Acute Ischemic Stroke

last updated: May 10, 2017

Orlando Debesa

Evolution from Acute to Chronic Infarction

Hemorrhagic Conversion

Fogging Phenomenon

History

1995 NINDS tPA within 3 hrs

 

2008 ECASS 3 (3-4.5 hrs)

 

2015 endovascular mechanical thrombectomy trials

  • MR CLEAN

  • REVASCAT

  • EXTEND IA

  • SWIFT PRIME

  • ESCAPE

 

favorable outcome with tPA based on ranking score

 

after 2015 why things got better

  • Use of newer generation devices

  • imaging criteria

  • Higher revascularization rate

  • 2nd generation device

    • Stent retrieval devices

 

Mechanical thrombectomy

  • Used if excluded from tPA use

  • used if unknown time of onset

  • on blood thinners

  • post op patients

  • beyond tPA window

  • low platelets/abnormal coagulation studies

 

Case #1

tPA with hemorrhagic conversion; SSx: new HA and worsening weakness, sudden rise in BP

  • can happen also spontaneous if no tPA given

    • SITS-MOST study

    • NINDS

    • CASES

Management:

  • stop IV tPA and scan

  • Type and cross

  • Coats and fibrinogen

  • Cryop and plat, PCC

 

Things that increase risk of hemorrhagic conversion

  • Early stroke changes on CT

  • AGE

  • severity of stroke

Other factors

  • Heart failure  

 

Seizure after ischemic stroke (has 2 peaks)

  • Within 24 hrs

  • Between 6-12 months

 

Suspecting seizures

  • Mental status fluctuations

  • Worsening unexplained neurological findings

 

Malignant edema post ischemic stroke (happens usually 24 hrs later so send to ICU)

  • N/v within 1st 24 hrs

  • >180 BP

  • HF

  • younger age

  • Female

  • >50% MCA involvement

  • ICA (T occlusion)

Tx

  • Aggressive: hemicraniectomy (no difference in prognosis, will be disabled because 1/2 brain cut out); allow the brain to herniate out

  • Osmol therapy/ICP management

 

Large Cerebellar stroke

  • Do well with hemicraniectomy and have good QOL

  • emergent posterior fossa decompresson with partial removal of infarcted tissue

 

RICA Occlusion

  • Good collateral will prevent symptoms via anterior communicating artery but many variations

  • Hemorrhagic conversion, seizure can occur

  • Obese with shunt from left to right because of CO2 elevation (hypoventilation); reverse Robin Hood syndrome

  • the collaterals form pretty fast with occlusion

 

Medical complications of ischemic stroke

  • At least one medical complication in 95% of patients

    • PNA most common 5-7% (aspiration); need to be cleared

    • Mechanical ventilation

      • MM very high after ischemic stroke 70-76%

    • PE

    • Angioedema

      • 1-8% tx with alteplase

    • Macroglossia

      • usually brain stem injury

      • Automomic dysfunction

    • Cardiac complications

      • RANTTAS trial

      • Elevated troponin (poor prognosis sign)

        • Insular cortex

    • GI bleeding

Hypoxic-Ischemic Brain Injury

  • diffuse oedema with effacement of the CSF-containing spaces

  • decreased cortical gray matter attenuation with loss of normal gray-white differentiation

  • decreased bilateral basal ganglia attenuation

  • reversal sign: reversal of the normal CT attenuation of grey and white matter, demonstrated within the first 24 hours in a small number of these patients (case 2)

  • it has been proposed that this finding is due to the distension of deep medullary veins secondary to partial obstruction of venous outflow from the elevated intracranial pressure caused by diffuse oedema

  • the result is that the cerebral white matter is of higher attenuation than the cortical gray matter

  • white cerebellum sign: has been described in at least one study as a component of the reversal sign and in which there is diffuse oedema and hypoattenuation of the cerebral hemispheres with sparing of the cerebellum and brainstem, resulting in apparent high attenuation of the cerebellum and brainstem relative to the cerebral hemispheres

  • linear hyperdensity outlining the cortex as well as linear cortical enhancement (later and less evident signs) correspond to cortical laminar necrosis

  • falx cerebri and tentorium cerebelli can appear hyperdense to ischaemic brain parenchyma and is one of the causes of pseudo-subarachnoid haemorrhage

  • Both the reversal sign and the white cerebellum sign indicate severe injury and a poor neurologic outcome 

Treatment

Cardiac

  • TTE to rule out LV thrombus or LA thrombus IF MRI is negative then we recommend this as outpatient workup

  • EKG

  • Lipid panel, LDL goal < 70

Gastrointestinal

  • Swallow screen

Endocrine

  • Hemoglobin A1C

Neuro​

  • no tPA if receiving anticoagulation

  • Load with 325mg of Aspirin

  • Start Aspirin 81mg daily
    -CTA head and neck to r/o any flow limiting stenosis
    -MRI Brain w/o contrast to r/o ischemia

... but I would more especially commend the clinician who, in acute diseases, by which the bulk of mankind are cutoff, conducts the treatment better than others.
 
Hippocrates, 400 BC