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Glaucoma may be described as a complex of diseases and primary open-angle glaucoma (POAG) is but one of this constellation of conditions.
It is the most common of the glaucomas and accounts for about 90 per cent of the primary glaucomas. POAG is insidious, bilateral and frequently asymmetric in its presentation. Without treatment it will progress to cause blindness. It is probably genetically determined, having a multifactorial basis, and risk factors include advancing age, a family history of the disease, particularly in first degree relatives, myopia and systemic vascular difficulties such as diabetes.
In most cases, intraocular pressure (IOP) is elevated at some time, due, it is thought, to a compromise of the aqueous outflow facility. This, and/or a vascular insufficiency leads to retinal ganglion cell loss, optic nerve head changes and a loss of visual field. The only parameter that can definitively be manipulated in its treatment is IOP.
Symptoms
POAG is slowly progressive and is usually asymptomatic until late in the disease process when the patient may complain of blurred vision and, with severe bilateral damage to the visual fields, tunnel vision. Patients who are acute observers may notice a visual field loss at an earlier stage.
Signs
Most patients with POAG have IOP greater than 21mmHg at some time, or have an exaggerated diurnal curve. About one third of patients do not have elevated IOP (see Normal tension glaucoma). Single readings of IOP should be avoided, with measurements taken at different times of the day. Gonioscopy reveals open anterior chamber angles with normal structures.
A variety of optic disc changes may be seen including an increase in the cup to disc ratio, ideally photographically documented, thinning and notching of the neuro retinal rim, especially infratemporal and supratemporal, bayoneting of blood vessels as they pass over the edge of the cup, pallor-cup discrepancy and the appearance of splinter or Drance haemorrhages at the optic disc margin. A thinning of retinal nerve fibres leads to the appearance of retinal nerve fibre layer defects, best visualised with a red-free filter. Pupil dilatation and the utilisation of binocular stereoscopic examination techniques are essential.
Defects in the visual field characteristically respect the horizontal midline, and commence with small paracentral scotomas, potentially close to fixation. These may coalesce to form arcuate defects continuous with the blind spot. Typically, a nasal step is present and one hemifield is more affected. Late in the disease, tunnel vision may be present with the patient eventually being left with a temporal island in the visual field. It is important that visual fields are investigated at threshold in suspect cases and repeated. Newer technologies, such as frequency doubling and short wavelength automated perimetry, may aid in the earlier detection of visual field loss. In cases that are advanced but asymmetric, a relative afferent pupil defect may be elicited.
Prevalence, Differential Diagnosis, Management
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