1. Cataract and IOLs: FLACS, capsular tension ring (CTR), phakic IOLs, modern IOLs, accommodative IOLs
2. Retina and vitreous: BRVO management, ARMD, OCT, ERG, ROP, retinal imaging, FFA, pars plana vitrectomy, Pascal laser, silicone oil
3. Cornea and ocular surface: stem-cell therapy, ocular surface squamous neoplasia, amniotic membrane, collagen cross-linking/C3R, keratoprosthesis, lamellar keratoplasty, pterygium surgery, toxic contact lens reactions
4. Glaucoma: neuroprotection, glaucoma implants, OCT in glaucoma
5. Anterior segment / iris / diagnostic imaging: pupilloplasty, UBM
6. General ophthalmic technology and materials: OVDs, lasers, dyes, tissue adhesives/glues

1. Cataract and IOLs: FLACS, capsular tension ring (CTR), phakic IOLs, modern IOLs, accommodative IOLs
2. Retina and vitreous: BRVO management, ARMD, OCT, ERG, ROP, retinal imaging, FFA, pars plana vitrectomy, Pascal laser, silicone oil
3. Cornea and ocular surface: stem-cell therapy, ocular surface squamous neoplasia, amniotic membrane, collagen cross-linking/C3R, keratoprosthesis, lamellar keratoplasty, pterygium surgery, toxic contact lens reactions
4. Glaucoma: neuroprotection, glaucoma implants, OCT in glaucoma
5. Anterior segment / iris / diagnostic imaging: pupilloplasty, UBM
6. General ophthalmic technology and materials: OVDs, lasers, dyes, tissue adhesives/glues

1. Cataract and IOLs: FLACS, CTR, phakic IOLs, modern/accommodative IOLs
2. Retina and vitreous: BRVO, ARMD, OCT, ERG, ROP, FFA, retinal imaging, vitrectomy, lasers, silicone oil
3. Cornea and ocular surface: stem cells, amniotic membrane, OSSN, C3R, keratoplasty, KPro, pterygium, contact-lens toxicity
4. Glaucoma: neuroprotection, drainage implants, OCT
5. Imaging, lasers and materials: UBM, dyes, OVDs, tissue glues, lasers, pupilloplasty

Cataract and IOLs for MS Ophthalmology Theory

1. Femtosecond laser-assisted cataract surgery (FLACS)
2. Capsular tension ring (CTR)
3. Phakic intraocular lenses
4. Modern pseudophakic IOLs, including toric, multifocal, EDOF and accommodating IOLs
5. IOL selection, biometry and high-yield complications

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1. Foundation: IOL basics

Definition

Parts

• Optic: central refracting portion
• Haptics: peripheral supporting elements
• Overall diameter: optic + haptic-to-haptic length
• Optic diameter: commonly 6 mm for standard adult posterior chamber IOLs

Ideal IOL properties

• Biocompatible and inert
• Stable fixation and centration
• Optically clear, scratch-resistant
• Minimal inflammation, posterior capsule opacification (PCO), dysphotopsia and glistenings
• Injectable through a small incision
• Predictable effective lens position (ELP)

Classification

Materials: exam comparison

Design features that prevent PCO

• Sharp square posterior optic edge produces a capsular bend and contact inhibition of lens epithelial cell migration.
• In-the-bag placement and meticulous cortical clean-up further reduce PCO.
• PCO, if visually significant, is managed by Nd:YAG posterior capsulotomy.

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2. FLACS: Femtosecond Laser-Assisted Cataract Surgery

Definition

1. Corneal incisions
2. Anterior capsulotomy
3. Lens fragmentation/softening
4. Arcuate or limbal-relaxing incisions for astigmatism

Principle

Essential components

• Docking interface: applanation or liquid-filled interface
• Image-guidance system: commonly OCT-based
• Laser delivery platform
• Patient interface and suction mechanism
• Integrated or adjacent phacoemulsification system

Steps of FLACS

1. Pharmacological dilation and sterile preparation.
2. Docking of the laser interface to the eye.
3. Imaging and treatment planning.
4. Laser creation of:
   • Primary and side-port corneal incisions
   • Precisely centered capsulotomy
   • Lens fragmentation pattern
   • Arcuate keratotomy if planned
5. Transfer to operating microscope.
6. Opening of laser capsulotomy and removal of free capsule disc.
7. Hydrodissection, phacoaspiration and cortical clean-up.
8. IOL implantation in the capsular bag.

Benefits

• Highly reproducible capsulotomy size, circularity and centration
• Precise corneal incisions
• Lens prefragmentation may reduce effective phaco time and cumulative dissipated energy
• Astigmatic arcuate incisions can be planned precisely
• Useful in selected challenging cases:
  • Shallow anterior chamber
  • Dense cataract
  • Low endothelial reserve
  • White/intumescent cataract, with careful case selection
  • Premium IOL procedures where centration is especially important

Limitations

• High capital, consumable and maintenance costs
• Extra docking and workflow time
• Requires pupil dilation and adequate corneal clarity
• Not always feasible in deep-set eyes, marked kyphosis, severe tremor, poor cooperation, inability to lie flat, or significant conjunctival scarring
• Incomplete capsulotomy, capsular tags and incomplete fragmentation can occur
• Does not replace surgical judgement or conventional phaco skill

Complications

During docking

• Subconjunctival hemorrhage
• Corneal folds and imaging artefacts
• Transient rise in IOP from suction
• Loss of suction and incomplete treatment

During surgery

• Incomplete corneal incision
• Capsular tags, microadhesions or incomplete capsulotomy
• Anterior capsular tear if the capsule is pulled before identifying and releasing tags
• Incomplete nuclear fragmentation
• Miosis due to prostaglandin release
• Rare capsular block syndrome if hydrodissection is forceful in a gas-fragmented lens

FLACS versus conventional phaco: what to write as “recent evidence”

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3. Capsular Tension Ring (CTR)

Definition

Design

• Usually made of PMMA
• Open ring with eyelets at both ends
• Inserted into the capsular bag after capsulorhexis and preferably after adequate hydrodissection
• Available in different diameters

Principle

Indications

Zonular weakness or dialysis

• Pseudoexfoliation syndrome
• Traumatic zonular dialysis
• High myopia
• Marfan syndrome and other ectopia lentis states
• Previous vitreoretinal surgery
• Mature/hypermature cataract with weak zonules
• Lens subluxation of limited extent
• Prior acute angle-closure attack with zonulopathy, in selected cases

Prevention of capsular contraction and IOL decentration

• Pseudoexfoliation
• Retinitis pigmentosa
• High myopia
• Uveitis, selectively
• Conditions predisposed to capsular phimosis

Types

Surgical technique

1. Create a well-centered continuous curvilinear capsulorhexis.
2. Use dispersive OVD to maintain the bag and protect endothelium.
3. Perform gentle hydrodissection, avoiding extension of zonular damage.
4. Place capsular hooks or iris retractors, if severe focal dialysis.
5. Insert the CTR slowly into the capsular bag using an injector or forceps.
6. Ensure the leading eyelet does not engage or tear the capsulorhexis margin.
7. Complete phacoemulsification with reduced stress on the weak zonular area.
8. Implant IOL in the bag if support is adequate.
9. In major dialysis, use a Cionni-modified device or CTS with scleral fixation.

Timing of insertion: common viva point

• Early insertion: improves early bag stability but may trap cortex behind the ring and make cortical aspiration difficult.
• Late insertion: allows easier cortical clean-up but may allow further zonular stress during phaco.

Advantages

• Stabilizes capsular bag during surgery
• Reduces capsular folds and equatorial bag collapse
• Improves IOL centration
• May improve rotational stability of toric IOLs
• Reduces risk of late decentration in selected cases, although it cannot eliminate progressive zonulopathy

Limitations and complications

• Cortex may become trapped between ring and capsule
• Capsular tear may extend if the ring is inserted forcefully
• Can worsen a pre-existing zonular dialysis if incorrectly inserted
• Standard CTR is inadequate when zonular loss is extensive or progressive
• Late in-the-bag IOL-CTR complex subluxation can still occur, especially in pseudoexfoliation
• A CTR should not be used as a substitute for scleral fixation when support is grossly insufficient

Recent evidence

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4. Phakic Intraocular Lenses (pIOLs)

Definition

Place in refractive surgery

• Refractive error is too high for safe corneal laser ablation
• Cornea is thin or topographically unsuitable for laser refractive surgery
• Accommodation should be preserved
• The patient is a young adult with stable refraction

Classification

Posterior chamber phakic IOL / ICL

Central-port ICL

Indications

• Stable refraction, generally for at least one year
• Moderate-to-high myopia, with or without astigmatism
• Hyperopia in selected cases
• Age typically 21 years or older, according to device approvals and local practice
• Adequate anterior chamber depth
• Adequate endothelial cell density
• Healthy cornea, crystalline lens, retina and optic nerve
• Strong desire to preserve accommodation

Contraindications

• Progressive refraction or unstable keratoconus
• Shallow anterior chamber
• Low endothelial cell count
• Narrow/occludable angle
• Cataract or significant lens opacity
• Active uveitis
• Uncontrolled glaucoma
• Corneal endothelial disease
• Significant retinal pathology requiring treatment first
• Unrealistic expectations or inability to comply with follow-up

Preoperative work-up

1. Manifest and cycloplegic refraction
2. Corneal tomography and pachymetry
3. Anterior chamber depth, measured from endothelium to anterior lens surface
4. White-to-white and/or sulcus-to-sulcus measurement
5. Endothelial cell count
6. Gonioscopy
7. Dilated retinal examination, especially in high myopia
8. IOP, optic-nerve assessment and macular OCT if indicated
9. Lens-vault prediction and sizing assessment using ultrasound biomicroscopy, anterior-segment OCT or device-specific nomograms

Vault

• Low vault: risk of anterior subcapsular cataract
• Excessive vault: angle crowding, pigment dispersion and secondary angle closure
• Ideal target varies by device and imaging method, but an adequate central vault with open angles is the goal.

Complications

Recent advances

• Central-port posterior chamber ICLs
• Toric pIOLs
• Improved vault prediction using AS-OCT and UBM
• Larger optic zones and customized sizing
• Diffractive phakic lenses for carefully selected presbyopic patients, but evidence remains limited

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5. Pseudophakic IOLs: Modern IOL Options

A. Monofocal IOL

Advantages

• Best contrast sensitivity
• Lowest rate of halos and glare
• Broadest suitability in eyes with retinal disease, glaucoma, corneal irregularity or uncertain visual potential
• Predictable and economical

Disadvantage

• Near spectacles are usually needed.

Aspheric monofocal IOL

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B. Toric IOL

Principle

Indications

• Regular corneal astigmatism
• Cataract patient seeking reduced spectacle dependence
• Adequate capsular support
• Reliable keratometry and stable ocular surface

Contraindications / caution

• Irregular astigmatism, unstable keratoconus, corneal scar or severe dry eye
• Poor capsular support
• Unreliable biometry
• Marked zonulopathy unless support is secured

Key points

• Accurate biometry and posterior corneal astigmatism consideration are essential.
• Marking can be manual, image-guided or digitally guided.
• Rotation matters: each degree of toric IOL rotation causes roughly 3.3% loss of cylindrical correction. At 30 degrees, the intended astigmatic correction is effectively lost.

Complications

• Misalignment/rotation
• Residual refractive astigmatism
• IOL tilt or decentration
• Need for early surgical repositioning if substantial rotation occurs

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C. Multifocal IOL

Principle

• Diffractive optics
• Refractive zones
• Hybrid designs

Advantages

• Greater spectacle independence at distance and near

Limitations

• Halos and glare
• Reduced contrast sensitivity, especially in dim illumination
• Neuroadaptation required
• Residual refractive error, dry eye, decentration or PCO can cause major dissatisfaction

Avoid or use cautiously in

• Significant ocular surface disease
• Corneal irregularity
• Macular disease, diabetic maculopathy, epiretinal membrane
• Advanced glaucoma or impaired contrast sensitivity
• Optic neuropathy
• Unrealistic patient expectations
• Occupations requiring excellent night contrast, depending on individual needs

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D. Trifocal IOL

Advantages

• Stronger near and intermediate spectacle independence than many bifocal designs

Disadvantages

• Dysphotopsia and contrast trade-off remain
• Needs precise centration and refractive targeting
• Not ideal for eyes with retinal or optic-nerve disease

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E. Extended Depth-of-Focus (EDOF) IOL

Principle

Advantages

• Often fewer halos than traditional multifocal lenses
• Good distance and intermediate vision
• Useful for computer users

Limitations

• Fine near tasks may still require spectacles
• Dysphotopsia and contrast effects can still occur
• Terminology and optical mechanisms vary between platforms

Important viva distinction

• Multifocal IOL: several discrete foci.
• EDOF IOL: elongated focus, usually better intermediate performance and often less severe dysphotopsia.
• Monofocal-plus/enhanced monofocal: improved intermediate range but not a true EDOF by all definitions.

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F. Accommodating IOL

Definition

Mechanisms

1. Single-optic movement: anterior movement of the optic during attempted accommodation.
2. Dual-optic systems: relative movement of two optics changes overall power.
3. Fluid-based or shape-changing designs: aim to alter curvature or refractive power.

Theoretical advantage

Limitations

• True, sustained objective accommodation has been difficult to demonstrate consistently.
• Capsular fibrosis and haptic restriction may reduce movement over time.
• Near outcomes may be partly due to depth of focus, pupil miosis or residual myopia rather than true accommodation.
• Current use is less widespread than monofocal, toric, multifocal, trifocal and EDOF designs.

Exam conclusion

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6. IOL Power Calculation and Modern Biometry

Essential formula concept

• Axial length
• Corneal power
• Anterior chamber depth / lens position predictors
• Lens thickness
• White-to-white in some formulas
• Desired postoperative refraction
• Effective lens position (ELP)

Common formula evolution

High-yield choices

• Short eyes: modern formulas such as Barrett Universal II, Kane, Hoffer QST and Holladay 2 may be useful.
• Long/high-myopic eyes: use modern formulas and consider axial-length adjustment where appropriate.
• Post-refractive surgery eyes: use no-history methods, tomography-derived corneal data and dedicated calculators where available.
• Toric IOLs: include posterior corneal astigmatism and surgically induced astigmatism.

Causes of refractive surprise

• Keratometry error, especially dry eye
• Incorrect axial length, especially posterior staphyloma
• Incorrect IOL constant
• Wrong IOL selection or implantation
• Unpredicted ELP
• Corneal edema or irregular astigmatism
• Prior refractive surgery
• IOL tilt, decentration or rotation

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7. How to Select an IOL: Clinical Algorithm

Step 1: Determine visual potential

• Cornea and ocular surface
• Macula: OCT if indicated
• Optic nerve and glaucoma status
• Diabetic retinopathy
• Amblyopia and previous retinal surgery

Step 2: Determine refractive objective

• Distance target with reading glasses
• Monovision
• Distance + intermediate
• Maximum spectacle independence

Step 3: Assess corneal astigmatism

• Regular and significant: consider toric IOL
• Irregular: treat ocular surface/corneal condition first; avoid routine toric or multifocal decisions until measurements are reliable

Step 4: Assess suitability for presbyopia correction

Step 5: Assess capsular support

• Good support: in-the-bag PCIOL
• Mild zonulopathy: CTR + PCIOL
• Major zonulopathy: modified CTR/CTS with scleral fixation, or consider secondary fixation strategy
• No capsular support: scleral-fixated, iris-fixated or selected ACIOL depending on anatomy and surgeon expertise

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8. Common Long-Answer Questions and Model Opening Lines

“Write a short note on FLACS.”

“Describe capsular tension ring.”

“Discuss phakic IOL.”

“Write a note on accommodating IOL.”

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9. Rapid Revision Pearls

• FLACS: more precise capsulotomy and incisions, but no proven overall long-term superiority or cost-effectiveness over standard phaco.
• CTR: supports the bag, not the weak zonules themselves. Use a Cionni ring or CTS with scleral fixation if zonular loss is major.
• Standard CTR: can trap cortex. Do not insert forcefully.
• Phakic IOL: preserves accommodation; assess ACD, ECD, angle, retina and vault.
• Low pIOL vault: cataract risk.
• High pIOL vault: angle crowding/pigment/IOP risk.
• Toric IOL: 1 degree of rotation loses about 3.3% cylinder effect.
• Multifocal/trifocal IOL: better spectacle independence, but halos and lower contrast sensitivity.
• EDOF: distance-to-intermediate range with less near performance than trifocal in many designs.
• Accommodating IOL: variable evidence for sustained true accommodation.
• Hydrophobic acrylic square-edge IOL: standard modern choice for low PCO risk.
• Avoid silicone IOL when silicone-oil tamponade is likely in future retinal surgery.

Retina and Vitreous: MS Ophthalmology Theory Revision

1. Branch retinal vein occlusion (BRVO)
2. Age-related macular degeneration (AMD/ARMD)
3. OCT and OCT angiography
4. Electroretinography (ERG)
5. Retinopathy of prematurity (ROP)
6. Retinal lasers, including Pascal
7. Pars plana vitrectomy (PPV)
8. Silicone oil and other endotamponades
9. Retinal imaging modalities
10. Fundus fluorescein angiography (FFA)

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1. Branch Retinal Vein Occlusion (BRVO)

Definition

Pathogenesis

1. Venous narrowing
2. Turbulent blood flow
3. Endothelial injury
4. Thrombus formation
5. Venous obstruction

• Raised intraluminal venous pressure
• Capillary leakage causing macular edema
• Retinal hemorrhage
• Capillary nonperfusion and ischemia
• Increased VEGF production, causing macular edema and neovascularization

Risk factors

Ocular

• Hypertension-related arteriosclerosis
• Primary open-angle glaucoma
• Raised IOP
• Short axial length, reported in some populations

Systemic

• Hypertension
• Diabetes mellitus
• Dyslipidemia
• Smoking
• Obesity
• Renal disease
• Hyperhomocysteinemia
• Myeloproliferative disorders
• Thrombophilia, especially in young, bilateral, recurrent, or atypical RVO

Classification

By site

• Major BRVO: first-order branch vein occlusion, commonly superotemporal
• Macular BRVO: smaller macular venous branch involved
• Hemispheric retinal vein occlusion: one hemiretina involved, often considered intermediate between BRVO and CRVO

By perfusion

• Perfused BRVO
• Ischemic BRVO: extensive capillary nonperfusion, higher risk of retinal/disc neovascularization

Clinical features

Symptoms

• Painless unilateral decrease in vision
• Metamorphopsia
• Central or paracentral scotoma
• Often incidentally detected if macula is spared

Signs

• Dilated, tortuous vein
• Flame-shaped and dot-blot retinal hemorrhages
• Cotton-wool spots
• Retinal edema
• Macular edema if macular circulation is affected
• Collateral vessels later
• Neovascularization of retina or disc in ischemic disease
• Vitreous hemorrhage as a late complication

Investigations

Management

A. Treat systemic risk factors

• BP control
• Diabetes control
• Lipid management
• Smoking cessation
• Assessment for glaucoma
• Selective hematologic work-up where indicated

B. Macular edema

• Ranibizumab
• Aflibercept
• Bevacizumab, widely used off-label in many settings
• Faricimab, a bispecific antibody targeting VEGF-A and angiopoietin-2

• Initial loading followed by pro re nata regimen
• Treat-and-extend protocol
• Individualized OCT-guided treatment

C. Intravitreal corticosteroid

• In pseudophakia
• When anti-VEGF response is suboptimal
• If injection burden is difficult
• In anti-VEGF contraindication or selected inflammatory phenotypes

• IOP elevation
• Cataract, particularly in phakic eyes
• Need for repeat treatment

D. Laser photocoagulation

• Grid laser for macular edema: historical role, now usually secondary to anti-VEGF therapy.
• Sector scatter laser: indicated for retinal/disc neovascularization associated with nonperfusion, not prophylactically merely because ischemia exists.

Prognosis

• Baseline VA
• Duration/severity of macular edema
• Foveal ischemia
• Integrity of ellipsoid zone and external limiting membrane on OCT
• Disorganization of retinal inner layers, DRIL
• Development of neovascularization/vitreous hemorrhage

Recent advances

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2. Age-Related Macular Degeneration (AMD/ARMD)

Definition

Risk factors

Non-modifiable

• Increasing age
• Family history/genetic susceptibility
• White ethnicity
• Complement-pathway gene variants, including CFH and ARMS2/HTRA1 associations

Modifiable

• Smoking, the strongest modifiable risk factor
• Hypertension/cardiovascular risk factors
• Obesity
• Poor diet and low antioxidant intake
• Excess ultraviolet exposure is less clearly established

Classification

1. Early AMD

• Medium drusen
• Mild RPE pigmentary abnormalities
• Usually no visual symptoms

2. Intermediate AMD

• Large drusen, typically at least 125 micrometers
• Numerous medium drusen
• Noncentral geographic atrophy

3. Late AMD

A. Dry AMD

• Drusen and RPE dysfunction
• Geographic atrophy (GA): sharply demarcated RPE and photoreceptor loss

B. Neovascular or wet AMD

• Subretinal fluid
• Intraretinal fluid
• Pigment epithelial detachment
• Hemorrhage
• Fibrosis/disciform scar

Classification of macular neovascularization

Clinical features

• Painless central visual loss
• Metamorphopsia
• Micropsia
• Difficulty recognizing faces and reading
• Central scotoma
• Reduced contrast and dark adaptation

Investigations

Management

Dry AMD

1. Smoking cessation
2. Control cardiovascular risk factors
3. Amsler monitoring and urgent review for new distortion/scotoma
4. Low-vision support where necessary
5. AREDS2 supplementation for selected intermediate AMD or advanced AMD in one eye

• Vitamin C
• Vitamin E
• Zinc
• Copper
• Lutein
• Zeaxanthin

Geographic atrophy: major advance

• Pegcetacoplan, a C3 inhibitor
• Avacincaptad pegol, a C5 inhibitor

Neovascular AMD

• Ranibizumab
• Aflibercept
• Bevacizumab, off-label in many regions
• Brolucizumab, used cautiously because of intraocular inflammation/retinal vasculitis concerns
• Faricimab: VEGF-A and Ang-2 inhibition
• Higher-dose aflibercept formulations in some regions for interval extension

• Fixed dosing
• Pro re nata
• Treat-and-extend, widely used in routine practice

Polypoidal choroidal vasculopathy

• Anti-VEGF is foundational.
• Photodynamic therapy may be added in selected cases, especially persistent polypoidal lesions or recurrent hemorrhage.

Recent advances

• OCT-guided treat-and-extend regimens
• Faricimab and high-dose aflibercept for reducing injection burden in selected patients
• Complement inhibition for geographic atrophy
• Home monitoring and AI-assisted fluid detection
• Long-acting delivery systems and gene therapy remain areas of active development rather than routine universal care

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3. Optical Coherence Tomography (OCT)

Definition

Principle

• A reference beam
• A sample beam reflected from ocular tissues

Types

Retinal OCT applications

• Diabetic macular edema
• BRVO/CRVO macular edema
• Neovascular AMD
• Central serous chorioretinopathy
• Epiretinal membrane
• Vitreomacular traction
• Macular hole
• Myopic maculopathy
• Retinal dystrophies
• Hydroxychloroquine monitoring
• Optic nerve/RNFL and ganglion-cell analysis in glaucoma

Important OCT signs

OCT-Angiography

Principle

Advantages

• Noninvasive
• Rapid
• Layer-by-layer vascular segmentation
• Identifies nonexudative MNV
• Useful in diabetic retinopathy, AMD, retinal vein occlusion, macular telangiectasia and inherited retinal disease

Limitations

• Does not show leakage
• Motion artifact
• Projection artifact
• Segmentation errors, especially in edema/PED
• Poor images with media opacity or poor fixation
• Slow-flow lesions may be missed

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4. Fundus Fluorescein Angiography (FFA)

Definition

Principle

• Is a water-soluble orange dye
• Absorbs blue light near 490 nm
• Emits yellow-green fluorescence near 530 nm
• Is largely protein-bound intravascularly
• Is excreted by the kidneys

Phases of FFA

1. Choroidal flush: patchy background choroidal fluorescence
2. Arterial phase
3. Arteriovenous/capillary phase
4. Early venous phase: laminar flow
5. Late venous phase
6. Recirculation phase

Hyperfluorescence: causes

Hypofluorescence: causes

Indications

• Diabetic retinopathy and macular edema
• BRVO/CRVO evaluation
• Macular ischemia
• Neovascular AMD
• Central serous chorioretinopathy
• Retinal vasculitis
• Choroiditis
• Cystoid macular edema
• Retinal neovascularization
• Unexplained visual loss with suspected vascular/retinal pathology

Contraindications and adverse effects

Relative contraindications

• Previous severe fluorescein reaction
• Pregnancy, depending on risk-benefit analysis
• Severe asthma or major allergy history requires caution

Complications

• Nausea and vomiting, common minor effects
• Yellow discoloration of skin
• Bright yellow urine
• Extravasation pain/tissue irritation
• Urticaria
• Bronchospasm
• Anaphylaxis, rare but potentially fatal

FFA versus ICGA

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5. Electroretinography (ERG)

Definition

Principle

Components

Types

Full-field ERG

• Retinitis pigmentosa
• Cone-rod dystrophy
• Congenital stationary night blindness
• Drug toxicity
• Widespread retinal dysfunction
• Unexplained reduced vision when a diffuse retinal dystrophy is suspected

Pattern ERG

Multifocal ERG

• Occult macular dystrophy
• Hydroxychloroquine toxicity
• Macular dysfunction with normal fundus
• Early regional retinal dysfunction

Electro-oculography

• Best vitelliform macular dystrophy

Dark-adapted versus light-adapted responses

Classic ERG patterns

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6. Retinopathy of Prematurity (ROP)

Definition

Pathogenesis: two-phase model

Phase 1: Hyperoxia and vaso-obliteration

• Relative hyperoxia suppresses VEGF and IGF-1
• Normal retinal vascular growth is interrupted
• Peripheral retina remains avascular

Phase 2: Hypoxia-driven neovascularization

• Avascular retina becomes hypoxic
• VEGF rises
• Pathological neovascularization and fibrovascular proliferation develop
• Traction can cause retinal detachment

Risk factors

• Lower gestational age
• Lower birth weight
• Prolonged supplemental oxygen exposure
• Sepsis
• Apnea/respiratory distress
• Poor postnatal weight gain
• Anemia/transfusions
• Intraventricular hemorrhage
• Poor neonatal care and oxygen monitoring

International Classification of ROP

Zones

• Zone I: circle centered on optic disc, radius twice disc-fovea distance
• Zone II: from outer edge of zone I to nasal ora serrata and toward temporal equator
• Zone III: residual temporal crescent of peripheral retina

Stages

Plus disease

Aggressive ROP

Treatment indication: Type 1 ROP

• Zone I, any stage with plus disease
• Zone I, stage 3 without plus disease
• Zone II, stage 2 or 3 with plus disease

• Zone I, stage 1 or 2 without plus
• Zone II, stage 3 without plus

Treatment

A. Laser photocoagulation

• Well-established treatment
• Definitive peripheral ablation
• Less concern about prolonged systemic VEGF suppression compared with anti-VEGF

• Technically demanding in small infants
• More myopia
• May be difficult in posterior zone I disease
• Peripheral field is ablated
• Does not allow normal peripheral vascularization

B. Intravitreal anti-VEGF

• Bevacizumab
• Ranibizumab
• Aflibercept in some settings

• Very effective in zone I/posterior aggressive disease
• Rapid regression
• Preserves more peripheral retina
• May induce less myopia than laser
• Useful where media opacity or poor pupil dilation makes laser difficult

• Late recurrence/reactivation can occur, sometimes months later
• Requires long-term follow-up until peripheral vascularization is complete
• Systemic absorption and long-term neurodevelopmental/systemic safety remain important concerns
• Optimal agent and lowest effective dose remain unsettled

C. Surgery

• Lens-sparing vitrectomy for selected stage 4 disease
• Vitrectomy with or without lensectomy for advanced tractional detachment
• Anatomical success and visual outcome worsen markedly in stage 4B and stage 5 disease

Current evidence

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7. Retinal Lasers

Principle of retinal photocoagulation

• Wavelength
• Power
• Spot size
• Duration
• Retinal pigmentation
• Media clarity
• Lens used

Common laser wavelengths

Types of retinal laser

PRP: indications

• Proliferative diabetic retinopathy
• Ischemic CRVO with neovascularization or high risk
• Ocular ischemic syndrome
• Proliferative sickle retinopathy
• Selected retinal vasculitis and Eales disease

Complications of retinal laser

• Pain
• Iatrogenic retinal break, rare
• Macular edema
• Reduced peripheral field after PRP
• Reduced night vision
• Reduced color/contrast sensitivity
• Choroidal effusion, exudative RD, rare
• Accidental foveal burn
• Bruch membrane rupture/secondary CNV, rare

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8. Pascal Laser

Full form

Definition

Principle

• 2 × 2
• 3 × 3
• 4 × 4
• Arc
• Grid
• PRP arrays

Advantages

• Faster delivery of PRP
• More uniform spot pattern
• Less total procedure time
• Often better tolerated
• Potentially less collateral thermal diffusion with short pulses
• Useful in PRP, sector laser and pattern macular treatment

Limitations

• Shorter pulse duration requires higher power to achieve the intended burn
• Lesion intensity must be titrated carefully
• Less flexibility in irregular peripheral anatomy in some situations
• Cost and availability limitations
• A dense or excessively intense pattern can still produce significant field effects

Pascal versus conventional laser

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9. Pars Plana Vitrectomy (PPV)

Definition

Anatomical basis

• Ora serrata anteriorly
• Ciliary body posteriorly

• Phakic adult eye: approximately 3.5-4 mm posterior to limbus
• Pseudophakic/aphakic eye: approximately 3-3.5 mm posterior to limbus
• In children: distance is adjusted according to age and globe size

Instrument systems

• 20 gauge: older, larger, sutured
• 23 gauge
• 25 gauge
• 27 gauge: very small, less flow, useful in selected fine maneuvers

1. Infusion cannula
2. Vitreous cutter
3. Illumination probe

Indications

Vitreous hemorrhage

• Non-clearing diabetic vitreous hemorrhage
• Dense hemorrhage preventing retinal evaluation/treatment
• Vitreous hemorrhage associated with retinal tear/detachment
• Selected trauma

Retinal detachment

• Pseudophakic RRD
• Giant retinal tear
• Posterior breaks
• RRD with PVR
• Nonvisualized breaks due to hemorrhage/media opacity
• Complex or recurrent RD

Diabetic retinopathy

• Tractional RD threatening or involving macula
• Combined tractional-rhegmatogenous RD
• Non-clearing vitreous hemorrhage
• Dense premacular/subhyaloid hemorrhage, selected cases
• Severe fibrovascular traction

Macular disease

• Epiretinal membrane
• Full-thickness macular hole
• Vitreomacular traction
• Selected myopic traction maculopathy

Other

• Endophthalmitis, depending on visual acuity/severity
• Retained lens fragments
• Intraocular foreign body
• Diagnostic vitreous biopsy
• Dislocated IOL or lens material
• Severe posterior segment trauma

Goals in retinal detachment surgery

1. Remove vitreoretinal traction
2. Identify and treat all retinal breaks
3. Flatten retina and drain subretinal fluid if required
4. Create chorioretinal adhesion using laser/cryo
5. Maintain retinal apposition with internal tamponade

Basic surgical steps

1. Preoperative retinal mapping and consent
2. Conjunctival displacement in transconjunctival systems
3. Create pars plana ports
4. Confirm infusion cannula position before opening infusion
5. Core vitrectomy
6. Induce posterior vitreous detachment, if not already present
7. Peripheral vitreous shaving with scleral depression
8. Remove membranes where indicated
9. Identify all breaks
10. Drain subretinal fluid, often through a break or drainage retinotomy
11. Fluid-air exchange
12. Endolaser retinopexy
13. Gas or silicone-oil tamponade, if needed
14. Close/suture leaking ports

Complications

Intraoperative

• Iatrogenic retinal break
• Lens touch
• Suprachoroidal hemorrhage
• Choroidal detachment
• Retinal incarceration at port
• Incomplete membrane removal
• Infusion misdirection

Postoperative

• Cataract progression, especially nuclear sclerosis in phakic patients
• Elevated IOP or hypotony
• Endophthalmitis
• Corneal edema
• Cystoid macular edema
• Recurrent RD/PVR
• Epiretinal membrane
• Retinal toxicity, rare
• Visual-field defects
• Need for reoperation

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10. Silicone Oil

Definition

Mechanism

• Supporting the retina against the RPE
• Preventing fluid from entering retinal breaks
• Maintaining chorioretinal adhesion while laser scars mature

Types

• Conventional silicone oil: commonly 1,000 or 5,000 centistokes
• Heavy silicone oil: denser than water, designed to tamponade inferior pathology, but has limited long-term use due to complications/emulsification concerns

Indications

• Complex RRD with PVR
• Giant retinal tears
• Recurrent retinal detachment
• Severe diabetic tractional/combined RD
• Retinal detachment with proliferative vitreoretinopathy
• Ocular trauma
• Cases requiring long-term tamponade
• Patients unable to posture for gas tamponade
• Need for early air travel or situations where gas is unsuitable

Advantages compared with gas

• Long-term support
• No expansion with nitrous oxide/altitude in the same manner as gas
• No strict prolonged face-down positioning in some cases, although positioning can still be clinically important
• Fundus can be examined through oil
• Appropriate for complex disease

Disadvantages

• Usually requires a second surgery for removal
• Less favorable visual outcomes than gas in uncomplicated RRD, partly because oil is used in more complex eyes
• Emulsification and anterior-segment complications

Complications

Pupillary block prevention

Silicone oil removal

• Retina is stable
• Adequate chorioretinal adhesion is established
• Oil-related complications develop
• Risk of redetachment is acceptable

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11. Other Vitreous Substitutes

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12. Retinal Imaging Modalities: Exam Table

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13. High-Yield Recent Advances

• Anti-VEGF treatment remains first-line for vision-threatening macular edema due to BRVO and for neovascular AMD.
• Faricimab targets VEGF-A and Ang-2 and may allow longer treatment intervals in some RVO and AMD patients, but superiority in durability over existing agents is not yet established.
• OCT-A is valuable for noninvasive vascular mapping, but FFA remains important when leakage and dynamic perfusion assessment are needed.
• Swept-source OCT gives deeper choroidal and vitreoretinal imaging.
• Geographic atrophy complement inhibitors can slow lesion enlargement but require counseling about limited functional recovery and risk of neovascular conversion.
• ROP anti-VEGF preserves peripheral retina and may reduce myopia, but requires prolonged surveillance for late reactivation and raises systemic-safety questions.
• Small-gauge vitrectomy with high-speed cutters has improved surgical efficiency and reduced tissue traction.
• Heads-up 3D vitreoretinal surgery, intraoperative OCT, digital visualization, robotic assistance and AI-supported imaging are evolving adjuncts.
• Pascal and micropulse lasers aim for more efficient or tissue-sparing laser delivery, but appropriate case selection and endpoint titration remain central.

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14. One-Minute Viva Answers

What is the difference between FFA and OCT-A?

What is the first-line treatment for BRVO macular edema?

What are the major complications of silicone oil?

What does a negative ERG indicate?

What is plus disease in ROP?

What is the role of PPV in diabetic retinopathy?

Cornea and Ocular Surface: MS Ophthalmology Theory Revision

1. Limbal stem-cell deficiency and stem-cell therapy
2. Amniotic membrane transplantation
3. Ocular surface squamous neoplasia
4. Corneal collagen cross-linking / C3R
5. Lamellar keratoplasty, especially DALK
6. Keratoprosthesis
7. Pterygium surgery
8. Toxic contact-lens-related ocular surface disease

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1. Limbal Stem Cells and Limbal Stem-Cell Deficiency (LSCD)

Normal limbal stem cells

Location

Functions

• Lifelong regeneration of corneal epithelium
• Maintenance of transparent, avascular corneal surface
• Healing after epithelial injury
• Prevention of conjunctivalization

Stem-cell niche

• Palisades of Vogt
• Limbal stromal fibroblasts
• Blood vessels and extracellular matrix
• Corneal nerves
• Melanocytes and immune cells

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Limbal Stem-Cell Deficiency

Definition

Etiology

Clinical features

• Persistent or recurrent epithelial defects
• Reduced vision, photophobia, pain and redness
• Whorl-like or late fluorescein staining
• Loss of limbal palisades of Vogt
• Superficial corneal vascularization
• Conjunctivalization of cornea
• Fibrovascular pannus and scarring
• Recurrent erosions
• In advanced disease: keratinization and symblepharon

Diagnosis

• Fluorescein staining pattern
• Impression cytology showing conjunctival goblet cells on cornea
• In vivo confocal microscopy
• Anterior-segment OCT
• Corneal epithelial markers, where available

Staging concept

• Partial LSCD: a sector or portion of limbus affected
• Total LSCD: entire limbus affected
• Unilateral versus bilateral LSCD is critical because it determines the donor source.

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Management of LSCD

Step 1: Restore the ocular surface

• Stop toxic topical medications and preservatives where possible
• Treat dry eye and lid disease
• Preservative-free lubricants
• Control inflammation: topical steroids, ciclosporin/tacrolimus in selected cases
• Manage exposure, lagophthalmos and trichiasis
• Treat infection and neurotrophic keratopathy if present
• Autologous serum tears or platelet-rich plasma in selected patients
• Scleral lens for surface protection and visual rehabilitation

Step 2: Stem-cell restoration

SLET: high-yield answer

1. Harvest a small limbal biopsy from healthy fellow eye.
2. Secure cryopreserved or fresh amniotic membrane over recipient cornea.
3. Divide donor biopsy into small explants.
4. Place explants on membrane.
5. Cover with bandage contact lens.
6. Cells expand across the membrane and repopulate the corneal surface.

Important principle

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2. Amniotic Membrane Transplantation (AMT)

Definition

Biological properties

• Promotes epithelial migration and adhesion
• Provides a basement-membrane scaffold
• Reduces inflammation and inflammatory-cell infiltration
• Reduces fibrosis and myofibroblast activation
• Inhibits angiogenesis
• Reduces pain by covering exposed corneal nerves
• Has antimicrobial and anti-scarring effects

Types

Orientation: common

• AMT orientation, techniques, indications and complications
• OSSN
• C3R/corneal cross-linking
• DALK and keratoprosthesis
• Pterygium surgery
• Contact-lens toxicity

Cornea and Ocular Surface: MS Ophthalmology Theory Notes

Topics

1. Limbal stem-cell deficiency and stem-cell therapy
2. Amniotic membrane transplantation
3. Ocular surface squamous neoplasia
4. Corneal collagen cross-linking, CXL/C3R
5. Lamellar keratoplasty, especially DALK
6. Keratoprosthesis
7. Pterygium surgery
8. Toxic contact-lens-related ocular surface disease

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1. Limbal Stem-Cell Deficiency and Stem-Cell Therapy

Normal limbus and stem-cell function

Functions

• Continuous renewal of corneal epithelium
• Healing after epithelial trauma
• Maintenance of a transparent, avascular corneal surface
• Barrier function preventing conjunctival epithelial migration onto cornea

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Limbal stem-cell deficiency (LSCD)

Definition

Causes

Clinical features

• Persistent/recurrent epithelial defect
• Photophobia, irritation, pain, redness
• Reduced vision
• Late fluorescein staining in a whorl or vortex pattern
• Loss of palisades of Vogt
• Conjunctivalization of cornea
• Superficial corneal vascularization and fibrovascular pannus
• Recurrent erosions, scarring, calcification
• In severe disease: keratinization, symblepharon and dry eye

Diagnosis

• Fluorescein staining
• Slit-lamp evaluation of limbus and palisades
• Impression cytology: conjunctival goblet cells on the cornea strongly support LSCD
• In vivo confocal microscopy
• Anterior segment OCT
• Corneal epithelial phenotype markers, in specialist centers

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Management of LSCD

Principle

Conservative management

• Stop toxic medication and minimize preservatives
• Preservative-free lubricants
• Treat blepharitis, meibomian-gland dysfunction and dry eye
• Control inflammation with carefully supervised topical steroid
• Topical ciclosporin or tacrolimus in selected inflammatory disease
• Autologous serum tears or platelet-rich plasma tears
• Punctal occlusion, tarsorrhaphy, epilation of trichiasis
• Scleral lenses for surface protection and optical rehabilitation
• Treat exposure, infection and neurotrophic keratopathy

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Surgical restoration of limbal stem cells

A. Conjunctival limbal autograft

• Tissue is harvested from the healthy contralateral eye.
• Transplanted to affected eye after removing conjunctivalized corneal tissue.
• Suitable for unilateral complete LSCD.
• Donor-site damage is possible if excessive limbus is harvested.

B. SLET: Simple limbal epithelial transplantation

Steps

1. Excise fibrovascular pannus and abnormal epithelium from recipient cornea.
2. Place cryopreserved amniotic membrane over bare corneal surface.
3. Harvest a small limbal biopsy from healthy contralateral eye.
4. Divide biopsy into multiple small explants.
5. Arrange explants over amniotic membrane.
6. Secure with fibrin glue or sutures and apply a bandage contact lens.

Advantages

• Small donor biopsy
• Less risk to donor eye than CLAU
• Does not need a cell-culture laboratory
• Cost-effective
• Particularly practical for unilateral chemical-burn-related LSCD

C. CLET

D. Allograft procedures

• Living related donor limbal tissue, or
• Cadaveric keratolimbal allograft.

Emerging advances

• Cultivated epithelial sheets
• Oral-mucosal epithelial transplantation
• Induced pluripotent stem-cell approaches
• Mesenchymal stem-cell-derived exosomes
• Biomaterial scaffolds and 3D engineered limbal niches

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2. Amniotic Membrane Transplantation (AMT)

Definition

Properties and mechanisms

• Promotes epithelial migration, adhesion and differentiation
• Provides basement-membrane substrate
• Suppresses inflammation
• Reduces fibroblast activation and scarring
• Reduces neovascularization
• Reduces pain by covering exposed corneal nerves
• Has anti-protease and anti-microbial properties

Types

• Cryopreserved amniotic membrane
• Dehydrated amniotic membrane
• Sutured graft
• Fibrin-glue-assisted graft
• Sutureless/self-retained membrane device
• Multilayer membrane for deep ulcers or perforation risk

Orientation: viva question

• For a graft/inlay, place the epithelial/basement-membrane side up, facing the regenerating corneal epithelium.
• The stromal side is placed against the host tissue.
• In an overlay/patch technique, the membrane acts mainly as a biological dressing, although standard orientation is still generally maintained.

Surgical techniques

1. Inlay or graft technique

• Persistent epithelial defect
• Corneal ulcer
• Stromal thinning
• Post-pterygium or post-tumor excision defect
• Partial LSCD

2. Overlay or patch technique

• Acute chemical injury
• Acute Stevens-Johnson syndrome
• Severe ocular-surface inflammation
• Extensive epithelial defect

3. Multilayer technique

• Corneal melt
• Descemetocele
• Small corneal perforation, often with tissue adhesive or bandage lens

Indications

AMT in acute ocular burns

Complications

• Membrane displacement, folding or dissolution
• Infection, uncommon
• Pyogenic granuloma
• Incomplete epithelialization
• Recurrence of underlying inflammation
• Transmission risk is extremely low with screened, processed tissue but must be discussed

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3. Ocular Surface Squamous Neoplasia (OSSN)

Definition

Histological spectrum

1. Squamous epithelial dysplasia
2. Conjunctival intraepithelial neoplasia, CIN
3. Carcinoma in situ
4. Invasive squamous cell carcinoma

Risk factors

• Ultraviolet-B exposure and outdoor work
• Older age
• Male sex in many populations
• HIV infection and immunosuppression
• HPV association, though causality and subtype contribution vary
• Xeroderma pigmentosum
• Chronic ocular-surface inflammation
• Smoking
• Prior irradiation
• Vitamin A deficiency in some settings

Clinical features

• Usually unilateral, interpalpebral, nasal limbal lesion
• Gelatinous, papilliform, leukoplakic or nodular mass
• Prominent feeder vessels
• Corneal epithelial extension may appear as a gray, translucent, elevated lesion
• May mimic pterygium, pinguecula, papilloma, actinic keratosis or amelanotic melanoma

Investigations

• Slit-lamp photography and lesion mapping
• High-resolution anterior-segment OCT:
  • Thickened hyperreflective epithelium
  • Abrupt transition between normal and abnormal epithelium
  • Helpful to distinguish OSSN from pterygium
• Ultrasound biomicroscopy if intraocular extension suspected
• Impression cytology, selected cases
• Excision biopsy for histopathology where diagnosis is uncertain or lesion requires removal
• Orbital imaging if deep invasion is suspected

Management

A. Surgical excision: “no-touch technique”

Principles

1. Avoid directly grasping tumor to prevent seeding.
2. Wide conjunctival margins, commonly 3-4 mm of clinically normal tissue where feasible.
3. Alcohol-assisted epitheliectomy for corneal component.
4. Excise lesion with involved Tenon tissue if needed.
5. Apply double freeze-thaw cryotherapy to conjunctival margins.
6. Send specimen for histopathology.
7. Reconstruct surface with conjunctival autograft or amniotic membrane if required.

B. Topical chemotherapy or immunotherapy

Choosing surgery versus medical treatment

• Histological diagnosis is needed
• Invasion is suspected
• Lesion is focal and easily excisable
• Patient may not comply with prolonged topical therapy
• Resources are limited
• Isolated corneal lesion requires diagnostic clarification

Follow-up

Major complication of treatment

• Large lesions
• More than 6 clock hours of limbal involvement
• Recurrent lesions
• Corneal involvement
• Repeated surgery or topical mitomycin-C

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4. Corneal Collagen Cross-Linking: CXL / C3R

Definition

Main indications

• Documented progressive keratoconus
• Progressive post-LASIK or post-PRK ectasia
• Pellucid marginal degeneration, selected cases
• Keratoglobus or other ectasias, selected cases
• PACK-CXL: photoactivated chromophore for infectious keratitis, as adjunctive treatment in selected refractory infections

Evidence of progression

• Increase in Kmax
• Increase in manifest cylinder or myopia
• Progressive thinning
• Worsening corrected vision
• Change in posterior corneal curvature/elevation
• Serial topographic/tomographic worsening

Dresden protocol: conventional epithelium-off CXL

1. Remove central 8-9 mm corneal epithelium.
2. Instill 0.1% riboflavin in dextran solution for approximately 30 minutes.
3. Confirm stromal saturation and adequate corneal thickness.
4. Expose cornea to UVA at 370 nm, 3 mW/cm² for 30 minutes.
5. Total radiant exposure is 5.4 J/cm².
6. Apply antibiotic, bandage contact lens and postoperative anti-inflammatory regimen.

Safety criterion

Mechanism

Types

Complications

• Severe pain in early postoperative days
• Delayed epithelial healing
• Sterile infiltrates
• Infectious keratitis
• Corneal haze/scarring
• Endothelial damage in excessively thin cornea
• Herpes simplex keratitis reactivation
• Rare loss of corrected vision

Recent evidence

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5. Lamellar Keratoplasty and DALK

Classification of corneal transplantation

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Deep anterior lamellar keratoplasty (DALK)

Definition

Indications

• Keratoconus
• Stromal corneal scars with healthy endothelium
• Stromal dystrophy
• Postinfectious stromal opacity after infection is controlled
• Some cases of corneal ectasia

Contraindications

• Endothelial dysfunction
• Significant Descemet membrane scarring
• Deep stromal scar adherent to Descemet membrane, relative contraindication
• Acute hydrops with severe Descemet membrane disruption, depending on case

Big-bubble technique

1. Partial-depth trephination.
2. Insert needle deeply into stroma.
3. Inject air to create a cleavage plane between posterior stroma and Descemet membrane.
4. Remove anterior stroma.
5. Open and remove residual posterior stromal tissue.
6. Place donor graft with donor Descemet membrane removed.
7. Suture graft.

Advantages over PK

• Preserves host endothelium
• Very low risk of endothelial rejection
• Better long-term endothelial survival
• Reduced risk of catastrophic open-sky complications
• Stronger wound architecture
• Useful in young keratoconus patients

Disadvantages and complications

• Technically demanding
• Descemet membrane perforation
• Conversion to PK may be required
• Double anterior chamber if Descemet membrane detaches
• Interface haze
• Residual stromal bed can reduce optical quality
• Suture-related astigmatism and infection
• Recurrence of disease in graft, uncommon depending on disease

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6. Keratoprosthesis

Definition

Main types

• Boston Type I keratoprosthesis
• Boston Type II keratoprosthesis
• Osteo-odonto-keratoprosthesis, OOKP
• Other specialist devices, including tibial osteokeratoprosthesis

Boston Type I KPro

Indications

• Multiple failed corneal grafts
• Severe bilateral corneal opacity with poor graft prognosis
• Chemical injury, selected cases
• Aniridia
• Severe herpetic disease, selected cases
• Some eyes with autoimmune ocular-surface disease, although outcomes are more guarded

Contraindications or poor-prognosis factors

• No light perception or poor optic-nerve/macular potential
• Uncontrolled glaucoma
• Active ocular inflammation
• Severe dry keratinized surface without adequate reconstruction
• Inability to comply with lifelong follow-up

Complications

• Glaucoma progression
• Retroprosthetic membrane
• Sterile keratolysis
• Infectious keratitis/endophthalmitis
• Retinal detachment
• Device extrusion
• Vitreous hemorrhage
• Need for lifelong antimicrobial prophylaxis and bandage contact lens in typical Boston Type I KPro care

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7. Pterygium and Pterygium Surgery

Definition

Risk factors

• Chronic ultraviolet exposure
• Outdoor work
• Dust, wind and dry climate
• Chronic ocular-surface irritation
• Geographic “pterygium belt” exposure

Indications for surgery

• Progressive corneal encroachment threatening visual axis
• Induced irregular astigmatism or reduced vision
• Persistent inflammation/irritation despite conservative care
• Restricted motility or diplopia, uncommon
• Cosmetic concern after informed discussion
• Suspicion of dysplasia/OSSN, especially atypical, nodular, leukoplakic, rapidly growing or unusually vascular lesions

Surgical options

Conjunctival autograft technique

1. Excise pterygium head from cornea.
2. Remove fibrovascular body and Tenon tissue carefully.
3. Polish residual corneal tissue as needed.
4. Harvest superior bulbar conjunctival graft, often including limbal tissue.
5. Place graft over bare sclera with limbal edge oriented toward limbus.
6. Secure with sutures or fibrin glue.

Fibrin glue versus sutures

• Glue shortens operative time and improves comfort.
• Sutures are inexpensive and secure, but cause more postoperative inflammation and foreign-body sensation.

Mitomycin-C

• Delayed epithelial healing
• Scleral thinning or melt
• Necrotizing scleritis
• Secondary infection
• Corneal edema
• Cataract or glaucoma, rarely due to intraocular toxicity

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8. Toxic Contact-Lens-Related Ocular Surface Disease

Definition

Major mechanisms

1. Hypoxia: reduced oxygen transmission, especially with overnight wear
2. Mechanical injury: tight lens, poor fit, edge trauma, lens deposits
3. Solution toxicity: preservatives, hydrogen peroxide not neutralized, surfactants
4. Inflammatory/hypersensitivity reaction
5. Microbial infection: particularly Pseudomonas in contact-lens-associated keratitis

Clinical syndromes

Toxic keratitis: high-yield point

Management approach

1. Stop contact-lens wear immediately.
2. Remove lens and retain it/case for culture if microbial keratitis is suspected.
3. Assess epithelial defect, infiltrate size/location, AC reaction and vision.
4. Use preservative-free lubrication.
5. Treat lid disease, dry eye and fit problems.
6. Change to daily disposable lens or a preservative-free peroxide system only after complete recovery.
7. Avoid topical steroid until infection is excluded or controlled.
8. Educate: no overnight wear, no water exposure, no swimming/showering with lenses, strict hand hygiene and lens-case replacement.

Red flags for microbial keratitis

• Moderate/severe pain
• Reduced vision
• Central/paracentral infiltrate
• Epithelial defect over infiltrate
• Anterior-chamber reaction/hypopyon
• Rapid progression
• Contact-lens wearer with red painful eye

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Rapid Exam Revision

One-line definitions

• LSCD: failure of limbal stem-cell function causing conjunctivalization and epithelial instability of cornea.
• AMT: biological ocular-surface graft or dressing that promotes epithelialization and reduces inflammation, fibrosis and angiogenesis.
• OSSN: spectrum from conjunctival epithelial dysplasia to invasive squamous cell carcinoma.
• CXL: riboflavin-UVA photochemical strengthening of corneal stromal collagen to arrest ectatic progression.
• DALK: stromal corneal transplant preserving host Descemet membrane and endothelium.
• KPro: artificial cornea for repeated graft failure or very poor prognosis for conventional grafting.
• Pterygium: fibrovascular conjunctival growth crossing limbus onto cornea.

Most important viva distinctions

Recent-advance pearls

• SLET offers practical in vivo expansion of limbal epithelial cells using a small biopsy from the fellow eye.
• High-resolution anterior-segment OCT helps diagnose and monitor OSSN noninvasively.
• Topical interferon alpha-2b, 5-FU and mitomycin-C have shifted OSSN care from surgery-only to individualized medical-surgical management.
• Conventional epi-off CXL remains the reference treatment for progressive keratoconus.
• Accelerated, transepithelial and iontophoresis-assisted CXL are evolving alternatives, but may not have identical biomechanical effect.
• Cryopreserved amniotic membrane is particularly important in acute SJS/TEN and selected moderate ocular chemical burns.

Glaucoma: MS Ophthalmology Theory Revision

Topics

1. Basics of aqueous humor dynamics and IOP
2. Classification of glaucoma
3. Primary open-angle glaucoma (POAG)
4. Primary angle-closure disease (PACD)
5. Secondary glaucomas
6. Glaucoma evaluation: gonioscopy, disc, fields and OCT
7. Medical and laser treatment
8. Trabeculectomy
9. Glaucoma drainage devices / implants
10. MIGS
11. Neuroprotection in glaucoma
12. Recent advances and rapid viva points

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1. Fundamentals: Aqueous Humor and IOP

Aqueous humor production

Mechanisms

• Active secretion: major mechanism
• Ultrafiltration
• Diffusion

Functions

• Maintains IOP and globe shape
• Provides nutrition to avascular cornea and lens
• Removes metabolites
• Transports ascorbate and other substances
• Maintains optical clarity

Aqueous flow pathway

Conventional or trabecular pathway

Unconventional or uveoscleral pathway

• Ciliary muscle
• Supraciliary space
• Suprachoroidal space
• Sclera and venous circulation

Intraocular pressure

Goldmann equation

• F = aqueous formation rate
• C = outflow facility
• Pv = episcleral venous pressure

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2. Definition of Glaucoma

• Retinal ganglion-cell death
• Retinal nerve fiber layer loss
• Characteristic optic-disc cupping
• Corresponding visual-field defects

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3. Classification of Glaucoma

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4. Primary Open-Angle Glaucoma (POAG)

Definition

Risk factors

Pathogenesis

IOP-dependent mechanisms

• Increased resistance to aqueous outflow at trabecular meshwork
• Mechanical stress at lamina cribrosa
• Retinal ganglion-cell axonal compression
• Impaired axoplasmic flow
• Optic-nerve head ischemia

IOP-independent mechanisms

• Vascular dysregulation
• Low perfusion pressure
• Oxidative stress
• Mitochondrial dysfunction
• Glutamate excitotoxicity
• Neuroinflammation
• Genetic susceptibility

Clinical features

Symptoms

• Gradual peripheral-field loss
• Difficulty with dark adaptation
• Late tunnel vision
• Central vision affected only in advanced disease

Signs

• Raised IOP may be present
• Open angle on gonioscopy
• Optic-disc cupping
• Rim thinning/notching, especially inferotemporal and superotemporal
• Vertical cup enlargement
• RNFL wedge defects
• Disc hemorrhage
• Corresponding visual-field defects

Optic-disc changes

ISNT rule

Glaucomatous disc signs

• Progressive cup enlargement
• Vertical cup-to-disc asymmetry greater than about 0.2
• Focal rim notch
• Laminar-dot sign
• Bayonetting of vessels
• Nasal displacement of vessels
• Peripapillary atrophy
• Disc hemorrhage

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5. Visual Field Defects in Glaucoma

Early defects

• Increased pattern standard deviation
• Paracentral scotoma
• Nasal step of Roenne
• Seidel scotoma

Established defects

• Arcuate scotoma of Bjerrum
• Double arcuate scotoma
• Temporal wedge defect

Advanced disease

• Central island
• Temporal island
• Tubular field or tunnel vision

Important rule

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6. Diagnosis and Work-up of Glaucoma

1. Visual acuity and refraction
2. Slit-lamp examination
3. Goldmann applanation tonometry
4. Pachymetry
5. Gonioscopy
6. Dilated optic-disc assessment
7. Disc photographs
8. Visual-field testing
9. OCT RNFL and macular ganglion-cell analysis
10. Assessment of systemic risk, medications and family history

Gonioscopy

Why it is essential

• Open
• Narrow/occludable
• Closed
• Synechially closed
• Abnormally pigmented
• Neovascularized
• Recessed after trauma

Angle structures from anterior to posterior

Shaffer grading

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7. OCT in Glaucoma

Role

Main OCT parameters

RNFL pattern

• Superior peak
• Inferior peak
• Thinner nasal and temporal sectors

OCT interpretation: limitations

• Do not diagnose glaucoma from a color code alone.
• “Red disease” means false-positive abnormal classification.
• “Green disease” means falsely reassuring normal classification.
• Myopia, tilted disc, peripapillary atrophy, poor signal strength, segmentation error, retinal disease and media opacity can mislead.
• Always correlate OCT with disc appearance and visual field.

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8. Medical Treatment of Glaucoma

Therapeutic goal

• Baseline IOP
• Severity of damage
• Rate of progression
• Age and life expectancy
• Fellow-eye status
• Corneal thickness
• Risk factors such as disc hemorrhage or low perfusion pressure

• Mild disease: 20%-30% reduction
• Moderate disease: 30%-40% reduction
• Severe/progressive disease: often 40%-50% or more

Topical anti-glaucoma drugs

First-line medical choice

• Strong efficacy
• Once-daily dosing
• Limited systemic effects

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9. Laser Treatment

A. Selective Laser Trabeculoplasty (SLT)

Principle

Indications

• POAG
• Ocular hypertension
• Pseudoexfoliative glaucoma
• Pigmentary glaucoma, cautiously
• Alternative to first-line drops
• Poor adherence or intolerance to drops
• Add-on treatment

Advantages

• Outpatient procedure
• Repeatable in many cases
• Reduces dependence on drops
• Avoids preservative toxicity

Complications

• Transient IOP spike
• Mild anterior uveitis
• Peripheral anterior synechiae, rare
• Corneal edema, rare
• Limited response in heavily scarred or advanced angle disease

B. Argon Laser Trabeculoplasty

C. Laser Peripheral Iridotomy (LPI)

Indications

• Acute angle closure after initial IOP control
• Primary angle closure
• Occludable/narrow angle at risk of pupillary block
• Fellow eye of acute angle-closure attack
• Iris bombe from posterior synechiae

Mechanism

Complications

• IOP spike
• Inflammation
• Corneal burn
• Hyphema
• Dysphotopsia
• Closure of iridotomy

D. Laser Peripheral Iridoplasty

• Plateau iris
• Persistent appositional angle closure after LPI
• Some acute angle-closure settings when LPI cannot be done immediately

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10. Primary Angle-Closure Disease

Classification

Mechanisms

• Relative pupillary block
• Plateau iris configuration
• Thick/anterior lens
• Short axial length
• Hypermetropia
• Ciliary-body rotation
• Lens enlargement with age

Acute angle closure

Symptoms

• Severe ocular pain
• Headache
• Halos around lights
• Blurred vision
• Nausea and vomiting

Signs

• Markedly raised IOP
• Ciliary injection
• Corneal edema
• Shallow anterior chamber
• Mid-dilated fixed pupil
• Closed angle

Emergency management

1. Analgesic and antiemetic
2. Topical aqueous suppressants
3. Systemic acetazolamide unless contraindicated
4. Hyperosmotic agent such as mannitol if severe and medically suitable
5. Topical steroid
6. Pilocarpine once IOP has fallen enough for iris sphincter to respond
7. Definitive LPI when cornea clears
8. Prophylactic LPI in fellow eye, if indicated

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11. Trabeculectomy

Definition

Indications

• Progressive glaucoma despite maximum tolerated medical therapy and/or laser
• Advanced glaucoma requiring very low target IOP
• Poor adherence to medical therapy
• Rapid progression
• Inadequate response to MIGS or prior treatment
• Selected pediatric or secondary glaucomas

Basic steps

1. Conjunctival peritomy
2. Hemostasis
3. Mitomycin-C or 5-FU application where indicated
4. Partial-thickness scleral flap
5. Deep scleral block and internal ostium/sclerostomy
6. Peripheral iridectomy
7. Adjustable/releasable scleral flap sutures
8. Conjunctival watertight closure
9. Formation of diffuse posterior bleb

Antimetabolites

• Mitomycin-C: stronger anti-fibrotic effect
• 5-Fluorouracil: intraoperative or postoperative use

Complications

Early

• Hypotony
• Shallow/flat anterior chamber
• Choroidal detachment
• Hyphema
• Bleb leak
• Malignant glaucoma
• Suprachoroidal hemorrhage
• Bleb failure due to fibrosis

Late

• Bleb leak
• Bleb-related infection or blebitis
• Endophthalmitis
• Hypotony maculopathy
• Cataract
• Dysesthesia
• Encapsulated bleb
• Ptosis

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12. Glaucoma Drainage Devices (GDDs)

Definition

Components

1. Tube
2. Plate/end plate
3. Tube-covering graft: sclera, cornea, pericardium or synthetic material
4. Conjunctival covering

Classification

Indications

• Previous failed trabeculectomy
• Extensive conjunctival scarring
• Neovascular glaucoma
• Uveitic glaucoma
• Post-keratoplasty glaucoma
• Aphakic/pseudophakic glaucoma
• Iridocorneal endothelial syndrome
• Epithelial ingrowth
• Complex pediatric glaucoma
• Traumatic glaucoma
• Refractory glaucoma after multiple surgery

Surgical principles

1. Select quadrant, commonly superotemporal.
2. Secure plate posteriorly beneath rectus muscles.
3. Create a scleral tunnel.
4. Insert tube into anterior chamber, ciliary sulcus, or pars plana.
5. Cover tube with patch graft.
6. Ensure watertight conjunctival closure.

Non-valved implant

Complications

Tube position

• Anterior chamber placement is standard in many eyes.
• Sulcus placement may reduce endothelial risk in pseudophakic eyes.
• Pars plana placement requires prior or concurrent adequate vitrectomy.

Ahmed versus Baerveldt: classic comparison

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13. MIGS: Minimally Invasive Glaucoma Surgery

Definition

Main categories

Indications

• Mild-to-moderate open-angle glaucoma
• Cataract surgery combined with IOP-lowering intervention
• Medication intolerance or poor adherence
• Target IOP not extremely low
• Open angle with accessible trabecular meshwork

Limitations

• Conventional trabecular MIGS cannot lower IOP below episcleral venous pressure.
• Not generally suitable as sole therapy for severe rapidly progressive glaucoma needing very low IOP.
• Bleb-forming “MIGS” may achieve lower pressures but have bleb-related risks.

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14. Neuroprotection in Glaucoma

Definition

Why it is needed

• Normal-tension glaucoma
• Advanced glaucoma
• Eyes with vascular dysregulation
• Eyes with disc hemorrhage or low ocular perfusion pressure

Proposed mechanisms of ganglion-cell damage

• Mechanical laminar stress
• Ischemia and reperfusion injury
• Oxidative stress
• Mitochondrial dysfunction
• Excitotoxicity from glutamate
• Calcium influx and apoptosis
• Neuroinflammation
• Reduced neurotrophic-factor support

Potential neuroprotective strategies

Exam conclusion on neuroprotection

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15. High-Yield Secondary Glaucomas

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16. Recent Advances in Glaucoma

• Selective laser trabeculoplasty is increasingly used as first-line or early treatment for open-angle glaucoma.
• Preservative-free fixed combinations reduce drop burden and ocular-surface toxicity.
• Rho-kinase inhibitors offer a new pharmacological mechanism by improving trabecular outflow.
• Sustained-release delivery systems and drug-eluting implants are evolving, with availability varying by country.
• MIGS has expanded options for mild-to-moderate open-angle glaucoma, especially with cataract surgery.
• Bleb-forming microshunts occupy an intermediate space between trabeculectomy and traditional MIGS.
• Swept-source OCT, BMO-MRW, macular GCIPL and OCT angiography improve structural assessment, but do not replace optic-disc examination and perimetry.
• Artificial intelligence is being developed for disc-photo, OCT and visual-field interpretation, but needs clinician oversight and validation across populations.
• Neuroprotection through mitochondrial/metabolic pathways, including nicotinamide, remains investigational.

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Rapid Viva Answers

What is the most important modifiable risk factor in glaucoma?

What is the definitive test to classify angle as open or closed?

What is the first-line treatment for most POAG patients?

What is the hallmark of glaucoma on OCT?

Why is a thin cornea important?

What is a trabeculectomy?

When do you prefer a tube shunt?

What is the only proven neuroprotective treatment?

What is the difference between PAC and PACG?

1. Cataract and IOLs: FLACS, capsular tension ring (CTR), phakic IOLs, modern IOLs, accommodative IOLs
2. Retina and vitreous: BRVO management, ARMD, OCT, ERG, ROP, retinal imaging, FFA, pars plana vitrectomy, Pascal laser, silicone oil
3. Cornea and ocular surface: stem-cell therapy, ocular surface squamous neoplasia, amniotic membrane, collagen cross-linking/C3R, keratoprosthesis, lamellar keratoplasty, pterygium surgery, toxic contact lens reactions
4. Glaucoma: neuroprotection, glaucoma implants, OCT in glaucoma
5. Anterior segment / iris / diagnostic imaging: pupilloplasty, UBM
6. General ophthalmic technology and materials: OVDs, lasers, dyes, tissue adhesives/glues

1. Cataract and IOLs: FLACS, CTR, phakic IOLs, modern/accommodative IOLs
2. Retina and vitreous: BRVO, ARMD, OCT, ERG, ROP, FFA, retinal imaging, vitrectomy, lasers, silicone oil
3. Cornea and ocular surface: stem cells, amniotic membrane, OSSN, C3R, keratoplasty, KPro, pterygium, contact-lens toxicity
4. Glaucoma: neuroprotection, drainage implants, OCT
5. Imaging, lasers and materials: UBM, dyes, OVDs, tissue glues, lasers, pupilloplasty

1. Femtosecond laser-assisted cataract surgery (FLACS)
2. Capsular tension ring (CTR)
3. Phakic intraocular lenses
4. Modern pseudophakic IOLs, including toric, multifocal, EDOF and accommodating IOLs
5. IOL selection, biometry and high-yield complications

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1. Foundation: IOL basics

Definition

Parts

• Optic: central refracting portion
• Haptics: peripheral supporting elements
• Overall diameter: optic + haptic-to-haptic length
• Optic diameter: commonly 6 mm for standard adult posterior chamber IOLs

Ideal IOL properties

• Biocompatible and inert
• Stable fixation and centration
• Optically clear, scratch-resistant
• Minimal inflammation, posterior capsule opacification (PCO), dysphotopsia and glistenings
• Injectable through a small incision
• Predictable effective lens position (ELP)

Classification

Materials: exam comparison

Design features that prevent PCO

• Sharp square posterior optic edge produces a capsular bend and contact inhibition of lens epithelial cell migration.
• In-the-bag placement and meticulous cortical clean-up further reduce PCO.
• PCO, if visually significant, is managed by Nd:YAG posterior capsulotomy.

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2. FLACS: Femtosecond Laser-Assisted Cataract Surgery

Definition

1. Corneal incisions
2. Anterior capsulotomy
3. Lens fragmentation/softening
4. Arcuate or limbal-relaxing incisions for astigmatism

Principle

Essential components

• Docking interface: applanation or liquid-filled interface
• Image-guidance system: commonly OCT-based
• Laser delivery platform
• Patient interface and suction mechanism
• Integrated or adjacent phacoemulsification system

Steps of FLACS

1. Pharmacological dilation and sterile preparation.
2. Docking of the laser interface to the eye.
3. Imaging and treatment planning.
4. Laser creation of:
   • Primary and side-port corneal incisions
   • Precisely centered capsulotomy
   • Lens fragmentation pattern
   • Arcuate keratotomy if planned
5. Transfer to operating microscope.
6. Opening of laser capsulotomy and removal of free capsule disc.
7. Hydrodissection, phacoaspiration and cortical clean-up.
8. IOL implantation in the capsular bag.

Benefits

• Highly reproducible capsulotomy size, circularity and centration
• Precise corneal incisions
• Lens prefragmentation may reduce effective phaco time and cumulative dissipated energy
• Astigmatic arcuate incisions can be planned precisely
• Useful in selected challenging cases:
  • Shallow anterior chamber
  • Dense cataract
  • Low endothelial reserve
  • White/intumescent cataract, with careful case selection
  • Premium IOL procedures where centration is especially important

Limitations

• High capital, consumable and maintenance costs
• Extra docking and workflow time
• Requires pupil dilation and adequate corneal clarity
• Not always feasible in deep-set eyes, marked kyphosis, severe tremor, poor cooperation, inability to lie flat, or significant conjunctival scarring
• Incomplete capsulotomy, capsular tags and incomplete fragmentation can occur
• Does not replace surgical judgement or conventional phaco skill

Complications

During docking

• Subconjunctival hemorrhage
• Corneal folds and imaging artefacts
• Transient rise in IOP from suction
• Loss of suction and incomplete treatment

During surgery

• Incomplete corneal incision
• Capsular tags, microadhesions or incomplete capsulotomy
• Anterior capsular tear if the capsule is pulled before identifying and releasing tags
• Incomplete nuclear fragmentation
• Miosis due to prostaglandin release
• Rare capsular block syndrome if hydrodissection is forceful in a gas-fragmented lens

FLACS versus conventional phaco: what to write as “recent evidence”

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3. Capsular Tension Ring (CTR)

Definition

Design

• Usually made of PMMA
• Open ring with eyelets at both ends
• Inserted into the capsular bag after capsulorhexis and preferably after adequate hydrodissection
• Available in different diameters

Principle

Indications

Zonular weakness or dialysis

• Pseudoexfoliation syndrome
• Traumatic zonular dialysis
• High myopia
• Marfan syndrome and other ectopia lentis states
• Previous vitreoretinal surgery
• Mature/hypermature cataract with weak zonules
• Lens subluxation of limited extent
• Prior acute angle-closure attack with zonulopathy, in selected cases

Prevention of capsular contraction and IOL decentration

• Pseudoexfoliation
• Retinitis pigmentosa
• High myopia
• Uveitis, selectively
• Conditions predisposed to capsular phimosis

Types

Surgical technique

1. Create a well-centered continuous curvilinear capsulorhexis.
2. Use dispersive OVD to maintain the bag and protect endothelium.
3. Perform gentle hydrodissection, avoiding extension of zonular damage.
4. Place capsular hooks or iris retractors, if severe focal dialysis.
5. Insert the CTR slowly into the capsular bag using an injector or forceps.
6. Ensure the leading eyelet does not engage or tear the capsulorhexis margin.
7. Complete phacoemulsification with reduced stress on the weak zonular area.
8. Implant IOL in the bag if support is adequate.
9. In major dialysis, use a Cionni-modified device or CTS with scleral fixation.

Timing of insertion: common viva point

• Early insertion: improves early bag stability but may trap cortex behind the ring and make cortical aspiration difficult.
• Late insertion: allows easier cortical clean-up but may allow further zonular stress during phaco.

Advantages

• Stabilizes capsular bag during surgery
• Reduces capsular folds and equatorial bag collapse
• Improves IOL centration
• May improve rotational stability of toric IOLs
• Reduces risk of late decentration in selected cases, although it cannot eliminate progressive zonulopathy

Limitations and complications

• Cortex may become trapped between ring and capsule
• Capsular tear may extend if the ring is inserted forcefully
• Can worsen a pre-existing zonular dialysis if incorrectly inserted
• Standard CTR is inadequate when zonular loss is extensive or progressive
• Late in-the-bag IOL-CTR complex subluxation can still occur, especially in pseudoexfoliation
• A CTR should not be used as a substitute for scleral fixation when support is grossly insufficient

Recent evidence

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4. Phakic Intraocular Lenses (pIOLs)

Definition

Place in refractive surgery

• Refractive error is too high for safe corneal laser ablation
• Cornea is thin or topographically unsuitable for laser refractive surgery
• Accommodation should be preserved
• The patient is a young adult with stable refraction

Classification

Posterior chamber phakic IOL / ICL

Central-port ICL

Indications

• Stable refraction, generally for at least one year
• Moderate-to-high myopia, with or without astigmatism
• Hyperopia in selected cases
• Age typically 21 years or older, according to device approvals and local practice
• Adequate anterior chamber depth
• Adequate endothelial cell density
• Healthy cornea, crystalline lens, retina and optic nerve
• Strong desire to preserve accommodation

Contraindications

• Progressive refraction or unstable keratoconus
• Shallow anterior chamber
• Low endothelial cell count
• Narrow/occludable angle
• Cataract or significant lens opacity
• Active uveitis
• Uncontrolled glaucoma
• Corneal endothelial disease
• Significant retinal pathology requiring treatment first
• Unrealistic expectations or inability to comply with follow-up

Preoperative work-up

1. Manifest and cycloplegic refraction
2. Corneal tomography and pachymetry
3. Anterior chamber depth, measured from endothelium to anterior lens surface
4. White-to-white and/or sulcus-to-sulcus measurement
5. Endothelial cell count
6. Gonioscopy
7. Dilated retinal examination, especially in high myopia
8. IOP, optic-nerve assessment and macular OCT if indicated
9. Lens-vault prediction and sizing assessment using ultrasound biomicroscopy, anterior-segment OCT or device-specific nomograms

Vault

• Low vault: risk of anterior subcapsular cataract
• Excessive vault: angle crowding, pigment dispersion and secondary angle closure
• Ideal target varies by device and imaging method, but an adequate central vault with open angles is the goal.

Complications

Recent advances

• Central-port posterior chamber ICLs
• Toric pIOLs
• Improved vault prediction using AS-OCT and UBM
• Larger optic zones and customized sizing
• Diffractive phakic lenses for carefully selected presbyopic patients, but evidence remains limited

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5. Pseudophakic IOLs: Modern IOL Options

A. Monofocal IOL

Advantages

• Best contrast sensitivity
• Lowest rate of halos and glare
• Broadest suitability in eyes with retinal disease, glaucoma, corneal irregularity or uncertain visual potential
• Predictable and economical

Disadvantage

• Near spectacles are usually needed.

Aspheric monofocal IOL

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B. Toric IOL

Principle

Indications

• Regular corneal astigmatism
• Cataract patient seeking reduced spectacle dependence
• Adequate capsular support
• Reliable keratometry and stable ocular surface

Contraindications / caution

• Irregular astigmatism, unstable keratoconus, corneal scar or severe dry eye
• Poor capsular support
• Unreliable biometry
• Marked zonulopathy unless support is secured

Key points

• Accurate biometry and posterior corneal astigmatism consideration are essential.
• Marking can be manual, image-guided or digitally guided.
• Rotation matters: each degree of toric IOL rotation causes roughly 3.3% loss of cylindrical correction. At 30 degrees, the intended astigmatic correction is effectively lost.

Complications

• Misalignment/rotation
• Residual refractive astigmatism
• IOL tilt or decentration
• Need for early surgical repositioning if substantial rotation occurs

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C. Multifocal IOL

Principle

• Diffractive optics
• Refractive zones
• Hybrid designs

Advantages

• Greater spectacle independence at distance and near

Limitations

• Halos and glare
• Reduced contrast sensitivity, especially in dim illumination
• Neuroadaptation required
• Residual refractive error, dry eye, decentration or PCO can cause major dissatisfaction

Avoid or use cautiously in

• Significant ocular surface disease
• Corneal irregularity
• Macular disease, diabetic maculopathy, epiretinal membrane
• Advanced glaucoma or impaired contrast sensitivity
• Optic neuropathy
• Unrealistic patient expectations
• Occupations requiring excellent night contrast, depending on individual needs

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D. Trifocal IOL

Advantages

• Stronger near and intermediate spectacle independence than many bifocal designs

Disadvantages

• Dysphotopsia and contrast trade-off remain
• Needs precise centration and refractive targeting
• Not ideal for eyes with retinal or optic-nerve disease

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E. Extended Depth-of-Focus (EDOF) IOL

Principle

Advantages

• Often fewer halos than traditional multifocal lenses
• Good distance and intermediate vision
• Useful for computer users

Limitations

• Fine near tasks may still require spectacles
• Dysphotopsia and contrast effects can still occur
• Terminology and optical mechanisms vary between platforms

Important viva distinction

• Multifocal IOL: several discrete foci.
• EDOF IOL: elongated focus, usually better intermediate performance and often less severe dysphotopsia.
• Monofocal-plus/enhanced monofocal: improved intermediate range but not a true EDOF by all definitions.

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F. Accommodating IOL

Definition

Mechanisms

1. Single-optic movement: anterior movement of the optic during attempted accommodation.
2. Dual-optic systems: relative movement of two optics changes overall power.
3. Fluid-based or shape-changing designs: aim to alter curvature or refractive power.

Theoretical advantage

Limitations

• True, sustained objective accommodation has been difficult to demonstrate consistently.
• Capsular fibrosis and haptic restriction may reduce movement over time.
• Near outcomes may be partly due to depth of focus, pupil miosis or residual myopia rather than true accommodation.
• Current use is less widespread than monofocal, toric, multifocal, trifocal and EDOF designs.

Exam conclusion

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6. IOL Power Calculation and Modern Biometry

Essential formula concept

• Axial length
• Corneal power
• Anterior chamber depth / lens position predictors
• Lens thickness
• White-to-white in some formulas
• Desired postoperative refraction
• Effective lens position (ELP)

Common formula evolution

High-yield choices

• Short eyes: modern formulas such as Barrett Universal II, Kane, Hoffer QST and Holladay 2 may be useful.
• Long/high-myopic eyes: use modern formulas and consider axial-length adjustment where appropriate.
• Post-refractive surgery eyes: use no-history methods, tomography-derived corneal data and dedicated calculators where available.
• Toric IOLs: include posterior corneal astigmatism and surgically induced astigmatism.

Causes of refractive surprise

• Keratometry error, especially dry eye
• Incorrect axial length, especially posterior staphyloma
• Incorrect IOL constant
• Wrong IOL selection or implantation
• Unpredicted ELP
• Corneal edema or irregular astigmatism
• Prior refractive surgery
• IOL tilt, decentration or rotation

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7. How to Select an IOL: Clinical Algorithm

Step 1: Determine visual potential

• Cornea and ocular surface
• Macula: OCT if indicated
• Optic nerve and glaucoma status
• Diabetic retinopathy
• Amblyopia and previous retinal surgery

Step 2: Determine refractive objective

• Distance target with reading glasses
• Monovision
• Distance + intermediate
• Maximum spectacle independence

Step 3: Assess corneal astigmatism

• Regular and significant: consider toric IOL
• Irregular: treat ocular surface/corneal condition first; avoid routine toric or multifocal decisions until measurements are reliable

Step 4: Assess suitability for presbyopia correction

Step 5: Assess capsular support

• Good support: in-the-bag PCIOL
• Mild zonulopathy: CTR + PCIOL
• Major zonulopathy: modified CTR/CTS with scleral fixation, or consider secondary fixation strategy
• No capsular support: scleral-fixated, iris-fixated or selected ACIOL depending on anatomy and surgeon expertise

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8. Common Long-Answer Questions and Model Opening Lines

“Write a short note on FLACS.”

“Describe capsular tension ring.”

“Discuss phakic IOL.”

“Write a note on accommodating IOL.”

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9. Rapid Revision Pearls

• FLACS: more precise capsulotomy and incisions, but no proven overall long-term superiority or cost-effectiveness over standard phaco.
• CTR: supports the bag, not the weak zonules themselves. Use a Cionni ring or CTS with scleral fixation if zonular loss is major.
• Standard CTR: can trap cortex. Do not insert forcefully.
• Phakic IOL: preserves accommodation; assess ACD, ECD, angle, retina and vault.
• Low pIOL vault: cataract risk.
• High pIOL vault: angle crowding/pigment/IOP risk.
• Toric IOL: 1 degree of rotation loses about 3.3% cylinder effect.
• Multifocal/trifocal IOL: better spectacle independence, but halos and lower contrast sensitivity.
• EDOF: distance-to-intermediate range with less near performance than trifocal in many designs.
• Accommodating IOL: variable evidence for sustained true accommodation.
• Hydrophobic acrylic square-edge IOL: standard modern choice for low PCO risk.
• Avoid silicone IOL when silicone-oil tamponade is likely in future retinal surgery.

1. Branch retinal vein occlusion (BRVO)
2. Age-related macular degeneration (AMD/ARMD)
3. OCT and OCT angiography
4. Electroretinography (ERG)
5. Retinopathy of prematurity (ROP)
6. Retinal lasers, including Pascal
7. Pars plana vitrectomy (PPV)
8. Silicone oil and other endotamponades
9. Retinal imaging modalities
10. Fundus fluorescein angiography (FFA)

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1. Branch Retinal Vein Occlusion (BRVO)

Definition

Pathogenesis

1. Venous narrowing
2. Turbulent blood flow
3. Endothelial injury
4. Thrombus formation
5. Venous obstruction

• Raised intraluminal venous pressure
• Capillary leakage causing macular edema
• Retinal hemorrhage
• Capillary nonperfusion and ischemia
• Increased VEGF production, causing macular edema and neovascularization

Risk factors

Ocular

• Hypertension-related arteriosclerosis
• Primary open-angle glaucoma
• Raised IOP
• Short axial length, reported in some populations

Systemic

• Hypertension
• Diabetes mellitus
• Dyslipidemia
• Smoking
• Obesity
• Renal disease
• Hyperhomocysteinemia
• Myeloproliferative disorders
• Thrombophilia, especially in young, bilateral, recurrent, or atypical RVO

Classification

By site

• Major BRVO: first-order branch vein occlusion, commonly superotemporal
• Macular BRVO: smaller macular venous branch involved
• Hemispheric retinal vein occlusion: one hemiretina involved, often considered intermediate between BRVO and CRVO

By perfusion

• Perfused BRVO
• Ischemic BRVO: extensive capillary nonperfusion, higher risk of retinal/disc neovascularization

Clinical features

Symptoms

• Painless unilateral decrease in vision
• Metamorphopsia
• Central or paracentral scotoma
• Often incidentally detected if macula is spared

Signs

• Dilated, tortuous vein
• Flame-shaped and dot-blot retinal hemorrhages
• Cotton-wool spots
• Retinal edema
• Macular edema if macular circulation is affected
• Collateral vessels later
• Neovascularization of retina or disc in ischemic disease
• Vitreous hemorrhage as a late complication

Investigations

Management

A. Treat systemic risk factors

• BP control
• Diabetes control
• Lipid management
• Smoking cessation
• Assessment for glaucoma
• Selective hematologic work-up where indicated

B. Macular edema

• Ranibizumab
• Aflibercept
• Bevacizumab, widely used off-label in many settings
• Faricimab, a bispecific antibody targeting VEGF-A and angiopoietin-2

• Initial loading followed by pro re nata regimen
• Treat-and-extend protocol
• Individualized OCT-guided treatment

C. Intravitreal corticosteroid

• In pseudophakia
• When anti-VEGF response is suboptimal
• If injection burden is difficult
• In anti-VEGF contraindication or selected inflammatory phenotypes

• IOP elevation
• Cataract, particularly in phakic eyes
• Need for repeat treatment

D. Laser photocoagulation

• Grid laser for macular edema: historical role, now usually secondary to anti-VEGF therapy.
• Sector scatter laser: indicated for retinal/disc neovascularization associated with nonperfusion, not prophylactically merely because ischemia exists.

Prognosis

• Baseline VA
• Duration/severity of macular edema
• Foveal ischemia
• Integrity of ellipsoid zone and external limiting membrane on OCT
• Disorganization of retinal inner layers, DRIL
• Development of neovascularization/vitreous hemorrhage

Recent advances

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2. Age-Related Macular Degeneration (AMD/ARMD)

Definition

Risk factors

Non-modifiable

• Increasing age
• Family history/genetic susceptibility
• White ethnicity
• Complement-pathway gene variants, including CFH and ARMS2/HTRA1 associations

Modifiable

• Smoking, the strongest modifiable risk factor
• Hypertension/cardiovascular risk factors
• Obesity
• Poor diet and low antioxidant intake
• Excess ultraviolet exposure is less clearly established

Classification

1. Early AMD

• Medium drusen
• Mild RPE pigmentary abnormalities
• Usually no visual symptoms

2. Intermediate AMD

• Large drusen, typically at least 125 micrometers
• Numerous medium drusen
• Noncentral geographic atrophy

3. Late AMD

A. Dry AMD

• Drusen and RPE dysfunction
• Geographic atrophy (GA): sharply demarcated RPE and photoreceptor loss

B. Neovascular or wet AMD

• Subretinal fluid
• Intraretinal fluid
• Pigment epithelial detachment
• Hemorrhage
• Fibrosis/disciform scar

Classification of macular neovascularization

Clinical features

• Painless central visual loss
• Metamorphopsia
• Micropsia
• Difficulty recognizing faces and reading
• Central scotoma
• Reduced contrast and dark adaptation

Investigations

Management

Dry AMD

1. Smoking cessation
2. Control cardiovascular risk factors
3. Amsler monitoring and urgent review for new distortion/scotoma
4. Low-vision support where necessary
5. AREDS2 supplementation for selected intermediate AMD or advanced AMD in one eye

• Vitamin C
• Vitamin E
• Zinc
• Copper
• Lutein
• Zeaxanthin

Geographic atrophy: major advance

• Pegcetacoplan, a C3 inhibitor
• Avacincaptad pegol, a C5 inhibitor

Neovascular AMD

• Ranibizumab
• Aflibercept
• Bevacizumab, off-label in many regions
• Brolucizumab, used cautiously because of intraocular inflammation/retinal vasculitis concerns
• Faricimab: VEGF-A and Ang-2 inhibition
• Higher-dose aflibercept formulations in some regions for interval extension

• Fixed dosing
• Pro re nata
• Treat-and-extend, widely used in routine practice

Polypoidal choroidal vasculopathy

• Anti-VEGF is foundational.
• Photodynamic therapy may be added in selected cases, especially persistent polypoidal lesions or recurrent hemorrhage.

Recent advances

• OCT-guided treat-and-extend regimens
• Faricimab and high-dose aflibercept for reducing injection burden in selected patients
• Complement inhibition for geographic atrophy
• Home monitoring and AI-assisted fluid detection
• Long-acting delivery systems and gene therapy remain areas of active development rather than routine universal care

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3. Optical Coherence Tomography (OCT)

Definition

Principle

• A reference beam
• A sample beam reflected from ocular tissues

Types

Retinal OCT applications

• Diabetic macular edema
• BRVO/CRVO macular edema
• Neovascular AMD
• Central serous chorioretinopathy
• Epiretinal membrane
• Vitreomacular traction
• Macular hole
• Myopic maculopathy
• Retinal dystrophies
• Hydroxychloroquine monitoring
• Optic nerve/RNFL and ganglion-cell analysis in glaucoma

Important OCT signs

OCT-Angiography

Principle

Advantages

• Noninvasive
• Rapid
• Layer-by-layer vascular segmentation
• Identifies nonexudative MNV
• Useful in diabetic retinopathy, AMD, retinal vein occlusion, macular telangiectasia and inherited retinal disease

Limitations

• Does not show leakage
• Motion artifact
• Projection artifact
• Segmentation errors, especially in edema/PED
• Poor images with media opacity or poor fixation
• Slow-flow lesions may be missed

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4. Fundus Fluorescein Angiography (FFA)

Definition

Principle

• Is a water-soluble orange dye
• Absorbs blue light near 490 nm
• Emits yellow-green fluorescence near 530 nm
• Is largely protein-bound intravascularly
• Is excreted by the kidneys

Phases of FFA

1. Choroidal flush: patchy background choroidal fluorescence
2. Arterial phase
3. Arteriovenous/capillary phase
4. Early venous phase: laminar flow
5. Late venous phase
6. Recirculation phase

Hyperfluorescence: causes

Hypofluorescence: causes

Indications

• Diabetic retinopathy and macular edema
• BRVO/CRVO evaluation
• Macular ischemia
• Neovascular AMD
• Central serous chorioretinopathy
• Retinal vasculitis
• Choroiditis
• Cystoid macular edema
• Retinal neovascularization
• Unexplained visual loss with suspected vascular/retinal pathology

Contraindications and adverse effects

Relative contraindications

• Previous severe fluorescein reaction
• Pregnancy, depending on risk-benefit analysis
• Severe asthma or major allergy history requires caution

Complications

• Nausea and vomiting, common minor effects
• Yellow discoloration of skin
• Bright yellow urine
• Extravasation pain/tissue irritation
• Urticaria
• Bronchospasm
• Anaphylaxis, rare but potentially fatal

FFA versus ICGA

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5. Electroretinography (ERG)

Definition

Principle

Components

Types

Full-field ERG

• Retinitis pigmentosa
• Cone-rod dystrophy
• Congenital stationary night blindness
• Drug toxicity
• Widespread retinal dysfunction
• Unexplained reduced vision when a diffuse retinal dystrophy is suspected

Pattern ERG

Multifocal ERG

• Occult macular dystrophy
• Hydroxychloroquine toxicity
• Macular dysfunction with normal fundus
• Early regional retinal dysfunction

Electro-oculography

• Best vitelliform macular dystrophy

Dark-adapted versus light-adapted responses

Classic ERG patterns

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6. Retinopathy of Prematurity (ROP)

Definition

Pathogenesis: two-phase model

Phase 1: Hyperoxia and vaso-obliteration

• Relative hyperoxia suppresses VEGF and IGF-1
• Normal retinal vascular growth is interrupted
• Peripheral retina remains avascular

Phase 2: Hypoxia-driven neovascularization

• Avascular retina becomes hypoxic
• VEGF rises
• Pathological neovascularization and fibrovascular proliferation develop
• Traction can cause retinal detachment

Risk factors

• Lower gestational age
• Lower birth weight
• Prolonged supplemental oxygen exposure
• Sepsis
• Apnea/respiratory distress
• Poor postnatal weight gain
• Anemia/transfusions
• Intraventricular hemorrhage
• Poor neonatal care and oxygen monitoring

International Classification of ROP

Zones

• Zone I: circle centered on optic disc, radius twice disc-fovea distance
• Zone II: from outer edge of zone I to nasal ora serrata and toward temporal equator
• Zone III: residual temporal crescent of peripheral retina

Stages

Plus disease

Aggressive ROP

Treatment indication: Type 1 ROP

• Zone I, any stage with plus disease
• Zone I, stage 3 without plus disease
• Zone II, stage 2 or 3 with plus disease

• Zone I, stage 1 or 2 without plus
• Zone II, stage 3 without plus

Treatment

A. Laser photocoagulation

• Well-established treatment
• Definitive peripheral ablation
• Less concern about prolonged systemic VEGF suppression compared with anti-VEGF

• Technically demanding in small infants
• More myopia
• May be difficult in posterior zone I disease
• Peripheral field is ablated
• Does not allow normal peripheral vascularization

B. Intravitreal anti-VEGF

• Bevacizumab
• Ranibizumab
• Aflibercept in some settings

• Very effective in zone I/posterior aggressive disease
• Rapid regression
• Preserves more peripheral retina
• May induce less myopia than laser
• Useful where media opacity or poor pupil dilation makes laser difficult

• Late recurrence/reactivation can occur, sometimes months later
• Requires long-term follow-up until peripheral vascularization is complete
• Systemic absorption and long-term neurodevelopmental/systemic safety remain important concerns
• Optimal agent and lowest effective dose remain unsettled

C. Surgery

• Lens-sparing vitrectomy for selected stage 4 disease
• Vitrectomy with or without lensectomy for advanced tractional detachment
• Anatomical success and visual outcome worsen markedly in stage 4B and stage 5 disease

Current evidence

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7. Retinal Lasers

Principle of retinal photocoagulation

• Wavelength
• Power
• Spot size
• Duration
• Retinal pigmentation
• Media clarity
• Lens used

Common laser wavelengths

Types of retinal laser

PRP: indications

• Proliferative diabetic retinopathy
• Ischemic CRVO with neovascularization or high risk
• Ocular ischemic syndrome
• Proliferative sickle retinopathy
• Selected retinal vasculitis and Eales disease

Complications of retinal laser

• Pain
• Iatrogenic retinal break, rare
• Macular edema
• Reduced peripheral field after PRP
• Reduced night vision
• Reduced color/contrast sensitivity
• Choroidal effusion, exudative RD, rare
• Accidental foveal burn
• Bruch membrane rupture/secondary CNV, rare

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8. Pascal Laser

Full form

Definition

Principle

• 2 × 2
• 3 × 3
• 4 × 4
• Arc
• Grid
• PRP arrays

Advantages

• Faster delivery of PRP
• More uniform spot pattern
• Less total procedure time
• Often better tolerated
• Potentially less collateral thermal diffusion with short pulses
• Useful in PRP, sector laser and pattern macular treatment

Limitations

• Shorter pulse duration requires higher power to achieve the intended burn
• Lesion intensity must be titrated carefully
• Less flexibility in irregular peripheral anatomy in some situations
• Cost and availability limitations
• A dense or excessively intense pattern can still produce significant field effects

Pascal versus conventional laser

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9. Pars Plana Vitrectomy (PPV)

Definition

Anatomical basis

• Ora serrata anteriorly
• Ciliary body posteriorly

• Phakic adult eye: approximately 3.5-4 mm posterior to limbus
• Pseudophakic/aphakic eye: approximately 3-3.5 mm posterior to limbus
• In children: distance is adjusted according to age and globe size

Instrument systems

• 20 gauge: older, larger, sutured
• 23 gauge
• 25 gauge
• 27 gauge: very small, less flow, useful in selected fine maneuvers

1. Infusion cannula
2. Vitreous cutter
3. Illumination probe

Indications

Vitreous hemorrhage

• Non-clearing diabetic vitreous hemorrhage
• Dense hemorrhage preventing retinal evaluation/treatment
• Vitreous hemorrhage associated with retinal tear/detachment
• Selected trauma

Retinal detachment

• Pseudophakic RRD
• Giant retinal tear
• Posterior breaks
• RRD with PVR
• Nonvisualized breaks due to hemorrhage/media opacity
• Complex or recurrent RD

Diabetic retinopathy

• Tractional RD threatening or involving macula
• Combined tractional-rhegmatogenous RD
• Non-clearing vitreous hemorrhage
• Dense premacular/subhyaloid hemorrhage, selected cases
• Severe fibrovascular traction

Macular disease

• Epiretinal membrane
• Full-thickness macular hole
• Vitreomacular traction
• Selected myopic traction maculopathy

Other

• Endophthalmitis, depending on visual acuity/severity
• Retained lens fragments
• Intraocular foreign body
• Diagnostic vitreous biopsy
• Dislocated IOL or lens material
• Severe posterior segment trauma

Goals in retinal detachment surgery

1. Remove vitreoretinal traction
2. Identify and treat all retinal breaks
3. Flatten retina and drain subretinal fluid if required
4. Create chorioretinal adhesion using laser/cryo
5. Maintain retinal apposition with internal tamponade

Basic surgical steps

1. Preoperative retinal mapping and consent
2. Conjunctival displacement in transconjunctival systems
3. Create pars plana ports
4. Confirm infusion cannula position before opening infusion
5. Core vitrectomy
6. Induce posterior vitreous detachment, if not already present
7. Peripheral vitreous shaving with scleral depression
8. Remove membranes where indicated
9. Identify all breaks
10. Drain subretinal fluid, often through a break or drainage retinotomy
11. Fluid-air exchange
12. Endolaser retinopexy
13. Gas or silicone-oil tamponade, if needed
14. Close/suture leaking ports

Complications

Intraoperative

• Iatrogenic retinal break
• Lens touch
• Suprachoroidal hemorrhage
• Choroidal detachment
• Retinal incarceration at port
• Incomplete membrane removal
• Infusion misdirection

Postoperative

• Cataract progression, especially nuclear sclerosis in phakic patients
• Elevated IOP or hypotony
• Endophthalmitis
• Corneal edema
• Cystoid macular edema
• Recurrent RD/PVR
• Epiretinal membrane
• Retinal toxicity, rare
• Visual-field defects
• Need for reoperation

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10. Silicone Oil

Definition

Mechanism

• Supporting the retina against the RPE
• Preventing fluid from entering retinal breaks
• Maintaining chorioretinal adhesion while laser scars mature

Types

• Conventional silicone oil: commonly 1,000 or 5,000 centistokes
• Heavy silicone oil: denser than water, designed to tamponade inferior pathology, but has limited long-term use due to complications/emulsification concerns

Indications

• Complex RRD with PVR
• Giant retinal tears
• Recurrent retinal detachment
• Severe diabetic tractional/combined RD
• Retinal detachment with proliferative vitreoretinopathy
• Ocular trauma
• Cases requiring long-term tamponade
• Patients unable to posture for gas tamponade
• Need for early air travel or situations where gas is unsuitable

Advantages compared with gas

• Long-term support
• No expansion with nitrous oxide/altitude in the same manner as gas
• No strict prolonged face-down positioning in some cases, although positioning can still be clinically important
• Fundus can be examined through oil
• Appropriate for complex disease

Disadvantages

• Usually requires a second surgery for removal
• Less favorable visual outcomes than gas in uncomplicated RRD, partly because oil is used in more complex eyes
• Emulsification and anterior-segment complications

Complications

Pupillary block prevention

Silicone oil removal

• Retina is stable
• Adequate chorioretinal adhesion is established
• Oil-related complications develop
• Risk of redetachment is acceptable

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11. Other Vitreous Substitutes

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12. Retinal Imaging Modalities: Exam Table

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13. High-Yield Recent Advances

• Anti-VEGF treatment remains first-line for vision-threatening macular edema due to BRVO and for neovascular AMD.
• Faricimab targets VEGF-A and Ang-2 and may allow longer treatment intervals in some RVO and AMD patients, but superiority in durability over existing agents is not yet established.
• OCT-A is valuable for noninvasive vascular mapping, but FFA remains important when leakage and dynamic perfusion assessment are needed.
• Swept-source OCT gives deeper choroidal and vitreoretinal imaging.
• Geographic atrophy complement inhibitors can slow lesion enlargement but require counseling about limited functional recovery and risk of neovascular conversion.
• ROP anti-VEGF preserves peripheral retina and may reduce myopia, but requires prolonged surveillance for late reactivation and raises systemic-safety questions.
• Small-gauge vitrectomy with high-speed cutters has improved surgical efficiency and reduced tissue traction.
• Heads-up 3D vitreoretinal surgery, intraoperative OCT, digital visualization, robotic assistance and AI-supported imaging are evolving adjuncts.
• Pascal and micropulse lasers aim for more efficient or tissue-sparing laser delivery, but appropriate case selection and endpoint titration remain central.

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14. One-Minute Viva Answers

What is the difference between FFA and OCT-A?

What is the first-line treatment for BRVO macular edema?

What are the major complications of silicone oil?

What does a negative ERG indicate?

What is plus disease in ROP?

What is the role of PPV in diabetic retinopathy?

Cornea and Ocular Surface: MS Ophthalmology Theory Revision

1. Limbal stem-cell deficiency and stem-cell therapy
2. Amniotic membrane transplantation
3. Ocular surface squamous neoplasia
4. Corneal collagen cross-linking / C3R
5. Lamellar keratoplasty, especially DALK
6. Keratoprosthesis
7. Pterygium surgery
8. Toxic contact-lens-related ocular surface disease

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1. Limbal Stem Cells and Limbal Stem-Cell Deficiency (LSCD)

Normal limbal stem cells

Location

Functions

• Lifelong regeneration of corneal epithelium
• Maintenance of transparent, avascular corneal surface
• Healing after epithelial injury
• Prevention of conjunctivalization

Stem-cell niche

• Palisades of Vogt
• Limbal stromal fibroblasts
• Blood vessels and extracellular matrix
• Corneal nerves
• Melanocytes and immune cells

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Limbal Stem-Cell Deficiency

Definition

Etiology

Clinical features

• Persistent or recurrent epithelial defects
• Reduced vision, photophobia, pain and redness
• Whorl-like or late fluorescein staining
• Loss of limbal palisades of Vogt
• Superficial corneal vascularization
• Conjunctivalization of cornea
• Fibrovascular pannus and scarring
• Recurrent erosions
• In advanced disease: keratinization and symblepharon

Diagnosis

• Fluorescein staining pattern
• Impression cytology showing conjunctival goblet cells on cornea
• In vivo confocal microscopy
• Anterior-segment OCT
• Corneal epithelial markers, where available

Staging concept

• Partial LSCD: a sector or portion of limbus affected
• Total LSCD: entire limbus affected
• Unilateral versus bilateral LSCD is critical because it determines the donor source.

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Management of LSCD

Step 1: Restore the ocular surface

• Stop toxic topical medications and preservatives where possible
• Treat dry eye and lid disease
• Preservative-free lubricants
• Control inflammation: topical steroids, ciclosporin/tacrolimus in selected cases
• Manage exposure, lagophthalmos and trichiasis
• Treat infection and neurotrophic keratopathy if present
• Autologous serum tears or platelet-rich plasma in selected patients
• Scleral lens for surface protection and visual rehabilitation

Step 2: Stem-cell restoration

SLET: high-yield answer

1. Harvest a small limbal biopsy from healthy fellow eye.
2. Secure cryopreserved or fresh amniotic membrane over recipient cornea.
3. Divide donor biopsy into small explants.
4. Place explants on membrane.
5. Cover with bandage contact lens.
6. Cells expand across the membrane and repopulate the corneal surface.

Important principle

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2. Amniotic Membrane Transplantation (AMT)

Definition

Biological properties

• Promotes epithelial migration and adhesion
• Provides a basement-membrane scaffold
• Reduces inflammation and inflammatory-cell infiltration
• Reduces fibrosis and myofibroblast activation
• Inhibits angiogenesis
• Reduces pain by covering exposed corneal nerves
• Has antimicrobial and anti-scarring effects

Types

Orientation: commonI’ve stopped researching. The cornea and ocular surface module was paused during amniotic membrane transplantation.

• AMT orientation, techniques, indications and complications
• OSSN
• C3R/corneal cross-linking
• DALK and keratoprosthesis
• Pterygium surgery
• Contact-lens toxicity# Cornea and Ocular Surface: MS Ophthalmology Theory Notes

Topics

1. Limbal stem-cell deficiency and stem-cell therapy
2. Amniotic membrane transplantation
3. Ocular surface squamous neoplasia
4. Corneal collagen cross-linking, CXL/C3R
5. Lamellar keratoplasty, especially DALK
6. Keratoprosthesis
7. Pterygium surgery
8. Toxic contact-lens-related ocular surface disease

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1. Limbal Stem-Cell Deficiency and Stem-Cell Therapy

Normal limbus and stem-cell function

Functions

• Continuous renewal of corneal epithelium
• Healing after epithelial trauma
• Maintenance of a transparent, avascular corneal surface
• Barrier function preventing conjunctival epithelial migration onto cornea

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Limbal stem-cell deficiency (LSCD)

Definition

Causes

Clinical features

• Persistent/recurrent epithelial defect
• Photophobia, irritation, pain, redness
• Reduced vision
• Late fluorescein staining in a whorl or vortex pattern
• Loss of palisades of Vogt
• Conjunctivalization of cornea
• Superficial corneal vascularization and fibrovascular pannus
• Recurrent erosions, scarring, calcification
• In severe disease: keratinization, symblepharon and dry eye

Diagnosis

• Fluorescein staining
• Slit-lamp evaluation of limbus and palisades
• Impression cytology: conjunctival goblet cells on the cornea strongly support LSCD
• In vivo confocal microscopy
• Anterior segment OCT
• Corneal epithelial phenotype markers, in specialist centers

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Management of LSCD

Principle

Conservative management

• Stop toxic medication and minimize preservatives
• Preservative-free lubricants
• Treat blepharitis, meibomian-gland dysfunction and dry eye
• Control inflammation with carefully supervised topical steroid
• Topical ciclosporin or tacrolimus in selected inflammatory disease
• Autologous serum tears or platelet-rich plasma tears
• Punctal occlusion, tarsorrhaphy, epilation of trichiasis
• Scleral lenses for surface protection and optical rehabilitation
• Treat exposure, infection and neurotrophic keratopathy

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Surgical restoration of limbal stem cells

A. Conjunctival limbal autograft

• Tissue is harvested from the healthy contralateral eye.
• Transplanted to affected eye after removing conjunctivalized corneal tissue.
• Suitable for unilateral complete LSCD.
• Donor-site damage is possible if excessive limbus is harvested.

B. SLET: Simple limbal epithelial transplantation

Steps

1. Excise fibrovascular pannus and abnormal epithelium from recipient cornea.
2. Place cryopreserved amniotic membrane over bare corneal surface.
3. Harvest a small limbal biopsy from healthy contralateral eye.
4. Divide biopsy into multiple small explants.
5. Arrange explants over amniotic membrane.
6. Secure with fibrin glue or sutures and apply a bandage contact lens.

Advantages

• Small donor biopsy
• Less risk to donor eye than CLAU
• Does not need a cell-culture laboratory
• Cost-effective
• Particularly practical for unilateral chemical-burn-related LSCD

C. CLET

D. Allograft procedures

• Living related donor limbal tissue, or
• Cadaveric keratolimbal allograft.

Emerging advances

• Cultivated epithelial sheets
• Oral-mucosal epithelial transplantation
• Induced pluripotent stem-cell approaches
• Mesenchymal stem-cell-derived exosomes
• Biomaterial scaffolds and 3D engineered limbal niches

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2. Amniotic Membrane Transplantation (AMT)

Definition

Properties and mechanisms

• Promotes epithelial migration, adhesion and differentiation
• Provides basement-membrane substrate
• Suppresses inflammation
• Reduces fibroblast activation and scarring
• Reduces neovascularization
• Reduces pain by covering exposed corneal nerves
• Has anti-protease and anti-microbial properties

Types

• Cryopreserved amniotic membrane
• Dehydrated amniotic membrane
• Sutured graft
• Fibrin-glue-assisted graft
• Sutureless/self-retained membrane device
• Multilayer membrane for deep ulcers or perforation risk

Orientation: viva question

• For a graft/inlay, place the epithelial/basement-membrane side up, facing the regenerating corneal epithelium.
• The stromal side is placed against the host tissue.
• In an overlay/patch technique, the membrane acts mainly as a biological dressing, although standard orientation is still generally maintained.

Surgical techniques

1. Inlay or graft technique

• Persistent epithelial defect
• Corneal ulcer
• Stromal thinning
• Post-pterygium or post-tumor excision defect
• Partial LSCD

2. Overlay or patch technique

• Acute chemical injury
• Acute Stevens-Johnson syndrome
• Severe ocular-surface inflammation
• Extensive epithelial defect

3. Multilayer technique

• Corneal melt
• Descemetocele
• Small corneal perforation, often with tissue adhesive or bandage lens

Indications

AMT in acute ocular burns

Complications

• Membrane displacement, folding or dissolution
• Infection, uncommon
• Pyogenic granuloma
• Incomplete epithelialization
• Recurrence of underlying inflammation
• Transmission risk is extremely low with screened, processed tissue but must be discussed

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3. Ocular Surface Squamous Neoplasia (OSSN)

Definition

Histological spectrum

1. Squamous epithelial dysplasia
2. Conjunctival intraepithelial neoplasia, CIN
3. Carcinoma in situ
4. Invasive squamous cell carcinoma

Risk factors

• Ultraviolet-B exposure and outdoor work
• Older age
• Male sex in many populations
• HIV infection and immunosuppression
• HPV association, though causality and subtype contribution vary
• Xeroderma pigmentosum
• Chronic ocular-surface inflammation
• Smoking
• Prior irradiation
• Vitamin A deficiency in some settings

Clinical features

• Usually unilateral, interpalpebral, nasal limbal lesion
• Gelatinous, papilliform, leukoplakic or nodular mass
• Prominent feeder vessels
• Corneal epithelial extension may appear as a gray, translucent, elevated lesion
• May mimic pterygium, pinguecula, papilloma, actinic keratosis or amelanotic melanoma

Investigations

• Slit-lamp photography and lesion mapping
• High-resolution anterior-segment OCT:
  • Thickened hyperreflective epithelium
  • Abrupt transition between normal and abnormal epithelium
  • Helpful to distinguish OSSN from pterygium
• Ultrasound biomicroscopy if intraocular extension suspected
• Impression cytology, selected cases
• Excision biopsy for histopathology where diagnosis is uncertain or lesion requires removal
• Orbital imaging if deep invasion is suspected

Management

A. Surgical excision: “no-touch technique”

Principles

1. Avoid directly grasping tumor to prevent seeding.
2. Wide conjunctival margins, commonly 3-4 mm of clinically normal tissue where feasible.
3. Alcohol-assisted epitheliectomy for corneal component.
4. Excise lesion with involved Tenon tissue if needed.
5. Apply double freeze-thaw cryotherapy to conjunctival margins.
6. Send specimen for histopathology.
7. Reconstruct surface with conjunctival autograft or amniotic membrane if required.

B. Topical chemotherapy or immunotherapy

Choosing surgery versus medical treatment

• Histological diagnosis is needed
• Invasion is suspected
• Lesion is focal and easily excisable
• Patient may not comply with prolonged topical therapy
• Resources are limited
• Isolated corneal lesion requires diagnostic clarification

Follow-up

Major complication of treatment

• Large lesions
• More than 6 clock hours of limbal involvement
• Recurrent lesions
• Corneal involvement
• Repeated surgery or topical mitomycin-C

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4. Corneal Collagen Cross-Linking: CXL / C3R

Definition

Main indications

• Documented progressive keratoconus
• Progressive post-LASIK or post-PRK ectasia
• Pellucid marginal degeneration, selected cases
• Keratoglobus or other ectasias, selected cases
• PACK-CXL: photoactivated chromophore for infectious keratitis, as adjunctive treatment in selected refractory infections

Evidence of progression

• Increase in Kmax
• Increase in manifest cylinder or myopia
• Progressive thinning
• Worsening corrected vision
• Change in posterior corneal curvature/elevation
• Serial topographic/tomographic worsening

Dresden protocol: conventional epithelium-off CXL

1. Remove central 8-9 mm corneal epithelium.
2. Instill 0.1% riboflavin in dextran solution for approximately 30 minutes.
3. Confirm stromal saturation and adequate corneal thickness.
4. Expose cornea to UVA at 370 nm, 3 mW/cm² for 30 minutes.
5. Total radiant exposure is 5.4 J/cm².
6. Apply antibiotic, bandage contact lens and postoperative anti-inflammatory regimen.

Safety criterion

Mechanism

Types

Complications

• Severe pain in early postoperative days
• Delayed epithelial healing
• Sterile infiltrates
• Infectious keratitis
• Corneal haze/scarring
• Endothelial damage in excessively thin cornea
• Herpes simplex keratitis reactivation
• Rare loss of corrected vision

Recent evidence

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5. Lamellar Keratoplasty and DALK

Classification of corneal transplantation

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Deep anterior lamellar keratoplasty (DALK)

Definition

Indications

• Keratoconus
• Stromal corneal scars with healthy endothelium
• Stromal dystrophy
• Postinfectious stromal opacity after infection is controlled
• Some cases of corneal ectasia

Contraindications

• Endothelial dysfunction
• Significant Descemet membrane scarring
• Deep stromal scar adherent to Descemet membrane, relative contraindication
• Acute hydrops with severe Descemet membrane disruption, depending on case

Big-bubble technique

1. Partial-depth trephination.
2. Insert needle deeply into stroma.
3. Inject air to create a cleavage plane between posterior stroma and Descemet membrane.
4. Remove anterior stroma.
5. Open and remove residual posterior stromal tissue.
6. Place donor graft with donor Descemet membrane removed.
7. Suture graft.

Advantages over PK

• Preserves host endothelium
• Very low risk of endothelial rejection
• Better long-term endothelial survival
• Reduced risk of catastrophic open-sky complications
• Stronger wound architecture
• Useful in young keratoconus patients

Disadvantages and complications

• Technically demanding
• Descemet membrane perforation
• Conversion to PK may be required
• Double anterior chamber if Descemet membrane detaches
• Interface haze
• Residual stromal bed can reduce optical quality
• Suture-related astigmatism and infection
• Recurrence of disease in graft, uncommon depending on disease

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6. Keratoprosthesis

Definition

Main types

• Boston Type I keratoprosthesis
• Boston Type II keratoprosthesis
• Osteo-odonto-keratoprosthesis, OOKP
• Other specialist devices, including tibial osteokeratoprosthesis

Boston Type I KPro

Indications

• Multiple failed corneal grafts
• Severe bilateral corneal opacity with poor graft prognosis
• Chemical injury, selected cases
• Aniridia
• Severe herpetic disease, selected cases
• Some eyes with autoimmune ocular-surface disease, although outcomes are more guarded

Contraindications or poor-prognosis factors

• No light perception or poor optic-nerve/macular potential
• Uncontrolled glaucoma
• Active ocular inflammation
• Severe dry keratinized surface without adequate reconstruction
• Inability to comply with lifelong follow-up

Complications

• Glaucoma progression
• Retroprosthetic membrane
• Sterile keratolysis
• Infectious keratitis/endophthalmitis
• Retinal detachment
• Device extrusion
• Vitreous hemorrhage
• Need for lifelong antimicrobial prophylaxis and bandage contact lens in typical Boston Type I KPro care

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7. Pterygium and Pterygium Surgery

Definition

Risk factors

• Chronic ultraviolet exposure
• Outdoor work
• Dust, wind and dry climate
• Chronic ocular-surface irritation
• Geographic “pterygium belt” exposure

Indications for surgery

• Progressive corneal encroachment threatening visual axis
• Induced irregular astigmatism or reduced vision
• Persistent inflammation/irritation despite conservative care
• Restricted motility or diplopia, uncommon
• Cosmetic concern after informed discussion
• Suspicion of dysplasia/OSSN, especially atypical, nodular, leukoplakic, rapidly growing or unusually vascular lesions

Surgical options

Conjunctival autograft technique

1. Excise pterygium head from cornea.
2. Remove fibrovascular body and Tenon tissue carefully.
3. Polish residual corneal tissue as needed.
4. Harvest superior bulbar conjunctival graft, often including limbal tissue.
5. Place graft over bare sclera with limbal edge oriented toward limbus.
6. Secure with sutures or fibrin glue.

Fibrin glue versus sutures

• Glue shortens operative time and improves comfort.
• Sutures are inexpensive and secure, but cause more postoperative inflammation and foreign-body sensation.

Mitomycin-C

• Delayed epithelial healing
• Scleral thinning or melt
• Necrotizing scleritis
• Secondary infection
• Corneal edema
• Cataract or glaucoma, rarely due to intraocular toxicity

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8. Toxic Contact-Lens-Related Ocular Surface Disease

Definition

Major mechanisms

1. Hypoxia: reduced oxygen transmission, especially with overnight wear
2. Mechanical injury: tight lens, poor fit, edge trauma, lens deposits
3. Solution toxicity: preservatives, hydrogen peroxide not neutralized, surfactants
4. Inflammatory/hypersensitivity reaction
5. Microbial infection: particularly Pseudomonas in contact-lens-associated keratitis

Clinical syndromes

Toxic keratitis: high-yield point

Management approach

1. Stop contact-lens wear immediately.
2. Remove lens and retain it/case for culture if microbial keratitis is suspected.
3. Assess epithelial defect, infiltrate size/location, AC reaction and vision.
4. Use preservative-free lubrication.
5. Treat lid disease, dry eye and fit problems.
6. Change to daily disposable lens or a preservative-free peroxide system only after complete recovery.
7. Avoid topical steroid until infection is excluded or controlled.
8. Educate: no overnight wear, no water exposure, no swimming/showering with lenses, strict hand hygiene and lens-case replacement.

Red flags for microbial keratitis

• Moderate/severe pain
• Reduced vision
• Central/paracentral infiltrate
• Epithelial defect over infiltrate
• Anterior-chamber reaction/hypopyon
• Rapid progression
• Contact-lens wearer with red painful eye

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Rapid Exam Revision

One-line definitions

• LSCD: failure of limbal stem-cell function causing conjunctivalization and epithelial instability of cornea.
• AMT: biological ocular-surface graft or dressing that promotes epithelialization and reduces inflammation, fibrosis and angiogenesis.
• OSSN: spectrum from conjunctival epithelial dysplasia to invasive squamous cell carcinoma.
• CXL: riboflavin-UVA photochemical strengthening of corneal stromal collagen to arrest ectatic progression.
• DALK: stromal corneal transplant preserving host Descemet membrane and endothelium.
• KPro: artificial cornea for repeated graft failure or very poor prognosis for conventional grafting.
• Pterygium: fibrovascular conjunctival growth crossing limbus onto cornea.

Most important viva distinctions

Recent-advance pearls

• SLET offers practical in vivo expansion of limbal epithelial cells using a small biopsy from the fellow eye.
• High-resolution anterior-segment OCT helps diagnose and monitor OSSN noninvasively.
• Topical interferon alpha-2b, 5-FU and mitomycin-C have shifted OSSN care from surgery-only to individualized medical-surgical management.
• Conventional epi-off CXL remains the reference treatment for progressive keratoconus.
• Accelerated, transepithelial and iontophoresis-assisted CXL are evolving alternatives, but may not have identical biomechanical effect.
• Cryopreserved amniotic membrane is particularly important in acute SJS/TEN and selected moderate ocular chemical burns.

Glaucoma: MS Ophthalmology Theory Revision

Topics

1. Basics of aqueous humor dynamics and IOP
2. Classification of glaucoma
3. Primary open-angle glaucoma (POAG)
4. Primary angle-closure disease (PACD)
5. Secondary glaucomas
6. Glaucoma evaluation: gonioscopy, disc, fields and OCT
7. Medical and laser treatment
8. Trabeculectomy
9. Glaucoma drainage devices / implants
10. MIGS
11. Neuroprotection in glaucoma
12. Recent advances and rapid viva points

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1. Fundamentals: Aqueous Humor and IOP

Aqueous humor production

Mechanisms

• Active secretion: major mechanism
• Ultrafiltration
• Diffusion

Functions

• Maintains IOP and globe shape
• Provides nutrition to avascular cornea and lens
• Removes metabolites
• Transports ascorbate and other substances
• Maintains optical clarity

Aqueous flow pathway

Conventional or trabecular pathway

Unconventional or uveoscleral pathway

• Ciliary muscle
• Supraciliary space
• Suprachoroidal space
• Sclera and venous circulation

Intraocular pressure

Goldmann equation

• F = aqueous formation rate
• C = outflow facility
• Pv = episcleral venous pressure

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2. Definition of Glaucoma

• Retinal ganglion-cell death
• Retinal nerve fiber layer loss
• Characteristic optic-disc cupping
• Corresponding visual-field defects

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3. Classification of Glaucoma

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4. Primary Open-Angle Glaucoma (POAG)

Definition

Risk factors

Pathogenesis

IOP-dependent mechanisms

• Increased resistance to aqueous outflow at trabecular meshwork
• Mechanical stress at lamina cribrosa
• Retinal ganglion-cell axonal compression
• Impaired axoplasmic flow
• Optic-nerve head ischemia

IOP-independent mechanisms

• Vascular dysregulation
• Low perfusion pressure
• Oxidative stress
• Mitochondrial dysfunction
• Glutamate excitotoxicity
• Neuroinflammation
• Genetic susceptibility

Clinical features

Symptoms

• Gradual peripheral-field loss
• Difficulty with dark adaptation
• Late tunnel vision
• Central vision affected only in advanced disease

Signs

• Raised IOP may be present
• Open angle on gonioscopy
• Optic-disc cupping
• Rim thinning/notching, especially inferotemporal and superotemporal
• Vertical cup enlargement
• RNFL wedge defects
• Disc hemorrhage
• Corresponding visual-field defects

Optic-disc changes

ISNT rule

Glaucomatous disc signs

• Progressive cup enlargement
• Vertical cup-to-disc asymmetry greater than about 0.2
• Focal rim notch
• Laminar-dot sign
• Bayonetting of vessels
• Nasal displacement of vessels
• Peripapillary atrophy
• Disc hemorrhage

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5. Visual Field Defects in Glaucoma

Early defects

• Increased pattern standard deviation
• Paracentral scotoma
• Nasal step of Roenne
• Seidel scotoma

Established defects

• Arcuate scotoma of Bjerrum
• Double arcuate scotoma
• Temporal wedge defect

Advanced disease

• Central island
• Temporal island
• Tubular field or tunnel vision

Important rule

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6. Diagnosis and Work-up of Glaucoma

1. Visual acuity and refraction
2. Slit-lamp examination
3. Goldmann applanation tonometry
4. Pachymetry
5. Gonioscopy
6. Dilated optic-disc assessment
7. Disc photographs
8. Visual-field testing
9. OCT RNFL and macular ganglion-cell analysis
10. Assessment of systemic risk, medications and family history

Gonioscopy

Why it is essential

• Open
• Narrow/occludable
• Closed
• Synechially closed
• Abnormally pigmented
• Neovascularized
• Recessed after trauma

Angle structures from anterior to posterior

Shaffer grading

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7. OCT in Glaucoma

Role

Main OCT parameters

RNFL pattern

• Superior peak
• Inferior peak
• Thinner nasal and temporal sectors

OCT interpretation: limitations

• Do not diagnose glaucoma from a color code alone.
• “Red disease” means false-positive abnormal classification.
• “Green disease” means falsely reassuring normal classification.
• Myopia, tilted disc, peripapillary atrophy, poor signal strength, segmentation error, retinal disease and media opacity can mislead.
• Always correlate OCT with disc appearance and visual field.

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8. Medical Treatment of Glaucoma

Therapeutic goal

• Baseline IOP
• Severity of damage
• Rate of progression
• Age and life expectancy
• Fellow-eye status
• Corneal thickness
• Risk factors such as disc hemorrhage or low perfusion pressure

• Mild disease: 20%-30% reduction
• Moderate disease: 30%-40% reduction
• Severe/progressive disease: often 40%-50% or more

Topical anti-glaucoma drugs

First-line medical choice

• Strong efficacy
• Once-daily dosing
• Limited systemic effects

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9. Laser Treatment

A. Selective Laser Trabeculoplasty (SLT)

Principle

Indications

• POAG
• Ocular hypertension
• Pseudoexfoliative glaucoma
• Pigmentary glaucoma, cautiously
• Alternative to first-line drops
• Poor adherence or intolerance to drops
• Add-on treatment

Advantages

• Outpatient procedure
• Repeatable in many cases
• Reduces dependence on drops
• Avoids preservative toxicity

Complications

• Transient IOP spike
• Mild anterior uveitis
• Peripheral anterior synechiae, rare
• Corneal edema, rare
• Limited response in heavily scarred or advanced angle disease

B. Argon Laser Trabeculoplasty

C. Laser Peripheral Iridotomy (LPI)

Indications

• Acute angle closure after initial IOP control
• Primary angle closure
• Occludable/narrow angle at risk of pupillary block
• Fellow eye of acute angle-closure attack
• Iris bombe from posterior synechiae

Mechanism

Complications

• IOP spike
• Inflammation
• Corneal burn
• Hyphema
• Dysphotopsia
• Closure of iridotomy

D. Laser Peripheral Iridoplasty

• Plateau iris
• Persistent appositional angle closure after LPI
• Some acute angle-closure settings when LPI cannot be done immediately

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10. Primary Angle-Closure Disease

Classification

Mechanisms

• Relative pupillary block
• Plateau iris configuration
• Thick/anterior lens
• Short axial length
• Hypermetropia
• Ciliary-body rotation
• Lens enlargement with age

Acute angle closure

Symptoms

• Severe ocular pain
• Headache
• Halos around lights
• Blurred vision
• Nausea and vomiting

Signs

• Markedly raised IOP
• Ciliary injection
• Corneal edema
• Shallow anterior chamber
• Mid-dilated fixed pupil
• Closed angle

Emergency management

1. Analgesic and antiemetic
2. Topical aqueous suppressants
3. Systemic acetazolamide unless contraindicated
4. Hyperosmotic agent such as mannitol if severe and medically suitable
5. Topical steroid
6. Pilocarpine once IOP has fallen enough for iris sphincter to respond
7. Definitive LPI when cornea clears
8. Prophylactic LPI in fellow eye, if indicated

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11. Trabeculectomy

Definition

Indications

• Progressive glaucoma despite maximum tolerated medical therapy and/or laser
• Advanced glaucoma requiring very low target IOP
• Poor adherence to medical therapy
• Rapid progression
• Inadequate response to MIGS or prior treatment
• Selected pediatric or secondary glaucomas

Basic steps

1. Conjunctival peritomy
2. Hemostasis
3. Mitomycin-C or 5-FU application where indicated
4. Partial-thickness scleral flap
5. Deep scleral block and internal ostium/sclerostomy
6. Peripheral iridectomy
7. Adjustable/releasable scleral flap sutures
8. Conjunctival watertight closure
9. Formation of diffuse posterior bleb

Antimetabolites

• Mitomycin-C: stronger anti-fibrotic effect
• 5-Fluorouracil: intraoperative or postoperative use

Complications

Early

• Hypotony
• Shallow/flat anterior chamber
• Choroidal detachment
• Hyphema
• Bleb leak
• Malignant glaucoma
• Suprachoroidal hemorrhage
• Bleb failure due to fibrosis

Late

• Bleb leak
• Bleb-related infection or blebitis
• Endophthalmitis
• Hypotony maculopathy
• Cataract
• Dysesthesia
• Encapsulated bleb
• Ptosis

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12. Glaucoma Drainage Devices (GDDs)

Definition

Components

1. Tube
2. Plate/end plate
3. Tube-covering graft: sclera, cornea, pericardium or synthetic material
4. Conjunctival covering

Classification

Indications

• Previous failed trabeculectomy
• Extensive conjunctival scarring
• Neovascular glaucoma
• Uveitic glaucoma
• Post-keratoplasty glaucoma
• Aphakic/pseudophakic glaucoma
• Iridocorneal endothelial syndrome
• Epithelial ingrowth
• Complex pediatric glaucoma
• Traumatic glaucoma
• Refractory glaucoma after multiple surgery

Surgical principles

1. Select quadrant, commonly superotemporal.
2. Secure plate posteriorly beneath rectus muscles.
3. Create a scleral tunnel.
4. Insert tube into anterior chamber, ciliary sulcus, or pars plana.
5. Cover tube with patch graft.
6. Ensure watertight conjunctival closure.

Non-valved implant

Complications

Tube position

• Anterior chamber placement is standard in many eyes.
• Sulcus placement may reduce endothelial risk in pseudophakic eyes.
• Pars plana placement requires prior or concurrent adequate vitrectomy.

Ahmed versus Baerveldt: classic comparison

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13. MIGS: Minimally Invasive Glaucoma Surgery

Definition

Main categories

Indications

• Mild-to-moderate open-angle glaucoma
• Cataract surgery combined with IOP-lowering intervention
• Medication intolerance or poor adherence
• Target IOP not extremely low
• Open angle with accessible trabecular meshwork

Limitations

• Conventional trabecular MIGS cannot lower IOP below episcleral venous pressure.
• Not generally suitable as sole therapy for severe rapidly progressive glaucoma needing very low IOP.
• Bleb-forming “MIGS” may achieve lower pressures but have bleb-related risks.

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14. Neuroprotection in Glaucoma

Definition

Why it is needed

• Normal-tension glaucoma
• Advanced glaucoma
• Eyes with vascular dysregulation
• Eyes with disc hemorrhage or low ocular perfusion pressure

Proposed mechanisms of ganglion-cell damage

• Mechanical laminar stress
• Ischemia and reperfusion injury
• Oxidative stress
• Mitochondrial dysfunction
• Excitotoxicity from glutamate
• Calcium influx and apoptosis
• Neuroinflammation
• Reduced neurotrophic-factor support

Potential neuroprotective strategies

Exam conclusion on neuroprotection

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15. High-Yield Secondary Glaucomas

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16. Recent Advances in Glaucoma

• Selective laser trabeculoplasty is increasingly used as first-line or early treatment for open-angle glaucoma.
• Preservative-free fixed combinations reduce drop burden and ocular-surface toxicity.
• Rho-kinase inhibitors offer a new pharmacological mechanism by improving trabecular outflow.
• Sustained-release delivery systems and drug-eluting implants are evolving, with availability varying by country.
• MIGS has expanded options for mild-to-moderate open-angle glaucoma, especially with cataract surgery.
• Bleb-forming microshunts occupy an intermediate space between trabeculectomy and traditional MIGS.
• Swept-source OCT, BMO-MRW, macular GCIPL and OCT angiography improve structural assessment, but do not replace optic-disc examination and perimetry.
• Artificial intelligence is being developed for disc-photo, OCT and visual-field interpretation, but needs clinician oversight and validation across populations.
• Neuroprotection through mitochondrial/metabolic pathways, including nicotinamide, remains investigational.

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Rapid Viva Answers

What is the most important modifiable risk factor in glaucoma?

What is the definitive test to classify angle as open or closed?

What is the first-line treatment for most POAG patients?

What is the hallmark of glaucoma on OCT?

Why is a thin cornea important?

What is a trabeculectomy?

When do you prefer a tube shunt?

What is the only proven neuroprotective treatment?

What is the difference between PAC and PACG?

5. Anterior segment / iris / diagnostic imaging

1. Pupilloplasty
   • Indications: traumatic mydriasis, iris defects, dysphotopsia, surgical iris loss
   • Techniques: McCannel, Siepser slipknot, single-pass four-throw, cerclage
   • Complications and selection of technique
2. Ultrasound biomicroscopy (UBM)
   • Principle, probe frequencies and image interpretation
   • Indications: angle-closure mechanism, plateau iris, ciliary body tumors, iris lesions, IOL position, trauma
   • UBM versus AS-OCT

6. General ophthalmic technology and materials

1. Ophthalmic viscosurgical devices (OVDs)
   • Cohesive, dispersive, viscoadaptive and viscous-dispersive types
   • Soft-shell technique
   • Uses in cataract, glaucoma and endothelial protection
   • Postoperative IOP rise and other complications
2. Ophthalmic lasers
   • Basic laser physics: wavelength, coherence, collimation, tissue interaction
   • Argon/532 nm, diode, Nd:YAG, femtosecond, excimer
   • Retinal photocoagulation, YAG capsulotomy/iridotomy, SLT, cyclophotocoagulation
3. Ophthalmic dyes
   • Fluorescein, rose bengal, lissamine green, trypan blue, indocyanine green, brilliant blue G
   • Mechanism, indications, interpretation, toxicities
4. Tissue adhesives / glues
   • Cyanoacrylate, fibrin glue and newer biomaterials
   • Corneal perforation, conjunctival autograft, amniotic membrane and lamellar graft fixation
   • Technique, contraindications and complications

Big-picture overview

• UBM versus AS-OCT
• Cohesive versus dispersive OVD
• Nd:YAG versus argon laser
• Fluorescein versus rose bengal versus lissamine green
• Cyanoacrylate versus fibrin glue
• Siepser versus McCannel pupilloplasty

1. Pupilloplasty
2. UBM
3. OVDs
4. Lasers
5. Dyes
6. Tissue glues