Category: Uncategorized

Rx of Granular Corneal Dystrophy in the USA in 2015

Q by Doctor Randy:

Dear All, 

I have not seen the patient yet, but was called by a colleague who wanted to refer a 55 year old patient with the above to me for “corneal laser treatment”. I asked of the patient had any ocular surface disease/recurrent erosions, and was told that the only problem was decreased acuity form the opacities themselves. No irregular astigmatism, no cataracts. 

How would those of you advise those of us who only have access to “USA technology” to proceed to treat such a patient? 

A by doctor Will:
    I have performed PTK on a handful of Granular Dystrophy patients who were experiencing reduced vision  The problem in Granular Dystrophy is that the opacities are breaking through the anterior stromal surface.  Removing the epithelium reveals a highly irregular surface 
    The goal with PTK is to just smooth out the surface, not eliminate opacities. 
    After smoothing out the stromal surface with PTK – patients will note  improved vision – both on Snellen testing as well as report improved quality of vision 
    Following the PTK – There will be plenty of opacities remaining.   
    Overall – the PTK procedure should be a very superficial treatment.  I have had one patient require a repeat PTK 6-7 years after the first treatment – and I expect that the PTK lasts for 5-10 years, depending on the patient.  So focusing as much on corneal smoothing while preserving as much corneal tissue is key, in my opinion. 

I hope this helps
Answer by Emil Chynn, MD:
When we treat granular dystrophy or scars, as long as there’s a significant refractive error, we try to treat that, too. Then the issue always arises re if abnormal tissue ablates at a faster or slower rate than normal cornea stroma
We (meaning myself and the various doctors who’ve worked with me) have concluded this is impossible to predict. So then we just shoot our normal nomogram. And have been pleasantly surprised that our refractive outcomes have come out close to plano
Regarding differential ablation rates and leaving bumps and lumps, if you employ a PRK nomogram and ablation profile, as long as your scars are mostly central and superficial, you wind up shaving off a substantial amount of the opacities. I’ve used many different agents to mask, and now there are dozens of tears out with varying viscosities. Unfortunately the predictability of outcomes when using any masking agent is lower than if you don’t use one.
Luckily as many of us have pointed out the epithelium can cover and mask a huge amount of surface irregularity. Therefore after myopic ablation, since you’re creating a “top hat” profile afterwards, it seems like the epithelium is more able to cover up the residual pathology than the original pathology, because the epithelium is going to try to recreate a more normal “dome” shape. There’s also epithelial hyperplasia, which can be encouraged with topical NSAIDs. So these are two often-ignored factors that contribute significantly to a smoother front refractive surface after PRK of opacities, even without using a masking agent in an attempt to differentially and preferably ablate scars or dystrophic deposits over normal stroma

PRK or not to PRK

Q by Doctor P:

I have a 37 yo high myope  (-9.00) with 500 u corneas.
She has a small area in the left nasal cornea of endothelial haze
No other signs/symptoms
No history of HSV etc.
specular right and left eyes
clearly abnormal OS>OD (increased coefficient of variation, lower cell count, weird dark centers OS>OD)
Would you offer PRK?
Answer by Doctor Ronal from Brazil:
Me not PRK for this case , too much myopia
yes.  Artisan
Answer by Doctor P:
I thought about ICL or Artisan but I would be more worrier about endothelial decompensation with an intraocular procedure rather than modern surface ablation…
Answer by Doctor Jim:
It’s natural to reflexively back away from this patient.  But lets look at the case objectively.

On a Visx with a Blend / Large zone ablation this would be 129 u (less with a small zone and/or no blend).  Assuming 50 u epithelium, this produces a RSB of 321 u and a PTA of 35.8%.  Those numbers are acceptable to many of us, per a recent conversation.  Also, with CCT of 500 u, it seems unlikely that there is currently any significant endothelial pump failure.
(1)  Would the PRK negatively impact the clinical course of the endothelial abnormality?  To my knowledge, ablations have not been shown to impact the endothelium, and endothelial transplantation should not be compromised by the ablation as long as there is no ectasia.
(2) Would the endothelial abnormality negatively impact the clinical course of PRK?  Without any evidence of corneal edema currently, the epithelium should heal properly.  It seems possible that, if the epithelial-stromal attachment is weaker than normal, as I noted in a previous thread, bullous keratopathy might be more likely after PRK, but this would be treated with endothelial transplantation anyway at that point even without the history of PRK.
It would be valuable to the patient to prognosticate on the future of the endothelial issue, if possible, but I would offer this patient PRK.
Answer by Emil Chynn:
It’s incorrect that “ablations are not known to affect the endothelium”
This was studied during FDA trails of the excimer laser I believe. The acoustic shockwave during ablation kills endothelial cells
I recall FDA trial data showed a small decrement in endothelial cell count densities, that then was flat, rather than progressive, indicating a one-time decrement, with no further accelerated induced loss
Because we’re normally born with excess endothelial cells, FDA extrapolated that this small one-time loss wouldn’t cause clinical edema later in life
At this is my 20-year old recollection as a PI for one of the excimer laser FDA trials.
Marc might have a more accurate recollection or maybe even some citations
Hope this helps
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The role of non-peer-reviewed research (and forums like Keranet)

I’m not sure what the point of your original question was. You seem to be implying that if one of us shares his or her vast experience accumulated over decades of careful observations, until it’s published it isn’t in some sense “real” (or believable)
We are all very busy and unfortunately have to earn livings as well as contribute to the advancement of science in our field. I’m sure if Bill Gates decided to give any of us a stipend of $1mil/yr under the stipulation that we would drop all our other obligations and focus only on advancing the science, our careers and practice patterns would take a dramatically different trajectory!
There are many levels of “research” and to try to draw any line in the sand between “real” and “not real” is both impossible and pointless
For example, one possible “hierarchy” of research “quality” might look as follows
NEI funded multi-center controlled trial
Drug company funded research for FDA trial
Device company funded research for FDA
Meta analyses
Multicenter trial, top peer-reviewed journal
Multicenter trial, ok peer-reviewed journal
Singlecenter trial, top PR journal
Singlecenter trial, ok PR journal
Poster at AAO ASCRS or ESCRS
Publication in non-peer-reviewed journal
Large nonpublished observations (k-net?)
Drug company dinner talk
Published case report
Pearls an older doctor gives in the hallway
Observations from small sample sizes
As you can see, any line you draw in this hierarchy is necessarily arbitrary. Worse, you’d be ignoring important sources of “real life” validation and information (ie the items towards the bottom of this list)
Once something is published it doesn’t become “real”. It just becomes “more public”
If you perform research under IRB it isn’t automatically “safer and more ethical”. You’ve merely formalized the ethical review process that I’m sure we all engage in carefully ourselves, weighing the (acceptably low) risks to our specific patients against the (higher) chance of finding a substantial benefit for all our future patients (and those of other surgeons, if shared properly on forums like Keranet)
One of the main reasons I’ve rejoined Keranet as an active participant, after a hiatus of nearly a decade, is I’m planning on retiring soon, and have realized that my plan to publish many things I’ve learned about ASA in peer-reviewed journals isn’t going to happen. Fellows graduate and don’t have the time to turn posters into papers. We get older, have family obligations, and our careers, like our lives, pass by so quickly
The giants in our field seem to be able to “do it all.”  But we don’t ever see the full burden of their sacrifice.

Trephine for ASA and alternate alcohol



I’d like to try your technique.

Can you share what your preferred trephine for ASA is (vendor, size, catalog #) ?

For yours and the group’s interest: I’ve been using a corneal light protector sponge saturated with 70% Isopropyl alcohol (yep good old rubbing alcohol!) for 12 secs followed by chilled BSS rinse. The epi comes off beautifully but not with a clean outer edge like a trephine.

I think the clean epi removal and ice cold BSS both after alcohol and after ablation are most helpful for pain control. I use Oasys 8.4,  NSAIDS for only 2 days, FML tapered over 3-4 months.



A by Emil Chynn MD:

it’s the same exact thing, ie using a mechanical microkeratome which uses a blunt separator that’s too blunt to go into the cornea, to push off the epithelium in one clean sheet, without needing any EtOH (in most cases), where the surgeon can choose to replace the epithelium or not (about 50% of surgeons do and 50% do not, bc they have observed quicker brand-new epithelium when they stimulate epi regrowth by leaving the area denuded for a few days w a BCL, surprisingly wo any increase in discomfort, and sometimes epi-off is actually more comfortable, probably bc the old epi isn’t dying off and releasing cytokines and other inflammatory mediators)

there has been a movement to renaming this procedure epiLASEK rather than epiLASIK, as it is clearly closer to LASEK (ie another ASA or Advanced Surface Ablation procedure) than LASIK, and the former (better) nomenclature is also more clear to the consumer/lay patient (ie they understand it is different than LASIK)
this is also why i have a problem w “bladeless” LASIK, as we all know that many lay patients think that this means there is no flap being cut at all, when in reality it means a flap is being cut with a laser. i do understand the branding/marketing value of this term, as it reduces fear, but i have actually seen a few patients over the last 20 yrs come in w flap dislocations from extreme sports after “bladeless” LASIK, and they were SHOCKED that they had a flap, and said “if my doctor had been more clear/honest w me that i had a flap cut into my cornea w a laser, i would have been more careful and worn eye protection”
long answer to a short question, but i hope it will be helpful and perhaps stimulate discussion!:)


This Cornea and Refractive Surgery……


Are there corneal thicknesses below which you would avoid any refractive surgery?

I am considering PRK on this 34 y/o woman. Stable refraction for years. No family history of corneal disease

-3.00 -1.00 x 180
-3.00 -1.00 x 180



before 2005 or so we mostly worried about RSB, like if they had a RSB over 250 the chance of ectasia would be low

past 2005 (approx) reports started to come out of iatrogenic KC with RSBs well over 250, some even in the 300s
but in cases where STARTING PACHY was low, ie below 500
now i won’t perform a case if LOWEST STARTING PACHY is below 475 ANYWHERE, as i had a case like the above:(
admittedly, there is no firm cut-off #, the 475 is as arbitrary as the 250–but it does help, and you need to use something
hope this helps;)

Epithelial Reattachment Following Surface Ablation


Dear All,

I’ve noticed during PRK enhancements over prior PRK, even years later, using a brush, that the epithelium is quite obviously not as adherent over the ablation zone as it generally is during primary PRK’s.  This phenomenon would probably not be apparent during alcohol-assisted enhancements, since that method loosens the epithelium before the surgeon touches it.

The loss of the normal Bowman’s Membrane could be integral to the pathogenesis, although it also seems to me that the epithelium is also less well attached over the surrounding unablated Bowman’s.  This is apparently not a clinically significant phenomenon other than the possibility that the cornea may be less resistant to epithelial trauma.  Still, I feel a little uncomfortable not knowing what to tell patients, particularly those who engage in high-contact sports, about when the abrasion resistance will return to 100%.

Has anyone else noticed this phenomenon and/or noted an interval after which epithelial attachment seems to have recovered?



I’ve not noticed the epithelium being looser after a true ASA. Indeed I often perform an ASA instead of a PTK in pts w RES as a solution to their RES and refractive error


ASA for High Astigmatism


New pt came to see me earlier this week for a refractive evaluation.  26yo male with past ocular hx of high astigmatism, no family hx of keratoconus.  Highly motivated, and understands higher likelihood for enhancement.  I was thinking of ASA for him, but wanted some input.
BCVA OD:  +0.5-4.50×005 20/25   pach 588
BCVA OS:  +2.25-6.00×180 20/25  pach 544
I am currently using the VISX S4 platform.  I have not ever attempted to treat this level of cylinder.  Thoughts?


i’m on the same laser (VISX S4 IR) so my experience should be very relevant to your outcomes
on this platform, i can reliably eliminate about up to 4D of cyl with LASEK
back when i was doing LASIK on the same laser, i could only reliably eliminate 3D or so of cyl
i’m not sure of the reason, but my conjecture is that perhaps the flap is obscuring/diminishing some of the laser effect
i’m curious if anyone else has observed they can reliably treat higher cyl with ASA vs LASIK
i don’t know what the group’s consensus is, or the literature statistics show
but i have actually never seen a patient who has significant hyperopia eventually manifest as a true KC patient
the left eye is another matter. obviously, there’s no way to reliably get rid of 6D of cyl with any laser procedure
so i would just tell him that i’d be able to reliably get rid of at least 4D, perhaps leaving him with 1D of cyl
however, he might also be left with some residual hyperopia
so if his residual Rx is +.50 – 2.00 x 180, his SE = -.50, which is compatible with a UCVA of 20/25
even if he had a residual Rx that was worse and an UCVA of 20/40, i bet he might elect not to enhance anyway
as he would presumably be 20/20 OD, so 20/20 w both eyes open anyway
so i’d just tell him all of this (depending on how much he would understand, of course)
which is really probably a better “informed consent” than just saying something generic like “you might need enhancement”
i disagree with jim that if there is a higher chance of enhancement, then LASIK would be preferred
many recent studies in the literature have quantified the risk of epithelial ingrowth
it has been estimated to be about 1% in primary cases (this includes visually insignificant ingrowth, of course)
and about 10% in secondary cases
so if you think you might need to enhance someone (eg there’s no way you can get rid of >4D of cyl all at once)
if you then elect to perform a LASIK, you are basically saying you’re ok with a 11% risk of epi ingrowth
in my opinion, that’s a very high number to be ok with, especially as a “better default”
i really think the issue is that most surgeons are performing LASIK the vast majority of cases (like 90%)
so if you’re only doing 10% surface, you’re not so motivated to do an epiLASEK or whatever, so you do a PRK
then the recovery is very long, and then perhaps the bias shifts away from ASA to incisional surgery
i did an epiLASEK on my secretary who was -4.50, and she was 20/15 and with 0 discomfort 72 hours afterwards
i guess if she had LASIK she could have been so by 48 hours, but that 24 hour savings is clinically unimportant
hope this helps, and pls feel free to call back if you need any more specific advice;)

Dr. Chynn on The invention and basic science of the excimer laser

Fluence/mm2/sec but then got bogged down by the math and units and didn’t want to post something I wasn’t confident about
I guess we should just say:
“Haze can be induced by the (mild) thermal damage caused when the excimer laser photo disrupts covalent bonds of the collagen stroma. This is why techniques such as chilling the cornea with cold or frozen BSS after ablation reduce the incidence of haze. It’s also why you may wish to turn down the pulse frequency or Hz if that’s something you can adjust for your longer ablations–especially if your laser is one of the “faster” brands”
Speaking of basic science, coincidentally last week I met the true inventor of the excimer laser. Not ST or FL, who had use patents, both of whom actually first trained me on their competing excimers when I was at Columbia in 1992. James Wynn PhD the guy who had the original patent at IBM. He and his co-researchers received the Lasker Prize (the “pre-Nobel”) and the Congressional Medal of Freedom from Obama for this work. Now he’s trying to use the excimer to ablate skin lesions, making use of the fact that at 293nm the laser is blocked by blood, so it stops penetrating on its own once it hits the deeper dermis.
This was at a meetup group of Physician Entrepreneurs that some of you may want to join. They have chapters in nyc and sf and a couple of other cities. If you email me privately I’ll put you in touch w the organizer (as K-net is supposed to be confined to anterior segment issues, the recent illuminating post on finger numbness from guitar-playing notwithstanding. I still think Jimmy Page was the best rock guitarist ever
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ASA v PRK protocols


Inspired by Emil, I made epithelial flaps for two patient on my last LVC day.  One patient 20/20- POD#1 the other 20/30 POD#1 and 20/20 OD and 20/25 OS POW#1 (-3.50 preop MRx).  Second patient had discomfort on POD#4; I think it likely was from a very tight CTL fit and not the technique.

Here’s what I did.  Thank you for sharing your thoughts and feedback with me.

Gentle superficial trephination with 8.75 mm trephine.
33% etoh for 5 seconds in 9.00 mm well incorporating trephine edges for 360 degrees.
Chilled BSS.
Lifted intact epithelial flap with spatula leaving a perfectly smooth stromal bed with perfect circular epithelial edge for 360 degrees.

Thank you,
C. H.


I’d concur that it’s important not to panic if you get an IOP spike post ASA and to not then cut the steroid. Had a couple of cases where a Fellow d/c’d the steroid prematurely and then haze started even months postop on higher Rxs

Just add some glaucoma drop and stay the course. Usually I add Alphagan as that helps with night glare too

– See more at:


I have a 26 yo healthy female (only med is a birth control pill, which she has been on for years) with the following refractive error:
Current wear in glasses:
OD:  -2.50+1.00×83
OS:  -1.75+1.25x96Manifest June 2014:
OD: -2.25+1.75×80
OS: -1.75+1.50×100Manifest Dec 2014:
OD: -2.50+1.00×85
OS: -1.75+1.25×95

Her topos from June and December 2014 are attached in pdf format.  The inferior portion of the anterior float appears steeper. It is mild and not changing over a few months. The B-A curves are within normal limits.
I plan to reevaluate in June.

She wants LASIK. I suggested PRK as an option for her.  I am inclined to avoid LASIK given my concern with the inferior area.

Would you consider PRK to be safe in this situation. Or would you steer the patient away from refractive surgery all together?


ASA (advanced surface ablation) is almost always safer in these cases. Done properly with her low age and Rx recovery should be quick and painless"</p

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