GLAUCOMA

dr. Liesa Zulhidya, Sp.M

- RSUD Dr. Soedarso

 FK Universitas Tanjungpura
AQUEOUS HUMOR PRODUCTION AND DRAINAGE
 PHYSIOLOGY AND PATHOPHYSIOLOGY
OF AQUEOUS HUMOR CIRCULATION
 Rate of production is about 2-6 μL/min.

Total anterior and posterior chamber  0.2 – 0.4

mL.
 Important for the optical imaging and helps to ensure several things:
– Uniformly smooth curvature of the surface of the cornea.
– Constant distance between the cornea, lens, and retina.
– Uniform alignment of the photoreceptors of the retina and
the pigmented epithelium on Bruch’s membrane, which is
normally taut and smooth.
 PATHOPHYSIOLOGY
 Closed-Angle

 Open-Angle
 DEFINITION

Glaucoma is all forms of the disease have in common a

characteristic potentially progressive optic neuropathy
that is associated
1. optic disk cupping
2. visual field loss
3. usually associated with elevated intraocular pressure.
 EPIDEMIOLOGY

 In the US, glaucoma is the leading cause of

preventable blindness.
 Primary open-angle glaucoma  most common
form among blacks and whites
 Primary angle closure (PAC)  high prevalence in
individuals of Asian descent.
 CLINICAL ASSESSMENT IN
GLAUCOMA
1. Tonometry
2. Illumination of Anterior Chamber
3. Slit Lamp
4. Gonioscopy
5. Visual Field
6. Funduscopy
 TONOMETRY

Average IOP in general population  16 mmHg.

The normal range of intraocular pressure is 11–21
mm Hg, two SD either side of the average considered
as normal.
If the intraocular pressure is consistently elevated in
the presence of normal optic disks and visual fields,
the patient should be observed periodically as a
glaucoma suspect.
 MEASURING INTRAOCULAR PRESSURE

 Palpation
 If the examiner can indent the
eyeball, which fluctuates
under palpation, pressure is
less than 20 mmHg.
 An eyeball that is not resilient
but rock hard is a sign of
about 60–70 mmHg of
pressure (acute angle closure
glaucoma).
Schiøtz indentation
tonometry
 The lower the intraocular pressure,
the deeper the tonometer pin sinks
and the greater distance the needle
moves.
 GOLDMANN
APPLANATION
TONOMETRY (GAT)
 Most common method of
measuring intraocular
pressure
PNEUMATIC NONCONTACT TONOMETRY

Electronic tonometer directs a 3 ms blast of air against

the cornea.
 Oblique Illumination of the Anterior
Chamber
 The anterior chamber is illuminated by a beam of light tangential to
the plane of the iris.
 In eyes with an anterior chamber of normal depth, the iris is
uniformly illuminated. This is a sign of a deep anterior chamber with an
open angle
 In eyes with a shallow anterior chamber and an angle that is
partially or completely closed, the iris protrudes anteriorly and is not
uniformly illuminated
14
SLIT-LAMP EXAMINATION

The central and

peripheral depth of
the anterior chamber
should be evaluated on
the basis of the thickness
of the cornea.
GONIOSCOPY
 Gonioscopy allows direct visualization of the angle structures
 Gonioscopy can differentiate the following conditions:

1. Open angle: visualize the full extent of the trabecular

meshwork, the scleral spur, and the iris processes
2. Narrowed: Being able to see only Schwalbe’s line or a
small portion of the trabecular meshwork
3. Closed angel : unable to see Schwalbe’s line
17
OPTIC DISK ASSESSMENT

The normal optic disk has a central depression—the

physiologic cup
Cup-disk ratio > 0.5 or significant asymmetry between
the two eyes is highly suggestive of glaucomatous
atrophy.
V
19
GLAUCOMATOUS CHANGES IN THE OPTIC
NERVE
Glaucoma produces typical changes in the shape of the
optic cup.
Progressive destruction of nerve fibers, fibrous and vascular
tissue, and glial tissue will be observable.
This tissue atrophy leads to an increase in the size of the
optic cup and to pale discoloration of the optic disk
Glaucoma  concentric enlargement of the optic cup or
preferential superior and inferior cupping with focal notching
of the rim of the optic disk
The optic cup also increases in depth as the lamina cribrosa is
displaced backward. As cupping develops, the retinal vessels
on the disk are displaced nasally.
CLASSIFICATION OF GLAUCOMA

1. Primary Open Angle Glaucoma

2. Primary Angle Closure Glaucoma
3. Secondary Glaucoma
4. Primary Congenital Glaucoma
PRIMARY OPEN ANGLE GLAUCOMA

Commonly bilateral disease of adult onset.

Characterized by:
 IOP > 21 mmHg
 Glaucomatous optic nerve damage
 An open anterior chamber angle
 Characteristic visual field loss as damage
progresses.
 Absence of signs of secondary glaucoma or a non-
glaucomatous cause for optic neuropathy.
PRIMARY OPEN ANGLE GLAUCOMA

Degenerative process in the trabecular

meshwork, including deposition of extracellular
material within the meshwork and beneath the
endothelial lining of Schlemm’s canal  reduction in
aqueous drainage leading to a rise in intraocular
pressure.
Symptoms :
 The majority of patients  do not experience any subjective
symptoms for years  Without treatment, progress insidiously to
complete blindness.
 headache, burning sensation, or blurred or decreased vision that
the patient may attribute to lack of eyeglasses or insufficient
correction.
 rings of color around light sources at night,
 PRIMARY OPEN ANGLE GLAUCOMA
Aim: prevent functional impairment of vision within the
patient’s lifetime. The only proven method  lowering IOP.
Indications for Initiating Treatment
 Glaucomatous changes in the optic cup: Medical treatment should be initiated
where there are signs of glaucomatous changes in the optic cup or where there is a
difference of more than 20% between the optic cups of the two eyes.
 Medical Therapy:
 Principle:
 Inhibit aqueous humor production.
 Increase trabecular outflow.
 Increase uveoscleral outflow
 Beta Blocker, Carbonic Anhydrase Inhibitors
 Medical therapy is the treatment of choice for primary open angle glaucoma.
 Surgery is indicated only where medical therapy fails.
PRIMARY ANGLE CLOSURE GLAUCOMA

 Definiton:
Occlusion of the trabecular meshwork by the peripheral iris. This
blocks aqueous outflow, and the intraocular pressure rises
rapidly
 Acute episodic increase in intraocular pressure to several
times the normal value (10 – 21 mm Hg) due to sudden
blockage of drainage.
 Production of aqueous humor and trabecular resistance are
normal
PRIMARY ANGLE CLOSURE GLAUCOMA

Symptoms
Acute onset of intense pain
Redness
Nausea and vomiting
Diminished visual acuity
Prodromal symptoms:
Blurred Vision, Colored
Halo's
 PRIMARY ANGLE CLOSURE GLAUCOMA
Treatment
Emergency  Immediate treatment by an Ophtalmologist
Treatment is initially directed at reducing the intraocular pressure.
Reduce the intraocular pressure:
1. Systemic  Intravenous and oral  Carbonic Anhydrase Inhibitor
(Acetazolamid)
2. Topical Agents  such as pilocarpine 2%, beta-blockers and
apraclonidine, and, if necessary, hyperosmotic (Hyperosmotic solution
(Glycerin/Mannitol), Topical steroids to reduce secondary intraocular
inflammation
3. Relieve pain  analgesic agents, antiemetic agents, and sedatives
4. Allow the cornea to clear (important for subsequent surgery)  Surgical
Management (shunt between the posterior and anterior chambers):
 Iridectomy and Laser Iridotomy
SECONDARY GLAUCOMA

Open angle
1. pre-trabecular, in which aqueous outflow is
obstructed by a membrane covering the
trabeculum
2. Trabecular, in which the obstruction occurs as
a result of ‘clogging up’ of the meshwork
3. Post-trabecular in which the trabeculum itself
is normal but aqueous outflow is impaired as a
result of elevated episcleral venous pressure.
Angle-closure
 With pupillary block
 Without pupillary
block
SECONDARY GLAUCOMA
 Forms:
 Pseudoexfoliative glaucoma. Deposits of amorphous acellular material
form throughout the anterior chamber and congest the trabecular meshwork.
 Pigmentary glaucoma. The disorder is characterized by release of pigment
granules from the pigmentary epithelium of the iris that congest the trabecular
meshwork.
 Cortisone glaucoma. Increased deposits of mucopolysaccharides in the
trabecular meshwork presumably increase resistance to outflow; this is
reversible when the steroids are discontinued.
 Inflammatory glaucoma. Two mechanisms contribute to the increase in
intraocular pressure:
 1. The viscosity of the aqueous humor increases as a result of the influx of protein
from inflamed iris vessels.
 2. The trabecular meshwork becomes congested with inflammatory cells and cellular
debris.
 Phacolytic glaucoma. This is acute glaucoma in eyes with mature or
hypermature cataracts. Denatured lens protein passes through the intact lens
capsule into the anterior chamber and is phagocytized.
PRIMARY CONGENITAL GLAUCOMA

PCG is rare, incidince 1:10000. Commonly affect

boys.
Involvement: bilateral
Caused by impaired aqueous outflow due to
maldevelopment of the anterior chamber angle.
Diagnosis
 Corneal haze, large (buphthalmos) or asymmetrical eyes,
waterign, photophobia or blepharospasm.
JUVENILE GLAUCOMA
Diagnostic Consideration
Measurement of IOP
Optic Disk Ophtalmoscopy
Inspection of Cornea
Gonioscopy

Treatment: Childhood glaucomas are treated surgically.

The prognosis improves the earlier surgery is performed
TREATMENT OF GLAUCOMA
Thank you