2. Stroke
Injury or death of brain tissue due to oxygen deprivation;
usually due to an interruption of blood flow
Characterized by abrupt onset of focal neurologic deficit
that is attributable to a focal vascular cause
Also referred to as “Brain Attack” or “Cerebrovascular
Accident” (CVA)
3. Introduction
Clinically stroke is
A sudden onset non convulsive neurologic deficit
characterized by the rapid appearance (usually over
minutes) of a focal deficit of brain function
Including a hemiplegia with or without signs of focal
higher cerebral dysfunction (such as aphasia),
hemisensory loss, visual field defect or brain-stem deficit
In stroke the evidence of brain dysfunction ( neurologic
deficit) lasts for at least 24h or more
4. Introduction
Transient Ischemic Attack (TIA)
“Mini-stroke”
a temporary focal neurologic deficit lasting < 24 hours
(typically < 30 minutes)
Caused by brief interruption of blood supply to part of
the brain
35% of untreated patients will develop a stroke within
5 years of TIA
5. Introduction
Stroke can be either
Ischemic (88% )
Hemorrhagic (12%)
Ischemic stroke:
Caused either by
In situ thrombosis of an intracranial vessel,
typically affecting the small penetrating arteries or
Occlusion of an intracranial vessel by an embolus
that arises from a distant site (e.g., cardiogenic
embolus)
Hypoperfusion caused by flow-limiting stenosis of a
major extracranial artery
5
7. Ischemic Stroke
Normal cerebral blood flow: 50 mL/100 g per minute
Arterial occlusion-----severe reductions in cerebral blood
flow-----infarction
Tissue that is ischemic but maintains membrane integrity
is referred to as the ischemic penumbra ----- surrounds the
infarct core------salvageable through therapeutic
intervention
8. Hemorrhagic stroke
Hemorrhagic stroke
less common but lethal
Pathogenesis: mechanical effect (mass effect) of blood and
neurotoxicity of the blood components and their degradation
products
Includes
Subarachnoid hemorrhage
Intracerebral hemorrhage
Subdural hematomas
9. Hemorrhagic stroke
Subarachnoid hemorrhage
Occurs when blood enters the subarachnoid space
(where cerebrospinal fluid is housed)
Caused by trauma, rupture of an intracranial
aneurysm, or rupture of an arteriovenous
malformation
10. Hemorrhagic stroke
Intracerebral hemorrhage
Occurs when a blood vessel ruptures within the
brain parenchyma itself, resulting in the formation of
a hematoma
Associated with uncontrolled high blood pressure,
antithrombotic or thrombolytic therapy
11. Hemorrhagic stroke
Subdural hematomas
Collections of blood below the dura (covering of the
brain)
Caused by trauma
14. Nonmodifiable risk
factors
Age
Risk doubles for each
decade after 55 years of
age
Sex
Men >>>> women
Women more likely to
die from stroke
Low birth weight
Race/ethnicity
family history
Modifiable risk factors
Arterial hypertension:3-4x
DM-2-4x
Smoking -2-3x
Atrial fibrillation: 5% to
20% per year
Dyslipidemia
TIA
Prior stroke
Carotid disease
Excessive alcohol
High fibrinogen
High homocystein
Low folate
Anticardiolipin Ab
Obesity
15. Clinical Presentation
General
The patient may have cognitive or language deficits
Symptoms
Weakness on one side of the body
Inability to speak
Loss of vision
Vertigo or falling
Headache severe with hemorrhagic stroke
16. Clinical Presentation
Signs
Neurologic dysfunction
Hemiparesis or monoparesis
Hemisensory deficit
Vertigo and double vision
Aphasia: anterior circulation strokes
Dysarthria
Visual field defects
altered levels of consciousness
18. Clinical Presentation
Laboratory Tests
Hypercoagulable states: protein C deficiency, protein
S, antithrombin III, and antiphospholipid antibody
Diagnostic Tests
CT scan of the head
Area of hyperintensity (white): hemorrhage and
Normal or hypointense (dark): infarction
MRI of the head: ischemia detected with higher
resolution and earlier than the CT scan
Carotid Doppler (CD): Stenosis in the carotid arteries
supplying blood to the brain (extracranial disease)
ECG: AF
Echocardiography: Valve or wall motion
abnormalities
19. Treatment
Desired Outcomes
To reduce the ongoing neurologic injury
To decrease mortality and long-term disability
To prevent complications secondary to immobility and
neurologic dysfunction and
To prevent stroke recurrence
21. Treatment
General Approach to Treatment
Respiratory and cardiac support
Determine whether the lesion is ischemic or
hemorrhagic
Ischemic stroke
Evaluate for reperfusion therapy
22. Treatment
General Approach to Treatment
Do not treat elevated blood pressure unless it exceeds
220/120 mm Hg, or there is evidence of
Aortic dissection
Acute myocardial infarction (AMI)
Pulmonary edema, or
Hypertensive encephalopathy
SAH: if an aneurysm is found by angiography,
endovascular coiling or clipping
ICH: EVD if
There is intraventricular blood and evolving
hydrocephalus
23. Acute Ischemic Stroke
Blood Pressure Treatment
Short acting agents should be used
Labetalol IV: 10-20 mg doubled every 10-20
minutes(max: 300 mg) or infusion of 2-8 mg/min
Nicardipine IV: infusion 5 mg/hr – 15 mg.hr
Nitroprusside IV: infusion 0.5 mcg/kg/min
Selection of agents depends on the elevation in BP
24. Pharmacologic Therapy
Ischemic Stroke
Acute treatment
Two agents with class I recommendations
IV tissue plasminogen activator (tPA) within 4.5 hours
of onset
0.9 mg/kg over 1 hour, with 10% given as initial bolus
over 1 minute
avoid antithrombotic (anticoagulant or antiplatelet)
therapy for 24 hours
Monitor: blood pressure, response, and hemorrhage
Monitor BP every 15 minutes for 2 hours after start of
infusion, then every 30 minutes for 6 hours, and every
60 minutes for 16 hours
Aspirin within 48 hours of onset
160-325 mg QD
27. Pharmacologic Therapy
Early aspirin therapy
Reduce long-term death and disability
Should never be given within 24 hours of the
administration of tPA
Increase the risk of bleeding
28. Pharmacologic Therapy
Antiplatelet therapy
Cornerstone of antithrombotic therapy for the
secondary prevention of ischemic stroke
should be used in noncardioembolic strokes
First-line antiplatelet agents
Aspirin: 62-325 mg QD
Clopidogrel: 75 mg QD
Extended-release dipyridamole plus aspirin (ERDP-
ASA): 200 mg/25 mg BID
29. Pharmacologic Therapy
Secondary prevention of ischemic stroke
In patients with atrial fibrillation and a presumed cardiac
source of embolism
Oral anticoagulation
Warfarin, dabigatran (direct thrombin inhibitor),
rivaroxaban, and apixaban (direct factor Xa
inhibitors)
INR: 2.5
30. Pharmacologic Therapy
Statins
reduce the risk of stroke by 30% in patients with CAD
and elevated plasma lipids
Ischemic stroke patients, regardless of baseline
cholesterol, be treated with high-intensity statin therapy
Atorvastatin: 80 mg/day
Simvastatin: 80 mg/day
31. Pharmacologic Therapy
Prophylaxis of Deep Vein Thrombosis (DVT)
Decreased mobility owing to stroke: risk of DVT
increases
LMWH or UFH
Enoxaparin: 1 mg/kg/day
UFH: 5,000 units three times daily
32. Hemorrhagic Stroke
SAH: can cause delayed cerebral ischemia (DCI) between
4 and 21 days after the bleed
Cause: vasospasm of the cerebral vasculature
Treatment: nimodipine 60 mg every 4 hours for 21 days
34. Treatment
Management of ICH involves a combination of medical
and surgical interventions
Use of antipyretic medications to lower body
temperature to normothermia in febrile patients with
stroke
Hyperglycemia in the first 24 hours after stroke is
associated with adverse outcomes
Insulin treatment for elevated serum glucose >140 to
185 mg/dL
35. Treatment
All anticoagulant and antiplatelet drugs should be
discontinued acutely for at least one to two weeks after the
onset of hemorrhage
Anticoagulant effect should be reversed immediately with
appropriate agents
Vitamin K, unactivated prothrombin complex concentrate
(also called factor IX complex)
High doses (ie, 10 to 20 mg) of intravenous vitamin K can
fully reverse warfarin-induced anticoagulation
36. Intracranial pressure control
Increased ICP
Contribute to brain injury and neurologic
deterioration
Management of elevated ICP
Elevate the head of the bed to 30 degrees, once
hypovolemia is excluded
Analgesia and sedation, particularly in unstable,
intubated patients: reduce cerebral metabolism
37. Intracranial pressure control
IV mannitol
Dose: initial bolus of 1 g/kg, followed by infusions of
0.25 to 0.5 g/kg every six hours
The goal of therapy is to achieve plasma
hyperosmolality (300 to 310 mosmol/kg) while
maintaining an adequate plasma volume
Side effects: pulmonary edema, hyponatremia and
metabolic acidosis, and hyperkalemia
38. Evaluation Of Therapeutic Outcomes
Monitoring of the Pharmaceutical Care Plan
Monitor for the development of
Neurologic worsening (recurrence or extension)
complications (thromboembolism or infection), or
Adverse effects from pharmacologic or non-
pharmacologic interventions