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Glaucoma

Definition of Glaucoma
Glaucoma is an optic disc neuropathy which is
characterized by:
High intra ocular pressure (IOP) > 21 mmHg,
Optic nerve fibers death optic disc damage,
Progressive visual field defect,
Cause of third permanent blindness.

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Incidence
Primary glaucoma is:
hereditary
female > male
especially at age > 40 years

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Incidence

Congenital glaucoma since in the intrauterine


Infantile glaucoma
after birth until 2 years
Juvenile glaucoma
age 10 - 15 years
Secondary glaucoma: glaucoma as a complication
from other eye disease

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Aqueous humor secretion


80% is secreted by non pigmented ciliary
epithelium via active metabolic process that
depends on a number of enzymatic systems
(carbonic anhydrase enzyme),
20% is produced by passive processes as
ultrafiltration and diffusion.

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Aqueous outflow
AH fills posterior chamber
Trabecular route

pupil
90 %

Schlemms canal

uveoscleral route (10%)

suprachoroidal space
leaves the eye
through episcleral vein
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anterior chamber

ciliary body

venous system in the ciliary body


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Aqueous outflow
Uveal
meshwork
b. Corneoscleral
meshwork
c. Schwalbes line
d. Schlemms canal
e. Collector
channels
f. Ciliary body
g. Scleral spur
a.

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Aqueous outflows,
influenced by:

High intra ocular pressure (IOP),


High episcleral pressure,
Aqueous viscosity: exudate, blood cell,
Ciliary block, pupillary block, posterior synechia,
Narrow / closed anterior chamber angle,
Narrowing of trabecular meshwork pore,
Macrophage, lens cell at the trabecular meshwork.
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Trabecular Meshwork
The TM is located at the anterior chamber
angle, which consists:

Descemet membrane
Sclera
Iris
Ciliary body

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Schwalbes line
scleral spur
iris processus
angle recess

Intra Ocular Pressure (IOP)


Normal IOP < 21 mm Hg,
IOP > 21 mm Hg glaucoma suspect,
Diurnal fluctuation of IOP in 24 hours:
IOP higher in the morning
IOP lower in the afternoon and evening

Ocular hypertension: IOP > 21 mmHg without any


nerve fiber damage,
Normal tension glaucoma: normal IOP, but
presenting glaucomatous signs.
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Pathogenesis of
Glaucomatous Damage
There are two current theories:
The indirect ischaemic theory: IOP -- nerve
fiber death + interfering micro circulation of
the optic disc,
Direct mechanical theory: IOP -- damage on
retinal nerve fiber at the optic disc.

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Classification of the glaucomas


According to:
Outflow impairment: open angle and angle
closure glaucoma,
contributing factors to IOP : primary and
secondary glaucoma,
Age: congenital, infantile, juvenile, adult.

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Primary glaucomas
High IOP is not associated with any ocular
disorder
Open angle
Angle closure
Congenital (developmental)

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Secondary glaucoma

Aqueous outflow alters by ocular / non ocular disorders


IOP :
Secondary open angle glaucoma: pretrabecular,
trabecular and post-trabecular,
Secondary angle closure glaucoma caused by
apposition between the peripheral iris and trabeculum,
Pathogenesis: anterior forces / posterior forces
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Tonometry
Two main methods of measuring IOP:
applanation force to flatten the cornea
indentation force to indent the cornea

The main types of tonometer:


The Schiotz tonometer uses a plunger with a
preset weight to indent the cornea. The amount
of indentation is converted into mmHg by use
of Friedenwald tables.
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Tonometry
The main types of tonometer:
Goldmann tonometer consists of double prism with
3.06 mm in diameter, applanation, more accurate,
Perkins tonometer, hand held, applanation,
The air puff tonometer, non contact, applanation, jet of
air to flatten the cornea.
Tono-pen
Gas Tonometer
Electrical Tonometer
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Schiotz Tonometer

Portable, simple, low cost,


Measure the depth of indentation of
cornea by a plunger with
specific weight (5 gr; 7,5 gr ; 10 gr)
The indentation represented in
Schiotz scale is converted into
mmHg by Freidenwald table,
Low accuracy because it is
influenced by ocular rigidity (high
myop, DM, corneal leucoma).
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Goldmanns Applanation
Tonometer
More accurate, not influenced by ocular
rigidity
The foot plate is smaller (3.06 mm)
Disadvantages: cannot be applied to

Corneal edema
Keratitis, corneal ulcer
Keratokonus
High astigmatism
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Non Contact Tonometer

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Tonography
To estimate outflow facility of HA,
Principle: to express the fluid flow from the
eye by continuous pressing to the eye
Place Schiotz tonometer for 2-4 minutes,
Compare IOP at 0 to 4 minutes outflow
facility (C),
Normal C > 0.18.
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Provocation Test
Water drinking test, dark room test,
midriatic test, steroid test,
Positive if IOP at the end of the tests are
more than 8 mmHg,
Indications:
Narrow / closed angle glaucoma
Normal tension glaucoma
Bias IOP
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Gonioscopy
Three main purposes of gonioscopy:
To Identify the abnormal angle structure,
To Estimate the width of the chamber angle,
To Visualize the angle during these following
procedures: goniotomy, laser trabeculoplasty.

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Identification of angle
structures
Schwalbes line (an opaque line) is a peripheral
termination of Descemet membrane,
Trabecular meshwork has a ground glass
appearance stretching from Schwalbes line to scleral
spur.
Consists of two parts:
The anterior: nonfunctional, non pigmented
part, whitish color,
The posterior: functional, pigmented part,
greyish-blue translucent.
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Identification of angle
structures
Schlemms canal: slightly darker line,
behind the posterior trabeculum,
Scleral spurs: anterior of sclera, narrow, dense, often
shiny, whitish band. As a landmark for laser
trabeculoplasty.
Ciliary body stands behind the scleral spur as dull
brown band. The width depends on iris insertion.
Curve of the corner at the margin of the ciliary body
Iris processes
Iris processes, small extension of the anterior surface
\ of the iris, inserted at the level of scleral spur.
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Angle classification by Shaffer


Grade IV
III
II
I
Grade 0

: 45 degrees angle
: 20 - 25 degrees angle
: 20 degrees angle closed
: 10 degrees angle closed
: closed angle, iridocorneal contact.

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Ophthalmoscopy of the optic disc


1.2 million axons passes across the retina and enter the
optic disc,
Fibers from the macula papillomacular bundle, straight
to the optic disc, most resistant,
Fibers from temporal of macula an arcuate path around
the papillomacular bundle supero and inferotemporal of
the optic disc, vulnerable to glaucomatous damage.

Nerve fiber layer


anatomy

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Ophthalmoscopy of the optic disc

Normal nerve fiber layer


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Diffuse nerve fiber atrophy


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Ophthalmoscopy of the optic disc


The optic cup, pale depression in the center of the optic
cup, absent of nerve fiber,
The neuroretinal rim, tissue between the outer edge of the
cup and the outer margin of the disc, the color is pinkish
orange, uniform width, contains nerve fibers,
Nerve fibers death thinning of retinal rim,
High IOP posterior bowing of lamina cribrosa,
nasalisation of central retinal vessels.

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Ophthalmoscopy of the optic disc


The cup-disc ratio: fraction of vertical and
horizontal diameter cup and diameter of the
disc, normal c/d ratio is 0.3 or less.

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Optic disc changes in glaucoma

Normal disc with small cup


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Optic disc changes in glaucoma


Cup and disc ratio > 0.6,
Peripapillary atrophy at temporal region,
Splinter-shaped hemorrhage on the disc
margin.

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Optic disc changes in glaucoma

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Normal Visual Field Examination

Nasally
: 60 degrees
Temporally : 95 degrees
Superiorly : 50 degrees
Inferiorly : 70 degrees
The blind spot is located temporally 10-20 degrees
Visual field is an island of vision surrounded by the sea of
darkness, the sharpest is at the top of the island.

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Visual Fields in Glaucoma


Baring of the blind spot
Localized paracentral scotoma at 10 - 20 degrees of
fixation at superior and inferior quadrant extension to
the blind spot Byerrum scotoma ring scotoma with
nasal step of Roenne,

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Visual Fields in Glaucoma


Peripheral scotoma that spreads and coalesces to the
paracentral scotoma
Leaving central island and accompanying temporal island,
even if the central vision is still normal
Temporal island total blindness

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Classification

Primary open-angle glaucoma


Secondary open-angle glaucoma
Primary closed-angle glaucoma
Secondary closed-angle glaucoma
Primary congenital glaucoma
Secondary congenital glaucoma
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Primary Open-Angle Glaucoma


(Simple Glaucoma)

Bilaterally, not necessarily symmetrical,


absence of secondary causes of high IOP,
Glaucomatous optic nerve damage,
Open and normal angle, IOP > 21 mmHg,
Adult onset, hereditary, steroid
responsiveness,
Glaucomatous visual field defects, central
tunnel vision,
Minimal clinical signs.
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Management of Primary Open


Angle Glaucoma
Initial therapy is usually medical, except in
advanced cases,
Argon laser trabeculoplasty (ALT) if IOP is
uncontrolled despite maximal tolerated medical
therapy,
Trabeculectomy with / without antimetabolic drug
in refractory glaucoma,
Artificial filtering shunt: Achmed valve, Molteno
tube, Krupin- Denver valve.
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Surgical Indications for


Simple Glaucoma
Uncontrolled IOP by maximal medical
treatment
Progressive disc damage and visual field
defect
Drugs intolerance
Unable to buy the drugs
Poor compliance
Unable to do the regular control
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Primary Closed-Angle
Glaucoma

Obstruction of aqueous outflow as a result of closure of the


angle by the peripheral iris
Anatomically predisposed, bilateral,
Predisposition:
Crowded anterior segment
Relatively anterior location iris lens diaphragm,
Shallow anterior chamber,
Narrow entrance to the chamber angle.
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PACG stage
Five overlapping stages:

Latent
Intermittent (sub acute)
Acute (congestive and post congestive)
Chronic
Absolute

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Latent angle-closure glaucoma


Shallow anterior chamber, convex-shape
iris lens diaphragm, close iris to cornea,
normal IOP, occludable angle,
Treatment:
Good fellow eye without treatment, follow
up,
PACG fellow eye laser iridotomy.
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Intermittent
angle-closure glaucoma
Rapid partial closure anterior chamber angle
and reopening of the angle after some rest,
Precipitating factors: physiological mydriasis,
watching TV in dark room, prone position,
reading, sewing, emotion, stress,
Transient blurring of vision, halo, headache,
Recovery after some rest.

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Acute congestive
angle-closure glaucoma
Presentation:
Rapidly progressive impairment of
vision, sometimes the vision 1/300 0,
Eye ache and frontal headache,
Congestion, nausea, vomiting.

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Acute congestive
angle-closure glaucoma
Examination
Ciliary and conjunctival injection
IOP > 50 mmHg, dilated pupil,
unreactive.
Cornea: epithelial edema, KP(+), vesicle
Ant chamber: shallow PAS, flare /
cell (+),
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Acute congestive
angle-closure glaucoma
Wide pupil, slow / negative light
reflex,
Papilla edema, retinal edema,

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Acute congestive
angle-closure glaucoma

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Acute congestive
angle-closure glaucoma
Differential diagnosis:
Red eyes:
conjunctivitis, iridocyclitis

Silent eyes:
simple glaucoma, ocular hypertension

Glaucomatous visual field defect:


anomaly of the optic nerve and retina

Papillary atrophy:
anomaly at optic nerve

Congenital megalocornea without high IOP

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Acute congestive
angle-closure glaucoma
Treatment:
Immediately decrease IOP with maximal drugs,
Wait for 24 hours evaluation,
Normal IOP, deep AC, open angle
iridectomy,
High IOP, permanent AC closure > 50%
trabeculectomy,
The fellow eye: preventive iridectomy.
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Postcongestive
angle-closure glaucoma

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Chronic closed-angle glaucoma


Clinical features of chronic CAG are similar as
POAG except gonioscopy of the angle is closed,
There are three mechanism of CCAG:
Creeping PAS laser iridotomy / trabeculectomy
After intermittent and laser iridotomy drug >
Combination of POAG with narrow angle laser
iridotomy + medical trabeculectomy

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Chronic closed-angle glaucoma


Signs and therapy are similar as simple
glaucoma:
Trabeculectomy,
Laser iridoplasty to make an angle,
Argon Laser Trabeculopasty (ALT)

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Primary Congenital Glaucoma


65% of patients are male, 1: 10.000,
Inheritance is autosomal recessive, bilateral,
Maldevelopment of the trabeculum and iridotrabecular
junction, abscent of angle recess, trabeculodysgenesis,
The iris insertion can be flat or concave,
Poor prognosis.

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Primary Congenital Glaucoma


Clinical signs:
Depends on the age of the onset and the level of
IOP,
According to the age of the onset there are 3
types:
True congenital glaucoma (40%). IOP elevated since
in the intrauterine buphthalmos,
Infantile glaucoma (55%) manifesting after birth,
Juvenile glaucoma: IOP at 10-35 years of age, with
clinical manifestation same as POAG.

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Primary Congenital
Glaucoma
Examinations:
Corneal haze, lacrimation, photophobia and
blepharospasm,
Buphthalmos if IOP before the age of 3 usually
associated with axial myop, subluxated lens,
Break of Descemet membrane, endothelial
decompensation permanent stromal edema,
Reversible glaucomatous cupping.

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Primary Congenital Glaucoma


Treatments:
Initial drug treatment,
Goniotomy if cornea is still clear,
Trabeculotomy at corneal clouding,
Trabeculectomy and trabeculotomy,
Trabeculectomy with antimetabolic agent,
--Outcome of the operation is poor.

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Secondary Glaucoma
Inflammation and residual inflammation of
the uveal tissue: iridocyclitis, posterior
synechia,
Immature cataract, hipermature cataract,
Lens luxation, lens subluxation,
Ischemic retina,
Sub choroidal bleeding,
Congenital anomaly of the eye
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Secondary Glaucoma

Pigmentary gl.
- Neovascular gl.
Inflammatory gl. - Phacolytic glaucoma
Red cell gl.
- Ghost cell glaucoma
Angle recession glaucoma
Iridocorneal endothelial syndrome
Pseudoexfoliative glaucoma
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Therapy
Nerve fiber damage caused by glaucoma is
irreversible,
Principle of the therapy is to decrease IOP
medically or surgically to maintain the current
condition,
The purpose of decreasing the IOP is to reduce
progressivity of the nerve fiber damage and visual
field defect,
Early findings.
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Indications of Medical Treatment


Simple glaucoma
Acute / chronic closed angle glaucoma
Maintain the diurnal IOP
Lower IOP before operation

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Reducing aqueous production


Carbonic anhydrase inhibitor
acetazolamide 250 mg qid orally,
dorzolamide eye drop tid,

Beta-adrenergic antagonist:
beta-blocker (timolol maleat 0.25-0.5%) bid,
betaxolol 0.25% - 0.5% bid.

Adrenergic agonist:
depefeprine 0.5% - 2% bid.
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Other antiglaucoma drugs


Parasympathomimetic agents:
pilocarpin eye drop 2-4%, 2-6 x / day
carbachol 0.75% used after cataract operation

Increase the latanoprost uveoscleral flow


Hyperosmotic fluid
glycerol 50% 1-2 ml/kg body weight, drink all at once,
manitol 20% swift infusion preoperative, 1.5-3 ml/kg
body weight.
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Surgical treatment
Peripheral iridectomy:
Acute attack glaucoma, with good trabecular meshwork,
Preventive treatment from acute attack for the fellow
eye.

Trabeculectomy for all types of glaucoma,


Goniotomy for congenital glaucoma if the cornea is
still clear,
Trabeculotomy for congenital glaucoma if the
cornea is edema.
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Surgical treatment
Treatment for absolute glaucoma:
cyclocryo coagulation destroys the ciliary body
to decrease HA production,
enucleation if all treatment is not successful.

Laser treatment:
iridotomy
gonioplasty
trabeculoplasty
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Good Prognosis
Early and right diagnosis,
Adequate control of IOP by medical /
surgical treatment,
Compliance of the patients to check their
IOP and use medical treatment,
Case finding among glaucoma family.
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Thank
you
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