Interesting Retinal Cases

A 66 y/o patient with large cups and thin rims OU, cataract and measurement artifact on OCT, the results are surprising 😅

By 𝐷𝑟. 𝑆𝑡𝑒́𝑝ℎ𝑎𝑛𝑒 𝐹𝑖𝑡𝑜𝑢𝑠𝑠𝑖 🇫🇷, 𝑀𝑖𝑎𝑚𝑖, 𝐹𝑙𝑜𝑟𝑖𝑑𝑎
With ࣪ ˖ ✩𝒵𝒶𝒾𝓇𝒶✩ ࣪ ˖
At Blinking Owl Eyecare ™️

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Another episode of Glaucoma Yes or No

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I am wearing color Navy blue.
👕: All-day scrub zip polo
👖: All-shift scrub jogger

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Oxidative stress drives AMD
• Key triggers: UV exposure, smoking, and poor diet.
• Guide patients on prevention: Advise quitting smoking, consistent UV protection, and encouraging a diet rich in leafy greens for long-term eye health.

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• Location of drusen
Normal aging: may be outside the macula, scattered in peripheral retina
Dry AMD: drusen primarily within the macula

• Laterality
Normal aging: can be unilateral or asymmetric
Dry AMD: typically bilateral (often asymmetric)

• Size / appearance
Normal aging: small, isolated drusen
AMD: larger, more numerous drusen often with RPE changes

• Macular involvement
Normal aging: macula unaffected
AMD: macular pathology present → central retinal involvement

• Visual impact
Normal aging: usually asymptomatic
AMD: gradual ↓ central vision, reduced contrast sensitivity

• Associated findings
Normal aging: no significant pigmentary abnormalities
AMD: RPE mottling, pigment migration, geographic atrophy (advanced cases)

• Progression
Normal aging: often stable over time
Dry AMD: progressive degenerative macular disease

• Key clinical pearl
Not all drusen = dry AMD
Small clusters of extramacular, unilateral drusen without macular changes may simply represent normal age-related retinal changes rather than dry AMD.

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• Definition
Progressive corneal ectasia → stromal thinning + anterior protrusion → irregular astigmatism

• Epidemiology
→ onset: teens to early adulthood
→ often bilateral, asymmetric

• Pathophysiology
→ structural weakening of corneal collagen
→ non-inflammatory

• Risk factors
→ eye rubbing
→ atopy (allergies, eczema, asthma)
→ family history
→ connective tissue disorders

• Symptoms
→ progressive blur
→ increasing astigmatism
→ frequent Rx changes
→ ghosting, halos, monocular diplopia

• Refraction clues
→ increasing cyl
→ irregular astigmatism
→ reduced BCVA with glasses
→ scissors reflex on retinoscopy

• Slit lamp signs
→ Vogt’s striae (fine vertical stress lines)
→ Fleischer ring (iron deposition)
→ corneal thinning, conical protrusion
→ ± apical scarring (advanced)

• Topography / Tomography
→ inferior steepening
→ asymmetric bow-tie
→ posterior elevation (early detection)

• Complication
→ acute corneal hydrops (Descemet break → stromal edema)

• Management
Early: glasses / soft toric CL
Moderate: RGP / scleral lenses
Progression: corneal cross-linking (CXL)
Advanced: INTACS or corneal transplant

• Key clinical pearl
Young patient with changing astigmatism + ↓ BCVA → think keratoconus and get topography early

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• Anatomic location
Preseptal: infection anterior to orbital septum (eyelid/periorbital tissues)
Orbital: infection posterior to septum (orbit)

• Common source
Preseptal: skin trauma, insect bite, chalazion/hordeolum
Orbital: sinusitis (especially ethmoid) → direct spread

• Pain
Preseptal: localized, anterior (eyelid), no pain with EOMs
Orbital: deep orbital pain + pain with EOMs

• Eye movements
Preseptal: full, painless
Orbital: restricted, painful EOMs

• Vision
Preseptal: normal
Orbital: ↓ VA possible, ± RAPD

• Proptosis
Preseptal: absent
Orbital: present

• Systemic signs
Preseptal: mild or none
Orbital: patient looks systemically ill, not just a swollen eyelid

• Anterior segment
Preseptal: lid edema/erythema only
Orbital: may have chemosis, conjunctival injection

• Imaging
Preseptal: not routinely needed
Orbital: CT orbit/sinuses indicated

• Management
Preseptal: oral antibiotics, close follow-up
Orbital: admission to hospital with IV antibiotics + urgent imaging

• Key clinical pearl
Any pain with EOMs, ↓ vision, or proptosis → treat as orbital cellulitis until proven otherwise

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• Etiology
Chalazion: sterile granulomatous inflammation from blocked meibomian gland
Hordeolum: acute bacterial infection (usually staph)

• Onset
Chalazion: gradual, chronic
Hordeolum: rapid, acute

• Pain
Chalazion: typically painless
Hordeolum: painful, tender

• Location
Chalazion: deeper, within tarsal plate/ Meibomian gland
Hordeolum:
• External: lash follicle / Zeis or Moll gland
• Internal: meibomian gland

• Appearance
Chalazion: firm, non-erythematous nodule (may have mild redness)
Hordeolum: erythematous, swollen, may point with pustule

• Course
Chalazion: persists, may enlarge slowly
Hordeolum: often drains spontaneously within days- release of pus

• Management
Chalazion: warm compress, lid hygiene, consider steroid injection or surgical removal if persistent

Hordeolum:
External: warm compress, topical antibiotics
Internal: warm compress, oral antibiotics may be needed

Clinical pearl:
Beware of preseptal spread in internal hordeolum

Clinical pearl:
Recurrent/persistent “chalazion” → rule out sebaceous gland carcinoma

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