Ischemic events to the eye can occur after cervical carotid dissections.1 Ocular vaso-occlusions usually occur within 1 month after the onset of dissection. We report a case of traumatic common carotid occlusion, presumably caused by dissection, which led to an ischemic event to the right eye 4 months after trauma.
A 19-year-old woman complained of acute painless visual loss in her right eye 7 days prior to our examination. Four months earlier, she was involved in a motor vehicle crash as a restrained passenger. She sustained sternal and rib fractures and bilateral pneumothoraces, requiring 2 chest tubes. She did not have any neurological or ocular symptoms and was discharged 1 week after the trauma. Her medical history was notable for sickle cell trait and cigarette use of half a pack per day. She had discontinued her oral contraceptives 1 month prior to the motor vehicle crash.
Visual acuity was 20/40 OD and 20/30 OS, and there was a right relative afferent pupillary defect. Goldmann visual fields showed a superonasal quadrantic defect in the right eye and were full in the left eye. Results of a fundus examination showed a branch retinal artery occlusion of the inferotemporal arcade in the right eye with a partial cherry-red spot (Figure 1). She was complaining of intermittent numbness in her right arm and her radial pulse was decreased on the right side, with asymmetric blood pressures (right arm, 72/51 mm Hg; left arm, 110/61 mm Hg).
Fundus photography shows a branch retinal artery occlusion in the inferotemporal arcade of the right eye. Arrows outline the area of edema resulting from the occlusion.
Carotid ultrasound examinations showed an occlusive thrombus in the right common carotid artery extending into the internal and external arteries. Angiography confirmed total occlusion of the innominate artery with no demonstrable flow in the right carotid system, even in its supraclinoid portion (Figure 2). The eye was most likely supplied by the external carotid artery by retrograde flow from distal branches of the internal maxillary artery and thyrocervical trunks. Warfarin was used as long-term anticoagulation therapy with no further sequelae.
Left, Aortic arch angiogram shows total occlusion of the right innominate artery (arrow). Right, Cerebral angiogram, anteroposterior view, after left internal carotid injection, shows intracerebral flow of right carotid system assumed by the left carotid via the anterior communicating artery and the right posterior communicating artery. The right ophthalmic artery fills from left-sided flow (arrow).
Traumatic dissections can result from multiple nonpenetrating injuries such as motor vehicle crashes, chiropractic manipulation, falls, and hanging.1,2 Dissection of the carotid arteries is an important cause of cerebrovascular ischemic events in young adults,2 and embolism is the most commonly presumed mechanism.
Common carotid dissections are almost always traumatic and can result either from direct trauma or extension of a dissection of the aorta or the innominate artery.3 Our patient most likely had a traumatic innominate and common carotid dissection that led to an internal carotid thrombus and, eventually, an embolus that produced a branch retinal artery occlusion. As our patient was a restrained passenger, with a seat belt over her right shoulder, and was asymptomatic for 4 months, we can only postulate that a dissection was the cause of the thrombosis. An anterograde thrombus occluding the common carotid artery likely progressively extended into the internal carotid artery and eventually reached the level of the ophthalmic artery, with a resultant embolus then lodging in the inferotemporal retinal artery.
Ocular strokes have been reported after carotid dissection. Newman et al1 reported 2 cases of central retinal artery occlusion following previously undiagnosed carotid artery dissection. In 1 of the cases, the patient had been in a motor vehicle crash 1 week prior to his ocular stroke.
Our patient's ischemic event occurred 4 months after her accident. In a prospective series of 80 patients with internal carotid dissection, Biousse et al4 reported that the majority of strokes (82%) occurred in the first 7 days, and the latest occurred 31 days after the first symptoms of dissection. In a retrospective series of 21 patients with traumatic carotid dissection, Mokri2 reported ischemic events in 15 patients (71%), 6 of whom had focal cerebral symptoms 2 months to 10 years after the trauma.
Of interest in our case was the lack of any cervical pain, headache, or Horner syndrome, the most common symptoms in cervical artery dissections.2,4 Acute, painless, monocular vision loss in a young adult can be caused by carotid dissection, either traumatic or spontaneous. The diagnosis of either common carotid or internal carotid dissection should be entertained when a patient is seen with an ocular stroke, even as long as 4 months after trauma.
This work was supported in part by a departmental grant from Research to Prevent Blindness Inc, New York, NY, and CORE grant P30-EYO 6360 from the National Eye Institute, National Institutes of Health, Bethesda, Md.
Corresponding author: Nancy J. Newman, MD, Neuro-Ophthalmology Unit, Emory Eye Center, 1365B Clifton Rd NE, Atlanta, GA 30322 (e-mail: firstname.lastname@example.org).
Godfrey DG, Biousse V, Newman NJ. Delayed Branch Retinal Artery Occlusion Following Presumed Blunt Common Carotid Dissection. Arch Ophthalmol. 1998;116(8):1120-1121. doi: