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  2. Endothelial Dystrophies

  2.1 Fuchs Endothelial Corneal Dystrophy

  Fuchs Endothelial Corneal Dystrophy is a slowly progressive, bilateral disease predominately seen in women in their fifth or sixth decades of life. It is the most common indication for endothelial transplantation in the United States[88, 109]. First recognized by Ernst Fuchs in 1910, the original cases exhibited central corneal clouding, loss of corneal sensation, and formation of epithelial bullae[22,24]. Closer examination reveals endothelial cell loss and formation of guttae which are excrescences of extracellular matrix products in DM. In the more common late-onset form, patients present with corneal guttae in their early 40s, but are asymptomatic. Over time, patients experience blurred vision as a result of the onset and progression of corneal edema and require treatment. A rarer early-onset form of FECD appears in the early decades of life and progress similarly to the classic type of FECD.

  On specular microscopy, endothelial cells demonstrate increased cell size (polymegethism) and irregularity (polymorphism); guttae appear as dark shadows (Fig. 1B)[23]. Descemet membrane is also affected and appears abnormally thick due to increased extracellular matrix material deposition. Endothelial pigmentation may also appear as the cells act as functional macrophages. Cases of chronic and advanced uncontrolled swelling may lead to painful bullae and subepithelial fibrosis that may affect the long-term visual outcomes after endothelial transplants[26,99]. (Figs. 1A, 1C) Initially, FECD may be treated with hypertonic sodium chloride drops and ointment to reverse corneal edema. Severe cases may require corneal transplantation.

  Just as the advent of the biomicroscope slit lamp permitted the discovery of FECD, advances in genetic and molecular analysis have brought to light the complex pathophysiology of this disease. However, the etiology of FECD is still incompletely understood. In this section, we discuss the clinical features, risk factors, molecular mechanisms, and genes which have been implicated in FECD. Innovative treatments will likely rest on a comprehensive understanding of the pathogenesis of this disease.

  2.1a Corneal Guttae and Progression to Symptomatic Edema —The different clinical manifestations of guttae lend to an understanding of progression to visually significant corneal edema. “Primary corneal guttata”, or primary central corneal guttata, is defined as the presence of persistent excrescences in central DM that rarely advances to FECD over time[80,144]. Given the occasional progression of “primary cornea guttata” to FECD, some believe that “primary cornea guttata” may be a precursor of FECD[37]. Others suggest that severe primary corneal guttata should be defined as early FECD[1,58,89]. Further research will determine the relationship between “primary corneal guttata” to FECD and the factors that determine clinical progression. Secondary corneal guttae, or pseudoguttae, are areas of endothelial edema arising from degenerative corneal disease, trauma, or inflammation which resolve after treating the underlying problem[37,86]. Hassall-Henle bodies are small transparent growths in peripheral DM of normal aging corneal tissue with no clinical implications[37]. Finally, in FECD, progressive guttae formation in the central and peripheral DM, and sufficient endothelial cell loss cause stromal edema and light scatter with subsequent blurred vision[80,144].

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