- Email: [email protected]
Cogan syndrome presenting after uneventful laser in situ keratomileusis
CASE REPORT
Cogan syndrome presenting after uneventful laser in situ keratomileusis Minoru Tomita, MD, PhD, Ayako Chiba, BS, Naoko Inoue, BA, Tukezban Huseynova, MD, Tadahiko Tsuru, MD, PhD, George O. Waring IV, MD
We report 2 cases of Cogan syndrome that developed after uneventful laser in situ keratomileusis. In the first case, an 8-month postoperative biomicroscopy revealed bilateral interface neovascularization, white intrastromal deposits, and anterior chamber cells and flare. In the second case, white cell infiltration and neovascularization were observed in the deep corneal stroma of the patient’s right eye 18 months postoperatively. Based on these observations, which are consistent with typical interstitial keratitis, and the patients’ history of Meniere-like disease, such as vertigo and mild hearing loss, Cogan syndrome was diagnosed in both patients. Topical steroids were prescribed. Intensive treatments with corneal irrigation and topical steroids showed effective outcomes in both cases. Financial Disclosure: No author has a financial or proprietary interest in any material or method mentioned. J Cataract Refract Surg 2013; 39:1260–1266 Q 2013 ASCRS and ESCRS
Cogan syndrome is a rare disease characterized by nonsyphilitic interstitial keratitis, often associated with ocular inflammation, vestibulo-auditory dysfunction such as Meniere syndrome, and various systemic manifestations.1–3 Although Cogan syndrome occurs most commonly in young adults without any sex predominance, the pathologic causes have not been determined.4–6 Interstitial keratitis may be unilateral or bilateral, and common ocular symptomatology includes, but is not limited to, decreased visual acuity, photophobia, ocular discomfort, and lacrimation. Vestibulo-auditory symptoms include vertigo, tinnitus, and/or the loss of hearing. Cogan syndrome has been classified into 2 types, typical and atypical, based on the ocular Submitted: January 13, 2013. Final revision submitted: March 10, 2013. Accepted: March 11, 2013. From the Shinagawa LASIK Center (Tomita, Chiba, Inoue, Huseynova, Tsuru), Chiyoda-ku, Tokyo, Japan; the Department of Ophthalmology (Tomita), Wenzhou Medical College, Wenzhou, China; and the Storm Eye Institute (Waring), Medical University of South Carolina, Charleston South Carolina, USA. Naoko Inoue provided editorial assistance. Corresponding author: Minoru Tomita, MD, PhD, Shinagawa LASIK Center, Yurakucho ITOCiA 14th floor, 2-7-1 Yurakucho Chiyoda, Tokyo 100-0006, Japan. E-mail: [email protected].
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manifestations or the interval between the onset of ocular manifestations and any vestibulo-auditory dysfunction. According to the original reports of typical Cogan syndrome, ocular findings are confined to the anterior segment and the onset of vestibulo-auditory symptoms are within 2 years of the onset of ocular symptoms.2,3,7 In atypical Cogan syndrome, ocular manifestations are varied, including but not limited to keratitis, episcleritis, scleritis, anterior uveitis, glaucoma, retinitis, and optic neuritis. In addition, vestibulo-auditory symptoms can appear more than 2 years before or after ocular manifestations.2–4,6 Since the original description in 1945,1 Cogan syndrome has been well documented in the literature.2–5,7 To our knowledge, only 1 case of Cogan syndrome has been reported after laser in situ keratomileusis (LASIK).7 With the increasing number of LASIK procedures worldwide, it is helpful to differentiate Cogan syndrome from keratitis such as diffuse lamellar keratitis (DLK), which is more typically found after LASIK. In this report, we present 2 cases of Cogan syndrome after uneventful LASIK and describe the management of both cases and the outcomes. CASE REPORTS Case 1 A 28-year-old man with a 12-year history of soft contact lens use to correct myopia and astigmatism had bilateral LASIK in March 2009 at Shinagawa LASIK Center. The 0886-3350/$ - see front matter http://dx.doi.org/10.1016/j.jcrs.2013.05.025
CASE REPORT: COGAN SYNDROME AFTER LASIK
medical history was notable for only atopic dermatitis. The preoperative examination was remarkable for a small peripheral stromal opacity in the left eye that was thought to be related to the contact lens use and was negative for signs of prior inflammatory episodes, including an absence of corneal neovascularization. The preoperative uncorrected (UDVA) and corrected (CDVA) distance visual acuities were 20/250 and 20/10, respectively, in the right eye and 20/250 and 20/10, respectively, in the left eye. The preoperative manifest refraction was 3.75 1.0 170 and 4.50 0.25 35 in the right eye and left eye, respectively. Uneventful LASIK was performed in both eyes with the Intralase FS60 (Abbott Medical Optics, Inc.) and the Allegretto Wave Eye-Q 400Hz (Alcon Laboratories, Inc.). Three months postoperatively, the UDVA and CDVA were 20/10 in both eyes and slitlamp examinations were within normal limits. Eight months after the LASIK procedure, the patient returned to the center complaining of decreased vision and a foreign-body sensation in the left eye. The UDVA and CDVA were 20/16 and 20/10, respectively, in the right eye and 20/20 and 20/16, respectively, in the left eye, respectively. Slitlamp examination showed bilateral superior stromal neovascularization and bilateral asymmetric diffuse interface inflammation consistent with DLK. In the right eye, mild diffuse interface inflammation was seen. The left eye was notable for severe diffuse interface inflammation including white exudates and clumped cells extending over half the cornea. Dexamethasone sodium m-sulfobenzoate 0.1% and moxifloxacin hydrochloride 0.5% ophthalmic solutions were prescribed hourly for 9 days. Six days after the topical therapy was started, the patient reported partial improvement in the subjective acuities but continued difficulty, more so in the left eye. The biomicroscopy was notable for persistent bilateral superior interstitial keratitis 9 days after the topical therapy was started and also for bilateral superior coalescent granular intrastromal opacities along with associated intrastromal neovascularization (Figure 1). Most of the deposits were located in the interface between the corneal flap and the stromal bed.
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Because of the patient’s condition and the location of the inflammation, a lifted-flap interface irrigation was performed in the left eye using a balanced salt solution containing 0.9% methylprednisolone sodium succinate. During the irrigation, white granular deposits and lipid crystals were flushed from the interface but no histopathology was performed. After the cornea in the left eye was irrigated, 0.2 mL of dexamethasone sodium phosphate 0.4% was injected subconjunctivally. Dexamethasone sodium m-sulfobenzoate 0.1%, moxifloxacin hydrochloride 0.5%, and sodium hyaluronate 0.3% ophthalmic solutions were prescribed bilaterally every hour for a week. As the patient was only mildly symptomatic in the right eye and no interface inflammation was observed at the time of follow-up, no irrigation was performed in the right eye. One day after the interface irrigation, the UDVA and CDVA in the left eye were 20/20 and 20/16, respectively, and the patient’s subjective acuity improved dramatically. One week after irrigation, the acuity improved subjectively and both UDVA and CDVA were 20/16. A sodium hyaluronate 0.1% ophthalmic solution was prescribed for 2 months until the next examination. Further questioning revealed a history of episodic vertigo consistent with Meniere-like symptomatology with a similar onset of decreasing visual acuity. Given this history and the episode of interstitial keratitis, atypical Cogan syndrome was diagnosed. After informed consent was obtained, a systemic examination including serological evaluation, vestibulo-auditory examinations, cranial magnetic resonance imaging (MRI), and computed tomography (CT) was performed. Serologic evaluation included complete blood cell counts, C-reactive protein, rheumatoid factor, antinuclear antibodies, serum complements syphilitic panels, human leukocyte antigens, antiviral immunoglobulins to herpes simplex virus (HSV) immunoglobulin G (IgG), varicella zoster virus (VZV IgG), and the human T-lymphotropic virus-1. Remarkable imaging results included frontonasal sinusitis and serologic evaluations that were positive for antiviral antibodies to herpes simplex and varicella zoster. Two months after the irrigation in the left eye, the interstitial keratitis had subsided. The UDVA and CDVA were 20/ 12.5 in both eyes. Three months after irrigation, the UDVA and CDVA were 20/10 in the right eye and remained 20/ 12.5 in the left eye.
Case 2
Figure 1. Case 1: Slitlamp view of the left eye 8 months after LASIK, indicating patchy exudates and neovascularization.
A 29-year-old woman with a 13-year history of soft contact lens use had bilateral LASIK in September 2007 at Shinagawa LASIK Center. The preoperative examinations were remarkable as the UDVA and CDVA were 20/800 and 20/ 12.5, respectively, in the right eye and 20/800 and 20/16, respectively, in the left eye. The manifest refraction was 12.00 diopters sphere and 10.50 0.50 90 in the right eye and left eye, respectively. The preoperative slitlamp examinations were within normal limits. Uneventful LASIK was performed with the Intralase FS60 and Allegretto Wave Eye-Q 400 Hz. One week postoperatively, the UDVA and CDVA were 20/20 and 20/20, respectively, in both eyes. Subsequent examinations were performed at the patient’s neighborhood clinic. Eighteen months after the LASIK procedure, the patient returned complaining of decreased visual acuity in the right eye. The physical examination results were remarkable for a UDVA of 20/40 and a CDVA of 20/25 in the
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Figure 2. Case 2: Corneal topography maps indicating subepithelial corneal infiltrates with opacities in the deep stroma.
right eye. Biomicroscopy of the right eye revealed superior intrastromal corneal neovascularization and focal opacities near the terminal portion of the neovascularization in the paracentral cornea. Both UDVA and CDVA in the left eye were 20/16, and the slitlamp examination was within normal limits. Dexamethasone sodium m-sulfobenzoate 0.1% and moxifloxacin hydrochloride 0.5% ophthalmic solutions were prescribed topically 5 times a day in the right eye. Two weeks after the initiation of the topical therapy, the UDVA and CDVA in the right eye improved to 20/32 and 20/20, respectively. The slitlamp examination revealed stable intrastromal neovascularization and opacities in the periphery of the central cornea. Dexamethasone sodium m-sulfobenzoate 0.1% ophthalmic solution use continued 4 times a day for 1 month in the right eye. One month after the topical treatment was started, the UDVA and CDVA in the right eye improved to 20/25 and 20/16, respectively. The dexamethasone sodium m-sulfobenzoate 0.1% course continued 4 times a day for 7 months with a slow taper. Monthly checks were performed, and the patient was stable during the treatment. Three months after the treatment was discontinued, the UDVA and CDVA remained stable but subepithelial corneal infiltrates with deep stromal opacities were noted in the right eye (Figures 2 and 3). Optical coherence tomography (Casia SS1000; Tomey Corp.) showed that the portions with highreflected densities coincided with the sites of pathological change in the deep stroma (Figure 4). Dexamethasone sodium m-sulfobenzoate 0.1% was prescribed 5 times a day for 2 weeks in the right eye. On further clinical review, the patient reported a history of Meniere disease-like symptoms including vertigo and mild hearing loss in the lower vocal ranges as she experienced decreasing visual acuity. The patient was referred to an otolaryngologist for evaluation and management of the Meniere disease. Betahistine mesilate was prescribed for a month, and the symptoms resolved. The patient had a complete systemic evaluation, the same as described for Case 1. The MRI was remarkable for paranasal sinusitis in the left maxillary sinus. In addition, the chest CT was translucent in the right upper lobe and both
lower lobes consistent with possible viral pneumonitis (Figure 5). Serologic and audiometric evaluations were negative except for viral antibodies, which were positive for HSV IgG and VZV IgG. Since the corneal haze and neovascularization were observed in the deep stroma, irrigation of the stromal bed was not performed. Dexamethasone sodium m-sulfobenzoate 0.1% was prescribed 5 times a day again in the right eye for 1 month. The patient remained stable on the interim visits, and the topical steroid use was discontinued. One year after the diagnosis of typical Cogan syndrome was made, the active interstitial keratitis had subsided completely. Although slight intrastromal scarring and neovascularization remained, the UDVA and CDVA were 20/25 and 20/20, respectively, in the right eye and 20/16 and 20/12.5, respectively, in the left eye. The patient experienced no
Figure 3. Case 2: Slitlamp view of the right eye showing corneal neovascularization and granular deposits.
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Figure 4. Case 2: Optical coherence tomography image of the right eye showing areas with high-reflected density coinciding with sites of pathological change in the deep stroma.
further dizziness or vertigo, with unremarkable follow-up visits to the otolaryngologist.
DISCUSSION Cogan syndrome was first described by David Cogan in 1945.1 He described 4 patients who had experienced nonsyphilitic interstitial keratitis and vestibuloauditory symptoms. Since then, cases of typical and atypical Cogan syndrome have been reported by several authors.1–6 However, case reports of Cogan syndrome after LASIK are rare.7 Cogan syndrome is an uncommon disease whose etiology is still unknown, so diagnostic criteria and treatment options have not been well established.5 Usually Cogan syndrome has been diagnosed based on the characteristic ocular findings and vestibuloauditory dysfunctions, as they were in our cases.1–3,5 Treatment is typically topical and/or systemic corticosteroids for the interstitial keratitis and vestibuloauditory dysfunction.2–4,6 The patient described in Case 1 suffered from Meniere disease–like dizziness prior to the development
of nonsyphilitic interstitial keratitis. Further diagnostic evaluation including serology, cranial MRI, CT, and audiometry were not remarkable for this particular etiology. Although some Cogan syndrome cases with paranasal sinusitis have been reported, the association with Cogan syndrome is unknown.3,8 In addition to the typical ocular and vestibulo-auditory findings, paranasal sinusitis was detected in both patients by cranial MRI. Although Cupps9 stated that sinusitis is not a diagnostic prerequisite for Cogan syndrome, previous reports show a potential association with Cogan syndrome and paranasal sinusitus.3,8,10,11 Further study of the correlation between Cogan syndrome and paranasal sinusitis is needed. According to Gluth et al.6 in their half-century literature review, one-third of patients exhibited ophthalmic signs and symptoms as the initial presentation of Cogan syndrome. Although rare, Cogan syndrome should be considered when interstitial keratitis or other associated findings are noted. As mentioned above, the Case 1 patient presented a history of atopic dermatitis, which may play a role as a host factor in the development of interface
Figure 5. Case 2: Chest CT images showing translucent lesions were observed in the upper lobe (A) and the S6 segment of the lower lobes (B and C). J CATARACT REFRACT SURG - VOL 39, AUGUST 2013
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keratitis. The allergic tendency in patients may predispose them to develop a more dramatic inflammatory response than that which occurs in individuals with fewer allergic tendencies. Eye complications in atopic dermatitis cases can be a source of substantial morbidity. Generally, patients report photophobia and pruritus.12 A Dennie-Morgan fold, infraorbital darkening, eyelid dermatitis, and blepharitis are common in these cases.12 Atopic keratoconjunctivitis often presents with bilateral itchy watery eyes and copious mucoid discharge.13 Papillary hypertrophy, hyperemia, scarring, and shrinking of the fornices, punctate corneal staining, scarring, ulceration, and vascularization can also occur.14 None of the symptoms described above were observed in Case 1. Cogan syndrome was the initial diagnosis in Case 1 as the patient had an episode of vertigo associated with interstitial keratitis.1,3,7 Although intensive treatment with topical corticosteroids improved his visual acuity, the patient complained of decreased visual acuities; therefore, irrigation of the interface between the corneal flap and the stromal bed was performed. Treatment of Cogan syndrome using irrigation has not been reported. In this case, it appeared to be effective for Cogan syndrome after LASIK. In patients with Cogan syndrome, corneal inflammation commonly recurs.3,4,7 Thus, careful long-term follow-up evaluations are warranted. Some diseases may result in symptoms similar to those of Cogan syndrome, especially infections such as syphilis, tuberculosis (TB), and/or viral infections. The differential diagnosis of Cogan syndrome with congenital syphilis is summarized in Figure 6. Acquired syphilis is rarely associated with sudden deafness.15 Tuberculosis can rarely cause interstitial keratitis and can be associated with deafness indirectly because of the use of streptomycin for the treatment of TB. However, TB keratitis usually causes single isolated gray-to-yellow spot lesions with
minimal vascularization.16 Many viral infections have also been associated with interstitial keratitis. Herpes zoster infections are recognizable due to the presence of skin or mucosal membrane lesions.17 Although both of our patients were positive for HSV and VZV serology, neither had a history of ocular herpetic disease. In some cases, herpes infections could produce vestibulo-auditory symptoms due to infection of the hearing nerve (cranial nerve VIII). When a nerve becomes infected, it tends to swell. Unfortunately, the hearing nerve (along with the facial nerve) goes through a bony canal called the internal auditory canal, which is a passageway through the skull to the ear. This bony passage does not enlarge to accommodate the nerve as it swells, causing the nerve to become “strangulated,” leading to hearing loss. This situation is akin to the loss of smell when that nerve is infected during a cold or Bell palsy, which can lead to facial paralysis. Neither patient had these conditions.18,19 The patient presented in Case 2 developed both ocular and vestibulo-auditory symptoms in the same period. In addition, pneumonitis was suspected after the chest CT examination. Some studies have reported an association of Cogan syndrome with upper respiratory tract infections.1,2,11,20 Corneal neovascularization and calcified opacities in the deep corneal stroma are common symptoms of Cogan syndrome.5,21 Based on these clinical findings, typical Cogan syndrome was diagnosed in Case 2. If a significant visual loss along with growing lesions or increased opacity occurs, surgical treatments such as deep lamellar keratoplasty will be considered.4,21 We presented 2 cases of Cogan syndrome, 1 typical and 1 atypical, that developed after uneventful LASIK. Although the correlation between LASIK and Cogan syndrome is not known, it deserves further investigation. Typically, DLK occurs in the lamellar interface within the first postoperative week, often within the
Figure 6. Characteristics of interstitial keratitis and vestibulo-auditory dysfunction in congenital syphilis and Cogan syndrome (IK Z interstitial keratitis). J CATARACT REFRACT SURG - VOL 39, AUGUST 2013
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first 24 hours, and is characterized by an inflammatory cellular reaction after LASIK,22 but it does not generally produce neovascularization.7 After a topical corticosteroid-drop treatment, DLK after LASIK typically subsides.23 However, surgeons should take Cogan syndrome into account as a possible differential diagnosis for late-onset DLK.7 It should be noted that late-onset DLK has been associated with some conditions able to induce ocular inflammation,24–29 such as allergic and adenoviral conjunctivitis or iritis,29 but it has not been associated with Cogan syndrome or other types of interstitial keratitis. Cogan syndrome might appear if there is some systemic condition resulting in interstitial keratitis after LASIK surgery. Consultation with all Cogan syndrome patients in general should include a review of Meniere disease– like symptoms and any hearing loss. When young patients present with Meniere disease–like symptoms,3 the development of corneal neovascularization,3,4 decreased vision,3 opacity or precipitates in the corneal stroma3,4 as late postoperative complications following LASIK,7 surgeons should consider the possibility of Cogan syndrome and carry out further evaluations. Treatments including intensive topical corticosteroids and an irrigation of the stromal bed lamellar flap interface can be effective for Cogan syndrome after LASIK.
REFERENCES 1. Cogan DG. Syndrome of nonsyphilitic interstitial keratitis and vestibuloauditory symptoms. Arch Ophthalmol 1945; 33:144–149 2. Haynes BF, Kaiser-Kupfer MI, Mason P, Fauci AS. Cogan syndrome: studies in thirteen patients, long-term follow-up, and a review of the literature. Medicine 1980; 59:426–441 try O, Papo T, 3. Grasland A, Pouchot J, Hachulla E, Ble Vinceneux P, Study Group for Cogan’s syndrome. Typical and atypical Cogan’s syndrome: 32 cases and review of the literature. Rheumatology 2004; 43:1007–1015. Available at: http://rheumatology.oxfordjournals.org/content/43/8/1007.full. pdf. Accessed March 12, 2013 4. Miserocchi E, Baltatzis S, Foster CS. A Case of atypical Cogan’s syndrome with uncommon corneal findings. Cornea 2001; 20:540–542 € Karaku an H. A case of atypical € c‚uk S, Dog 5. Aksu M, Ersoy AO, Cogan’s syndrome and review of literature. Turk J Medical Sci 1998; 28:705–707. Available at: http://journals.tubitak.gov.tr/ medical/issues/sag-98-28-6/sag-28-6-25-97032.pdf. Accessed March 12, 2013 6. Gluth MB, Baratz KH, Matteson EL, Driscoll CLW. Cogan syndrome: a retrospective review of 60 patients throughout a half century. Mayo Clin Proc 2006; 81:483–488 ~oz G, Pe rez-Santonja JJ, Vidal MT, 7. Javaloy J, Barrera C, Mun JL. Spontaneous bilateral, recurrent, late-onset diffuse laAlio mellar keratitis after LASIK in a patient with Cogan’s syndrome. J Refract Surg 2008; 24:548–550
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8. Mimura T, Funatsu H, Usui T, Yamagami S, Noma H, Amano S. Topical ocular drug delivery to inner ear disease and sinusitis. South Med J 2006; 99:1287–1289 9. Cupps T. Autoimmune-mediated sinus and midfacial diseases. In: Gershwin ME, Incaudo GA, eds, Diseases of the Sinuses; A Comprehensive Textbook of Diagnosis and Treatment. Totowa, NJ, Human Press, 1996; 381–402 10. Gran JT, Nordva˚g BY, Storesund B. An overlap syndrome with features of atypical Cogan syndrome and Wegener’s granulomatosis. Scand J Rheumatol 1999; 28:62–64 11. Ikeda M, Okazaki H, Minota S. Cogan’s syndrome with antineutorophil cytoplasmic autoantibody [letter]. Ann Rheum Dis 2002; 61:761–762. Available at: http://www.ncbi.nlm.nih.gov/pmc/ articles/PMC1754200/pdf/v061p00761.pdf. Accessed March 12, 2013 12. Gelmetti C. Extracutaneous manifestations of atopic dermatitis. Pediatr Dermatol 1992; 9:380–382 13. Leung DYM, Tharp M, Boguniewicz M. Atopic dermatitis (atopic eczema). In: Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI, eds, Fitzpatrick’s Dermatology in General Medicine, 5th ed. New York, NY, McGraw-Hill, 1999; 1464–1480 14. Dixon WS. Ocular allergies. Prac Allergy Immunol 1995; 10:84–88 15. Arnold GE, Ohsaki K. Two cases of sudden deafness; one from acquired syphilis and one associated with possible collagen disease. Ann Otol Rhinol Laryngol 1963; 72:605–620 16. Pau H. Differential Diagnosis of Eye Disease. Philadelphia, PA, WB Saunders, 1978; 154 17. Marcy SM, Kibrick S. Mumps. In: Hoeprich PD, ed, Infectious Diseases: A Modern Treatise of Infectious Processes, 2nd ed. Hagertown, MD, Harper Row, 1977; 621 18. Stachler RJ, Chandrasekhar SS, Archer SM, Rosenfeld RM, Schwartz SR, Barrs DM, Brown SR, Fife TD, Ford P, Ganiats TG, Hollingsworth DB, Lewandowski CA, Montano JJ, Saunders JE, Tucci DL, Valente M, Warren BE, Yaremchuk KL, Robertson PJ. Clinical practice guideline: sudden hearing loss. Otolaryngol Head Neck Surg 2012; 146(3 suppl):S1–S35. Available at: http://oto.sagepub.com/content/146/3_suppl/S1.full.pdf. Accessed March 12, 2013 19. Moon IS, Lee JD, Kim J, Hong S-J, Lee W-S. Intratympanic dexamethasone is an effective method as a salvage treatment in refractory sudden hearing loss. Otol Neurotol 2011; 32:1432–1436 20. Norton EWD, Cogan DG. Syndrome of nonsyphilitic interstitial keratitis and vestibuloauditory symptoms; a long-term followup. AMA Arch Ophthalmol 1959; 61:695–697 21. Cogan DG, Kuwabara T. Late corneal opacities in the syndrome of interstitial keratitis and vestibulo-auditory symptoms. Acta Ophthalmol Suppl 1989; 192:182–187 22. Linebarger EJ, Hardten DR, Lindstrom RL. Diffuse lamellar keratitis: diagnosis and management. J Cataract Refract Surg 2000; 26:1072–1077 23. Shen Y-C, Wang C-Y, Fong S-C, Tsai H-Y, Lee Y-F. Diffuse lamellar keratitis induced by toxic chemicals after laser in situ keratomileusis. J Cataract Refract Surg 2006; 32:1146–1150 JL, Pe rez-Santonja JJ, Tervo T, Tabbara KF, Vesaluoma M, 24. Alio Smith RJ, Maddox B, Maloney RK. Postoperative inflammation, microbial complications, and wound healing following laser in situ keratomileusis. J Refract Surg 2000; 16:523–538 25. Holland SP, Mathias RG, Morck DW, Chiu J, Salde SG. Diffuse lamellar keratitis related to endotoxins released from sterilizer reservoir biofilms. Ophthalmology 2000; 107:1227–1233; discussion by EJ Holland, 1233–1234
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26. Shah MN, Misra M, Wihelmus KR, Koch DD. Diffuse lamellar keratitis associated with epithelial defects after laser in situ keratomileusis. J Cataract Refract Surg 2000; 26:1312–1318 27. Harrison DA, Periman LM. Diffuse lamellar keratitis associated with recurrent corneal erosions after laser in situ keratomileusis. J Refract Surg 2001; 17:463–465 28. Keszei VA. Diffuse lamellar keratitis associated with iritis 10 months after laser in situ keratomileusis. J Cataract Refract Surg 2001; 27:1126–1127 n A. Diffuse lamellar kerati€ ell JL, Wolley-Dod C, Ada 29. Gris O, Gu tis and corneal edema associated with viral keratoconjunctivitis
2 years after laser in situ keratomileusis. J Cataract Refract Surg 2004; 30:1366–1370
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First author: Minoru Tomita, MD, PhD Shinagawa LASIK Center, Tokyo, Japan
Cogan syndrome presenting after uneventful laser in situ keratomileusis Minoru Tomita, MD, PhD, Ayako Chiba, BS, Naoko Inoue, BA, Tukezban Huseynova, MD, Tadahiko Tsuru, MD, PhD, George O. Waring IV, MD
We report 2 cases of Cogan syndrome that developed after uneventful laser in situ keratomileusis. In the first case, an 8-month postoperative biomicroscopy revealed bilateral interface neovascularization, white intrastromal deposits, and anterior chamber cells and flare. In the second case, white cell infiltration and neovascularization were observed in the deep corneal stroma of the patient’s right eye 18 months postoperatively. Based on these observations, which are consistent with typical interstitial keratitis, and the patients’ history of Meniere-like disease, such as vertigo and mild hearing loss, Cogan syndrome was diagnosed in both patients. Topical steroids were prescribed. Intensive treatments with corneal irrigation and topical steroids showed effective outcomes in both cases. Financial Disclosure: No author has a financial or proprietary interest in any material or method mentioned. J Cataract Refract Surg 2013; 39:1260–1266 Q 2013 ASCRS and ESCRS
Cogan syndrome is a rare disease characterized by nonsyphilitic interstitial keratitis, often associated with ocular inflammation, vestibulo-auditory dysfunction such as Meniere syndrome, and various systemic manifestations.1–3 Although Cogan syndrome occurs most commonly in young adults without any sex predominance, the pathologic causes have not been determined.4–6 Interstitial keratitis may be unilateral or bilateral, and common ocular symptomatology includes, but is not limited to, decreased visual acuity, photophobia, ocular discomfort, and lacrimation. Vestibulo-auditory symptoms include vertigo, tinnitus, and/or the loss of hearing. Cogan syndrome has been classified into 2 types, typical and atypical, based on the ocular Submitted: January 13, 2013. Final revision submitted: March 10, 2013. Accepted: March 11, 2013. From the Shinagawa LASIK Center (Tomita, Chiba, Inoue, Huseynova, Tsuru), Chiyoda-ku, Tokyo, Japan; the Department of Ophthalmology (Tomita), Wenzhou Medical College, Wenzhou, China; and the Storm Eye Institute (Waring), Medical University of South Carolina, Charleston South Carolina, USA. Naoko Inoue provided editorial assistance. Corresponding author: Minoru Tomita, MD, PhD, Shinagawa LASIK Center, Yurakucho ITOCiA 14th floor, 2-7-1 Yurakucho Chiyoda, Tokyo 100-0006, Japan. E-mail: [email protected].
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manifestations or the interval between the onset of ocular manifestations and any vestibulo-auditory dysfunction. According to the original reports of typical Cogan syndrome, ocular findings are confined to the anterior segment and the onset of vestibulo-auditory symptoms are within 2 years of the onset of ocular symptoms.2,3,7 In atypical Cogan syndrome, ocular manifestations are varied, including but not limited to keratitis, episcleritis, scleritis, anterior uveitis, glaucoma, retinitis, and optic neuritis. In addition, vestibulo-auditory symptoms can appear more than 2 years before or after ocular manifestations.2–4,6 Since the original description in 1945,1 Cogan syndrome has been well documented in the literature.2–5,7 To our knowledge, only 1 case of Cogan syndrome has been reported after laser in situ keratomileusis (LASIK).7 With the increasing number of LASIK procedures worldwide, it is helpful to differentiate Cogan syndrome from keratitis such as diffuse lamellar keratitis (DLK), which is more typically found after LASIK. In this report, we present 2 cases of Cogan syndrome after uneventful LASIK and describe the management of both cases and the outcomes. CASE REPORTS Case 1 A 28-year-old man with a 12-year history of soft contact lens use to correct myopia and astigmatism had bilateral LASIK in March 2009 at Shinagawa LASIK Center. The 0886-3350/$ - see front matter http://dx.doi.org/10.1016/j.jcrs.2013.05.025
CASE REPORT: COGAN SYNDROME AFTER LASIK
medical history was notable for only atopic dermatitis. The preoperative examination was remarkable for a small peripheral stromal opacity in the left eye that was thought to be related to the contact lens use and was negative for signs of prior inflammatory episodes, including an absence of corneal neovascularization. The preoperative uncorrected (UDVA) and corrected (CDVA) distance visual acuities were 20/250 and 20/10, respectively, in the right eye and 20/250 and 20/10, respectively, in the left eye. The preoperative manifest refraction was 3.75 1.0 170 and 4.50 0.25 35 in the right eye and left eye, respectively. Uneventful LASIK was performed in both eyes with the Intralase FS60 (Abbott Medical Optics, Inc.) and the Allegretto Wave Eye-Q 400Hz (Alcon Laboratories, Inc.). Three months postoperatively, the UDVA and CDVA were 20/10 in both eyes and slitlamp examinations were within normal limits. Eight months after the LASIK procedure, the patient returned to the center complaining of decreased vision and a foreign-body sensation in the left eye. The UDVA and CDVA were 20/16 and 20/10, respectively, in the right eye and 20/20 and 20/16, respectively, in the left eye, respectively. Slitlamp examination showed bilateral superior stromal neovascularization and bilateral asymmetric diffuse interface inflammation consistent with DLK. In the right eye, mild diffuse interface inflammation was seen. The left eye was notable for severe diffuse interface inflammation including white exudates and clumped cells extending over half the cornea. Dexamethasone sodium m-sulfobenzoate 0.1% and moxifloxacin hydrochloride 0.5% ophthalmic solutions were prescribed hourly for 9 days. Six days after the topical therapy was started, the patient reported partial improvement in the subjective acuities but continued difficulty, more so in the left eye. The biomicroscopy was notable for persistent bilateral superior interstitial keratitis 9 days after the topical therapy was started and also for bilateral superior coalescent granular intrastromal opacities along with associated intrastromal neovascularization (Figure 1). Most of the deposits were located in the interface between the corneal flap and the stromal bed.
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Because of the patient’s condition and the location of the inflammation, a lifted-flap interface irrigation was performed in the left eye using a balanced salt solution containing 0.9% methylprednisolone sodium succinate. During the irrigation, white granular deposits and lipid crystals were flushed from the interface but no histopathology was performed. After the cornea in the left eye was irrigated, 0.2 mL of dexamethasone sodium phosphate 0.4% was injected subconjunctivally. Dexamethasone sodium m-sulfobenzoate 0.1%, moxifloxacin hydrochloride 0.5%, and sodium hyaluronate 0.3% ophthalmic solutions were prescribed bilaterally every hour for a week. As the patient was only mildly symptomatic in the right eye and no interface inflammation was observed at the time of follow-up, no irrigation was performed in the right eye. One day after the interface irrigation, the UDVA and CDVA in the left eye were 20/20 and 20/16, respectively, and the patient’s subjective acuity improved dramatically. One week after irrigation, the acuity improved subjectively and both UDVA and CDVA were 20/16. A sodium hyaluronate 0.1% ophthalmic solution was prescribed for 2 months until the next examination. Further questioning revealed a history of episodic vertigo consistent with Meniere-like symptomatology with a similar onset of decreasing visual acuity. Given this history and the episode of interstitial keratitis, atypical Cogan syndrome was diagnosed. After informed consent was obtained, a systemic examination including serological evaluation, vestibulo-auditory examinations, cranial magnetic resonance imaging (MRI), and computed tomography (CT) was performed. Serologic evaluation included complete blood cell counts, C-reactive protein, rheumatoid factor, antinuclear antibodies, serum complements syphilitic panels, human leukocyte antigens, antiviral immunoglobulins to herpes simplex virus (HSV) immunoglobulin G (IgG), varicella zoster virus (VZV IgG), and the human T-lymphotropic virus-1. Remarkable imaging results included frontonasal sinusitis and serologic evaluations that were positive for antiviral antibodies to herpes simplex and varicella zoster. Two months after the irrigation in the left eye, the interstitial keratitis had subsided. The UDVA and CDVA were 20/ 12.5 in both eyes. Three months after irrigation, the UDVA and CDVA were 20/10 in the right eye and remained 20/ 12.5 in the left eye.
Case 2
Figure 1. Case 1: Slitlamp view of the left eye 8 months after LASIK, indicating patchy exudates and neovascularization.
A 29-year-old woman with a 13-year history of soft contact lens use had bilateral LASIK in September 2007 at Shinagawa LASIK Center. The preoperative examinations were remarkable as the UDVA and CDVA were 20/800 and 20/ 12.5, respectively, in the right eye and 20/800 and 20/16, respectively, in the left eye. The manifest refraction was 12.00 diopters sphere and 10.50 0.50 90 in the right eye and left eye, respectively. The preoperative slitlamp examinations were within normal limits. Uneventful LASIK was performed with the Intralase FS60 and Allegretto Wave Eye-Q 400 Hz. One week postoperatively, the UDVA and CDVA were 20/20 and 20/20, respectively, in both eyes. Subsequent examinations were performed at the patient’s neighborhood clinic. Eighteen months after the LASIK procedure, the patient returned complaining of decreased visual acuity in the right eye. The physical examination results were remarkable for a UDVA of 20/40 and a CDVA of 20/25 in the
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Figure 2. Case 2: Corneal topography maps indicating subepithelial corneal infiltrates with opacities in the deep stroma.
right eye. Biomicroscopy of the right eye revealed superior intrastromal corneal neovascularization and focal opacities near the terminal portion of the neovascularization in the paracentral cornea. Both UDVA and CDVA in the left eye were 20/16, and the slitlamp examination was within normal limits. Dexamethasone sodium m-sulfobenzoate 0.1% and moxifloxacin hydrochloride 0.5% ophthalmic solutions were prescribed topically 5 times a day in the right eye. Two weeks after the initiation of the topical therapy, the UDVA and CDVA in the right eye improved to 20/32 and 20/20, respectively. The slitlamp examination revealed stable intrastromal neovascularization and opacities in the periphery of the central cornea. Dexamethasone sodium m-sulfobenzoate 0.1% ophthalmic solution use continued 4 times a day for 1 month in the right eye. One month after the topical treatment was started, the UDVA and CDVA in the right eye improved to 20/25 and 20/16, respectively. The dexamethasone sodium m-sulfobenzoate 0.1% course continued 4 times a day for 7 months with a slow taper. Monthly checks were performed, and the patient was stable during the treatment. Three months after the treatment was discontinued, the UDVA and CDVA remained stable but subepithelial corneal infiltrates with deep stromal opacities were noted in the right eye (Figures 2 and 3). Optical coherence tomography (Casia SS1000; Tomey Corp.) showed that the portions with highreflected densities coincided with the sites of pathological change in the deep stroma (Figure 4). Dexamethasone sodium m-sulfobenzoate 0.1% was prescribed 5 times a day for 2 weeks in the right eye. On further clinical review, the patient reported a history of Meniere disease-like symptoms including vertigo and mild hearing loss in the lower vocal ranges as she experienced decreasing visual acuity. The patient was referred to an otolaryngologist for evaluation and management of the Meniere disease. Betahistine mesilate was prescribed for a month, and the symptoms resolved. The patient had a complete systemic evaluation, the same as described for Case 1. The MRI was remarkable for paranasal sinusitis in the left maxillary sinus. In addition, the chest CT was translucent in the right upper lobe and both
lower lobes consistent with possible viral pneumonitis (Figure 5). Serologic and audiometric evaluations were negative except for viral antibodies, which were positive for HSV IgG and VZV IgG. Since the corneal haze and neovascularization were observed in the deep stroma, irrigation of the stromal bed was not performed. Dexamethasone sodium m-sulfobenzoate 0.1% was prescribed 5 times a day again in the right eye for 1 month. The patient remained stable on the interim visits, and the topical steroid use was discontinued. One year after the diagnosis of typical Cogan syndrome was made, the active interstitial keratitis had subsided completely. Although slight intrastromal scarring and neovascularization remained, the UDVA and CDVA were 20/25 and 20/20, respectively, in the right eye and 20/16 and 20/12.5, respectively, in the left eye. The patient experienced no
Figure 3. Case 2: Slitlamp view of the right eye showing corneal neovascularization and granular deposits.
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Figure 4. Case 2: Optical coherence tomography image of the right eye showing areas with high-reflected density coinciding with sites of pathological change in the deep stroma.
further dizziness or vertigo, with unremarkable follow-up visits to the otolaryngologist.
DISCUSSION Cogan syndrome was first described by David Cogan in 1945.1 He described 4 patients who had experienced nonsyphilitic interstitial keratitis and vestibuloauditory symptoms. Since then, cases of typical and atypical Cogan syndrome have been reported by several authors.1–6 However, case reports of Cogan syndrome after LASIK are rare.7 Cogan syndrome is an uncommon disease whose etiology is still unknown, so diagnostic criteria and treatment options have not been well established.5 Usually Cogan syndrome has been diagnosed based on the characteristic ocular findings and vestibuloauditory dysfunctions, as they were in our cases.1–3,5 Treatment is typically topical and/or systemic corticosteroids for the interstitial keratitis and vestibuloauditory dysfunction.2–4,6 The patient described in Case 1 suffered from Meniere disease–like dizziness prior to the development
of nonsyphilitic interstitial keratitis. Further diagnostic evaluation including serology, cranial MRI, CT, and audiometry were not remarkable for this particular etiology. Although some Cogan syndrome cases with paranasal sinusitis have been reported, the association with Cogan syndrome is unknown.3,8 In addition to the typical ocular and vestibulo-auditory findings, paranasal sinusitis was detected in both patients by cranial MRI. Although Cupps9 stated that sinusitis is not a diagnostic prerequisite for Cogan syndrome, previous reports show a potential association with Cogan syndrome and paranasal sinusitus.3,8,10,11 Further study of the correlation between Cogan syndrome and paranasal sinusitis is needed. According to Gluth et al.6 in their half-century literature review, one-third of patients exhibited ophthalmic signs and symptoms as the initial presentation of Cogan syndrome. Although rare, Cogan syndrome should be considered when interstitial keratitis or other associated findings are noted. As mentioned above, the Case 1 patient presented a history of atopic dermatitis, which may play a role as a host factor in the development of interface
Figure 5. Case 2: Chest CT images showing translucent lesions were observed in the upper lobe (A) and the S6 segment of the lower lobes (B and C). J CATARACT REFRACT SURG - VOL 39, AUGUST 2013
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keratitis. The allergic tendency in patients may predispose them to develop a more dramatic inflammatory response than that which occurs in individuals with fewer allergic tendencies. Eye complications in atopic dermatitis cases can be a source of substantial morbidity. Generally, patients report photophobia and pruritus.12 A Dennie-Morgan fold, infraorbital darkening, eyelid dermatitis, and blepharitis are common in these cases.12 Atopic keratoconjunctivitis often presents with bilateral itchy watery eyes and copious mucoid discharge.13 Papillary hypertrophy, hyperemia, scarring, and shrinking of the fornices, punctate corneal staining, scarring, ulceration, and vascularization can also occur.14 None of the symptoms described above were observed in Case 1. Cogan syndrome was the initial diagnosis in Case 1 as the patient had an episode of vertigo associated with interstitial keratitis.1,3,7 Although intensive treatment with topical corticosteroids improved his visual acuity, the patient complained of decreased visual acuities; therefore, irrigation of the interface between the corneal flap and the stromal bed was performed. Treatment of Cogan syndrome using irrigation has not been reported. In this case, it appeared to be effective for Cogan syndrome after LASIK. In patients with Cogan syndrome, corneal inflammation commonly recurs.3,4,7 Thus, careful long-term follow-up evaluations are warranted. Some diseases may result in symptoms similar to those of Cogan syndrome, especially infections such as syphilis, tuberculosis (TB), and/or viral infections. The differential diagnosis of Cogan syndrome with congenital syphilis is summarized in Figure 6. Acquired syphilis is rarely associated with sudden deafness.15 Tuberculosis can rarely cause interstitial keratitis and can be associated with deafness indirectly because of the use of streptomycin for the treatment of TB. However, TB keratitis usually causes single isolated gray-to-yellow spot lesions with
minimal vascularization.16 Many viral infections have also been associated with interstitial keratitis. Herpes zoster infections are recognizable due to the presence of skin or mucosal membrane lesions.17 Although both of our patients were positive for HSV and VZV serology, neither had a history of ocular herpetic disease. In some cases, herpes infections could produce vestibulo-auditory symptoms due to infection of the hearing nerve (cranial nerve VIII). When a nerve becomes infected, it tends to swell. Unfortunately, the hearing nerve (along with the facial nerve) goes through a bony canal called the internal auditory canal, which is a passageway through the skull to the ear. This bony passage does not enlarge to accommodate the nerve as it swells, causing the nerve to become “strangulated,” leading to hearing loss. This situation is akin to the loss of smell when that nerve is infected during a cold or Bell palsy, which can lead to facial paralysis. Neither patient had these conditions.18,19 The patient presented in Case 2 developed both ocular and vestibulo-auditory symptoms in the same period. In addition, pneumonitis was suspected after the chest CT examination. Some studies have reported an association of Cogan syndrome with upper respiratory tract infections.1,2,11,20 Corneal neovascularization and calcified opacities in the deep corneal stroma are common symptoms of Cogan syndrome.5,21 Based on these clinical findings, typical Cogan syndrome was diagnosed in Case 2. If a significant visual loss along with growing lesions or increased opacity occurs, surgical treatments such as deep lamellar keratoplasty will be considered.4,21 We presented 2 cases of Cogan syndrome, 1 typical and 1 atypical, that developed after uneventful LASIK. Although the correlation between LASIK and Cogan syndrome is not known, it deserves further investigation. Typically, DLK occurs in the lamellar interface within the first postoperative week, often within the
Figure 6. Characteristics of interstitial keratitis and vestibulo-auditory dysfunction in congenital syphilis and Cogan syndrome (IK Z interstitial keratitis). J CATARACT REFRACT SURG - VOL 39, AUGUST 2013
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first 24 hours, and is characterized by an inflammatory cellular reaction after LASIK,22 but it does not generally produce neovascularization.7 After a topical corticosteroid-drop treatment, DLK after LASIK typically subsides.23 However, surgeons should take Cogan syndrome into account as a possible differential diagnosis for late-onset DLK.7 It should be noted that late-onset DLK has been associated with some conditions able to induce ocular inflammation,24–29 such as allergic and adenoviral conjunctivitis or iritis,29 but it has not been associated with Cogan syndrome or other types of interstitial keratitis. Cogan syndrome might appear if there is some systemic condition resulting in interstitial keratitis after LASIK surgery. Consultation with all Cogan syndrome patients in general should include a review of Meniere disease– like symptoms and any hearing loss. When young patients present with Meniere disease–like symptoms,3 the development of corneal neovascularization,3,4 decreased vision,3 opacity or precipitates in the corneal stroma3,4 as late postoperative complications following LASIK,7 surgeons should consider the possibility of Cogan syndrome and carry out further evaluations. Treatments including intensive topical corticosteroids and an irrigation of the stromal bed lamellar flap interface can be effective for Cogan syndrome after LASIK.
REFERENCES 1. Cogan DG. Syndrome of nonsyphilitic interstitial keratitis and vestibuloauditory symptoms. Arch Ophthalmol 1945; 33:144–149 2. Haynes BF, Kaiser-Kupfer MI, Mason P, Fauci AS. Cogan syndrome: studies in thirteen patients, long-term follow-up, and a review of the literature. Medicine 1980; 59:426–441 try O, Papo T, 3. Grasland A, Pouchot J, Hachulla E, Ble Vinceneux P, Study Group for Cogan’s syndrome. Typical and atypical Cogan’s syndrome: 32 cases and review of the literature. Rheumatology 2004; 43:1007–1015. Available at: http://rheumatology.oxfordjournals.org/content/43/8/1007.full. pdf. Accessed March 12, 2013 4. Miserocchi E, Baltatzis S, Foster CS. A Case of atypical Cogan’s syndrome with uncommon corneal findings. Cornea 2001; 20:540–542 € Karaku an H. A case of atypical € c‚uk S, Dog 5. Aksu M, Ersoy AO, Cogan’s syndrome and review of literature. Turk J Medical Sci 1998; 28:705–707. Available at: http://journals.tubitak.gov.tr/ medical/issues/sag-98-28-6/sag-28-6-25-97032.pdf. Accessed March 12, 2013 6. Gluth MB, Baratz KH, Matteson EL, Driscoll CLW. Cogan syndrome: a retrospective review of 60 patients throughout a half century. Mayo Clin Proc 2006; 81:483–488 ~oz G, Pe rez-Santonja JJ, Vidal MT, 7. Javaloy J, Barrera C, Mun JL. Spontaneous bilateral, recurrent, late-onset diffuse laAlio mellar keratitis after LASIK in a patient with Cogan’s syndrome. J Refract Surg 2008; 24:548–550
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8. Mimura T, Funatsu H, Usui T, Yamagami S, Noma H, Amano S. Topical ocular drug delivery to inner ear disease and sinusitis. South Med J 2006; 99:1287–1289 9. Cupps T. Autoimmune-mediated sinus and midfacial diseases. In: Gershwin ME, Incaudo GA, eds, Diseases of the Sinuses; A Comprehensive Textbook of Diagnosis and Treatment. Totowa, NJ, Human Press, 1996; 381–402 10. Gran JT, Nordva˚g BY, Storesund B. An overlap syndrome with features of atypical Cogan syndrome and Wegener’s granulomatosis. Scand J Rheumatol 1999; 28:62–64 11. Ikeda M, Okazaki H, Minota S. Cogan’s syndrome with antineutorophil cytoplasmic autoantibody [letter]. Ann Rheum Dis 2002; 61:761–762. Available at: http://www.ncbi.nlm.nih.gov/pmc/ articles/PMC1754200/pdf/v061p00761.pdf. Accessed March 12, 2013 12. Gelmetti C. Extracutaneous manifestations of atopic dermatitis. Pediatr Dermatol 1992; 9:380–382 13. Leung DYM, Tharp M, Boguniewicz M. Atopic dermatitis (atopic eczema). In: Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI, eds, Fitzpatrick’s Dermatology in General Medicine, 5th ed. New York, NY, McGraw-Hill, 1999; 1464–1480 14. Dixon WS. Ocular allergies. Prac Allergy Immunol 1995; 10:84–88 15. Arnold GE, Ohsaki K. Two cases of sudden deafness; one from acquired syphilis and one associated with possible collagen disease. Ann Otol Rhinol Laryngol 1963; 72:605–620 16. Pau H. Differential Diagnosis of Eye Disease. Philadelphia, PA, WB Saunders, 1978; 154 17. Marcy SM, Kibrick S. Mumps. In: Hoeprich PD, ed, Infectious Diseases: A Modern Treatise of Infectious Processes, 2nd ed. Hagertown, MD, Harper Row, 1977; 621 18. Stachler RJ, Chandrasekhar SS, Archer SM, Rosenfeld RM, Schwartz SR, Barrs DM, Brown SR, Fife TD, Ford P, Ganiats TG, Hollingsworth DB, Lewandowski CA, Montano JJ, Saunders JE, Tucci DL, Valente M, Warren BE, Yaremchuk KL, Robertson PJ. Clinical practice guideline: sudden hearing loss. Otolaryngol Head Neck Surg 2012; 146(3 suppl):S1–S35. Available at: http://oto.sagepub.com/content/146/3_suppl/S1.full.pdf. Accessed March 12, 2013 19. Moon IS, Lee JD, Kim J, Hong S-J, Lee W-S. Intratympanic dexamethasone is an effective method as a salvage treatment in refractory sudden hearing loss. Otol Neurotol 2011; 32:1432–1436 20. Norton EWD, Cogan DG. Syndrome of nonsyphilitic interstitial keratitis and vestibuloauditory symptoms; a long-term followup. AMA Arch Ophthalmol 1959; 61:695–697 21. Cogan DG, Kuwabara T. Late corneal opacities in the syndrome of interstitial keratitis and vestibulo-auditory symptoms. Acta Ophthalmol Suppl 1989; 192:182–187 22. Linebarger EJ, Hardten DR, Lindstrom RL. Diffuse lamellar keratitis: diagnosis and management. J Cataract Refract Surg 2000; 26:1072–1077 23. Shen Y-C, Wang C-Y, Fong S-C, Tsai H-Y, Lee Y-F. Diffuse lamellar keratitis induced by toxic chemicals after laser in situ keratomileusis. J Cataract Refract Surg 2006; 32:1146–1150 JL, Pe rez-Santonja JJ, Tervo T, Tabbara KF, Vesaluoma M, 24. Alio Smith RJ, Maddox B, Maloney RK. Postoperative inflammation, microbial complications, and wound healing following laser in situ keratomileusis. J Refract Surg 2000; 16:523–538 25. Holland SP, Mathias RG, Morck DW, Chiu J, Salde SG. Diffuse lamellar keratitis related to endotoxins released from sterilizer reservoir biofilms. Ophthalmology 2000; 107:1227–1233; discussion by EJ Holland, 1233–1234
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26. Shah MN, Misra M, Wihelmus KR, Koch DD. Diffuse lamellar keratitis associated with epithelial defects after laser in situ keratomileusis. J Cataract Refract Surg 2000; 26:1312–1318 27. Harrison DA, Periman LM. Diffuse lamellar keratitis associated with recurrent corneal erosions after laser in situ keratomileusis. J Refract Surg 2001; 17:463–465 28. Keszei VA. Diffuse lamellar keratitis associated with iritis 10 months after laser in situ keratomileusis. J Cataract Refract Surg 2001; 27:1126–1127 n A. Diffuse lamellar kerati€ ell JL, Wolley-Dod C, Ada 29. Gris O, Gu tis and corneal edema associated with viral keratoconjunctivitis
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First author: Minoru Tomita, MD, PhD Shinagawa LASIK Center, Tokyo, Japan