Acute Ischemic Stroke
Etiology & Patophysiology
Causes category :
1. Global hypoperfusion
2. Thrombus (blood vessel clot)
3. Embolic (clot somewhere that broke off and circulated, blocking cerebral vessel)
4. Other causes (vasculitis, dissection, hypercoagulable state)
Global hypoperfusion
Lead to watershed infarcts
Causes : significant cardiogenic shock (cardiac arrest), lack of oxygen (severe acute
respiratory failure), I.C.A stenosis & low BP (too much anti-HTN), septic shock, cardiac
surgery
Thrombus
Large Vessel Thrombus : I.C.A. (extra & intracranial), M.C.A (prox segment/M1),
Vertebral/basillar A.
Small vessel :
Come off the MCA and supply basal ganglia lenticulostriae artery
Small pontine branches
RF of thrombus :
Modifieble :
Hypertension (m/c)
DM type 1 or 2 (hyperglycemia)
Hyperlipidemia
Smoking
Obesity
Non modifiable :
Old age (>65 yrs)
Male
Family history
Genetic hyperlipidemia
Risk factor atherosclerotic plaque stenosis, occlusion of cerebral vessel with high
blood pressure, piece of covering the plaque got removed inner cheesy material got
exposed (super thrombotic) little platelet adhere to the cheesy material platelet plug
formed, fibrin mesh formed blood clot on top of thrombus blockage of blood flow
Embolic causes (m/c of ischaemic stroke)
1)Arterial to arterial emboli : Aortic arch to I.C.A leading to infarction. Could be due to I.C.A.
plaque or aortic arch plaque the plaque that’s on vessel wall rupture freely circulated
in the blood vessel infarction
2)Cardiac embolic cause
L.A. thrombus
ineffective atrial contraction (A.Fib or AFL to some degree)
Valve issue (mechanical valve
Rheumatic heart disease (super prone to form clot)
infective endocarditis (IV drug user, etc)
Stasis of BF, hypercoagula, endhotelial dysfunction Virchow triad
L..V. thrombus
L.V. aneurysm
Ant/Lat. MI stasis of blood flow ec weakend pumping function
HF w/ reduced EF (30-35%)
Paradoxical Embolus
ASD : Patent foramen ovale (P.F.O.), atrial septal aneurysm
PFO abnormal hole between atrial patient w/ DVT clot breaks off come up via
IVC to right atrial patient w/ PFO the emboli could go straight to left atrial and to cerebral
circulation
Embolic locations :
- M.C.A. usually proximal (M1 segment)
- P.C.A.
- Smaller segment (M2/M3)
On imaging, if theres multiple lesion think about embolic cause
Vasculitis (autoimmune, infection) injury to the vessel/pathogen attack the cerebral
vessel blood clot formed
Dissection (trauma, iatrogenic, connective tissue disease like ehlers-danlos syndrome)
Hypercoagulable disorder (factor V leiden, protein C and S deficiency, anti-thrombin 3
deficiency, pro-thrombin gene mutation, anti-phospolipid syndrome, polisitemia, Heparin
Induced Thrombocytopenia)
CLINICAL FEATURES see other vids
DIAGNOSIS
Stat Non Contrast CT-Scan R/O hemmoragic stroke (ICH/SAH)
Hyperdense sign hyperdense MCA/Basillar artery
Hypodensity as infark (cerebral tissue)
CT-Angiogram w/ contrast (see where contrast cant get past the clot)
MRI
DWI hyperintense on infark (bright)
ADC hypointense (darker on infark)
ECHO (T.E.E./T.T.E)
Point of care glucose wanna know hypo/hyperglycemia sometimes hypoglycemia into
a lesser degree hyperglycemia can present a stroke mimics
Patient w/ low glucose before you give them TPA correct the glucose level first
Check INR INR >1.7 ??
INR >1.7 + warfarin take into consideration bcs anticoagulated + TPA increased risk of
bleeding
PT/INR/PTT
CBC