ACUTE ISCHEMIC STROKE

OVERVIEW
• a condition in which there is an inadequate supply of blood and oxygen
to a portion of the myocardium
• It typically occurs when there is an imbalance between myocardial
oxygen supply and demand.
• The most common cause of myocardial ischemia is atherosclerotic
disease of an epicardial coronary artery (or arteries) sufficient to cause
a regional reduction in myocardial blood flow and inadequate perfusion
of the myocardium supplied by the involved coronary artery.
INCIDENCE
• IHD causes more deaths and disability and incurs greater economic costs
than any other illness in the developed world.
• IHD is the most common, serious, chronic, life-threatening illness in the United
States, where 15.5 million persons have IHD, and 3.4 million people aged ≥40
years have angina pectoris. Although there is regional variation, about 4% of
the population has sustained a myocardial infarction.
• Genetic factors, a high-fat and energy-rich diet, smoking, and a sedentary
lifestyle are associated with the emergence of IHD. In the United States and
Western Europe, IHD is growing among low-income groups, but primary
prevention has delayed the disease to later in life across socioeconomic groups.
ETIOLOGY
• Obesity, insulin resistance, and type 2 diabetes mellitus are increasing
and are powerful risk factors for IHD. These trends are occurring in the
general context of population growth and as a result of the increase in
the average age of the world’s population. With urbanization in
countries with emerging economies and a growing middle class,
elements of the energy-rich Western diet are being adopted.
 PATHOPHYSIOLOGY
• Acute occlusion of an intracranial vessel causes reduction in blood flow to the brain region it supplies.
• The magnitude of flow reduction is a function of collateral blood flow, and this depends on individual vascular
anatomy (which may be altered by disease), the site of occlusion, and systemic blood pressure.
• A decrease in cerebral blood flow to values <20 mL/100 g tissue per minute cause ischemia without infarction
unless prolonged for several hours or days; values <16–18 mL/100 g tissue per minute cause infarction within
an hour; and values zero causes death of brain tissue within 4–10 min
• If blood flow is restored to ischemic tissue before significant infarction develops, the patient may experience
only transient symptoms, and the clinical syndrome is called a transient ischemic attack (TIA).
• Focal cerebral infarction occurs via two distinct pathways:
(1) a necrotic pathway in which cellular cytoskeletal breakdown is rapid, due principally to energy failure of
the cell
(2) an apoptotic pathway in which cells become programmed to die.
Cascade of Cerebral Ischemia
ARTERY-TO-ARTERY EMBOLIC STROKE
Thrombus formation on atherosclerotic plaques may embolize to intracranial arteries producing
an artery-to-artery embolic stroke. Less commonly, a diseased vessel may acutely thrombose.
Carotid Atherosclerosis
Atherosclerosis within the carotid artery occurs most frequently within the common carotid
bifurcation and proximal internal carotid artery; the carotid siphon (portion within the cavernous
sinus) is also vulnerable to atherosclerosis.
Intracranial atherosclerosis produces stroke either by an embolic mechanism or by in situ
thrombosis of a diseased vessel.
Dissection of the internal carotid or vertebral arteries or even vessels beyond the circle of Willis
is a common source of embolic stroke in young (age <60 years) patients.
The dissection is usually painful and precedes the stroke by several hours or days. Ehlers-Danlos
type IV, Marfan’s disease, cystic medial necrosis, and fibromuscular dysplasia are associated with
dissections. Trauma and Spinal manipulative therapy is associated with vertebral artery dissection
and stroke.
 SMALL VESSEL STROKE
• The term lacunar infarction refers to infarction following atherothrombotic or
lipohyalinotic occlusion of a small artery in the brain. The term small-vessel stroke
denotes occlusion of such a small penetrating artery and is now the preferred term.
Small-vessel strokes account for ~20% of all strokes.
• The MCA stem, the arteries comprising the circle of Willis (A1 segment, anterior and
posterior communicating arteries, and P1 segment), and the basilar and vertebral
arteries all give rise to 30- to 300-μm branches that penetrate the deep gray and white
matter of the cerebrum or brainstem. Each of these small branches can occlude either by
atherothrombotic disease at its origin or by the development of lipohyalinotic thickening.
• Thrombosis of these vessels causes small infarcts that are referred to as lacunes (Latin for
“lake” of fluid noted at autopsy).
• These infarcts range in size from 3 mm to 2 cm in diameter. Hypertension and age are the
principal risk factors.
MANAGEMENT
GOALS OF TREATMENT:
prevent or reverse brain injury.
Attend to the patient’s airway, breathing, and circulation (ABCs), and treat hypoglycemia or hyperglycemia
if identified by finger stick testing.
Perform an emergency non- contrast head CT scan to differentiate between ischemic stroke and
hemorrhagic stroke;
 MANAGEMENT
6 categories of treatment:

(1) medical support

(2) IV thrombolysis
(3) endovascular revascularization
(4) antithrombotic treatment
(5) neuroprotection
(6) stroke centers and rehabilitation.
PROGNOSIS
Overall mortality rate at 30 days after stroke- 28%
Prognosis varies depending on the stroke severity and on the patient’s
premorbid condition, age, and poststroke complications.
Acute ischemic stroke has been associated with acute cardiac
dysfunction and arrhythmia.
References
Kasper, Dennis L., Hauser, Stephen L., Fauci, Anthony S. Et al.. Harrison’s
Principles of Internal Medicine 20th ed. Chapter 420