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Misleading tonometry after LASIK
LETTERS
depth and thus the final cornea trauma.—J.L. Gu¨ell, MD, PhD, M. Calatayud, MD Reference 1. Budak K, Friedman NJ, Koch DD. Limbal relaxing incisions with cataract surgery. J Cataract Refract Surg 1998; 24:503–508
Misleading Tonometry After LASIK
W
e read with interest the report by Rehany and coauthors1 on a pocket of interface fluid developing after laser in situ keratomileusis (LASIK) in a glaucoma patient. Lyle and Jin2 first reported this condition but mistakenly attributed it to associated epithelial ingrowth. We reported a similar patient with a steroidinduced elevation of intraocular pressure (IOP) after LASIK who had a pocket of fluid under the interface in the left eye.3 This interface fluid led to a misleadingly low Goldmann tonometry reading, so the steroid-induced glaucoma was not diagnosed for several months. We diagnosed the elevated IOP by performing tonometry on the peripheral cornea. The patient had severe visual loss. We hypothesized that the steroid-induced IOP elevation caused transudation of fluid across the competent endothelium. Whereas this normally would have accumulated as microcystic edema in the epithelium, the resistance to fluid accumulation was lower in the potential space of the interface so fluid accumulated there instead. Rehany and coauthors postulate that glaucoma may have been a predisposing factor, but our patient did not have preexisting glaucoma. There are ow 3 case reports of this syndrome.1–3 We believe it is important for LASIK practitioners and general eyecare providers to be alert to this syndrome. With increasing numbers of patient having LASIK, increasing numbers of post-LASIK patients will be placed on steroid for rehabilitation from cataract surgery, for uveitis, or for other ocular disorders. Practitioners need to be aware that peripheral cornea tonometry may be needed to accurately assess the IOP in these postoperative patients, even long after LASIK surgery. ROBERT K. MALONEY, MD References 1. Rehany U, Bersudsky V, Rumelt S. Paradoxical hypotony after laser in situ keratomileusis. J Cataract Refract Surg 2000; 26: 1823–1826 2. Lyle WA, Jin GJC. Interface fluid associated with diffuse lamellar keratitis and epithelial ingrowth after laser in situ keratomileusis. J Cataract Refract Surg 1999; 25:1009 –1012 650
3. Najman-Vanier J, Smith RJ, Maloney RK. Interface fluid after LASIK: misleading tonometry can lead to end-stage glaucoma (letter). J Cataract Refract Surg 2000; 26:471
Reply: We appreciate Dr. Maloney’s comments. Indeed, when we wrote our report before the comment from Maloney and coauthors to the Lyle and Jin report was published, we were looking for similar cases to collaborate these findings. We thought that such collaboration would enhance the validity of our findings and the proposed theory for the development of post-LASIK paradoxical hypotony. In our paper, we did mention that we were aware of at least 2 patients without a history of glaucoma who developed post-LASIK paradoxical hypotony. The common denominator in all previous patients, whether glaucomatous, was the accumulation of fluid in the corneal flap–stromal bed interface, which masked the real IOP. In addition, all patients had steroid-induced glaucoma and interstitial keratitis. We may conclude that any patient with an intralamellar fluid pocket may have increased IOP. This should be assessed by Schiotz tonometry, manual palpation, or applanation tonometry through the peripheral cornea. Patients with high IOP according to these measurements, even when the IOP obtained by applanation tonometry through the central cornea is exceedingly low, should be treated with antiglaucoma medications. Carbonic anhydrase inhibitors and hyperosmotic agents may be particularly effective in these patients. Topical corticosteroids should be replaced with topical cyclosporine-A and nonsteroidal antiinflammatory drugs or discontinued. Systemic corticosteroids may be added when this complication is associated with severe diffuse intralamellar inflammatory response. Some patients may require elevation of the corneal flap, irrigation, and reposition. It is worthwhile to document the use of corticosteroids and the presence of preceding interstitial keratitis and to perform specular microscopy to ascertain whether they are common to all patients and could support our theory for the development of post-LASIK paradoxical hypotony. In conclusion, it is crucial after LASIK to avoid prolonged instillation of topical corticosteroids and to diagnose and treat this condition as early as possible to prevent irreversible visual field loss.—Uri Rehany, MD, Valery Bersudsky, MD, Shimon Rumelt, MD
Chronic or Saccular Endophthalmitis: Diagnosis and Management n a recent article, Dr. Teichmann1 refers to our paper2 as an example of a primarily aggressive approach to the treatment of chronic postoperative endophthalmitis (intraocular lens removal, total capsulectomy, anterior vitrectomy). Various conservative treatments have been tried but have had limited success. This is probably due to the fact that Propionibacterium and
I
J CATARACT REFRACT SURG—VOL 27, MAY 2001
depth and thus the final cornea trauma.—J.L. Gu¨ell, MD, PhD, M. Calatayud, MD Reference 1. Budak K, Friedman NJ, Koch DD. Limbal relaxing incisions with cataract surgery. J Cataract Refract Surg 1998; 24:503–508
Misleading Tonometry After LASIK
W
e read with interest the report by Rehany and coauthors1 on a pocket of interface fluid developing after laser in situ keratomileusis (LASIK) in a glaucoma patient. Lyle and Jin2 first reported this condition but mistakenly attributed it to associated epithelial ingrowth. We reported a similar patient with a steroidinduced elevation of intraocular pressure (IOP) after LASIK who had a pocket of fluid under the interface in the left eye.3 This interface fluid led to a misleadingly low Goldmann tonometry reading, so the steroid-induced glaucoma was not diagnosed for several months. We diagnosed the elevated IOP by performing tonometry on the peripheral cornea. The patient had severe visual loss. We hypothesized that the steroid-induced IOP elevation caused transudation of fluid across the competent endothelium. Whereas this normally would have accumulated as microcystic edema in the epithelium, the resistance to fluid accumulation was lower in the potential space of the interface so fluid accumulated there instead. Rehany and coauthors postulate that glaucoma may have been a predisposing factor, but our patient did not have preexisting glaucoma. There are ow 3 case reports of this syndrome.1–3 We believe it is important for LASIK practitioners and general eyecare providers to be alert to this syndrome. With increasing numbers of patient having LASIK, increasing numbers of post-LASIK patients will be placed on steroid for rehabilitation from cataract surgery, for uveitis, or for other ocular disorders. Practitioners need to be aware that peripheral cornea tonometry may be needed to accurately assess the IOP in these postoperative patients, even long after LASIK surgery. ROBERT K. MALONEY, MD References 1. Rehany U, Bersudsky V, Rumelt S. Paradoxical hypotony after laser in situ keratomileusis. J Cataract Refract Surg 2000; 26: 1823–1826 2. Lyle WA, Jin GJC. Interface fluid associated with diffuse lamellar keratitis and epithelial ingrowth after laser in situ keratomileusis. J Cataract Refract Surg 1999; 25:1009 –1012 650
3. Najman-Vanier J, Smith RJ, Maloney RK. Interface fluid after LASIK: misleading tonometry can lead to end-stage glaucoma (letter). J Cataract Refract Surg 2000; 26:471
Reply: We appreciate Dr. Maloney’s comments. Indeed, when we wrote our report before the comment from Maloney and coauthors to the Lyle and Jin report was published, we were looking for similar cases to collaborate these findings. We thought that such collaboration would enhance the validity of our findings and the proposed theory for the development of post-LASIK paradoxical hypotony. In our paper, we did mention that we were aware of at least 2 patients without a history of glaucoma who developed post-LASIK paradoxical hypotony. The common denominator in all previous patients, whether glaucomatous, was the accumulation of fluid in the corneal flap–stromal bed interface, which masked the real IOP. In addition, all patients had steroid-induced glaucoma and interstitial keratitis. We may conclude that any patient with an intralamellar fluid pocket may have increased IOP. This should be assessed by Schiotz tonometry, manual palpation, or applanation tonometry through the peripheral cornea. Patients with high IOP according to these measurements, even when the IOP obtained by applanation tonometry through the central cornea is exceedingly low, should be treated with antiglaucoma medications. Carbonic anhydrase inhibitors and hyperosmotic agents may be particularly effective in these patients. Topical corticosteroids should be replaced with topical cyclosporine-A and nonsteroidal antiinflammatory drugs or discontinued. Systemic corticosteroids may be added when this complication is associated with severe diffuse intralamellar inflammatory response. Some patients may require elevation of the corneal flap, irrigation, and reposition. It is worthwhile to document the use of corticosteroids and the presence of preceding interstitial keratitis and to perform specular microscopy to ascertain whether they are common to all patients and could support our theory for the development of post-LASIK paradoxical hypotony. In conclusion, it is crucial after LASIK to avoid prolonged instillation of topical corticosteroids and to diagnose and treat this condition as early as possible to prevent irreversible visual field loss.—Uri Rehany, MD, Valery Bersudsky, MD, Shimon Rumelt, MD
Chronic or Saccular Endophthalmitis: Diagnosis and Management n a recent article, Dr. Teichmann1 refers to our paper2 as an example of a primarily aggressive approach to the treatment of chronic postoperative endophthalmitis (intraocular lens removal, total capsulectomy, anterior vitrectomy). Various conservative treatments have been tried but have had limited success. This is probably due to the fact that Propionibacterium and
I
J CATARACT REFRACT SURG—VOL 27, MAY 2001