To the Editor:
In the April 2003 National Panel Report "Cataract Surgeons Settle Down," the panelists were apparently asked if they used antibiotics in the infusion bottle as a prophylactic measure against endophthalmitis. It should be noted that, since it's nearly impossible to control the dosage of medication when used in this manner, many surgeons have abandoned this technique and simply inject the antibiotics intracamerally at the end of the procedure. I feel that injecting steroids, non-steroidals and antibiotics that provide both gram-positive and gram-negative coverage, such as ceftazadime and vancomycin, is possibly the best way to prevent endophthalmitis. Since the eye is a closed container, the chance of developing resistance is remote.
We've performed 35,000 cataract procedures since our last case of endophthalmitis, using the following protocol:
• use ultraviolet lights in the operating room to help kill bacteria;
• pass all irrigating solutions through a 0.22 micropore filter;
• instill a dilute Betadine solution pre- and postoperatively; and
• measure intraocular pressures within
the first 20-30 minutes after surgery to check for hypotony and reduce the risk of ocular bacterial influx.
I don't prescribe topical antibiotics since I already administer antibiotics intraocularly and then make sure the wound is watertight.
James P. Gills, MD
Tarpon Springs, Fla.
To the Editor:
I read your Glaucoma Issue with interest. Some of the comments [in the National Panel article, "A Paradigm Shift Hits Glaucoma," p. 46] were quite amazing, such as the one from "a surgeon from Pennsylvania" who recommended an argon laser trabeculoplasty in a 16-year-old boy with juvenile onset open-angle glaucoma, with no signs of the pigment dispersion syndrome. I also wondered why the "surgeon from Texas" said, "If the intraocular pressure is greater than 10-12 mmHg, this boy can go blind" despite the information that the baseline intraocular pressure was 30 mmHg. The number of opinions that were presented as if they were more than basically unsupported opinion was disturbing.
However, the main point of this letter is to congratulate you for the article ["Glaucoma Care at the Fringes," p. 78] pointing out how difficult it is for people with low income to get satisfactory care. Were we truly interested in improving the health of patients with glaucoma, we would be spending a lot more time on issues like that, and a lot less on technologies which are expensive and of questionable value.
Congratulations on your sensitivity to this important issue and your preparation of a fine article dealing with it.
George L. Spaeth, MD
Louis J. Esposito Research Professor
Wills Eye Hospital/Jefferson Medical College
To the Editor:
I have read the attractive article, "The Value of Genetic Testing in Glaucoma," by Amy M. Bovell and Karim F. Damji. (June 2003, Glaucoma Management, p. 76) Now there is a new way to see this argument. If you read my paper (Izzotti A, Sacca SC, Cartiglia C, De Flora S. Oxidative deoxyribonucleic acid damage in the eyes of glaucoma patients. Am J Med 2003 Jun 1;114(8):638-46.), you will be able to find a new way for the appraisal of the genetics of primary open-angle glaucoma.
This paper showed that the oxidative DNA damage of trabecular meshwork—as values of 8-hydroxy-2"-deoxyguanosine levels—is statistically significantly higher in POAG specimens than in controls. We have demonstrated a good statistical correlation between oxidative DNA damage and daily average intraocular pressure values. In addition, the levels of the oxidative DNA damage in human trabecular meshwork are directly proportional with the indexes of visual field damage.
In our paper we give evidence that the lack of GSTM1 [Glutathione S-transferase M1] seems associated with open-angle glaucoma patients and its oxidative stress increased in trabecular meshwork cells, especially when the antioxidant defense weakens with age. Moreover, this study supports the hypothesis that oxidative DNA damage would be the primum movens of human trabecular meshwork alterations in POAG. I hope that your readers will be interested in this article.
Sergio C. Saccà, MD
Clinica Oculistica Ospedale S.Martino
To the Editor:
The recent letter by Kenneth Hoffer: "Reflections on the origins of LASEK, 1990" reminded me of the evolution of LASEK at the Massachusetts Eye and Ear Infirmary in Boston in the mid-90s.
While waiting for my cornea fellowship to start at the MEEI in July 1995 and under the suggestion of Jonathan Talamo, MD, I spent a month in Monterrey, Mexico where they were doing PRK with the Schwind laser. They had started removing the epithelium using dilute alcohol but quickly abandoned the practice to the more conventional scraping method. In reviewing the charts it was found that the alcohol patients did better than the mechanically scraped ones.1 As PRK became available in the United States, we did a larger and more detailed study evaluating alcohol removal of the epithelium (using a regular Hoffer marker), which confirmed the prior findings.2 On November 6, 1996 while doing alcohol-assisted PRK at the MEEI, I decided to replace back the corneal epithelium on two patients instead of throwing it away. Dr. Dimitri Azar and I called it "Epithelial-flap PRK." The results have been published.3 Those were the days of the emergence of LASIK, and we decided instead to continue along that route for a while. Dr. Azar has made important modifications to the LASEK technique as well as important basic science research about it.4,5 From my perspective, I do thin-flap LASIK with a Carriazo-Barraquer manual microkeratome with a 110-µm plate obtaining flaps from 80 to 120 µm in the majority of cases and leaving at least 300 µm of untouched cornea. No striae or undue irregular astigmatism due to the flaps has been noted. This leads to a safe, predictable and rapidly recovering refractive procedure. On the rare occasion I perform LASEK.
In summary, LASEK is an important refractive alternative. Dr. Hoffer should be commended for his foresight, Dr. Azar for continuously improving upon the surgical technique, and Dr. Camellin for independently developing and popularizing it. I just happened to be at the right place at the right time to be involved in what is nowadays called LASEK.
Juan-Carlos Abad, MD
1. Dilute ethanol versus mechanical debridement before photorefractive keratectomy (PRK). Abad JC, Talamo JH, Vidaurri-Leal J, Helena MC, Cantu-Charles C. J Cataract Refract Surg 1996; 22:1427-1433.
2. A prospective evaluation of alcohol-assisted versus mechanical debridement before photorefractive keratectomy (PRK). Abad JC, An B, Power WJ, Foster CS, Azar DT, Talamo JT. Ophthalmology 1997;104:1566-1575.
3. Azar DT, Ang RT, Lee J-B, Kato T, Chen CC, Jain S, Gabison E, Abad JC. Laser Subepithelial Keratomileusis: Electron Microscopy and Visual Outcomes of Flap Photorefractive Keratectomy. Curr Opin Ophthalmol 2001;12:323-328.
4. Chen, CC, Chang J-H, Lee JB, Javier J, Azar DT. Human corneal epithelial cell viability and morphology after dilute alcohol exposure. Invest Ophthalmol Vis Sci 43:2593-2602, 2002
5. Feit R, Taneri S, Azar DT, Chen CC, Ang RT. LASEK results. Ophthalmol Clin North Am 2003;16:127-35.