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Glaucoma: Basic Knowledge

Glaucoma: Basic Knowledge
Glaucoma is a disorder in which increased intraocular pressure damages the optic nerve. This eventually leads to blindness in the affected eye.


Basic Knowledge



Glaucoma is a disorder in which increased intraocular pressure damages the optic nerve. This eventually leads to blindness in the affected eye.

Primary glaucoma refers to glaucoma that is not caused by other oculardisorders.

Secondary glaucoma may occur as the result of another ocular disorder oran undesired side effect of medication or other therapy.


Glaucoma is thesecond most frequent cause of blindnessindeveloping countries after diabetes mellitus. Fifteen to twenty per cent of all blind persons lost their eyesight as a result of glaucoma. In Germany, approxi-mately 10% of the population over 40 has increased intraocular pressure. Approximately 10% of patients seen by ophthalmologists suffer from glau-coma. Of the German population, 8 million persons are at risk of developing glaucoma, 800 000 have already developed the disease (i.e., they have glau-coma that has been diagnosed by an ophthalmologist), and 80 000 face the risk of going blind if the glaucoma is not diagnosed and treated in time.

Early detection of glaucoma is one of the highest priorities for the pub-lic health system.

Physiology and pathophysiology of aqueous humor circulation (Fig. 10.1):

The average normal intraocular pressure of 15 mm Hg in adults is significantly higher than the average tissue pressure in almost every other organ in the body. Such a high pressure 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.

The aqueous humor is formed by the ciliary processes and secreted into the posterior chamber of the eye (Fig. 10.1 [A]). At a rate of about 2 – 6 µl per minute and a total anterior and posterior chamber volume of about 0.2 – 0.4 ml, about 1 – 2% of the aqueous humor is replaced each minute.

The aqueous humor passes through the pupil into the anterior chamber. As the iris lies flat along the anterior surface of the lens, the aqueous humor can-not overcome this pupillary resistance (first physiologic resistance; Fig. 10.1 [B]) until sufficient pressure has built up to lift the iris off the surface of the lens. Therefore, the flow of the aqueous humor from the posterior chamber into the anterior chamber is not continuous but pulsatile.

Any increase in the resistance to pupillary outflow (pupillary block) leads to an increase in the pressure in the posterior chamber; the iris inflates anteri-orly on its root like a sail and presses against the trabecular meshwork (Table 10.2). This is the pathogenesis of angle closure glaucoma.

Various factors can increase the resistance to pupillary outflow (Table10.1). The aqueous humor flows out of the angle of the anterior chamber through two channels:

  The trabecular meshwork (Fig. 10.1 [C]) receives about 85% of the out-flow, which then drains into the canal of Schlemm. From here it is conducted by 20 – 30 radial collecting channels into the episcleral venous plexus (D).

A uveoscleral vascular system receives about 15% of the outflow, which joins the venous blood (E).

The trabecular meshwork (C) is the second source of physiologic resistance. The trabecular meshwork is a body of loose sponge-like avascular tissue between the scleral spur and Schwalbe’s line. Increased resistance in present in open angle glaucoma.


Glaucoma can be classified according to the specificpathophysiology (Table 10.2).

The many various types of glaucoma are nearly all attributable to increased resistance to outflow and not to heightened secretion of aqueous humor.


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