Glaucoma

ANATOMY AND PHYSIOLOGY

APPLIED ANATOMY
Ciliary body- aqueous poduction
Angle of anterior chamber
Gonioscopic grading of the angle width
Grade

Angle witdth

Configuration

Chances of closure Structures visible

on gonioscopy

IV

35-45

Wide open

Nil

SL, TM, SS, CBB

III

20-35

Open angle

Nil

SL, TM, SS

II

20

Moderately
narrow

Possible

SL, TM

10

Very narrow

High

SL only

Closed

Closed

None of the angle

structures visible

APPLIED ANATOMY
Aqueous outflow system

APPLIED PHYSIOLOGY
Aqueous humour and its production
Volume
Anterior chamber: o.25 mL
Posterior chamber: 0.06 mL

Functions:

Maintains a proper intraocular pressure

Metabolic role
Maintains optical transparency
Takes place of lymph that is absent within the eyeball

APPLIED PHYSIOLOGY
Aqueous humour and its production
Refractive index: 1.336
Composition
Water: 99.9%
Solids: 0.1%

Proteins
Amino acid
Non-colloid constituents
Oxygen

Note: composition of aqueous is similar to plasma

except:
High concentrations of ascorbate, pyruvate and lactate
Low concentration of protein, urea and glucose

APPLIED PHYSIOLOGY
Aqueous humour and its production
Anterior chamber VS. posterior chamber
HCO in posterior chamber is higher than in the
anterior chamber
Cl concentration in posterior chamber is lower than in
the anterior chamber
Ascorbate concentration of posterior aqueous is
slightly higher than that of anterior chamber aqueous

APPLIED PHYSIOLOGY
Aqueous humour and its production
Production
2.3 l/min
Three mechanisms
Ultrafiltration
Secretion
Diffusion

Control of aqueous formation

APPLIED PHYSIOLOGY
Drainage of aqueous humour
Trabecular (conventional) outflow
Uveoscleral (unconventional) outflow

APPLIED PHYSIOLOGY
Maintenance of intraocular pressure
Normal IOP: 10-21 mmHg
Local factors

Rate of aqueous formation

Resistance to aqueous outflow (drainage)
Increased episcleral venous pressure
Dilatation of pupil

APPLIED PHYSIOLOGY
Maintenance of intraocular pressure
General factors

Heredity
Age
Sex
Diurnal variation of IOP
Postural variations
Blood pressure
Osmotic pressure of blood
General anaesthetics

GENERAL CONSIDERATIONS

DEFINITION OF GLAUCOMA
It is not a single disease process
Group of disorders
Characterized by a progressive optic
neuropathy
Characteristic apperance of the optic disc
Specific pattern of irreversible visual field
defects
Associated with raised IOP

CLASSIFICATION OF GLAUCOMA
Congenital and developmental glaucomas
Primary congenital glaucoma (w/o associated
anomalies)
Developmental glaucoma (w/associated
anomalies)

Primary adult glaucomas

Primary open angle glaucomas (POAG)
Primary angle closure glaucoma (PACG)
Primary mixed glaucoma

Secondary glaucomas

PATHOGENESIS OF GLAUCOMATOUS
OCULAR DAMAGE
Progressive optic neuropathy
Death of retinal ganglion cells (RGCs)
Blockage of neurothrophins from the brain
RGCs are unable to maintain normal function and
undergo apoptosis and also trigger apoptosis of
adjacent vells
RGC death is associated with loss of retinal nerve
fibers

PATHOGENESIS OF GLAUCOMATOUS
OCULAR DAMAGE
Etiology
Primary insults
Raised IOP (Mechanical theory)
Pressure independent factors (Vascular insufficiency
theory)

Failure of autoregulatory mechanism of blood flow

Vasospasm
Systemic hypotension
Other factors: e.g. acute blood loss

Secondary insults (Excitotoxicity theory)

CONGENITAL/DEVELOPMENTAL
GLAUCOMAS

TERMINOLOGY
Group of diverse disorders in which abnormal
high intraocular pressure results due to
developmental abnormalities of the angle of
anterior chamber obstructing the drainage of
aqueous humour
Types:
Primary developmental/congenital glaucoma
Developmental glaucoma with associated ocular
anomalies

PRIMARY DEVELOPMENTAL/
CONGENITAL GLAUCOMA
Abnormally high IOP which results due to
developmental anomaly of the angle of the
anterior chamber
Not associated with any other ocular or
systemic anomaly

PRIMARY DEVELOPMENTAL/
CONGENITAL GLAUCOMA
True congenital glaucoma
IOP is raised during intrauterine life and child is
born with ocular enlargment
40% of cases

Infantile glaucoma
Disease manifests prior to the childs 3rd birthday
50% of cases

Juvenile glaucoma
Develop pressure rise between 3-16 years of life
10% of cases

PRIMARY DEVELOPMENTAL/
CONGENITAL GLAUCOMA
Prevalence and genetic pattern
Sporadic
10% of cases exhibit an autosomal recessive
inheritance with incomplete penetrance
65% of patients are males
Diseases is bilateral in 75% cases
Disease affects only 1 child in 10,000 births

PRIMARY DEVELOPMENTAL/
CONGENITAL GLAUCOMA
Pathogenesis
Trabeculodysgenesis
Flat iris insertion
more common
Iris inserts flatly and abruptly into the thickened
trabeculum either at or anterior to scleral spur or
posterior to scleral spur

Concave iris insertion

Less common
Superficial iris tissue sweeps over the iridotrabecular
junction and the trabecululm and thus oscures the scleral
spur and ciliary body

PRIMARY DEVELOPMENTAL/
CONGENITAL GLAUCOMA
Clinical features
Photophobia, blepharospasm, lacrimation and eye
rubbing
Corneal signs:
Oedema
Enlargement
Tears and breaks in Descemets membrane

Sclera becomes thin and appears blue

Anterior chamber becomes deep
Iris may show iridodonesis and atrophic patches

PRIMARY DEVELOPMENTAL/
CONGENITAL GLAUCOMA
Clinical features
Lens becomes flat and may even subluxate
Optic disc may show variable cupping and atrophy
IOP is raised
Axial myopia

PRIMARY DEVELOPMENTAL/
CONGENITAL GLAUCOMA
Examination (Evaluation)
Measurement of IOP
Schiotz tonometer
Perkins applanation tonometer

Measurement of corneal diameter

Ophthalmoscopy
Gonioscopic examination

PRIMARY DEVELOPMENTAL/
CONGENITAL GLAUCOMA
Differential diagnosis
Cloudy cornea
Trauma, mucopolysaccharidosis, interstitial keratitis and corneal
endothelial dystrophy

Large cornea
Megalocornea

Lacrimation
Congenital nasolacrimal duct blockage

Photophobia
Keratitis or uveitis

Raised IOP in infants

Retinoblastoma, retinopathy of prematurity, persistent primary
hyperplastic vitreous, traumatic glaucoma and secondary
congenital glaucomas

PRIMARY DEVELOPMENTAL/
CONGENITAL GLAUCOMA
Treatment
Surgical but IOP must be lowered by use of
medications
Surgical procedures:
Goniotomy
Trabeculotomy
Combined trabeculotomy and trabeculectomy

DEVELOPMENTAL GLAUCOMAS WITH

ASSOCIATED ANOMALIES
Glaucoma associated with iridocorneal
dysgenesis
Glaucoma associated with aniridia
Glaucoma associated with ectopia lentis
syndromes
Glaucoma associated with phakomatosis
Miscellaneous conditions

PRIMARY OPEN ANGLE GLAUCOMA

AND RELATED CONDITIONS

PRIMARY OPEN ANGLE GLAUCOMA

No obvious systemic or ocular cause of rise in
the intraocular pressure
Eyes with open angle of the anterior chamber
Chronic simple glaucoma of adult onset
Slowly progressive raised IOP associated with
optic disc cupping and specific visual field
defects
POAG

PRIMARY OPEN ANGLE GLAUCOMA

Etiopathogenesis
Predisposing and risk factors

Heredity
Age
Race
Myopes
Diabetics
Cigarette smoking
High blood pressure
Thyrotoxicosis

PRIMARY OPEN ANGLE GLAUCOMA

Etiopathogenesis
Pathogenesis of rise in IOP
Due to decrease in the aqueous outflow facility due to
increased resistance to aqueous outflow caused by
age-related thickening and sclerosis of the trabeculae
and an absent of giant vacuoles in the cell lining the
canal of Schlemm

Corticosteroid responsiveness
More likely to respond to 6 weeks topical steroid
therapy with a significant rise of IOP

PRIMARY OPEN ANGLE GLAUCOMA

Incidence of POAG
1 in 100 of the general population above the age
40 years

PRIMARY OPEN ANGLE GLAUCOMA

Clinical features
Symptoms
Insidious and usually asymptomatic until it has caused a
significant loss of visual field
Mild headache and eyeache
Defect in the visual field
Reading and close work often present increasing
difficulties
Delayed dark adaptation

PRIMARY OPEN ANGLE GLAUCOMA

Clinical features
Signs
Anterior segment
Intraocular pressure changes
Optic disc changes

Examinations techniques
Direct ophthalmoscopy and indirect ophthalmoscopy
Slit-lamp biomicroscopy using a + 90D lens, Hruby lens
or Goldmann contact lens

 Recording and documentation techniques

Serial drawings, photography and photogrammertry
Confocal scanning laser topography i.e., Heidelberg
retinal tomograph (HRT)
Optical coherence tomography
Scanning laser polarimetry i.e., Nerve fibre analyser
(NFA)

PRIMARY OPEN ANGLE GLAUCOMA

Clinical features
Early glaucomatous changes

Vertically oval cup

Asymmetry of the cups
Large cup
Splinter hemorrhages
Pallor areas on disc
Atrophy of retinal nerve fibre layer

PRIMARY OPEN ANGLE GLAUCOMA

Clinical features
Advanced glaucomatous changes in the optic disc

Marked cupping
Thinning of neuroretinal rim
Nasal shifting of retinal vessels
Pulsations of the retinal arterioles
Lamellar dot sign

PRIMARY OPEN ANGLE GLAUCOMA

Clinical features
Glaucomatous optic atrophy
All the neural tissue is destroyed and the optic nerve
head appears white and deeply excavated
Pathphysiology of disc changes
Mechanical effect
Raised IOP forces the lamina criborosa backwards and
squeezes the nerve fibres
Vascular factors
Contribute in ischemic atrophy of the nerve fibres
Cavernous optic atrophy

PRIMARY OPEN ANGLE GLAUCOMA

Visual field defects
Anatomical basis of field defects
Distribution of retinal nerve fibres
Superior and inferior radiating fibres (srf and irf)
Papillomacular bundle (pmb)
Superior and inferior arcuate fibres (saf and iaf)

Arrangement of nerve fibres within optic nerve head

PRIMARY OPEN ANGLE GLAUCOMA

Visual field defects
Progression of field defects
1.
2.
3.
4.
5.
6.
7.
8.
9.

Isopter contraction
Baring of blind spot
Small wing-shaped paracentral scotoma
Seidels scotoma
Arcuate or Bjerrums scotoma
Ring or double arcuate scotoma
Roennes central nasal step
Peripheral field defects
Advanced glaucomatous field defects

PRIMARY OPEN ANGLE GLAUCOMA

Diagnosis of glaucoma field defects on HGA
single field prinout
Criteria to grade glaucomatous field defects:

Sr.

Parameter

No.

Criteria for glaucomatous field defects

Early defects

Moderate defects

Severe defects

Mean deviation (MD)

< -6 dB

-6 dB 12 dB

> - 12 dB

Corrected pattern
standard deviation
(CPSD)

Depressed to
the p<5%

Depressed to the
p <5%

Depressed to the p
<5%

Pattern deviation plot

Points depressed
below the p < 5%
or
Points decreased
below the p <1%

< 18 (25%)

< 37 (50%)

> 37 (>50%)

< 10

< 20

> 20

Glaucoma Hemifield
Test (GHT)

Outside normal
limits

Outside normal
limits

Outside normal
limits

Sensitivity in central 5
degree

No point <
15dB

One hemifield
may have point
sensitivity <15dB
No point has 0 dB

Both hemifield have

points with
sensitivity <15dB
Any point has 0 dB

PRIMARY ANGLE-CLOSURE
GLAUCOMA

SECONDARY GLAUCOMAS

SURGICAL PROCEDURES FOR

GLAUCOMA