BRIEF REPORTS Delayed Mustard Gas Keratopathy: Clinical Findings and Confocal Microscopy Uwe Pleyer, MD, Zacharias Sherif, Holger Baatz, MD, and Christian Hartmann, MD, PHD PURPOSE:
To describe the clinical manifestations and confocal microscopic findings in a patient with delayed mustard gas keratopathy. METHOD: Case report. A 32-year-old veteran who had participated in the Iran-Iraq conflict was exposed to mustard gas in 1988. Ocular abnormalities in 1996 and 1998 and corneal confocal microscopic findings in 1998 are presented. RESULTS: In 1996, slit-lamp examination disclosed bilateral limbal changes with tortuous blood vessels and full-thickness corneal alterations. In 1998, the right eye had porcelain-white episcleral changes and adjacent peripheral ulcerative keratopathy. Confocal microscopy demonstrated irregular-appearing epithelial and basal epithelial cells. The anterior stroma was remarkable for spindle-like keratocytes, diffuse fibrillar inhomogeneities and the presence of highly reflective material. CONCLUSIONS: Mustard gas keratopathy is a uncommon cause of ocular damage, but it may lead to delayed ocular damage. (Am J Ophthalmol 1999;128:506 –507. © 1999 by Elsevier Science Inc. All rights reserved.)
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1988. At that time he was hospitalized for 7 months for treatment of skin lesions. In August 1996 the patient’s best-corrected visual acuity was 20/32 in both eyes. Corneal sensation was reduced bilaterally. At the 7 o’clock position (RE) and 3 o’clock position (LE) irregular conjunctival and corneal epithelium with positive fluorescein staining was seen. We also noticed limbal and corneal stromal changes with tortuous and varicose vessels and intracorneal bleeding. The central cornea was hazy, demonstrating stromal deposits. No intraocular inflammation was present and intraocular pressure was normal. The patient was treated for 3 weeks with topical betamethasone 0.1% four times daily and ocular lubricants in both eyes. Corticosteroids were discontinued because the symptoms and clinical condition did not change, and treatment was restricted to unpreserved artificial tears. In December 1998 the patient had irregular astigmatism and changed axis on examination; visual acuity had decreased to RE: 20/40 and the left eye remained stable. The right eye had porcelain-white episcleral changes and adjacent peripheral ulcerative keratopathy (Figure 1). Confocal microscopy demonstrated irregular-appearing epithelial and basal epithelial cells in both central corneas. Within the anterior corneal stroma spindlelike keratocytic nuclei close to Bowman layer could be delineated. These
ULFUR MUSTARD IS STILL A THREAT OF CHEMICAL
warfare. We describe an ocular injury after mustard gas exposure. A 32-year-old man was initially examined with recurrent pain, photophobia, and blurred vision. His symptoms first occurred several months earlier but increased in severity. The medical history was unremarkable for previous systemic or ocular diseases. However, he had served in the Iranian army and had been severely affected by mustard gas warfare during the Iran-Iraq conflict in March Accepted for publication April 28, 1999. From the Department of Ophthalmology, Charite´, Campus Virchow Hospital, D-13353 Berlin, Germany. This work was supported by DFG (Pl 150/9-1) and Charite´ research grant (Pl). Inquiries to Uwe Pleyer, MD, Department of Ophthalmology, Charite´, Augustenburger Platz 1, D-13353 Berlin; fax: 49-30-450 54901; e-mail:
[email protected]
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1999 BY
FIGURE 1. Porcelain-white episcleral changes and adjacent peripheral corneal ulceration (arrow) in the right eye of the patient initially seen in December 1998, 10 years after mustard gas exposure.
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FIGURE 2. Confocal images of the patient’s 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 fibrils and surrounded by highly reflective diffuse fibrillar material. (Confocal microscopy; objective 40/0.75).
keratocytes were gradually incorporated into a network of interlacing fibrils and surrounded by highly reflective diffuse fibrillar 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 film 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. Opacification 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. Specific protein denaturants and selective enzyme inhibitors. In: Eye injuries. Springfield, Illinois: Charles C. Thomas Publishers, 1970:308 –309. 2. Hochmeister M, Vycudilik W. Morpho-toxikologische Befunde nach Kampfgaseinwirkung (S-Lost). Beitr Gerichtl Med 1989;47:533–538. 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;82:121–147.
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:
[email protected]
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