Hollenhorst plaque

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Fundus photograph of right retina with labelled ischemic area and cholesterol embolus (“Hollenhorst plaque”)
Right eye findings. a Fundus photo showing superior pale retina. b Presence of Hollenhorst plaque in the superotemporal vessel (arrow)
Hollenhorst plaque
ophthalmoscope) and yellow.[1] This is a medical exam finding, and is not a medical condition, though it may be related to cardiovascular conditions such as atherosclerosis of the internal carotid artery.[1] It was first described by American ophthalmologist Robert Hollenhorst in 1961.[2]

Cause

A Hollenhorst plaque is the result of embolization (breaking off) of cholesterol forming an

atheromatous plaque. This occurs in a blood vessel that is upstream of the eye, such as the internal carotid artery on the same side as the eye (ipsilateral), or the aorta.[1] This cholesterol embolus is then able to travel via the bloodstream to distal (downstream) vessels.[1] When it reaches the tiny blood vessels in the retina of the eye, the plaque may become lodged, where it is visible on eye exam by a physician as a bright crystal (the Hollenhorst plaque).[1] The plaques most commonly lodge at vessel bifurcations, meaning areas where the blood vessel branches into two or more smaller vessels.[1]

Associated conditions

Hollenhorst plaques may cause retinal occlusion, where the plaque blocks blood flow through the retinal vessels, resulting in temporary or permanent vision loss in the affected eye.[1] However, while Hollenhorst plaques do become lodged in retinal arteries, they generally do not fully prevent blood flow so do not cause ischemia.[1] Once a Hollenhorst plaque is discovered in a retinal vessel, it may further migrate and lodge elsewhere, break into smaller pieces, or dissolve and disappear entirely.[1]

While Hollenhorst plaques generally not cause problems with health of the eye, they may be a sign of systemic health issues, particularly of the

peripheral vascular disease).[2] Appearance of retinal plaques is associated with strokes and may be a risk factor for stroke, however because plaques may disappear on their own, discovery of plaques is not predictive of an impending stroke.[2] Risk of death after a stroke may be increased in those who are noted to have Hollenhorst plaques compared to stroke patients who do not.[2] The most common condition associated with appearance of a Hollenhorst plaque is carotid artery disease, including carotid artery stenosis (narrowing of the space inside the vessel).[3]

Management

Standard workup and recommendations

Hollenhorst plaques still require more research, and because of this, there is a wide range of testing that a physician may or may not choose to complete. While there are many possible options, the American Academy of Ophthalmology recommends the following steps be taken when an asymptomatic plaque is first noted.[1]

Other testing and management options

While there is disagreement among medical professionals on what testing is considered necessary, several forms of testing are not shown to be effective in evaluating patients for cardiovascular disease after a retinal cholesterol embolus is found.[1] This recommendation is for patients who do not have any symptoms or concerning past medical history, and testing is ultimately decided by the physician on a case-by-case basis for the individual patient. These include:

  • Daily aspirin. While this is commonly used for prevention of cardiovascular events in high-risk patients, there is currently no evidence to support use of daily aspirin in patients with an asymptomatic Hollenhorst plaque.[1]
  • Referral for
    echocardiogram. This is a test commonly performed; however, much like the carotid Doppler ultrasound, a negative test does not rule out the heart as a potential source of the retinal embolus. This is not part of the standard workup due to the limited research available, but may be ordered for certain patients at the discretion of the primary care physician.[1]
  • Kidney function testing. While Hollenhorst plaques have shown a possible association with chronic kidney disease, testing for kidney function is not routinely recommended. This is because the presentation of kidney disease is often severe and sudden.[1] While patients should be screened for concerning symptoms (new uncontrolled hypertension, skin lesions, gastrointestinal symptoms, fever, weight loss, malaise), it is unlikely that a patient without symptoms would have kidney disease. For this reason testing is not standard in asymptomatic patients.[1]
  • Carotid Auscultation. When physicians listen via a stethoscope placed on the neck, they may hear a bruit, which indicates turbulent flow through a blood vessel. While this may be useful in detecting unknown carotid disease, it is not accurate enough to rule out disease.[1] It is estimated that 44% of patients who do not have a bruit on auscultation will still have significant stenosis of the carotid artery.[1]
  • Carotid endarterectomy. This is a surgical procedure that is used to restore blood flow in a stenosed carotid artery. At this time, it is not recommended that patients with an asymptomatic Hollenhorst plaque have this procedure, as it does not change the risk of stroke.[4]

Eponym and discovery

The phenomenon is named after the American ophthalmologist Robert Hollenhorst.

The first recorded description of "bright" retinal emboli was made in 1927 by TH Butler. While other retinal emboli had been described, the bright nature of these differentiated them from prior descriptions.[2]

Hollenhorst further described finding bright plaques in 1958, at the same time they were independently described by German researchers R. Witmer and A. Schmid via a case study.[2][5][6] They further hypothesized that these plaques were composed of cholesterol. However, it was Hollenhorst who went on to establish the link between these bright emboli and cerebrovascular disease.[2] He further discovered the relationship between presence of these plaques, and increased mortality from cardiovascular disease. In his study of patients with carotid artery disease, he noticed that the plaques occurred on the same side as the affected artery.[2] In 1960 he expanded his research, and noted that the plaques could be made to move by applying pressure to the eye.[2] Additionally, he found that the plaques often occurred after a patient had had carotid artery surgery.[2]

In 1961, Hollenhorst published “Significance of Bright Plaques in Retinal Arterioles” in the

Macaca rhesus monkeys. They found development of similar retinal plaques in these animals.[2] In 1963, the cholesterol composition was confirmed by researchers via autopsy of a patient who died during carotid surgery.[2]

Hollenhorst continued to study these plaques, detailing associations with their appearance and cerebral ischemic events. He also noted that survival these patients was decreased compared to those without plaques.[2]

Work continued on this topic, and studies include the 1997 Blue Mountain Eye Study conducted in Australia and the Beaver Dam Eye Study in Wisconsin, of which patients have been followed up for the past 15 years.[1][7][8] In 2005, one study looked at data from both the Atherosclerosis Risk in Communities (ARIC) study, and the Cardiovascular Health Study (CHS) and suggested evaluation composed of cardiovascular workup and smoking cessation.[1][9] Other work continued to build on this and includes 2008 the Los Angeles Latino Eyes Study (LAKES) study,[1][10] and the 2017 Singapore Epidemiology of Eye Disease Study (SEEDS).[1][11]

References

External links