The first records of a bright retinal embolism can be found as early as 1927 by T. Harrison Butler (Kaufman 2024).
Robert W. Hollenhorst described the Hollenhorst plaques named after him in 1958. Independently of this, the German researchers Witmer and Schmid also described these retinal plaques in the same year (Graff-Radford 2015).
Hollenhorst plaques (HP) are cholesterol emboli that are localized in the retina of the eye (Herold 2020).
According to Kaufman (2024), the prevalence of retinal embolisms in people over the age of 49 is 1.4%. The prevalence also increases with age. HPs account for around 80 % of all retinal embolisms.
Cholesterol crystals in retinal vessels are found in approx. 11% of patients with cholesterol embolism syndrome (Endres 2022).
Patients with arterial branch occlusion (AAV) are usually between 50 and 60 years of age. Men are more frequently affected than women (Erb 2011).
Hollenhorst plaques are caused by atheromatous diseases of the carotid artery or the aortic arch (Graff-Radford 2015).
The plaques consist of cholesterol and are recognizable as crystalline deposits (Kasper 2015).
HPs have been found to be significantly associated with arterial hypertension, a history of vascular surgery, general vascular disease and smoking (history of smoking) (Kaufman 2024).
The source of retinal emboli are ulcerating plaques distal to the bifurcation of the common carotid artery into its outer and inner branches (Kaufman 2024).
Hollenhorst plaques are typically localized in the retina of the eye (Herold 2020). However, localizations of the CNS, liver, pancreas, spleen, prostate, testicles, adrenal gland and thyroid gland have also been described (Endres 2022).
Hollenhorst plaques are generally asymptomatic (Ghoneim 2023). However, cases of transient monocular blindness also occur (Kaufman 2024).
The diagnosis is made on the basis of the patient's history and the characteristic findings of the retina on funduscopy (Mehta 2024). The HPs typically appear as yellowish fragments at an arterial bifurcation (Kaufman 2024). The Hollenhorst plaques show a characteristic refraction that makes them appear larger than the vessel (Augustin 2001).
In addition, once HPs have been diagnosed, the following tests can be used:
Treatment of the HPs is not necessary. The complete blockage of a vessel is an exception (Kaufman 2024). If complications occur, appropriate treatment should be administered immediately (Kaufman 2024).
Asymptomatic HPs are a poor predictor of future embolic events. They are definitely a risk variable for apoplexy, as a meta-analysis of 1,343 asymptomatic patients shows. 17.8% had a current history of apoplexy or TIA. During follow-up, 12% suffered an apoplexy, TIA or died (Kaufman 2024).
Patients with retinal embolisms should be referred to their GP for a bilateral carotid duplex examination. They should also be informed about appropriate lifestyle changes and how to combat risk factors such as arterial hypertension, diabetes mellitus, hyperlipidemia, obesity, lack of exercise and cigarette smoking (Kaufman 2024).