Definition :

• Glaucoma is characterized by progressive optic neuropathy.
• This results in characteristic apperance of the optic disc with a specific pattern of irreversible visual field defects.
• This may or may not be associated with the raised intraocular pressure.
• Thus raised intraocular pressure is a risk factor for Glaucoma but not the only risk factor for the development of Glaucoma.

Classification :

• Congenital / Developmental Glaucomas
• Primary adult Glaucomas
• Secondary Glaucomas
  • Congenital or Developmental Glaucomas
    • Primary congenital/ developmental glaucoma ( without associated anomalies )
    • Secondary congenital/ developmental glaucoma ( with associated anomalies )
  • Primary adult Glaucomas
    • Primary open angle Glaucomas (POAG)
    • Primary angle – closure glaucoma (PACG)
    • Primary mixed mechanism glaucoma
  • Secondary Glaucomas
    • Secondary open – angle glaucomas
    • Secondary angle – closure glaucomas

Epidemiology :

Global prevalence of Glaucoma

• 2 % of people with age over 40 years
• 10 % of people with age over 80 years

POAG versus PACG in different ethnic groups

Ethnic group	POAG : PACG
Indian	1:1
Urban Chinese	1:2
Mongolian	1:3
European, African and Hispanic	5:1

Glaucoma blindness

Global	8.0%
India	12.8%

Types :

• Congenital/Developmental Glaucoma :
  • Primary congenital or developmental
    • Congenital
    • Infantile
    • Juvenile
  • Developmental associated with ocular anomalies
• Primary Adult glaucomas :
  • Primary open angle glaucoma
  • Primary Angle closure Glaucoma
  • Primary mixed mechanism Glaucoma
• Secondary Glaucoma :
  • Lens induced
  • Pigmentory
  • Steroid induced
  • Neovascular
  • Traumatic
  • Introcular tumors
  • Aphakic
  • Pseudoexfoliative

Primary Open angle galucoma or Chronic simple Glaucoma :

• Characterized by :
  • Slowly progressive raised IOP (>21 mmHg)
  • Open normal appearing anterior chamber angle.
  • Characteristic optic disc cupping
  • Special visual filed defects.
• More common the Angle closure Glaucoma.

Etiology :

• Increased IOP
• Hereditary : due to the following genes
  • Myocillin C
  • Optineurin
  • WD repeat domain 36
• Age : Usually at 5th to 7th decades
• Race : Occurs more in black than white race
• Myopes
• Thinner central corneal thickness
• Diabetes
• Cigarette smoking
• High BP
• Thyrotoxicosis
• Corticosteroids

Pathogenesis :

• Rise in IOP occurs due to decrease in aqeous outflow.
• This occurs due to increase in resistance to aqeous outflow.
• Causes :
  • Age related thickening and sclerosis of the trabecular meshwork.
  • Absence of vacuoles in the cells lining the canal of schlemm.
  • Narrowing of the intertrabecular meshwork.
  • Amorphous material deposition in the Juxtacanalicular space.

Clinical features :

Symptoms :

• The symptoms are not significant until it causes significant loss of the visual field. Apart from that the symptoms includes Headache, Eye ache, Frequent change in the presbyopic correction, Scotoma, Difficulty in dark adaptation and also significant loss of vision and blindness.

Signs :

• Anterior segment :
  • Normal or low central corneal thickness.
• IOP changes :
  • In the initial stages the IOP tends to remain normal.
  • Later on the IOP tends to show Diurnal variation.
  • So IOP is checked for every 3 to 4 hours for 24 hours.
  • Variation of IOP of :
    • > 5 mmHg (Schiotz) – Suspicious
    • > 8 mmHg – Diagnostic
    • In the later stages the IOP remains greater than 21 mmHg permanently.
• Visual field defects :
  • Visual defects in Glaucoma :
    • Isopteric contraction :
      • Generalized constriction of central and peripheral field.
      • Earliest visual field defect.
    • Baring of Blind Spot :
      • Exclusion of blind spot from the central field.
    • Paracentral scotoma :
      • Earliest clinically significant Visual field defect.
      • Found either Below or Above the Blind spot in the Bjerrum’s area.
    • Siedel’s scotoma :
      • The paracentral scotoma joins the Bjerrum’s area to form the sickle cell shaped Siedel’s scotoma.
    • Arcuate or Bjerrum’s Scotoma :
      • Extension of the Siedel’s scotoma in the area above or below the fixation point.
    • Ring or Double arcuate Scotoma :
      • Two arcuate scotoma joins together to form the Ring or Double arcuate Scotoma.
    • Roenne’s central nasal step :
      • Two arcuate Scotoma runs in different arcs and meet to form sharp right angle defect.
    • Tubular vision

 

 

Optic nerve head changes :

• Early Glaucomatous changes :
  • Vertically oval cup
  • Assymetry of the cup
  • Large cup with cup disc ratio > 0.5
  • Atrophy of retinal nerve fibre layer
  • Pallor on the disc
  • Splinter Hemorrhages
• Late Glaucomatous changes :
  • Marked Cupping
  • Total Bean pot cupping
  • Thinning of Neuroretinal rim
  • Lamellar dot sign
  • Pulsation of retinal arterioles at disc margin
  • Total disc pallor

Diagnosis :

• Atleast two of the following first three findings must be positive to confirm Primary Open Angle Glaucoma in the presence of Normal Open Angle Glaucoma which is confirmed by Gonioscopy.
  • IOP > 21 mmHg on more than one occasion and variation of >8 mmHg measured by Schiotz tonometry.
• Glaucomatous changes in Disc / Optic nerve head as seen by :
  • Direct Ophthalmoscopy
  • Indirect Ophthalmoscopy
  • Slit lamp biomicroscopy using Hruby or Goldman contact lens
• Typical visual field changes : as seen in Perimetry.
• Defects in nerve fibre layer

Treatment :

• Investigations
  • Tonomtery :
    • Applanation is preffered over Schiotz
  • Central corneal thickness ( CCT ) : Low CCT ( < 545 microns )
  • Diurnal variation test
  • Gonioscopy : Wide open angle of AC
  • Optic disc changes
  • Slit lamp examination
  • Perimetry
  • Nerve fibre layer analyzer
  • Provocative tests.
• Medical therapy :
  • Topical Beta Blockers like Timolol, Betaxolol, Levobunolol, Carteolol are the Drug of Choice.
  • Topical Prostaglandin Anaalogues like Bimatoprost, Latanoprost, Travoprost are the second drug of choice.
• Argon or Laser Trebaculoplasty :
  • It is the choice of treatment when the IOP does not decrease inspite of the medical therapy.
• Filteration surgery :
  • It is done when IOP is not controlled Inspite of proper Medical therapy and Trabeculoplasty.
  • Trabeculectomy is done.

Primary Angle Closure glaucoma

• It is a type of primary angle glaucoma where rise in IOP occurs due to the Blockage of aqeous outflow caused by the closure of narrower angle of the anterior chamber.
• It is characterized by the apposition of peripheral iris against the trabecular meshwork.
• This is the second most common type of Glaucoma.
• Females are usually affected more than that of the males.

Etiopathogenesis :

• Predisposing factors :
  • Age : 6th and 7th decade of life
  • Gender : Female : Male ( 4:1)
  • Rare : Common in Caucasians and Chinese
  • Shallow anterior chamber, Short eye, Hypermetropic eye, Large lens, Anterior location of iris Lens Diaphragm and also smaller corneal diameter are also the predisposing factors.
• Precipitating factors :
  • Dim Light, Emotional stress and also Use of Mydriatics are the Precipitaing factors.

Pathogenesis :

• Pupillary Block mechanism
• Plateau iris configuration
• Phacomorphic mechanism

Classification :

• ISEGO classification :
  • Primary angle closure suspect (PACS)
  • Primary angle closure
  • Primary angle closure glaucoma
• Clinical classification :
  • Latent PACG
  • Subacute PACG
  • Acute PACG
  • Chronic PACG

	Latent PACG	Subacute PACG	Acute PACG	Chronic PACG
Characteristics	Shallow anterior chamber	Shallow anterior chamber	Sudden occlusion of entire angle with resultant acute rise of the IOP	Constantly elevated IOP Decreased visual acuity Visual field defects like POAG Eyeball is White and Not congested
Symptoms	Halos around the light Transient haziness of vision	Halos around the light Transient blurring of vision Headache Browache Eyeache	Sudden painful LOV Colored Halos Nausea Prostrations Vomiting Redness Photophobia Lacrimation	Painfull blind eye and is irritable
Signs	Gonioscopic finding – Narrow angle < 20 degree	Eye is white but not congested	Shallow anterior chamber Semidilated, vertically oval, fixed pupil, non reactive to both light and accomodation. IOP is increased Lid edema Conjuctiva is chemosed, congested, red Cornea is edematous, insensitive and cloudy Iris is discolored Angle of AC is closed Optic disc is edematous, Hyperaemic Fellow eye – Shalow AC, Narrow angle	Perilimbal Reddish Blue zone, Caput Medusae, Hazy cornea, Atrophic iritis, Stony hard eyeball, Raised IOP, Fixated Dilated Pupil, Optic disc atropy
Tests	Prone Darkroom provocative test – Phyisological test IOP > 8 mmHg Mydriatic or Cycloplegic provocative tests – Not phyiological IOP > mmHg – Dilated with Mydriatics	Provocative tests are positive	Provocative tests are positive	Provocative tests are positive

Treatment :

• Definitive treatment :
  • Surgery – Trabeculectomy, Deep Sclerotomy and also Viscoanulostomy

Congenital Glaucoma :

• Primary Congenital Glaucoma (PCG) refers to the high IOP that results due to developmental anomaly of the angle of the anterior chamber that is not associated with any other ocular or systemic anomaly.
• Depending upon the age the developmental glaucomas are classified into
  • Newborn Glaucoma
  • Juvenile Glaucoma
  • Buphthalmos

Pathogenesis :

• Maldevelopment, from the neural crest cells, of trabeculum including iridotrabecuar junction (Trabeculodysgenesis )is responsible for impaired aqeous outflow resulting in the raised IOP.

Symptoms :

• Lacrimation
• Photophobia
• Blepharospasm

Signs :

• Lacrimation, Photophobia and Blepharospasm often occurs as a triad along with the history of Eye rubbing.
• Corneal signs including Corneal Oedema, Corneal enlargement, Haab’s striae and also Hazy Cornea occurs.
• Sclera becomes thin and appears blue due to the underlying uveal tissue.
• Moreover the anterior chamber becomes deep.
• Iris may show iridodonesis and atrophic patches in the late stage.
• Lens become antero – posteriorly flat.
• Optic disc may show cupping and atrophy especially after third year.
• IOP is raised with no significance.

Examination :

• Measurement of IOP, Corneal Diameter, Slit lamp examination, Ophthalmoscopy and also Gonioscopic examination is carried out.

Treatment :

• Medical Treatment :
  • Hyperosmotic agents
  • Carbonic anyhydrase inhibitors
  • Beta blockers
• Surgical Procedures :
  • Incisional angle surgery
    • Goniotomy
    • Trabeculotomy
  • Filteration surgery
    • Trabeculectomy
    • Combined Trabeculotomy and Trabeculectomy
  • Glaucoma drainage devices