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ULY CLINIC

ULY CLINIC

20 Septemba 2025, 02:05:14

Vision loss

Vision loss
Vision loss
Vision loss

Vision loss — the inability to perceive visual stimuli — can be sudden or gradual, temporary or permanent. The deficit may range from slight impairment to total blindness. Causes include ocular, neurologic, systemic disorders, trauma, or drug-related toxicity. Early and accurate diagnosis is crucial for optimal visual outcomes.


Pathophysiology

  • Ocular causes: Cataracts, glaucoma, retinal artery or vein occlusion, macular degeneration, vitreous hemorrhage, or trauma impair light perception or image formation.

  • Neurologic causes: Optic neuritis, optic atrophy, pituitary tumors, stroke, or cortical lesions disrupt transmission of visual signals to the brain.

  • Systemic/metabolic causes: Diabetes mellitus, hypertension, temporal arteritis, or infections may damage ocular structures or retinal vasculature.

  • Drug-induced toxicity: Chloroquine, ethambutol, digoxin, quinine, or methanol impair retinal or optic nerve function.

  • Trauma: Penetrating, blunt, or chemical injury may acutely damage ocular structures and cause partial or total vision loss.


History and Physical Examination

History
  • Onset: sudden vs gradual.

  • Pattern: unilateral or bilateral, partial or total, transient or persistent.

  • Symptoms: photophobia, eye pain, floaters, visual field defects, halos around lights.

  • Associated systemic conditions: hypertension, diabetes, thyroid disease, rheumatic or vascular disorders, infections, cancer.

  • Ocular history: previous eye disease, trauma, surgery, or family history of eye disorders.


Examination Tip: Testing Visual Acuity
  • Snellen letter chart (patients >6 years, literate):Patient sits or stands 20′ (6 m) from chart, covers one eye, and reads the smallest line visible. Record fraction: numerator = distance from chart, denominator = distance a normal eye reads that line. Normal vision = 20/20.

  • Snellen symbol chart (children 3–6 years or illiterate patients):Patient indicates direction of the E’s arms. Record fraction as above.

  • If unable to read largest letter at 20′, move closer and record actual distance (e.g., 3/200).


Physical Examination
  • Assess visual acuity with best available correction.

  • Inspect eyelids, conjunctiva, sclera for edema, redness, drainage, or lacerations.

  • Check lid closure and ptosis.

  • Examine cornea and iris for scars, irregularities, or foreign bodies.

  • Evaluate pupils: size, shape, direct and consensual light reflex, accommodation.

  • Assess extraocular muscles via six cardinal fields of gaze.


Medical causes

Cause

Onset

Key Features

Associated Findings

Pathophysiology

Management

Amaurosis fugax

Transient

Recurrent unilateral vision loss, seconds to minutes

Transient weakness, hypertension, elevated IOP

Temporary retinal ischemia

Identify source of emboli, vascular risk management

Cataract

Gradual

Painless visual blurring, milky white pupil

Progressive loss of vision

Lens opacity → impaired light transmission

Surgical extraction

Concussion

Acute

Blurred or double vision, temporary vision loss

Headache, LOC changes, amnesia, nausea, vomiting

Transient CNS dysfunction post-trauma

Supportive care, rest, monitor for complications

Diabetic retinopathy

Gradual

Visual blurring

Retinal edema, hemorrhage, microaneurysms

Retinal vascular damage due to hyperglycemia

Glycemic control, laser therapy, anti-VEGF injections

Endophthalmitis

Acute

Severe unilateral pain, vision loss

Redness, discharge, history of trauma or surgery

Intraocular infection/inflammation

Intravitreal antibiotics, surgery if needed

Glaucoma (acute angle-closure)

Acute

Eye pain, halos, nausea, vomiting

Rock-hard eye, nonreactive pupil, cloudy cornea

Sudden IOP elevation → optic nerve damage

Pressure-reducing drops, IV acetazolamide, ophthalmology consult

Glaucoma (chronic open/angle closure)

Gradual

Peripheral vision loss, aching eyes

Halo vision, reduced night vision

Progressive optic nerve damage

Eye drops, laser/surgery

Macular degeneration

Gradual

Central vision loss

Blurring, distorted vision

Retinal macular degeneration

Anti-VEGF therapy, low-vision aids

Ocular trauma

Acute

Sudden unilateral or bilateral vision loss

Eyelid edema, laceration, intraocular content extrusion

Mechanical or penetrating injury

Emergency ophthalmology evaluation

Optic neuritis

Acute/subacute

Unilateral vision loss, eye pain

Sluggish pupillary response, hyperemic optic disk

Inflammation/demyelination of optic nerve

Corticosteroids, treat underlying cause

Optic atrophy

Gradual

Progressive visual field loss

Color vision changes, optic disk pallor

Degeneration of optic nerve fibers

Address underlying cause; visual rehabilitation

Pituitary tumor

Gradual

Blurred vision, hemianopia

Diplopia, nystagmus, ptosis, headache

Compression of optic chiasm

Surgery, radiation, endocrine management

Retinal artery occlusion

Acute

Sudden unilateral vision loss

Sluggish direct pupillary response

Arterial obstruction → retinal ischemia

Ophthalmology emergency, ocular massage, vasodilation

Retinal detachment

Acute or gradual

Painless visual field defect, shadow/curtain

Floaters, sudden vision loss

Separation of retina from underlying epithelium

Surgical repair

Retinal vein occlusion

Acute

Unilateral decrease in visual acuity

Variable vision loss

Retinal venous obstruction → edema/hemorrhage

Laser therapy, anti-VEGF therapy

Stevens-Johnson syndrome

Acute

Corneal scarring, vision loss

Conjunctivitis, systemic symptoms

Immune-mediated mucocutaneous reaction

Ophthalmology care, supportive therapy

Temporal arteritis

Acute/subacute

Vision loss, blurring

Throbbing unilateral headache, malaise, fever

Inflammation of temporal arteries → ischemia

High-dose corticosteroids

Rift Valley fever

Acute

Vision loss

Fever, myalgia, encephalitis in severe cases

Retinal inflammation

Supportive care, manage systemic disease

Drugs

Gradual

Vision loss, visual field defects

Retinal pigmentation changes, optic neuropathy

Drug-induced retinal or optic nerve toxicity

Discontinue offending drug, supportive therapy


Emergency interventions

  • Sudden vision loss may indicate central retinal artery occlusion or acute angle-closure glaucoma — urgent ophthalmology consultation required.

  • Central retinal artery occlusion: ocular massage, increase CO₂ levels (rebreathing or Venturi mask) to restore retinal blood flow.

  • Acute angle-closure glaucoma: measure IOP, administer pressure-lowering eye drops, IV acetazolamide.


Special considerations

  • Vision loss can cause significant anxiety.

  • Orient patient to surroundings, ensure safety, announce presence when approaching.

  • Darken room for photophobia; advise sunglasses.

  • Avoid contamination of the unaffected eye; maintain hand hygiene.

  • Prepare for surgery if indicated.


Patient counseling

  • Educate on environmental safety to prevent injury.

  • Stress importance of hand hygiene and avoiding rubbing eyes.

  • For progressive or permanent vision loss, refer to low-vision or social support services.


Pediatric pointers

  • Causes include optic nerve glioma, retinoblastoma, congenital infections (rubella, syphilis), retrolental fibroplasia, Marfan syndrome, retinitis pigmentosa, amblyopia.

  • Early detection is critical for treatment and vision preservation.


Geriatric pointers

  • Reduced visual acuity may result from morphologic retinal changes, decreased rod/cone function, or ocular diseases (cataract, glaucoma, macular degeneration).

  • Difficulty looking upward is common.

  • IOP increases with age; monitor for glaucoma.


References

  1. Biswas J, Krishnakumar S, Ahuja S. Manual of Ocular Pathology. New Delhi, India: Jaypee – Highlights Medical Publishers; 2010.

  2. Gerstenblith AT, Rabinowitz MP. The Wills Eye Manual. 7th ed. Philadelphia (PA): Lippincott Williams & Wilkins; 2012.

  3. Levin LA, Albert DM. Ocular Disease: Mechanisms and Management. 3rd ed. London (UK): Saunders Elsevier; 2010.

  4. Roy FH. Ocular Differential Diagnosis. Clayton, Panama: Jaypee – Highlights Medical Publishers, Inc.; 2012.

  5. American Academy of Ophthalmology. AAO Basic and Clinical Science Course. San Francisco (CA): AAO; 2021.

  6. Kanski JJ, Bowling B. Clinical Ophthalmology: A Systematic Approach. 9th ed. London (UK): Elsevier; 2011.

  7. Morgan ML, Katsnelson J. Ophthalmology Review Manual. 5th ed. Philadelphia (PA): Wolters Kluwer; 2017.

  8. Foroozan R. Acute visual loss: Approach to diagnosis and management. Ophthalmol Clin North Am. 2018;31:1–12.

  9. Kanski JJ, Salmon JF. Clinical Ophthalmology: A Systematic Approach. 8th ed. Elsevier; 2016.

  10. American Optometric Association. Comprehensive Eye and Vision Examination Guidelines. St. Louis (MO): AOA; 2020.

  11. Wong TY, Mitchell P. The eye in systemic disease. Lancet. 2007;370:1361–1373.

  12. Choudhury P, Choudhury A. Pediatric ocular emergencies. Indian J Ophthalmol. 2011;59:97–103.

  13. Taylor D. Geriatric ophthalmology: Age-related changes in vision and ocular anatomy. Clin Geriatr Med. 2015;31:285–300.

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