GLAUCOMA
- Any of
- ↑↑ IOP
- Visual field defect
- Fundus changes → Cupping
- C:D ratio > 0.3

Theories of Glaucoma
Theory | Key Factor | Mechanism | Outcome |
Mechanical | ↑ IOP | Narrowing of lamina cribrosa openings in sclera → ↓ Axoplasmic outflow (ON dysfunction) | Optic atrophy |
Ischemic/Vascular | IOP independent / Structural vascular changes | ↓ Perfusion of optic disc | Optic atrophy |
- Ganglion cells are affected in glaucomatous optic atrophy

Pathophysiology & Types
- Optic neuropathy:
- Progressive, characteristic optic disc changes.
- Irreversible visual field defects.
- IOP: Normal (11-21 mmHg) or raised.
- Glaucoma occurs due to:
- Increased aqueous production.
- Decreased aqueous clearance.
- Aqueous Flow:
- Ciliary processes secrete aqueous → Trabecular meshwork (site of outflow) → Schlemm’s canal → Aqueous vein → Episcleral vein.


Feature | Primary Open Angle Glaucoma (POAG) | Primary Angle Closure Glaucoma (PACG) |
CF | Gradual painless LOV | Sudden painful LOV |
Angle between iris & cornea | Wide | Narrow |
Pathology | Defective trabecular meshwork | Anterior displacement of iris |
Cause | • Myopia • > 40 yrs • Family history | Pupil block → Eg: after movie theatre Mid dilated fixed pupil |
Anterior Chamber (AC) | Deep | Shallow |
Treatment | Drugs f/b B/L Laser Trabeculoplasty / Trabeculectomy | Iridectomy / Iridotomy If anterior synachiae > 270 degree • Trabeculectomy + Mitomycin C |


Malignant glaucoma
- After Intraocular Surgery
- Common in Hypermetropic eyes
- Causes Ciliary block & aqueous misdirection → Glaucoma
- Rx
- Atropine
- Cycloplegic → Relieves ciliary block
- NOTE: Atropine C/I in POAG

ANS
- Laser iridotomy Ineffective once synechial closure exceeds 270°
- Trabeculectomy with mitomycin C
High-Risk Factors for Progression of Ocular Hypertension to POAG
- Ageing
- Raised IOP
- > 30 mmHg
- Central Corneal Thickness (CCT)
- < 550 microns
- Optic Disc Changes
- Increased Cup : Disc ratio > 0.7
- Splinter Hemorrhages
- Pattern Standard Deviation (PSD) on Humphrey Visual Field Analyzer
Investigations
Optic Disc Examination
- Direct ophthalmoscopy:
- Magnification 15 times.
- Visualizes central fundus.
- Disadvantage: No binocular vision.
- Slit lamp biomicroscopy:
- Magnification with +90 D lens.

Visual Field Examination (Perimetry)
- Manual
- listers perimeter

- Automated
- Humphrey field analyser


- Kinetic:
- Moving targets (not preferred).
- Static:
- Idle targets (e.g., Humphrey Field Analyzer (HFA)).
- Normal Visual Field:
- Horizontally oval with an infero-nasal notch.
- Superior: Minimum Visual field
- Temporal: Maximum Visual field

IOP Measurement (Tonometry)

- Indentation tonometry:
- Schiotz tonometer (not preferred).
- Non-contact tonometry:
- Choice for screening in camps.
- Puff air
- Ocular response analyser (Advanced)
- Tonopen
- For scarred cornea
- Rebound tonometer
- For self-monitoring
- Self monitoring to prevent Rebound
- Transpalpebral tonometry
- Diaton, Proview
- Visualized through eyelid.
- Fixed area tonometers:
- Goldmann’s
- Mackey marg:
- Choice for edematous irregular cornea.
- Mnemonic: Margam illathapo Mackey marg
- Goldmann’s Applanation tonometry
- Principle: Imbert Fick law (Pressure = Force/Area).
- Uses fluorescein dye and cobalt blue light
- Gold standard.
- Mnemonic: Gold is gold
- Most commonly done

- Pascals tonometer
- Now better than Goldmann
- Pascal was a better man
- Maklakov tonometer
- Variable application surface
- Makkalkk variable swabavam


Examination of Anterior Chamber Angle
- Closed Her in Anterior Chamber
- Heri Ick () gone (Gonioscopy) when Flashed (Oblique flashlight) light
- Van Herick’s Method:
- Compares
- peripheral anterior chamber depth (PACD) and
- corneal thickness (CT) using slit lamp
- PACD = CT:
- Open angle.
- PACD < 1/4 CT:
- Shallow AC (closed/closing angle).
- Mnemonic: Her in a Van → with slit lamp check her thickness → Anterior chamber

- Oblique Flashlight Test:
- Shadow over nasal iris ⇒ Angle closure glaucoma.

- Gonioscopy:
- Best method
- But gold standard is Goldman
- Principle: Overcomes total internal reflection.
- Contraindication: Dilated pupil.
- Direct gonioscope:
- Richardson/ Koeppe
- Structures seen: Mnemonic: I can see till schwalbe line
- Iris
- Ciliary body.
- Scleral spur.
- Trabecular meshwork.
- Schwalbe’s line (Peripheral termination of Descemet’s membrane).


Primary Open Angle Glaucoma (POAG)



- Mnemonic:
- POAG → Open → Open (Optineurin) My (Myocilin) World 360 degree (WDR 36)
- Old people (Senile) become Alpha (Alpha is specific) → Rims (Neuroretinal rim)
- Amina (Lamina) in net (Bayonetting) dress with cups (Vertical cupping)
- and dots (Laminar dot sign)
- Chronic disease.
- Common in age >50 years.
- Positive family history.
- Genes: WDR 36, optineurin, myocilin.
Symptoms
- Headache.
- Delayed dark adaptation.
- Frequent change in presbyopic spectacles.
Enlarged blind spot is seen in
- POAG
- Papilledema
- Medullated nerve fibers
- Optic disc drusen
- Coloboma of optic disc and myopic disc with crescent.
Criteria
- IOP >21 mmHg OR
- >5 mmHg difference between both eyes.
- > 8 mmHg difference in diurnal variation
Other signs
- RAPD or Marcus Gunn Pupil
Optic Disc Changes
- Loss of neuroretinal rim (inferior).
- Vertical cupping (c/d ratio >0.5).
- Bayonetting sign (double angulation of blood vessel)
- Laminar dot sign.
- Peripapillary atrophy:
- Alpha zone: Specific.
- Beta zone: Also seen in myopia.
Visual Field Changes




- Earliest sign on perimetry:
- Isopter contraction (Constriction of peripheral VF)

- Baring of blind-spot.
- In bjerrum area affecting nerve fibres
- Paracentral scotoma
- Earliest clinically visible manifestation
- Seidel’s scotoma:
- Comma shaped, connects with blind spot.
- Bjerrum/Arcuate scotoma:
- Arches to opposite side, affects arcuate nerve fibres in Bjerrum’s area.
- Ring/Double arcuate scotoma:
- Central vision spared
- Roenne’s nasal step:
- Due to unequal contraction of upper & lower hemispheres.
- → Loss of Central vision
- → Loss of temporal island vision (last to be lost).
Normal Tension Glaucoma (NTG)
- Defined by: OD changes + VF changes + Normal IOP.
- Commonly associated with:
- Raynaud phenomena.
- migraine.
- ↓ blood flow velocity in ophthalmic artery.
- Rx: Lifestyle changes
Adrenochrome deposits
- Seen in conjunctiva
- After chronic use of topical epinephrine for Glaucoma

Medical Management (Topical drugs):
Drug Class | Mechanism of Action |
Prostaglandin analogs | • ↑ Uveoscleral outflow |
Nitric Oxide (NO) | • ↑ Trabecular outflow |
β-blockers | • ↓ Aqueous production |
Carbonic Anhydrase Inhibitors | • ↓ Aqueous production |
α-Agonists | • ↓ Aqueous production + • ↑ Trabecular outflow (Apraclonidine) / • ↑ Uveoscleral outflow (Brimonidine) |
Rho Kinase Inhibitor | • ↓ Aqueous production • ↑ Trabecular outflow via: → Actin-myosin contraction → ↓ Episcleral venous pressure |
Mechanism | Drug Classes |
↑ Trabecular outflow | • Nitric Oxide • α-Agonists → Apraclonidine • Rho Kinase Inhibitor Trap → No () Trap, A clone () → its Risky () |
↑ Uveoscleral outflow | • Prostaglandin analogs • α-Agonists → Brimonidine UV put PGs in Brim |
↓ Aqueous production | • β-blockers • Carbonic Anhydrase Inhibitors (CAIs) • α-Agonists • Rho Kinase Inhibitor All inhibitors + α agonist → ↓ Aquous pdn |
Prostaglandin F2α (PGF2α):
- Latanoprost (DOC).
- Increases uveoscleral outflow.
- Side effects:
- Hypertrichosis.
- Bimatoprost → FDA approved for hypotrichosis
- Hyperpigmentation of iris.
- Cystoid macular edema.
- Uveitis
- Contraindicated in patients with signs of uveitis
- like aqueous flare, corneal precipitants
- Reactivation of Herpes keratitis
- Take h/o previous corneal/herpetic infections
- Mnemonic:
- PGs got herpes () at a CME ().
- They are afraid of UV (Uveitis, ↑ Uveoscleral outflow).
- Drug: Latanoprostene bunod (Prodrug)
- MOA: On administration, breaks down → Latanoprost + Butadenol (Unstable)
- Latanoprost → ↑ Uveoscleral outflow
- Butadenol breakdown → Nitric oxide ↑↑
- Nitric oxide → Relaxes trabecular meshwork → ↑ Trabecular outflow
β-blockers:
- Timolol (non-selective).
- Decreases aqueous production.
- Side effects:
- Corneal anesthesia on continuous use (especially Timolol)
- Nasolacrimal duct (NLD) blockage.
- Blepharoconjunctivitis
- Aphakic cystoid macular edema:
- Specific to Betaxolol
- Mnemonic: Beta blocker → Beat the eye → No pain bcz corneal anasthesia () → But got NLD blockage () and Conjunctivitis ()
α-agonists:
- Apraclonidine:
- Decreases aqueous production + increases trabecular outflow.
- More preferred agent for glaucoma.
- DOC for post laser rise in IOP.
- Side effects:
- Eyelid retraction,
- mydriasis (d/t α₁ > α₂ agonism)
- follicular conjunctivitis
- Mnemonic:
- Apraclonidine → Appan → Open our eyes (Mydriasis and eye lid retraction) → Give flower (Follicular conjunctivitis) → Wipe our tears (↓ aquous pdn and ↑outflow) → All this after laser surgery
- Brimonidine:
- Contraindicated in children and infants
- 2nd line agent for glaucoma.
- Decreases aqueous production (+ ↑ Uveoscleral outflow)
- CNS suppression due to crossing of BBB.
- Drowsiness
- apnea
- depression
- UV put everyone on Brim → Cause depression
- Not recommended for Children
Carbonic anhydrase inhibitors:
- Acetazolamide - emergency drug.
- Dorzolamide: Rx of childhood glaucoma
- MOA:
- Inhibit CA II isoform on sphincter pupillae & ciliary muscle
- ↓ Aqueous production
- Mnemonic: Car nte dooril child kudungi (Car → Dorzolamide → For childhood)
Pilocarpine
- S/E
- Miosis
- NLD stenosis
Rho kinase inhibitors:
- Netarsudil
- Dual action drug
- ↓ Aqueous production
- ↑ Trabecular outflow by:
- Promoting actin-myosin contraction
- ↓ Episcleral venous pressure
- Side effects:
- Congestion/hyperemia
- Corneal verticillata: (Spindle shaped deposits)
- Subconjunctival haemorrhage
NOTE
- Vortex Keratopathy / cornea verticillata
- Whorl like/Spindle pattern
- Also seen in Queen () Ami () Tame () with Netram () in Indian () Fabric () dress
- Chloroquine
- Amiodarone
- Tamoxifene
- Netarsudil (Rho kinase ⛔),
- Indomethacin
- Fabry’s disease
- Phenothiazines
- NOT Methotrexate

Surgical Management:
- Increases trabecular outflow.
1. CLOSED SURGERY
Laser trabeculoplasty:
- Acts on trabecular meshwork (TM).
- Improves aqueous outflow.
- Best response:
- Pseudoexfoliation
- Pigmentary glaucoma

- Photocoagulation
- Argon laser (514 nm)
- SLT (Selective LT) (532 nm)
- TOC for prophylaxis in other eye
- Mnemonic: Do Urgent (Argon) Laser in POAG, but Selective (SLT) laser in other eye
Indications
- OAG uncontrolled on medical therapy
- OAG with poor compliance
- OAG with poor drug tolerance
- Pseudoexfoliative glaucoma.
- Pigmentary glaucoma.
- Angle-closure glaucoma
- Only after patent iridotomy.
- Or Anterior Synechiae > 270 degree
- Temporary IOP control
- When glaucoma surgery must be deferred
Contraindications
- Inflammatory glaucoma
- Advanced glaucoma
- Poor visualization of TM
- Due to synechiae.
- Laser cannot act on TM.
2. OPEN SURGERY
a. Penetrating Surgery
- Trabeculectomy:
- Best surgery.
- Creating fistula b/w AC and subtenon space → Aqueous drainage.

b. Non-penetrating Surgery:
- Viscocanalostomy
- Deep sclerectomy
SURGERY WITH IMPLANTS
- Done for resistant glaucoma.
1. Seton Surgery
- Implants a glaucoma drainage device.
- Parts:
- Tube → Inserted into AC (Sub-tenon or subconjunctivally) → Enables outflow.
- Plate → Positioned in sub-tenon space → Collects fluid.
- Types of Drainage Device
- Non-valved:
- Continuous outflow.
- Examples:
- Express mini shunt (made of stainless steel) → like express train
- Baerveldt device → 4 Bore wells
- Malteno device → Malt → Motta
- Valved:
- Stops outflow when required.
- Example: Ahmed Glaucoma Valve (AGV).
- Ahmed’s Sperm

2. MIGS (Minimally Invasive Glaucoma Surgery).
- Stents through TM (Trabecular Meshwork) → Enables outflow.
- Advantages:
- Small incision
- ↓ Chance of post-operation infection (e.g., Endophthalmitis)

Ex-PressTM implant


Ahmed glaucoma valve

Molteno implant

Baerveldt implant


Primary Angle Closure Glaucoma (PACG)

- Acute disease.
- Other Causes:
- TCA → Clomipramine, Amitryptilline
- Citalopram
Pathogenesis

Relative pupillary block (pupillary margin touches lens)
- → No aqueous flow (posterior to anterior chamber)
- → Iris pushed forward (Iris bombe)
- → Irido-trabeculo-corneal contact
- → Peripheral anterior synechiae formation
- → PACG.
Clinical Features
- Headache.
- Severe eye pain (IOP >40 mmHg, rock hard eye).
- High IOP disrupts endothelium causing corneal edema.
- Distorted vision (due to hazy cornea).
- Redness of eye.
- Vomiting.
- Halos around lights (prismatic dispersion due to corneal edema).
Signs

- Eclipse sign:
- Shadow over nasal iris
- Oblique flashlight test
- Posterior synechiae
- adhesion between pupillary margin & lens
- Anterior synechiae
- between iris and cornea
- Both anterior and posterior synechiae are seen
- Vogt’s triad: VOGT → Vertically Oval, Glaucomflecken, aTrophy Iris
- Iris aTrophy.
- Glaucomflecken
- Lens epithelium necrosis → white or grey lens opacities
- Vertically oval mid-dilated pupil (fixed).



- Note: ACG is precipitated in dark places (e.g., movie halls).
Treatment
- Initial Treatment:
- IV Mannitol (DOC)
- Oral acetazolamide
- Pilocarpine eyedrops
- miotic, given after ↓IOP;
- pulls iris to center and opens angle
- Mnemonic: Pilocarpine → Put a carpet and relax → parasymp → miosis
- Atropine should not be given
- Definitive Treatment:
- Laser iridotomy (TOC):
- Nd-YAG Laser
- Performed between 11 o’clock & 1 o’clock
- Equalizes pressure.

- If anterior synechiae > 270 degree
- Trabeculectomy + Mitomycin C
NOTE: Complicated cataract
- Causes - Mnemonic: UMAR:
- Uveitis (m/c).
- Myopia.
- Angle closure glaucoma.
- Retinitis pigmentosa.

- Appearance: Breadcrumb + Polychromatic lustre.
- Site: Posterior subcapsular cataract.
- Mnemonic: Umar ate bread with different coloured ingredients → Posterior complicated ayi
Congenital Glaucoma


Blue in congenital ophthal | ㅤ |
Congenital glaucoma | Blue sclera |
Developmental cataract | Blue dot cataract |
Signs

- Open angle Glaucoma due to Trabecular dysgenisis
- Hazy cornea
- Earliest sign
- Buphthalmos:
- Enlarged eyeballs.
- Deep AC.
- Increased axial length (myopia).
- Corneal diameter >13 mm.
- Blue sclera.
- Haabs striae
Striae | ㅤ | ㅤ |
Haab’s striae | • Horizontal breaks in Cornea | • Congenital glaucoma |
Vogt’s striae | • Vertical stretching • In Slit lamp • Vogt → Valich stretch cheyth • Striae → Stretch → Slit lamp | • Keratoconus |
- Cornea ↑↑, Axial length ↑↑↑, Anterior chamber ↑↑
- Mnemonic:
- Child (Congenital) haab (Haab) glowing (glaucoma) blue () eye
Gonioscopic Findings
- Anterior iris insertion
- Barkan membrane
- Loch Ness monster phenomenon: Loops of vessels visible
- Mnemonic: Monster (Lochness monster) came Barking (Barkan membrane) → Child with blue eyes Gone (Gonioscopy)

Treatment
- Trabeculectomy + trabeculotomy (TOC).
- Trabeculectomy: Cutting of some TM
- Trabeculotomy: Formation of holes in the remaining TM
- If cornea is clear
- Goniotomy
- Needle piercing of Trabecular Meshwork using a gonioscope for visualization.
- Can be performed if cornea is clear (if onset >2 yrs)
Secondary Congenital/Developmental Glaucoma
- Mechanism: irido trabeculo corneal dysgenesis
- Causes:
- Axenfeld-Rieger syndrome
- Glaucoma in 50% cases
- Posterior embryotoxon:
- Anteriorly displaced Schwalbe's line
- Peter's anomaly
- Aniridia: Ectopia lentis and glaucoma
- Phacomatosis: NF, Sturge weber syndrome
- Phac () peter () with no iris () but axe ()
Secondary Glaucoma

Lens Induced:

Secondary angle closure | ㅤ |
↳ Phacomorphic | • Intumescent cataract • Morph into |
Secondary open angle | ㅤ |
↳ Phacolytic | • Morgagnian cataract • Agni → Lysis |
↳ Pseudoexfoliation | • M/c/c • M/c A/w old age Secondary OAG • Target sign ↳ Deposit of exfoliative material on lens • Fnocks ↳ Deposit of pseudohotodisruptionexfoliative material on pupillary margin • Pseudo Ex is m/c → Horrifying () → Target () Flocks () • Hoarfrost sign |
↳ Pigmentary | • Krukenberg spindles (characteristic). |
↳ Neovascular glaucoma | • Neovascularization of Iris/Rubeosis Iridis • Hyphema → 2° OAG • Causes: ◦ Proliferative Diabetic Retinopathy (PDR) ◦ Ischemic CRVO. |






