Cases reported "Keratitis"

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1/18. Interface fluid associated with diffuse lamellar keratitis and epithelial ingrowth after laser in situ keratomileusis.

    We report a case in which diffuse interface keratitis began 1 week after bilateral uneventful laser in situ keratomileusis (LASIK). A layer of fluid in the interface with epithelial ingrowth was noted in the left eye 20 days postoperatively. The same complication occurred in the right eye 5 months after LASIK. Dry-eye syndrome and steroid-induced intraocular pressure elevation occurred in this patient with pre-existing ocular hypertension. A long course of interface inflammation was resistant to topical steroids. Surgical removal of the epithelial ingrowth and drainage of the fluid, combined with medical treatment, resulted in resolution of the inflammation. The cytopathologic examination of the fluid showed epithelial cells without signs of inflammation. The clinical features of this case represent a new complication of LASIK.
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2/18. Interface fluid after laser in situ keratomileusis.

    We report a case in which raised intraocular pressure (IOP) was associated with interface fluid after uneventful bilateral laser in situ keratomileusis (LASIK). The patient presented with diffuse lamellar keratitis in both eyes 3 weeks postoperatively that was treated aggressively with topical corticosteroids. A steroid-induced rise in IOP resulted in interface fluid accumulation and microcystic edema. Measurements with the Goldmann tonometer revealed an IOP of 3.0 mm Hg in both eyes. However, Schiotz tonometry recorded a pressure of 54.7 mm Hg in both eyes. Reduction in the dosage of topical corticosteroid and medical treatment of the raised IOP resulted in resolution of the microcystic edema and interface fluid accumulation. This case highlights the inaccuracies of IOP measurement after LASIK and the resulting complications.
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3/18. Steroid-induced glaucoma after laser in situ keratomileusis associated with interface fluid.

    PURPOSE: To report the ocular manifestations and clinical course of eyes developing interface fluid after laser in situ keratomileusis (LASIK) surgery from a steroid-induced rise in intraocular pressure. DESIGN: Retrospective, noncomparative interventional case series. PARTICIPANTS/INTERVENTION: We examined six eyes of four patients who had diffuse lamellar keratitis develop after uneventful myopic LASIK surgery and were treated with topical corticosteroids. PRINCIPAL OUTCOME MEASURE: Slit-lamp findings, intraocular pressure measurements, and visual field loss. RESULTS: All eyes had a pocket of fluid develop in the lamellar interface between the flap and the stromal bed associated with a corticosteroid-induced rise in intraocular pressure. However, because of the interface fluid, intraocular pressure was normal or low by central corneal Goldmann applanation tonometry in all eyes. The elevated intraocular pressure was diagnosed by peripheral measurement in several cases after months of elevated pressure. All six eyes had visual field defects develop. Three eyes of two patients had severe glaucomatous optic neuropathy and decreased visual acuity develop as a result of undiagnosed steroid-induced elevated intraocular pressure. CONCLUSIONS: A steroid-induced rise in intraocular pressure after LASIK can cause transudation of aqueous fluid across the endothelium that collects in the flap interface. The interface fluid leads to inaccurately low central applanation tonometry measurements that obscure the diagnosis of steroid-induced glaucoma. Serious visual loss may result.
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4/18. Confocal microscopic findings in a case of delayed-onset bilateral diffuse lamellar keratitis after laser in situ keratomileusis.

    We report a case of bilateral diffuse lamellar keratitis (DLK) with delayed onset after a bilateral laser in situ keratomileusis (LASIK) procedure. A thorough history, review of systems, and laboratory evaluation revealed no pertinent medical history or risk factors for delayed-onset DLK after LASIK. Confocal microscopic examination of both corneas demonstrated a large number of activated keratocytes in the flap interface, particulate debris of variable size distributed throughout the interface, and scattered inflammatory cells. It was then decided to lift and wash both corneal flaps and interfaces. Scrapings for stains and cultures were also taken from both flap beds and were negative. After treatment with prednisolone acetate 1% and topical cyclosporin A 0.5%, the DLK resolved in both eyes with residual faint, diffuse, corneal haze. The patient developed a steroid-induced elevation in intraocular pressure that resolved after the topical corticosteroids were stopped.
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5/18. Elevated intraocular pressure-induced interlamellar stromal keratitis.

    PURPOSE: To describe a series of cases (Elevated intraocular pressure Induced Interlamellar Stromal keratitis (PISK)) that appears to be identical to post-laser in situ keratomileusis (LASIK) diffuse lamellar keratitis (DLK), but was present at a later time frame and was associated with a significant elevation of intraocular pressure (IOP). Unlike DLK, this syndrome is not steroid responsive, but resolves with a lowering of the IOP. DESIGN: Retrospective, noncomparative, small case series. PARTICIPANTS: The medical records of four LASIK patients with IOP-induced interface changes for the 1-year period March 2000 to March 2001 were reviewed retrospectively. MAIN OUTCOME MEASURE: Slit-lamp appearance. RESULTS: In the four cases presented, the slit-lamp findings and visual degradation appeared identical to DLK. All cases, however, presented outside of the first postoperative week and were not associated with any antecedent trauma. All four cases failed to respond to high-dose topical steroids. Significant IOP elevations were noted in all cases, and the interface changes responded dramatically to both a lowering of the IOP and a discontinuation or lowering of the topical steroids. CONCLUSIONS: Elevated IOP-induced post-LASIK interface keratitis (PISK) is a poorly documented phenomena. Because the condition may be caused by or worsened by frequent topical steroids, early recognition is important. Treatment consists primarily of normalizing the IOP.
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6/18. intraocular pressure-induced interlamellar keratitis after LASIK surgery.

    PURPOSE: To describe a case of interlamellar stromal keratitis induced by increased intraocular pressure (IOP) after LASIK surgery. methods: Case report and review of the literature. RESULTS: A 53-year-old white man with a history of treated ocular hypertension underwent uncomplicated LASIK surgery. The postoperative course was complicated by markedly elevated IOP induced by topical corticosteroid drops used to treat what appeared to be diffuse lamellar keratitis. Because IOPs remained uncontrolled despite maximal therapy, topical steroids were discontinued after a total of 9 weeks. The IOP rapidly returned to normal range with complete resolution of the corneal findings. Humphrey visual field analysis, confocal scanning laser imaging of the optic nerve, and stereoscopic disc photographs all demonstrated that significant glaucomatous field loss and optic atrophy developed over this 8-week period. DISCUSSION: The IOP should be immediately evaluated in patients who present with interlamellar stromal keratitis more than 1 week after LASIK. If the IOP is elevated, corticosteroid drops should be discontinued to prevent permanent visual loss. Furthermore, if a glaucoma specialist examines a patient with a history of LASIK and unexplained visual field loss, the medical record should be reviewed to determine if the postoperative course was complicated by this diffuse lamellar keratitis-like phenomenon.
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7/18. Herpes zoster virus sclerokeratitis and anterior uveitis in a child following varicella vaccination.

    PURPOSE: To report a case of herpes zoster virus sclerokeratitis with anterior uveitis following vaccination with live attenuated varicella vaccine (Oka strain). DESIGN: Case report. methods: The case records of the patient were reviewed retrospectively. Pertinent literature citations were identified using medline. RESULTS: A 9-year-old boy presented with herpes zoster ophthalmicus 3 years following vaccination with live attenuated varicella vaccine (Oka strain). Examination of the affected eye revealed a moderate follicular response on the palpebral conjunctiva, decreased corneal sensation, mildly elevated intraocular pressure, diffuse anterior scleritis with marginal keratitis, and a moderately severe anterior uveitis. Amplified dna from fluid taken from the base of a cutaneous vesicle produced wild-type varicella zoster virus (VZV) dna, not Oka strain. CONCLUSIONS: Herpes zoster virus infection needs to be considered in all patients who present with scleritis, keratitis, or anterior uveitis, regardless of their varicella vaccination status.
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8/18. Delayed onset diffuse lamellar keratitis following enhancement LASIK surgery.

    BACKGROUND: Diffuse lamellar keratitis (DLK) is a relatively uncommon complication of the refractive procedure, laser-assisted in situ keratomileusis (LASIK). If detected and diagnosed in a timely fashion, it can be treated and should resolve with minimal sequelae. If untreated, or misdiagnosed and treated incorrectly, there may be loss of visual acuity. Optometrists should be familiar with this condition, its signs, symptoms and correct treatment protocol. CASE history: A 58-year-old male Caucasian developed delayed onset diffuse lamellar keratitis, seemingly in the absence of an epithelial defect, 25 days following an enhancement LASIK procedure to his right eye. The DLK in this patient is delayed longer than typically reported in the literature. Subsequent management with topical steroids was complicated as the patient was a steroid responder and developed a markedly raised intraocular pressure that was managed with a topical anti-glaucoma agent. The diagnosis, pathogenesis and issues relevant to the treatment of this condition are discussed. CONCLUSION: Optometrists, particularly those actively participating in the shared care of refractive surgery patients, must be familiar with diffuse lamellar keratitis so that diagnosis is not delayed. As the number of cases of refractive surgery in australia increases, optometrists will encounter this condition more frequently.
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9/18. In vivo confocal microscopic findings in patients with steroid-induced glaucoma after LASIK.

    OBJECTIVE: To report the confocal microscopic findings of 2 different cases of steroid-induced glaucoma after LASIK. DESIGN: Observational case report of 2 cases. methods: Two cases of steroid-induced glaucoma after LASIK were selected. Examination with a white-light tandem slit-scanning confocal microscope was performed in addition to routine slit-lamp biomicroscopy. MAIN OUTCOME MEASURES: In vivo confocal findings at the flap interface. RESULTS: In both cases, the interfaces were identified at a deeper level than expected. Confocal microscopic examination did not show mononuclear cells and granulocytes typically seen in patients with classic diffuse lamellar keratitis. CONCLUSION: Our findings confirm that steroid-induced glaucoma after LASIK is not associated with the collection of inflammatory cells. The treatment option of lowering the intraocular pressure is effective in treating the disease, even without anti-inflammatory medications. Confocal in vivo microscopy is a useful tool to study the course of steroid-induced glaucoma after LASIK in humans.
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10/18. Pressure-induced interface keratitis: a late complication following LASIK.

    PURPOSE: Interface inflammation is a common complication of laser in situ keratomileusis (LASIK). The most well-described presentation is diffuse lamellar keratitis (DLK), which typically develops early after LASIK and responds quickly to topical steroids. In this report, we describe a novel presentation of interface inflammation that resembles DLK in appearance but presents late in the postoperative period, is associated with increased intraocular pressure, and is exacerbated by steroid treatment. methods: A retrospective case series and chart review of all patients treated in our tertiary care private practice for late-onset interface inflammation associated with elevated intraocular pressure. RESULTS: Ten eyes in 6 patients with late-onset interface inflammation and increased intraocular pressure were identified. At presentation, all patients were presumed to have classic DLK and were treated initially with aggressive topical steroids. Eight of the 10 eyes were receiving topical steroids at the time of presentation. The average time of presentation was 17 days after LASIK (range, 7-34). Elevated intraocular pressure was noted on average 28 days after presentation (range, 8-69). Lamellar inflammation was exacerbated by topical steroids. Resolution of the interface inflammation did not occur until intraocular pressure was controlled. CONCLUSIONS: This case series describes a clinically distinct form of interface inflammation that presents late and is associated with elevated intraocular pressure. The lamellar inflammation was refractory to topical steroids and only resolved when pressure was controlled. These findings suggest that elevated intraocular pressure can contribute to interface inflammation. Postoperative assessment of intraocular pressure is essential in patients presenting with flap inflammation.
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