Glaucoma is the leading cause of irreversible blindness in the world.
It is characterised by progressive loss of the visual field, due to a progressive atrophy of the optic nerve, by unidentified nerve cell loss and, without treatment, can end in blindness.
The changes caused by glaucoma can be prevented by early diagnosis and subsequent close follow-up. All vision loss in glaucoma is completely irreversible.
Glaucomatous lesions are related to increased intraocular pressure and other factors. However, as ocular pressure is the element on which we can act, it is on this that we focus our attention.
The eye continuously produces (in the ciliary body, an organ located behind the iris in the periphery) aqueous humour liquid which passes through the pupil into the anterior part of the eye and is eliminated into the circulation through holes in the angle between the cornea and iris, called the trabecular meshwork. When there is a balance between production and elimination, the eye pressure remains stable. If there is more production than elimination, or elimination is hindered by resistance to the passage of aqueous humour through the trabecular meshwork, the pressure inside the eye rises, exceeding the perfusion pressure of the blood vessels irrigating the optic nerve. As a result, the irrigation of the optic nerve decreases, the nerve fibres die, with progressive loss of vision.
The progressive destruction of the optic nerve initially causes a slow loss of the peripheral visual field, which goes unnoticed by the vast majority of people. If it is not detected, the field closes further and further, until a tubular field remains, through which clear vision can still be seen. The patient has great difficulty in orienting himself, because he sees as if through a spyglass. This later leads to a total loss of vision.
In most cases of glaucoma we find an increase in intraocular pressure, some degree of optic nerve atrophy and characteristic visual field losses.
Types of Glaucoma
Usually when making the diagnosis we find only bilateral high eye pressure with no other signs, or one eye with more advanced glaucoma and the other at the beginning with no symptoms. Later, if left untreated it becomes bilateral. Painless initially, later if the pressure is very high with deafening pain around the eye and in the head on the same side.
The loss of vision is initially limited, of the peripheral visual field not identifiable in everyday life. As it gets worse the patient realises that something is wrong. He knocks on someone else's shoulder, cannot see the doorframe and eventually consults the ophthalmologist.
The visual field narrows until it reaches a tubular vision, in which case he can distinguish objects, but at a distance, without seeing what is around him, as if he were looking through a spyglass. Later he ends up losing his vision completely.
There is also low-tension glaucoma, in which the eye pressure is normal, but all the signs described in the previous case are present.
In acute or closed angle glaucoma there is an abrupt increase in intraocular pressure due to the closure of the angle of the anterior chamber by dilation of the pupil. As the angle is sufficiently narrow, the iris tissue ends up closing the trabecular meshwork, which, as already mentioned, is situated at the vertex of this angle, thus acutely increasing the ocular pressure enormously, due to the impossibility of draining the aqueous humour. The patient has severe pain which is almost impossible to bear, the eye is very red due to congestion of the superficial blood vessels and the pupil is dilated. Typically this type of glaucoma occurs in eyes with a small anterior segment (hypermetropes) and large crystallines (increased volume as may happen with age-related opacification of the lens in cases with a small anterior chamber).
Secondary glaucoma results from eye diseases that end up in one way or another causing glaucoma. It is the case we talked about earlier of the increase in volume of the crystalline lens by cataract, the prolonged use of steroids causing in a glaucoma similar to the simple chronic one.
When iris pigment disperses and is deposited in the trabecular meshwork region, it can lead to pigmentary glaucoma, similar in its evolution to simple chronic glaucoma.
Neovascular glaucoma results from the formation of new blood vessels in the iris reaching the trabecular meshwork, preventing the elimination of aqueous humour. It is usually associated with retinal vascular diseases such as diabetic retinopathy and venous occlusions. Secondary glaucoma is generally very difficult to treat because the anatomical alterations are very marked.
Congenital glaucoma is a special case, detected at birth, as babies are born with very large eyes (buftalmos).