GLAUCOMA

Liesa Zulhidya
Definition

Glaucoma is All forms of the disease have in common a

characteristic potentially progressive optic neuropathy that is
associated (Trias Glaucoma)
1. optic disk cupping
2. visual field loss
3. usually associated with elevated intraocular pressure
Leads to blindness in the affected eye
Epidemiology

Worldwide, glaucoma is the leading cause of irreversible

blindness.
About 60 million people have glaucoma. An estimated 3
million Americans are affected, and of these cases, about
50% are undiagnosed.
About 6 million people are blind from glaucoma
Movement of
fluid in the
eye
Physiology and pathophysiology of aqueous
humor circulation

• volume is about 250 μL, and its rate of production is about 2.5
μL/min.
• Thats value is 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

• The aqueous humor is formed by the

ciliary processes and secreted into
the posterior chamber of the eye
• 2 Physiologic Resistance of Aqueos
Flow:
• 1st Resistance: Pupil  Closed-
Angle
• 2nd Resistance: Trabecular
Meshwork  Open-Angle
Classification
CLINICAL ASSESSMENT
IN GLAUCOMA
1. Tonometry
2. Illumination of Anterior Chamber
3. Slit Lamp
4. Gonioscopy
5. Visual Field
6. Funduscopy
Tonometry

• The normal range of intraocular pressure is 11–21

mm Hg
• In the elderly, average intraocular pressure is
higher, giving an upper limit of 24 mm Hg.
• 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.
 Applanation tonometry

• most common method of

measuring intraocular
pressure
• A flat tonometer tip has a
diameter of 3.06 mm for
applanation of the cornea over
a corresponding area (7.35
mm2).
• This method eliminates the
rigidity of the sclera as a
source of error
Pneumatic non-contact tonometry

• The tonometer records the deflection of the cornea and

calculates the intraocular pressure on the basis of this
deformation.
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
Slit-Lamp Examination

• The central and peripheral depth of the anterior chamber

should be evaluated on the basis of the thickness of the
cornea.
• An anterior chamber that is less than three times as deep
as the thickness of the cornea in the center with a
peripheral depth less than the thickness of the cornea
suggests a narrow angle.
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
 Optic Disk Assessment

• The normal optic disk has a central depression—the

physiologic cup
• 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 nerve is the eye’s “glaucoma memory.”
• The end result of glaucomatous cupping is the so-called
“bean-pot” cup
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
Early glaucoma showing inferior focal Typical glaucomatous cupping. Note the nasal
notching of the neuroretinal rim (arrow). displacement of the vessels and hollowed-out
appearance of the optic disk except for a thin
border.

Glaucomatous (“bean-pot”) cupping of the

optic disk.
Visual Field Testing

• Detecting glaucoma as early as possible requires

documenting glaucomatous visual field defects at the
earliest possible stage
• Glaucomatous visual field defects initially manifest
themselves in the superior paracentral nasal visual field
or, less frequently, in the inferior field, as relative
scotomas that later progress to absolute
Classification of glaucoma
1. Primary Open Angle Glaucoma
2. Primary Angle Closure Glaucoma
3. Secondary Glaucoma
4. Juvenile Glaucoma
Primary Open Angle Glaucoma

• Definiton:
• Primary open angle glaucoma begins in middle-aged and
elderly patients with minimal symptoms that
progressively worsen.
• The angle of the anterior chamber characteristically
remains open throughout the clinical course of the
disorder.
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
• Primary open-angle glaucoma (POAG) is a commonly
bilateral disease of adult onset. It is characterized by:
 IOP >21 mmHg at some stage.
Glaucomatous optic nerve damage.
An open anterior chamber angle.
Characteristic visual field loss as damage progresses.
Absence of signs of secondary glaucoma or a
nonglaucomatous cause for the optic neuropathy.
Primary Open Angle Glaucoma
• 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:
• Sufficient iris bombé develops to cause
occlusion of the anterior chamber
angle 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 – 20 mm Hg)
due to sudden blockage of
drainage.
• Production of aqueous humor and
trabecular resistance are normal
 Primary Angle Closure Glaucoma
• Etiology:
• Anatomically predisposed
eyes with shallow anterior
chambers
• Iatrogenic pharmacologic
mydriasis and systemic
psychotropic drugs
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

• sudden onset of visual loss accompanied by excruciating pain

• Halos
• nausea and vomiting.
• Other findings:
• increased intraocular pressure
• a shallow anterior chamber
• a steamy cornea
• a fixed, moderately dilated pupil
• ciliary injection.
Primary Angle Closure Glaucoma

• sudden onset of visual loss accompanied by excruciating

pain
• Halos
• nausea and vomiting.
• Other findings:
• increased intraocular pressure
• a shallow anterior chamber
• a steamy cornea
• a fixed, moderately dilated pupil
• ciliary injection.
Primary Angle Closure Glaucoma
Treatment
• Emergency  Immediate treatment by an Ophtalmologist
• Treatment is initially directed at reducing the intraocular
pressure.
• Reduce the intraocular pressure:
• Systemic  Intravenous and oral  Carbonic Anhydrase Inhibitor
(Acetazolamid)
• 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
• Relieve pain  analgesic agents, antiemetic agents, and sedatives
• Allow the cornea to clear (important for subsequent surgery) 
Surgical Management (shunt between the posterior and anterior
chambers):
• Iridectomy and Laser Iridotomy
Secondary Glaucoma
Close angle
1. Relative pupillary Block
2. Non Relative Pupillary Block
 Open angle the meshwork
1. pre-trabecular, 3. Post-trabecular
in which in which the
aqueous trabeculum
outflow is itself is normal
obstructed by a but aqueous
membrane outflow is
covering the impaired as a
trabeculum result of
elevated
2. Trabecular, in
episcleral
which the
venous
obstruction
pressure.
occurs as a
result of
‘clogging up’ of (A) Pre-trabecular obstruction; (B) trabecular obstruction;
(C) angle closure with pupillary block; (D) angle closure
without pupillary block
• Forms:
Secondary Glaucoma
• 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.
Juvenile Glaucoma

• Any abnormal increase in

intraocular pressure during
the first years of life will cause
dilatation of the wall of the
globe, and especially of the
cornea. The result is a
characteristic, abnormally
large eye (buphthalmos) with
a progressive increase in
corneal diameter. This is also
referred to as hydrophthalmos
or hydrophthalmia.
 Juvenile Glaucoma

• Etiology
• The iris inserts anteriorly far in the
trabecular meshwork
• Embryonic mesodermal tissue in
the form of a thin transparent
membrane (Barkan’s membrane)
covers the trabecular meshwork
and impedes the flow of aqueous
humor into the canal of Schlemm.
 Juvenile Glaucoma

• Symptoms
• photophobia, epiphora, corneal
opacification, and unilateral or
bilateral enlargement ofthe
cornea.
• Children with this disorder are
irritable, poor eaters, and rub
their eyes often.
 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