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GLAUCOM

A
Dr. NENI K. PARIMO, Sp.M

GLAUCOMA
Definition
A damage of optic nerve head (Papil N.Opticus)
characterized by:
- Excavation of optic nerve papil
- Narrowing of visual field
Primarily caused by increase of intra ocular pressure

Intra Ocular Pressure (IOP)


High IOP > 22 mmHg

IOP examination:
Digital
Schiotz indentation tonometer
Applanation tonometer
- Contact
- Non-contact
Digital
- Estimation
- Comparing right and left eye
- Technique
pressing the eyeball with two
pointing

Schiotz Tonometer
points on scale conversion to mmHg
Applanation Tonometer
indicates mmHg

IOP Examination with Schiotz tonometer:


Give inform consient to the patient
Patient lies in bed

Apply topical Pantocaine 0.5% on eye


Tonometry with 5.5g weight is tested on the steel plate
points at zero
Tonometry is put over cornea
Read the scale convert by provided table to mmHg
If the reading is < 3, the weight is added (replaced) by
7.5g or 10g

Optic Nerve Papil


- Normal C/D Ratio 0.2 0.3
- Excavation > 0.6

Visual Field Examination :


Confrontation Test
Tangent Screen
Goldman Perimetry
Computerized - Octopus
- Humphrey

Glaucoma Classification
A. Primary Glaucoma
1. Open angle / simple chronic glaucoma
2. Chronic closed angle glaucoma / chronic congestive
glaucoma
3. Acute closed angle glaucoma / acute congestive glaucoma
According to gonioscopy

B. Secondary Glaucoma
1. Lens Dislocation
Cataract
3. Uveitis
4.
Hyphema
5. Corticosteroid
6. Rubeosis iridis

C. Congenital Glaucoma
D. Absolute Glaucoma No vision / LP

2.

A. Primary Glaucoma
Dynamics of Humor Aqueous :
Production cilliary body nonepithelium
Posterior chamber pupil anterior chamber
Conventional Trabeculair Meshwork Schlemms canal
( + 80 85% )
Non conventional Uvea-sclera ( 15 20% )

Open angle glaucoma/ chronic simple glaucoma


- chronic
- progressive
- bilateral
Symptoms :
- white eye with blurred vision
- frequent bumping
on movement / walking
- tunnel vision
Signs :
- IOP > 22 mmHg
- open angle
- visual field narrowing
- enlargement of C/D Ratio

Restriction of the Visual Field

Pathophysiology
- Degeneration of trabecula, Schlemms canal
- Genetic aspect

Treatment
A. Medication
-- Asetazolamide tablets /Carbonic anhydrase inhibitor 125
250 mg 4 x 250 mg/ day
--

Beta Adrenergic Blocking Agent Timolol 0.25% 0.50% eyedrops 2 x1 /day

-- Selective Receptor 1 Betaxolol 0.25% - 0.50% 2 x/day


-- Pilocarpin 1- 4% 4 6 x/day
-- Prostaglandin Analogue : Latanoprost, Travaprost
1x 1 drop at evening

B. Laser Trabeculoplasty
- If medication fails

C. Surgery
- If medication and Laser trabeculoplasty
fails
- Most common Trabeculektomy

Pathway of aqueus egress following trabeculectomy

- Low Tension Glaucoma


Intra ocular pressure within normal limits
Signs of glaucoma present
Damage of the optic nerve excavation
Visual field defect

- Ocular hypertension
High IOP > 22mmHg
No sign of glaucomatous optic nerve damage

Acute Primary Angle Closure Glaucoma ( Acute PACG)

Pathophysiology
- Pupillary block
- No pupillary block / cilliary block
Most common: pupillary block

Pupillary block
1. Predisposing factors:
- Narrow angle
- Shallow anterior
chamber
- Short eye / axial length
- Small
corneal diameter
- Age
2. Triggering factors
- Mid mydriasis
- Swollen lens
-

Symptoms :
- Eye pain
- Dizziness, nausea, vomiting
- Halo / seeing rainbows blurred vision
Signs:
-

IOP > 22 mmHg


PCI + CI
Corneal edema bullous keratopathy
Shallow anterior chamber
Flare
Atrophy of the iris
Mid Mydriasis
Glaucomflecken (cataract due to IOP )

PAINFUL RED EYE WITH VISUAL LOSS


REFER IMMEDIATELY

Definitive treatment :
- Iridectomy / laser iridotomy
- Trabeculektomy
Management:
- Medical therapy for preparation of definitive treatment
- Definitive treatment:
< 48 72 jam iridectomy / laser iridotomy
> 48 72 jam trabeculectomy
- Fellow eye preventive iridectomy / laser iridotomy

Medical Therapy :
- Glyserin p.o. 1ml/KgBW in 50% solution (mixed
with water)
- Acetazolamide, initial dose 500mg 4 x 250 mg
- Timolol 0.5% 2 x 1 drop
- Pilocarpin 2% 4 6 x 1 drop
- Treat pain analgesics
- Mannitol i.v 1 2 g/KgBW Preparation for
surgery if IOP is not reduced

Chronic Closed angle Glaucoma (Chronic PACG)

Pathophysiology
- Intermittent pupillary block
- No pupillary block / cilliary block intermittently
Most common by pupillary block

Signs & Symptoms


Same as Acute PACG but less severe

Treatment
Same as Acute PACG

B. Secondary Glaucoma
1. Lens Dislocation
2. Cataract there are 2 pathogenesis :
1. Phacomorphic
- intumescent

cataract
pupillary block closed angle glaucoma

2. Phacolytic
- Hyper
mature cataract

3. Hyphema
blood particle trabecular meshwork obstruction
open angle glaucoma

4. Uveitis there are 2 pathogenesis :


1. Pupillary seclusion iris bombe PAS closed
angle glaucoma
2. Infllamatory cells inflamasi trabecular meshwork
obstruction open angle glaucoma

5. Corticosteroid use
- Trabecular meshwork damage
6. Rubeosis iridis
anterior

Formation of fibrovascular tissue at


chamber angle

C. Congenital Glaucoma
Symptoms :
Light irritability
Cranky
Tearing
Eyeball enlargement
Signs :
High IOP
Epiphora
Blepharospasm
Photophobia
Buftalmos

OD Bulpthalmos.

OS Bulpthalmos

Treatment:
Goneotomy surgery
Trabeculotomy surgery
Trabeculectomy surgery

D. Absolute Glaucoma
Is the end stage of all kinds of glaucoma, where the
vision is zero / Light Perception ( - )

Terima Kasih
Atas perhatiannya

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