Cases reported "Ocular Hypertension"

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1/14. Increased intraocular pressure and visual field defects in high resistance wind instrument players.

    OBJECTIVE: In this twofold study, part 1 aimed to determine whether the playing of high resistance wind instruments elevates intraocular pressure (IOP) and if so, to investigate the mechanism of IOP elevation and whether its magnitude differs while playing high resistance versus low resistance instruments. The purpose of part 2 was to evaluate whether high resistance players have a greater incidence of glaucomatous changes than other musicians. DESIGN: Three case reports and a cross-sectional study. PARTICIPANTS: Two players of high resistance instruments and one player of high and low resistance wind instruments participated in part 1 of the study. Nine high resistance wind players, 12 low resistance wind players, and 24 nonwind players were recruited among professional musicians in the boston area to participate in part 2. INTERVENTION: In part 1, IOP and uveal thickness changes were measured by pneumatonometry and ultrasound biomicroscopy in two participants playing their high resistance wind instruments (trumpet and oboe) and in a third participant playing both high (trumpet) and low (clarinet and saxaphone) resistance instruments. Each musician in part 2 underwent medical and musical history, measurement of IOP, Humphrey visual field testing, slit-lamp examination, gonioscopy, and dilated examination. MAIN OUTCOME MEASURES: intraocular pressure and uveal thickness changes, and visual field loss and optic nerve head appearance were the main parameters measured in part 1 and part 2, respectively. RESULTS: In part 1, pneumatonometry showed IOP elevation dependent on the force of blowing, and ultrasound biomicroscopy revealed uveal thickening associated with IOP elevation. The magnitude of IOP elevation was dependent on the amount of expiratory resistance provided by the particular instrument. Part 2 showed that life hours of high resistance wind instrument playing had a significant relationship to abnormal visual field (P = 0.03) and corrected pattern standard deviation (CPSD) scores (P = 0.007) in univariate logistic regression and univariate linear regression, respectively. A 0.011-unit increase in CPSD for each 1000 life hours of high resistance wind playing was found. CONCLUSIONS: High and low resistance wind musicians experience a transient rise in their IOP while playing their instruments as a result least in part of uveal engorgement. The magnitude of IOP increase is greater in high resistance wind players versus low resistance wind players. High resistance wind musicians had a small but significantly greater incidence of visual field loss (abnormal fields and increased CPSD scores) than other musicians, which was related to life hours of playing. The cumulative effects of long-term intermittent IOP elevation during high resistance wind instrument playing may result in glaucomatous damage, which could be misdiagnosed as normal-tension glaucoma.
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2/14. Ockham's glaucoma.

    The combination of characteristic optic nerve head cupping, arcuate visual field loss and ocular hypertension would usually be thought sufficient to diagnose glaucoma. Only in the absence of elevated intraocular pressure, when normal tension glaucoma may be suspected, would intracranial imaging normally be performed to exclude occult pathology. A case is presented which illustrates the continuing need for vigilance, and an open mind, years after an apparently straight-forward diagnosis has been made.
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3/14. Optic neuropathy in children with lyme disease.

    Involvement of the optic nerve, either because of inflammation or increased intracranial pressure, is a rare manifestation of lyme disease. Of the 4 children reported here with optic nerve abnormalities, 2 had decreased vision months after disease onset attributable to optic neuritis, and 1 had headache and diplopia early in the infection because of increased intracranial pressure associated with Lyme meningitis. In these 3 children, optic nerve involvement responded well to intravenous ceftriaxone therapy. The fourth child had headache and visual loss attributable to increased intracranial pressure and perhaps also to optic neuritis. Despite treatment with ceftriaxone and steroids, he had persistent increased intracranial pressure leading to permanent bilateral blindness. Clinicians should be aware that neuro-ophthalmologic involvement of lyme disease may have significant consequences. If increased intracranial pressure persists despite antibiotic therapy, measures must be taken quickly to reduce the pressure.
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4/14. Late normalization of melanocytomalytic intraocular pressure elevation following excision of iris melanocytoma.

    BACKGROUND: Melanocytoma of the iris is a rare tumor which may sometimes undergo necrosis that could result in elevated intraocular pressure through pigment dispersion. Only nine similar patients have been previously reported. methods: A 27-year-old woman presented with a dark brown iris stromal mass located between the 4 and 8 o'clock positions in the inferior quadrant. Her left visual acuity was 20/60. The tumor encroached on the lens and caused focal cataract. There was massive pigmented debris over the iridocorneal angle and the intraocular pressure was 42 mmHg. RESULTS: Fine needle aspiration biopsy did not suggest malignancy. A wide sector iridectomy was performed and histopathological examination of the lesion revealed melanocytoma of the iris. There was no ciliary body involvement. In the postoperative period, intraocular pressure, which persisted in the mid-twenties, was successfully lowered with topical dorzolamide and betaxolol drops. These drugs were continued for 2 years while the angle pigmentation gradually disappeared. There has been no documented glaucomatous damage to the optic nerve and visual fields. A year after the cessation of the drops, the left intraocular pressure stabilized and did not rise above 15 mmHg. Her left visual acuity remained 20/25. CONCLUSION: In contrast to previously reported cases, the normalization of intraocular pressure in this patient took 26 months, a period that could be associated with the self-clearing process of pigment from the iridocorneal angle. Close follow-up with medical treatment averted a pressure lowering surgical procedure in this case.
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5/14. Glaucomatous optic nerve head changes with scanning laser ophthalmoscopy.

    PURPOSE: To determine whether there are angiographic differences among normal, preperimetric and advanced glaucoma eyes using indocyanine green angiography with SLO. This method was chosen because of its sensibility to detect peripapillary capillary vessels. methods: Scanning laser opthalmoscopy was preformed on normal eyes, preperimetric glaucomas and advanced glaucomas. MATERIAL: The authors used a confocal SLO (Heidelberg Retina Angiograph-HRA) CONCLUSION: Several changes may be seen on peripapillary capillary vessels at the different glaucomatous stages. DISCUSSION: In normal subjects HRT shows preservation of the disc/cup area ratio; indocyanine green angiography shows normal prepapillary plexus pattern on the neuroretinal rim and cup. Subjects on glaucomatous preperimetric stage reveal a decrease in the disc/cup area ratio as a result of an increase of the cup area secondary to a reduction of the neuroretinal rim area. ICG at this hipertensive stage shows an increase in prepapillary plexus visualization, which may be a consequence of increased blood flow while autoregulation is still operative. Subjects with advanced glaucoma show prominent decrease in the disc/cup area ratio as well as marked capillary droupout in ICG angiography.
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6/14. Visual-field loss with optic nerve drusen and ocular hypertension: a case report.

    BACKGROUND: patients with optic nerve drusen are often asymptomatic and free of visual symptoms. However, ocular complications such as visual-field defects may develop. This article presents the case of a patient with optic nerve drusen, ocular hypertension, and a visual-field defect. The diagnosis and management of patients with such findings will be presented. CASE REPORT: A 75-year-old man came to the eye clinic with a history of being treated for glaucoma. On examination, optic nerve drusen were found in both eyes. Subsequent testing revealed ocular hypertension and a visual-field defect that could be related to either optic nerve drusen or glaucoma. After re-establishment of baseline intraocular pressures (IOP) and re-initiation of treatment, the patient is being monitored for IOP control and visual-field progression. CONCLUSION: optic nerve drusen and glaucoma can both cause visual-field defects. When a patient manifests optic nerve drusen, ocular hypertension, and visual-field defects, a diagnostic and management dilemma exists. Regardless of the etiology for the field defects, a treatment regimen designed to reduce the intraocular pressure to a level that potentially reduces the risk of ocular sequelae is recommended.
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7/14. Refractory ocular hypertension secondary to intravitreal injection of triamcinolone acetonide.

    PURPOSE: to report a case of severe ocular hypertension occurring as a complication after a single intravitreal injection of triamcinolone acetonide for the treatment of a diabetic cystoid macular edema. methods: interventional case report. RESULTS: a 63-year-old pseudophakic diabetic woman developed a severe and relatively sudden IOP increase to 50 mm Hg one month after receiving a single 4-mg intravitreal injection of triamcinolone acetonide for a chronic progressive macular cystoid edema. Previously the patient who did not develop corticosteroid-induced glaucoma secondary to her cataract surgery was treated with topical beta-blockers for a mild chronic bilateral ocular hypertension. A deep sclerectomy had to be performed in emergency to avoid optic nerve damage and allowed to successfully control the IOP with a 5 month follow-up. Concomitantly visual acuity could be increased from 0.05 before the intravitreal injection to 0.4. CONCLUSIONS: Although unfrequent in the literature, this observation confirms the risk of occurrence of a severe ocular hypertension after intravitreal injection of triamcinolone. A close monitoring of IOP is mandatory after intravitreal injection, especially in patients with altered trabecular function. This potentially devastating complication has to be weighed up with the benefices of intravitreal injection of triamcinolone for improving visual acuity in patients with clinically significant diabetic macular edema.
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8/14. Neurosensory detachment arising from a fractured inner-limiting membrane secondary to chronically elevated intraocular pressure.

    Diffuse optic nerve excavation and focal rim loss mimicking an optic pit have never been reported to predispose patients to serous detachments despite their relative frequency among patients with glaucoma. Recent reports of idiopathic macular schisis detachments occurring in the setting of elevated intraocular pressure without evidence of a contributing comorbidity have caused some to speculate that alternative mechanisms exist with the capacity to engender these retinal complications. Experimental simian research has unveiled the capacity of chronically elevated intraocular pressure to yield conduction portals between the posterior hyaloid face and the subretinal space by inducing microscopic fractures in the inner-limiting membrane. To our knowledge, this is the first case report providing objective evidence of an idiopathic neurosensory detachment resulting from a fractured inner-limiting membrane arising in the setting of chronically elevated intraocular pressures. CASE REPORT: A 34-year old black man presented with transient eye pain and fluctuating vision in his left eye with his current spectacle prescription. A 2-year history of right eye blindness from glaucoma was uncovered. Funduscopic evaluation revealed a broad neurosensory detachment in the setting of an excavated optic nerve in the patient's right eye. Optical coherence tomography confirmed the hydrodynamic separation of the sensory retina from the retinal pigmented epithelium and permitted visualization of a fractured inner-limiting membrane with a contiguous communication between the posterior hyaloid face and the subretinal space at the nasal limit of the detachment. fluorescein angiography studies identified the absence of chorioretinal vascular compromise contributing to the minimal expansion of the dye into serous cavity late into the study. No optic pit was discernible using optical coherence tomography imaging or fluorescein angiography. CONCLUSIONS: Although glaucomatous damage of the optic nerve has rarely been shown to predispose an individual to serous complications within the macula, recent reports attest to its pathogenic capacity and propose a theory to explain their infrequent clinical coexistence. This case provides additional support for the mounting evidence to support the role of a compromised inner-limiting membrane in inducing a macular detachment in the setting of chronically elevated intraocular pressure without evidence of preexisting optic pits.
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9/14. triamcinolone acetonide-induced ocular hypertension.

    PURPOSE: The aim of this study is to report on the clinical course of a patient showing markedly increased intraocular pressure (IOP) caused by intravitreal triamcinolone acetonide. methods: A 33-year-old patient received an intravitreal injection of approximately 20 mg of triamcinolone acetonide (TA) as treatment of otherwise therapy-resistant uveitis. She experienced an IOP rise to values over 40 mmHg for a period for more than 3 months, despite maximal antiglaucomatous medical therapy. Peak IOP was 55 mmHg. RESULTS: Neither confocal scanning laser tomography nor qualitative assessment of optic disc photographs nor perimetry showed development of glaucomatous changes. scanning laser polarimetry of the retinal nerve fiber layer suggested a slight loss in the nasal upper fundus quadrant. CONCLUSIONS: Relatively young patients with a pronounced TA-induced rise in IOP, unresponsive to maximal antiglaucomatous medication, may not necessarily undergo antiglaucomatous surgery if the rise in IOP does not last longer than approximately 3 months.
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10/14. Mechanisms of visual loss in severe proptosis.

    Vision loss in orbital hypertension secondary to sudden space-occupying lesions is usually attributed to one of three causes: central retinal artery occlusion, direct compressive optic neuropathy, or compression of optic nerve vasculature. Accepted modes of decompressive therapy include lateral canthotomy and cantholysis; drainage of localized orbital air, hematoma, or abscess; and bony wall decompression. Five cases are presented in which orbital hypertension caused severe proptosis with traction on the optic nerve and tenting of the posterior globe. Another mechanism contributing to visual loss is proposed in these cases: ischemic optic neuropathy due to stretching of nutrient vessels. In these cases, rapid posterior decompression should theoretically be favored to reduce orbital pressure and relieve traction on the optic nerve vasculature.
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