Glaucoma

Catherine Qui-Macaraig, MD
UST Hospital
Cardinal Santos Medical Center
American Eye Center
Glaucoma
An optic neuropathy with:
o Optic disc cupping
o Visual eld loss
o Usu! "ith increased #O$
G%AUCOMA is an optic neuropathy
characteri&ed 'y optic cupping and visual
feldloss.
Theories on #O$ damaging ner(e
intraocular pressure inter)eres with 'lood
*ow in the optic ner(e+ which has 'een
made suscepti'le 'y )actors that reduce
the a'ility o) 'lood *ow to autoregulate in
the optic ner(e head!
Another current theory is that pressure,
induced de)ormation o) the lamina cri'rosa
harms the a-ons passing through it!
Optic .isc
Has a central depression, the physiologic
cup
Cup si&e, dependent on 'ers and opening
in sclera
Hyperopes, small cup
Myopes, 'ig cup
Physiologic cup
Central depression
Si&e depends on the 'ul/ o) the 'ers that
)orm the optic ner(e and the scleral
opening passing through it
Glaucomatous optic atrophy
%oss o) dis/ su'stance
.etected as enlargement o) the optic disc
cup
Optic ner(e
.iagnosis 0 clinical practice
1ecognition o) 2signs3 o) glaucoma
4euroretinal rim 5cup
Vessels
$eripapillary area
1etinal ner(e 'er layer
1ecognition o) change )rom 'aseline
The Cup: si&e
4ormal c5d 6!7
4ormal C5. 6!8
larger than normal with a C5. ratio o) 6!8!
Howe(er there is a good neural rim as seen on the
temporal side 9your right: suggesting normal
retinal )unction
Generali&ed enlargement o) the cup
;ounger patients
Male < )emale9slightly:
Mar/ed ele(ated #O$
4o signicant systemic associations
1are optic disc hemorrhages
.i=use 14>% de)ects 5di=use V> loss
$hysiologic Cup, signicant hyperopia
The disc here is small and compact and
o)ten more (ascular in appearance than
normal!
?ecause the eye is small and the disc more
compact+ the physiologic cup is o)ten
missing
$hysiologic Cup, myopic disc
appears larger+ and o)ten slopes
temporally!
The physiologic cup appears larger and has
no deniti(e edge temporally!
.isc Changes in G%
.isc Changes in G%
Enlarged cup and pallor in area o) cupping
Concentric or supero,in)erior cupping
>ocal notching o) rim
4asal displacement o) (essels
?ean pot cupping: end,stage
.isc Changes in G%
Enlarged cup and pallor in area of
cupping
Concentric or supero,in)erior cupping
>ocal notching o) rim
4asal displacement o) (essels
?ean pot cupping: end,stage
Optic disc si&e assessment
Sophisticated techni@ues
$lanimetry
Scanning laser tomography
Oct
Easy techni@ues
Comparing with light spot o) direct
ophthalmoscopy
Measurement o) disc diameter at the slit
lamp
Asymmetry o) the optic cups
.isc Changes in G%
Enlarged cup and pallor in area o) cupping
Concentric or supero,in)erior cupping
Focal notching of rim
4asal displacement o) (essels
?ean pot cupping: end,stage
Focal Notching of the Rim
#n)erior notch
loss o) tissue )orming a notch at the in)erior
pole!
The openings in the lamina cri'rosa
92laminar dots3: are (isi'le in the notch
right to the disc margin+ a monocular clue
that tissue is a'sent in this region! The
course o) the in)erior temporal (enous
tri'utary disappears as it passes o(er the
sharp in)erior disc margin!
Superior 4otch
this neural retinal rim is a'sent 9A11O":
.isc Changes in G%
Enlarged cup and pallor in area o) cupping
Concentric or supero,in)erior cupping
>ocal notching o) rim
Nasal displacement of retinal vessels
Bean pot cupping: end-stage
?ean $ot Cupping
$rogression o) cup
$eripapillary Atrophy
Optic 4er(e Head and 4er(e >i'er %ayer
#maging
Visual loss in glaucoma
1etinal ganglion cell atrophy
Thinning o) the inner nuclear and retinal
ner(e 'er layer
A-onal loss in the optic ner(e
4er(e >i'er %ayer E(aluation
Ganglion cell death causes (isual eld loss
in G%
retinal 4>% is composed o) the a-ons o)
these ganglion cells+ astrocytes+ and
neuroglia
4>% e(aluation: >or the early diagnosis o)
glaucoma and o) glaucomatous progression
As much as A6B o) the 4>% may 'e lost
'e)ore a (isual,eld de)ect is detected 'y
perimetric testing!
4ormal 4>%
>rom the nasal retina the 'ers ta/e a
straight course toward the disc! A-ons
originating temporal to the )o(ea arc
around the macula to enter the upper and
lower poles o) the optic ner(e head! The
macula 'ers pass directly to the temporal
@uadrant o) the disc in the papillomacular
'undle
1etinal ner(e 'er layer 914>%:
NFL Anormalities
4>% loss may 'e di=use or locali&ed
di=use loss o) striations
)ocal areas o) less (isi'le+ or loss o)+
striations in an arcuate or wedge
distri'ution
increased prominence o) medium,si&ed
(essels
1etinal ner(e 'er layer in glaucoma
A cur(ed wedge represents the loss o)
ner(e 'er 'undles corresponding to a
sector o) the disc mar/ed 'y a splinter
hemorrhage 9small cur(ed arrow:! Optic
disc hemorrhages precede retinal ner(e
'er layer de)ects in ocular hypertension!
Assessment o) the Optic 4er(e
.irect Ophthalmoscopy 9C.:
#ndirect Ophthalmoscopy 97.:
>undus $hotograph
>undus $hotography
the Topcon #magenet
a pair o) stereo images are shown at the
top with )our operator,pro(ided control
points on the right image+ and the
calculated cup margin and elliptical disc
margin are superimposed on the le)t image
gray,scale representations o) intensity
(alues in an original pair o) digiti&edstereo
images!
digitally ltered (ersions o) these original
stereoimages+ with each column
corresponding to the same perspecti(e
Humphrey 1etinal Analy&er
a grid o) points selected in the le)t stereo
imagewas matched to corresponding points
in the right stereo image+ using a cross,
correlation operation that identies pairs
o)corresponding points 'y the similarity o)
a window o) intensity (alues around each
point!
Optical coherence tomography 9OCT:
a noncontact+ nonin(asi(e cross,sectional
imaging techni@ue that produces high,
resolution measurements o) the eye!
#ntraocular $ressure
.etermined 'y rate o) a@ueous production
and resistance to out*ow )rom the eye
4ormal range: D6 0 CA mmHg
#4T1AOCU%A1 $1ESSU1E 9#O$:
Rate of a!ueous production"
Resistance to a!ueous out#o$
%&P can e monitored y applanation
tonometry
Portale: Per'in(s" )onopen
Schiot& Tonometer
#ndentation tonometer
Applanation)onometer
Tono,pen
Noncontact )onometer
$neumatotonometer
#O$ and Central Corneal Thic/ness
$achymeter
measures corneal thic/ness
)hic' corneas * high %&P
)hin corneas * relatively lo$ %&P
A@ueous Humor
Optical transparency
4utrition
Structural integrity
Made 'y ciliary processes o) the ciliary
'ody
>ills anterior and posterior cham'ers o) eye
Composition similar to plasma 'ut with
higher ascor'ate+ pyru(ate and lactateE
%ower protein+ urea+ and glucose
A@ueous *ow
A@euous humor is )ormed 'y acti(e
secretion )rom the ciliary processes 9A:!
.rainage occurs through the out*ow
pathways+ principally )rom the tra'ecular
meshwor/ 9?: and SchlemmFs canal 9C: into
the a!ueous (eins 9.:!
A smaller proportion o) the a!ueous
humor ma/es its way directly into the
ciliary 'ody 9u(eoscleral pathway: and is
drained 'y way o) the ciliary muscle+ the
suprachoroidal space+ and the sclera 9E:!
A@ueous out*ow systemis comprised o):
tra'ecular meshwor/
SchlemmFs canal
the a@ueous (eins
)raecular +esh$or'
u(eal meshwor/, more supercial
corneoscleral meshwor/, deeper
Gu-tacanalicular connecti(e tissue 9HCT:
adGacent to SchlemmFs canal
Ciliary muscle
o attached to TM I increases pore si&e
Gonioscopy
Allows direct (isuali&ation o) the angle
structures:
o .ar/, Schwal'eJs line
o Upper light,non,ltering meshwor/
o .ar/,posterior ltering meshwor/
o %ight,scleral spur
o .ar/ ciliary 'ody 'and
Visual >ield E-amination
$erimetry
a must in the diagnosis and )ollow,up o)
glaucoma
E-amines the central 76 degrees o) the
eld and peripheral K6 degrees
>or detection o) scotoma+ a 'lind or
partially 'lind area in the (isual eld
Visual eld de)ects are not detected until
there is a'out A6B retinal ganglion loss!
)ypes of Glaucoma
$rimary Glaucoma
O$E4 A4G%E
o impaired out*ow )rom a'normal
drainage system
4O1MA% TE4S#O4
A4G%E C%OSU1E
o impaired a@ueous access to out*ow
drainage system
Acute
Su'acute
Chronic
$lateu iris
Glaucoma suspect
high #O$E i) the (isual,eld e-amination is
normal
normal 92low3: tension glaucoma
&ptic disc cupping
,isual -eld loss
%&P 0 within normal range
4ormal Tension Glaucoma
Ocular Hypertension
. &ptic disc cupping
. ,isual -eld loss
Elevated %&P
Ocular Hypertension ris/ )or G%
Angle
O$E4: >ull (iew o) the tra'ecular meshwor/
9TM: scleral spur+ iris processes
4A11O": Only Schwal'eJs line and small
portion o) TM
C%OSE.: 4o (iew o) Schwal'eJs line
$rimary Acute Angle Closure G%
Sudden and se(ere 'lurring
Se(ere pain+ nausea and (omiting
#ncreased intraocular pressure 9#O$:
Acute angle closure glaucoma isan
ophthalmic emergency!
+anagement
/yperosmotic agent
o reduces (itreous (olume
o ma/es the 'lood hypertonic+ thus
drawing out the water out o) the
(itreous
o #V Mannitol
Oral glycerin mi-ed with dalandan Guice
Pilocarpine eye drops
o #ncrease a@ueous out*ow 'y action
on the TMthrough contraction o)
the ciliary muscle
o $upillary constriction
&ral aceta0olamide
o Car'onic anhydrase inhi'itor
o Can suppress a@ueous production
A6 0 K6B
o 4ot )or long term use
o CL6 mg ta' tid
1urgical &ptions
$eripheral #ridectomy
Su'acute Angle Closure G%
1ecurrent short episodes o) inc! #O$
$ain+ #ncrease #O$+ Ciliary *ush or
circumcorneal inGection
?lurred (ision+ halos around lights+
Attac/s o)ten in the e(ening+
resol(es o(ernight
Gonioscopy: 4arrow angle
T-: %aser $eripheral iridotomy
#ris $lateau
Chronic Angle Closure Glaucoma
o Genetically narrrow angles
o .e(elop $AS gradually
o Symptoms li/e $OAG
o Treatment:
o tra'eculectomy
Primary &pen-Angle GL 2P&AG3
Ele(ated #O$ 0 treata'le )actor
Optic .is/ Cupping
Visual >ield de)ect
Open angle
$athophysiology
.eposition o) e-tracellular material
o within the TM and
o 'eneath the endothelial lining o) the
SchlemmJs canal
)ypes
4uvenile-onset
o Chromosome D mutation in
myocilin gene
o LB )amilial+ 7B non)amilial
Adult onset
o Chromosome 7 autosomal
dominant
GL 1creening
>irst degree relati(es o) those with $OAG
1egular screening e(ery two years )rom
age 7L years and annually )rom age L6
GL Follo$-up
Once a glaucoma+ always a glaucoma
1egular )ollow up+ a lifetime o) )ollow,up
$eriodic #O$ measurement + Visual eld
test or perimetry + 14>% thic/ness
5ongenital Glaucoma
D! $rimary Congenital G%
a'normality in the anterior cham'er
angle
C! Anterior segment de(elopmental anomalies
7! .e(elopmental anomalies assJd with otherocular
or e-traocular a'normalities
Mani)est
L6B at 'irth
M6B in the rst K months
86B end o) the rst year
EARL6:
o Epiphora
o #ncrease #O$
o Glaucomatous optic disc cupping
o $hotopho'ia+ loss o) corneal luster
LA)E:
o corneal diameter greater than D6!L mm
o increased anterior cham'er depth
o corneal opacity
/aa(s1triae:
traumatic rupture o) descemetJs
mem'rane
5ongenital Glaucoma
E-amination under anesthesia!
9#O$+ Gonioscopy+ Optic dis/:
Treatment is surgical! Success rate is a'out
L6B!
Medical treatment is temporarily gi(en!
Goniotomy
o procedure o) choice
>ailure o) medical and surgical treatment:
cyclodestructi(e procedures
Cryotheraphy
.iode laser+ diathermy+ thermal ;AG
Endoscopic laser 0 ciliary 'ody
Anterior 1egment 7ysgenesis
Autosomal dominant
Mutations in chromosome A and D7
Glaucoma de(elop in L6B o) cases
, late childhood or
, early adulthood
PER%P/ERAL &PA5%)%E1
A4T! SEGME4T .;SGE4ES#S
ANE4>E%.J S A4OMA%;
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O SEGME4T .E>ECT
1E#GE1JS A4OMA%;
$E1#$HE1A% A?4O1MA%#T#ES
O O #1#S CHA4GES
ANE4>E%.,1#EGE1JS S;4.1OME
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.EVE%O$ME4TA% .E>ECT
ANE4>E%.JS A4OMA%;
?#%ATE1A%
$1OM#4E4T+ A4TE1#O1%; .#S$%ACE.
SCH"A%?EJS %#4E
OCCAS#O4A% MEGA%O O1 M#C1OCO14EA
GO4#OSCO$;
O $1OM#4E4T SCH"A%?EJS
%#4E!E4%A1GEME4T 5 .#S$%ACE.
O T#SSUE ST1A4.S ?1#.GE THE
A4G%E
O O$E4 A4G%E
O V#S#?%E T1A?ECU%A1 MESH"O1P
O SC%E1A% S$U1 O?SCU1E. ?;
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#1#S CHA4GES
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CO1ECTO$#A
ECTO$#O4 UVEAE
#1#S AT1O$H; "#TH HO%E >O1MAT#O4
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ANE4>E%.,1#EGE1JS S;4.1OME
L6B .EVE%O$ G%AUCOMA
ASSOC#ATE. "#TH
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O ST1A?#SMUS
O .E1MO#.
O 1ET#4A% .ETACHME4T
O CHO1#O1ET#4A% CO%O?OMA
O H;$O$%AS#A , CHO1O#.
O H;$O$%AS#A , O$T#C 4E1VE
ENT1AOCU%A1 S;M$TOMS
MAN#%%A1; H;$O$%AS#A
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M#C1O.O4T#A
H;$O.O4T#A
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1OU4. CENTRAL O$AC#T;
A?SE4T CO14EA% E4.OTHE%#UM I
.ESCEMETJS
ST1OMA% TH#44#4G
9 O5, : #1#S ST1A4.S#4 THE $OSTE1#O1
CO14EA
A4#1#.#A
, (estigial iris
, glaucoma 'e)ore adolescence
, re)ractory to medical or surgical treatment
1econdary Glaucoma
D! $igmentary G%
C! $seudo,E-)oliation Syndrome
7! Changes in the U(eal Tract
U(eitis
Ciliary ?ody Swelling
Tumor
A! Changes in the lens
%ens .islocation
#ntumescence o) the %ens
$hacolytic Glaucoma
U(eitis
#O$ can 'e high!
o #n*ammatory cells 'loc/ the TM
#O$ can 'e low!
o Ciliary 'ody shutdown!
Sometimes+ when in*ammation is 'eing controlled+
#O$ starts to rise!
Secclusiopupillae
7K6 degree posterior synechiae
#ris 'om'e
Acute angle closure G%
#ntensi(e mydriasis
T-: %aser iridotomy 5 Surgical iridectomy
$seudo,e-)oliation Syndrome
Fla'e-li'e deposits of -rillary
material in the
, anterior lens capsule
, ciliary process
, &onule
, posterior iris sur)ace
, anterior cham'er
, TM
$igmentary G%
A'normal deposition o) pigment in the TM+
posterior corneal sur)ace 9Pru/en'erg
spindle: and iris transillumination de)ects
Ele(ated #O$ a)ter e-ercise and pupillary
dilatation
Pru/en'ergJs spindle
Myopic males+ 'etween CL to A6 years
#) w5o G%: $igmentary .ispersion
Syndrome
Autosomal dominant+ chromosome M
%aser Tra'eculoplasty+
Tra'eculectomy with mitomycin
Angle recession
Neovascular Glaucoma
retinal ischemia
o inCentral retinal (ein occlusion or
proli)erati(e dia'etic retinopathy
1turge-8eer 1yndrome
$ort wine stain or (enous angiomata or
ne(us *ammeus in the distri'ution o)
the C4 V
1aised episcleral (enous pressure due
to hemangioma o) the episclera
Carotid,ca(ernous stula
Anterior cham'er anomalies
o A6B de(elop
choroidalhemangioma on the
same side
o %eptomeningealangiodysplasia
o) the 'rain and mninges
8L B Gac/sonianse&ures
K6B mental retardation
Cere'rocortical atrophy
Steroid 0 #nduced G%
$eriocular< Topical < Systemic
Topical:
.e-amethasone < $rednisolone
acetate<>luoromethalone acetate
#O$ increase a)ter prolonged use+
usually months
#O$ increase right a)ter it is used
9steroid responders:
$eriodic tonometry and
ophthalmoscopy to all patients using
steroids!
#CE Syndrome
+anagement of Glaucoma
Most glaucoma is treata'le 'ut not cura'le
A! Medical Treatment o) $OAG
Suppression o) a@ueous production
>acilitation o) A@ueous Out*ow
1eduction o) Vitreous Volume
Miotics+ mydriatics and Cycloplegics
A! Suppression o) a@ueous production
D! ?eta,adrenergic 'loc/ers
C! Alpha,adrenergic agonist
7! Topical car'onic anhydrase inhi'itor
A! Systemic car'onic anhydrase inhi'itor
Beta-adrenergic loc'ers
timolol maleate+ le(o'unolol+ metipranolol+
carteolol
'eta-olol 0 greater selecti(ity )or ?D
receptors
C5#: CO$. 9ASTHMA: and cardiac
conduction de)ects
Alpha-adrenergic agonist
, apraclonidine:
decreases #O$ a)ter %aser t-+ allergic
reaction is common
, brimonidine:
also increases a@ueous out*ow through
u(eoscleral pathway
allergies also common
)opical caronic anhydrase inhiitor
, dor&olamide 0 com'ined with timolol
, 'rin&olamide 0 less irritation
1ystemic caronic anhydrase inhiitor
, aceta&olamide
, metha&olamide 9 not a(aila'le:
, dichlorphenamide 9out in the mar/et:
HC6 OCOC
SE: meta'ollic acidosisE hypo/alemiaE
aplastic anemiaE paresthesias
4ot )or long,term use
?! >acilitation o) A@ueous Out*ow
D! $arasympathomimetic agents
$ilocarpine
Car'achol
.emecarium 'romide
Echothipate iodide
Through contraction o) ciliary muscle
SE: miosisE accomodati(e spasm
$ilocarpine
Muscarinic agonist
'inds to receptors in the ciliary muscle+
causing contraction o) the muscle and
displacement o) the scleral spur+ thus
opening SchlemmFs canal and )acilitating
humor *ow out o) the eye
C! $rostaglandin analogues
%atanoprost 9Nalatan:+
Tra(oprost 9Tra(atan:+
?imatoprost 9%umigan:
prostaglandins act through the
uncon(entional out*ow pathway+ i!e!+ inc!
u(eoscleral out*ow
ConG! 1ednessE dar/ 'rows I irisE growth o)
lashesE reacti(ation o) u(eitis I macular
edema 9latanoprost:
increase in a@ueous out*ow
some decrease in a@ueous production
ne(er use in narrow anterior cham'er
angle
C! 1eduction o) Vitreous Volume
Hyperosmotic agents, ma/e 'lood
hypertonic
Glycerin 9Glycerol: Dml5/g, mi-ed with
lemon Guice Qcaution in .M
Mannitol5 Urea
.! Miotics+ mydriatics and Cycloplegics
Constrict,
o primary angle closure
.ilate,
o angle closure secondary to iris
'om'e and posterior synechiae
1urgical and Laser )reatment
$eripheral #ridectomy
%aser tra'eculoplasty
Glaucoma drainage surgery
Cyclodestructi(e procedures
Peripheral %ridectomy
$upillary 'loc/ in angle closure
glaucoma, a@ueous )ails to go into
anterior cham'er
Laser %ridotomy
hole in peripheral iris with ;AG laser
Laser )raeculoplasty
e(enly spaced 'urns around the
circum)erenceo) the tra'ecular
meshwor/! 4o attempt was made to
penetrate through the tra'ecular
meshwor/ to SchlemmFs canal with this
procedure!the desired tissue reaction is
'lanching o) the tra'ecular meshwor/+
with or without minimal 'u''le
)ormation+ demonstrated on the le)t!
>or $OAG, Allows a
decrease in meds
1eturn o) iop to
pretreatment le(els in C,L
yrs!
Can 'e repeated
May ha(e ad(erse e=ects
on later drainage
procedures
Glaucoma 7rainage Procedure-
)raeculectomy
?ypass+ )rom anterior cham'er to
su'conGuncti(al and or'ital tissues
Accelerates cataract )ormation
Complication: 'rosis in episcleral tissues
o ;oung patients
o ?lac/s
o U(eitis
o $re(ious ltering surgery
?aer(eldt #mplant
Viscocanalostomy
.ilating sclemmJs canal with high
molecular weight (iscoelastic su'stance
5yclodestructive Procedures
Cyclocryotherapy 0
o )ree&ing ciliary 'ody to induce
shutdown o) ciliary 'ody production
o) a@ueous