Primary Glaucoma

GLAUC MAJOHN PAUL A. TADAY, RN, MD-MPA LEVEL 2

GLAUCOMA: CLASSIFICATION

CONGENITAL & DEVELOPMENTAL GLAUCOMAS1

PRIMARY ADULT GLAUCOMAS1

SECONDARY GLAUCOMAS1

ABSOLUTE GLAUCOMA2

GLAUCOMA: CLASSIFICATION

PRIMARY GLAUCOMAGENERAL INFORMATION

PRIMARY GLAUCOMA: DEFINITION

OPTIC DISK CUPPING

VISUAL FIELD LOSS

OCULAR HYPERTENSION cases with constantly

IOP w/o any assoc. glaucomatous damage

NORMAL or LOW TENSION GLAUCOMA cases

with cupping of the disc and/or visual field

defects with a normal or IOP, NTG/LTG

PRIMARY OPEN-ANGLE GLAUCOMA & PRIMARY ANGLE-CLOSURE GLAUCOMA

• Refers to collection of diseases with chronic optic

neuropathy showing DISTINCTIVE CHANGES

• Mostly associated with IOP

• Normal or low-tension glaucoma also possible1

PRIMARY GLAUCOMA: EPIDEMIOLOGY

INCIDENCE ~60M people affected (Worldwide)

• Expected to from 64M (2015) to 76M (2020),

and 111M (2040)3

• 3M people (US) & 50% undiagnosed

RACE African Countries (highest prevalence)3

• Blacks & Whites (POAG > PCAG)

• China & Asians (PCAG – 90% of cases)

• Japan (Normal-tension glaucoma most common)

• Philippines (POAG = PCAG)4

AGE the mean IOP after 40 y/o possibly d/t

facility of aqueous outflow2

GENDER in older age

groups IOP with age

greater in females2

PRIMARY GLAUCOMA: PHYSIOLOGY

• Pathophysiology revolves around the

AQUEOUS HUMOUR DYNAMICS

• CILIARY BODY aqueous production

• ANGLE OF ANTERIOR CHAMBER formed by

root of iris, anterior-most part of ciliary body,

scleral spur, trabecular meshwork and

Schwalbe’s linePRINCIPAL OCULAR STRUCTURES:


• AQUEOUS OUTFLOW SYSTEM

TRABECULAR MESHWORK (CONVENTIONAL)



UVEOSCLERAL

OUTLOW

(UNCONVEN-

TIONAL)



UVEAL MESHWORK

CORNEOSCLERAL MESHWORK

JUXTACANALICULAR

(ENDOTHELIAL) MESHWORK

• TRABECULAR MESHWORK sieve-

like structure through which aqueous

humour leaves the eye

• SCHLEMM’S CANAL endothelial

lined oval channel to the aqueous

vein and intrascleral plexus



• COLLECTOR CHANNELS called

“Intrascleral Aqueous Vessels”, about

25-35 in number, terminate into

episcleral veins

AQUEOUS HUMOUR PRODUCTION:

• ULTRAFILTRATION

• SECRETION (ACTIVE TRANSPORT)

• DIFFUSION (PASSIVE TRANSPORT)


VACUOLATION THEORY

1 – Non-vacuolated stage

2 – Stage of early infolding of basal surface of

the endothelial cell

3 – Stage of macrovacuolar structure formation

4 – Stage of vacuolar transcellular channel

formation

5 – Stage of occlusion of the basal infolding

• “Most Accepted View” in aqueous humor flow

• Transcellular spaces exist in the endothelial

cells OPEN AS A SYSTEM OF VACUOLES

AND PORES, primarily in response to pressure

PRIMARY GLAUCOMA: MAJOR TYPES

OPEN ANGLE CLOSED ANGLE

PRIMARY OPEN ANGLEGLAUCOMA

PRIMARY OPEN ANGLE GLAUCOMA

DEFINITION• A type of primary glaucoma

• (–) obvious systemic or ocular cause

•IOP OPEN ANGLE of anterior chamber

• A.k.a. “CHRONIC SIMPLE GLAUCOMA OF

ADULT ONSET”

EPIDEMIOLOGY• Varies in different populations & 1/3 of all cases of glaucoma• RACE 4X more common & 6X more likely to cause blindness in BLACKS• AGE 5th & 7th decades• INCIDENCE affects ~ 1/100 of the population (of either sex) >40 y/o


ETIOLOGY &

PATHOPHYSIOLOGY

PREDISPOSING AND RISK FACTORS

• HEREDITY polygenic inheritance, 4%

risk in the offspring of patients

• AGE risk with age

• RACE more severe in black

• MYOPES nearsighted person

• DIABETICS higher prevalence

• SMOKING higher risk

• HIGH BLOOD PRESSURE

• THYROTOXICOSIS does not cause

IOP, but prevalence more in Graves’

ophthalmic patients than the normals IOP

AQUEOUS OUTFLOW FACILITY

RESISTANCE TO AQUEOUS OUTFLOW

TRABECULAR MESHWORK

THICKENING & SCLEROSIS

ABSENCE OF GIANT VACUOLES (CANAL

OF SCHLEMM)

CAUSE UNCERTAIN

UNCONTROLLED


VISUAL FIELD DEFECTS

FORCES THE LAMINA

CRIBROSA BACKWARDS

MECHANICAL EFFECTS

VASCULAR EFFECTS

DAMAGING CASCADE

ISCHAEMIC

ATROPHY

SQUEEZES THE

NERVE FIBRES

VISUAL FIELD LOSS

DEATH OF RETINAL

GANGLION CELLS (RGC’s)

LARGE CAVERNS OR LACUNAE ARE

FORMED (CAVERNOUS OPTIC ATROPHY)


CLINICAL MANIFESTATIONSSYMPTOMS

• Insidious & usually ASYMPTOMATIC

• Mild headache & eyeache

• Frequent changes in presbyopic

glasses

• Delayed dark adaptation

SIGNS• ANTERIOR SEGMENT SIGNS

pupil reflex becomes sluggish &cornea may show slight haze (LATESTAGES)

SIGNS

• IOP CHANGES IOP falls during

the evening (most patients) in Diurnal

Variation Test


SIGNS

• OPTIC DISC CHANGES seen on

fundoscopic exam

• VERTICALLY OVAL CUP d/t

selective loss of neural rim tissue in

the inferior and superior poles

• ASYMMETRY OF THE CUPS

difference of > 0.2 b/w two eyes

OPTIC DISK CUPPING

1. EARLY GLAUCOMATOUS CHANGES

Reveals one or more of the following

signs:

NORMAL


• LARGE CUP 0.6 or more

(Normal cup size – 0.3 to 0.4) may

occur d/t concentric expansion

• SPLINTER HAEMORRHAGES

present on/near optic disc margin

• PALLOR AREAS present on disc

• ATROPHY OF RETINAL NERVE FIBRE

LAYER seen with red free light

1. EARLY GLAUCOMATOUS CHANGES

Reveals one or more of the following

signs:

NORMAL EARLY CHANGE


• MARKED CUPPING cup size 0.7

to 0.9, excavation may even reach

the disc margin

• THINNING OF NEURORETINAL RIM

seen as a crescentric shadow

adjacent to the disc margin

• NASAL SHIFTING OF RETINAL

VESSELS appearance of being

broken off at the margin –

BAYONETTING SIGN

2. ADVANCED GLAUCOMATOUS CHANGES

Reveals one or more of the following signs:

NORMAL LATE CHANGE


• PULSATIONS OF THE RETINAL

ARTERIOLES may be seen at the

disc margin (a PATHOGNOMIC

SIGN of glaucoma), when IOP is

very high

• LAMELLAR DOT SIGN pores in

the lamina cribrosa are slit-shaped

and are visible up to the margin of

the disc

2. ADVANCED GLAUCOMATOUS CHANGES


NORMAL LATE CHANGE


• As the damage progresses, all the

NEURAL TISSUE of the disc is

destroyed and the OPTIC NERVE

HEAD appears white & excavated

3. GLAUCOMATOUS OPTIC ATROPHY


NORMAL OPTIC ATROPHY


• VISUAL FIELD DEFECTS usually run

parallel to the changes at optic nerve

head & progresses if IOP is not controlled

• SRF & IRF superior and inferiorradiating fibres from nasal half

• PMB PAPILLOMACULAR BUNDLEfrom macular area

• SAF & IAF superior & inferior

arcuate fibres from the temporal half

ANATOMICAL BASIS OF FIELD DEFECTS

• DISTRIBUTION OF RETINAL NERVE FIBRES





• From peripheral part – lie deep in the

retina but occupy the most peripheral

(superficial) part of the optic disc

• Fibres originating closer to the nerve

head – lie superficially and occupy a

more central (deep) portion of the disc.

EARLY LOSS IN THE VISUAL FIELD REGIONS

RETENTION OF CENTRAL VISION TILL END

ANATOMICAL BASIS OF FIELD DEFECTS

• ARRANGEMENT OF NERVE FIBRES WITHIN

OPTIC NERVE HEAD

• ARCUATE FIBERS (SAF & IAF) occupy the

superior & inferior temporal half of optic

nerve head – most sensitive to damage

• MACULAR FIBRES most resistant to theglaucomatous damage





PROGRESSION OF FIELD DEFECTS

• ISOPTER CONTRACTION mildgeneralized constriction of central aswell as peripheral field

EARLIEST

VISUAL FIELD

DEFECT

• BARING OF BLIND SPOT exclusion

of the blind spot from the central

field d/t inward curve of the outer

boundary of 30° central field

• SMALL WING-SHAPED PARACENTRAL

SCOTOMA appear below or above

the blind spot in BJERRUM'S AREA

EARLIEST

CLINICALLY

SIGNIFICANT

FIELD DEFECT

• SEIDEL’S SCOTOMA “Sickle-shaped”

in time, paracental scotoma joins the

blind spot


• ARCUATE OR BJERRUM’S SCOTOMA

formed by extension of Seidel’s scotoma

in an area either above or below the

fixation point to reach the horizontal line

• RING / DOUBLE ARCUATE SCOTOMA

develops when the two arcuate

scotomas join together

• ROENNE'S CENTRAL NASAL STEP two

arcuate scotomas run in different arcs and

meet to form a sharp right-angled defect

at the horizontal meridian

• PERIPHERAL FIELD DEFECTS

can appear in early and

late stages

• ADVANCED FIELD DEFECTS

eventually only a small

island of central vision

(TUBULAR VISION) are left



DIAGNOSTIC FACTORS• CRITERIA to diagnose EARLY, MODERATE and SEVERE glaucomatous field defects


• TONOMETRY measures the IOP

TWO BASIC TYPES OF TONOMETERS:

INDENTATION (IMPRESSION)

2. Schiotz TonometerAPPLANATION

1. Goldmann

Tonometer


• DIURNAL VARIATION TEST

useful in detection of early cases

A – Normal slight morning rise

B – Morning rise seen in 20% cases

C – Afternoon rise seen in 25%

D – Biphasic variation seen in 55%

• SLIT-LAMP EXAMINATION to R/O

causes of 2° Open Angle Glaucoma

• WATER DRINKING TEST eyes with

glaucoma with greater response to

water drinkinga. 8 hours fasting, then baseline IOP

b. Patient drinks 1L of water, then IOP noted

q 15min for 1 hour

c. Rise of 8 mmHg or more (DIAGNOSTIC)

• NERVE FIBRE LAYER ANALYZER to

detect damage in retinal nerve fibres


• PERIMETRY detect visual field defects

TWO CLASSIFICATIONS OF PERIMETERS:

GOLDMANN’S PERIMETER

1. Manual PerimeterLISTER’S PERIMETER

2. Automated Perimeter

HUMPHREY FIELD ANALYSER

• ADVANTAGES OF AUTOMATED:

1. Level of precision & consistency

2. data storage capability & ease

3. Statistical comparison


• GONIOSCOPY primary importance in POAG is

to rule out other forms of glaucoma

GOLDMANN’S GONIOLENS & TECHNIQUE OF GONIOSCOPY

• APPLICATIONS OF GONIOSCOPY:

1. Classification of glaucoma into open angle and

closed angle based on configuration of the angle

2. Localization of foreign bodies, abnormal blood

vessels or tumors in the angle.

3. Demonstration of extent of peripheral anterior

synechiae and hence planning of glaucoma surgery

4. Direct goniolens is used during goniotomy


SHAFFER’S

SYSTEM OF

GRADING THE

ANGLE WIDTH

MOST COMMONLY USED

OCULARHYPERTENSION

OCULAR HYPERTENSION

DEFINITION• “Glaucoma Suspect”

• IOP constantly >21mmHg but NO OPTIC

DISC or VISUAL FIELD CHANGES

ETIOLOGIC FACTORS

HIGH RISK FACTORS

• IOP CONSTANTLY >28 mmHg

• SIGNIFICANT DIURNAL VARIATION difference

of > 8mmHg

• Significantly positive WATER DRINKING TEST

• Association with SPLINTER HEMORRHAGES

• RETINAL NERVE FIBER LARGE DEFECTS

• PARAPAPILLARY CHANGES

• CENTRAL CORNEAL THICKNESS < 555 μm

Should be CAREFULLY MONITORED

by an ophthalmologist, should be

treated as cases of POAG in the

presence of HIGH RISK FACTORS

OCULAR HYPERTENSION

OTHER RISK FACTORS

• SIGNIFICANT ASYMMETRY in the cup size of

the two eyes difference of more than 0.2

• Strong FAMILY HISTORY of glaucoma

• When associated with HIGH MYOPIA,

DIABETES or PIGMENTARY CHANGES in the

anterior chamber

MANAGEMENT• WITH HIGH RISK FACTORS treated on

the lines of POAG (aim is to reduce IOP by20%)

• NO HIGH RISK FACTORS annuallyfollowed by examination of optic disc,perimetry and record of IOP, treatment notrequired till glaucomatous damage isdocumented

NORMAL TENSIONGLAUCOMA

NORMAL TENSION GLAUCOMA

DEFINITION• (NTG), A.k.a LOW TENSION GLAUCOMA,

typical glaucomatous DISC CHANGES, but

WITH / WITHOUT VISUAL FIELD DEFECTS

• Associated with IOP constantly <21 mmHg

EPIDEMIOLOGY

• Variant of POAG (16% of all

cases of POAG)

• AGE prevalence >40 y/o is

0.2%

ETIOLOGY & PATHOPHYSIOLOGY

OPTIC NERVE

SUSCEPTIBLE

CHRONIC LOW

VASCULAR

PERFUSION

PREDISPOSING AND RISK FACTORS

• Raynauld phenomenon

• Migraine

• Nocturnal systemic hypotension

• Overtreated systemic hypertension

• blood flow velocity (ophthalmic artery)

VASCULAR EFFECT ONLY!


CLINICAL MANIFESTATIONS• Disc changes & visual field defects

(Similar to POAG)

• NORMAL IOP

• Other features of NTG are some

ASSOCIATIONS mentioned

DIFFERENTIAL DIAGNOSIS• POAG early stages POAG may

present with normal IOP

• Congenital optic disc anomalies• APPROXIMATELY 60% HAVE

PROGRESSIVE VISUAL FIELD LOSS


MANAGEMENT• MEDICAL TREATMENT to IOP IOP

by 30% (about 12-14 mmHg)a. BETAXOLOL DOC d/t in addition toIOP, also optic nerve blood flow

b. Other Beta Blockers and Adrenergicdrugs (DIPIVERAFRINE) be avoided(causes nocturnal systemic hypotension& are likely to affect adversely theoptic nerve perfusion)

c. NEUROPROTECTIVE DRUGS maybe preferred like “Brimonidine”

d. PROSTAGLANDIN ANALOGUES

greater ocular hypotensive effect

• TRABECULECTOMY considered

when progressive field loss occurs

despite IOP in lower teens

• SYSTEMIC Ca2+ BLOCKERS for

confirmed peripheral vasospasm

• SYSTEMIC BP MONITORING

PRIMARY ANGLE-CLOSURE

GLAUCOMA

PRIMARY ANGLE-CLOSURE GLAUCOMA

DEFINITION• A type of primary glaucoma, (–) obvious

systemic or ocular cause

• IOP occurs d/t BLOCKAGE of the

aqueous humour outflow

• Closure of a NARROWER ANGLE of the

anterior chamber

EPIDEMIOLOGY• AGE more common in 5th decade of life

• GENDER F>M (Ratio 4:1)

• RACE South-East Asian, Chinese (50% of

all primary glaucoma) or Inuit/ Eskimos2

• SEASON higher in rainy season

• FAMILY HISTORY inherited

• TYPE OF PERSONALITY common in

individuals with unstable vasomotors


ETIOLOGY & PATHOPHYSIOLOGY

I. ANATOMICAL FACTORS

• HYPERMETROPIA with shallow

anterior chamber

• Iris-lens DIAPHRAGM placed

anteriorly

• NARROW ANGLE of anterior

chamber, which may be d/t:

a. Small eyeball

b. Relatively large size of the

lens & smaller diameter of

the cornea

c. Bigger size of the ciliary

body

II. GENERAL FACTORS

• AGE• GENDER• RACESEASON• FAMILY HISTORY• TYPE OF PERSO-

NALITY

PREDISPOSING

RISK FACTORS

The following factors may

PRECIPITATE an attack:

• DIM ILLUMINATION

• EMOTIONAL STRESS

• MYDRIATIC DRUGS like

Atropine, Tropicamide

PRECIPITATING

FACTORS INCREASED

AMOUNT OF

APPOSITION B/W

IRIS

ANTERIORLY

PLACED LENS WITH

CONSIDERABLE

PRESSURE

NORMAL PUPILMILD PUPIL DILATATION


RELATIVE

PUPIL

BLOCK

AQUEOUS HUMOR COLLECTS IN THE POSTERIOR CHAMBER

PUSHES THE PERIPHERAL FLACCID IRIS ANTERIORLY

IRIS

BOMBE

APPOSITIONAL

ANGLE CLOSURE

SYNECHIAL

ANGLE CLOSURE

ATTACK OF IOP

MAY LAST LONGER

ACUTE PACG

CHRONIC PACG

Results from the following

CIRCUMSTANCES:

• CREEPING SYNECHIAE

• SUBACUTE PACG ATTACKS

• MIXED MECHANISM


CLINICAL MANIFESTATIONS:

LATENT PRIMARY ANGLE-CLOSURE

GLAUCOMA “Glaucoma suspect”

SUBACUTE OR INTERMITTENT PACG

ACUTE ANGLE-CLOSURE GLAUCOMA

POSTCONGESTIVE

ANGLE-CLOSURE GLAUCOMA

CHRONIC PACG

FIVE DIFFERENT CLINICAL ENTITIES





INDICATES DECREASED AXIAL ANTERIOR

CHAMBER DEPTH

• Eyes with shallow anterior chamberwith an OCCLUDABLE ANGLE

• SYMPTOMS absent• ECLIPSE SIGN elicited by shining a

penlight across the anterior chamberfrom temporal side, noting a shadowon the nasal side




• GONIOSCOPIC EXAMINATION it

shows very narrow angle (SHAFFER

GRADE 1)

• SLIT-LAMP BIOMICROSCOPIC SIGNS:

a.axial anterior chamber depth

b.Convex shaped iris lens diaphragm

c. Close proximity of the iris to cornea

in the periphery








• VAN HERICK SLIT-LAMP GRADING

used when gonioscope is not available

(FAIR ACCURACY)

• Peripheral Anterior Chamber Depth

(PACD) compared to the adjacent

corneal thickness (CT) and the

presumed angle width

• CLINICAL COURSE if without Tx,

may follow any of the following:

a. IOP may remain NORMAL

b. SUBACUTE or ACUTE angle-closure

glaucoma may occur subsequently

c. CHRONIC angle-closure glaucoma

may develop without passing

through subacute or acute stage



VAN HERICK METHOD OF

SLIT-LAMP GRADING

A – Grade IV

B – Grade III

C – Grade II

D – Grade I

E – Grade 0

GRADES:Grade 4 (WIDE OPEN ANGLE)

• PACD = 3/4 to 1 CT

Grade 3 (MILD NARROW)

• PACD = ¼ to ½ CT

Grade 2 (MODERATE NARROW)

• PACD = ¼ CT

Grade 1 (EXTREMELY NARROW)

• PACD < ¼ CT

Grade 0 (CLOSED ANGLE)

• PACD Nil




• Attack of TRANSIENT IOP (40-50mmHg) (last for minutes to 1-2 hours)

• Usually PRECIPITATED by:a. PHYSIOLOGICAL MYDRIASIS

reading in dim light, watching TV orcinema in darkened room, or duringanxiety (Sympathetic Overactivity)

b. PHYSIOLOGICAL SHALLOWINGOF ANTERIOR CHAMBER afterlying in prone position


• SYMPTOMS unilateral transient

blurring of vision, coloured halos

around light, headache, browache

and eyeache on the affected side

COLOURED HALOS AROUND LIGHT




• During PE, eye is white & not congested

• All the signs described in LATENT PACG

can be elicited in this phase ALSO

• CLINICAL COURSE if without Tx,

may follow any of the following:

a. Attack of ACUTE PACG

b. CHRONIC PACG without passing

through acute stage





• Attack of Acute PACG occurs d/t a

sudden total angle closure leading to

SEVERE RISE in IOP


SIGHT THREATENING EMERGENCY!

SYMPTOMS• PAIN sudden onset of very severe pain

that radiates along the CN-V branches

• NAUSEA, VOMITING, PROSTRATIONS

• Rapid progress of VISION LOSS also

with redness, photophobia & lacrimation

(PRESENT IN ALL CASES)

• PAST HISTORY ~5% (+)Hx of typical

previous transient attacks of subacute

angle-closure glaucoma

SIGNS

• LIDS may be edematous

• CONJUNCTIVA congested

• CORNEA edematous & insensitive

• ANTERIOR CHAMBER very shallow

• ANGLE OF ANTERIOR CHAMBER

closed completely (SHAFFER GRADE0)

• IRIS may be discoloured





•NOTE CILIARY CONGESTION,

•CORNEAL EDEMA & MIDDILATED PUPIL

DISCOLOURED IRISVERY SHALLOW –ANTERIOR CHAMBER

SIGNS

• IOP it is usually markedly elevated,

b/w 40-70 mmHg (NV:10-21mmHg)

• PUPIL semi-dilated, vertically oval

and fixed, usually non-reactive to both

light & accommodation

• OPTIC DISC edematous, hyperemic

• FELLOW EYE shows shallow anterior

chamber and a narrow angle





PUPIL NON-REACTIVE TO BOTH LIGHT & ACCOMMODATION

EDEMATOUS & HYPEREMIC OPTIC DISC




POSTCONGESTIVE


• VOGT’S TRIAD seen with any type

of post-congesive glaucoma & in

treated acute congestive glaucoma:

a. GLAUCOMFLECKEN an anterior

sub-capsular lenticular opacity

b. PATCHES OF IRIS ATROPHY

c. SLIGHTLY DILATED NON-REACTING

PUPIL due to sphincter atrophy PATCHES OF IRIS ATROPHYSLIGHTLY DILATED NON-

REACTING PUPIL

GLAUCOMFLECKEN

VOGT’S TRIAD




POSTCONGESTIVE


1.POSTSURGICAL POSTCONGESTIVE

PACG after laser peripheral

iridotomy (PI) treatment for an

attack of acute PACG

FOUR CLINICAL SETTINGS

• Clinical status of eye after an attack of

acute PACG with or without treatment

• With normalized IOP post-laser Tx,

the eye usually “QUITENS” after some

time with/without s/s of acute attack

• With raised IOP after unsuccessful Tx,

there occurs a STATE OF CHRONIC

CONGESTIVE GLAUCOMA




POSTCONGESTIVE


2.SPONTANEOUS ANGLE OPENING

may very rarely occur in some cases

and the attack of acute PACG may

subside itself without treatment

FOUR CLINICAL SETTINGS

• Clinical status of eye after an attack of

acute PACG with or without treatment

3. CHRONIC CONGESTIVE PACG

continuation of acute congestive angle-

closure glaucoma when no Tx or when is

unsuccessful

a. EYE permanently congested, pain

reduced d/t “ACCLAMATIZATION”

b. IOP remains constantly raised

c. LID & CONJUCTIVAL EDEMA

d. OPTIC DISC may show cupping

e. Other features are similar to acute

congestive angle-closure glaucoma

4. CILIARY BODY SHUT DOWN

temporary cessation of aqueous humor

secretion due to ischemic damage

a. IOP is low, PAIN is “MARKEDLY”

• Similar to POAG, EXCEPT that the

angle in Chronic PACG is narrow

• IOP constantly raised

• EYEBALL it is usually remains white

(without congestion) & PAINLESS

• OPTIC DISC may show cupping

• VISUAL FIELD DEFECTS like POAG

• GONIOSCOPY variable degree of

angle closure




CHRONIC PACG

PAINLESS EYEBALL


ABSOLUTE PACG if no Tx for chronic

phase, with/without sub-acute attacks,

gradually passes into “FINAL PHASE”

a. PAINFUL BLIND EYE irritability & now

completely blind (NO LIGHT PERCEPTION)

b. PERILIMBAL REDDISH BLUE ZONE slight

ciliary flush around the cornea d/t dilated

anterior veins

c. CORNEA clear but insensitive

d. ANTERIOR CHAMBER very shallow

e. IRIS becomes atrophic

f. PUPIL fixed, dilated, greenish hue

g. OPTIC DISC shows atrophy

h. INTRAOCULAR PRESSURE high

i. EYEBALL becomes stony hard

PERILIMBAL REDDISH BLUE ZONE

PAINFUL BLIND EYE INSENSITIVE

CORNEA


DIAGNOSTIC FACTORS:

CLINICAL ENTITY DIAGNOSIS

LATENT PRIMARY ANGLE-

CLOSURE GLAUCOMA

DIAGNOSIS MADE BY:

• CLINICAL SIGNS described beforehand

• PROVOCATIVE TESTS designed to precipitate closure of

the angle in the ophthalmologist’s office, where it can be

treated promptly

a. PRONE-DARKROOM TEST it is the most popular & best

physiological provocative test for PACG

b. MYDRIATIC PROVOCATIVE TEST not preferred now

SUBACUTE PRIMARY ANGLE-

CLOSURE GLAUCOMA

ACUTE, POSTCONGESTIVE,

CHRONIC, ABSOLUTE PACG*DIAGNOSIS USUALLY OBVIOUS FROM THE CLINICAL SIGNS1


PRONE-DARKROOM TEST

MYDRIATIC PROVOCATIVE TEST

DIAGNOSTIC FACTORS:


CORNEAL ULCERATION

STAPHYLOMA FORMATION

ATROPHIC BULBI

D/T prolonged epithelial edema & insensitivity

Sclera becomes very thin and atrophic,

ultimately bulges out (CILIARY staphyloma &

EQUATORIAL staphyloma)

Ciliary body degenerates, IOP and the

eyeball shrinks

COMPLICATIONS

If untreated, d/t prolonged IOP the following may occur:

CORNEAL

ULCERATION

STAPHYLOMA

FORMATION

ATROPHIC BULBI

REFERENCES

1 – Khurana's Ophthalmology - 4th Edition 2007

2 – Vaughan and Asbury's Ophthalmology - 17th Edition 2007

3 – http://eyewiki.aao.org/Glaucoma_in_the_Developing_World

4 – http://roqueeyeclinic.com/eye-conditions/glaucoma/80-glaucoma-classification-epidemiology

-- DR. JOSE RIZAL

Philippine National Hero

Ophthalmologist

END

Health & Medicine

Primary Glaucoma