2. CVA
• Y 65 yrs old man was admitted to the hospital at 14/10/20 and presented with acute unilateral left-hand
weakness for 14hrs associated with slurred speech, dysphagia, incontinence of the urine and altered
mental status.
• PMHx: know case of HTN
• PSHx: none
• DHx: No known drug allergy, no current meds
• SHx: khat, cigarette,
• Ohx: night shift guard
3. EXAMINATION
Admission stats: 150/90, 104, 37.4, 22, 94%
HEENT: Mouth deviated to right-side, right eye deviated to right
C/P: Tachycardia with normal rhythm
Abdomen: unremarkable
Neuro-MSK: left-hand motor weakness (0/5) with hypotonia and normal sensory
modalities. The rest limbs were normal.
4. LABS AND IMAGES
• White count: 4.8
• Hb: 17mg/dl
• Platelets: normal range
• U/A: 5-6 wbc on hpf, proteins ++
• Creatinine: 0.9mg/dl
• Cholesterol: 158mg/dl
• CT scan: infraction of RMCA
5. OVERVIEW OF STROKE AND TIA
• The term stroke is applied to a sudden focal neurologic syndrome caused by
cerebrovascular disease.
• 5th common cause of death in low in-come countries (WHO , 2016)
• CVD refers to an abnormality of the brain caused by pathology of blood vessels
such as:
a. Occlusion by embolus or thrombus
b. Vessel rupture
c. Altered permeability of the vessel wall
d. Increased viscosity
6. PATHOGENESIS
• The primary vascular disorder may be atherosclerosis, hypertensive
arteriosclerotic change, arteritis, aneurysmal dilatation, or a developmental
malformation.
• The secondary parenchymal changes in the brain resulting from the vascular lesion
could be ischemia, with or without infarction, and hemorrhage.
• varicella zoster infection has been identified as a risk factor for ischemic and
hemorrhagic strokes and TIA (increases risk by 30%).
7. TRANSIENT ISCHEMIC ATTACK
• Brain ischemia without infarction has been recently defined by the
American Stroke Association as a transient ischemic attack (TIA).
Ischemic stroke has been defined as infarction and may result in
temporary or permanent cognitive, motor, and/or sensory deficits.
• The latest guideline on TIA from the American Stroke Association has
removed all references to duration of symptoms.
9. WORK-UP
• Patients with TIA should have imaging within 24 hours or ASAP after their
symptoms to determine if any infarction is present. Also order CT or MR
angiography of intracranial and neck vessels, echo, and blood work:
chemistries, BS, lipids, CBC. Order an ECG to rule out atrial fibrillation
(AF).
10. CLASSIFICATION OF STROKES
• Strokes are classified as ischemic or hemorrhagic.
• Ischemic strokes can be thrombotic or embolic.
• Ischemic strokes (87% of all strokes):
• Hemorrhagic strokes are mainly caused by:
• • Intracerebral hemorrhage (ICH)
• • Subarachnoid hemorrhage (SAH)
11. CLINICAL FEATURES AND RISK FACTORS
Risk factors:
• Smoking
• HTN
• Diabetes
• High cholesterol level
• Heart and blood vessel disease
• Clinical features: Weakness, aphasia, apraxia, dysarthria, dystonia, personality
changes, urinary incontinence, N/V,……………
15. ASSESSMENT
• History and Physical exam: To distinguish between other disorders in the
differential diagnosis of stroke.
• Vital sign: Hypertension, fever (may worsen brain ischemia), breathing
(may be increased in hemorrhage).
• Non-contrast computed tomography (CT) is typically the first diagnostic
study in patients with suspected stroke.
16. ASSESSMENT
• The main advantages of CT are widespread access (not in Africa) and speed of
acquisition. CT is highly sensitive for the diagnosis of hemorrhage in the acute setting.
• MRI is more sensitive than CT for the early diagnosis of brain infarction
• In patients with ischemia who do not yet have brain infarction, both CT and MRI may be
normal.
• Small subarachnoid hemorrhages can be missed by either CT or MRI. Lumbar puncture
may be needed to make the diagnosis in such patients
17. ASSESSMENT
• The history, physical examination, serum glucose, oxygen saturation, and a non-
contrast CT scan are sufficient in most cases to guide acute therapy.
• Other tests are considered based upon individual patient characteristics, but the
absence or unavailability of any additional tests need not be a reason to delay
therapy if otherwise indicated.
18. MANAGEMENT
• The goals in the initial phase include:
• Ensuring medical stability, with particular attention to airway, breathing, and circulation
• Quickly reversing any conditions that are contributing to the patient's problem
• Determining if they are candidates of intravenous thrombolytic therapy
• Moving toward uncovering the pathophysiologic basis of the patient's neurologic
symptoms
19. MANAGEMENT
• Fluids: choose isotonic saline without dextrose. Hypotonic fluids can
exacerbate cerebral edema
• Hypoglycemia: Hypoglycemia can cause focal neurologic deficits
mimicking stroke, and severe hypoglycemia alone can cause neuronal
injury. It is important to check the blood sugar and rapidly correct low
serum glucose (<60 mg/dL [3.3 mmol/L]) at the first opportunity
20. MANAGEMENT
• Hyperglycemia: is common in patients with acute stroke and is associated with
poor functional outcome.
• Hyperglycemia may augment brain injury by several mechanisms including
increased tissue acidosis from anaerobic metabolism, free radical generation, and
increased blood brain barrier permeability.
• The American Heart Association/American Stroke Association guidelines for
acute ischemic stroke recommend treatment for hyperglycemia to achieve serum
glucose concentrations in the range of 140 to 180 mg/dL
21. MANAGEMENT
• Swallowing assessment: NPO and NG tube
• Head and Body position: keeping the head in neutral alignment with the body
and elevating the head of the bed to 30 degrees for patients in the acute phase of
stroke.
• Fever: May contribute to brain injury in patients with an acute stroke. The source
of fever should be investigated and treated, and antipyretics should be used to
lower temperature in febrile patients with acute stroke. The favorable range is ≤
37Ċ
22. MANAGEMENT
• Blood pressure: Bp is maintained ≤180/110 mmHg in patients who are
eligible to thrombolytics.
• Patients who are not eligible to thrombolytics, reduction of Bp in the acute
phase is not advised unless the patient’s BP is ≥220/120 mmHg.
• The choice of the control of BP in the acute phase is; labetalol, nicardipine
and clevidipine
23. ISCHEMIC STROKE MANAGEMENT
For eligible patients with acute ischemic stroke, intravenous alteplase is first-line
therapy, provided that treatment is initiated within 4.5 hours of clearly defined
symptom onset. Because the benefit of alteplase is time dependent, it is critical to
treat patients as quickly as possible.
Mechanical thrombectomy is indicated for patients with acute ischemic stroke due
to a large artery occlusion in the anterior circulation who can be treated within 24
hours of the time last known to be well
24. ISCHEMIC STROKE MANAGEMENT
• Antithrombotic therapy with aspirin initiated within 48 hours of stroke onset.
• If the patient has got thrombolytics, start aspirin after 24 hours.
• Adding dipyridamole with aspirin adds effacacy
• If the patient is contraindicated to aspirin, start clopidogrel
• Aspirin and clopidogrel are not co-administered in stroke.
25. ISCHEMIC STROKE MANAGEMENT
• Statin therap: There is clear evidence that long-term intensive statin therapy is associated
with a reduced risk of recurrent ischemic stroke and cardiovascular events.
• SSRIs: There is some evidence from small randomized controlled trials suggesting that
early initiation of selective serotonin-reuptake inhibitors (SSRIs) after ischemic stroke for
patients with hemiparesis but without depression enhances motor recovery and reduces
dependency.
• Prevention of bedsore, physiotherapy and psychological support is important.
• Behavioral and lifestyle changes: including smoking cessation, exercise, weight
reduction for obese patients, and a Mediterranean style diet