The Skinny on Salzmann Nodular Degeneration

The majority of worrisome corneal pathologic findings involve thinning and necrosis, but it’s crucial that we as primary eye care providers do not neglect the possibility of raised corneal lesions. When we think about elevated lesions of the cornea, conditions such pterygia or even phlyctenules most readily come to mind. However, the most common raised corneal lesion is the Salzmann nodule, also known as Salzmann nodular degeneration (SND; Figure).

WHAT IS SND?

SND was first described by ophthalmology pioneer Maximillian Salzmann, MD, who was best known for his work in glaucoma and gonioscopy. SND is a close cousin of dry eye and anterior basement membrane dystrophy, and typically presents as a gray or blueish raised lesion of the epithelium and Bowman layer. It is best viewed with indirect illumination and is usually round or oval in shape and located peripherally; however, considerable variation and variability can be found in SND presentations.¹

In one retrospective study, 28% of the nodules were found in the superior-nasal quadrant, 23% in the superior-temporal quadrant, 20.5% in the inferior-nasal quadrant, 18% in the inferior-temporal quadrant, and 10% were located centrally.¹

Although sometimes an asymptomatic finding, the typical symptoms associated with SND mirror those of dry eye and ocular surface disease (OSD), including foreign body sensation and decreased vision, which is the most common complaint, reported in about 85.5% of patients.¹

This process is not completely understood, but it is generally thought that mechanical irritation and/or chronic inflammation leads to poor and extended wound repair processes, which causes disruption of the basement membrane and Bowman layer.¹ Differentiation and anterior migration of stromal fibroblasts and myofibroblasts, which deposit excessive, disorganized subepithelial extracellular matrix material, then forms these nodules.¹

EFFECTS ON THE OCULAR SURFACE

SND can cause central corneal flattening and astigmatism, which may lead to fluctuating or inadequate improvement by refractive error correction and inaccurate preoperative measurements for refractive and cataract surgeries.¹ The visual symptoms of SND can also be mistaken for or even cause an overestimation of the visual effects of early lens changes, leading to inadequate or incomplete improvement in patients postoperatively. SND can also cause a refractive shift, once it is removed from the anatomy.

As is the case with many ocular surface pathologies, treatment strategies for SND typically follow a stepwise approach targeting inflammation, (increasing) lubrication, and (avoiding) evaporation.¹

Topical steroids, cyclosporine, lifitegrast ophthalmic solution 5% (Xiidra, Bausch + Lomb), semifluorinated alkanes, and various ocular lubricants may be used as treatments, as well as doxycycline or amniotic membranes.¹ The anterior and superficial location of this pathology also lends itself well to procedural removal.¹

BE AS THOROUGH AS POSSIBLE

When assessing patients with signs or symptoms of OSD, remember to completely evaluate the ocular surface and watch closely for SND to best tailor and personalize your therapies.