FIGURE 2. Confocal images of the patients right eye in December 1998.

(Left) Spindle-shaped irregular keratocytes (arrow) of the anterior stroma. (Right) Fibroblasts are interconnected by a three-dimensional network of brils and surrounded by highly reective diffuse brillar material. (Confocal microscopy; objective 40/0.75).

keratocytes were gradually incorporated into a network of interlacing brils and surrounded by highly reective diffuse brillar inhomogeneities (Figure 2). The compact nature of these changes prevented clear visualization of corneal endothelium in this area, but endothelial cells appeared normal in the remaining parts of the cornea. Mustard gas may cause immediate and delayed ocular damage. Immediate effects may result from its alkylating effect,1,2 which is facilitated in aqueous solutions such as the tear lm and may result in cell necrosis and inhibition of cell proliferation.3 In less than 1% of victims a delayed type of keratopathy occurs with a long asymptomatic period of up to 40 years after initial exposure.4 As seen in our patient, delayed keratopathy typically is seen with corneal ulceration and persistent porcelain-like episcleral appearance. Opacication of the cornea is seen predominantly in the lower and central portions, whereas the upper part is protected by the eyelid. Inhibition of respiratory enzymes resulting in formation of free radicals has been suggested as the underlying pathomechanism affecting predominantly germinative epithelial cells in the skin, the respiratory tract, and at the ocular surface.3 Moreover, degenerative processes and immune reactions against altered corneal proteins have been suggested as causes of long-term damage.4,5 Our confocal images of spindle-like keratocytes may favor necrotic changes after injury. Treatment of delayed mustard gas keratopathy is aimed at reducing ocular irritation and improving vision. Ocular lubricants, therapeutic contact lenses, and lamellar or penetrating keratoplasty have been used.4 Transplantation of amnion membrane or limbal stem cells may prove to be a successful concept for the treatment of this disorder. VOL. 128, NO. 4

REFERENCES

1. Zagora E. Specic protein denaturants and selective enzyme inhibitors. In: Eye injuries. Springeld, Illinois: Charles C. Thomas Publishers, 1970:308 309. 2. Hochmeister M, Vycudilik W. Morpho-toxikologische Befunde nach Kampfgaseinwirkung (S-Lost). Beitr Gerichtl Med 1989;47:533538. 3. Aasted A, Darre E, Wulf HC. Mustard gas: clinical, toxicological and mutagenic aspects based on modern experience. Ann Plast Surg 1987;19:330 333. 4. Solberg Y, Alcalay M, Belkin M. Ocular injury by mustard gas. Surv Ophthalmol 1997;41:461 466. 5. Maumenee AE, Scholz RO. The histopathology of ocular lesions produced by sulfur and nitrogen mustards. Bull John Hopkins Hosp 1948;82:121147.

Iatrogenic Cataract After LaserAssisted In Situ Keratomileusis

Kunihiko Nakamura, MD, Hiroko Bissen-Miyajima, MD, Hiroyuki Arai, MD, Ikuko Toda, MD, Yoshiko Hori, MD, Shigeto Shimmura, MD, and Kazuo Tsubota, MD
PURPOSE:

To report a case of corneal opacity and iatrogenic cataract after laser-assisted in situ keratomileusis.
Accepted for publication May 20, 1999. From the Department of Ophthalmology, Tokyo Dental College, Chiba, Japan (K.N., H.B.-M., I.T., Y.H., S.S., K.T.); the Minami Aoyama Eye Clinic, Tokyo, Japan (H.A., I.T., Y.H.); and the Department of Ophthalmology, Keio University School of Medicine, Tokyo, Japan (K.N., H.B.-M., S.S., K.T.). Inquiries to Kunihiko Nakamura, MD, Department of Ophthalmology, Tokyo Dental College, 5-11-13 Sugano, Ichikawa, Chiba 272-8513, Japan; fax: 81-47-325-4456; e-mail: QYJ15752@nifty.ne.jp

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Case report. A 44-year-old man was initially seen with a traumatic cataract, corneal stromal opacity, and defect of the endothelium in the right eye after laser-assisted in situ keratomileusis performed by a plastic surgeon who had no ophthalmologic training. RESULTS: It was speculated that repeated ablations resulted in corneal perforation. We immediately performed phacoemulisication to remove the cataract and to prevent phacolytic glaucoma. However, visual acuity remained 20/200 because of the corneal stromal opacity, and penetrating keratoplasty was performed 2 months later, which improved best-corrected visual acuity to 20/30. CONCLUSIONS: This case demonstrated that laser-assisted in situ keratomileusis can cause devastating damage to the eye. (Am J Ophthalmol 1999;128:507509. 1999 by Elsevier Science Inc. All rights reserved.)

METHOD:

ASER-ASSISTED IN SITU KERATOMILEUSIS IS A MORE

FIGURE 1. Slit-lamp appearance of the patients right eye. Corneal stromal opacity under the ap created by a microkeratome and a defect in the endothelium at the center of the cornea were observed. The rupture of the anterior lens capsule extended from the 1 oclock to the 7 oclock position, and the mass of lens cortex herniated into the anterior chamber.

complex procedure than photorefractive keratectomy. Although maneuvers required for laser-assisted in situ keratomileusis have recently been simplied, it still demands a well-trained ophthalmologist who knows the basic principles and is familiar with the surgical instruments to minimize and manage complications. With laser-assisted in situ keratomileusis becoming simpler and more popular, many surgeons have entered the eld of refractive surgery, many of whom lack a thorough knowledge of the procedure. This tendency can result in severe complications. We report our experience in treating a patient with an iatrogenic cataract and corneal opacity after laser-assisted in situ keratomileusis by a nonophthalmologist.

CASE: A 44-year-old man underwent bilateral laserassisted in situ keratomileusis at a private clinic by a plastic surgeon who had no ophthalmologic training. He had markedly decreased visual acuity in his right eye 2 weeks postoperatively. He was examined by an ophthalmologist at another clinic and referred to our clinic for treatment of cataract and corneal scarring. Examination disclosed a best-corrected visual acuity of RE: hand motions and LE: 20/30 and intraocular pressure of RE: 23 mm Hg and LE: 15 mm Hg. The right eye had corneal stromal opacity under the ap created by a microkeratome and a defect in the endothelium at the center of the cornea. The mass of lens cortex herniated through the ruptured anterior lens capsule into the anterior chamber. Fundus examination was impossible because of the dense cataract (Figure 1). According to the information obtained from the patient, his previous best-corrected visual acuity was RE: 20/20 before the three laser-assisted in situ keratomileusis procedures. The rst operation consisted of the corneal ap and excimer laser ablation to correct myopia. The second operation included redetaching the ap and additional

FIGURE 2. Slit-lamp appearance of the patients right eye after a phacoemulsication procedure and corneal transplantation. Best-corrected visual acuity improved to 20/30.

ablation to correct astigmatism. However, the patient could not attain satisfactory uncorrected visual acuity, and a third operation was performed 3 months after the second surgery to treat residual myopia. At this time, corneal perforation occurred during laser ablation. The surgeon then apparently sutured the stromal bed of the perforated site and replaced the corneal ap. When the patient was referred to our clinic, we decided to perform phacoemulsication to remove the cataract and to prevent phacolytic glaucoma. After cataract surgery, best-corrected visual acuity remained 20/200 because of the stromal opacity and irregular astigmatism of the cornea. Penetrating keratoplasty was performed 2 months later, and best-corrected visual acuity improved to 20/30 (Figure 2).
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OCTOBER 1999

Complications of laser-assisted in situ keratomileusis may occur in each step of the procedure, including the use of the microkeratome, excimer laser, or postoperative management. Severe complications have been reported such as corneal perforation caused by inappropriate assembly of the microkeratome,1 displacement of the corneal ap,2 and melting of the corneal ap because of progressive epithelial ingrowth.3 This patient had irregular corneal thickness, and accidental perforation of the corneal stromal bed resulted from the inexperience of the surgeon. It is speculated that the anterior lens capsule was ruptured by inappropriate suturing of the stromal bed to seal the perforation site. Surgeons performing laser-assisted in situ keratomileusis should be aware of potentially devastating complications.
REFERENCES

ciprooxacin, whereas from 1995 to 1998, 4.1% (8/ 196) of ocular isolates showed in vitro resistance (P .014). CONCLUSIONS: Ciprooxacin-resistant P. aeruginosa has been identied in recent clinical ocular specimens. Ciprooxacin resistance among ocular isolates of P. aeruginosa is a local and worldwide concern. (Am J Ophthalmol 1999;128:509 510. 1999 by Elsevier Science Inc. All rights reserved.)

IPROFLOXACIN IS A COMMONLY USED ANTIBIOTIC IN

1. Moner JIB, Granados JIB. Intrastromal keratomileusis: complications associated with the microkeratome. In: Buratto L, Brint SF, editors. LASIK principles and techniques. Thorofare, New Jersey: Slack, 1998:365369. 2. Hoffman CJ, Rapuano CJ, Cohen EJ, Laibson PR. Displacement of corneal lenticule after automated lamellar keratoplasty. Am J Ophthalmol 1994;118:109 111. 3. Castillo A, Diaz-Valle D, Gutierrez AR, Toledano N, Romero F. Peripheral melt of ap after laser in situ keratomileusis. J Refract Surg 1998;14:61 63.

Emerging Ciprooxacin-Resistant Pseudomonas aeruginosa

Nauman A. Chaudhry, MD, Harry W. Flynn, Jr, MD, Timothy G. Murray, MD, Homayoun Tabandeh, MD, Mozart O. Mello, Jr, MD, and Darlene Miller, MS, MPH
To report a clinical series of ciprooxacinresistant ocular isolates of Pseudomonas aeruginosa from a tertiary care ophthalmic center. METHODS: Review of in vitro sensitivities of all ocular isolates of P. aeruginosa between July 1991 and September 1998. In vitro resistance was dened as a minimum inhibitory concentration of 4 or more g per ml. RESULTS: Nine of 423 ocular isolates of P. aeruginosa showed in vitro resistance to ciprooxacin. From 1991 to 1994, 0.44% (1/227) of ocular isolates were resistant to
Accepted for publication May 22, 1999. From the Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami School of Medicine, Miami, Florida. Presented in part at the annual meeting of the Association for Research in Vision and Ophthalmology, Ft Lauderdale, Florida, 1999. Reprint requests to Timothy G. Murray, MD, Bascom Palmer Eye Institute, 900 NW 17th St, University of Miami School of Medicine, Miami, FL 33136; fax: (305) 326-6417. PURPOSE:

ophthalmic practice.1 It is a broad-spectrum uoroquinolone with coverage against most gram-positive and gram-negative organisms, including Pseudomonas aeruginosa. The emergence of ciprooxacin-resistant ocular isolates is a growing concern.25 This study was conducted to examine the susceptibility of ocular isolates of P. aeruginosa to ciprooxacin. In the microbiology department of the Bascom Palmer Eye Institute, a review of in vitro sensitivities of all ocular isolates of P. aeruginosa between January 1991 and December 1998 was performed. In vitro resistance was dened as a minimum inhibitory concentration (MIC) of 4 or more g per ml. The sensitivities were tested with the automated Vitek test system (bioMerieux Vitek Inc, Missouri) and conrmed with the conventional disk diffusion method and the E test (AB Biodisk, Remel, Lenexa, Kansas). During the 8-year study period, a total of 499 ocular isolates of P. aeruginosa were identied; 76 isolates were excluded because of multiple cultures from the same patients. Of the 423 ocular isolates included in this study, nine showed in vitro resistance to ciprooxacin. The source of ocular specimens included cornea (4), conjunctiva (2), orbital tissue (2), and lacrimal sac (1). All isolates were sensitive to gentamicin (Table 1). The isolates were not tested for other uoroquinolones because resistance to ciprooxacin implies resistance to all other clinically available uoroquinolones, including ooxacin, noroxacin, lomeoxacin, and enoxacin.6 To study the trend in susceptibility of ciprooxacin to ocular P. aeruginosa, we studied the susceptibility pattern between 1991 to 1994 and 1995 to 1998 (Figure 1). During the 1991 to 1994 interval, 227 ocular isolates were tested, and only one (0.44%) showed in vitro resistance to ciprooxacin. Between 1995 and 1998, 196 isolates were studied and eight (4.1%) were resistant to ciprooxacin. The change in susceptibility was statistically signicant (P .014; Fisher exact test). Reported ciprooxacin-resistant ocular isolates include coagulase-negative Staphylococcus, Staphylococcus aureus, Streptococcus viridans, Corynbacterium pseudodiphtheriticum, Xanthomonas maltophila, and Mycobacterium chelonae.15 The possible mechanisms for acquired resistance include a decrease in the susceptibility of DNA gyrase to the 509

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