GLAUCOMA

PGMI ABADILLA ANGELA MARIE

CONTENTS

 ANATOMY  OPEN ANGLE

 HISTORY  CLOSE ANGLE

 DEFINITION

 CLASSIFICATION

 INVESTIGATION OF
GLAUCOMA
 PATHOPHYSIOLOGY

 CLINICAL FEATURES

 DIAGNOSIS
ANATOMY
ANATOMY
ANTERIOR CHAMBER
 BOUND IN FRONT BY
POSTERIOR SURFACE OF
CORNEA AND ANGLE RECESS
 APEX OF ANGLE

 AVERAGE DIAMETER: 11 – 12
MM
 AXIAL DEPTH: 3 – 3.5MM

 VOLUME: 0.2 – 0.3MM

 SHALLOWEST PART:
IRIDOCORNEAL JUNCTION
 DEEPEST PART: PUPILLARY
AREA
ANATOMY
POSTERIOR CHAMBER
 SPACE IN FRONT BY THE
IRIS, BACK OF THE LENS,
AND SUSPENSORY
LIGAMENT
 BASE: CILIARY PROCESS

 APEX: PUPILLARY
MARGIN OF THE IRIS
 VOLUME: 0.06ML

INCLUDES 3
COMPARTMENTS:
-PREZONULAR
-ZONULAR
-RETROZONULAR
ANATOMY
ANGLE OF ANTERIOR
3 STRUCTURES
CHAMBER

 BOUND BEHIND BY 1. DESCEMET’S

THE ROOT OF THE MEMBRANE
IRIS, IN FRONT BY 2. SCLERAL
THE MESHWORK
CORNEOSCLERAL
3. UVEAL MESHWORK
TRABECULUM AND
ANTERIORMOST PART
OF THE CILIARY
BODY

ANATOMY
OUTFLOW APPARATUS
CONSIST OF:
 TRABELACUR MESHWORK
 CANAL OF SCHLEMM
 COLLECTOR CHANNEL
TRABECULAR MESHWORK
 ARISES BEFORE THE
APPARENT TERMINATION OF
DESCEMET’S MEMBRANE
CANAL OF SCHLEMM
 CONDUCTS THE AQUEOUS
HUMOR FROM THE
TRABECULAR MESHWORK TO
THE EPISCLERAL VENOUS
NETWORK VIA THE COLLECTOR
CHANNELS
COLLECTOR CHANNELS
 DEEP PLEXUS
MADE UP OF: BRANCHES OF THE
ANTERIOR CILIARY VEINS
DRAINS INTO: INTRASCLERAL
PLEXUS
 AQUEOUS VEINS ARE THOSE 8
COLLECTOR CHANNELS THAT
DIRECTLY DRAINS INTO
EPISCLERAL PLEXUS
ANATOMY
INNER CANALS OR
AFFERENT
COMMUNICATIONS
 FINE
 TORTOUS

 ENDOTHELIAL LINED

 OBLIQUE SPACES
HISTORY
 HIPPOCRATES USED THE  1835 – MACKENZIE
TERM GLAUCOS WHILE PROVED THE ESSENTIAL
DESCRIBING BLINDNESS IN FEATURE – RAISED
SENILE PEOPLE OCULAR TENSION
 1st SUGGESTION OF
 1857 – VON GRAEFE
AFFECTION – “MIGRAINE
DIVIDED THE AFFECTION
OF THE EYE” OR
INTO 3 GROUPS: ACUTE,
“HEADACHE OF THE PUPIL”
CHRONIC AND
 1ST EXCELLENT
SECONDARY
DESCRIPTION OF
 1938 – OTTO BARKAN
GLAUCOMA WITH RAISED
OCULAR TENSION WAS ESTABLISHED THE
GIVEN BY ANTOINE – CONCEPT OF ACUTE
PIERRE DEMOURS GLAUCOMA.
DEFINITION
 IS A STATE CHARACTERIZED BY A PERSISTENT
OR INTERMITTENT ELEVATION OF THE
INTRAOCULAR PRESSURE FROM ANY CAUSE
LEADING TO A TEMPORARY OR PERMANENT
FUNCTIONAL AND OR STRUCTURAL DAMAGE
TO THE EYE
CLASSIFICATION
PRIMARY GLAUCOMA INFANTILE PRIMARY
ADULT PRIMARY GLAUCOMA
GLAUCOMAS JUVENILE PRIMARY
 CHRONIC SIMPLE GLAUCOMA
 CLOSED ANGLE MIXED PRIMARY
4 PHASES: GLAUCOMA
i. PREGLAUCOMA
ii. INTERMITTENT OR
SUBACUTE
iii. ACUTE

iv. CHRONIC
CLASSIFICATION
SECONDARY GLAUCOMA
THIS TYPE IS DUE TO A SPECIFIC ANOMALY OR
PREEXISTING OCULAR DISEASE
INVESTIGATION OF GLAUCOMA
 TONOMETRY – METHOD OF ESTIMATION OF THE
INTRAOCULAR PRESSURE
CLASSIFIED AS: DIGITAL AND INSTRUMENTAL
-IMPRESSION OR INDENTATION TONOMETRY:
SCHIOTZ TONOMETER
-APPLANATION TONOMETRY: GOLDMANN
APPLANATION TONOMETER
INVESTIGATION OF GLAUCOMA
 PERIMETRY AND SCOTOMETRY
 OCULAR RIGIDITY

 GONIOSCOPY

 EXAMINATION OF THE ANGLE OF THE

ANTERIOR CHAMBER BY A GONIOPRISM
PATHOPHYSIOLOGY OF GLAUCOMA
The eye produces fluid called aqueous humor secreted by the ciliary
body into the posterior chamber of the eye, the space between iris and
the lens.
This fluid flows to the pupil into the anterior chamber between the iris
and the cornea.
From here it drains through a sponge like structure located at the base
of the iris called trabecular meshwork. In a healthy a the rate of fluid
secretion balances to the rate of drainage.
People with glaucoma the drainage is blocked fluid then builds up in
the chambers and increases pressure within the eye. The pressure
pushes the lens back and presses the vitreous body which in turn
compresses and damages the blood vessels and nerve fibers running at
the back of the eye. This damage results in patches of vision loss which
depends on which nerve fibers are affected. If this is left untreated may
cause blindness.
CLINICAL FEATURES
 Chronic simple glaucoma: bilateral affection, very slow
progress and is insidious in onset.
 The early symptoms: aches about the eyes and mild
headaches.
 Any subject above the age of 40 years requiring
especially frequent change in presbyopic glasses should
be examined for any evidence of this affection.
 First evidence of the underlying glaucoma is signs of
central retinal vein.
DIAGNOSIS
 Tonometry
 Gonioscopy

 Perimetry

 Ophthalmoscopy

Ophthalmoscopic Signs in Glaucoma:

 Optic Disk

 Retinal Blood Vessel

 Nerve Fiber Layer of Retina

OPEN ANGLE GLAUCOMA
DEFINITION
 Primary open angle glaucoma (POAG) is a subset of the
glaucomas defined by an open, normal appearing
anterior chamber angle and raised intraocular pressure
(IOP), with no other underlying disease.
 Secondary open-angle glaucoma is a condition in which
an ocular disorder causes a persistently high intraocular
pressure and the aqueous humor has free access to the
trabecular meshwork. During the early stages of
secondary open-angle glaucoma, the optic disk and
visual fields are normal. It may either be monocular or
binocular.
PRIMARY OPEN ANGLE GLAUCOMA
RISK FACTORS CLINICAL FEATURES

 AGE: <40 Y/O  ASYMPTOMATIC

 AFRICAN-CARIBBEAN  IOP > 21mmHg

 1ST DEGREE  VISUAL FIELD

RELATIVE; HIGHER IN DEFECT: focal defects
SIBLINGS respecting the horizontal
 STEROID INDUCED meridian and generalized
IOP ELEVATION depression
 VASCULAR DISEASE
AND MYOPIA
PRIMARY OPEN ANGLE GLAUCOMA
PATHOPHYSIOLOGY TREATMENT

Pressure builds when the  MEDICAL (TOPICAL):

aqueous humour accumulates in PROSTAGLANDIN
the chambers
ANALOGUE (PGA), B-
BLOCKER, A2-AGONIST,
CARBONIC
Pressure ANHYDRASE
INHIBITOR
 SURGICAL

Damage or loss of nerve fibers PROCEDURE: LASER

causes a permanently decreased TRABECULOPLASTY –
of visual field 1ST LINE TREATMENT
FOR FRAIL
PRIMARY ANGLE-CLOSURE
GLAUCOMA
PRIMARY ANGLE CLOSURE GLAUCOMA
 Primary angle-closure glaucoma is the term that should
be used only when primary angle closure has resulted in
optic nerve damage and visual field loss.
 Risk Factors: increased age, female gender, family
history of glaucoma, Southeast Asian, Chinese, or Inuit
ethnic background
ACUTE ANGLE CLOSURE

 “Acute Glaucoma”  Blocks aqueous outflow,

occurs when sufficient increased IOP rapidly
iris develops to cause  Occurs in the evening
occlusion of the anterior
chamber angle by the
peripheral iris.
CLINICAL FINDINGS OTHER FINDINGS…

 SUDDENT ONSET OF  INCREASED IOP

VISUAL LOSS (WITH  SHALLOW ANTERIOR
EXCRUCIATING PAIN, CHAMBER
HALOS, NAUSEA AND  STEAMY CORNEA
VOMITING)
 MODERATELY
DILATED PUPIL
 CILIARY INJECTION
 DELAYED TREATMENT: PERIPHERAL IRIS
ADHERE TO THE TRABECULAR MESHWORK –
PRODUCING IRREVERSIBLE OCCLUSION OF THE
ANTERIOR CHAMBER ANGLE REQUIRING
SURGERY
 OPTIC NERVE IS DAMAGED
TREATMENT
 OPHTHALMIC EMERGENCY
 INITIALLY IOP SHOULD BE REDUCED

INTRAVENOUS AND ORAL ACETAZOLAMIDE

 BETA BLOCKERS

 APRACLONIDINE

IOP UNDER CONTROL: LASER PERIPHERAL

IRIDOTOMY SHOULD BE UNDERTAKEN TO FORM A
PERMANENT CONNECTION BETWEEN ANTERIOR
AND POSTERIOR CHAMBERS – TO PREVENT
RECURRENCE OF IRIS BOMBE
SUBACUTE ANGLE CHRONIC ANGLE
CLOSURE CLOSURE
 RECURRENT SHORT  WITH EXTENSIVE VISUAL
EPISODES OF UNILATERAL FIELD LOSS IN BOTH EYES
PAIN, REDNESS, AND  FINDINGS: RAISED IOP,
BLURRING OF VISION NARROW ANTERIOR
ASSOCIATED WITH HALOS
CHAMBER ANGLES WITH
AROUND LIGHTS
AMOUNTS OF PERIPHERAL
 ATTACKS OCCUR IN THE
ANTERIOR SYNECHIAE
EVENING AND RESOLVES AND OPTIC DISK AND
OVERNIGHT
VISUAL FIELD CHANGES
 DIAGNOSIS CAN BE
 INITIAL MANAGEMENT:
CONFIRMED WITH
GONIOSCOPY
LASER PERIPHERAL
IRIDOTOMY
 TREATMENT: LASER
PERIPHERAL IRIDOTOMY
THANK YOU
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