Approach to the adult with acute persistent visual loss
- Thellea Leveque, MD, MPH
Thellea Leveque, MD, MPH
- Clinical Associate Professor, Department of Ophthalmology
- University of Washington School of Medicine
Acute vision loss is a frightening experience for patients and has the potential for long-term visual consequences. The many causes of acute vision loss and the time-sensitive need for evaluation and treatment pose diagnostic and therapeutic challenges .
A careful history is key to narrowing the differential diagnosis and will allow for a more focused physical examination. Prompt diagnosis and treatment may influence the visual outcome.
This topic will present an overview of the approach to patients with acute persistent visual loss. Transient visual loss, the differential diagnosis of the red eye, and specific causes of acute vision loss are discussed separately. (See "Amaurosis fugax (transient monocular or binocular visual loss)" and "Evaluation of the red eye".)
DEFINITION OF TERMS
Acute transient visual loss (TVL) is defined as a sudden deficit in visual function in one or both eyes lasting less than 24 hours. It is caused by a temporary vascular occlusion in the circulation to the eye or visual cortex, or by neuronal depression after a seizure or migraine . Acute persistent visual loss (PVL) may be defined as lasting at least 24 hours and is typically not caused by transient ischemia . (See "Amaurosis fugax (transient monocular or binocular visual loss)".)
To achieve clear vision, light must follow an unhindered path from the front to the back of the eye, traveling through the cornea, aqueous humor, lens, and vitreous humor to the retina (figure 1). Refracted by the cornea and lens (and perhaps also by glasses or contact lenses), light is focused onto the retina where it is transformed into an electrochemical signal by photoreceptors and supporting cells. The signal is transmitted via the optic nerve through the visual pathways to the occipital lobes.To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:
- Borooah S, Dhillon A, Dhillon B. Gradual loss of vision in adults. BMJ 2015; 350:h2093.
- Burde R, Savino P, Trobe J. Clinical Decisions in Neuro-ophthalmology, 3rd ed, Mosby, 2002.
- Trobe JD. The Physician's Guide to Eye Care, 2nd ed, The Foundation of the American Academy of Ophthalmology, San Francisco 2001.
- Rumelt S, Brown GC. Update on treatment of retinal arterial occlusions. Curr Opin Ophthalmol 2003; 14:139.
- London NJ, Brown G. Update and review of central retinal vein occlusion. Curr Opin Ophthalmol 2011; 22:159.
- Balcer LJ. Clinical practice. Optic neuritis. N Engl J Med 2006; 354:1273.
- Liu GT, Volpe NJ, Galetta SL. Vision loss: Disorders of the Chiasm. In: Neuro-Ophthalmology Diagnosis and Management, WB Saunders Company, 2001.
- Lois N, Wong D. Pseudophakic retinal detachment. Surv Ophthalmol 2003; 48:467.
- Schein OD, Buehler PO, Stamler JF, et al. The impact of overnight wear on the risk of contact lens-associated ulcerative keratitis. Arch Ophthalmol 1994; 112:186.
- Taban M, Behrens A, Newcomb RL, et al. Acute endophthalmitis following cataract surgery: a systematic review of the literature. Arch Ophthalmol 2005; 123:613.
- Miguel A, Henriques F, Azevedo LF, Pereira AC. Ophthalmic adverse drug reactions to systemic drugs: a systematic review. Pharmacoepidemiol Drug Saf 2014; 23:221.
- Thoo S, Cugati S, Lee A, Chen C. Successful treatment of fingolimod-associated macular edema with intravitreal triamcinolone with continued fingolimod use. Mult Scler 2015; 21:249.
- Liu CY, Francis JH, Brodie SE, et al. Retinal toxicities of cancer therapy drugs: biologics, small molecule inhibitors, and chemotherapies. Retina 2014; 34:1261.
- Fraser S, Siriwardena D. Interventions for acute non-arteritic central retinal artery occlusion. Cochrane Database Syst Rev 2002; :CD001989.
- Hazin R, Dixon JA, Bhatti MT. Thrombolytic therapy in central retinal artery occlusion: cutting edge therapy, standard of care therapy, or impractical therapy? Curr Opin Ophthalmol 2009; 20:210.
- Rahman W, Rahman FZ. Giant cell (temporal) arteritis: an overview and update. Surv Ophthalmol 2005; 50:415.
- Saw SM, Gazzard G, Friedman DS. Interventions for angle-closure glaucoma: an evidence-based update. Ophthalmology 2003; 110:1869.
- Choong YF, Irfan S, Menage MJ. Acute angle closure glaucoma: an evaluation of a protocol for acute treatment. Eye (Lond) 1999; 13 ( Pt 5):613.
- Ross WH. Visual recovery after macula-off retinal detachment. Eye (Lond) 2002; 16:440.
- DEFINITION OF TERMS
- Media problems
- - Keratitis
- - Corneal edema
- - Hyphema
- - Lens changes
- - Vitreous hemorrhage
- - Uveitis
- Retinal problems
- - Retinal artery occlusion
- - Retinal vein occlusion
- - Retinal detachment
- - Acute maculopathy
- Optic nerve problems
- - Ischemic optic neuropathy
- - Optic neuritis
- - Papilledema
- Chiasmal problems
- Retrochiasmal disorders
- - Homonymous hemianopia
- - Cortical blindness
- Psychogenic problems
- APPROACH TO THE PATIENT
- Physical examination
- Patient triage
- Immediate treatment
- - Central retinal artery occlusion
- - Giant cell arteritis
- - Acutely elevated intraocular pressure
- Emergent referral