Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344232 (blurred vision)
 2,072 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To minimize the risk of visual loss in diabetic patients, recognition of early signs of oculopathy is essential. Diabetes-associated third-nerve palsy is manifested by unilateral ptosis and exotropia. Symptoms of closed-angle glaucoma are intense pain, halos around lights, and blurred vision. Open-angle glaucoma does not necessarily produce symptoms and is treated medically. A gradual decrease in visual acuity, sometimes associated with photophobia and difficulty in night driving, and monocular diplopia, are manifestations of cataract. The patient with "background" retinopathy usually complains of blurred or distorted central vision. Once the macula is involved, vision progressively decreases. Although the relationship of metabolic control to retinopathy has not been settled, evidence indicates that good medical control of the disease may delay onset of vascular complications.
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PMID:Four common ocular complications of diabetes--and how to treat them. 71 Aug 91

A 33 year old man developed acute oliguric failure lasting 66 days, eight days after admission with multiple gun shot wounds. On day 99 after admission, serum calcium was elevated mildly at 2.54 mmol/l (normal range 2.1-2.5 mmol/l). Serum parathormone was undetectable. He was discharged soon afterwards. He presented again on day 164 with nausea, vomiting and blurred vision. Fundoscopy revealed an ischaemic retinopathy and extensive keratopathy. Serum calcium was 3.48 mmol/l and serum creatinine 262 umol/l (normal range 40-110 umol/l). Repeat parathormone was undetectable and there was no evidence of myeloma, sarcoidosis or malignancy. Following treatment with intravenous saline and frusemide, serum calcium fell to a nadir of 3.05 mmol/l. On day 168 an infusion of sodium clodronate 300 mg was given. Twenty-four hours later serum calcium was 2.65 mmol/l and 48 hours later calcium was 2.26 mmol/l. Normocalcaemia was maintained for 17 days and severe hypercalcaemia never recurred. This is the first report in which biphosphonates have been successfully used to treat hypercalcaemia following acute renal failure thus obviating the need for further dialysis.
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PMID:Severe hypercalcaemia four months after acute oliguric renal failure--successful treatment with intravenous clodronate. 138 45

A 22-year-old woman presenting with recurrent transient episodes of vertebro-basilar artery syndrome and blurred vision was initially diagnosed as suffering from a collagen disease affecting the retina and CNS. Treatment with systemic steroids induced an apparent remission. However, a rapid deterioration of her condition prompted a reevaluation of the diagnosis and treatment. Ophthalmoscopic examination disclosed numerous ischemic foci in both eyes, scattered superficial hemorrhages, and neovascular tufts on the optic nerves. The possibility that both the cerebral and ocular phenomena were the results of systemic showering of emboli was raised. Careful two-dimensional echo cardiography revealed a mitral mass compatible with myxoma of the left atrium. The difficult differential diagnosis of combined encephalopathy and retinopathy is discussed.
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PMID:Bilateral retinopathy and encephalopathy. 292 Sep 7

Diabetes mellitus is a major cause of visual impairment and blindness. Cataracts and retinal vascular abnormalities (retinopathy) are the major defects occurring in the eyes. The frequency of these defects increases with the duration of diabetes. Many believe that the occurrence of eye disease in children with diabetes is rare. Blurry vision, an early manifestation of cataractogenesis, occurs in nearly all children with diabetes. Retinopathy, which is extremely rare prior to puberty, occurs in 70-90% of adolescents with diabetes of more than 10 years' duration. Proliferative retinopathy and blindness due to diabetes also occur in adolescents. Regular, careful ophthalmologic examinations by retinal specialists are indicated for the adolescents at risk. Those at risk are adolescent females with HLA DR3 and DR4 as well as those with limited joint mobility. Early recognition is essential to prevent the blindness that follows untreated proliferative retinopathy.
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PMID:Ophthalmologic complications of insulin-dependent diabetes mellitus in children and adolescents. 633 75

Funduscopic examination of two young adults complaining of blurred vision revealed small symmetrical macular lesions suggestive of solar retinopathy. Although both patients had recently looked at the sun for less than one minute, it is common to look at the sun for longer periods (ie, sunsets) without incurring visual symptoms of retinal lesions. Our biophysical analysis revealed the important parameters of solar retinopathy and the minimum exposure to the sun that would produce such lesions. Under ideal optical conditions, solar retinopathy can occur following extremely short observations of the sun.
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PMID:Solar retinopathy. A biophysical analysis. 648 17

The ophthalmologic safety of antimalarial drugs is well established, but absolute safety cannot be assured. Three types of side effects may develop. Corneal deposits and neuromuscular-associated blurred vision are always reversible and therefore benign. Visual loss has occurred in patients with retinopathy. Retinopathy may be divided into true retinopathy and premaculopathy. It is true retinopathy that may be associated with visual loss, while premaculopathy consists of subtle visual field and funduscopic abnormalities. These premaculopathic changes are generally completely reversible with drug discontinuation and have not been shown to progress. Hydroxychloroquine appears safer than chloroquine when currently accepted equivalent doses are used. Fewer than 20 patients with true retinopathy caused by hydroxychloroquine have been reported; more patients have developed true retinopathy when taking chloroquine. The safety profile is most dependent on low daily dose and regular ophthalmologic monitoring. The optimal strategy of ophthalmologic testing has not yet been determined, but visual acuity, funduscopic examination and visual field examination should be monitored. Self-administered ophthalmologic testing with Amsler grids may contribute additional safety but is not a replacement for physician testing.
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PMID:Ophthalmologic safety profile of antimalarial drugs. 848 66

We examined cone and rod electroretinograms to ganzfeld stimuli in a patient with crystalline retinopathy. The 54-year-old man complained of night blindness, blurred vision, and metamorphopsia in both eyes. His visual acuity was 10/200 in the right eye and 10/20 in the left eye; his subjective dark-adaptation threshold was elevated 1 log unit, and he made one tritan error on the Farnsworth Panel D-15. Specular microscopic examinations revealed tiny crystalline deposits in the limbal cornea bilaterally. Ophthalmoscopically, crystalline deposits were found in the posterior fundi. His light-adapted cone electroretinograms to white stimuli were diminished (about 30% of those of normal controls), with normal implicit times. His dark-adapted rod electroretinogram amplitudes were 10% of those of normal controls. The S-cone electroretinogram was not detectable to different spectral stimuli with strong white background, while the L-M-cone responses appeared normal in waveforms with reduced amplitude. These ERG results indicated that the patient's S-cone system is more highly impaired than the L-M-cone system, supporting the psychophysical evidence that the S-cone system is more vulnerable than other cone systems in retinal diseases.
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PMID:Nondetectable S-cone electroretinogram in a patient with crystalline retinopathy. 884 31

Purtscher's retinopathy is characterized by sudden visual loss in severely traumatized patients and is associated with multiple areas of superficial retinal whitening located primarily in the posterior pole. Visual outcome in Purtscher's retinopathy is variable, and there is no well-defined treatment. We report on a patient with immediate blurred vision in the right eye after a traffic accident. Ophthalmoscopy revealed multiple whitish patches scattered over the macular and peripapillary areas in the right eye. Fluorescein angiography showed multifocal retinal arteriolar occlusion in the early phase and staining of the involved retinal vessels and optic nerve head in the late phase. Indocyanine green angiography (ICG) showed rarefaction of choroidal vessels in the peripapillary area of the right eye at early phase. The late phase ICG study revealed multifocal hypofluorescent patches in the macular and peripapillary areas. Megadose steroid therapy was given with good visual response in the first 2 weeks, and the patient's vision had recovered completely when followed-up 10 months later.
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PMID:Pathogenesis and neuroprotective treatment in Purtscher's retinopathy. 974 75

Progressive outer retinal necrosis syndrome is a recently recognized variant of necrotizing herpetic retinopathy, developing in patients with acquired immune deficiency syndrome (AIDS) or other conditions causing immune compromise. We report a case in which the diagnosis of retinal necrosis syndrome was made before the diagnosis of AIDS was confirmed. A 41-year-old man presented with a 1-month history of blurred vision in his left eye. Ophthalmologic examination revealed extensive retinal necrosis with total retinal detachment in his left eye and multifocal deep retinal lesions scattered in the posterior fundus as well as in the peripheral retina in his right eye. The serologic test for human immunodeficiency virus (HIV) was positive. Despite intravenous acyclovir treatment for 1 week, the lesions in the right eye showed rapid progression. High doses of intravitreal ganciclovir were then given in addition to intravenous acyclovir. After combined treatment for 1 month, the lesions became quiescent and the visual acuity improved to 20/30. Although the patient soon developed full-blown AIDS, the vision in his right eye remained undisturbed. Physicians should suspect progressive outer retinal necrosis syndrome in any patient with rapidly progressive necrotizing retinopathy and test the patient for HIV infection. Aggressive combined antiviral agent therapy should be considered to save vision.
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PMID:Progressive outer retinal necrosis syndrome as an early manifestation of human immunodeficiency virus infection. 1008 72

Sun-gazing is the main cause of solar retinopathy. A 20-year-old inebriated man lying in a park gazed at the sun for approximately three hours at noon. Forty-eight hours after sun-gazing, the patient experienced the symptoms of blurred vision, erythropsia, and central scotoma in the left eye. Visual acuity decreased from 6/6 to 6/60 in the left eye and fundi examinations showed a round, yellowish-white discoid lesion on the left fovea and a smaller one on the right fovea. Fluorescein angiography showed early dye leakage in the fovea of the left eye, that increased gradually in size and became fuzzy at the foveal border in the late phase. A small, central scotoma of the left eye was also found in the visual field test. One month later, the lesion in the fovea of the left eye became smaller and was surrounded by a coarse pigmented halo. Fluorescein angiography showed a window defect in the retinal pigment epithelium. Visual field testing disclosed that the central scotoma persisted, but became smaller. Six months after sun-gazing, a lamellar hole in the fovea of the left eye was detected by optical coherence tomography. The visual acuity was 6/6 in the right eye and 6/60 in the left eye, and was unchanged at the end of the six-month follow-up period.
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PMID:Solar retinopathy: a case report. 1063 3


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