REBEL Core Cast 97.0 – Acute Vision Loss II

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Definition: Decrease of visual acuity due to a non-traumatic cause.  Transient vision loss defined as vision loss <24 hours. Persistent vision loss defined as loss of vision >24 hours. (Bagheri 2015).

Causes: There are multitude of causes of vision loss. This post focuses on the following pathologies:

• Glaucoma
• Giant Cell Arteritis
• Vitreous Detachment
• Retinal Detachment
• Central Retinal Vein Occlusion
• Central Retinal Artery Occlusion
• Amaurosis Fugax

Vitreous Detachment (Guluma 2018)

Definition: Separation between the posterior vitreous cortex and the internal limiting membrane (ILM) of the retina (which is the most external portion of the retina).

Background

• Risk factors – Increasing age, myopia (nearsightedness)
• Many older individuals have essentially asymptomatic vitreous detachments.
• Often occurs as the vitreous shrinks with increasing age, pulling away from the retina.

Symptoms

• Floaters > flashers
• No change in visual fields
• May have decreased visual acuity.

Signs

• Shafer’s sign (tobacco dust)
• May see a Weiss ring when the posterior vitreous (PV) detaches from the optic disc margin
• Visualization with ultrasound.

Emergency Department Management:

• Emergency ophthalmology consultation.
• Emergency surgical management indicated if concomitant retinal tear, vitreous hemorrhage, or retinal detachment.

Retinal Detachment (Hollands 2009)

Pathophysiology

• Posterior vitreous shrinks with advancing age (aka synchysis senilis), pulling on the retina.
• Pulling can cause tears in the retina (10-15% of the time) (Hollands 2009)
• Tear allows liquefied vitreous leaks in, causing the retina to separate from the retinal pigment epithelium (33-46% of the time) (Hollands 2009)

Symptoms

• Blurry vision/decreased peripheral vision
• Flashers(photopsia)/floaters
  • 14% of pts referred to ophthalmology with flashers/floaters end up having retinal tears.
  • Photopsia is from vitreoretinal traction, floaters are from vitreous cells/blood in the eye.
  • Symptom characteristics (Hollands 2009)
    • Any flashers/floaters:  (+) LR 1.2 and (–) LR 0.9.
    • >10 floaters, (+) LR 8.1-36

Signs

• Pigmented cells (‘‘tobacco dust’’ aka Shafer’s sign) in the vitreous and occasionally in the anterior chamber (caused by pigmented epithelial cells that spilled into vitreous)
• Visual field loss
• Vitreous hemorrhage: (+) LR 10
• Visualization on ultrasound

Emergency Department Management

• Emergency ophthalmology consultation for possible surgical repair

Central Retinal Vein Occlusion (CRVO) (McAllister 2012)

Background

• Pathophysiology not fully understood; possibly due to thrombus located in the central retinal vein (CRV), in the region of the lamina cribrosa
• Second most common cause of vision loss due to  retinal vascular disease (Most common cause: Diabetic retinopathy)

Symptoms

• Floaters – CRVO can cause neovascularization which causes leaky vessels leading to debris in vitreous.
• Blurry vision
• Glaucoma symptoms – due to leaky vessels.
• May be asymptomatic

Signs

• Visual acuity deficit – Variable degree.
• Funduscopic exam-
  • Flame-shaped, dot and blot hemorrhages
  • Retinal edema: May be limited to a certain section of the retina (if branch occlusion) or in all quadrants (if central vein occluded) (aka pizza pie eye)
  • May have macular edema

Emergency Department Management

• Ophthomology consultation
• Treatment traditionally laser for neovascularization complications, although newer treatments are emerging.

Central Retinal Artery Occlusion (CRAO)

Background

• • Anatomy: First branch of the internal carotid artery is the ophthalmic artery which splits into the posterior ciliary and central retinal arteries which supply the eye.
  • Causes:
    • Carotid artery stenosis (most common)
    • Cardioembolic sources also important cause.

Symptoms

• Sudden painless monocular vision loss
• May have some temporal sparing.

Signs

• APD in affected eye
• Funduscopic exam: Whitening of ischemic inner retinal layers with sparing in the foveal region (which is supplied by the intact choroidal circulation) creating the classic “cherry-red spot”

Emergency Department Management

• Emergency ophthalmology consult, stroke work-up
• Treatment options:
  • No clinical trials have demonstrated improvement with any treatment compared with observation.
  • Management options described in the literature
    • Tissue plasminogen activator (tPA)
    • Ocular massage
    • Ocular pressure lowering agents / maneuvers
    • Topical agents such as timolol
    • IV agents such as acetazolamide or mannitol
    • Anterior chamber paracentesis
    • Vasodilatory Agents (nitroglycerin, pentoxifylline, isosorbide, carbogen, breathing into a bag – causes increase in CO₂ leading to vasodilation)

Read More

Bhatia K, Sharma R: Eye Emergencies in Adams J.G. et al, Emergency Medicine Clinical Essentials ed 2. Philadelphia: Elsevier, 2013  (Ch) 26:  p. 209-225

Walker R, Adhikari S.: Eye Emergencies, in Tintinalli J et al (eds): Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, Seventh Edition New York City: McGraw-Hill 2016 (Ch) 241

Guluma K, Lee JE. Ophthalmology, in Marx J et al (eds): Rosens Emergency Medicine: Concepts and Practice, ed 9. Philadelphia: Elsevier, 2018 (Ch) 61: p. 790-819

Core Ultrasound: Vitreous vs Retinal Detachment

Post Created By: Anand Swaminathan MD, MPH

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)