Vision Loss (Acute)

Definitions 📚

• Acute persistent vision loss: defined as lasting at least 24 hours, with potential for long-term vision loss depending on the underlying pathology

• Acute transient vision loss: defined as sudden deficit < 24 hours, with sudden nature of onset implicating temporary vascular occlusion (”amaurosis fugax”) or change in electrical activity (i.e. post-seizure neuronal depression, migraine)

Qualifiers 🧠

• Painless vs. painful
• “Red” vs. Normal-appearing eye
• Unilateral vs. bilateral
• Visual field cuts
• +/- Relative afferent pupillary defect

Anatomic Localization: Pain 🔥

• Neither the retina (retinal pigment epithelium → internal limiting membrane) nor the brain (neurons) harbor pain fibers, so any pathology resulting in a pain-predominant syndrome immediately excludes these posterior structures; however, if retinal disease is accompanied by pain, this suggests concurrent inflammation of the optic nerve (i.e. “neuroretinitis”)

• Importantly, GCA as an important cause of vision loss in patients > 50 can result in temporal arteritis-related headache, & one should consider atypical pain reporting if other signs point toward GCA

• Finally, optic neuritis (i.e. inflammatory rather than ischemic optic nerve disease) is the one posterior structure that can result in pain due to nociceptive innervation of the “sheath” of the optic nerve: the sheath is tugged during EOMs, thus painful EOMs may localize pathology to an inflamed optic nerve/sheath

Localization: Inspection → Fundoscopy 🔎

• Unless posterior uveitis is “spilling over” into the anterior chamber (”pan-uveitis”), posterior pathology does not generally result in a “red eye”; therefore, the presence of redness generally localizes pathology to the anterior eye structures

• If there is no redness, fundoscopy may or may not inform on localization:

1. Paleness + cherry-red spot → central retinal artery occlusion (CRAO)
2. “Blood & thunder” → central retinal vein occlusion
3. Retinal whitening → posterior uveitis
4. U/l papilledema + splinter hemorrhages → anterior ischemic optic neuropathy
5. B/l papilledema → ↑ ICP

• Importantly, a normal fundoscopic exam does not rule-out:

Localization: Laterality & Visual Field Pattern ↔️

• Just like the rarity of bilateral cellulitis, bilateral disease of the anterior structures is generally uncommon; therefore, the presence of bilateral visual field defects most commonly localizes to the chiasmal → retrochiasmal compartments (i.e. bitemporal vs. homonymous hemianopia)

• Importantly, many patients with homonymous hemianopia from a retrochiasmal stroke do not report bilateral vision loss, as they will only notice the temporal field cut (e.g. being surprised by objects as they emerge from the temporal field), & not the nasal field cut of the other eye

Medication-related Disease 💊

• Anticholinergics, topiramate (angle-closure)
• Digoxin (yellow vision)
• Sildenafil (ischemic optic neuropathy, blue vision)
• OCPs (ischemic, retinal, or optic nerve events)
• Sulfonamides (myopia)
• Rifabutin (uveitis)

• Approach to the adult with acute persistent visual loss

• Uveitis: Etiology, clinical manifestations, and diagnosis

• Case 21-2026: A 28-Year-Old Man with Headache and Vision Loss in the Right Eye