New research has demonstrated a relationship between malfunction of beneficial enzymes found within the eye’s surface and an accompanying chemical imbalance that leads to toxic damage and thinning of eye tissue. Because keratoconus can be found in extended families, this improper functioning of beneficial enzymes appears to have genetic causes about 5% of the time. Eye damage from keratoconus also can be linked to factors such as overexposure to sunlight, improper fittings of contact lenses, excessive rubbing of the eye, and continual (chronic) eye irritation.

• Keratoconus is usually detected when the patients reach their 20’s. For some, it may advance over several years. For others the progression might reach a certain point and stop.
• Keratoconus is not visible to the naked eye except during the later stage of the disease. In severe cases the cone shape is visible to an observer when the patient looks down and the upper lid is lifted. When looking down, the lower lid is no longer shaped like an arc, but bows outward around the pointed cornea. This is called Munson’s sign.
• Special corneal test called ‘Topography’ provides the doctor with detail about the cornea’s shape and is used to detect the progression of the disease. A ‘Pachymeter’ may also be used to check the thickness of the cornea.

The first line of treatment for patients with keratoconus is to fit rigid gas permeable (RGP) contact lenses. Because this type of contact lens is not flexible, it creates a smooth, evenly shaped surface to see through. However, because of the cornea’s irregular shape, these lenses can be very challenging to fit. This process often requires a great deal of time and patience. When vision deteriorates to the point that contact lenses no longer provide satisfactory vision, corneal transplant may be necessary to replace the diseased cornea with a healthy one.