POAG AND PACGAN INTRODUCTION

JAYENDRA JHA OPTOMETRIST

C.L GUPTA EYE INSTITUTEMORADABAD

HISTORICAL ASPECTS

• The glaucoma term is derived from the old greek

word “glaukos” which means “greyish-blue”

• Hippocrates defined glaucoma as “a disease of the

elderly patients in which the pupilla becomes blue”.

– A person with a swollen cornea and a rapidly

developing cataract and chronic (long-term)

elevated pressure inside the eye

c. 460 BC–c. 380 BC

WHAT IS THE INTRAOCULAR PRESSURE

• Pressure insıde the eye is termed ”intraocular pressure (IOP)”

• Eye pressure is measured in millimeters of mercury (mmHg)

• “Normal eye pressure” is not a stable number(s), it ranges from 10

to 21 mmHg

• Elevated IOP is an eye pressure of “greater than 21 mmHg”

WHAT IS GLAUCOMA

• Currently, glaucoma is defined as “a progressive optic

neuropathy which causes permanent blindness by damaging

the optic nerve and the periferal visual field”.

• Glaucoma affects 3% of the society and the second frequent

reason of permanent blindness (especially in developed

countries).

• The prevalance is higher in elderly population.

RISK FACTORS

• IOP

• AGE

• RACE

• FAMILY HISTORY

• DIABETES MELLITUS

• REFRACTIVE ERROR

• VASCULAR DISEASE

CLASSIFICATION OF GLAUCOMA

• Various classifıcations are available.

• Many classifications are based on etiology, anatomy and clinical

presentation.

• CLASSIFICATION BY THE TIME OF ONSET IS AS;

– Congenital glaucoma

– Acquired glaucoma

• Primary glaucoma

• Secondary glaucoma

CLASSIFICATION OF THE ACQUIRED GLAUCOMAS

PRIMARY OPEN ANGLE GLAUCOMA•Normal pressure glaucoma•Ocular hypertensıon

SECONDARY OPEN ANGLE GLAUCOMAS•Pseudoexfoliatıon glaucoma•Pigmentary glaucoma•Phacolytic glaucoma •Secondary to ocular inflammation•Secondary to high episcleral venous pressure•Secondary to steroid therapy

PRIMARY ANGLE CLOSURE GLAUCOMA

•Acute angle closure glaucoma•Subacute angle closure glaucoma

SECONDARY ANGLE CLOSURE GLAUCOMAS •Due to peripheral anterior synechiae •Swollen lens or pupillary seclusion anterior movement of the iris-lens diaphragm

•Neovascular glaucoma• Plateau iris syndrome

PRIMARY OPEN ANGLE GLAUCOMA

• POAG is described as optic nerve damage from multiple possible causes that is chronic and progresses over time

• A loss of optic nerve fibers is characteristic of the disease

• POAG characteristics are open anterior chamber angle, high intraocular pressure in the eye ,visual field abnormalities and cupping and atrophy of the optic disc

• The exact cause of POAG is unknown

• The most important (and well known) cause of POAG is increased

IOP

• The cause of the high IOP is generally accepted to be because of an

imbalance in the productıon and drainage of fluid in the eye (aqueous

humor)

• The fluid is continually being produced but cannot be drained

because of the improperly functioning drainage channels (called

trabecular meshwork)

POAG CAUSES ?

RAISING THE IOP!!

PRIMARY ANGLE CLOSURE GLAUCOMA

• PACG is characterised by apposition of peripheral iris against the

trabecular meshwork obstructing aqueous outflow

• Generally seen in hyperopic eyes than myopic eyes

• PACG is typically associated with greater speed of progresssion

and visual morbidity than POAG

OUTFLOW PATHWAYS AND RESISTANCE POINTS

GLAUCOMATOUS DAMAGE

• The basis of the glaucomatous damage

is the loss of retinal ganglion cells.

• The ganglion cells constituting the

retinal nerve fiber layer and their axons

dies during the glaucomatous damage

process.

SYMPTOMS

• Most cases are asymptomatic until the visual field abnormalities

become prominent and affect central vision.

• Thus, annual routine examinatıon is essential for early

diagnosis.

• In PACG, some patient present acute pain and headache

SIGNS

CHRONIC PRESENTATION• VA is normal unless advanced stages• Anterior chamber is shallow• IOP elevation may be only intermittent

ACUTE ANGLE CLOSURE• VA is usually 20/200 or HM• IOP is usually very high (50-100 mmHg)• Conjunctival hyperaemia, corneal oedema• Unreactive mid- dilated oval pupil• Fellow eye generally shows an occludable angle

THE EVALUATION OF GLAUCOMA PATIENTS

• Visual acuity (best corrected)

• Biomicroscopy (clues to specific diagnosis...)

• Measurement of intraocular pressure

– Applanation tonometry

– Noncontact tonometry

• Pachymetry

• Evaluation of the anterior chamber angle

• Perimetry

• Funduscopy

TONOMETRY

• Tonometry is a method used to measure the pressure inside the eye

• Because IOP varies from hour to hour in any individual (diurnal

variation), measurements may be taken at different times of day

(morning and night)

– A difference in pressure between morning and night of 5 mmHg

or more may suggest glaucoma

• A difference in pressure between the two eyes of 3 mmHg or more

may suggest glaucoma

THE TECHNIQUES OF IOP MEASUREMENTS

APPLANATION TONOMETRY

SCHIOTZ TONOMETER

PERRKINS HAND HELD TONOMETER

TONOPEN XLNON CONTACT TONOMETER

PACHYMETRY

Normal central corneal thickness is variable

500-520 microns

Thinner cornea (CCT < 500 m) can give

falsely low pressure readings

Severe glaucoma patients may be failed

diagnose

A thick cornea (>600 m) can give falsely

high pressure readings

Unnecessary treatments !!

GONIOSCOPY

SL:Schwalbe’s lıneTM:Trabecular MeshworkSS:Scleral SpurCBB:Ciliary Body Band

•Gonioscopy is performed to check

the drainage angle of an eye

•A special contact lens(goniolens)

is placed on the eye

•This test is important to

determine if the angles are open,

narrowed, or closed

•Open angle: long term,slowly,

insidious disease

•Close (narrow): risk of PACG.

VISUAL FIELD TESTING

• VF testing to check the patients peripheral vision

• Typically by using an automated visual field machine

• This test is done to rule out any visual defects due to glaucoma

• VF defects may not be apperent until over 40% of the optic nerve

fiber layer has been lost

• VF testıng may need to be repeated

– A low risk of glaucomatous damage, the test may be performed

once a year

– A high risk of glaucomatous damage, test may be performed as

frequently as every 2 months

NORMAL VF

AUTOMATED VISUAL FIELD ANALYZER

STAGES OF GLAUCOMATOUS VISUAL FIELD DEFECTS

EARLY STAGE MODERATE STAGE END STAGE

OPTIC NERVE HEAD EXAMINATION

• Each optic nerve head is examined for any damage or abnormalities

• This may require dilation of the pupils to ensure an adequate examination of the optic nerves

• Fundus photographs,which are pictures of optic disc are taken for future reference and comparison

• Different imagıing studies may be conducted to document the status of optic nerve and to detect changes over time

FUNDOSCOPIC CHANGES

NORMAL OPTIC DISC

GLAUCOMATOUS OPTIC DISCS

CONFOCAL SCANNING LASER OPHTHALMOSCOPY

HEIDELBERG RETINA TOMOGRAPHY

NORMAL OD GLAUCOMATOUS OD

NORMAL TENSION GLAUCOMA

• People can have optic nerve

damage without having

elevated IOP

• The main reason of this

condition is vascular

insufficiency (ocular

ischemia)

• People can have elevated pressures without signs of optic nerve damage or visual field loss

• They are considered as a risk for glaucoma

• These people are known as glaucoma suspect

OCULAR HYPERTENSION

TWO DIFFERENT SITUATION

GENERAL TREATMENT OPTIONS FOR GLAUCOMA

• MEDICAL THERAPY

• LASER THERAPY

• SURGICAL THERAPY

THE GOAL OF GLAUCOMA TREATMENT IS

REDUCE THE PRESSURE BEFORE IT CAUSES

GLAUCOMATOUS LOSS OF VISION

•CHOLINERGICS•Pilocarpıne

•PROSTAGLANDINS•Latanoprost•Travoprost•Bimatoprost

MEDICAL THERAPY

•ADRENERGIC ANTAGONISTS(BETA BLOCKERS)•Nonselective

Timolol Levobunolol

Metipranolol•Selective

Betaxolol•ADRENERGIC AGONISTS

(SELECTIVE ALPHA-2 AGONISTS)•Apraclonidıne•Brimonidine

•CARBONIC ANHYDRASE INHIBITORS•Systemic

•Acetozolamide•Topical

•Dorzolamide•Brinzolamide

AQUEUS SUPPRESANTS

OUTFLOW FACILITATIVE DROGS

FIXED COMBINATIONS

TIMOLOL MALEAT

+Dorzolamide Latanoprost

+ +Travoprost

LASER THERAPY

• LASER TRABECULOPLASTY

– Argon laser trabeculoplasty (Argon

Laser)

– Selective laser trabeculoplasty

(ND:YAG)

• CYCLOPHOTOCOAGULATION

– Transscleral (ND:YAG, Diode)

– Transpupillary (Argon)

– Transvitreal (During vitrectomy)

– Endoscopic (Argon)

ARGON LASER TRABECULOPLASTY

DIODE LASER TRANSSCLERAL CYCLOPHOTOCOAGULATION

SURGICAL THERAPY

SHUNT (IMPLANT) SURGERY (AHMED GLAUCOMA VALVE)

FILTRATION SURGERY

(TRABECULECTOMY)

NON PENETRATING SURGERY

KEY POINTS• Glaucoma is progressive Optic neuropathy causes irreversible

vision loss.

• Glaucoma is not treatable entity, only further progression is restricted by timely intervention.

• Awareness about glaucoma is only the major action to restrict the progression entity.

• Medical or surgical therapy can only restrict its progression speed.

REFRENCES

• Comprehensive ophthalmology – A K Khurana Sixth Edition The Health Sciences Publishers

• Clinical Ophthalmology – Jack J Kanski &Brad Bowling Seventh Edition, Elsevier Saunders

• Shields Textbook of Glaucoma – R. Rand Allingham Sixth Edition

• Educational Sites (Wikipedia, Webmd.com….)

• The Glaucoma Book

THANK YOU