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Transient ipsilateral mydriasis following carotid artery stenting
Evan Luther1, Emily Swafford1, Vasu Saini1
1Department of Neurological Surgery, University of Miami Miller School of Medicine, Miami, FL, USA.
Insights
Transient mydriasis (pupil dilation) after carotid stenting is a rare but possible complication. This case highlights that it can be benign and resolve on its own, even without neurological deficits.
Area of Science:
- Neurology
- Vascular Surgery
- Ophthalmology
Background:
- Hyperperfusion hemorrhage is a feared complication of carotid revascularization.
- Ipsilateral mydriatic pupil after carotid endarterectomy (CEA) or stenting (CAS) warrants neurosurgical evaluation for hyperperfusion injury.
Observation:
- A case of benign, transient ipsilateral mydriasis following CAS is presented.
- The patient developed anisocoria with a poorly reactive pupil post-procedure.
- Imaging revealed no acute pathology, and symptoms resolved spontaneously within 48 hours.
Findings:
- The mydriasis was attributed to transient ischemia of parasympathetic structures in the internal carotid artery (ICA) due to device placement.
- Sympathetic stimulation during angioplasty is also a potential cause.
Implications:
- While ipsilateral mydriasis requires assessment after carotid revascularization, it can be a self-limiting condition.
- This finding is particularly true when no other focal neurological deficits are present.
Background And Importance:
One of the most feared and devastating complications of carotid revascularization procedures is hyperperfusion hemorrhage. The acute onset of an ipsilateral mydriatic pupil following carotid endarterectomy (CEA) or carotid artery stenting (CAS) should prompt immediate neurosurgical evaluation to rule out hyperperfusion injury.
Clinical Presentation:
We describe a case of benign, transient ipsilateral mydriasis following CAS. After undergoing right common and internal carotid artery (ICA) angioplasty and stenting with distal embolic protection, the patient developed anisocoria with a right-sided 5 mm minimally reactive pupil. Imaging demonstrated no acute pathology, and the mydriasis resolved spontaneously within 48 hours. We hypothesise that the pathophysiologic mechanism is secondary to transient ischemia of parasympathetic structures within the petrous/cavernous ICA from arterial ostium occlusion that occurred during device placement. Alternatively, sympathetic stimulation during angioplasty is also plausible.
Conclusions:
Although an ipsilateral mydriatic pupil following carotid revascularization necessitates evaluation, it may represent a self-limiting process especially in the absence of other focal neurologic deficits.
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