This document provides an overview of stroke, including its definition, types, risk factors, pathophysiology, clinical presentation, diagnosis, treatment both initially and long-term, and management considerations. The two main types of stroke are ischemic (87%) and hemorrhagic (13%). Risk factors include modifiable factors like hypertension and non-modifiable factors like age. Treatment involves stabilizing the patient, diagnosing with imaging, treating the cause, preventing complications, and long-term prevention with medications like aspirin, statins, and anticoagulants depending on the cause of stroke.

1. Stroke
Ni’ma bader

2.  Definition:
• Rapidly developing nurological dysfunction
due to acute vascular pathology not related to
trauma.
• There are two types of stroke:
• Ischemic. 87%
• Hemorrhagic. 13%
-subarachnoid hemorrhage.
-intracerebral hemorhage

3. Ischemic stroke:
• Ischemic strokes occur when blood flow is
reduced to a part of the brain or all of the
brain, resulting in tissue damage. The
reduction in blood flow can be due to
decreased systemic perfusion, severe stenosis
or blood vessel occlusion.
• They are classified to: large artery
atherosclerosis, cardioembolsim, small vessel
occlusion or other unusual etiology.

4. Hemorrhagic stroke
 Hemorrhagic strokes are characterized by too
much blood in the closed cranial cavity.
 Hemorrhagic strokes are often associated
with uncontrolled hypertension and
antithrombotic/thrombolytic therapy. They
are less common than ischemic strokes but
more lethal.

5. Risk factors:
Non-modifiable:
 Age.
 Race.
 Sex.
 Low birth weight.
 Genetic factors.
Modifiable:
 Hypertension.
 Cigarette smoking.
 Diabetes.
 Atrial fibrillation.
 Dyslipidemia.
 Asymptomatic carotid stenosis.
 Sickle cell disease.
 Poor diet.
 Obesity.
 Physical inactivity.
 Other cardiac diseases (coronary
heart disease, heart failure,
PAD).

6.  Pathophysiology (ischemic stroke)

7.  Hemorrhagic stroke
• The presence of blood in the brain parenchyma
causes mechanical compression of vulnerable
tissue and subsequent activation of
inflammation and neurotoxins.

8. Clinical presentation:
Symptoms:
– Weakness on one side of the body.
– Inability to speak.
– Loss of vision.
– Vertigo, falling.
– Headache (can be very severe with hemorrhagic
stroke).

9.  Signs:
– Hemiparesis, monoparesis, hemisensory deficits.
– Vertigo and double vision (posterior circulation
involvement).
– Aphasia (anterior circulation stroke).
– Dysarthia.
– Visual field deficits.
– Altered level of consciousness.

10. INITIAL ASSESSMENT
• The history, physical examination, serum
glucose, oxygen saturation, and a noncontrast
CT scan are sufficient in most cases to guide
acute therapy.

11.  Approach to treatment:
1. Airway, breathing and circulation
2. History and physical examination
3. Neurologic evaluation (NIHSS)
4. Immediate laboratory studies
5. Neuroimaging
6. Cardiac studies

12.  STROKE MANAGEMENT ISSUES
1. Fluids:
a. isotonic saline without dextrose is the agent of
choice
b. avoid excess free water as in ½ isotonic saline
a. avoid fluids containing glucose
a. fluid management must be individualized on the
basis of cardiovascular status, electrolyte
disturbances.

13. 2. Hypoglycemia.
3. Hyperglycemia (stress hyperglycemia):
1. Defined as a blood glucose level >126 mg/dL.
2. Can present regardless of diabetes.
3. It is associated with reduced benefit from recanalization
with thrombolytic.
4. Treat if glucose >180 mg/dL.
5. Goal is serum glucose concentrations in the range of 140 to
180 mg/dL.

14. 4. Swallowing assessment:
Dysphagia is common after stroke and is a major risk factor
for developing aspiration pneumonia.
5. Head and body position
– keep the head of bed in the position that is most
comfortable for the patient.
– Elevate the head of the bed to 30 degrees if the at risk
for:
• Elevated intracranial pressure (ie, intracerebral hemorrhage,
cerebral edema >24 hours from stroke onset)
• Aspiration (eg, those with dysphagia and/or diminished
consciousness)
• Cardiopulmonary decompensation or oxygen desaturation (eg,
those with chronic cardiac and pulmonary disease).

15. Mobilization
• Mobilization of stable patients after 24 hours
may lessen the likelihood of major complications
such as pneumonia, deep vein thrombosis,
pulmonary embolism, and pressure sores after
stroke.
• Exceptions; those who exhibit neurologic
deterioration upon assuming more upright
postures.
• very early mobilization, within 24 hours of
symptom onset, may be harmful.

16.  Fever
– Increase mortality rates, greater disability, more
dependence, worse functional outcome, greater
severity, and longer ICU and hospital stays.
– R/O primary CNS infection such as meningitis.
– maintain normothermia for at least the first several
days after an acute stroke.

17.  Permissive hypertension
• Treat if BP > 220/120 mmHg
• BP goals in the first 24-48h post stroke:
– No IV tPA : <220/120 mmHg
– IV tPA : <185/110 mmHg
• first-line: labetalol, nicardipine and clevidipine
• second-line: nitroprusside (if DBP >120 mmHg)

18. • In ICH patients with blood pressure between
150 and 220 mm Hg systolic, early treatment
designed to achieve a pressure of less than
140 mm Hg systolic has been shown to be safe
and improve functional outcome.

19. Fibrinolytics

20. • Endovascular thrombectomy with a stent
retriever is indicated after tPA but within 6
hours, for patients with proximal vessel
occlusion and a small core injury on imaging.

21. Alteplase:
• No proven mortality benefits.
• Reduce disability 3 months post-stroke
• Indicated within 4.5h of stroke onset.
• tPA: 0.9mg/kg ( max 90mg), 10% as IV bolus,
remainder over 1h.

22.  ANTIPLATELET AGENTS
• Aspirin:
– Reduce stroke recurrence, death and disability.
– Start within 24-48h of stroke onset.
• Aspirin vs. ticagrelor: ticagrelor not superior to
aspirin.
• Antiplatelet agents is not an alternative to
intravenous thrombolysis .

23. • symptomatic atherosclerotic intracranial large artery
stenosis, we suggest dual antiplatelet therapy with
aspirin plus clopidogrel for 90 days, followed by
antiplatelet monotherapy.
• parenteral anticoagulation rather than aspirin only for
select patients with acute cardioembolic ischemic
stroke or TIA who have intracardiac thrombus, as these
patients are at high risk for recurrent ischemic stroke.

24. • Secondary hemorrhagic transformation of an
ischemic infarct vs. aspirin use?
• Early anticoagulation is associated with a
higher mortality and worse outcomes
compared with aspirin treatment initiated
within 48 hours of ischemic stroke onset

25. • Early anticoagulation :
– no proven benefit.
– If used:
• Heparin: administer as IV infusion rather than bolus.
• Enoxaparin: 1 mg/kg dose every 12 hours

26. Secondary prevention

27. • ASA vs. ASA & ERDP
– the combination demonstrated a significant
advantage over the ASA-alone therapy.
– High dc rate because of headache (15%)
• ERDP-ASA vs. clopidogrel
– the risk of recurrent stroke was similar for the two
antiplatelet agents, but clopidogrel was better
tolerated with less bleeding and headache.

28. • ASA vs. clopidogrel:
– clopidogrel is slightly more effective than ASA and
had a similar incidence of adverse effects.

29. • ASA Plus Clopidogrel for secondary
prevention:
– No add benefit, increased bleeding risk

30. Aspirin
• lowest effective dose is 50 mg/day.
• most common adverse effects: Upper GI
discomfort and bleeding (both are dose
related).
• Caution when used with NSAIDs.

31. Extended-Release Dipyridamole Plus
ASA
• MOA:
– inhibit platelet aggregation by inhibiting
phosphodiesterase, leading to accumulation of
cAMP and cGMP intracellularly, which prevent
platelet activation.
– dipyridamole also enhances the antithrombotic
potential of the vascular wall.
– High dc rate because of headache

32. Oral Anticoagulants
• The treatment of choice for the prevention of
stroke in patients with atrial fibrillation
• target INR of 2.5
• NOAC including dabigatran, rivaroxaban, and
apixaban have significant advantages over
warfarin in terms of ease of dosing and less
food and drug interactions. Also all three agents
have been shown to be as effective as, and in
some cases, superior to, warfarin in reducing
recurrent events and intracranial hemorrhage.

33. Statins
• Use regardless of lipid profile
– high intensity statin (atorvastatin 40-80mg).
– If not tolerated use moderate intensity statins. (eg:
atorvastatin 10-20 mg, rosuvastatin 5-10mg,..)

34. Heparin
• Use low dose.
• Potential but unproven uses for treatment
doses of heparins include:
– bridge therapy in patients being initiated on
warfarin
– carotid dissection
– continuous worsening of ischemia despite
adequate antiplatelet therapy.

35. Dosing
 aspirin: 50 to 100 mg daily
clopidogrel: 75 mg daily
Aspirin-extended release dipyridamole: 25mg-
200mg BID.

36. Glycemic control:
 Patients with diabetes mellitus have
approximately twice the risk of ischemic
stroke compared with those without diabetes.
 Tight glycemic control reduces microvascular
complications.
 A goal of therapy for most people should be
A1C less than or equal to 7.

37. GI ulcer prophylaxis
 When to administer prophylaxis?
 If on mechanical ventilation for >48 hours.
 Coagulopathy.
 History of GI ulceration or bleeding within the past year.
 Traumatic brain injury, traumatic spinal cord injury, or
severe burn injury.
 Two or more of the following risk factors: sepsis, intensive
care unit stay lasting >1 week, occult GI bleeding lasting ≥6
days, or high-dose glucocorticoid therapy.
 Prophylaxis is through proton pump inhibitors or H2
antagonists.

38. DVT prophylaxis:
 DVT is common in patients after stroke, and more common for
those who suffer hemiparesis. It can lead to PE which holds a high
risk for mortality.
 DVT prophylaxis could be through intermittent pneumatic
compression (IPC) starting at presentation , for patients within 72
hours of acute ischemic stroke onset who have restricted mobility.
 C/I to IPC: leg ischemia because of PVD, leg ulceration, dermatitis or
severe leg edema.
 If patient has already been at bed rest or immobilized without VTE
prophylaxis for >72 hours, don’t use IPC.
 They can also take anticoagulants starting at presentation and
within 48 hours such as heparin 5000 units BID or TID or enoxaparin
40mg daily.

39. • Smoking cessation is also important.
• Carotid endarterectomy.