A condition in which the intraocular pressure (fluid pressure inside the eyes) causes impaired vision. Aqueous humour (watery fluid) is secreted into the front of the eye by the ciliary body (a structure behind the iris) to maintain the eye’s shape and nourish the tissues. Excess fluid drains away at the edge of the iris. In glaucoma, however, this excess fluid may not be able to escape. It causes compression and obstruction of the blood vessels that supply the retina and the optic nerve. This, in turn, may destroy nerve fibres and cause gradual loss of vision.
Types, causes and symptoms
The most common form of glaucoma is chronic simple (open-angle) glaucoma. It rarely occurs before the age of 40, and tends to run in families. In this condition, the outflow of aqueous humour is gradually blocked over a period of years, causing a slow rise in pressure. There are often no symptoms until visual loss is advanced. In acute (closed-angle) glaucoma, the outflow of aqueous humour is rapidly blocked, and the pressure rises suddenly. This may cause a severe, dull pain in and above the eye, fogginess of vision, and the perception of haloes around lights at night. Nausea and vomiting may occur, and the eye may become red with a dilated pupil.
Congenital glaucoma is due to an abnormality in the drainage angles of the eyes that develops before birth.
Glaucoma can also be caused by injury or an eye disease such as uveitis or lens dislocation. A less common form, called normal-pressure or low-tension glaucoma, occurs in people whose intraocular pressure is normal or only slightly raised but causesthe same damage to the retina and optic nerve as excessively high fluid pressure. This condition is not well understood; and it seems that the pressure, although not considered to be excessive, is too high for the tissues to withstand, and thus causes damage.
Diagnosis and treatment
Tonometry is used to check for glaucoma by measuring the pressure within the eye. Ophthalmoscopy may show depression of the head of the optic nerve due to the increase in pressure. Tests of the visual field will be needed to assess whether vision has already been damaged, because longstanding or severe glaucoma can result in loss of peripheral vision. Prompt treatment is essential to prevent permanent loss of vision.
Chronic simple glaucoma can usually be controlled with eye-drops, such as timolol, or tablets that reduce pressure in the eye. Treatment needs to be continued for life. If drugs are ineffective, surgery or laser treatment can unblock the drainage channel at the edge of the iris or create an artificial channel.
Acute glaucoma requires emergency drug treatment, often in hospital.
Sugery or laser treatment may be needed in order to prevent a further attack. The usual procedure is iridectomy, in which a small opening is made at the edge of the iris so that aqueous humour can drain more easily, Treatment for normal-pressure glaucoma is the same as for open-angle glaucoma, but is aimed at reducing the intraocular pressure to an even lower level than normal.
Glaucoma in more detail - technical
Glaucoma: Introduction
Glaucoma is an acquired chronic optic neuropathy characterized by optic disk cupping and visual field loss. It is usually associated with elevated intraocular pressure. In the majority of cases, there is no associated ocular disease (primary glaucoma) (Table 1).
Table 1. Glaucoma Classified According to Etiology.
| A. Primary glaucoma | 3. Due to lens changes (phacogenic) |
| 1. Open-angle glaucoma | a. Dislocation |
| a. Primary open-angle glaucoma (chronic open-angle glaucoma, chronic simple glaucoma) | b. Intumescence |
| b. Normal-tension glaucoma (low-tension glaucoma) | c. Phacolytic |
| 2. Angle-closure glaucoma | 4. Due to uveal tract changes |
| a. Acute | a. Uveitis |
| b. Subacute | b. Posterior synechiae (seclusio pupillae) |
| c. Chronic | c. Tumor |
| d. Plateau iris | d. Ciliary body swelling |
| B. Congenital glaucoma | 5. Iridocorneoendothelial (ICE) syndrome |
| 1. Primary congenital glaucoma | 6. Trauma |
| 2. Glaucoma associated with other developmental ocular abnormalities | a. Hyphema |
| a. Anterior chamber cleavage syndromes | b. Angle contusion/recession |
| Axenfeld's syndrome | c. Peripheral anterior synechiae |
| Reiger's syndrome | 7. Postoperative |
| Peter's syndrome | a. Ciliary block glaucoma (malignant glaucoma) |
| b. Aniridia | b. Peripheral anterior synechiae |
| 3. Glaucoma associated with extraocular developmental abnormalities | c. Epithelial downgrowth |
| a. Sturge-Weber syndrome | d. Following corneal graft surgery |
| b. Marfan's syndrome | e. Following retinal detachment surgery |
| c. Neurofibromatosis 1 | 8. Neovascular glaucoma |
| d. Lowe's syndrome | a. Diabetes mellitus |
| e. Congenital rubella | b. Central retinal vein occlusion |
| C. Secondary glaucoma | c. Intraocular tumor |
| 1. Pigmentary glaucoma | 9. Raised episcleral venous pressure |
| 2. Exfoliation syndrome | a. Carotid-cavernous fistula |
| b. Sturge-Weber syndrome | |
| 10. Steroid-induced | |
| D. Absolute glaucoma: The end result of any uncontrolled glaucoma is a hard, sightless, and often painful eye. |
About 60 million people have glaucoma. An estimated 3 million Americans are affected, and of these cases, about 50% are undiagnosed. About 6 million people are blind from glaucoma, including approximately 100,000 Americans, making it the leading cause of preventable blindness in the United States. Primary open-angle glaucoma, the most common form among blacks and whites, causes insidious asymptomatic progressive bilateral visual loss that is often not detected until extensive field loss has already occurred. Blacks are at greater risk than whites for early onset, delayed diagnosis, and severe visual loss. Angle-closure glaucoma accounts for 10–15% of cases in whites. This percentage is much higher in Asians and in Inuit. Primary angle-closure glaucoma may account for over 90% of bilateral blindness due to glaucoma in China. Normal-tension glaucoma is the most common type in Japan.
The mechanism of raised intraocular pressure in glaucoma is impaired outflow of aqueous resulting from abnormalities within the drainage system of the anterior chamber angle (open-angle glaucoma) or impaired access of aqueous to the drainage system (angle-closure glaucoma) (Table 2). Treatment is directed toward reducing the intraocular pressure and, when possible, correcting the underlying cause. Although in normal-tension glaucoma intraocular pressure is within the normal range, reduction of intraocular pressure may still be beneficial.
Table 2. Glaucoma Classified According to Mechanism of Intraocular Pressure Rise.
| A. Open-angle glaucoma | B. Angle-closure glaucoma |
| 1. Pretrabecular membranes: All of these may progress to angle-closure glaucoma due to contraction of the pretrabecular membranes. | 1. Pupillary block (iris bombé) |
| a. Neovascular glaucoma | a. Primary angle-closure glaucoma |
| b. Epithelial downgrowth | b. Seclusio pupillae (posterior synechiae) |
| c. ICE syndrome | c. Intumescent lens |
| 2. Trabecular abnormalities | d. Anterior lens dislocation |
| a. Primary open-angle glaucoma | e. Hyphema |
| b. Congenital glaucoma | 2. Anterior lens displacement |
| c. Pigmentary glaucoma | a. Ciliary block glaucoma |
| d. Exfoliation syndrome | b. Central retinal vein occlusion |
| e. Steroid-induced glaucoma | c. Posterior scleritis |
| f. Hyphema | d. Following retinal detachment surgery |
| g. Angle contusion or recession | 3. Angle crowding |
| h. Iridocyclitis (uveitis) | a. Plateau iris |
| i. Phacolytic glaucoma | b. Intumescent lens |
| 3. Posttrabecular abnormalities | c. Mydriasis for fundal examination |
| a. Raised episcleral venous pressure | 4. Peripheral anterior synechiae |
| a. Chronic angle closure | |
| b. Secondary to flat anterior chamber | |
| c. Secondary to iris bombé | |
| d. Contraction of pretrabecular membranes |
Intraocular pressure can be reduced by decreasing aqueous production or increasing aqueous outflow, using medical, laser, or surgical treatments. Medications, usually administered topically, are available to reduce aqueous production or increase aqueous outflow. Surgically bypassing the drainage system is useful in most forms of glaucoma if there is a failure to respond to medical treatment. In recalcitrant cases, laser, cryotherapy, or diathermy can be used to ablate the ciliary body to reduce aqueous production. Improving access of aqueous to the anterior chamber angle in angle-closure glaucoma may be achieved by peripheral laser iridotomy or surgical iridectomy if the cause is pupillary block, miosis if there is angle crowding, or cycloplegia if there is anterior lens displacement. In the secondary glaucomas, consideration must always be given to treating the primary abnormality.
In all patients with glaucoma, the necessity for treatment and its effectiveness are assessed by regular determination of intraocular pressure (tonometry), inspection of optic disks, and measurement of visual fields.
The management of glaucoma is best undertaken by an ophthalmologist, but detection of asymptomatic cases is dependent on the cooperation and assistance of all medical personnel, particularly optometrists. Ophthalmoscopy to detect optic disk cupping and tonometry to measure intraocular pressure should be part of the routine ophthalmologic examination of all patients over 35 years of age. They are especially important in patients with a family history of glaucoma and in high-risk groups such as blacks, who should undergo regular screening every 2 years from age 35 and annually from age 50.