Download MBBS (Bachelor of Medicine, Bachelor of Surgery) Ophthalmology PPT 42 Primary Open Angle Glaucoma Lecture Notes
Primary open angle glaucoma
Acknowledgement
? Figures and photographs - Courtesy
Kanski's Clinical Ophthalmology
2
Learning Objectives
? At the end of this class the students shall be able to :
? Define primary open angle glaucoma(POAG).
? Understand the pathophysiology and the
risk factors of POAG.
? Understand the clinical features of POAG.
? Understand the fundamentals of managing
primary open angle glaucoma
3
What is glaucoma ?
? The term glaucoma is derived from the
Greek word "glaukos" meaning "gray blue"
? Is the second leading cause of blindness
worldwide
? The third most common cause of blindness
in India
? Not reversible
? More than 50% of patients unaware of
disease.
4
Definition of POAG
? Chronic, progressive optic neuropathy
characterised by morphological changes at
the optic nerve head and retinal nerve fibre
layer leading to characteristic visual field
changes, in the absence of other ocular
diseases or congenital anomalies (with or
without a raised IOP)
5
Etiopathogenesis
? Multifactorial aetiology
? Risk factors include:
?Elevated Intra Ocular Pressure(IOP)
(More than 21 mm Hg)
?Optic disc cupping
?Increasing Age : More common in 5th to 7th
decades of life
?Race: More common and severe in Black
population
6
Etiopathogenesis
?Heredity/ Family History: Risk of about
10% in siblings; 4% in off springs
?Diabetes
?Systemic Hypertension
? Myopia
?Thin central corneas
?Steroid usage
? ??Migraine, Cigarette smoking,Graves
disease
7
Pathogenesis of POAG
? Decrease in aqueous outflow facility due to
increased resistance to outflow leads to rise
in IOP
? Two theories of axonal loss in optic disc
? 1. Mechanical: Distortion of lamina cribrosa
leading to impaired axoplasmic flow
2. Vascular: Optic disc ischaemia with
defective autoregulation of blood vessels
8
FORMATION OF AQUEOUS HUMOR
CILIARY PROCESSES
-approx. 70-80 radial folds in the pars plicata which form
the site of aqueous production.
-Zonular fibers attach primarily in the valleys of the ciliary
processes and also along the pars plana
DIFFUSION
SECRETION
(80-90%)
ULTRA-
FILTRATION
FORMATION PROCESSES 10
Formation of aqueous humor
? Diffusion and ultrafiltration are both
passive mechanisms so no active cellular
partcipation occurs.
? Active secretion is an active process.
? Rate of formation of aqueous humor in a
healthy human eye is-
2 - 3 microlitres/minute
11
Table 1. Constituents of Human Aqueous Humor*
Constituent (?mol/mL) Anterior Chamber
Aqueous
Plasma
Ascorbate
1.06
0.04
Bicarbonate
22.0
26.0
Calcium
2.5
4.9
Chloride
131.0
107.0
Glucose
2.8
5.9
Lactate
4.5
1.9
Magnesium
1.2
1.2
Phosphate
0.6
1.1
Potassium
22.0
26.0
Sodium
152.0
148.0
Urea
6.1
7.3
Protein (gm/dL)
0.024
7.0
12
pH
7.21
7.4
Differences between
aqueous humor & plasma
AQUEOUS PLASMA
-Marked deficit of
0.024 7.0
proteins
gm/dl gm/dl
-Marked excess of
1.06 0.04
Ascorbate
micromol/ml micromol/ml
-Excess of Lactate
4.5 1.9
micromol/ml micromol/ml
-Excess of Chloride &
certain amino acids
13
Functions of aqueous humor
*Maintaining IOP :
-important for early ocular development &
maintaining global integrity throughout life.
*Serves as a vascular system for the avascular
structures of the eye: cornea, lens & TM.
- by providing substrates & nutrients & removing
metabolites.
14
Functions of aqueous humor
*Delivering high concentration of Ascorbate:
- scavenges free radicals & protects against UV
rays & other radiations.
*Local paracrine signaling & immune responses.
*Colourless & transparent medium as part of eye's
optical system.
15
Aqueous humor outflow
16
Major amount of aqueous humor leaves the
eye by
BULK FLUID FLOW
i.e. fluid flows along normal pressure
gradient through non-energy dependent
process
17
Ciliary processes
Aqueous Humor in PC
through pupil
Anterior Chamber
18
Trabeculo-canalicular outflow
*It is the main outlet for aqueous from the AC
*70-90% of total aqueous is drained by this route
TRABECULAR MESHWORK
-A sponge work of
connective tissue
beams arranged as
super-imposed
perforated sheets.
-It's extracellular spaces
contain hydrophilic
glycosaminoglycans &
collagen.
20
-Inner portion
Uveal meshwork
-Outer portion
Corneoscleral meshwork
-In between
Juxta-canalicular
(endothelial)meshwork
21
Uveal meshwork
Corneo-scleral meshwork
Juxta-canalicular tissue
Endothelial lining of SC
Schlemm's Canal
22
UVEAL MESHWORK
-Extends from the iris
root & ciliary body to
schwalbe's line.
-Trabeculae are cord
like, 2-3 layer thick.
-Openings of 25-75
microns size.
23
CORNEOSCLERAL MESHWORK
-Extends from SS to the
lateral wall of scleral
sulcus
-Flattened perforated
sheets, 8-15 layers
-Openings of 5-50
microns size
24
JUXTACANALICULAR
(ENDOTHELIAL) MESHWORK
-The outermost portion
of TM which mainly
offers the normal
resistance to
aqueous outflow .
-Connects the
corneoscleral
meshwork with
schlemm's canal
25
? Veins from the anterior part of ciliary body form the
Ciliary venous plexus
Anterior ciliary veins & Episcleral veins
communicate with Schlemm's canal
26
Schlemm's Canal
20-30 Collector channels Aqueous Vein
Intra-scleral venous plexus
Episcleral venous plexus
& Anterior Ciliary vein
27
UNCONVENTIONAL
OUTFLOW
*responsible for 10-25% of total aqueous outflow
UVEO-SCLERAL OUTFLOW
29
Trans-corneal outflow
- Aqueous humor from anterior chamber
goes into tear film through cornea.
- Very little aqueous passes through this
pathway.
- Total volume of fluid transferred is limited
by high hydraulic resistance of the cornea.
30
ANGLE OF ANTERIOR
CHAMBER
- The peripheral recess of anterior chamber is known as
the angle of anterior chamber.
- It is clinically visualized by gonioscopy.
- Starting at the root of iris & progressing anteriorly
towards the cornea, the following structures can be
identified in a normal angle in an adult :
1) Ciliary body band (CBB) & root of iris
2) Scleral spur (SS)
3) Trabecular meshwork (TM)
4) Schwalbe's line (SL)
31
32
---------
Grade
IV
III
II
I
0
33
34
Clinical features of POAG
Symptoms
? Usually asymptomatic in early cases
? Mild headache and eye ache
? Frequent changes in presbyopic glasses
? Delayed dark adaptation
? Loss of peripheral vision
? Loss of central vision(late cases)
35
Signs of POAG
? Normal anterior segment
? Pupil reaction to light may be sluggish(in
advanced cases only)
? Elevated IOP(More than 21 mm Hg) with
diurnal variation more than 5-8 mmHg
? Optic disc changes (Progressive,
asymmetric)
? Visual field defects
36
37
Optic disc changes in glaucoma
? Early changes
o Retinal nerve fibre layer atrophy
o Vertically oval cup
o Asymmetry of the cups(More than 0.2
difference)
o Large cup(CD more than 0.6)
o Splinter haemorrhages
38
Advanced glaucomatous disc changes
? Marked cupping (More than 0.7)
? Thinning of NRR (Neuroretinal rim)
? Lamellar dot sign
? Vascular alterations
o Nasal shifting of retinal vessels
o Bayonetting sign(convoluted path due to NRR
loss)
o Baring of circumlinear vessels and overpass
vessels
o Multiple haemmorrhages at disc
? Glaucomatous optic atrophy
39
40
41
Recording and documenting disc changes
? Serial drawings (10 square grid) after
seeing fundus by ophthalmoscopy/slit
lamp with +90D/+78D lens
? Disc photography
? HRT(Heidelberg retinal tomography)
? OCT (Optical coherence tomography)
? NFA(Nerve fibre analyser)
42
43
Visual field defects in glaucoma
? Arcuate nerve fibres in the superior and
inferior temporal portions of the optic disc:
Most sensitive to damage
? Macular fibres : Most resistant to damage
CENTRAL VISION IS PRESERVED TILL
THE LAST IN GLAUCOMA
44
Progression of field defects
? Isopter contraction: Generalised field
constriction
? Baring of blind spot : Non specific
(Exclusion of blind spot from central field)
? Paracentral scotoma: Wing shaped and
occurs above or below the blind spot in the
Bjerrum's area(10-25 degrees from
fixation)
Is the earliest clinically significant defect
45
Progression of field defects
? Seidel's scotoma: sickle shaped
Due to joining of blind spot and
paracentral scotoma
? Bjerrum's/Arcuate scotoma:
Extension of Seidel's scotoma to reach the
horizontal line.
? Double arcuate/ring scotoma
46
Progression of field defects
? Roenne's central nasal step:
Sharp right angled defect at the horizontal
meridian when arcuate scotomas run in
different arcs
? Peripheral field defects
? Advanced defects
Residual Tubular vision
Temporal island of vision
47
Quantification of visual field defects
? Visual field analyzer
Kinetic perimeter
Static perimeter (automated)
Testing more than once is required before
final interpretation
48
Enlarged blind spot
49
Superior arcuate scotoma
50
Bjerrum's scotoma
51
Roenne's nasal step
52
Double arcuate
10-2- Advanced VFD , macular split
53
Advanced glaucoma
54
Diagnostic work up/Investigations
? Tonometry
? Goniscopy: Open angles
? Perimetry: To detect visual field defects
? Slit lamp examination: To rule out causes
of secondary open angle glaucoma
? Fundus examination to document optic
disc changes
? Diurnal variation testing
? Provocative testing: Water drinking test 55
Diagnosis
? POAG: Raised IOP(More than 21 mm Hg),
glaucomatous optic disc cupping, visual
field changes.
? Ocular hypertension/glaucoma suspect:
Raised IOP
? NTG(Normal tension glaucoma):
glaucomatous optic disc cupping with or
without visual field changes with normal
IOP
56
Management of POAG
? Therapeutic choices
q Medical therapy
q Argon/Diode Laser Trabeculoplasty
q Filtration surgery
57
Basic principles of therapy
? Make a correct diagnosis
? Set a target IOP
? Start with a single drug to lower IOP
? Switch to another group of drugs if needed
? Add drugs from different groups
(Combination therapy)
? Control IOP on minimal medication
? Monitor therapy and reset target IOP
whenever needed
58
Topical drugs used for POAG therapy
? Prostaglandin/Prostamides
Latanoprost, Bimatoprost, Travoprost
? Beta blockers
Timolol maleate, Betaxolol
? Carbonic anhydrase inhibitors
Dorzolamide, Brinzolamide
? Sympathomimetics
Brimonidine, Apraclonidine
? Parasmpathomimetics
59
Pilocarpine
Systemic drugs used for POAG therapy
? Used rarely, for short term control of IOP
? Oral carbonic anhydrase inhibitors
Acetazolamide, Methazolamide
60
Laser treatment
? Indications
Target IOP not achieved with medical
therapy
Non compliance of medical therapy
Argon/ Diode Laser Trabeculoplasty (ALT)
Selective Laser Trabeculoplasty (SLT)
61
Surgical therapy
? Indications
v Target IOP not achieved with maximal
tolerated medical therapy and laser
trabeculoplasty
v Non compliance of medical therapy
v Non availability of laser therapy
v Advanced glaucoma
62
Surgical therapy
? Filtration surgery : Trabeculectomy
? Modified trabeculectomy :
Use of antifibrotic agents
Mitomycin/5FU
? Aqueous drainage devices:
Ahmed glaucoma valve
In cases with no/poor visual potential:
Cycloablative therapy with laser/cryo- Last 63
resort
This post was last modified on 07 April 2022