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Glaucoma Management - Ophthalmology Resident Guide

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1. Definition and Goal of Treatment

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2. Classification

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3. Primary Open-Angle Glaucoma (POAG)

Risk Factors

• IOP: The higher the IOP, the greater the risk. Asymmetry ≥4 mmHg is significant.
• Age: More common with advancing age.
• Race: 4x more prevalent in Black individuals; earlier onset and harder to control.
• Family history: 4x risk to siblings, 2x risk to offspring.
• Myopia: Associated with increased incidence and susceptibility.
• CCT: Thin central corneal thickness is an independent risk factor.
• Optic disc area: Larger discs are more vulnerable.
• Anti-VEGF therapy: Recurrent intravitreal injections (especially bevacizumab) may cause sustained IOP elevation.
• Genetics: MYOC gene (myocilin) and OPTN gene (optineurin) mutations; polygenic risk scoring is emerging.

Pathogenesis of Optic Neuropathy

Natural History (EMGT Data)

• High-tension glaucoma (HTG): -1.31 dB/year
• Normal-tension glaucoma (NTG): -0.36 dB/year
• Pseudoexfoliation glaucoma: -3.13 dB/year (most aggressive)

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4. Optic Disc Assessment

Glaucomatous Disc Changes

• Focal ischaemic - inferior notch (most common)
• Myopic - temporal crescent with inferior NRR loss
• Sclerotic - superior shelving and inferior notching
• Concentric - deep uniform cup enlargement

• Notching (focal thinning) - most significant
• Thinning of inferior or superior poles first
• Vertical C/D ratio enlargement (C/D >0.7 or asymmetry >0.2 is suspicious)

• Disc haemorrhage (Drance haemorrhage) - risk factor for progression; don't miss it without magnification
• Baring of circumlinear vessels - early NRR thinning
• Bayoneting of vessels - double angulation from NRR loss
• Laminar dot sign - exposed lamina cribrosa fenestrations in advancing glaucoma
• RNFL defects - wedge-shaped, best seen by red-free photography

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5. Visual Field Defects

1. Early: Small paracentral scotomas (often superonasal), increased response variability
2. Nasal step - sensitivity difference above/below horizontal midline (bounded by the horizontal raphe)
3. Temporal wedge (less common)
4. Arcuate defect - coalescence of paracentral scotomas, 10-20° from fixation
5. Ring scotoma - superior and inferior arcuates become continuous
6. End-stage - small central island + temporal island

• GHT (Glaucoma Hemifield Test) outside normal limits
• ≥3 non-edge points depressed on PSD at P<5%, at least one at P<1%
• Corrected PSD occurring in <5% of normal individuals

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6. Imaging in Glaucoma

• OCT (Optical Coherence Tomography): RNFL thickness, optic nerve head parameters, macular ganglion cell complex - essential for structural monitoring. Detects pre-perimetric loss.
• HRT (Heidelberg Retinal Tomography): 3D optic disc topography; Moorfields Regression Analysis
• GDx (Nerve Fibre Analyser): Scanning laser polarimetry for RNFL
• OCT Angiography: Emerging - detects reduced optic disc perfusion density in glaucoma

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7. IOP Measurement

• Goldmann applanation tonometry (GAT): Gold standard
• Correction for CCT: Readings are overestimated in thick corneas and underestimated in thin corneas (e.g. post-LASIK, corneal ectasia, low CCT in NTG patients)
• Diurnal curve / phasing: IOP fluctuation of >5 mmHg is significant; peak IOP often in the morning
• Target IOP: Individualized - typically aim for at least 20-30% reduction from baseline. AGIS data: <18 mmHg at all times significantly reduces progression risk.

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8. Medical Therapy

Drug Classes

Review Protocol

• First review after starting: 4-8 weeks
• If satisfactory: reassess at 3-6 months
• If no response: switch the drug
• If partial response: add a second agent
• Leave 5 minutes between drops (prevent washout)

Causes of Treatment Failure

• Inappropriate (too high) target pressure
• Poor adherence (≥25% of patients)
• Wide diurnal IOP fluctuations
• Check that morning drops were taken before clinic visit

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9. Laser Treatment

Selective Laser Trabeculoplasty (SLT)

• Selective photothermolysis of trabecular meshwork pigmented cells
• Suitable as first-line alternative to drops (LiGHT trial showed non-inferiority to medication as initial treatment)
• IOP reduction ~25-30%
• Repeatable (unlike ALT)
• Side effects: transient IOP spike, mild anterior uveitis

Argon Laser Trabeculoplasty (ALT)

• Thermal coagulation of trabecular meshwork
• Largely replaced by SLT
• Not easily repeatable

Laser Peripheral Iridotomy (LPI)

• Standard treatment for primary angle closure and prevention in fellow eye after APAC
• Creates alternative aqueous drainage route, bypasses pupillary block
• Nd:YAG laser (sometimes preceded by argon for pigmented irides)
• Prophylactic LPI in PAC suspects with narrow angles

Laser Iridoplasty (ALPI - Argon Laser Peripheral Iridoplasty)

• For plateau iris syndrome after LPI
• Burns peripheral iris stroma, contracting it away from trabeculum

Cyclodiode / Cyclophotocoagulation

• Destroys ciliary body epithelium to reduce aqueous production
• Used in refractory glaucoma, painful blind eyes, poor surgical candidates
• Risk: hypotony, phthisis bulbi

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10. Surgical Treatment

Trabeculectomy

• Guarded filtration surgery - creates a fistula with scleral flap
• First-choice incisional procedure for POAG
• Antimetabolites: Mitomycin C (MMC) or 5-FU applied intraoperatively to reduce scarring (essential in higher-risk eyes)
• Target IOP post-op: typically low teens

• Early: shallow AC, hypotony, choroidal effusion, bleb leak, encapsulated bleb
• Late: bleb-related endophthalmitis (0.5-1.5% lifetime risk), cataract, hypotony maculopathy, dysesthetic bleb

Glaucoma Drainage Devices (GDDs/Tubes)

• Tube shunts (Ahmed, Baerveldt, Molteno)
• Indicated when trabeculectomy has failed or is likely to fail (uveitic glaucoma, NVG, aniridic glaucoma, failed conjunctiva)
• Provide best long-term IOP control in complex cases
• Tube-Versus-Trabeculectomy (TVT) Study: similar efficacy at 5 years, tubes had fewer re-operations

Minimally Invasive Glaucoma Surgery (MIGS)

• iStent, iStent Inject, Hydrus Microstent (Schlemm's canal)
• Kahook Dual Blade goniotomy, OMNI (ab interno trabeculotomy)
• XEN Gel Stent (subconjunctival drainage)
• CyPass Micro-Stent (supraciliary) - withdrawn due to corneal endothelial loss
• Best suited for mild-moderate glaucoma, often combined with cataract surgery
• Lower complication profile than trabeculectomy; more modest IOP reduction

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11. Normal-Tension Glaucoma (NTG)

Definition

Key Differences from POAG

• IOP-independent vascular mechanisms are relatively more important
• Disc haemorrhages more frequent and associated with greater progression risk
• VF defects tend to be closer to fixation, deeper, steeper, and more localized
• More common in Japanese patients; more common in females; associated with migraine, Raynaud phenomenon, systemic hypotension
• Lower CCT on average than POAG

Treatment

• Prostaglandins are first-line
• Brimonidine may provide neuroprotection beyond IOP reduction (preferred over beta-blockers in NTG)
• Betaxolol (selective β1-blocker) preferred over timolol to avoid nocturnal BP dips
• SLT is a reasonable initial option
• Surgery when progression occurs despite IOP in low teens
• Control systemic vascular risk factors (diabetes, HTN, hyperlipidaemia)
• Systemic calcium-channel blockers to address vasospasm in selected cases
• Nocturnal hypotension: Reduce antihypertensive dose if large nocturnal BP dips detected; advise sleeping head-up 30° (reduces IOP ~20% in flat vs. 30° position in a third of patients)
• The Collaborative Normal-Tension Glaucoma Study showed 30% IOP reduction reduced progression rate

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12. Primary Angle-Closure Glaucoma (PACG)

Gonioscopy - Shaffer Grading

Classification

• PAC Suspect (PACS): Narrow angle on gonioscopy, no ITC, no PAS, normal IOP and disc
• Primary Angle Closure (PAC): ITC present, ± PAS or raised IOP, but no optic nerve damage
• Primary Angle-Closure Glaucoma (PACG): All of above + optic nerve/VF damage

Mechanisms

• Pupillary block (most common) - relative block at pupillary margin, aqueous diverts posteriorly, forward bowing of iris
• Plateau iris - anteriorly rotated ciliary processes, angle occlusion even after patent LPI
• Phacomorphic - large/intumescent lens pushes iris-lens diaphragm forward
• Malignant glaucoma (ciliolenticular block) - aqueous misdirected into vitreous cavity

Risk Factors

• Female sex, age ~62 at presentation
• Asian ethnicity (especially Far Eastern and South Asian)
• Hypermetropia, short axial length
• Positive family history
• Precipitants of acute attack: dim lighting, pharmacological mydriasis, parasympathetic antagonists, topiramate/sulfa drugs (ciliary body effusion), semi-prone position

Acute Primary Angle Closure (APAC) - Emergency Management

• IOP markedly elevated (often 50-80 mmHg)
• Conjunctival injection, corneal epithelial oedema
• Shallow AC, mid-dilated fixed pupil
• Glaukomflecken (anterior lens opacities)

1. Patient lies supine (gravity encourages lens to shift posteriorly)
2. Acetazolamide 500 mg IV if IOP >50 mmHg; oral if <50 mmHg (contraindicated: sulfonamide allergy, topiramate-induced attack)
3. Single drops of: apraclonidine 0.5-1% + timolol 0.5% + prednisolone 1% / dexamethasone 0.1% (3-5 min apart)
4. Pilocarpine 2% × 1-2 drops to affected eye (NOT if IOP >40 mmHg - ischaemia impairs action; also 1% to fellow eye prophylactically)
5. Analgesia + antiemetic as needed

• Central corneal indentation with squint hook or goniolens (forces aqueous into angle)
• 50% topical glycerol to clear corneal oedema first
• IV mannitol 20% (1-2 g/kg over 1 hour) or oral glycerol 50% (1 g/kg) or oral isosorbide
• Early Nd:YAG iridotomy after clearing oedema (iridoplasty as alternative)
• Paracentesis as last resort

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13. Secondary Glaucomas

Pseudoexfoliation Glaucoma (PXG)

• Most common secondary open-angle glaucoma worldwide
• PXF material (abnormal extracellular fibrillar material) clogs the TM
• Higher IOP, worse diurnal fluctuation, faster progression than POAG
• Responds well to SLT
• Associated with increased surgical complication risk (weak zonules - phacodonesis, capsular complications)
• Systemic: cardiovascular disease, dementia associations

Pigmentary Glaucoma

• Young myopic males
• Iris pigment (Krukenberg spindle on corneal endothelium) and heavy trabecular pigmentation
• Exercise or pupillary dilation can acutely spike IOP
• May spontaneously "burn out" as iris pigment depletes with age
• Laser iridotomy may reduce pigment dispersion (controversial)
• SLT very effective

Neovascular Glaucoma (NVG) - "100-Day Glaucoma"

• Caused by rubeosis iridis (iris neovascularization) from retinal ischaemia
• Main causes: ischaemic CRVO (35-50%), diabetes (10-15%), CRAO, ocular ischaemic syndrome
• Vessels at pupillary margin → iris surface → angle → fibrovascular membrane → angle closure
• Management:
  • Anti-VEGF (intravitreal): Rapidly reduces neovascularization, buys time for definitive treatment
  • Panretinal photocoagulation (PRP): Addresses ischaemic drive (definitive)
  • IOP-lowering drops (cyclodestructive procedures or GDD when refractory)
  • Trabeculectomy has poor outcomes; GDD preferred for surgical management

Steroid-Induced Glaucoma

• Topical > periocular > systemic > inhaled
• Posterior sub-Tenon's injections: prolonged risk (weeks-months after injection)
• Open-angle mechanism: steroid receptor activation reduces aqueous outflow through TM
• Managed by cessation/switching of steroid + standard IOP-lowering treatment
• May require surgery in resistant cases

Inflammatory (Uveitic) Glaucoma

• Mechanisms: trabeculitis/TM oedema (open-angle), PAS (angle-closure), seclusio pupillae and iris bombé (pupillary block), steroid effect
• Ciliary body shutdown in acute uveitis may mask underlying high IOP tendency
• Management: aggressive treatment of uveitis; use topical CAI or alpha-agonist (avoid prostaglandins - may worsen inflammation and CMO); cycloplegic to break posterior synechiae; LPI for iris bombé; surgery (trabeculectomy ± MMC or GDD) in refractory cases

Lens-Related Glaucoma

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14. Monitoring Protocol

• VF: MD worsening >1 dB/year OR Pointwise regression
• Structure: OCT RNFL significant thinning outside normal limits on serial comparison
• Always correlate structural and functional data

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15. Special Situations

Ocular Hypertension (OHT)

• IOP >21 mmHg without structural or functional damage
• OHTS data: 5-year risk of conversion to POAG ~10% untreated; treatment reduces this by 50%
• Treatment thresholds consider: IOP level, CCT (thin CCT dramatically increases risk), disc appearance, VF, age, race

Glaucoma Suspect

• Structural changes (suspicious disc, RNFL defect, OCT outside normal) WITHOUT VF loss = pre-perimetric glaucoma - treat or monitor closely

Glaucoma in Special Populations

• Children: Suspect congenital glaucoma if buphthalmos, epiphora, photophobia, Haab striae on cornea. IOP may be normal under GA. Treat surgically (goniotomy or trabeculotomy).
• Pregnancy: Avoid acetazolamide (teratogenic) and prostaglandins. Beta-blockers are relatively safe. Timolol may cause neonatal bradycardia.
• Pseudophakia: Capsular block syndrome, alpha-2 agonist still usable; prostaglandins are safe.

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16. Key Clinical Trials to Know

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17. Practical Tips for Residents

1. Always perform gonioscopy in a darkened room - PAC is more prevalent than previously realized.
2. Disc haemorrhage = red flag - risk factor for progression; magnification essential.
3. CCT must be measured in every glaucoma patient - it critically affects IOP interpretation and risk stratification.
4. Poor adherence is ubiquitous (≥25%) - ask about drop technique, timing, and cost at every visit.
5. Never rely on IOP alone - assess structure (disc, OCT) and function (VF) together.
6. In NTG, look for nocturnal BP dips - advise head-up sleeping position and avoid bedtime beta-blockers.
7. Anti-VEGF for NVG before any surgery - neovessels regress dramatically within days; reduces operative bleeding.
8. Pilocarpine in APAC is withheld if IOP >40 mmHg - ischaemic iris sphincter won't respond.
9. MIGS is for mild-moderate glaucoma combined with phaco - don't expect trabeculectomy-level IOP reduction.
10. The worse the baseline damage, the lower the target IOP - progressive loss of ganglion cells means each remaining cell counts more.

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