Angle-closure glaucoma is one of the most serious emergencies in ophthalmology it comes abruptly with such an elevated eye pressure that can become into blindness. There are some anatomic factors about the eye which can avoid this situation, if learnt.
Glaucoma is known to be the second leading cause of blindness in the Western world, and Angle-closure glaucoma (ACG) represents the 30% of the whole glaucoma. However, if we look at the incidence of acute crisis, ACG represents almost the 90% of cases. ACG is more frequent in people older than 60 years and women. There are no facts that relate ACG to genetics but it is frequently seen in small eyes, like hyperopic eyes, which is directly related to genetics, and it is needed to be taken into account.
ACG is characterized by the feeling of strong eye pain, red eye, and perception of halos around the lights, dilated pupils, nausea and vomits. These symptoms are due to a severe increase of intraocular pressure (IOP).
When we talk about the angle in the glaucoma context, we are referring to the gap degree between the root of the iris and the cornea (trabecular meshwork), which could be represented by two lines which define a virtual angle as we can see in the following picture (Figure 1).
Figure 1.- Scheme showing simultaneously the iris position in relation to the cornea, representing angles of 20º and 45º.
In current conditions, we consider 20º as the limit value of normality. Values which overcome 20º are considered regular, and the ones which are below 20º are considered pathological values, making up a narrow angle. Narrow angles involve a risk situation where an increase of IOP takes places. The true problem comes when the angle is so close to reduce the aqueous humour out-flow ( liquid inside the eye) or when the angle is completely closed, blocking the aqueous humour out-flow and their accumulation inside the eye like we are puffing up a ball, the consequence is a rapid increase of IOP, it is called an acute angle-closure glaucoma.
Figure 2.- On the right picture we see the anatomic structure of the anterior segment , and on the left one, we see the scheme showing the aqueous humour flow (blue) from the posterior to the anterior chamber, through the pupil, and reaching the trabecular meshwork in the angle.
There are different primary ACG pathogenic mechanisms but in the majority of cases it is started by blocking the pupil, especially in white race-population. The aqueous humour produced in the posterior chamber has to go to the anterior chamber in order to leave the eye (figure 2). This way through has to cross the pupil, and the iris must be lifted up over the anterior lens face, where the iris is laid on. This is why iris is submitted to this pressure differences between the posterior and the anterior faces, with a domed shape bowed anteriorly and narrowing the angle (Figure 3).
Figure 3.- Pathogenetic mechanism for angle-closer glaucoma. Aqueous humours in the posterior chamber lifting the iris and bowed anteriorly, narrowing the angle until blocking when iridotrabecular contact is produced (c).
When the pupil is semidilated, iris is relaxed and flaccid, and this is why it doesn’t resist to being pushed up anteriorly by the aqueous humour from the posterior chamber, making bulge to the front and getting closer to the trabecular methwork, untill they have contact and the angle gets completely closed, as we can see in the figure 3.
Beside small anterior chamber or a flaccid iris, there are some facts which are responsible of the angle closure and the start of acute glaucoma. The principal trigger fact is the media mydriasis: (1) Physiological, caused by the enviroment which are not so lightened, like cinemas, and (2) Pharmacological, most of the times caused by the instalation of mydriatic eye drops, such as alpha sympathomimetics or parasympatholytics, commonly used in the fundus eye exploration, to dilate the pupil to facilitate the exam.
Likewise, administration of any systemic medication of parasymptathicolitic effect, such as atropine, antidepressants, anti dizziness drugs, etc. may have the same effect: dilate the pupil causing iris retreat in the periphery closing up camerular angle. As a consequence of it, patients taking drugs such as muscular sedatives, antidepressants, tranquilizers, etc. should previously go to the ophthalmologist to check the eye ant to measure the angle in order to prevent an eventual acute glaucoma.
Until recently, evaluation of the angle has been very subjective, since it has relied on the ophtalmologist alone, on the way he visualized this anatomic structure trough a special lens (gonioscopy), with the intersubjective variations that such a method implies. Now we have new systems of image analysis that allow rendering objective anatomic structures in a very precise way. Iris root can be identified as well as the trabecular meshwork. Such new image-analysis systems integrate gauges able to calculate the angle as we can see in figure 4.
Figure 4.- Image of the angle taken with OCT where anatomic structures can be identified and the angle can be gauged and measured: 19 degrees in the image above and 43 degrees after opening the iris with YAG laser iridotomy ( asterisk).
With this technology we can analyse every patient and follow up the angle with aging (angle tends to reduce with age) or drugs that can alter it, as we have comment before, we can also see the treatment effect of opening the angle after YAG laser iridotomy, to prevent pressure increase or acute crisis.
In cases of family history with acute glaucoma, a detailed study of the anatomic structure of the eye, the anterior camera and iris morphology (iris plateau), is mandatory and if we detect changes in IOP or reduction of the angle values, the YAG laser iridology will be recommended treatment to avoid an acute crisis and a possible vision loss.