Fuch's Corneal Dystrophy
Fuchs' corneal dystrophy, or Fuchs' endothelial dystrophy, is a condition effecting the cornea, or lens of the eye, and most commonly affects older adults. The innermost cells of the cornea, called the endothelium, begin to degenerate. This tissue is normally responsible for regulating fluid within the cornea, as too much or too little fluid can negatively affect vision. Typically both eyes are affected simultaneously, and vision will gradually become cloudier as the disease progresses. The cornea may also swell and blister, leading to bullous keratopathy.
Some cases of FCD are hereditary, being passed from generation to generation. Just one parent having FCD results in a 50% chance of their child developing the disease later in life. However some people can develop the disease without any family history at all. In these cases, the root cause of the disease is not currently known. It is most commonly found in senior citizens, however it can develop in younger people and affects women more often than men.
Symptoms of FCD can develop slowly, or quickly, and not all those affected will exhibit the same symptoms. Some of the symptoms that may appear include:
- Appearance of light glare
- Sensitivity to light
- Pain or discomfort of the eye
- Blurry vision
- Appearance of halos around lights
- Poor night vision
- Poor morning vision that improves throughout the day
- Foreign body sensation
If any of these symptoms are experienced, it's strongly recommended to schedule a comprehensive eye exam with an eye care professional. The exam will allow the doctor to make a diagnosis, either of FCD, or any other potentially vision-threatening disorder, and prescribe the appropriate treatment.
To diagnose FCD specifically, a magnified image of the cornea is taken with a tool called a slit lamp, which allows the doctor to view all of its layers. The innermost layer, the one affected by FCD, we be examined to determine the amount of fluid within.
One of the earliest signs of FCD is a lower than normal number of endothelial cells within the cornea. This alone is not enough to cause a noticeable change in vision, meaning that few people ever notice it on their own without a medical diagnosis. The next symptoms likely to develop are the thinning or thickening of the cornea, and the growth of small lesions called guttata in the corneal endothelium. The thinning or thickening of the cornea is likely going to affect visual acuity, providing the first noticeable symptom that brings people to their eye doctor.
While there is currently no way for FCD to be prevented, it is possible for it to be treated. They method of treatment will entirely depend on its stage of development. In the early stages, vision can often be improved by removing excess water from the cornea with 5% sodium chloride (hypertonic) eye drops. If you have endothelial dystrophy and raised interocular pressure, glaucoma eye drops may be prescribed to help reduce the internal eye pressure.
The small lesions, epithelial bullae, that develop early on will eventually grow and rupture, creating painful abrasions on the surface of the eye. Once this occurs the damage is irreversible, and can only be fixed with a complete corneal transplant (penetrating keratoplasty or PK) or deep lamellar endothelial keratoplasty (DLEK), which is a surgical method to replace the endothelium that leaves the upper layers of the cornea untouched. This procedure has shown success for the treatment of Fuchs' dystrophy with potentially fewer risks than penetrating keratoplasty.
In recent years, an advanced form of DLEK called femtosecond laser-assisted Descemet stripping endothelial keratoplasty (FS-DSEK) has shown encouraging results for treatment of the disease.
Note that anyone that has been diagnosed with FCD should avoid LASIK or other refractive surgery methods. These eye surgeries are likely to exacerbate the condition, and most refractive surgeons won't operate on any one that has been diagnosed with the disease.
Author: John Dreyer Optometrist Bsc(Hons), MCOPTOM, DipCLP
Created: 30 Aug 2016, Last modified: 17 Jul 2019