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Acute Vision Loss

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2921. Acute posterior multifocal placoid pigment epitheliopathy associated with diffuse retinal vasculitis and late haemorrhagic macular detachment. (PubMed)

Acute posterior multifocal placoid pigment epitheliopathy associated with diffuse retinal vasculitis and late haemorrhagic macular detachment. A 20-year-old healthy man suffered rapid loss of bilateral central vision with placoid lesions at the level of the retinal pigment epithelium and choriocapillaris scattered in the posterior pole of the fundus. In addition, acute vasculitis of the retinal veins was remarkable and widespread throughout the posterior pole and midperiphery (...) . These inflammatory signs subsided in several weeks and were succeeded by recovery of the normal visual acuity with residual pigment derangements in the deep retina. Sixteen months after the onset of the disease choroidal neovascular membranes developed in the macular region of the left eye, followed by haemorrhagic macular detachment and marked visual loss. Significant increases in the serum cold agglutinin titre occurred as isolated laboratory findings concurrently with the acute stage of the disease

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1986 The British journal of ophthalmology

2922. Recurrent Giant Cell Reparative Granuloma of the Skull Base and the Paranasal Sinuses Presenting with Acute One-Sided Blindness (PubMed)

Recurrent Giant Cell Reparative Granuloma of the Skull Base and the Paranasal Sinuses Presenting with Acute One-Sided Blindness The etiology, pathogenesis, histopathologic diagnosis, prognosis, and treatment of giant cell reparative granulomas of the skull are controversial. We report a 14-year-old girl with an advanced recurrent giant cell reparative granuloma of the skull base and paranasal sinuses whose only clinical manifestation was a loss of vision. After undergoing endovascular catheter

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2002 Skull Base

2923. Treatment of acute retrolental fibroplasia by cryopexy. (PubMed)

Treatment of acute retrolental fibroplasia by cryopexy. Fifteen to 20% of premature infants weighing below 1500 g develop variable degrees of acute retrolental fibroplasia (RLF). Approximately 5% of those infants who develop RLF can be expected to become blind. A prospective study was carried out to evaluate if early cryopexy can prevent this blindness. The study showed that, among 533 infants admitted to the neonatal intensive care unit between July 1976 and December 1978, 55 had some degree (...) of active RLF. In 18 eyes of 9 infants in whom the retinopathy progressed beyond active stage II cryopexy treatment was applied to the avascular retina. In all the treated eyes the active retinopathy regressed, and there were no complications due to the procedure. The long-term follow-up showed that in 15 eyes there was good vision and that the remaining 3 eyes had some impairment of vision but were not blind. These results suggest that cryotherapy may prove useful in treating premature infants with RLF

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1980 The British journal of ophthalmology

2924. Coffee and doughnut maculopathy: a cause of acute central ring scotomas (PubMed)

, and neuroimaging.The patients were three women and two men whose ages ranged from 25 to 57 years. Four patients were heavy caffeine consumers while the fifth patient experienced an episode of hypotension. Vision loss was acute in all cases. The onset of vision loss was bilateral/simultaneous in three cases, bilateral/sequential in one case, and unilateral in one case. All affected eyes retained visual acuities of 20/25 or better. Colour vision was subnormal in three of four cases. Visual field defects were (...) field loss and its location, combined with the presence of temporal pallor in five eyes, suggest that the defect localises to the inner layers of the macula. While these cases could be considered an expansion of the clinical spectrum of acute macular neuroretinopathy, some may represent a distinct entity.

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2000 The British journal of ophthalmology

2925. Acute zonal occult outer retinopathy: a long-term follow-up study. (PubMed)

patients had residual visual field defects. Final visual acuity was 20/40 or better in 61 (68%) affected eyes. Nine patients (18%) were legally blind. The fundi of 90 affected eyes revealed no changes of AZOOR in 47 eyes (52%) and changes in the pigment epithelium and retina caused by AZOOR in 43 eyes (48%).Visual loss in AZOOR is characterized by one or more episodes of acute dysfunction, and in some cases, death of retinal receptor cells in one or more zones of one or both eyes. Central vision (...) was present in one eye of 31 patients (61%) and both eyes in 20 patients (39%). All patients presented with an acute loss of one or more zones of visual field, and 45 (88%) patients presented with photopsia. Corrected visual acuity was 20/40 or better in 68 (76%) of 90 affected eyes. Funduscopic examination was normal in 82 eyes and revealed signs of AZOOR in 8 eyes. Electroretinographic amplitudes were depressed in all affected eyes. The median delay in diagnosis of AZOOR was 17 months. During follow-up

2002 American Journal of Ophthalmology

2926. Acute acquired toxoplasma retinitis may present similarly to unilateral acute idiopathic maculopathy. (PubMed)

Acute acquired toxoplasma retinitis may present similarly to unilateral acute idiopathic maculopathy. To describe a patient with acquired toxoplasma retinitis that shared similarities with unilateral acute idiopathic maculopathy.Interventional case report.Interventional case report.A 39-year-old woman presented with sudden unilateral vision loss in the right eye after a flu-like illness. She had retinitis involving the fovea, subretinal fluid, thickening of the retinal pigment epithelium (...) , and a few vitreous cells; the retinitis resolved with antitoxoplasma antibiotic treatment.Acute acquired toxoplasma retinitis may present similarly to unilateral acute idiopathic maculopathy.

2004 American Journal of Ophthalmology

2927. What is the prognosis if there is a delay in treating visual loss from acute glaucoma? How many hours have we got in which to initiate treatment and how many hours means treatment is never going to im

@tripdatabase.com What is the prognosis if there is a delay in treating visual loss from acute glaucoma? How many hours have we got in which to initiate treatment and how many hours means treatment is never going to improve sight? We searched the NLH Specialist Library for Eyes and Vision and the TRIP and Medline databases but found little information to answer this question. Although a number of guidelines and other sources state acute angle glaucoma is an opthalamic emergency requiring immediate treatment (...) , none specify a finite period (or number of hours) in which treatment needs to be initiated in order to prevent visual loss. An American Optometric Association guideline states: “An acute angle closure attack is a true ophthalmic emergency and appropriate therapy must be instituted immediately to prevent vision loss.” [1] A practice guideline by the same organization notes: “ Acute primary angle closure …High IOP may be accompanied by nausea and vomiting. Acute attacks may be self-limited

2006 TRIP Answers

2928. Successful treatment of acute visual loss in Muckle-Wells syndrome with interleukin 1 receptor antagonist (PubMed)

Successful treatment of acute visual loss in Muckle-Wells syndrome with interleukin 1 receptor antagonist 16014694 2005 09 19 2008 11 20 0003-4967 64 8 2005 Aug Annals of the rheumatic diseases Ann. Rheum. Dis. Successful treatment of acute visual loss in Muckle-Wells syndrome with interleukin 1 receptor antagonist. 1245-6 Alexander T T Klotz O O Feist E E Rüther K K Burmester G-R GR Pleyer U U eng Case Reports Letter England Ann Rheum Dis 0372355 0003-4967 0 IL1RN protein, human 0 Interleukin (...) 1 Receptor Antagonist Protein 0 Receptors, Interleukin-1 0 Sialoglycoproteins IM Acute Disease Aged Autoimmune Diseases drug therapy Female Humans Interleukin 1 Receptor Antagonist Protein Receptors, Interleukin-1 antagonists & inhibitors Sialoglycoproteins therapeutic use Syndrome Vision, Low drug therapy 2005 7 15 9 0 2005 9 20 9 0 2005 7 15 9 0 ppublish 16014694 64/8/1245 10.1136/ard.2004.032060 PMC1755588

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2005 Annals of the Rheumatic Diseases

2929. Acute visual loss after initiation of antihypertensive therapy: case report (PubMed)

Acute visual loss after initiation of antihypertensive therapy: case report We report the case of a 50-year-old man who reported sudden, painless loss of vision in his left eye after starting antihypertensive therapy. Potential causes of acute painless unilateral visual loss are discussed, as is the initial management of hypertension in asymptomatic patients.

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2003 CMAJ: Canadian Medical Association Journal

2930. The management of acute visual loss after sinus surgery--two cases of rhinogenic optic neuropathy. (PubMed)

The management of acute visual loss after sinus surgery--two cases of rhinogenic optic neuropathy. Different causative mechanisms of ophthalmic complications during endonasal sinus surgery have been reported. Only a few cases of blindness caused by affections of the optic nerve due to inflammatory paranasal sinus disease have been described.Inflammatory optic neuropathy shall be considered among the causative factors for amaurosis after sinus surgery.We present two patients with dramatic visual (...) decrease occurring two weeks after sinus surgery as a result of inflammatory posterior paranasal sinus disease.Our therapy including surgical intervention in form of orbital or optic nerve decompression accompanied by systemic steroids and antibiotic therapy resulted in a significant increase of visual acuity in one case and a complete restoration of vision in the other case. In these two cases surgical intervention in the described fashion along with systemic steroids and antibiotic therapy

2006 Rhinology

2931. Acute visual loss in a child with autosomal recessive polycystic kidney disease: case report and review of the literature. (PubMed)

Acute visual loss in a child with autosomal recessive polycystic kidney disease: case report and review of the literature. Acute visual loss secondary to ischemic optic neuropathy in children is extremely rare. The causes are usually hypotension or anemia. We describe the clinical course of a 9-year-old boy with a functional renal transplant who presented to the emergency room hemodynamically stable after waking up with complete bilateral loss of vision (no light perception). Examination showed (...) that he had suffered massive nocturnal blood loss from esophageal varices secondary to portal hypertension. The patient's end-stage renal disease was secondary to autosomal recessive polycystic kidney disease (ARPKD), an entity comprised of renal cysts and hepatic fibrosis. Ophthalmologic findings in ARPKD are rarely cited in the literature. A literature search revealed 3 other cases of sudden visual loss reported in nonophthalmologic journals in patients with ARPKD. Funduscopic examination showed

2003 JAAPOS - Journal of the American Association for Pediatric Ophthalmology and Strabismus

2932. Hypercapnia invokes an acute loss of contrast sensitivity in untreated glaucoma patients (PubMed)

Hypercapnia invokes an acute loss of contrast sensitivity in untreated glaucoma patients It is widely accepted that hypercapnia results in increased retinal, choroidal, and retrobulbar blood flow. Reports of a visual response to hypercapnia appear mixed, with normal subjects exhibiting reduced temporal contrast sensitivity in some studies, while glaucoma patients demonstrate mid-peripheral visual field improvements in others. This suggests that under hypercapnic conditions a balance exists (...) hypercapnia.During room air breathing, compared with normal subjects, glaucoma patients had higher IOP (p = 0.0003) and lower contrast sensitivity at 3 cycles/degree (cpd) (p = 0.001). Mild hypercapnia caused a significant fall in contrast sensitivity at 6, 12, and 18 cpd (p < 0.05), only in the glaucoma group.Glaucoma patients with early disease exhibit central vision deficits as shown by contrast sensitivity testing at 3 cpd. Hypercapnia induces further contrast loss through a range of spatial frequencies (6

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2001 The British journal of ophthalmology

2933. Cerebral venous thrombosis presenting as acute visual loss (PubMed)

Cerebral venous thrombosis presenting as acute visual loss 11561555 2001 09 20 2008 11 20 0007-1161 85 9 2001 Sep The British journal of ophthalmology Br J Ophthalmol Cerebral venous thrombosis presenting as acute visual loss. 1140-1 Ko Y C YC Chen W T WT Lin P K PK Hsu W M WM Liu J H JH eng Case Reports Letter England Br J Ophthalmol 0421041 0007-1161 IM Acute Disease Female Humans Intracranial Thrombosis complications Middle Aged Vision, Low etiology 2001 9 20 10 0 2001 9 21 10 1 2001 9 20 10

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2001 The British journal of ophthalmology

2934. Acute visual loss by an Onodi cell (PubMed)

Acute visual loss by an Onodi cell 11032437 2000 10 06 2008 11 20 0007-1161 84 7 2000 Jul The British journal of ophthalmology Br J Ophthalmol Acute visual loss by an Onodi cell. 801-2 Klink T T Pahnke J J Hoppe F F Lieb W W eng Case Reports Letter England Br J Ophthalmol 0421041 0007-1161 IM Acute Disease Adult Ethmoid Sinus pathology Humans Magnetic Resonance Imaging Male Mucocele complications diagnosis Optic Nerve Diseases complications diagnosis Vision, Low etiology 2000 10 14 11 0 2000 10

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2000 The British journal of ophthalmology

2935. Sudden loss of vision caused by a vasculitic ophthalmic artery occlusion in a patient with ankylosing spondylitis and Crohn's disease (PubMed)

Sudden loss of vision caused by a vasculitic ophthalmic artery occlusion in a patient with ankylosing spondylitis and Crohn's disease 17057182 2006 12 11 2018 11 13 0007-1161 90 11 2006 Nov The British journal of ophthalmology Br J Ophthalmol Sudden loss of vision caused by a vasculitic ophthalmic artery occlusion in a patient with ankylosing spondylitis and Crohn's disease. 1438 Soomro H H Armstrong M M Graham E M EM Stanford M R MR eng Case Reports Letter England Br J Ophthalmol 0421041 0007 (...) -1161 IM Acute Disease Adult Blindness etiology Crohn Disease complications Female Humans Ophthalmic Artery Spondylitis, Ankylosing complications Vasculitis complications 2006 10 24 9 0 2006 12 12 9 0 2006 10 24 9 0 ppublish 17057182 90/11/1438 10.1136/bjo.2006.097097 PMC1857510 Postgrad Med J. 1995 Mar;71(833):170-2 7746779 Jpn J Ophthalmol. 1998 Sep-Oct;42(5):398-400 9822971 Am J Ophthalmol. 2000 Oct;130(4):528-30 11024432 Am J Gastroenterol. 2001 Apr;96(4):1116-22 11316157 J Gastroenterol. 1994

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2006 The British journal of ophthalmology

2936. A 16-year-old boy with progressive central vision loss in his left eye (PubMed)

A 16-year-old boy with progressive central vision loss in his left eye 15078843 2004 06 03 2018 11 13 0820-3946 170 8 2004 Apr 13 CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne CMAJ A 16-year-old boy with progressive central vision loss in his left eye. 1228 Morris Shaun S Department of Pediatrics, Hospital for Sick Children, Toronto, Ont. Hiraki Linda L Muise Aleixo A eng Case Reports Journal Article Canada CMAJ 9711805 0820-3946 AIM IM CMAJ. 2004 (...) Aug 17;171(4):310; author reply 310 15313971 Adolescent Blindness etiology Disease Progression Encephalomyelitis, Acute Disseminated complications diagnosis Humans Male 2004 4 14 5 0 2004 6 4 5 0 2004 4 14 5 0 ppublish 15078843 PMC385351 Mult Scler. 1997 Feb;3(1):43-6 9160345 Neurology. 2001 May 22;56(10):1308-12 11376179 Ann Neurol. 2001 Jul;50(1):121-7 11456302

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2004 CMAJ : Canadian Medical Association Journal

2937. Effects of flurbiprofen and indomethacin on acute cystoid macular edema after cataract surgery: functional vision and contrast sensitivity. (PubMed)

Effects of flurbiprofen and indomethacin on acute cystoid macular edema after cataract surgery: functional vision and contrast sensitivity. We examined the effect of acute cystoid macular edema (CME) on contrast sensitivity. Eyedrops were instilled into the surgically treated eye f1p4 times daily for two days preoperatively and for three months postoperatively. Angiographic and clinical CME were measured, as were contrast sensitivity and Snellen acuity. Jaeger visual acuity equivalents were (...) ; this also increased over time, most notably in the higher spatial frequencies. Flurbiprofen treatment improved contrast sensitivity in patients with and without CME significantly at 12 cycles per degree. Flurbiprofen-treated patients with CME in general had higher contrast sensitivity scores than vehicle-treated patients. In this population of patients having cataract surgery, treatment with flurbiprofen or indomethacin reduced the loss of functional vision associated with CME.

1995 Journal of cataract and refractive surgery

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