WHAT IS GLAUCOMA?

(FOR PATIENTS)

INTRODUCTION

• The term glaucoma is derived from the Greek word “glaukos” which means a bluish or greenish color of the pupil.

• In the 10^th century an Arab scholar, Ibn-Tabarri was the first to suggest that the eyes of glaucoma patients are harder than normal eyes.

• Richard Bannister (1622) gave the concept of “Glaucoma Triad”. This triad consists of: Raised intra-ocular pressure (IOP), optic disc changes (cupping) and visual field defects.

• The normal range of IOP is: 10-21 mmHg.

• IOP is maintained as a balance between aqueous formation and aqueous outflow. This is called “aqueous humor dynamics”.

• Later it was found that glaucoma could occur in the presence of normal levels of IOP. This is called “Normal Tension Glaucoma” (NTG).

• Conversely, high IOP can be present without any glaucomatous changes. This is known as “Ocular Hypertension” (OHT) or Glaucoma Suspects.

• Therefore, IOP is not the main criteria to define glaucoma.

•  Glaucoma is now defined as: A multifactorial neurodegenerative disorder.

• Glaucoma is the 2^nd leading cause of blindness world-wide.

PATHOGENESIS

• There are many theories regarding the pathogenesis of glaucoma.

• These include: Mechanical, vascular, biochemical, genetic and other theories.

• The mechanical theory explains the development of glaucoma by mechanical compression of the optic nerve head due to raised IOP.

• However, it fails to explain the development of NTG and progression of glaucoma in cases where IOP is normal.

•  The vascular theory explains glaucoma on the basis of deranged circulatory physiology and ischemia.

• Certain biochemical molecules have also been implicated in the development of glaucoma. These include: glycine, aspartate, glutamate and others.

•  Genetic linkage studies have revealed certain genes which have a very strong effect on disease causation. These include the MYOC and OPTN genes for familial POAG and CYP1B1 for congenital glaucoma.

TYPES OF GLAUCOMA

• There are several systems available to classify glaucomas.

• It can be based on etiology, where it defines the underlying disorder leading to alteration in aqueous humor dynamics or retinal ganglion cell (RGC) loss.

•  Classification based on etiology can categorize glaucoma into “primary” or “secondary” forms. 

• Primary glaucomas are those where the initial events leading to outflow obstruction and IOP elevation are confined to the anterior chamber angle or conventional outflow pathways with no apparent contribution from other ocular or systemic disorders.

Classification of glaucomas

OPEN ANGLE				DEVELOPMENTAL		ANGLE CLOSURE
Normal Tension (NTG)	Primary (POAG)		Secondary	Primary	Secondary	Primary (PACG)	Secondary
			Exfoliative Gl. Pigment dispersion Gl.	Poorly formed or incomplete regression of TM.	Secondary to congenital ocular abnormalities.		Phacomorphic Gl. Posterior segment tumors pushing the lens-iris diaphragm anteriorly.

INVESTIGATIONS

  

• TONOMETRY= It is the procedure to measure IOP.
  

• OPHTHALMOSCOPY= It is the procedure to observe the optic disc for signs of glaucoma (cupping) and fundus for cause of glaucoma (neovascularization, pigment dispersion).
  

•  PERIMETRY= It is the procedure to map and analyze the visual field.
  

• GONIOSCOPY= It is the procedure to observe the anterior chamber angle (differentiate between open and closed angle; look for secondary causes e.g. Neovascularization and pigment dispersion).
  

• PACHYMETRY= It is the procedure to measure the central corneal thickness (CCT). (IOP measured is erroneously low in thin CCT; patients with thin CCT have higher risk of glaucoma).
  

• RETINAL NERVE FIBER LAYER (RNFL) ANALYSIS= It is the procedure utilizing optical-coherence-tomography (OCT) to analyze the RNFL which becomes thinner with glaucoma progression.
  

TREATMENT

There are different methods available to control IOP. (IOP is the main risk factor and only risk factor which can be controlled presently).

1. Medical/pharmacologic

2. Laser

3. Surgical

4. Implants (MIGS, GDD, setons etc.)

5. Cyclodestructive procedures

Medical management:

·  INCREASE THE AQUEOUS OUTFLOW THROUGH TRABECULAR MESHWORK or UNCONVENTIONAL PATHWAYS=

·         Beta-blockers= Timolol, Betoxolol.

·         Prostaglandin analogues= Latanoprost, travoprost

·         Carbonic anhydrase inhibitors= Systemic: Acetazolamide; Topical: Dorzolamide

·         Alpha2 agonists= Brimonidine

·         REDUCE VITREOUS VOLUME (SHRINK THE VITREOUS)=

·         Hyperosmotic agents (systemic)= Mannitol, glycerol

Lasers:

·         Open angle glaucoma= Trabeculoplasty

·         Closed angle= Peripheral iridotomy

Surgical:

·         Trabeculotomy and Goniotomy (For developmental glaucomas)

·         Trabeculectomy

·         Non-penetrating glaucoma surgery (NPGS)

Implants:

·         Minimally Invasive Glaucoma Surgery (MIGS) = Express Mini Shunt; Xen Gel implant

·       Glaucoma Drainage Devices (GDDs) = Ahmed Glaucoma Valve; Baerveldt Glaucoma Valve; Molteno Glaucoma Valve

Cyclodestructive procedures (To destroy ciliary body, therefore reduce aqueous production):

·         Cyclocryotherapy/ Cyclocryopexy

·         Laser cyclophotocoagulation