INPATIENT WORKUP OF STROKE
To many, stroke admissions are not very exciting: it’s formulaic with the same tests ordered every time. But if you understand the reason behind the tests, it becomes much more interesting! Let’s explore together.
#neurology #meded #stroke #FOAMed
To many, stroke admissions are not very exciting: it’s formulaic with the same tests ordered every time. But if you understand the reason behind the tests, it becomes much more interesting! Let’s explore together.
#neurology #meded #stroke #FOAMed
Back in the 1990s, there was a study called the TOAST trial that categorized strokes by mechanism. That framework is very helpful to this day and I’ll be using it here.
This thread will focus on the most common cause: large artery atherosclerosis (LAA)
This thread will focus on the most common cause: large artery atherosclerosis (LAA)
PATHOPHYSIOLOGY
LAA is caused by the same common pathway that often causes other vascular diseases including MIs and PVD: atherosclerosis.
Risk factors include anything that causes vessel trauma: HTN, diabetes, smoking, FHx, and of course high LDL.
LAA is caused by the same common pathway that often causes other vascular diseases including MIs and PVD: atherosclerosis.
Risk factors include anything that causes vessel trauma: HTN, diabetes, smoking, FHx, and of course high LDL.
Large vessel disease occurs in vessels that have names, as a general rule (eg ICA, vertebral arteries, MCA, PCA), and can be intracranial or extracranial.
Some sub-mechanisms include:
- Plaque rupture and occlusion
- Athero-embolism
- Dissection
Some sub-mechanisms include:
- Plaque rupture and occlusion
- Athero-embolism
- Dissection
DIAGNOSIS
LAA is diagnosed based on imaging characteristics, both of the stroke itself and the blood vessels. The latter is critical for management, meaning we need vessel imaging to work it up.
Options include:
- CTA (preferred)
- MRA
- Carotid ultrasound
LAA is diagnosed based on imaging characteristics, both of the stroke itself and the blood vessels. The latter is critical for management, meaning we need vessel imaging to work it up.
Options include:
- CTA (preferred)
- MRA
- Carotid ultrasound
Generally speaking, CTA/MRA is better than ultrasound because you can evaluate the posterior circulation (ie vertebral, basilar, and PCAs) and intracranial vessels.
Carotid ultrasound can provide additional data on plaque characteristics, but it’s a more narrow-use test.
Carotid ultrasound can provide additional data on plaque characteristics, but it’s a more narrow-use test.
Generally speaking, LAA is going to cause either full-territory or embolic-appearing strokes confined to a single vascular territory. There are exceptions (such as athero-embolism “jailing” a small vessel causing a lacunar appearance) but this is a good rule of thumb.
TREATMENT
Depends on the location. For intracranial atherosclerotic disease (ICAD), trials have shown superiority in (initial) optimal medical management over surgical.
We always want to control vascular risk factors and in particular LDL, usually warranting statin therapy.
Depends on the location. For intracranial atherosclerotic disease (ICAD), trials have shown superiority in (initial) optimal medical management over surgical.
We always want to control vascular risk factors and in particular LDL, usually warranting statin therapy.
You may recall Virchow’s triad, which applies nicely here. Endothelial injury generally requires antiplatelet therapy. In the case of ICAD, we usually do 90 days of dual antiplatelet (eg aspirin and clopidogrel) followed by indefinite single antiplatelet therapy.
What about extracranial disease?
If it’s severe (>70%) and symptomatic (caused a stroke or TIA), studies have shown a benefit of surgical intervention. Select other populations can also benefit.
Options include carotid endarterectomy and stenting.
If it’s severe (>70%) and symptomatic (caused a stroke or TIA), studies have shown a benefit of surgical intervention. Select other populations can also benefit.
Options include carotid endarterectomy and stenting.
What about dissections?
This is a special case because the pathophysiology is often different - it can often be due to trauma.
Studies haven’t shown consistent superiority in single vs dual antiplatelet therapy (or even anticoagulation). Uniquely, they often heal with time.
This is a special case because the pathophysiology is often different - it can often be due to trauma.
Studies haven’t shown consistent superiority in single vs dual antiplatelet therapy (or even anticoagulation). Uniquely, they often heal with time.
SUMMARY
- Pathophysiology: atherosclerosis
- Diagnosis: vessel imaging (eg CTA)
Look especially for single-territory
infarcts
- Treatment:
> Intracranial: (dual) antiplatelet
> Extracranial: CEA or stenting
Plus traditional vascular risk factor management
- Pathophysiology: atherosclerosis
- Diagnosis: vessel imaging (eg CTA)
Look especially for single-territory
infarcts
- Treatment:
> Intracranial: (dual) antiplatelet
> Extracranial: CEA or stenting
Plus traditional vascular risk factor management
See part two on small vessel disease here ⬇️
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