secondary deviation

sec·on·dar·y de·vi·a·tion

sec·on·dar·y de·vi·a·tion

glaucoma

A progressive neuropathy which leads to retinal ganglion cell death and optic nerve atrophy. Glaucoma is characterized by optic disc cupping and visual field defects, usually associated with elevated intraocular pressure. It is commonly divided into open-angle and angle-closure types. If the cause of the glaucoma is a recognized ocular disease or injury (e.g. corneal laceration), it is called secondary, whereas if the cause is unknown it is called primary. Glaucoma is present in about 1% of the Caucasian population over the age of 40 years and about 3% over the age of 70 years, but these figures vary among different populations, tending to be lower in white populations and higher in non-white populations. See optic atrophy; glaucomatous cup; visual expander field; neuroprotection; cup-disc ratio; Marfan's syndrome; Sturge-Weber syndrome; tritanopia.
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." >Fig. G3 Typical evolution of field defects in primary open-angle glaucoma of the left eye (A and B, early field defects; C, more field defects with Roenne nasal step; D, Bjerrum scotoma; E and F, advanced field defects)" >Fig. G4 Advanced glaucomatous cupping in a POAG case. The entire neuroretinal rim has become thinner. Note the large cup-disc ratio

Table G1 Glaucoma medications
class	drug (common eye drop solution)
topical agents
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%)
prostamide	bimatoprost (0.03%)
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%)
systemic agents
carbonic anhydrase inhibitor	acetazolamide (tablet 250mg)
hyperosmotic agents	glycerol (oral solution)
	mannitol (intravenous)

position