Hollenhorst Plaque


Article Author:
Evan Kaufman
Navid Mahabadi


Article Editor:
Bhupendra Patel


Editors In Chief:
Chaddie Doerr


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
6/23/2019 1:08:05 PM

Introduction

Stroke is the third most common cause of death in the United States. Eighty percent of all strokes are due to occlusion of a vessel secondary to atherothrombosis or embolus. Hollenhorst plaques were discovered in 1961 by Dr. Robert Hollenhorst. He defined them as emboli cause by plaques of cholesterol. The appearance of these emboli indicate that they are yellow, refractile, and typically located at an arterial bifurcation.[1][2]

Etiology

Hollenhorst plaques tend to originate from carotid arteries or the aorta. This finding is consistent with carotid disease originating from atherosclerotic lesions. The initial assumption, among eye care providers, upon discovering a Hollenhorst plaque is that it originated from the stenosed, ipsilateral internal carotid artery. The direct anatomical route between the internal carotid artery (ICA) and central retinal artery (CRA) supports this assumption. The ophthalmic artery is the first branch of the ICA, which then leads into the CRA.[3][4]

Epidemiology

The Blue Mountains Eye study stated the prevalence of retinal emboli is 1.4% in the general population older than 49 years old. The prevalence increases with age. Retinal emboli are significantly more prevalent in men than in women. Hollenhorst plaques make up the majority of the retinal emboli at 80%. An estimated 10% of carotid emboli reach the retinal arteries.[5]

Pathophysiology

Ulcerated plaques just distal to the bifurcation of the common carotid artery into its external and internal branches may be a source of retinal emboli that can be asymptomatic or produce transient monocular blindness.[6][7]

A Hollenhorst plaque is a clinical sign. It is commonly a contributing factor in the diagnosis of retinal artery occlusion (RAO). In order for a Hollenhorst plaque to cause an RAO, the plaque must completely obstruct the vessel. RAOs can occur in the central retinal artery (CRAO) or one of its branches (BRAO). Hollenhorst plaques are only one possible cause of a CRAO/BRAO and should not be thought of as synonymous. As discussed in the differential diagnoses, other types of emboli exist with the ability to occlude. There are also non-embolic causes of retinal artery occlusion including nocturnal arterial hypotension and transient vasospasm. Hollenhorst plaques, like other types of retinal emboli, may not stay in one place. The plaque may dislodge and move to a smaller diameter vessel before it gets lodged again, or the plaque may dissolve completely. The presence of a Hollenhorst plaque is a confirming diagnosis; however, the absence of a plaque does not rule out the possibility of embolic occlusion.

If an RAO takes place, the most common symptom is sudden, painless vision loss. The fundus will display typical ischemic signs such as retinal whitening around the occluded vessel. The macular area will remain “cherry-red” due to its secondary outer retinal blood supply.If the plaque is only partially occluding the vessel, blood can still flow through the lumen, and no damage is currently occurring. This partial occlusion is what was taking place with our patient. This does not mean an RAO cannot occur in the future. A single eye can undergo more than one transient RAO as documented by Hayreh et al. in their clinical study of over 250 patients. Unfortunately, what the literature shows is that asymptomatic Hollenhorst plaques are a poor predictor of future embolic events.

History and Physical

Hollenhorst plaques serve as markers of past emboli events but are poor predictors of future events. These plaques may or may not cause an RAO. The discovery of asymptomatic emboli has a greater concern for a patient’s systemic health than visual health.

Statistics

The prevalence increased with age: 0.8% visible in participants ages 49 to 60, 1.4% in ages 60 to 69, 2.1% in ages 70 to 79. This prevalence then dropped to 1.5% in the population over 80 years old.

Retinal emboli were significantly more prevalent in men compared to women: 67%. The presentation of a single embolism (88%) was more prevalent than a presentation of multiple emboli (12%). Lastly, the majority of the emboli were cholesterol (80%), followed by platelet-fibrin (14%) and calcific (6%).[8]

Evaluation

Ocular testing may involve fluorescein angiography (FA) as a supplemental test. Expected results for an occlusion include: delay in the retinal arterial filling, delayed arteriovenous transit time, and variable amounts of residual retinal circulation. It is very rare to see a complete lack of retinal filling even though the vessel is completely occluded. The choroidal filling should be normal since the occlusion has occurred anterior to the ophthalmic artery. There is also a restoration of retinal circulation within days/weeks after an RAO via anastomoses with the central retinal artery; therefore, an FA is of little benefit if delayed.[4][9]

Treatment / Management

Unless a Hollenhorst plaque completely obstructs a vessel causing an RAO, no ocular treatment is necessary. All patients with retinal emboli should be referred to the patient’s primary care provider for bilateral carotid duplex. Ocular testing may involve fluorescein angiography (FA) as a supplemental test.[10][11]

Differential Diagnosis

Calcific emboli:  White, dull (non-refractile), due to their larger size typically found in the central retinal artery close to the optic disc. This finding is consistent with cardiac disease originating from heart valve calcifications.

Platelet-fibrin emboli: White/gray, dull (non-refractile), elongated. This can be a finding for both cardiac and carotid disease; however, cholesterol emboli are more common in carotid disease.

Talc emboli­: Small, white/yellow, highly refractile, typically located in the macular region. This finding is associated with intravenous drug abuse.

Lipid/fat emboli:  Usually cannot visualize the emboli, cotton wool spots are often seen. This finding is associated with long bone fractures and chest trauma, i.e., Purtscher retinopathy.

Tumor cells: These proliferative neoplastic cells which can fall off the main the main lesion and lodge in the retinal arterioles.

Septic emboli:  These deposits are associated with bacterial endocarditis

Prognosis

Atheromatous disease of the internal carotid artery can be associated with these Hollenhorst plaques and is usually an indicator of potential stroke. Carotid stenosis increase in stroke risk as 1.18 times for every 10% increase in stenosis. This risk of stroke rises less than 1% per year for a vessel that is less than 80% stenosed. Whereas a vessel that is greater than 90% stenosed rises at 4.8% per year.

Complications

The most common complication is a stroke.

Pearls and Other Issues

Cholesterol emboli aka Hollenhorst plaque:  Yellow, refractile, typically located at the  carotid artery bifurcation. They tend to originate from carotid arteries or the aorta. This finding is consistent with carotid disease originating from atherosclerotic lesions.

  • Hollenhorst plaques are considered to be the most common form of emboli
  • Hollenhorst plaques are a common finding in the aging population
  • Approximately 75% of Hollenhorst plaques seen in ophthalmic practice are asymptomatic

 

 

Enhancing Healthcare Team Outcomes

Even though there are several other causes of hollenhorst bodies, the most worrisome diagnosis is that of atherosclerosis of the internal carotid artery. Often the presence of a hollenhorst body is indicative of an impending stroke, especially in older individuals. Once a hollenhorst body has been diagnosed the management is multidisciplinary involving a neurologist, ophthalmologist, cardiologist, vascular surgeon, interventional radiologist, nurse, and a pharmacist. The patient should undergo a duplex ultrasound of the neck to determine the presence of atherosclerotic disease at the carotid bifurcation. If the lesion is ulcerated and more than 70% stenosis, the patient should be referred to the vascular surgeon or an interventional radiologist for stenting. The patient should be encouraged to lower his blood pressure and cholesterol, discontinue smoking and take an aspirin while awaiting surgery. The nurse should educate the patient on the possible symptoms of a stroke and when to return to the emergency room. When patients with carotid artery atherosclerosis are managed with elective surgery or stenting, the morbidity and mortality rates are less than 3%. [4][9](Level V)


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    Contributed by Dr. Evan J Kaufman, OD FAAO The university of Virginia, Department of Ophthalmology
Attributed To: Contributed by Dr. Evan J Kaufman, OD FAAO The university of Virginia, Department of Ophthalmology

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Hollenhorst Plaque - Questions

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A 66-year-old male has a Hollenhorst plaque. This plaque is composed of which of the following?



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What is the etiology of a Hollenhorst plaque?

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Which is the most appropriate test done after identifying a retinal Hollenhorst plaque?



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In a patient with emboli from the internal carotid artery to the ophthalmic artery, what will the fundoscopic exam reveal?

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A 71-year old presents to the clinic with complaints of sudden vision loss in his left eye. The episode lasted 45 seconds and felt like a curtain come over his eye. While awaiting for more studies, the ophthalmology resident assesses his eye. Microscopy of the lesion shown in the image will usually reveal?

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    Contributed by Dr. Evan J Kaufman, OD FAAO University of Virginia, Department of Ophthalmology
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82-year-old male presents to the clinic complaining of loss of vision in his right eye. Patients state that he woke up yesterday and noticed he could not see out of his right eye. Patient denies pain, flashes of light, and floaters. The patient has a past medical history of diabetes mellitus type 2, hypertension, peripheral arterial disease, and hyperlipidemia. On indirect ophthalmoscopy, the patient's fundus appears pale accompanied with a "cherry red" dot in the macula. What is the most likely underlying pathophysiology causing this patients ocular symptoms?



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82-year-old male presents to the clinic complaining of loss of vision in his right eye. Patients state that he woke up yesterday and noticed he could not see out of his right eye. Patient denies pain, flashes of light, and floaters. The patient has a past medical history of diabetes mellitus type 2, hypertension, peripheral arterial disease, hyperlipidemia, and transient ischemic attacks. Before the examination ends, the patient experiences a massive stroke and collapses onto the floor. He is rushed to the ED and passes away. On autopsy, the pathologist finds yellow emboli lodged in the central retinal artery that most likely explains the patient's ocular symptoms. What are the most likely composition and source of this emboli?



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75-year-old female presents to the clinic complaining of loss of vision in her left eye. Patients state that she occasionally loses vision in her eyes but it usually self resolves within 20 minutes. Yesterday she woke up and noticed she could not see out of her left eye and it has not self-resolved. She denies pain, flashes of light, and floaters. The patient has a past medical history of diabetes mellitus type 2, hypertension, peripheral arterial disease, hyperlipidemia, and amaurosis fugax. What is the most likely biochemical composition of the inciting embolism?

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A 65-year-old man with 20/20 visual acuity in both eyes was referred to the emergency room after presenting with an incidental finding in the left eye during a routine ophthalmic examination. Fluorescein angiography revealed significantly delayed vascular filling in his left eye with normal filling in his right eye. The patient agreed to be evaluated immediately in a local emergency room. There, the patient was found to have >90% proximal, left internal carotid artery narrowing. The patient underwent urgent vascular surgery with left internal carotid endarterectomy. The patient recovered rapidly and has remained asymptomatic. Four months later, fluorescein angiography revealed significantly normalized vascular filling of his left retinal circulation. What was the underlying pathophysiologic cause of the delayed vascular filling?



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A 75-year-old male presents for a routine ophthalmic exam complaining of episodes of transient, painless vision loss in his left eye. These episodes occur and resolve within a 15-minute timeframe. The patient current vision is 20/20 in both eyes. On fluorescein angiography, there is a vascular filling defect in the symptomatic left eye. The ophthalmologist suspects a Hollenhorst plaque that is lodged in the left central retinal artery. What is the next most appropriate step?



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Hollenhorst Plaque - References

References

Majstruk L,Giocanti-Aurégan A, [Multimodal imaging of a Hollenhorst plaque]. Journal francais d'ophtalmologie. 2016 Sep     [PubMed]
Coca MN,Palau AE,Morgan ML,Lee AG, Embolic anterior ischemic optic neuropathy associated with a Hollenhorst plaque. JAMA ophthalmology. 2015 Feb     [PubMed]
Lawlor M, Bakri et al.: is carotid ultrasound necessary in the evaluation of the asymptomatic Hollenhorst plaque? (Ophthalmology 2013;120:2747-8). Ophthalmology. 2014 Sep     [PubMed]
Bakri SJ,Luqman A,Pathik B,Chandrasekaran K, Is carotid ultrasound necessary in the evaluation of the asymptomatic Hollenhorst plaque? Ophthalmology. 2013 Dec     [PubMed]
Tokoyoda T,Tsujimoto I,Sugiura Y,Sezaki R, A hollenhorst plaque in cholesterol crystal embolism. Internal medicine (Tokyo, Japan). 2012     [PubMed]
Saric M,Kronzon I, Cholesterol embolization syndrome. Current opinion in cardiology. 2011 Nov     [PubMed]
Wolintz RJ, Carotid endarterectomy for ophthalmic manifestations: is it ever indicated? Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society. 2005 Dec     [PubMed]
Chawluk JB,Kushner MJ,Bank WJ,Silver FL,Jamieson DG,Bosley TM,Conway DJ,Cohen D,Savino PJ, Atherosclerotic carotid artery disease in patients with retinal ischemic syndromes. Neurology. 1988 Jun     [PubMed]
Dunlap AB,Kosmorsky GS,Kashyap VS, The fate of patients with retinal artery occlusion and Hollenhorst plaque. Journal of vascular surgery. 2007 Dec     [PubMed]
Schwarcz TH,Eton D,Ellenby MI,Stelmack T,McMahon TT,Mulder S,Meyer JP,Eldrup-Jorgensen J,Durham JR,Flanigan DP, Hollenhorst plaques: retinal manifestations and the role of carotid endarterectomy. Journal of vascular surgery. 1990 May     [PubMed]
Bunt TJ, The clinical significance of the asymptomatic Hollenhorst plaque. Journal of vascular surgery. 1986 Dec     [PubMed]

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