Hollenhorst Plaque

A 75-year-old female presented with several days of cloudy vision to her inferior left eye gaze and a dull 3/10 frontal headache, without any nausea, vomiting, or photophobia. She reported having a sharp pain to the same eye several weeks prior, which had since resolved. 

PHYSICAL EXAMINATION AND LABORATORY TESTS

Her past medical history was significant for diabetes, hypertension, hypothyroidism, and a remote smoking history. She appeared younger than her age, had a MMSE of 30/30, and her complete neurologic and physical exam was unremarkable with the exception of her fundus (Figure) and visual testing. Her C-reactive protein level was not elevated, and she had no temporal tenderness or jaw claudication. A brain CT revealed age-related atrophic changes only.

Figure. Hollenhorst plaque in retinal artery.

OUTCOME OF THIS CASE

She was started on enoxaparin, and admitted for an expeditious workup of a possible cerebrovascular accident associated with the Hollenhorst plaque in her left eye. Treatment focuses on the potential improvement of any underlying cardiovascular disease. Our patient was already well managed with respect to her diabetes, hypertension, and lipid profile. 

She was prescribed clopidogrel and discharged the next day to the care of her internal medicine doctor after finding no acute concerns on a brain MRI and echocardiogram. Follow on carotid ultrasound testing would prove significant for 75% blockage of her left carotid artery.

DISCUSSION

Robert Hollenhorst, MD, first identified these bright, refractile, golden yellow plaques in 1961. These cholesterol emboli have usually dislodged from atheroma of the ipsilateral carotid artery or possibly the aortic arch, and often lodge at the bifurcation of retinal arteries. The cholesterol emboli are somewhat malleable, allowing blood flow past the blockage, thus they rarely result in permanent retinal injury.¹ 

Considered an ominous indicator of a potential stroke or TIA, there is a direct correlation with symptomatic emboli (transient monocular vision loss or amarousis fugax) and carotid artery disease. An expeditious workup for the source of the thrombi should be initiated to include possible cardiac, hematologic, and extracranial arteriosclerotic disease possibilities.^2,3 However, an association to significant carotid disease in an incidentally found Hollenhorst plaque in an asymptomatic eye is less clear, and may not be a particularly good predictor of future CVA issues.^4,5

All opinions expressed in this manuscript are those of the authors and do not reflect upon the official policy of BUMED, Navy Department, and/or Department of Defense.

References

1.Miller NR. Embolic causes of transient monocular visual loss: Appearance, source, and assessment. In: Ophthalmology Clinics of North America. Katz B (ed). Philadelphia: W.B. Saunders; 1996:359.

2.Loftus CM. Carotid Endarterectomy: Principles and Technique. 2nd edition. Informa Health Care; 2006:7.

3.Adams HP, Hachinski V, Norris JW. Ischemic Cerebrovascular Disease. Oxford University Press; 2001:65-66.

4.Dunlap AB, Kosmorsky GS, Kashyap VS. The fate of patients with retinal artery occlusion and Hollenhorst plaque. J Vasc Surg. 2007;46(6):1125-1129.

5.Bunt TJ. The clinical significane of the asymptomatic Hollenhorst plaque. J Vasc Surg. 1986;4(6):559-562.