Introduction: We present three cases of carotid endarterectomy (CEA) followed by postoperative development of ipsilateral mydriasis without referable pathology.

Methods: Three patients were identified who underwent CEA with postoperative ipsilateral mydriasis. A literature review was conducted.

Results: Endarterectomy was offered to each patient for refractory TIA/strokes. Shunting was not utilized in the cases as neuromonitoring remained at baseline. Clamp time was 90 minutes in one case because of complex anatomy (occluded CCA). Post operatively all three of the patients awoke with a dilated, ipsilateral, nonreactive pupil. CT scan did not demonstrate any referable pathology. The patients were otherwise at their neurologic baseline and the mydriasis resolved over the ensuing days. Cases of post CEA Horner’s syndrome with a miotic pupil have been reported, with symptoms attributed to manipulation of the sympathetic plexus along the carotid artery. We report the first 3 cases of mydriasis following CEA.

Conclusions: We hypothesize that these cases are secondary to an ischemic phenomenon, specifically to the ciliary ganglion and/or the oculomotor nerve resulting in parasympathetic dysfunction. Blood supply to these nervous structures is from the ciliary arteries (originating from the ophthalmic artery), and branches off the intracavernous portion of the ICA (inferior cavernous sinus artery and meningohypophyseal artery), respectively. A similar finding of mydriasis following acute carotid injury has been reported, with ischemia also postulated as the etiology. These cases involved carotid dissection, aortic dissection with extension into the carotid, and giant cell arteritis. Ipsilateral pupillary dilation immediately following CEA is worrisome, since it may indicate large reperfusion hemorrhage. However, this post CEA mydriatic phenomenon can be a benign finding. We suggest these three cases, similar to reported cases of acute carotid injury followed by mydriasis, are the result of ischemia to susceptible structures. Whether certain patients undergoing CEA are more prone to this phenomenon remains unclear. Treating physicians should be aware that post CEA mydriasis may result from local ciliary ganglion or oculomotor nerve ischemia, rather than a devastating intracranial event.

Patient Care: This case series increases physician understanding regarding the etiology of pupillary dilation as it relates to carotid endarterectomy or other carotid insult, in addition to proposing a physiologic mechanism.

Learning Objectives: By the conclusion of this session, participants should understand 1) that unilateral mydriasis can occur after carotid endarterectomy or other carotid injury, 2) the proposed etiology of this post CEA mydriasis phenomenon

References: Chen et al., Mydriatic pupil as the presenting sign of aortic dissection. Am J Emerg Med 29:240.e5–240.e7, 2011 Koennecke et al., Mydriatic pupil as the presenting sign of common carotid artery dissection. Stroke 29:2653–2655, 1998 Perry., Horner’s Syndrome After Carotid Endarterectomy: A Case Report. Vasc Endovascular Surg 35:325–327, 2001 Prasad et al., Mydriatic pupil in giant cell arteritis. J Neurol Sci 284:196–197, 2009