Early symptoms include blurry vision upon wakening which improves during the morning,[2] as fluid retained in the cornea is unable to evaporate through the surface of the eye when the lids are closed overnight.

[citation needed] In moderate stages of the disease, an increase in guttae and swelling in the cornea can contribute to changes in vision and decreased sharpness throughout the day.

Corneal endothelial cells in end-stage FED are reduced in number and appear attenuated, causing progressive stromal edema (swelling).

Progressive endothelial cell loss causes relative influx of aqueous humor into the cornea, leading to swelling (corneal stromal edema), which results in blurred vision.

Hence, patients with a history of Fuchs' dystrophy may be at a greater risk of corneal edema after ocular surgery as they have fewer functioning endothelial cells.

[citation needed] The exact pathogenesis is unknown but factors include endothelial cell apoptosis, sex hormones, inflammation, and aqueous humor flow and composition.

While corneal thickness can be a valuable indicator of how the cornea is changing over time, it is affected by multiple factors and is not adequate itself as a screening tool to diagnose Fuchs dystrophy.

Medical management includes topical hypertonic saline, the use of a hairdryer to dehydrate the precorneal tear film, and therapeutic soft contact lenses.

[9] Injection of cultured endothelial cells is under investigation and in a series of 11 patients in Japan with bullous keratopathy, was able to clear corneal edema.

First assessed in a clinical setting, Fuchs himself estimated the occurrence of dystrophia epithelialis corneae to be one in every 2000 patients; a rate that is likely reflective of those who progress to advanced disease.

It was characterized by late onset, slow progression, decreased visual acuity in the morning, lack of inflammation, diffuse corneal opacity, intense centrally, and roughened epithelium with vesicle-like features.