Eye exam results.

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Yesterday’s eye exam was a bit of a mixed bag. My left eye (the more severely affected of the two) has got considerably worse since its topography was last measured, now distinctly conical at the visual axis – which explains its particularly poor vision. My right eye, however, was shown by topographic examination to be considerably less conical overall than my left, and has changed less over the last 12 months; it has undoubtedly worsened, but only slightly. Measurement of each eye’s corneal thickness also brought good news: both eyes are only slightly thinner than the average thickness of a healthy eye. This is a very encouraging sign, and means I have a greater range of treatment options available.

I am due to be fitted with new gas permeable or scleral rigid contact lenses, and my doctor believes that as a young person with continued degeneration and suitably thick corneas I will also benefit from corneal cross-linking (a process briefly explained in my previous post). This should greatly help my prognosis and hopefully reduce the likelihood I ever need a corneal transplant. However in the grand scheme of things I am fortunate as the cornea is just the window of the eye, and at the worst windows can always be replaced.

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Eyesore: what is keratoconus?

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By the time this is posted, I will have returned from the local eye hospital, where the progression of an eye condition I have called keratoconus will have been assessed. I have written this before setting off as sometimes the eye examination requires dilation of the pupils and other irritating procedures that can affect one’s vision for several hours, making using a computer difficult.

The condition causes the cornea – the clear, outermost layer of the front of the eye largely responsible for the eye’s ability to focus (by refracting light onto the retina) – to progressively thin, which results in cone-shaped bulging, rather than the usual dome shape of a healthy cornea. This can lead to a range of visual disturbances and symptoms including seeing multiple images or “ghosting” in a single eye, glare or halos around lights, sensitivity to light, and blurred vision. I personally find that ghosting and halos of light to be my most significant symptoms, particularly in situations with high levels of contrast such as when looking at headlights or streetlamps at night, whilst my daytime vision only suffers from blurring that is correctable with contact lenses.

Initially visual impairment can be corrected with glasses, but as the condition progresses one must upgrade to contact lenses; typically soft hydrogel contacts are first used, sometimes upgraded to rigid gas-permeable or large scleral lenses as required, and sometimes two kinds of lenses can be combined, or “piggy-backed”. If even contacts fail to correct vision a range of surgical procedures can be considered, from inserting rings (called Intacs) into the cornea to reinforce it and artificially restore a more dome-like shape to corneal transplants.

Whilst the underlying causes of the condition are poorly understood and as of yet no cures exist, a newer procedure called corneal cross-linking (or CXL) has shown promise for slowing, and even halting, progression of the disease. In CXL a riboflavin treatment and Ultraviolet-A radiation are combined to induce the formation of new bonds between collagen molecules in the cornea to recover and maintain mechanical strength. However, this treatment is only suitable for cases in which the condition is continuing to progress, but has not yet thinned or scarred excessively. If today’s investigations show my eyes as progressively worsening this treatment option may be considered, but we’ll have to wait and see.

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