A. Components of the Eye Exam
- History
- Time of onset
- Symptoms when patient first noticed bluriness
- Unilteral or bilateral
- Associated conditions or events
- Non-Ophthalmologist Visual Exam
- Visual Acuity
- Visual field
- Pupils
- Extraocular Muscle movements
- Anterior Segment (sclera, conjunctiva, cornea, anterior chamber, iris, lens)
- Posterior Segment (vitreous, retina, optic nerve)
- Visual Acuity
- Test one eye at a time
- Glass or contact lenses on if usually used
- Read standard chart
- Pinhole occlusion used if vision <20/40
- If cannot read chart, ask patient to count fingers on examiner's hands
- If cannot count fingers, determine distance where hand motions are detect
- If cannot detect hand motion, determine if patient can detect light
- Visual Field
- Neurologic disease or retinal detachment may change peripheral vision
- Test each eye separately
- Check nasal, temporal, superior and inferior quadrants
- Amsler's grid may be used: patient looks at central dot
- Patient then reports any areas of distortion or loss of visual field
- Grid is especially useful in retinal disease
- Pupils
- Pupils should be black, round, of same size, and reactive to light
- Nonblack pupil suggests opacification of lens, usually due to cataracts
- Misshapen or eccentric pupils after trauma
- Pupillary asymmetry may be only sign of serious eye injury on penlight exam (~20%)
- Normally, light shined in one pupil should cause both pupils to constrict
- Dilation of non-illuminated pupil is called afferent pupillary defect (APD)
- APD is a sign of optic nerve disease or injury (nerve and/or retinal damage)
- Extraocular Muscles (EOM)
- Diplopia is usually a manefestation of EOM disfunction
- This may be interpreted as blurry vision
- EOM testing should be done in all four quadrants
- Patient is asked to follow a penlight
- Movements of eyes together and separately should be smooth, unrestricted, symmetrical
- Limitations of gaze in any direction should be noted
- Anterior Segment
[Figure]: "Schematic of the Eye"
- Sclera, conjunctiva, cornea, anterior chamber, iris, lens
- Entire anterior segment can be visualized with penlight illumination and observation
- Sclera and conjunctiva examined for discharge, swelling, vascular prominence
- Corneal reflection of light is extremely important
- Reflection should be absolutely clear, sharp, and free of irregularities
- Blood collection in eye is called hyphema
- Pus collection in eye is called hypopyon
- Iris evaluated for alterations in shape and contour
- Lens should be clear; opacification may signify cataracts
- Posterior Segment
- Consists of vitreous, retina, optic nerve
- Direct ophthalmoscopy with pupil dilation is required for reasonable visualization
- This is most difficult part of the exam
- Pupil dilation with 1% topicamide and 2.5% phenylephrine recommended [1]
- Red reflex through direct ophthalmoscope should look the same from all directions
- Altered red reflex in cataracts, vitreal hemorrhage, retinal or choroidal detachment
- Margins of optic nerve should be flat and well demarcated
- Arteries and veins should be free of hemorrhages, exudates, and ischemic cotton-wool spots
B. Nonpathologic Causes of Blurred Vision
- Refractive Errors
- Amblyopia: lazy eye (see below)
- Strabismus: wandering eye
- Functional (perceptual or psychological) visual loss
C. Pathologic Causes of Sudden Blurred Vision
- Sudden, Unliteral, Painless Vision Loss
- Often from abnormality in posterior segment of eye
- Vitreous hemorrhage (usually in diabetics)
- Serous elevations of macula, including choroidal neovascular membranes
- Age-related macular degeneration (AMD)
- Retinal detachments
- Retinal-vein occlusions
- Retinal artery occlusion (temporary = amaurosis fugax)
- Central retinal artery occlusion - APD, cherry red spot on macula, plaque may be seen
- Sudden, Unliteral, Painful Vision Loss
- Usually involve cornea and anterior chamber
- Typically with red eye
- Corneal causes: abrasion, infection, edema
- Corneal infections with ulceration are emergencies
- Inflammaiton of iris, ciliary body, anterior uveal tract often associated with photophobia
- Traumatic hyphema usually associated with pain and reduced visual acuity
- Acute glaucoma causes pain and corneal edema
- Temporal (giant cell) arteritis (vasculitis) - presents in older patients, sometimes with scalp pain and arthropathy, very high erythrocyte sedimentation rate (ESR)
- Optic neuritis presents in younger persons, often associated with multiple sclerosis
- APD is present in temporal arteritis and optic neuritis
- Orbital cellulitis can be vision threatening, potentially life threatening
- Sudden, Bilateral, Painless Vision Loss
- Extremely rare
- May occur in poorly controlled diabetes
- Medications with anticholinergic agents or cholinergic agents
- Sudden, Bilateral, Painful Vision Loss
- Trauma to anterior segment: foreign bodies, chemicals, welder's exposure to UV radiation
- Corneal infections, iritis, and acute glaucoma may be biliateral
D. Pathologic Causes of Gradual Visual Loss
- Gradual, Unliteral, Painless Vision Loss
- Cataracts are most common cause, particularly in elderly
- Age-related macular degeneration (dry form)
- Rarely caused by slow compression on optic nerve (with optic atrophy)
- This may be caused by a pituitary or other brain tumor, or sinus tumor
- Vasculitis - giant cell arteritis (visual loss may be sudden), other vasculidites [2]
- Gradual, Unliteral, Painful Vision Loss
- Rare cause of vision loss
- Slowly progressive inflammatory or neoplastic disease
- Orbital granulomas or optic neuromas
- Gradual, Bilateral, Painless Vision Loss
- Cataracts and macular degeneration as above
- Ethambutol or hydroxychloroquine (very rare) toxicity
- Gradual, Bilateral, Painful Vision Loss
- Exceedingly rare
- Usually chronic inflammatory disease including sarcoidosis and autoimmune disorders
E. Amblyopia (Lazy Eye) [3,4]
- Defined as reduction in best-corrected visual acuity that is not directly attributable to any structural abnormality of the eye or visual path
- Most common cause of uncorrectable loss of vision in children
- Prevalance of 2%
- Usually occurs in children <3 years old (but can occur in ages 4-6)
- Screening at least by school entry (age 5-6) for all children is standard
- Earliest possible screening (when child can undertake visual acuity measurement) has been advocated, which is typically ~3 years old in many states in the USA
- Visual outcome ranges from 20/25 (nearly normal) to 20/200 (legally blind)
- Anisometropic amblyopia - only one eye is involved (most commonly)
- Isometropic amblyopia - both eyes are involved
- Three Categories
- Strabismic amblyopia: most common
- Refractive amblyopia: most difficult to detect
- Deprivation amblyopia: most severe in terms of vision loss
- Strabismic Amblyopia
- Deviating eye may turn in (esotropia), out (exotropia), up (hypertropia), down (hypotropia)
- Deviating eye input to brain is suppressed to prevent double vision
- This suppression may progress until all visual potential is lost in deviating eye
- Refractive Amblyopia
- Occurs when two eyes have significantly different refractive states
- Young child may rely on sight of the more focused eye
- The other eye will lose its visual potential
- Deprivation Amblyopia
- Typically affects children with unilateral or bilateral congenital cataracts
- May also occur with corneal or vitreous opacity or severe ptosis
- Excessive patching of one eye may similarly lead to deprivation amblyopia
- Treatment
- Appropriate optical correction using eye glasses or contact lenses
- Refractive error correction with spectacles may take up to 6 months
- Main choices are patching and atropine drops
- For strabismus, nearly full time occlusion of normal eye is prescribed
- Atropine may also be instilled into the normal eye to cause blurring ("penalization")
- Careful pediatric ophthalmological examination is critical
- Treatment is effective and results in better visual outcomes than no treatment
References
- Shingleton BJ and O'Donoghue MW. 2000. NEJM. 343(8):556

- Kathiresan S, Kelsey PB, Steere AC, et al. 2005. NEJM. 352(19):2003 (Case Record)

- Holmes JM and Clarke MP. 2006. Lancet. 367(9519):1343

- Simon JW and Kaw P. 2001. Am Fam Phys. 64(4):623
