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
I 10 Very narrow High SL only
0 0 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 3
rd
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. Isopter contraction
2. Baring of blind spot
3. Small wing-shaped paracentral scotoma
4. Seidels scotoma
5. Arcuate or Bjerrums scotoma
6. Ring or double arcuate scotoma
7. Roennes central nasal step
8. Peripheral field defects
9. 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 Criteria for glaucomatous field defects
No. Early defects Moderate defects Severe defects
1 Mean deviation (MD) < -6 dB -6 dB 12 dB > - 12 dB
2 Corrected pattern
standard deviation
(CPSD)
Depressed to
the p<5%
Depressed to the
p <5%
Depressed to the p
<5%
3 Pattern deviation plot
Points depressed
below the p < 5%
or
Points decreased
below the p <1%
< 18 (25%)
< 10
< 37 (50%)
< 20
> 37 (>50%)
> 20
4 Glaucoma Hemifield
Test (GHT)
Outside normal
limits
Outside normal
limits
Outside normal
limits
5 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