Cases reported "Myopia"

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1/49. Hyperoxic myopia in a closed-circuit mixed-gas scuba diver.

    A myopic shift occurred in a closed-circuit mixed-gas scuba diver using a 1.3 atm abs constant partial pressure of oxygen in a nitrogen-oxygen mix. This change was noticed after approximately 18 days of diving with a mean dive time of 4.04 h each day. The observed myopic shift was due to hyperoxic myopia, one sign of lenticular oxygen toxicity, and resolved over a 1 mo. period after diving was completed. On a subsequent drive trip, a myopic shift was found in both the index diver as well as two other divers breathing the same gasmix on similar profiles. diving communities should be aware of the risk of both lenticular and pulmonary oxygen toxicity when conducting intensive diving at oxygen partial pressures in the 1.3-1.6 atm abs range.
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2/49. 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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3/49. New-onset headache in an adolescent with MASS syndrome.

    A 15-year-old girl with the "MASS" phenotype (meeting several of the minor criteria for marfan syndrome) presents with a new onset low-pressure postural headache. Clinical features and magnetic resonance imaging suggested intracranial hypotension, which was confirmed with lumbar puncture. The pathophysiology and treatment of spontaneous intracranial hypotension are discussed.
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4/49. Premacular subhyaloid hemorrhage following laser in situ keratomileusis.

    PURPOSE: To report a case of premacular subhyaloid hemorrhage following laser in situ keratomileusis (LASIK). methods: Case report. RESULTS: The subhyaloid hemorrhage did not resolve over 1 month of observation, necessitating Nd:YAG posterior hyaloidotomy. CONCLUSION: The LASIK procedure can be associated with postoperative subhyaloid hemorrhage, presumably from rapid release of the microkeratome vacuum pressure.
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5/49. Visual field defect associated with laser in situ keratomileusis.

    PURPOSE: To report a case of visual field defect associated with laser in situ keratomileusis. methods: Case report. A 28-year-old woman with high myopia (-10D) and a family history of normal tension glaucoma underwent bilateral laser in situ keratomileusis keratorefractive surgery. Preoperatively, both eyes had normal intraocular pressure and visual field. RESULTS: At the first postoperative visit 1 day after apparently uncomplicated laser in situ keratomileusis, the patient reported a scotoma in the right eye. At 3-month follow-up, visual fields revealed the patient had developed a near-superior altitudinal visual field defect in the right eye. The defect did not progress over 1 year of follow-up examinations. CONCLUSION: Increased intraocular pressure associated with the microkeratome vacuum ring used during laser in situ keratomileusis may have precipitated optic nerve head ischemia and visual field defect.
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6/49. Optic neuropathy associated with laser in situ keratomileusis.

    PURPOSE: To report 4 cases of optic neuropathy following laser in situ keratomileusis (LASIK). SETTING: Tertiary Care ophthalmic practices. methods: In this retrospective observational case series, 4 patients who developed acute visual loss following LASIK are reported. All had clinical evidence of optic neuropathy. Two had optic disc edema and 2 had normal appearing optic discs initially. None of the patients experienced significant visual recovery, and all developed optic atrophy in the affected eye. RESULTS: All patients had evaluations for alternative etiologies of their optic neuropathy, with negative results. All patients were therefore presumed to have experienced an ischemic optic neuropathy following LASIK. CONCLUSIONS: patients who have LASIK may experience an acute anterior or retrobulbar optic neuropathy. The etiology is unknown but may be related to the marked increase in intraocular pressure that occurs during a portion of the procedure.
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7/49. Paradoxical hypotony after laser in situ keratomileusis.

    We present a case of paradoxically low (0 to 2 mm Hg) intraocular pressure (IOP) measured by Goldmann applanation and Tono-Pen tonometry in an eye with corticosteroid-induced high IOP after laser in situ keratomileusis. The patient complained of blurred vision and ocular pain in both eyes. The eyes were firm by palpation, and the IOP measured by Schiotz indentation tonometry was 38 mm Hg. An interface fluid pocket was identified by slitlamp examination, and the corneal surface became steeper. These findings resolved after flap relifting, interface irrigation, and addition of antiglaucoma medications. We postulate that the paradoxically low reading by applanation tonometry was due to fluid accumulation within the flap-bed interface. The applanation tonometry reflected the interface fluid pocket pressure rather than the real high IOP. An exceedingly low IOP should be verified by palpation or by Shiotz indentation tonometry, and interface fluid should be identified.
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8/49. Laser in situ keratomileusis-induced optic neuropathy.

    OBJECTIVE: To report a case of bilateral optic neuropathy after bilateral laser-assisted in situ keratomileusis (LASIK) surgery. DESIGN: Observational case report. methods: Complete eye examination with detailed evaluation of the optic nerve, detailed medical history, stereo disc photographs, GDx Nerve Fiber Analyzer testing, Humphrey 24-2 SITA visual field testing, diurnal intraocular pressure measurement, serologic evaluation, and magnetic resonance imaging of the brain and orbits. MAIN OUTCOME MEASURES: optic nerve status, visual field status, and visual acuity. RESULTS: A subject with previously healthy optic nerves had bilateral optic neuropathy develop after LASIK surgery. This neuropathy manifested with a subjective decrease in visual field, normal visual acuity, normal color vision, relative afferent pupillary defect, increased cupping of the optic nerve with focal neuroretinal rim defects, decreased nerve fiber layer thickness, and nerve fiber bundle-type visual field defects. The subject had no other risk factors for optic neuropathy. No other cause of neuropathy was identified. CONCLUSIONS: Optic neuropathy is a potential vision-threatening complication of LASIK surgery. This complication may be due to barotrauma or ischemia related to extreme elevation of intraocular pressure by the suction ring. Careful examination of the optic nerve before and after LASIK surgery is warranted.
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9/49. Interface fluid and diffuse corneal edema after laser in situ keratomileusis.

    PURPOSE: To report a new complication of interface fluid accumulation and corneal edema in an uneventful laser in situ keratomileusis (LASIK) procedure. methods: Uncomplicated bilateral LASIK for myopia using the Hansatome microkeratome was performed. One day postoperatively, the patient noted decreased visual acuity. The topical corticosteroid was changed from dexamethasone to prednisolone acetate 1% every 2 hours. Two weeks later the patient reported worsening visual acuity in both eyes. Uncorrected visual acuity was 20/200 in the right eye and 20/100 in the left. Slit-lamp biomicroscopy indicated significant fluid build-up in the interface. intraocular pressure (IOP) by Goldmann applanation tonometry was 15 mmHg in the right eye and 14 mmHg in the left. RESULTS: After 4 weeks, intraocular pressure by bidigital pressure was increased and high. The corticosteroid was discontinued and antiglaucoma medication lowered the intraocular pressure, which resulted in corneal clearing and disappearence of interface fluid in both eyes. CONCLUSIONS: Early recognition of this new complication of LASIK is necessary. The falsely low reading of IOP in the setting of interface fluid was the result of easy compressibility of the fluid-filled space and reflects the pressure of the interface fluid. This apparently low IOP reading can be an additional sign of the existence of interface fluid. The corticosteroid should be discontinued and antiglaucoma medication instituted. This should lead to a lowering of intraocular pressure and result in corneal clearing and disappearence of the interface fluid with improvement in visual acuity.
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10/49. 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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