GLAUCOMA

GLAUCOMA

  • Any of
    • ↑↑ IOP
    • Visual field defect
    • Fundus changes → Cupping
      • C:D ratio > 0.3
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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
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Pathophysiology & Types

  1. Optic neuropathy:
      • Progressive, characteristic optic disc changes.
  1. Irreversible visual field defects.
  1. 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.
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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
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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
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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.
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Visual Field Examination (Perimetry)

  • Manual
    • listers perimeter
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  • Automated
    • Humphrey field analyser
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  • 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
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IOP Measurement (Tonometry)

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  • 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
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  • Pascals tonometer
    • Now better than Goldmann
    • Pascal was a better man
  • Maklakov tonometer
    • Variable application surface
    • Makkalkk variable swabavam
Maklakov tonometer
Maklakov tonometer
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Examination of Anterior Chamber Angle

  • Closed Her in Anterior Chamber
    • Heri Ick () gone (Gonioscopy) when Flashed (Oblique flashlight) light
  • Van Herick’s Method:
    • notion image
    • 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:
    • notion image
    • Shadow over nasal irisAngle closure glaucoma.
  • Gonioscopy:
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    • Best method
      • But gold standard is Goldman
    • Principle: Overcomes total internal reflection.
    • Contraindication: Dilated pupil.
    • Direct gonioscope:
      • Richardson/ Koeppe
        • notion image
    • Structures seenMnemonic: 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)

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  • 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

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  • Earliest sign on perimetry:
    • Isopter contraction (Constriction of peripheral VF)
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  • 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
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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
        1. ↓ Aqueous production
        1. ↑ 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
    • notion image
      • 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
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  • 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.
      • notion image

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
    • notion image
    • 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)
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Ex-PressTM implant

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Ahmed glaucoma valve

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Molteno implant

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Baerveldt implant

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Primary Angle Closure Glaucoma (PACG)

Not Pigment dispersion → Vertically oval pupil
Not Pigment dispersionVertically oval pupil
  • Acute disease.
  • Other Causes:
    • TCA → Clomipramine, Amitryptilline
    • Citalopram

Pathogenesis

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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

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  • 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
      1. Iris aTrophy.
      1. Glaucomflecken
          • Lens epithelium necrosis → white or grey lens opacities
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      1. Vertically oval mid-dilated pupil (fixed).
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  • 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):
      • notion image
      • 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.
      • notion image
  • Appearance: Breadcrumb + Polychromatic lustre.
  • Site: Posterior subcapsular cataract.
  • Mnemonic: Umar ate bread with different coloured ingredients → Posterior complicated ayi

Congenital Glaucoma

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Symptoms

  • Triad
    • Photophobia
      • earliest symptom
    • Lacrimation
      • m/c symptom
    • Blepharospasm.
Blue in congenital ophthal
Congenital glaucoma
Blue sclera
Developmental cataract
Blue dot cataract

Signs

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  • 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
      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)
    • notion image

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

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Lens Induced:

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Secondary angle closure
Phacomorphic
Intumescent cataract
Morph into
Secondary open angle
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.
Pigmentary glaucoma
Pigmentary glaucoma
Pigmentary → Krukenberg spindle
Pigmentary → Krukenberg spindle
Neovascular glaucoma
Neovascular glaucoma
 
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