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Download MBBS Ophthalmology PPT 47 Primary Open Angle Glaucoma Lecture Notes

Download MBBS (Bachelor of Medicine, Bachelor of Surgery) Ophthalmology PPT 47 Primary Open Angle Glaucoma Lecture Notes

This post was last modified on 07 April 2022

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Acknowledgement

? Kanski's Clinical Ophthalmology (8th Edition).

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? Becker- Schaffer's Diagnosis and therapy of The

Glaucomas (8th Edition).

? Comprehensive Ophthalmology (A.K.Khurana)

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(7th Edition).

2

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Learning Objectives

? At the end of this class the students shall be able to :
? Define primary open angle glaucoma(POAG).

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? Comprehend the pathophysiology and
risk factors of POAG.
? Understand the clinical features of POAG.
? Understand the fundamentals of managing
primary open angle glaucoma

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3

4
Question

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Glaucoma is defined as:
? a. a group of diseases that have in common a

characteristic optic neuropathy associated with increased

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intraocular pressure.

? b. a group of diseases that have in common a

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characteristic optic neuropathy with associated visual

function loss.

? c. a group of diseases that have in common high

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intraocular pressure with or without optic neuropathy.

? d. a group of diseases that have in common a

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characteristic optic neuropathy with poor visual acuity.

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Definition of POAG

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? Chronic, progressive optic neuropathy

characterised by morphological changes at the

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optic disc and retinal nerve fibre layer leading to

characteristic visual field changes, in the absence

of other ocular diseases or congenital anomalies

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(with or without a raised IOP).

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Etiopathogenesis

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? Multifactorial aetiology
? Risk factors include:

? Elevated Intra Ocular Pressure(IOP)

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(More than 21 mm Hg)

? Optic disc cupping

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? Increasing Age : More common in 5th to 7th decades

? Race: More common and severe in Black population

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Etiopathogenesis

? Heredity/ Family History: Risk of about 10% in

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siblings; 4% in off springs

? Diabetes

? Systemic Hypertension

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? Myopia

? Thin central corneas

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? Steroid usage

? ?Migraine, Cigarette smoking

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Pathophysiology of POAG

? Decrease in aqueous outflow facility due to

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increased resistance to outflow leads to rise in IOP

? Two theories of axonal loss in optic disc
? 1. Mechanical: Distortion of lamina cribrosa

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leading to impaired axoplasmic flow

2. Vascular: Optic disc ischaemia with
defective autoregulation of blood vessels

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9

FORMATION OF AQUEOUS HUMOR

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CILIARY PROCESSES

-approx. 70-80 radial folds in the pars plicata which form

the site of aqueous production.

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-Zonular fibers attach primarily in the valleys of the ciliary

processes and also along the pars plana

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DIFFUSION

SECRETION
(80-90%)

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ULTRA-
FILTRATION

FORMATION PROCESSES 11

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Formation of aqueous humor

? Diffusion and ultrafiltration are both

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passive mechanisms so no active cellular

participation occurs.

? Active secretion is an active process.

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? Rate of formation of aqueous humor in a

healthy human eye is-

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2 - 3 microlitres/minute

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Table 1. Constituents of Human Aqueous Humor*

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Constituent (?mol/mL) Anterior Chamber

Aqueous

Plasma

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Ascorbate

1.06

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0.04

Bicarbonate

22.0

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26.0

Calcium

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2.5

4.9

Chloride

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131.0

107.0

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Glucose

2.8

5.9

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Lactate

4.5

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1.9

Magnesium

1.2

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1.2

Phosphate

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0.6

1.1

Potassium

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22.0

26.0

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Sodium

152.0

148.0

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Urea

6.1

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7.3

Protein (gm/dL)

0.024

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7.0

pH

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7.21

7.4

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Differences between

aqueous humor & plasma

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AQUEOUS PLASMA

-Marked deficit of

0.024 7.0

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proteins

gm/dl gm/dl

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-Marked excess of

1.06 0.04

Ascorbate

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micromol/ml micromol/ml



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-Excess of Lactate

4.5 1.9

micromol/ml micromol/ml

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-Excess of Chloride &

certain amino acids

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Functions of aqueous humor

*Maintaining IOP :
-important for early ocular development &

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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.

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Functions of aqueous humor

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*Delivering high concentration of Ascorbate:

- scavenges free radicals & protects against UV

rays & other radiations.

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*Local paracrine signaling & immune responses.

*Colourless & transparent medium as part of eye's

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optical system.

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Aqueous humor outflow

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Video of aqueous humor outflow

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Major amount of aqueous humor leaves the

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eye by


BULK FLUID FLOW

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i.e. fluid flows along normal pressure

gradient through non-energy dependent

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process

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Ciliary processes

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Aqueous Humor in PC



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through pupil

Anterior Chamber

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Trabeculo-canalicular outflow

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*It is the main outlet for aqueous from the AC

*70-90% of total aqueous is drained by this route

TRABECULAR MESHWORK

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-A sponge work of
connective tissue
beams arranged as
super-imposed

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perforated sheets.
- Extracellular spaces
contain hydrophilic

glycosaminoglycans &

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collagen.

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JUXTACANALICULAR

(ENDOTHELIAL) MESHWORK

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- Outermost portion of

TM which mainly

offers the normal

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resistance to

aqueous outflow

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- Connects the

corneoscleral

meshwork with

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schlemm's canal

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? Veins from the anterior part of ciliary body form the

Ciliary venous plexus


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Anterior ciliary veins & Episcleral veins

communicate with Schlemm's canal

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Schlemm's Canal

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20-30 Collector channels Aqueous Vein

Intra-scleral venous plexus


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Episcleral venous plexus
& Anterior Ciliary vein

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UNCONVENTIONAL

OUTFLOW

*responsible for 10-25% of total aqueous outflow

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UVEO-SCLERAL OUTFLOW

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Trans-corneal outflow

- Aqueous humor from anterior chamber

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goes into tear film through cornea.

- Very little aqueous passes through this

pathway.

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- Total volume of fluid transferred is limited

by high hydraulic resistance of the cornea.

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Clinical features of POAG

Symptoms
? Usually asymptomatic in early cases

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? Mild headache and eye ache
? Frequent changes in presbyopic glasses
? Delayed dark adaptation
? Loss of peripheral vision
? Loss of central vision(late cases)

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Signs of POAG

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? Normal anterior segment
? Pupil reaction to light may be sluggish(in

advanced cases only)

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? Elevated IOP(More than 21 mm Hg) with

diurnal variation more than 5-8 mmHg

? Optic disc changes (Progressive,

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asymmetric)

? Visual field defects

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Optic disc changes in glaucoma

? Early changes
o Retinal nerve fibre layer atrophy

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o Vertically oval cup

o Asymmetry of the cups(More than 0.2

difference)

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o Large cup(CD more than 0.6)

o Splinter haemorrhages

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Advanced glaucomatous disc changes

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? Marked cupping (More than 0.7)
? Thinning of NRR (Neuroretinal rim)
? Lamellar dot sign
? Vascular alterations
o Nasal shifting of retinal vessels

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o Bayonetting sign(convoluted path due to NRR

loss)

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o Baring of circumlinear vessels and overpass

vessels

? Glaucomatous optic atrophy

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Normal Optic Disc

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Glaucomatous optic disc

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Is this a normal or

Glaucomatous optic disc

glaucomatous disc ?

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Recording and documenting disc changes

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? Serial drawings (10 square grid) after

seeing fundus by ophthalmoscopy/slit

lamp with +90D/+78D lens

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? Disc photography
? HRT(Heidelberg retinal tomography)
? OCT (Optical coherence tomography)
? NFA(Nerve fibre analyser)

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View of optic disc by 90D lens examination

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Field of vision

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Visual field defects in glaucoma

? Arcuate nerve fibres in the superior and

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inferior temporal portions of the optic disc:

Most sensitive to damage
? Macular fibres : Most resistant to damage

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CENTRAL VISION IS PRESERVED TILL

THE LAST IN GLAUCOMA

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Progression of field defects

? Isopter contraction: Generalised field

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constriction

? Baring of blind spot : Non specific
(Exclusion of blind spot from central field)
? Paracentral scotoma: Wing shaped and

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occurs above or below the blind spot in the

Bjerrum's area(10-25 degrees from

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fixation)

Is the earliest clinically significant defect

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Progression of field defects

? Seidel's scotoma: sickle shaped
Due to joining of blind spot and
paracentral scotoma

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? Bjerrum's/Arcuate scotoma:
Extension of Seidel's scotoma to reach the
horizontal line.
? Double arcuate/ring scotoma

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Progression of field defects

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? Roenne's central nasal step:
Sharp right angled defect at the horizontal
meridian when arcuate scotomas run in
different arcs
? Peripheral field defects

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? Advanced defects
Residual Tubular vision
Temporal island of vision

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Quantification of visual field defects

? Visual field analyzer

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Kinetic perimeter
Static perimeter (automated)

Testing more than once is required before
final interpretation

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Enlarged blind spot

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Superior arcuate scotoma

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Bjerrum's scotoma

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Roenne's nasal step

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Double arcuate

10-2- Advanced VFD , macular split

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Advanced glaucoma

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Diagnostic work up/Investigations

? Tonometry

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? Goniscopy: Open angles
? Perimetry: To detect visual field defects
? Slit lamp examination: To rule out causes

of secondary open angle glaucoma

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? Fundus examination to document optic

disc changes

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? Diurnal variation testing
? Provocative testing: Water drinking test 50
Diagnosis

? POAG: Raised IOP(More than 21 mm Hg),

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glaucomatous optic disc cupping, visual
field changes.
? Ocular hypertension/glaucoma suspect:
Raised IOP
? NTG(Normal tension glaucoma):

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Glaucomatous optic disc cupping with or
without visual field changes with normal IOP


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Management of POAG

? Therapeutic choices

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q Medical therapy

q Argon/Diode Laser Trabeculoplasty

q Filtration surgery

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Basic principles of therapy

? Make a correct diagnosis

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? Set a target IOP
? Start with a single drug to lower IOP
? Switch to another group of drugs if needed
? Control IOP on minimal medications
? Monitor therapy and reset target IOP

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whenever needed

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Topical drugs used for POAG therapy

? Prostaglandin/Prostamides
Latanoprost, Bimatoprost, Travoprost
? Beta blockers

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Timolol maleate, Betaxolol
? Carbonic anhydrase inhibitors
Dorzolamide, Brinzolamide
? Sympathomimetics
Brimonidine, Apraclonidine

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? Parasympathomimetics
Pilocarpine

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Systemic drugs used for POAG therapy

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? Used rarely, for short term control of IOP
? Oral carbonic anhydrase inhibitors
Acetazolamide, Methazolamide

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Laser treatment

? Indications

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Target IOP not achieved with medical
therapy
Non compliance of medical therapy

Argon/ Diode Laser Trabeculoplasty (ALT)

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Selective Laser Trabeculoplasty (SLT)

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Surgical therapy

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? Indications
v Target IOP not achieved with maximal
tolerated medical therapy and laser
trabeculoplasty
v Non compliance of medical therapy

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v Non availability of laser therapy
v Advanced glaucoma

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Surgical therapy

? Filtration surgery : Trabeculectomy

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? Modified trabeculectomy :
Use of antifibrotic agents
Mitomycin/5FU
? Aqueous drainage devices:
Ahmed glaucoma valve

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In cases with no/poor visual potential:
Cycloablative therapy with laser/cryotherapy

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Conclusion

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? Primary open angle glaucoma is a

progressive optic neuropathy with

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characteristic optic disc and visual field

changes.

? Increased resistance to aqueous outflow

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leads to rise in IOP.

? Aim of management is to reduce IOP to

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minimize damage to optic disc and

resultant visual field defects.

59

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Question

Which of the fol owing is not a risk factor

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for the development of primary open

angle glaucoma?
a. positive family history.
b. advanced age.

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c. increased IOP.
d. increased corneal thickness.

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Question

You have been referred a case of open

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angle glaucoma. Which of the fol owing

would be an important point in

diagnosing the case?

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a. Shallow anterior chamber
b. Optic disc cupping
c. Narrow angle
d. Visual acuity and refractive error

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61

THANK YOU

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