INPATIENT STROKE WORKUP
Pt 3: Cardioembolic strokes
In a cardioembolic stroke, a blood clot starts in or passes through the heart but ends up in the brain. It’s managed differently than the other two types we’ve covered. Let’s jump in!
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Pt 3: Cardioembolic strokes
In a cardioembolic stroke, a blood clot starts in or passes through the heart but ends up in the brain. It’s managed differently than the other two types we’ve covered. Let’s jump in!
#neurotwitter #neurology #MedEd #FOAMed
PATHOPHYSIOLOGY
Cardioembolic strokes are generally caused by the other two corners of Virchow’s triad: stasis (eg afib) and hypercoagulability (eg paradoxical embolus from a DVT). Overactivity of secondary coagulation results in a thrombus which can embolize.
Cardioembolic strokes are generally caused by the other two corners of Virchow’s triad: stasis (eg afib) and hypercoagulability (eg paradoxical embolus from a DVT). Overactivity of secondary coagulation results in a thrombus which can embolize.
Some of the more important causes include:
- afib/aflutter
- paradoxical embolism via patent foramen ovale (PFO)
- ventricular thrombus
- afib/aflutter
- paradoxical embolism via patent foramen ovale (PFO)
- ventricular thrombus
IMAGING
The thrombi from cardioembolic strokes are typically larger than atheroembolic strokes (see pt 1) meaning the strokes generally fall in large vessel territories (not lacunes).
The unique feature is that it can hit any vascular territory, left/right/anterior posterior.
The thrombi from cardioembolic strokes are typically larger than atheroembolic strokes (see pt 1) meaning the strokes generally fall in large vessel territories (not lacunes).
The unique feature is that it can hit any vascular territory, left/right/anterior posterior.
Sometimes you will see strokes of different ages on MRI, suggesting the heart is flinging out multiple clots over a period of time. When these fall in variable vascular territories, it strongly suggests a central (cardio) embolic source.
DIAGNOSIS
To detect these strokes, we use two types of tools: electrical (EKG with/without ambulatory monitoring) and structural (TTE +/- TEE).
To detect these strokes, we use two types of tools: electrical (EKG with/without ambulatory monitoring) and structural (TTE +/- TEE).
TTEs are good at excluding ventricular thrombi but don’t get a good look at the left atrial appendage (LAA), which is where 90% of clots form in afib.
It can also show chronic atrial disease, low ejection fraction, valvular issues, and other thrombogenic conditions.
It can also show chronic atrial disease, low ejection fraction, valvular issues, and other thrombogenic conditions.
While getting a TTE, we almost always inject agitated saline contrast to look for a PFO. If no PFO is seen, we can usually exclude paradoxical embolus. If we see one, we may have to go DVT hunting in the limbs and pelvis via ultrasound and/or MRV/CTV.
If we have a high suspicion for either LAA thrombus or PFO, obtaining a TEE is a more sensitive test. It’s more invasive and isn’t considered standard care, but it can be important in unclear cases.
Afib can be detected as easily as via a simple EKG, but interpretation is tricky. What if they were only in afib for a few minutes secondary to heart strain from the stroke? Or what if they are back in NSR?
All stroke patients should have cardiac monitoring while inpatient.
All stroke patients should have cardiac monitoring while inpatient.
Afib is often paroxysmal and statistically you often won’t catch it while inpatient. These patients need prolonged, ambulatory cardiac monitoring. We have lots of possible devices, from a sticker to an implantable monitor.
TREATMENT
Most afib patients require chronic anticoagulation, and this is doubly true for stroke patients. Studies have shown superiority in DOACs (eg apixaban) over warfarin. If patients have contraindications to chronic AC, a LAA occlusive device gets almost the same benefit.
Most afib patients require chronic anticoagulation, and this is doubly true for stroke patients. Studies have shown superiority in DOACs (eg apixaban) over warfarin. If patients have contraindications to chronic AC, a LAA occlusive device gets almost the same benefit.
The decision to cardiovert is another important one. Options include both chemical and electrical cardioversion and generally requires either short term anticoagulation or a TEE to exclude thrombus.
Generally, this decision is up to the cardiologist.
Generally, this decision is up to the cardiologist.
Should you close a PFO?
Not necessarily. About 20% of the population has a PFO. Most strokes, even in patients with a PFO, were probably from something else.
The decision to close one is based off of size, imaging, patient age and risk, and scoring tools (eg RoPE score).
Not necessarily. About 20% of the population has a PFO. Most strokes, even in patients with a PFO, were probably from something else.
The decision to close one is based off of size, imaging, patient age and risk, and scoring tools (eg RoPE score).
Ventricular thrombi and valvular afib generally require warfarin over DOACs, which comes with all the typical headaches of warfarin management for both patient and provider.
SUMMARY:
- Imaging: strokes in multiple territories
- Workup: TTE with bubble, cardiac monitoring, +/- TEE
- Management
> Afib: AC (DOAC preferred) vs LAA occlusion
> PFO: refer for closure if high risk
> Ventricular thrombus: warfarin
- Imaging: strokes in multiple territories
- Workup: TTE with bubble, cardiac monitoring, +/- TEE
- Management
> Afib: AC (DOAC preferred) vs LAA occlusion
> PFO: refer for closure if high risk
> Ventricular thrombus: warfarin
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