02. Blurred Vision

Resident Editor: Patrick Azcarate, MD

Faculty Editor: Jennifer Tu, OD, FAAO

BOTTOM LINE

✔ Evaluate for emergency causes first

✔ Ask about time course, prior episodes, and associated symptoms

✔ Avoid topical anesthetics or corticosteroids until recommended by Ophthalmology

Background

  • Sudden visual acuity change or vision loss can be an ophthalmologic emergency.
  • The key is to promptly identify potentially vision-threatening conditions and refer early as appropriate. 
  • If concurrent red eye, consider: anterior uveitis, corneal abrasion/ulcer, trauma, foreign body, hyphema, episcleritis, scleritis, keratitis, orbital cellulitis, angle-closure glaucoma, chemical burn, and thermal/UV keratopathy.
  • This chapter will focus on etiologies not detailed in The Red Eye.

Signs and Symptoms

Assess:

  • Tempo: acute vs chronic; recurrent vs non-recurrent
  • Unilateral vs. Bilateral
  • Visual acuity loss vs visual field deficit vs diplopia (see Figure 2)
  • Associated symptoms (e.g., eye pain, floaters or other abnormal spots, headache, neurologic deficits, constitutional symptoms)
  • Pertinent Co-morbidities (e.g., migraine, DM, HTN, CVA, inflammatory disorder, malignancy)
  • Relevant Meds (e.g., anticholinergics, rifabutin, hydroxychloroquine, sildenafil)
  • Recent Procedures/trauma/psychological stress
  • Use of corrective lenses, esp. contact lenses

Etiologies of Blurred Vision

Chronic:

  • Refractive error: myopia, hyperopia, astigmatism, presbyopia
  • Related to ocular disease: cataract, macular degeneration or other macular disorder, glaucoma, corneal dystrophy/degeneration/scar, strabismus,  pterygium, blepharitis, dry eyes
  • Related to systemic disease or condition: poorly-controlled DM, trauma, pituitary adenoma, idiopathic intracranial hypertension (IIH), stroke
  • Related to medication use: Plaquenil, Ethambutol, Topamax, Corticosteroids

Acute:

  • Trauma: (micro)hyphema, iritis, cataract, retinal detachment, macular hole
  • Infectious: conjunctivitis, corneal ulcer, endophthalmitis, retinitis
  • Inflammatory: uveitis (episcleritis, scleritis, iritis, trabeculitis, vitritis, retinitis, optic neuritis)
  • Vascular: ischemic optic neuropathy, retinal artery/vein occlusion, cranial neuropathy
  • Neoplastic: ocular melanoma, choroidal metastasis, cancer-associated retinopathy

Evaluation

  • See the Ocular Exam section under Eye Anatomy and Physical Exam chapter for details of tests, with a focus on: visual acuity, direct observation, and ophthalmoscopy.
  • Be sure to check if visual acuity improves with pinhole occlusion—this indicates refractive error

Treatment

  • Determine the cause of the vision change and if emergent intervention is needed to preserve vision
  • Manage underlying co-morbidities or stop potentially offending medications contributing to blurred vision. Never prescribe topical anesthetics/corticosteroids alone or with antibiotics unless done in consultation with an ophthalmologist.

General approach

  • See flow chart

Common Causes

Cause

Specific Etiologies

Typical Presentation

Management

Refractive Error

Myopia (nearsightedness), hyperopia (farsightedness), astigmatism, presbyopia (age related loss of accommodation leading to impaired near vision)

Gradual onset, painless, bilateral, responsive to correction with pinhole occluder or refractive lenses

Routine referral for prescription corrective lenses

Acquired Cataracts

Age-related, metabolic (e.g., DM), trauma, chronic anterior uveitis, meds (steroids, phenothiazines,), prior ocular surgery (glaucoma filter, vitrectomy)

Progressive blurring over months to years with both near and far vision affected, glare, decreased color vision

diminished red reflex, difficulty visualizing fundus

Routine referral for surgical extraction

Age-Related Macular Degeneration

Idiopathic but risk factors include: age, genetics, HTN, hyperlipidemia, smoking

Dry: accumulation of drusen/macular atrophy

Wet: Dry signs AND choroidal neovascularization

Rapid or gradual onset of central vision loss with central scotomas

Drusen (yellow macular exudates), macular or vitreous hemorrhage

Amsler grid test

Urgent referral for  intravitreal anti-VEGF

Migraine

Classic migraine with aura

Possible precipitants: OCPs, EtOH, stress, tyramine foods

Temporary visual defects usually precede migraine HA sxs but can occur without (acephalegic migraine). Normal neuro exam.

Identify and avoid precipitants

Prophylactic and/or abortive migraine therapy

Medications

Reversible: amiodarone, retinoids, tamoxifen, linezolid, sildenafil

Irreversible: ethambutol, hydroxychloroquine

Varies

Stop offending meds and seek alternatives if possible

Optic Neuritis

MS, other demyelinating conditions, viral infections, syphilis, granulomatous disorders, meds (e.g., ethambutol), idiopathic

Onset over days, usually unilateral, pain with eye movement, focal neuro sxs

Visual field defects, decreased color vision, afferent pupillary defect, normal or edematous optic disc

Assess full neuro exam for MS

Consider CBC, RPR, ESR, CRP

Brain MRI with gadolinium

High-dose pulse systemic steroids

Urgent referral: eval for other ocular disease

Functional Loss

Conversion disorder

Malingering

Acute onset, recent severe psychological trauma, history of seeking personal gain

Reassurance, possible Psych referral

Routine referral for further evaluation to r/o organic blindness

Ophthalmologic Emergencies

Cause

Specific Etiologies

Typical Presentation

Management

Retinal Artery Occlusion

Emboli, atherosclerotic, hypercoaguable states, meds (e.g., OCPs, diuretics), collagen vascular diseases, giant cell arteritis

Acute painless vision loss/field defect, can be transient (amaurosis fugax) or permanent

Afferent papillary defect, retinal whitening, retinal arteriolar “box-carring”, Hollenhorst plaques, cherry-red spot

Urgent ophtho referral

 

Check BP, foused PE on carotids, CV, and neuro.

 

If age>50:

-If embolus identified, perform embolic W/U: carotid U/S, cardiac echo, Holter, EKG and start ASA

 

-If concurrent headache/PMR, jaw claudication: GCA evaluation and start high dose steroids

 

If age<50: hypercoag W/U and start anticoagulation

 

Retinal Vein Occlusion

HTN, atherosclerotic, hypercoaguable states, meds (e.g., OCPs, diuretics)

Subacute onset, usually unilateral, can be transient or permanent

+/- afferent pupillary defect, extensive retinal hemorrhage, dilated/tortuous veins, cotton wool spots, optic disc swelling

Urgent ophtho referral for possible photocoagulation/intravitreal anti-VEGF injections

 

Check BP and other pertinent PE based on suspected etiology

 

Consider fasting glucose, A1c, CBC, coags, lipid panel, ESR, ANA

 

Stop offending meds

 

Retinal Detachment

Recent eye surgery or trauma, DM or sickle cell retinopathy, high myopia, malignant HTN, neoplasm, may be spontaneous without clear inciting cause

“Flashing lights” , floaters, “curtain” moving over to obscure field of vision, periph/central visual field loss

Abnormal visual acuity and visual field testing, +/- afferent pupillary defect

Emergent referral for surgical repair

Giant Cell Arteritis

Inflammation of medium and large vessels with elastic lamina, primarily of the head (but also aortic arch and branches)

Usually unilateral but can progress to bilateral, HA, scalp tenderness, jaw claudication, fever

Palpable but nontender and nonpulsatile temporal artery, afferent pupillary defect, pale swollen optic disc, possible flame-shaped hemorrhages, +/- CN 3/4/6 palsies

Immediate steroids (Solumedrol 250mg IV q6h x 12 doses, then prednisone 80-100mg PO daily until path returns), and consider ulcer ppx

Check ESR and CRP stat, temporal artery biopsy can still be done within 1 week of starting steroids

Emergent referral

Endophthalmitis

Recent eye surgery or trauma, retained foreign body, septic emboli, fungemia

Eye redness, floaters, +/- pain

Conjunctival injection, discharge, hypopyon, diminished red reflex

Emergent referral for intravitreal antibiotics or vitrectomy if severe

References

Eva PR, Pascoe PT, Vaughan DG. Refractive change in hyperglycaemia: hyperopia, not myopia. Br J Ophthalmol 1982;66:500-505.

Fraunfelder FW and Fraunfelder FT. Adverse ocular drug reactions recently identified by the National Registry of Drug-Induced Ocular Side Effects. Ophthalmology. 2004. 111(7): 1275 – 1279.

Li J, Tripathi RC, Tripathi BJ. Drug-induced ocular disorders. Drug Safety 2008;31(2):127-141.

Palay DA and Krachmer JH (2005). Primary Care Ophthalmology. 2nd Edition. Elsevier Mosby.

Shingleton BJ and O’Donoghue MW. Blurred vision. N Eng J Med 2000;343:556-562.

Skuta GL, Cantor LB, Weiss JS. Fundamentals and Principles of Ophthalmology. 2012. American Academiy of Ophthalmology.