible within 4.5 hours of onset
III. Obtain CT scan to rule out hemorrhage
IV. Meet all inclusion and no exclusion criteria
V. Administer alteplase 0.9 mg/kg (maximum 90 mg) infused IV over 1 hour, with
10% given as initial bolus over 1 minute
VI. Avoid anticoagulant and antiplatelet therapy for 24 hours
VII. Monitor the patient closely for elevated BP, response, and hemorrhage.
Inclusion and Exclusion Criteria for tPA Use in Acute Ischemic Stroke
Inclusion criteria
 Age 18 years or older
 Clinical diagnosis of ischemic stroke causing a measurable neurologic deficit
 Time of symptom onset well established to be <4.5 hours before treatment would
begin
Exclusion criteria
 History of previous intracranial hemorrhage
 Symptoms suggestive of SAH
 Active internal bleeding
 Acute bleeding diathesis, including but not limited to a platelet count
<100,000/mm3
 Patient has received heparin within 48 hours, resulting in an elevated aPTT
 Recent anticoagulant use and elevated INR (>1.7) or PT (>15 seconds)
 Current use of direct thrombin inhibitors or direct factor Xa inhibitors with elevated
sensitive laboratory tests (such as aPTT, INR, platelet count, and ECT; TT; or
appropriate factor Xa activity assays)
 Significant head trauma or previous stroke within 3 months
 Arterial puncture at noncompressible site within 7 days
 Intracranial neoplasm, arteriovenous malformation, or aneurysm
 SBP >185 mm Hg or DBP >110 mm Hg
 Blood glucose <50 mg/dL (2.7 mmol/L)
 CT demonstrates multilobar infarction (hypodensity >1/3 cerebral hemisphere)
Inclusion and Exclusion Criteria for tPA Use in AIS
Cont’d

Relative exclusion criteria (considering risk to benefit in individual patients,

may be wise to administer tPA despite 1 or more of the following:
 Only minor or rapidly improving symptoms
 Pregnancy
 Seizure at onset with postictal residual impairments
 Major surgery or serious trauma within 14 days
 Gastrointestinal or urinary tract hemorrhage within 21 days
 Acute myocardial infarction within 3 months

Additional exclusion criteria if within 3–4.5 hours of onset

 Age greater than 80 years
 Current treatment with oral anticoagulants
 NIH Stroke Scale Score >25 (severe stroke)
 Imaging evidence of large infarct (>1/3 MCA territory)
 History of both stroke and diabetes
 Other IV fibrinolytics
 A single IV bolus of tenecteplase at 0.25 mg/kg (maximum 25 mg)
can be administered instead of IV alteplase in patients without
contraindications who are eligible for mechanical thrombectomy.

 The ease of administration gives tenecteplase (given as a single, intravenous

bolus) unique practical advantages compared with alteplase

 Evidence that tenecteplase is noninferior to alteplase for acute

ischaemic stroke

 IV defibrinogenating or IV fibrinolytic agents, other than alteplase

and tenecteplase, are not recommended.
 Antiplatelet treatment:
 Aspirin administration is recommended within 24 to 48 hours after
symptom onset.

 However, aspirin administration is typically delayed until 24 hours after

treating a patient with IV alteplase.

 Patients diagnosed with minor, noncardioembolic ischemic stroke who

have not received IV alteplase
 it is appropriate to initiate dual antiplatelet therapy with aspirin and
clopidogrel within 24 hours after symptom onset
 Secondary prevention of ischemic stroke
Use antiplatelet therapy in noncardioembolic stroke.
 Aspirin, clopidogrel, and extended release dipyridamole plus aspirin are all first-line agents
Patients with atrial fibrillation and a presumed cardiac source of embolism
 Oral anticoagulation with a vitamin K antagonist (warfarin), apixaban, dabigatran, or
rivaroxaban
Reduction of BP > 140/90 mm Hg in patients with stroke or TIA after the
acute period (first 7 days)
Patients experiencing ischemic stroke of presumed atherosclerotic origin who
have LDL-c > 100 mg/dL should be treated with high intensity statin therapy.
Low-molecular-weight heparin or low-dose subcutaneous unfractionated
heparin
 Dose: 5000 units TID
 It is recommended for prevention of deep vein thrombosis in hospitalized patients with
decreased mobility due to stroke and should be used in all but the most minor strokes
THERAPY OF HEMORRHAGIC
STROKE
Intracerebral hemorrhage
 Initiating treatment for elevated BP within 2 hours of ICH onset and
achieving the target BP within 1 hour may reduce HE risk and improve
outcomes

 Anticoagulation should be discontinued immediately in patients with

anticoagulant-associated ICH, and rapid reversal should be performed as
soon as possible

 Surgical management has reduced mortality for specific patients

compared to medical management alone.

 Surgical options for managing ICH include

 Minimally invasive hematoma evacuation with endoscopic or stereotactic
aspiration, external ventricular drain (EVD) insertion, and craniotomy
Subarachnoid Hemorrhage
 Early treatment of aneurysms is recommended to decrease the risk of
rebleeding

 Short-term antifibrinolytic therapy is considered a strategy to reduce the

rebleeding risk
 However, the routine use of tranexamic acid after SAH cannot be recommended

 Between the onset of SAH symptoms and the obliteration of the aneurysm,
AHA/ASA recommends maintaining SBP below 160 mm Hg.
 On the contrary, Europea Stroke Association suggests maintaining the SBP < 180
mm Hg
 Treatment with antiepileptic drugs is recommended in case a patient
experience seizures associated with SAH
 Short-term seizure prophylaxis may also be considered during the immediate
posthemorrhagic period

 Management of hydrocephalus involves diverting cerebrospinal fluid

through methods such as EVD or lumbar drainage

 Nimodipine should be administered to all patients to prevent delayed

cerebral ischemia, with oral administration preferred over IV
administration

 Additional treatment goals include pain control, euvolemia,

normothermia, and normoglycemia.