Hollenhorst Plaques
Title: Hollenhorst Plaque
Author (s): Beau Sylvester, BS, MSIV
Author Email: beausylvester@wustl.edu
Photographer: Lisa A. Messegee
Date: 8/29/22
Keywords/Main Subjects: Hollenhorst plaque, branch retinal artery occlusion, central, painless vision loss, embolus, stroke
Diagnosis: Branch Retinal Artery Occlusion
Description of Case: This is a basic ophthalmology review article on Hollenhorst plaques. Included are photos from a case of a branch retinal artery occlusion, demonstrating a Hollenhorst plaque visible on the color photo, with the corresponding retinal angiography imaging.
Images or video:
Figure A. Color fundus photo of a patient presenting with acute, superior central vision loss in the left eye. Arrow indicates a Hollenhorst plaque at the bifurcation of an inferior branch of the central retinal artery. Note the whitening of the retina downstream from the Hollenhorst plaque, indicating acute swelling and edema of the inner layers of the retina secondary to infarction.
Figure B. Fluorescein angiography of the same patient with a Hollenhorst plaque and acute vision loss. Arrow indicates silhouetted arterioles distal to the embolus with absent filling of fluorescein dye.
Summary of the Case: Images in this article are of a patient presenting with acute monocular vision loss in the left eye due to branch retinal artery occlusion by a Hollenhorst plaque.
Overview
Hollenhorst plaques are yellow, refractile cholesterol emboli that lodge in retinal arterioles and may lead to hypoperfusion of retina and corresponding vision loss.
Pathophysiology
Cholesterol emboli typically break off from atherosclerotic plaques of the carotid artery or aortic arch. The ophthalmic artery, which gives rise to the central retinal artery, is the first branch of the internal carotid artery (ICA), and atherosclerotic stenosis of the ipsilateral ICA is often suspected on detection of Hollenhorst plaques.[1] When a large embolus completely obstructs the proximal central retinal artery, the resulting central retinal artery occlusion (CRAO) may lead to complete vision loss in that eye. Occasionally, patients with a CRAO will have a small island of vision preserved from a collateral blood source from the cilioretinal artery which brances off the ophthalmic artery as well but separately from the central retinal artery. The embolus can get dislodged and allow reperfusion of part versus all of the retina and the resultant vision loss is transient. Emboli may embed in branches of the central retinal artery, often at bifurcations, causing branch retinal artery occlusion (BRAO) with a resulting patch of vision loss in that eye (Figure A).
Figure A: Emboli may embed in branches of the central retinal artery, often at bifurcations, causing branch retinal artery occlusion (BRAO) with a resulting patch of vision loss in that eye
Presentation
Hollenhorst plaques may be discovered in patients presenting with painless monocular vision loss due to CRAO or BRAO. However, asymptomatic emboli are not uncommon, with the Blue Mountains Eye study demonstrating a prevalence of retinal emboli in 1.4% of the population above the age of 49, 80% of which were Hollenhorst plaques.[2] The Beaver Dam Eye study demonstrated a similar prevalence and found that, after controlling for age, sex, and vascular risk factors, patients with retinal emboli were more likely to die with stroke listed as a cause.[3] In addition, a pooled analysis of both the Blue Mountains and Beaver Dam Eye studies demonstrated higher all-cause mortality over 10 to 12 years in patients with retinal emboli (56%) compared to those without (30%).[4]
Workup
Fluorescein angiography (FA) may be ordered to identify areas of hypoperfusion, with delayed arterial filling (Figure B) and arteriovenous transit time expected soon after retinal artery occlusion. Patients with Hollenhorst plaques with or without symptoms are at risk of carotid occlusive disease and should undergo duplex carotid ultrasonography to evaluate for stenosis and potential need for stenting or endarterectomy.1
Figure B: Fluorescein angiography (FA) may be ordered to identify areas of hypoperfusion, with delayed arterial filling.
Differential Diagnosis
Retinal artery occlusion should be differentiated from other causes of monocular vision loss. Giant cell arteritis can cause amaurosis fugax or transient vision loss that may progress to permanent vision loss, and workup should include erythrocyte sedimentation rate (ESR)/c-reactive protein (CRP) and assessment for polymyalgia rheumatica, with temporal artery biopsy indicated for high-risk patients.
Although Hollenhorst plaques account for 80% of retinal emboli, other types of emboli may be observed in retinal arterioles.[5] Calcific emboli are dull (non-refractile), white deposits that may break off from heart valve calcifications and appear hyperreflective with optical shadowing on optical coherence tomography (OCT).[6] Platelet-fibrin emboli are elongated, non-refractile, grey-white material observed occupying a segment of retinal arteriole discontinuously and may originate from carotid atheromatous disease or heart valve vegetations.[7] Talc and corn starch emboli are highly refractile, white/yellow particles that may occur as a result of intravenous use of crushed oral medications.[8] Fat emboli after trauma and long bone fracture can cause Purtscher’s retinopathy, with cotton wool spots and hemorrhages surrounding the optic nerve.[9] Although Roth spots (white-centered retinal hemorrhages) were once thought to be septic emboli from endocarditis, more recent histological evidence has shown that these non-specific lesions are fibrin thrombi rather than bacterial abscesses.[10]
Management
Aside from imaging and screening and treatment of vascular risk factors for secondary prevention, treatment of retinal artery occlusion is controversial, with various management strategies and no randomized controlled trials to inform care. There is some evidence to support treatment of CRAO similarly to other strokes with tissue plasminogen activator (tPA) within 4.5 hours of vision loss.[11]
References:
[1] Bakri SJ, Luqman A, Pathik B, Chandrasekaran K. Is carotid ultrasound necessary in the evaluation of the asymptomatic Hollenhorst plaque? Ophthalmology. 2013;120(12):2747-2748.e1.
[2] Mitchell P, Wang JJ, Li W, Leeder SR, Smith W. Prevalence of asymptomatic retinal emboli in an Australian urban community. Stroke. 1997; 28:63–66.
[3] Klein R, Klein BE, Moss SE, Meuer SM. Retinal emboli and cardiovascular disease: the Beaver Dam Eye Study. Trans Am Ophthalmol Soc. 2003; 101:173–180, discussion 180.
[4] Wang JJ, Cugati S, Knudtson MD, Rochtchina E, Klein R, Klein BE, Wong TY, Mitchell P. Retinal arteriolar emboli and long-term mortality: pooled data analysis from two older populations. Stroke. 2006;37(7):1833-6.
[5]Kaufman EJ, Mahabadi N, Patel BC. Hollenhorst Plaque. StatPearls [Internet] Updated 2022. Available at https://www.ncbi.nlm.nih.gov/books/NBK470445. Accessed September 1, 2022.
[6] Shah VA, Wallace B, Sabates NR. Spectral domain optical coherence tomography findings of acute branch retinal artery occlusion from calcific embolus. Indian J Ophthalmol. 2010;58(6):523-4.
[7] Wijman CA, Babikian VL, Matjucha IC. Monocular visual loss and platelet fibrin embolism to the retina. J Neurol Neurosurg Psychiatry. 2000;68(3):386-7.
[8] AtLee WE Jr. Talc and cornstarch emboli in eyes of drug abusers. JAMA. 1972;219(1):49-51.
[9] Mishra SK, Sharma V, Kamal VKBM, Kumar A. Purtscher’s retinopathy. QJM. 2020;113(7):495-496.
[10] Ling R, James B. White-centred retinal haemorrhages (Roth spots). Postgrad Med J. 1998;74(876):581-2.
[11] Mac Grory B, Schrag M, Biousse V, Furie KL, Gerhard-Herman M, Lavin PJ, Sobrin L, Tjoumakaris SI, Weyand CM, Yaghi S; American Heart Association Stroke Council; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Hypertension; and Council on Peripheral Vascular Disease. Management of Central Retinal Artery Occlusion: A Scientific Statement From the American Heart Association. Stroke. 2021;52(6):e282-e294.
Faculty Approval by: Griffin Jardine, MD
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Identifier: Moran_CORE_126041
