Wednesday, June 18, 2008

Abstract: Dry eye and refractive surgery


1) I could live without the Restasis/plug/Intralase cheerleading, but never mind

2) I am pleased to see the first three sentences of the Conclusions stated so nicely and I just wish these could be lifted verbatim and placed in every Informed Consent form for laser surgery, with a required verbal explanation by the physician.

3) I am just as disgusted with the last sentence of the Conclusions as I always am at this kind of a conclusion. Why laser these people with pre-existing dry eye at all?

Postrefractive surgery dry eye.
Curr Opin Ophthalmol. 2008 Jul;19(4):335-41.
Quinto GG, Camacho W, Behrens A.
The Wilmer Ophthalmological Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287-0005, USA.

PURPOSE OF REVIEW: To report the recently published literature on ocular surface changes after refractive surgery, as well as the outcomes of treatment modalities on postrefractive surgery dry eye.

RECENT FINDINGS: Cyclosporine, the first US Food and Drug Administration approved agent to treat the underlying pathological mechanism of chronic dry eye, has demonstrated promising results in dry eye patients. Further, there may be an additive effect of topical cyclosporine and punctal occlusion. Femtosecond lasers for corneal flaps in laser in-situ keratomileusis seem to induce fewer signs and symptoms of dry eye and may be attributed to the creation of thinner flaps.

SUMMARY: Dry eye is one of the most common complications after photorefractive keratectomy and laser in-situ keratomileusis. Keratorefractive surgery is known to cause damage to the corneal sensory nerves. Several studies have demonstrated a decrease in corneal sensation, tear secretion, and tear film stability several months after keratorefractive surgery. For patients with preoperative dry eye, the ocular surface must be treated accordingly prior to surgery.

Abstract: Review of recent published research

Dry eyes: etiology and management.
Curr Opin Ophthalmol. 2008 Jul;19(4):287-91.
Latkany R.

PURPOSE OF REVIEW: Until recently, the cause of dry eye syndrome was uncertain and the treatment was palliative. Since discovering that dry eyes are caused by inflammation, there has been an abundance of research focusing on anti-inflammatory therapies, other contributing causes, and better diagnostic testing. This review summarizes some of the interesting published research on ocular surface disease over the past year.

RECENT FINDINGS: The definition of dry eye now highlights the omnipresent symptom of blurry vision. The re-evaluation of ocular surface staining, tear meniscus height, and visual change will allow for a better diagnosis and understanding of dry eyes. Punctal plugs, and oral and topical anti-inflammatory use will strengthen our arsenal against ocular surface disease.

SUMMARY: Major progress has occurred in the past few years in gaining a better understanding of the etiology of dry eye syndrome, which will inevitably lead to more effective therapeutic options.

Abstract: Tear glands, tit for tat, and... is this interesting or is this interesting!

Well, kewl - someone's finally speaking my language (so to speak)!

OK so it's only rabbits but I found this extremely suggestive. Has it been all said and done long ago and I just never noticed? Seriously, maybe it's just leaky brain syndrome but I honestly don't remember coming across something like this before, simple as it is.

They cauterized shut the meibomian glands of one eye and observed the effects on the tear film. Aqueous tears (i.e. from the lacrimal glands) increased and goblet cell density (i.e. mucous-makers) DECREASED.

Just playing guessing games here as I'm only looking at an abstract not data but:

Let's agree to ignore the lacrimal gland increase on the basis that screwing with the rest of the tear system has left such a bad surface that the bunnies are getting lots of reflex tearing.

Now look at the goblet cells: We've just simulated severe MGD or MG atrophy, goblet cell density is down so presumably mucous production is down. I've always felt that the 'unexplained' element with some of the patients who have severe burning or other 'surface symptoms' (including the infamous 'menthol sensation), despite decent aqueous production and a relatively quiet LOOKING ocular surface, might have as a common factor poor mucus resulting in poor 'wetting' (in a feeble attempt to speak Dr. Holly's language). If so, this might explain why some of these patients can max out on antibiotics, heat treatment, bleph treatment etc and still be in symptomatic hell. Furthermore, it might also help explain why simply applying something that 'wets' better (like Dwelle) can seriously improve symptoms even if the MGs remain completely unproductive, something I was puzzling over in an earlier post using our DEZ member 'Rozjen''s remarkable experience as an example... So now what I really want to know is whether it just compensates for the absence of the substance that is normally responsible for tear adherence or, as suggested in earlier studies, also actually improves goblet cell density. In due course hopefully we'll actually nail this down. Oh for research dollars. It wouldn't really take all THAT much.

[Changes in lacrimal secretion in rabbits according to meibomian glands activity][Article in Romanian]
Oftalmologia. 2007;51(4):121-5.
Stan C, Visan O, Samoila O, Mogosan C, Craciun C, Mera M.

PURPOSE: The purpose of this issue is to create an experimental animal model of dry eye and study the alteration of lachrymal secretion in time.
MATERIALS AND METHODS: We used a group of 8 rabbits in which the Meibomian gland orifices of the right eye were individually closed by cauterization, the results being related to the sound left eye.
RESULTS: We studied: the quantitative alteration of the lachrymal secretion using Schirmer 1 test; the alteration of lachrymal film using rose-bengal and fluorescein staining; the variation in tear protein concentration and histopathological changes in conjunctiva.
CONCLUSIONS: We found histopatological changes in conjunctiva and in the lachrymal secretion consisting in conjunctival goblet-ceil density decrease and watery secretion increase, probably due to lachrymal viscousity decrease mechanism.

Abstract: Dry eye after cataract surgery

This is nothing more than a blurb... But there is so little out there on dry eye after cataract in mainstream peer reviewed journals that I'll take anything I can get. I would love to see the raw data to get any idea of the correlations between incision size, topical meds and severity/persistence of dry eye after surgery. (Any MD, or co-managing ODs out there that happen to have collected data to share?)

[Clinical correlations between dry eye and cataract surgery][Article in Romanian]
Nistor MC, Nistor C.
Oftalmologia. 2007;51(4):79-82.

Cataract procedure is sometimes followed by dry eye symptoms. The dimensions of the incisions, topical medication and other manoeuvres are responsible for these phenomena. I tried to objective them by break-up-time (BUT) and Schirmer test. The favourable outcomes of artificial tears confirm this theory.

Tuesday, June 17, 2008

BOTOX / Blepharospasm alert

As some of you know, BOTOX injections can be used to treat blepharospasm. Typically patients get injections every 3 months.

I have heard from two different patients quite recently who experienced sudden complications from an injection. In one case, the lid froze open, causing severe pain and great risk to the cornea. In another, there are less severe but still serious problems with lid closure.

I am very concerned about this. If I've personally heard of two in a row, make no doubt there's more of it happening out there somewhere. Furthermore, LID PARALYSIS AND INCOMPLETE LID CLOSURE ARE NOT LISTED AS RISKS anywhere that I can find. Allergan's site lists ptosis, dry eye and corneal inflammation as side effects. The FDA site lists 'droopy eyelid' lasting a few weeks. This is more serious than any of those, however.

DOCTORS, please be on the alert for this and by all means file a Medwatch report or make sure your rep does. If any of your patients experience this please make sure they learn about ALL available remedies including things like Tranquileyes moisture goggles which will help hold their lids closed at night. If that's not suitable for your patient for some reason we can help you find alternatives such as eyelid-friendly tapes or sleep masks.

PATIENTS, if any of you reading this have experienced this complication, please urge your doctor to report it to the FDA. Whether or not your doctor undertakes to do so, please also file a Medwatch report on your own.

Here is the link to the FDA site for adverse event reporting.

As we witnessed so recently with LASIK, failure to report adverse events associated with drugs and medical devices has serious repercussions:

(1) it cripples the FDA's ability to pursue post-market safety issues, and

(2) it prevents future patients from receiving accurate information about the risks they may be undertaking.

(Note that after it was widely reported that only 140 "consumer complaints" had been received by the FDA about LASIK in 8 years, more than 200 more complaints were filed in less than a month - uncomfortable testimony to the FDA's failure to make their reporting system known and to physicians' and/or manufacturers failures to report poor patient outcomes.)

As conscientious consumers and professionals let's do our part to make things safer for future patients!

Thanks everybody.