Читать книгу Fundamentals Of Glaucoma: A Guide For Ophthalmic Nurse Practitioners, Optometrists And Orthoptists - Группа авторов - Страница 12

Neil Bowley

Glaucoma has been known since antiquity, and yet a full understanding of the pathophysiological mechanisms is not known today; it is probable that an interplay of environmental and genetic factors results in the clinical presentation of glaucoma.

Glaucoma is a syndrome in which progressive damage occurs to the ganglion cells which form the optic nerve, therefore producing a corresponding visual field defect. The etiology of this damage is multifactorial. A combination of raised intraocular pressure, ischaemic injury, autoimmune dysregulation, trans-cribriform plate pressure differential and excitotoxicity have been postulated as contributory factors.

Most commonly, raised pressure within the eye is a key factor in developing glaucoma; however, elevated intraocular pressure and glaucoma are not synonyms. This misconception is common both with patients and non-ophthalmic medical professionals.

It is possible to have raised intraocular pressure and no glaucomatous nerve damage; similarly, it is possible to have a measured intraocular pressure within the ‘normal’ range and still have a progressive nerve damage.

The intraocular pressure is maintained by the secretion of the aqueous and its drainage as shown in Equation 1.

Equation 1. Intraocular pressure (IOP) calculation

A ‘normal’ intraocular pressure is between 10 and 21 mmHg, which encompasses 95% of the normal population.

A gross simplification of the flow of aqueous within the eye is shown in Fig. 2.1. The aqueous is produced by the ciliary body (shown in pink) at a rate of approximately 2.5 μl per minute (normal AC volume is approximately 170 μl). The aqueous passes between the posterior surface of the iris and the anterior lens, then on through the pupil into the anterior chamber of the eye. The aqueous is primarily returned to the episcleral veins by filtration through the trabecular meshwork, which is located at the interface of the anterior iris and the cornea, known as ‘the angle’. The ‘uveo-scleral’ outflow pathway, which does not rely on the trabecular meshwork, plays a smaller role in the recycling of aqueous. The aqueous is absorbed by the iris and the sclera directly and is returned passively to the blood.

The classification and correct identification of the specific type of glaucoma the patient has is important because it will alter how the patient’s condition is managed and the likely clinical course. The specific diagnosis can be made clinically with examination and testing as discussed in the following chapters.

Fig. 2.1. Normal movement of aqueous within the eye.

Currently; medical, LASER, and surgical therapies available to us rely on manipulation of the secretion, reabsorption and movement of the aqueous humour within, and out of the eye. Therefore, the classification of glaucomatous disease will focus on this anatomical and etiological mechanism. Two large sub-classifications of glaucoma are therefore possible; if the flow of aqueous present within the eye under study is unimpeded from ciliary body to the iridocorneal angle, the glaucoma is said to be ‘open angle’; if this passage of aqueous is structurally impeded, the glaucoma is defined as ‘closed angle’.