glaucoma(redirected from primary glaucoma)
Also found in: Dictionary, Thesaurus, Encyclopedia.
Causes and symptoms
The normal eye is filled with aqueous humor in an amount carefully regulated to maintain the shape of the eyeball. In glaucoma, the balance of this fluid is disturbed; fluid is formed more rapidly than it leaves the eye, and pressure builds up. The increased pressure damages the retina and disturbs the vision, such as by loss of side vision. If not relieved by proper treatment, the pressure will eventually damage the optic nerve, interrupting the flow of impulses and causing blindness.
Another form of adult primary glaucoma is angle-closure glaucoma (narrow angle glaucoma), which can be either acute or chronic. In this type of glaucoma the chamber angle is narrowed or completely closed because of forward displacement of the final roll and root of the iris against the cornea. This closure obstructs the flow of aqueous humor from the eyeball and permits a buildup of pressure.
Secondary glaucoma occurs as a result of a variety of disorders, such as uveitis, neoplastic disease, trauma, and degenerative changes in the eye.
Congenital glaucoma is due to the defective development of the structures in and around the anterior chamber of the eye and results in impairment of the aqueous humor.
Angle-closure glaucoma is usually treated surgically. If it becomes acute, it is a medical and surgical emergency. If the excessive intraocular pressure is not relieved promptly by medical and surgical means, nerve fibers in the optic disk are destroyed and vision is irretrievably lost. Laser surgical techniques for relief of intraocular pressure include iridotomy and trabeculoplasty.
Iridotomy involves perforation of the root of the iris, which provides an additional route for the escape of excess aqueous from the posterior to the anterior chambers and the trabecular meshwork.
In trabeculoplasty the spaces of the trabecular meshwork are enlarged by a series of microscopic lesions. Eventually scars form and contract, thus widening the spaces and allowing better aqueous flow.
Laser surgery can be done on an outpatient basis. A local anesthetic is used and patients feel only mild pricking sensations as the laser pulses strike and coagulate tissue. A retrobulbar anesthetic may be used to immobilize the eye during laser surgery.
Those most at risk for glaucoma are (1) diabetics, (2) persons with recently controlled hypertension, (3) African Americans (who have an incidence rate of glaucoma-related blindness that is eight times that seen in other ethnic groups), (4) those with a family history of glaucoma, (5) persons with facial hemangiomas or other nevi, and (6) victims of eye injury.
Patients who already have symptoms of glaucoma and are being treated with drugs must be informed about the nature of their eye disorder, the expected effects of each medication, and the importance of faithfully following the regimen of care. Since some patients experience undesirable side effects from these medications, they are told to report them promptly so that the medications can be evaluated by the ophthalmologist.
The combinations of drugs used to treat glaucoma in individual patients can vary considerably. In some cases patients may take as many as four or five drugs. They will need to know about each drug and may need help in devising a schedule for taking them.
Drugs are prescribed either to enhance the outflow of aqueous or to decrease its production, or both. Miotic drugs such as pilocarpine facilitate aqueous outflow by stretching the iris away from the trabecular meshwork. Pilocarpine also constricts the pupil, which reduces visual acuity. epinephrine, acetazolamide, methazolamide, and the beta-adrenergic blocking agenttimolol decrease production of aqueous.
Prescribed eyedrops and oral medications must be taken on an uninterrupted basis. Patients in acute care and long-term care facilities are sometimes allowed to keep their glaucoma medications at their bedsides if they are able to administer the eyedrops and medications themselves. If they are not able to do so, it is imperative that treatment for glaucoma not be neglected while caregivers are focusing their attention on more immediate medical needs of patients.
Care of the patient after laser surgery is relatively simple compared with treatment after more traditional surgery. The patient may experience mild headache and blurred vision for the first 24 hours after surgery and there will be transient distortion of the pupil and a mild iritis. Topical steroids and a cycloplegic to prevent movement of the ciliary muscle may be prescribed. The patient should be told to report any sudden severe eye pain immediately and to keep all appointments for follow-up care.
An elevated intraocular pressure may persist for a week or longer postoperatively and so glaucoma medications are continued until the follow-up visit and perhaps longer if intraocular pressure remains high.
glau·co·ma(glaw-kō'mă), Avoid the mispronunciation glow-kō'mă.
glaucoma/glau·co·ma/ (glaw-) (glou-ko´mah) a group of eye diseases characterized by an increase in intraocular pressure, causing pathological changes in the optic disk and typical visual field defects.glauco´matous
glaucomaOphthalmology A disorder characterized by ↑ intraocular pressure, which damages the optic nerve causing vision loss and eventually blindness Types Open-angle glaucoma–more common and of adult-onset; acute angle-closure glaucoma; in glaucoma, the fluid drains too slowly out of the anterior chamber of the eye, resulting in fluid buildup and damage to the optic nerve and eye and loss of vision; open-angle glaucoma is so named because the anterior angle of the eye stays open Clinical Initially, asymptomatic; later pain and narrowed visual field and blindness Diagnosis Air puff test or other tests that measure intraocular pressure management–surgery Surgery can also help fluid escape from the eye and thereby reduce the pressure, but is reserved for Pts whose pressure cannot be controlled with eyedrops, pills, or laser surgery High-risk groups Family Hx of glaucoma; anyone > age 60; blacks > age 40; glaucoma is 5 times more likely to occur in blacks than whites and about 4 times more likely to cause blindness in blacks
glaucoma(glaw-ko'ma) [L., cataract]
Glaucoma occurs when the aqueous humor drains from the eye too slowly to keep up with its production in the anterior chamber. Thus, narrowing or closure of the filtration angle that interferes with drainage through the canal of Schlemm causes intraocular fluid to accumulate, after which intraocular pressure increases. Glaucoma may develop, however, even if the filtration angle is normal and the canal of Schlemm appears to be functioning; the cause of this form of glaucoma is not known.
Glaucoma may not cause symptoms. It is best detected early by measurements of elevated intraocular pressure (IOP), often made by adjusting the raw values that are obtained for changes in corneal thickness (as demonstrated with a pachymeter or with optical coherence tomography). A normal tonometer reading ranges from 13 to 22. The frequent need to change eyeglass prescriptions, vague visual disturbances, mild headache, and impaired dark adaptation may also be present. The standard for determining visual loss in glaucoma is the visual-field test.
Open-angle glaucoma causes mild aching in the eyes, loss of peripheral vision, haloes around lights, and reduced visual acuity (esp. at night) that is uncorrected by prescription lenses. Acute angle-closure glaucoma (an ophthalmic emergency) causes excruciating unilateral pain and pressure, blurred vision, decreased visual acuity, haloes around lights, diplopia, lacrimation, and nausea and vomiting due to increased IOP. The eyes may show unilateral circumcorneal injection, conjunctival edema, a cloudy cornea, and a moderately dilated pupil that is nonreactive to light. It requires immediate treatment to reduce IOP.
Nonoperative treatment includes the use of miotics (eserine, pilocarpine), timolol maleate, intravenous mannitol, and parenteral acetazolamide. Experimental studies indicate that marijuana alleviates the symptoms of severe glaucoma. Control of associated disorders such as diabetes mellitus should be maintained. Operative treatment includes laser trabiculoplasty, trabiculectomy, paracentesis of the cornea, iridectomy (broad peripheral), cyclodialysis, anterior sclerotomy, sclerotomy with inclusion of the iris, as iridotasis or iridencleisis; sclerectomy. See: illustration; ciliarotomy; trabeculoplasty
CAUTION!Acute glaucoma may be precipitated in patients with closed-angle glaucoma by dilating the pupils. In glaucoma patients, cycloplegic drops are given only after trabeculectomy and only in the eye that had the procedure. Administering drops in an eye affected with glaucoma can precipitate an acute attack in an eye already compromised by elevated IOP.
Health care providers should wash their hands thoroughly before touching the patient's eye. Prescribed topical and systemic medications are administered and evaluated.
The patient is prepared physically and psychologically for diagnostic studies and surgery as indicated. If the patient has a trabeculectomy, prescribed cycloplegic drugs are administered to relax the ciliary muscle and decrease iris action, thus reducing inflammation and preventing development of adhesions.
After any surgery, an eye patch and shield are applied to protect the eye, the patient is positioned with the head slightly elevated, and general safety measures geared to the patient's level of sensory alteration are instituted. Usually, the patient is encouraged to ambulate as soon as possible following surgery.
Patients with glaucoma need to know that the disease can be controlled, but not cured. Fatigue, emotional upsets, excessive fluid intake, and use of antihistamines may increase IOP. Signs and symptoms such as vision changes or eye pain should be reported immediately. Both the patient and family are instructed in correct techniques for hand hygiene and eyedrop administration; the importance of adherence to the prescribed regimen; the need for regular follow-up care with an ophthalmologist; and any adverse reactions to report.
Information is provided to the patient and family as needed. Referral is made to local organizations and support groups.
Public education is carried out to encourage glaucoma screening for early detection of the disease. Because glaucoma is more common in African Americans than European Americans, all African Americans above age 35 (and earlier for those with a family history of glaucoma) should have an annual tonometric examination. Written information should be made available about detection and control of glaucoma.
narrow-angle glaucomaClosed-angle glaucoma.
primary open-angle glaucoma
glaucomaA rise in the pressure in the fluids within the eye of sufficient degree to cause internal damage and affect vision. There are several kinds of glaucoma, the commonest, chronic simple glaucoma, being almost symptomless but causing insidious and gradual narrowing of the fields of vision. Acute congestive glaucoma causes exquisite pain and sudden blinding. Subacute glaucoma causes eye-ache, misting of vision and the perception of rainbow coloured rings around lights. Glaucoma can be CONGENITAL. See also GONIOSCOPE.
glaucomaeye disease more common in the elderly and patients with diabetes mellitus, characterized by raised intraocular pressures, causing visual field defects and blindness; treated by topical beta-blocker agents
absolute glaucoma Final stage of the disease which has been either untreated or unsuccessfully treated. The eye is blind and hard, the optic disc is white and the pupil dilated.
acute angle-closure glaucoma (AACG) A form of raised intraocular pressure in which the pressure within the eye increases rapidly due to blockage of the trabecular meshwork. Symptoms include: intense pain, redness, blurred vision, haloes around lights, as well as nausea. Findings on examination include: reduced visual acuity, greatly elevated intraocular pressure (in the range of 40-50 mmHg), corneal epithelial oedema, semi-dilated and fixed pupil, shallow anterior chamber and mild aqueous cell and flare. Elevated intraocular pressure often causes glaucomatous optic nerve damage, as well as iris atrophy and damage to the anterior epithelial cells of the lens (glaukomflecken). Immediate treatment is imperative and includes systemic acetazolamide as well as topical medication. Surgery is often necessary. Syn. acute glaucoma; congestive glaucoma.
angle-closure glaucoma (ACG) Glaucoma in which the angle of the anterior chamber is blocked by the root of the iris which is in apposition to the trabecular meshwork and thus the aqueous humour cannot reach the drainage apparatus to leave the eye. (As the blockage persists, anterior synechia may result.) This condition occurs usually in anatomically shallow anterior chambers, as is often the case in hypermetropes. Angle-closure glaucoma can either be primary (PACG) or secondary following iritis, iridocyclitis, postoperative complications, traumatic cataract, tumours, etc. Moreover, angle-closure glaucoma is divided into acute and chronic. In chronic angle-closure glaucoma (CACG) there may never be an attack but intermittent periods of increased intraocular pressure caused by progressively extensive peripheral anterior synechia. Symptoms may be absent or there may be periodic episodes of mild congestion and blurred vision. Gonioscopy is essential to differentiate this condition from open-angle glaucoma. People most at risk are females, Chinese and South-East Asian and the average age at presentation is about 60 years. Anatomical predisposing factors are pupillary block and plateau iris. Treatment of angle-closure glaucoma is essentially surgical. However, initially therapeutic agents are used including miotics, hyperosmotic agents, which cause a rapid reduction of the IOP, beta-blockers and carbonic anhydrase inhibitors. Syn. closed-angle glaucoma; narrow-angle glaucoma. A subacute form of angle-closure glaucoma may occur as a result of episodes of elevated intraocular pressure caused by anterior synechia, intermittent pupillary block, or when in a dark room. Attacks tend to resolve spontaneously but treatment with prophylactic peripheral laser iridotomy is frequently undertaken. See anisocoria; cornea plana; iridoschisis; iris bombé; plateau iris; Shaffer and Schwartz van Herick method; Smith's method; provocative test; shadow test.
capsular glaucoma See pseudoexfoliation glaucoma.
chronic glaucoma See angle-closure glaucoma; open-angle glaucoma.
ciliary block glaucoma A secondary glaucoma, which occurs when aqueous fluid becomes misdirected into the vitreous cavity. The accumulating fluid then produces a displacement of the lens and iris, causing a narrowing of the anterior chamber angle with resultant raised intraocular pressure. This condition occurs most commonly following intraocular surgery, especially glaucoma surgery after the cessation of cycloplegic medications. Treatment consists of medical intervention (cycloplegics, β-adrenergic agents, carbonic anhydrase inhibitors and hyperosmotic agents) or puncture of the vitreous face with the Nd-YAG laser if medical treatment is unsuccessful. In phakic eyes, vitrectomy is sometimes required to open the anterior vitreous face. Syn. malignant glaucoma.
closed-angle glaucoma See angle-closure glaucoma.
compensated glaucoma See open-angle glaucoma.
congenital glaucoma Glaucoma occurring with developmental anomalies that are manifest at birth and interfere with the drainage of the aqueous humour causing an increase in intraocular pressure. This in turn causes stretching of the elastic coats of the eye, enlargement of the globe as the sclera and cornea stretch, optic atrophy, marked cupping of the optic disc and loss of vision. Most noticeable is the enlargement of the cornea. Congenital glaucoma is inherited as an autosomal recessive condition with incomplete penetrance. Immediate treatment is essential. Syn. buphthalmos; hydrophthalmos; infantile glaucoma.Glaucoma occurying after the age of about three years is more often referred to as juvenile glaucoma as it follows a course similar to adult glaucoma without enlargement of the globe. See goniotomy; luxation of the lens; Peter's anomaly; Rieger's syndrome; Sturge-Weber syndrome.
congestive glaucoma See angle-closure glaucoma.
glaucoma detection Tests that are used to diagnose glaucoma. They are: ophthalmoscopic viewing of the optic nerve head; tonometry; visual field assessment of typical glaucomatous defects; gonioscopy to assess the width of the anterior chamber; pachometry to measure central corneal thickness and anterior chamber depth as well as providing a correction factor for applanation tonometer results; and dimensional analysis of retinal structures including the thickness and topography of the retinal nerve fibre layer (RNFL) and of the optic nerve head, assessed by scanning laser polarimetry, confocal scanning laser ophthalmoscopy, optical coherence tomography, stereoscopic photography of the optic nerve head and red-free photography of the RNFL. Glaucomatous eyes lose retinal nerve fibres with consequent reduction in layer thickness and alteration of the topography of the optic nerve head. These changes frequently precede glaucomatous visual fields losses.
infantile glaucoma; juvenile glaucoma See congenital glaucoma.
inflammatory glaucoma A secondary glaucoma caused by an intraocular inflammation and characterized by elevated intraocular pressure, which may be transient. The most common cause is either active anterior uveitis or following previous episodes of inflammation. Glaucoma may occur as a result of trabecular meshwork blockage due to deposits of inflammatory debris, or because of complete posterior synechia (called seclusion pupillae) blocking the flow of aqueous causing iris bombe and angle-closure, or peripheral anterior synechia. The inflammatory process is treated along with a reduction of intraocular pressure. See Fuchs' heterochromic iridocyclitis; Posner-Schlossman syndrome.
low tension glaucoma See normal-tension glaucoma.
narrow-angle glaucoma See angle-closure glaucoma.
malignant glaucoma Elevated intraocular pressure occurring after filtration surgery for glaucoma in which the aqueous humour is diverted posteriorly pushing the vitreous body anteriorly and consequently shallowing the anterior chamber.
neovascular glaucoma A secondary glaucoma due to new vessel formation on the anterior surface of the iris blocking the exit of the aqueous humour through the angle of filtration. It may occur as a result of central retinal vein occlusion (this type typically develops within three months and is sometimes called 'ninety-day glaucoma'), or diabetes mellitus. Other causes include carotid artery occlusion, central retinal artery occlusion, retinal and choroidal tumours. The condition may initially be open-angle but eventually becomes angle-closure with severe loss of visual acuity, pain, congestion, high intraocular pressure, corneal oedema, aqueous flare, synechia and severe rubeosis iridis. The presence of new blood vessels on the iris and drainage angle distinguishes this condition from primary angle-closure glaucoma. Treatment includes topical steroids to decrease the inflammation, beta-blockers and carbonic anhydrase inhibitors to lower the intraocular pressure and laser treatment of the iris neovascularization and sometimes cyclodestructive procedures (e.g. cyclodiode laser therapy). See ectropion uvea; iris neovascularization.
ninety-day glaucoma See neovascular glaucoma.
normal-tension glaucoma (NTG) An ocular condition in which there is a glaucomatous cupping (often accompanied by disc haemorrhages) and visual field defects with an intraocular pressure of 21 mmHg or less. It is commonly regarded as a variant of primary open-angle glaucoma and it is typically associated with cardiovascular disease or migraine. Treatment with prostaglandin analogues is usually considered the best choice but if there are progressive visual field losses surgery may be needed. Syn. low-tension glaucoma.
open-angle glaucoma Glaucoma in which the angle of the anterior chamber is open and provides the aqueous humour free access to the drainage apparatus. It can occur: (1) As a primary open-angle glaucoma (POAG) (also called chronic simple glaucoma, compensated glaucoma, chronic glaucoma). The increased intraocular pressure leads to atrophy and excavation of the optic disc and typical defects of the visual field. It is the most common type of glaucoma (opinions of prevalence vary between 0.5% and 3% of the Caucasian population over 40 years and 2%-3% over the age of 70 years). Because of its insidious nature it is difficult to detect. It tends to occur more often in people after the age of 40, in people who have a family history of the disease, in African-Caribbeans, in people who have high myopia and in people who have diabetes mellitus. It is characterized by an almost complete absence of symptoms. Haloes around lights and blurring of vision occur in some patients when there has been a sudden increase in intraocular pressure or when the disease is very advanced. The diagnosis of this disease is made by demonstrating that the eye has a characteristic visual field loss (Figs. G3 and G4) and exaggerated diurnal fluctuations in intraocular pressure (>5 mmHg). POAG has been found to be caused by mutation in genes at several loci, including myocilin gene (MYOC) on chromosome 1q, optineurin gene (OPTN) on chromosome 10p, WD repeat containing protein 36 gene (WDR36) on chromosome 5q22, and others. (2) The other form is secondary open-angle glaucoma in which the intraocular pressure is elevated as a result of ocular trauma or iridocyclitis, crystalline lens abnormalities, etc. Management of open-angle glaucoma is usually by medication, unless this proves ineffective and surgery may be necessary. Formerly, pilocarpine (or carbachol) or adrenaline (epinephrine) drops were the most commonly used drugs. Nowadays,β-adrenergic blocking agents such as timolol maleate or betaxolol, which act by reducing aqueous humour formation and do not affect pupil size or accommodation, are employed as the initial treatment. Also used are the carbonic anhydrase inhibitors (e.g. acetazolamide) the α-adrenergic agonist (e.g. brimonidine), and the prostaglandin derivatives (e.g. latanoprost), which enhance the uveoscleral outflow. See optic atrophy; glaucomatous cup; ocular hypertension; plateau iris; pseudoexfoliation; baring of the blind spot; provocative test; shadow test; tunnel vision.
phacolytic glaucoma An open-angle glaucoma secondary to a hypermature or mature cataract. It is due to a leakage of lens proteins into the anterior chamber that blocks the outflow of aqueous humour through the trabecular meshwork. It is characterized by an acute onset of pain and redness with high intraocular pressure.
phacomorphic glaucoma A form of secondary angle-closure glaucoma in which the angle of the anterior chamber is closed due to swelling of the lens. Angle closure may be due to pupillary block or in some cases due to anterior pressure on the iris.
pigmentary glaucoma A secondary open-angle glaucoma caused by pigment granules released from the posterior surface of the iris impeding the aqueous outflow through the trabecular meshwork. This type of glaucoma develops in about one-third of patients with the pigment dispersion syndrome, especially myopic males. The pigments are believed to appear as a result of a posterior bowing of the iris rubbing against the zonule. The intraocular pressure is elevated and sometimes high after a sudden release of pigment following mydriasis or strenuous physical exercise with corneal oedema, redness and haloes. Treatment is usually by medication but if this proves ineffective, surgery may be required.
primary glaucoma See angle-closure glaucoma; open-angle glaucoma.
pseudoexfoliation glaucoma A secondary glaucoma caused by greyish-white, flake-like basement membrane material and pigment impeding the aqueous outflow through the trabecular meshwork. It usually appears in elderly patients who present with high intraocular pressure, optic disc changes and visual field defects. It is frequently resistant to drug therapy and may require surgery (e.g. laser trabeculoplasty). Syn. capsular glaucoma. See pseudoexfoliation; pseudoexfoliation syndrome.
secondary glaucoma Glaucoma occurring as a result of intraocular tumour, iritis, iridocyclitis, uveitis, rubeosis iridis, traumatic cataract, tumours, luxation of the lens, etc. See epithelial downgrowth; hyphaemia; Rieger's syndrome; ICE syndrome; pseudoexfoliation syndrome.
simple glaucoma See open-angle glaucoma.
glaucoma surgery See cyclodialysis; cyclodiode; filtration surgery; goniotomy; iridectomy; iridotomy; sclerectomy; deep sclerectomy; trabeculectomy; trabeculoplasty; trabeculotomy; viscocanalostomy.
|Table G1 Glaucoma medications|
|class||drug (common eye drop solution)|
|beta-blockers||betaxolol (0.25% or 0.5%), carteolol (1%),|
|timolol (0.25% or 0.5%, gel 0.1%)|
|levobunolol (0.5%), metipranolol (0.1%),|
|carbonic anhydrase inhibitors||brinzolamide (1%), dorzolamide (2%)|
|miotics||carbachol (3%), pilocarpine (0.5,1,2,3,4%)|
|prostaglandin analogues||latanoprost (0.005%), travoprost (0.004%)|
|sympathomimetics||apraclonidine (0.5%), brimonidine (0.2%), dipivefrine (0.1%)|
|combination drugs||timolol (0.5%) with brimonidine (0.2%)|
|timolol (0.5%) with dorzolamide (2%)|
|timolol (0.5%) with latanoprost (0.005%)|
|carbonic anhydrase inhibitor||acetazolamide (tablet 250mg)|
|hyperosmotic agents||glycerol (oral solution)|