Retinal drusen are small yellow dots  in the eye. They are visiblebetween the deepest or outermost layer of the retina, called Bruch’s membrane, and the underlying retinal pigment epithelium (RPE).

In most cases drusen is a phenomenon related to aging. Accompanying changes include atrophy of the RPE and disappearance of retinal pigment in various spots. These are together called age-related macular degeneration (AMD), a progressive condition that can cause loss of central vision. In fact, AMD is the cause of loss of vision in the majority of elderly patients.

Drusen are found in almost every patient with AMD but the converse is not true: AMD does not occur in most cases where drusen are found. Drusen do not cause any eye symptoms and so are detected only by fundoscopic examination of the eye.

Classification of Drusen

Drusen may be hard or soft. Hard drusen are less than 63 µm in diameter, and have well-defined margins. They are also not grouped. Larger drusen (up to 125 µm) are also called hard if they are flat. The same size of drusen is called soft if they are more substantial. Soft drusen may be indistinct or distinct. Again, based on the location, drusen may be either macular or peripheral. The morphology also varies, such as reticular drusen, and early-onset adult grouped drusen. They may be confused with exudates or cotton wool spots. With increasing age, the percentage of soft drusen goes up, though not the hard type.

Risk factors for Drusen formation

The following factors may contribute to drusen formation:

• Age
• Chronic retinal detachment
• Inherited macular dystrophies
• Type II membranoproliferative glomerulonephritis
• Phthisis bulbi

When choroidal pigmentation is seen along with drusen it implies that the lesion is of long standing and is therefore benign.

Drusen are made of various substances including protein, lipids and sugars, with dendritic cells. They may also be rich in chemical mediators of inflammation and sometimes show the presence of certain types of amyloid. Their origin is still in question. They may represent accumulated waste products from the RPE (“tombstones of dead RPE cells”) which grow around a nidus. The nucleus may be the result of inflammation or any other debris taken up by phagocytes. Thus the drusen goes through various stages of nucleation, expansion and coalescence. In many cases their natural history includes involution and disappearance.  Only about 3 of every 100 eyes with hard drusen develop AMD or other sequelae but this shoots up to between 26-34% with soft drusen.

Management

Drusen are difficult to predict as to their outcome. The only risk factors for the development of AMD which have been identified so far are smoking, aging and genetic susceptibility. It is important to have regular eye examinations once drusen are identified, because the wet type of AMD may set in with rapidity at any time, leading to severe central visual loss.

Photocoagulation of the affected eye was shown to cause the regression of drusen, but with an increased incidence of the dangerous condition called choroidal neovascularization. Antioxidants show some modest benefit in preventing the progression of drusen to severe AMD when used alone or in combination with zinc. However, this applied only to patients with large or multiple significant drusen, or those who had non-central geographic atrophy of the retina. However, it is known that some of these antioxidants, notably beta-carotene, increase the rate of occurrence of other more dangerous conditions such as lung cancer, and so the recommendations for their use are mixed.

Statins have also been used to treat drusen on the strength of their ability to bring down lipid levels in the blood and to lower the levels of inflammation, both of which appear to be significant in the pathogenesis of drusen. Their use requires further study.