Glaukoma

Definisi : penyakit mata yang ditandai dengan adanya peningkatan tekanan intraorbita dan
penurunan penglihatan yang disebabkan oleh glaucomatous optic neuropathy.
Klasifikasi glaukoma berdasarkan etiologi :

Table 111. Glaucoma Classified According to Etiology.

3. Due to lens changes (phacogenic)
A. Primary glaucoma
1. Open-angle glaucoma
a. Dislocation
a. Primary open-angle glaucoma (chronic b. Intumescence
open-angle glaucoma, chronic simple
glaucoma)
b. Normal-tension glaucoma (lowc. Phacolytic
tension glaucoma)
2. Angle-closure glaucoma
4. Due to uveal tract changes
a. Acute
a. Uveitis
b. Subacute
c. Chronic
d. Plateau iris
B. Congenital glaucoma
1. Primary congenital glaucoma
2. Glaucoma associated with other
developmental ocular abnormalities

b. Posterior synechiae (seclusio pupillae)

c. Tumor
d. Ciliary body swelling
5. Iridocorneoendothelial (ICE) syndrome
6. Trauma
a. Hyphema

a. Anterior chamber cleavage syndromes

Axenfeld's syndrome
Reiger's syndrome
Peter's syndrome
b. Aniridia
3. Glaucoma associated with extraocular
developmental abnormalities
a. Sturge-Weber syndrome
b. Marfan's syndrome
c. Neurofibromatosis 1
d. Lowe's syndrome

b. Angle contusion/recession
c. Peripheral anterior synechiae
7. Postoperative
a. Ciliary block glaucoma (malignant glaucoma)
b. Peripheral anterior synechiae
c. Epithelial downgrowth

e. Congenital rubella

b. Central retinal vein occlusion

c. Intraocular tumor
9. Raised episcleral venous pressure
a. Carotid-cavernous fistula
b. Sturge-Weber syndrome
10. Steroid-induced

C. Secondary glaucoma
1. Pigmentary glaucoma
2. Exfoliation syndrome

d. Following corneal graft surgery

e. Following retinal detachment surgery
8. Neovascular glaucoma
a. Diabetes mellitus

D. Absolute glaucoma: The end result of any

uncontrolled glaucoma is a hard, sightless, and
often painful eye.

Fisiologi aqueous humor

Volume 250 uL, produksi 2,5 uL/menit

Komposisi : kaya akan asam askorbat, laktat, piruvat, dan rendah protein, urea, glukosa
Diproduksi oleh korpus siliaris dan difiltrasi oleh prosesus siliaris
Aliran aqueous humor :

Faktor resiko :
Usia > 60 tahun
TIO tinggi
Ras (african-american, mexican-american)
Riwayat penyakit keluarga glaukoma
Kondisi medis lain : DM, hipotiroid, CVD, hipertensi, dll
Penyakit mata lain : trauma mata, ablasio retina, tumor, uveitis, iritis, miopia

Kortikosteroid berkepanjangan

Jenis glaukoma terbanyak : primary open-angle glaucoma dan acute angle-closure glaucoma
Primary Open-angle Glaucoma

Patofisiologi
The exact cause of glaucomatous optic neuropathy is not known, although many risk factors have been identified, to include
the following: elevated IOP, family history, race, age older than 40 years, and myopia.
Elevated IOP is the most studied of these risk factors because it is the main clinically treatable risk factor for glaucoma. Multiple
theories exist concerning how IOP can be one of the factors that initiates glaucomatous damage in a patient. Two of the major
theories include the following: (1) onset of vascular dysfunction causing ischemia to the optic nerve, and (2) mechanical
dysfunction via cribriform plate compression of the axons.
In addition to vascular compromise and mechanically impaired axoplasmic flow, contemporary hypotheses of possible
pathogenic mechanisms that underlie glaucomatous optic neuropathy include excitotoxic damage from excessive retinal
glutamate, deprivation of neuronal growth factors, peroxynitrite toxicity from increased nitric oxide synthase activity, immunemediated nerve damage, and oxidative stress. The exact role that IOP plays in combination with these other factors and their
significance to the initiation and progression of subsequent glaucomatous neuronal damage and cell death over time is still
under debate; the precise mechanism is still a hot topic of discussion.
In cases where POAG is associated with increased IOP, the cause for the elevated IOP generally is accepted to be decreased
facility of aqueous outflow through the trabecular meshwork. Occurrence of this increase in resistance to flow has been
suggested by multiple theories, to include the following:

An obstruction of the trabecular meshwork by accumulated material

A loss of trabecular endothelial cells
A reduction in trabecular pore density and size in the inner wall endothelium of the Schlemm canal
A loss of giant vacuoles in the inner wall endothelium of the Schlemm canal
A loss of normal phagocytic activity
Disturbance of neurologic feedback mechanisms
Other processes thought to play a role in resistance to outflow include altered corticosteroid metabolism, dysfunctional
adrenergic control, abnormal immunologic processes, and oxidative damage to the meshwork.

Epidemiology
Glaucoma is the second leading cause of blindness in the world (surpassed only by cataracts, a reversible condition). More
than 3 million people are bilaterally blind from POAG worldwide, and more than 2 million people will develop POAG each year.
Presentation
History

The initial patient interview is extremely important in the evaluation for POAG or other ocular diseases secondarily causing
elevated IOP.
Because of the silent nature of glaucoma, patients will not usually present with any symptoms or visual complaints until late in
the disease course, particularly with POAG. However, narrow/closed angle glaucoma and secondary glaucomas can cause
rapid closure of the trabecular meshwork, with an equally rapid rise in IOP, which is usually symptomatic, particularly when IOP
is equal to or greater than 35 mm Hg.
Significant attention should be given to the following:
Past ocular history includes the following:

History of eye pain or redness

Multicolored halos
Headache
Previous ocular disease, including cataracts
Uveitis
Diabetic retinopathy
Vascular occlusions
Other factors include the following:
Previous ocular surgery, including photocoagulation or refractive procedures
Ocular/head trauma
Past medical history - Any surgeries or pertinent vasculopathic systemic illnesses
Current medications, including any hypertensive medications (which may indirectly cause fluctuation of IOP) or
topical/systemic corticosteroids

Risk factors for glaucomatous optic neuropathy, strong implications are as follows:
History of elevated IOP; advanced age, particularly after 50 years; African American descent; positive family history of
glaucoma (first-degree relative, especially correlative if present in a sibling; relative risk 3.7-fold higher than if no family history
of glaucoma); myopia
Be specific when asking family history (Which family members? Was there actual visual loss from glaucoma or other causes
of visual field loss? Are they under control on one or more medications? Did they require surgery for adequate control?)
Possible implications are as follows:

Systemic cardiovascular disease

Diabetes mellitus
Migraine headache
Systemic hypertension
Vasospasm
Anecdotal risk factors are as follows:

Obesity
Smoking
Alcohol
History of stress
Anxiety

Open-angle glaucoma