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The Differential
of Decrease in Vision
By Mays Dairi, MD
Painful decrease in vision
Red eye
Non red eye
Non-painful decrease in vision
Sudden
Progressive |
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PAINFUL DECREASE IN VISION
Keratitis:
Bacterial ulcer (contact lens wearer),
Herpes simplex ophthalmicus
Symptoms: foreign body sensation, epiphora, purulent discharge,
Exam: corneal epithelial defect, uptake by fluorescein
Management: gram stain, culture, and antibiotics or antivirals (for herpes)
Acute angle
closure glaucoma
Risk factors: narrow anterior
chamber, hyperopia, Eskimos and Asians
Symptoms: very painful red eye, haloes around light (due to corneal
edema), nausea, vomiting
Exam: Fixed mid-dialated pupil, high intraocular pressure (>45), narrow
anterior chamber, dialated conjunctival, episcleral and iris vessels,
might see glaucomafleckens (not seen acutely, but if seen, indicate a
previous episode of angle closure).
Management: miotics, carbonic anhydrase inhibitors, mannitol, laser
iridotomy
Uveitis
(see the Red Eye
chapter)
Risk factors: reiter's, ankylosing
spondylitis, collagen vascular disease, sarcoidosis, granulomatous
infections, juvenile rheumatoid arthritis, syphilis
Symptoms: red eye, decreased vision (variable), tearing, photophobia
PE:keratic precipitates, cells in the anterior chamber, iris nodules,
hypopyon
Management: rheumatological and infectious work up, topical steroids
and cycloplegics for mild cases, oral steroids and immune suppressants
if severe.
Non Red Eye
Risk factors: multiple sclerosis,
syphilis, sarcoidosis, lyme disease, collagen vascular disease (SLE,
Wegener's)
Symptoms: pain around the eye, exacerbated by eye movement, subacute
visual deterioration, a decrease in contrast sensitivity, color vision
and visual field defect (central scotoma)
Exam: decreased contrast sensitivity, relative APD if unilateral
Management: rheumatologic work up, IV steroids
PAINLESS DECREASE IN VISION
Sudden decrease in vision
Risk factors: high myopia, glaucoma, family history, previous surgery,
and trauma
Symptoms: flashing lights (photopsia), floaters, and shadow across
visual field
Signs on Exam: APD, retinal folds
Treatment: pneumatic retinopexy, scleral buckle, pars plana vitrectomy
Retinal
vascular disease
Amaurosis fugax
Unilateral tansient visual loss
Cholesterol and/or fibrin platelet emboli
Exam: may be normal, may show Hollen-Horst plaques
Management: evaluate for cardiac or carotid disease. Aspirin therapy
Symptoms: sudden loss of vision in the visual field that corresponds
to the territory of the obstructed artery
Branch retinal artery occlusion:
90 % are due to emboli, cardiac or carotid in
origin.
Exam: ischemic whitening of the retina in the territory of the
obstructed artery, retinal arteries distal to the blockage are
attenuated, might see embolic material
Central retinal artery occlusion
In central retinal
artery obstruction, the blockage is within the optic nerve itself and
the site of obstruction could not visualized. It is believed however
that most cases are due to thrombus formation. It could also be due to
extrinsic nerve compression due to orbital or optic nerve tumors,
inflammation or trauma.
Exam: cherry
red spot in the macular area
Management:
There is no proven treatment for retinal artery occlusion. If caught
within 72 hours trials of dislodging the emboli (by massaging,
paracentesis, and lowering the intraocular pressure), or thrombus
dissolution, or increasing oxygenation to the retina, have been tried.
Risk factors: hypertension, diabetes
mellitus, and hyperviscosity syndromes
Symptoms: rapid unilateral painless loss of vision
Exam: dilated tortuous veins, cotton wool spots, and retinal hemorrhages
Management: panretinal photocoagulation for neovascularization
Cataract
Acute metabolic changes or trauma can
cause a cataract
Neurologic disease
Lesion involving the neuronal visual pathways: optic tract, chiasm,
Lateral geniculate nucleus, cortex
Symptoms: painless decrease in the visual field
Exam: ophthalmologic exam is usually normal, might find some associated neurologic findings
Management: LP, CT, MRI and manage accordingly
Weight loss, anorexia, fever, jaw claudications, headache,
scalp tenderness, proximal joint and muscle pain
Exam: altitudinal visual field defects, pale swollen optic nerve
High ESR
Management: start high dose steroids therapy, schedule for a temporal
artery biopsy within a few days (pathology results are the same up
till 1 week after treatment)
Gradual decrease in vision
Risk factors: trauma, metabolic disease (diabetes, some inborn errors
of metabolism), medications, old age
Symptoms: painless decrease in vision, myopic shift, glares
Exam: lens opacity
Management: surgical extraction and replacement with an intraocular
lens
Risk factors: elevated intraocular pressure, genetic predisposition,
African origin, myopia, exfoliation syndrome, pigment dispersion
syndrome, history of trauma to the eye, severe anemia...
Symptoms: patients don’t notice the damage until late in the disease
where by they notice a decrease in the peripheral visual field
Exam: high intraocular pressure, large cup to disc ratio, visual filed
defect
Management: decrease intraocular pressure by medications (beta
blockers, prostagandins, adrenergics, carbonic anhydrase inhibitors,
hyperosmotic agents, miotics), and surgery in refractive cases.
Retinopathies
Diabetic Retinopathy, hereditary
retinopathies, Age-related
Macular Degeneration.
Risk factors: endocrine disease, genetic factors, old age,
medications...
Management: prevention is the key term, the only thing current
management does is prevent the progression of the disease.
Corneal Dystrophies and
Ectasias
Hereditary,
non-inflammatory, commonly progressive changes in the cornea
interfering with clarity of vision
Risk factors:
family history
Symptoms:
progressive refractive error, recurrent erosions
Exam: changes in the corneal clarity (dystrophy), or change in the
curvature (ectasia)
Management: spectacle correction, penetrating keratoplasty
Non-Arteritic Ischemic Optic
Neuropathy
No systemic symptoms, associated with cardivascular
disease, diabetes and hypertension
Normal ESR (see retinal artery occlusion) |