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- v.328(7431); 2004 Jan 10
- PMC314054
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BMJ. 2004 Jan 10; 328(7431): 97–99.
PMCID: PMC314054
PMID: 14715605
ABC of Eyes
P T Khaw, P Shah, and A R Elkington
Copyright and License information PMC Disclaimer
This article has been corrected. See BMJ. 2004 March 27; 328(7442): 762.
The glaucomas are a range of disorders with a characteristic type of optic nerve damage. The glaucomas are the second commonest cause of blindness in the world, and the commonest cause of irreversible blindness. The most effective way of preventing this damage is to lower the intraocular pressure.
Normally, the ciliary body secretes aqueous, which flows into the posterior chamber and through the pupil into the anterior chamber. It leaves the eye through the trabecular meshwork, flowing into Schlemm's canal and into episcleral veins. The flow and drainage can be obstructed in several ways.ways.
Figure 1
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Normal aqueous drainage and possible sites of obstruction
Symptoms and signs
Raised intraocular pressure
The intraocular pressure is determined by the balance between aqueous production inside the eye and aqueous drainage out of the eye through the trabecular meshwork. Each normal eye makes about 2 μl of aqueous a minute—that is, about 70 l during the course of a lifetime. Normal intraocular pressure is 10-21 mm Hg, but it can drop as low as 0 mm Hg in hypotony and can exceed 70 mm Hg in some glaucomas.
The rate at which raised intraocular pressure causes optic nerve damage depends on many factors, including the pressure and whether glaucomatous damage is early or advanced. In general, pressures of 20-30 mm Hg usually cause damage over several years, but pressures of 40-50 mm Hg can cause rapid visual loss and also precipitate retinovascular occlusion.
Haloes around lights and cloudy cornea
The cornea is kept transparent by the continuous removal of fluid by the endothelial cells. When the pressure rises quickly (acute closed angle glaucoma), the cornea becomes waterlogged, causing a fall in visual acuity and creating haloes around lights (like looking at a light through frosted glass).
Pain
If the rise in pressure is slow, pain is not a feature of glaucoma until the pressure is extremely high. Pain is not characteristically a feature of primary open angle glaucoma.
Visual field loss
Pressure on the nerve fibres and chronic ischaemia at the optic nerve head cause damage to the retinal nerve fibres and usually result in characteristic patterns of field loss (arcuate scotoma). However, central vision is spared initially, and the patient does not notice the defect. Vision may still be 6/6 even at the terminal stage of glaucomatous field loss (tunnel vision)vision)
Figure 2
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Computerised visual field test print out showing tunnel vision
Optic disc changes
The optic disc marks the exit point of the retinal nerve fibres from the eye. With a sustained rise in intraocular pressure the nerve fibres atrophy, leaving the characteristic sign of chronic glaucoma—the cupped, pale optic disc.disc.
Figure 3
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Glaucomatous cupping of optic nerve
Venous occlusion
Raised intraocular pressure can impede blood flow in the venous system, increasing the risk of retinal venous occlusion.
This article is adapted from the 4th edition of the ABC of Eyes, which will be published by BMJ Books in February 2004 (www.bmjbooks.com).
Enlargement of the eye
In adults the eye cannot enlarge greatly because growth has ceased. In a young child, however, enlargement of the eye (buphthalmos or “ox-eye”) can occur with raised intraocular pressure, usually in children under 3 years old. Affected children may also be photophobic and have watering eyes and cloudy corneas.corneas.
Figure 4
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Enlarged watering eyes with cloudy corneas in a child with glaucoma
Primary open angle glaucoma
Primary open angle glaucoma is the most common form of glaucoma and is the third commonest cause of registration of blindness in the United Kingdom. The resistance to outflow through the trabecular meshwork gradually increases, for reasons not fully understood, and the pressure in the eye slowly increases, causing damage to the nerve. There may be other damage mechanisms, particularly ischaemia of the optic nerve head.head.
Table 1
Risk factors for primary open angle glaucoma
| • Level of intraocular pressure |
| • Increasing age (0.02% at age 40-49, up to 10% at age >80) |
| • African-Caribbean origin (five times risk of white people) |
| • Family history (risk 1 in 10 in first degree relatives) |
| • Thin corneas |
| • Large cup to disc ratio |
| • Myopia |
| • Genetic mutations (account for 3-4% of glaucoma) |
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Symptoms
Because the visual loss is gradual, patients do not usually present until severe damage has occurred. The disease can be detected by screening high risk groups for the signs of glaucoma. At present most patients with primary open angle glaucoma are detected by optometrists at routine examinations.
Signs
The eye is white and on superficial examination looks normal. The best diagnostic signs are changes in the optic disc. The cup to disc ratio increases as the nerve fibres atrophy. Asymmetry of disc cupping is also important, as the disease is often more advanced in one eye than the other. Haemorrhages on the optic disc are a poor prognostic sign.
Longer term changes in disc cupping are best detected by serial photography. The more recently introduced scanning laser ophthalmoscope may be able to detect structural changes in the nerve at an early stage of the disease.
Visual field loss is difficult to pick up clinically until considerable damage (loss of up to 50% of the nerve fibres) has occurred. Computerised field testing equipment may detect nerve fibre damage earlier, particularly if certain types of stimuli such as fine motion or blue on yellow targets are used. Computer assisted field testing is also the best method for detecting long term change and deterioration of visual fields.fields.
Figure 5
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Optic disc changes in glaucoma
The classic signs of glaucoma (field loss and optic disc cupping) often occur in patients who have pressures below the statistical upper limit of normal (21 mm Hg). However, many clinicians now believe that these two glaucomas are part of the same spectrum of pressure dependent optic neuropathies, although these patients are sometimes referred to as having normal tension glaucoma. Intraocular pressure phasing, taking multiple measurements throughout the day, is useful as it detects any spikes in pressure.
Patients with normal tension glaucoma may have appreciable vascular associated damage at the optic nerve head (ischaemia or vasospasm). Management of progressive normal tension glaucoma involves lowering intraocular pressure. Drug induced nocturnal hypotension should be considered in progressive normal tension glaucoma.glaucoma.
Figure 6
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Advanced scanning laser image of cupped optic nerve head
Acute angle closure glaucoma
Acute angle closure glaucoma is probably the best known type of glaucoma. Apposition of the lens to the back of the iris prevents the flow of aqueous from the posterior chamber to the anterior chamber. This is more likely to occur when the pupil is semidilated at night. Aqueous then collects behind the iris and pushes it on to the trabecular meshwork, preventing the drainage of aqueous from the eye, so the intraocular pressure rises rapidly.rapidly.
Figure 7
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Acute angle closure glaucoma
Symptoms
The eye becomes red and painful, and patients may be systemically unwell with nausea, vomiting, and severe pain or headache. Vision is blurred, and patients may notice haloes around lights. They may have a history of similar attacks that were aborted by going to sleep. During sleep the pupil constricts and may pull the peripheral iris out of the angle.
Groups at risk
This type of glaucoma usually occurs in longsighted people (hypermetropia), who tend to have shallow anterior chambers and shorter axial length eyes. With increasing age the lens tends to increase in size and crowd the anterior segment structures in these eyes. Women have shallower anterior chambers and live longer and therefore are more at risk of this type of glaucoma.
Signs
Visual acuity is impaired, depending on the degree of corneal oedema. The eye is red and tender to touch. The cornea is hazy because of oedema, and the pupil is semidilated and fixed to light. The attack begins with the pupil in the semidilated position and the rise in pressure makes the iris ischaemic and fixed in that position. On gentle palpation the affected eye feels much harder than the other. If the patient is seen shortly after an attack has resolved, none of these signs may be present, hence history is important.important.
Figure 8
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Development of acute angle closure glaucoma
Management
Emergency treatment is required to preserve the sight of the eye. If treatment is delayed, adhesions may form between the iris and the cornea (peripheral anterior synechiae), damaging the trabecular meshwork and necessitating surgical drainage. Angle closure glaucoma is a serious condition, and even with optimum management the patient may need multiple surgical procedures and have impaired vision.vision.
Table 2
Management of acute angle closure glaucoma
| If it is not possible to get the patient to hospital immediately, give acetazolamide 500 mg intravenously and instil pilocarpine 4% in the eye to constrict the pupil |
| In hospital |
| • Bring down intraocular pressure with drugs |
| • Give analgesia and antiemetic if required |
| • Make a hole in the peripheral iris, either with a laser or surgically, to restore aqueous flow (peripheral iridotomy) |
| • Treat other eye similarly as a prophylactic measure |
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Other types of glaucoma
If there is inflammation in the eye (anterior uveitis), adhesions may develop between the lens and iris (posterior synechiae). These adhesions block the flow of aqueous between the posterior and anterior chambers and cause forward ballooning of the iris and a rise in intraocular pressure. Adhesions may also develop between the iris and cornea (peripheral anterior synechiae), covering up the trabecular drainage meshwork. Inflammatory cells may also block the meshwork.meshwork.
Figure 9
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New vessels on the iris causing rubeotic glaucoma
Topical steroids may cause a gradual asymptomatic rise in intraocular pressure that can lead to blindness. Patients taking topical steroids over a long period should always be under ophthalmological supervision. The growth of new vessels on the iris (rubeosis) occurs both in diabetic patients and after occlusion of the central retinal vein resulting from retinal ischaemia. These vessels also block the trabecular meshwork causing rubeotic glaucoma, which is extremely difficult to treat.
The trabecular meshwork itself may have developed abnormally (congenital glaucoma) or been damaged by trauma to the eye. Patients who have had eye injuries have a higher chance than normal of developing glaucoma later in life. If there is a bleed in the eye after trauma, the red cells may also block the trabecular meshwork.
Notes
The ABC of Eyes is by P T Khaw, professor of ophthalmology at Moorfields Eye Hospital, London (p.khaw@ucl.ac.uk), P Shah, consultant ophthalmic surgeon at Birmingham and Midland Eye Centre, Birmingham (moc.12klat@hahs.f.p), and A R Elkington, emeritus professor of ophthalmology, University of Southampton.
The photographs were provided by PTK and Moorfields Eye Hospital and the line drawings were prepared by Alan Lacey, Moorfields Eye Hospital.
Competing interests: PS and PTK have received educational and research grants from pharmaceutical companies.
Articles from The BMJ are provided here courtesy of BMJ Publishing Group
