Embolic Stroke of Undetermined Source (ESUS) Criteria

ESUS Criteria

Non-lacunar Stroke on Imaging

No Extracranial or Intracranial Atherosclerosis ≥50%

No Major Cardioembolic Source

No Other Specific Cause Identified

Criteria Met: 0 / 4

ESUS Criteria Not Met

0 of 4 criteria met. All criteria must be present for ESUS diagnosis. Review for alternative stroke etiologies based on unmet criteria.

Diagnoses embolic stroke of undetermined source.

Why Use

Defines cryptogenic stroke based on criteria, rather than from the absence of available test results. Outlines sufficient diagnostic workup in ischemic strokes of unclear etiology not previously described. The prior TOAST stroke classification , a diagnosis of exclusion, classifies a high proportion of strokes as cryptogenic. Enables standardized diagnostic criteria for clinical trials. Used in many ongoing randomized controlled trials studying secondary stroke prevention in patients with cryptogenic strokes.

When to Use

Patients with ischemic stroke of unclear etiology.

Formula

Selection of the appropriate criteria (all 4 must be present): Ischemic stroke detected by CT or MRI that is not lacunar*. Absence of extracranial or intracranial atherosclerosis causing ≥50% luminal stenosis in arteries supplying the area of ischemia. No major risk cardioembolic source of embolism**. No other specific cause of stroke identified (e.g. arteritis, dissection, migraine/vasospasm, drug abuse). Note: diagnosis of ESUS requires a minimum diagnostic evaluation, including cardiac monitoring for >24 hours with automated rhythm detection, in addition to the above criteria. *Lacunar = subcortical infarct ≤1.5 cm (≤2.0 cm on MRI diffusion images) in largest dimension, including on MRI diffusion-weighted images, and in distribution of small, penetrating cerebral arteries of cerebral hemispheres and pons. **Permanent or paroxysmal atrial fibrillation, sustained atrial flutter, intracardiac thrombus, prosthetic cardiac valve, atrial myxoma or other cardiac tumors, mitral stenosis, recent (<4 weeks) MI, left ventricular ejection fraction <30%, valvular vegetations, or infective endocarditis.

Pearls / Pitfalls

Diagnosis of ESUS can be established after sufficient evaluation, including long-term cardiac monitoring for ≥24 hours, for occlusive large vessel atherosclerosis and high-risk cardioembolic sources in nonlacunar infarcts. Potential low-risk embolic sources are thought to comprise ESUS. Transesophageal echocardiography (TEE) is not required in ESUS; thus, aortic arch atherosclerosis (shaggy aorta) evaluation is not included. Studies used to develop ESUS were in predominantly Caucasian populations. An unknown proportion of ESUS patients may have non-embolic stroke mechanisms.

Management

Depending on clinical suspicion, further evaluation may include any of the following: Prolonged outpatient cardiac monitoring. TEE. Cardiac MRI. Transcranial Doppler with monitoring for emboli. Catheter angioplasty. Workup for occult cancer. Workup for non-embolic causes such as vasculitis. Secondary prevention in all noncardioembolic ischemic strokes includes anti-platelet therapy, blood pressure control, anti-lipid therapy, and lifestyle modifications. The benefit of anticoagulation therapy in ESUS without proven atrial tachyarrhythmia is unclear and the subject of ongoing clinical trials. Certain patients aged ≤60 years with ESUS and patent foramen ovale (PFO) may benefit from percutaneous PFO closure in addition to antiplatelet therapy. In patients with recurrent ESUS, switching antiplatelet agents or starting empiric anticoagulation therapy is reasonable.

Critical Actions

All ischemic strokes undergo the same acute therapy management regardless of etiology, including intravenous tPA or mechanical thrombectomy if indicated.

Advice

Strokes that meet ESUS criteria are thought to be due to sources of uncertain risk, including: Minor-risk potential cardioembolic sources. Occult paroxysmal atrial fibrillation. Undiagnosed malignancy. Arteriogenic emboli such as aortic arch atherosclerotic plaques or non-stenotic cerebral arteries. Paradoxical embolism through an atrial septal defect.