Case Three

Does this map resemble KC or CL induced corneal warpage? What distinguishes the two?

Slit lamp exam reveals no evidence of KC (that is no Vogt's striae, Fleischer's ring, or corneal scarring characteristics of KC).

Case Four

Male, age 55

Dx with KC 2 years ago.

Medical Hx: asthma, atopy, was on steroids and developed PSC OU, now refuses any medication except holistic meds, patient wheezes in exam chair. Wearing opaque tinted Freshlook lenses 20/50 OD, 20/200 OS.

Ophthalmic exam: topography consistent with KC and sagging cones OU + Vogt's striae OU, + Fleisher's ring OU, 4+ GPC OU.

Recommended immediate refit to GP OU with medical tx of GPC.

Patient refuses medical therapy, Proceed with GP only.

FINAL DISPENSED LENSES after multiple attempts to achieve best centration and fit:

• OD 6.80 9.0/7.0 -6.00 Boston ES 20/25
• OS 6.60 9.0/7.0 -7.75 Boston ES 20/30

Lenses position low OU but easy movement, patient comfortable, GPC resolving to Grade 3, patient asymptomatic from GPC.

6 month f/u: Unchanged from above, no change to lenses or wearing schedule.
1 yr f/u: Patient happy, no complaints, GPC remains at Grade 3 and asymptomatic
slit lamp exam reveals bilateral inferior neovascularization 2 mm OD, 2.3 mm OS.

Refits attempted at increasing centration fail (flatter lenses, smaller diameters, higher edge lift, etc, ) Refit to hyper Dk lenses of same parameters instead. Currently pending f/u.

Questions?

1) What is most probable mechanism of neovascularization?
2) How does his atopic disease and asthma play a role?
3) Is the GPC a concern?
4) How are hyper Dk lenses expected to perform in GPC control? For further
development of neovascularization?
5) What are other treatment options?
6) Is he a good candidate for a PK?