Glaucoma

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Print Close Window Note: Large images and tables on this page may necessitate printing in landscape mode. Copyright ©2007 The McGraw-Hill Companies. All rights reser e!. "ange #phthalmology > Chapter 11. Glaucoma > Glaucoma: Introduction Glaucoma is an acquired chronic optic neuropathy characteri ed by optic dis! cupping and "isual #ield loss. It is usually associated with ele"ated intraocular pressure. In the ma$ority o# cases% there is no associated ocular disease &primary glaucoma' &(able 11)1'. (able 11)1. Glaucoma Classi#ied *ccording to +tiology. A. $rimary gla%coma 1. .pen/angle glaucoma a. Primary open/angle glaucoma &chronic open/angle glaucoma% chronic simple glaucoma' b. 0ormal/tension glaucoma &low/ tension glaucoma' 1. *ngle/closure glaucoma a. *cute b. 4ubacute c. Chronic d. Plateau iris &. Congenital gla%coma 1. Primary congenital glaucoma 1. Glaucoma associated with other de"elopmental ocular abnormalities a. *nterior chamber clea"age syndromes *9en#eld:s syndrome ;eiger:s syndrome Peter:s syndrome ,. -ue to lens changes &phacogenic' a. -islocation b. Intumescence

c. Phacolytic 2. -ue to u"eal tract changes a. 3"eitis b. Posterior synechiae &seclusio pupillae' c. (umor d. Ciliary body swelling 5. Iridocorneoendothelial &IC+' syndrome 6. (rauma a. 7yphema b. *ngle contusion8recession c. Peripheral anterior synechiae <. Postoperati"e a. Ciliary bloc! glaucoma &malignant glaucoma'

b. *niridia ,. Glaucoma associated with e9traocular de"elopmental abnormalities a. 4turge/Weber syndrome b. >ar#an:s syndrome c. 0euro#ibromatosis 1 d. Lowe:s syndrome e. Congenital rubella C. 'econ!ary gla%coma 1. Pigmentary glaucoma 1. +9#oliation syndrome

b. Peripheral anterior synechiae c. +pithelial downgrowth

d. =ollowing corneal gra#t surgery e. =ollowing retinal detachment surgery ?. 0eo"ascular glaucoma a. -iabetes mellitus b. Central retinal "ein occlusion c. Intraocular tumor @. ;aised episcleral "enous pressure a. Carotid/ca"ernous #istula b. 4turge/Weber syndrome 1A. 4teroid/induced (. A)sol%te gla%coma: (he end result o# any uncontrolled glaucoma is a hard% sightless% and o#ten pain#ul eye.

*bout 6A million people ha"e glaucoma. *n estimated , million *mericans are a##ected% and o# these cases% about 5AB are undiagnosed. *bout 6 million people are blind #rom glaucoma% including appro9imately 1AA%AAA *mericans% ma!ing it the leading cause o# pre"entable blindness in the 3nited 4tates. Primary open/angle glaucoma% the most common #orm among blac!s and whites% causes insidious asymptomatic progressi"e bilateral "isual loss that is o#ten not detected until e9tensi"e #ield loss has already occurred. Clac!s are at greater ris! than whites #or early onset% delayed diagnosis% and se"ere "isual loss. *ngle/closure glaucoma accounts #or 1A)15B o# cases in whites. (his percentage is much higher in *sians and in Inuit. Primary angle/closure glaucoma may account #or o"er @AB o# bilateral blindness due to glaucoma in China. 0ormal/tension glaucoma is the most common type in Dapan. (he mechanism o# raised intraocular pressure in glaucoma is impaired out#low o# aqueous resulting #rom abnormalities within the drainage system o# the anterior chamber angle &open/angle glaucoma' or impaired access o# aqueous to the drainage system &angle/ closure glaucoma' &(able 11)1'. (reatment is directed toward reducing the intraocular pressure and% when possible% correcting the underlying cause. *lthough in normal/tension glaucoma intraocular pressure is within the normal range% reduction o# intraocular pressure may still be bene#icial. (able 11)1. Glaucoma Classi#ied *ccording to >echanism o# Intraocular Pressure ;ise.

A. #pen-angle gla%coma

&. Angle-clos%re gla%coma

1. Pretrabecular membranes: *ll o# these may progress to 1. Pupillary bloc! &iris angle/closure glaucoma due to contraction o# the pretrabecular bombE' membranes. a. 0eo"ascular glaucoma b. +pithelial downgrowth c. IC+ syndrome 1. (rabecular abnormalities a. Primary open/angle glaucoma b. Congenital glaucoma c. Pigmentary glaucoma d. +9#oliation syndrome e. 4teroid/induced glaucoma #. 7yphema g. *ngle contusion or recession h. Iridocyclitis &u"eitis' i. Phacolytic glaucoma ,. Posttrabecular abnormalities a. ;aised episcleral "enous pressure a. Primary angle/ closure glaucoma b. 4eclusio pupillae &posterior synechiae' c. Intumescent lens d. *nterior lens dislocation e. 7yphema 1. *nterior lens displacement a. Ciliary bloc! glaucoma b. Central retinal "ein occlusion c. Posterior scleritis d. =ollowing retinal detachment surgery ,. *ngle crowding a. Plateau iris b. Intumescent lens c. >ydriasis #or #undal e9amination 2. Peripheral anterior synechiae a. Chronic angle closure b. 4econdary to #lat anterior chamber c. 4econdary to iris bombE d. Contraction o# pretrabecular membranes

Intraocular pressure can be reduced by decreasing aqueous production or increasing aqueous out#low% using medical% laser% or surgical treatments. >edications% usually administered topically% are a"ailable to reduce aqueous production or increase aqueous out#low. 4urgically bypassing the drainage system is use#ul in most #orms o# glaucoma i# there is a #ailure to respond to medical treatment. In recalcitrant cases% laser% cryotherapy% or diathermy can be used to ablate the ciliary body to reduce aqueous production. Impro"ing access o# aqueous to the anterior chamber angle in angle/closure glaucoma may be achie"ed by peripheral laser iridotomy or surgical iridectomy i# the cause is pupillary bloc!% miosis i# there is angle crowding% or cycloplegia i# there is anterior lens displacement. In the secondary glaucomas% consideration must always be gi"en to treating the primary abnormality. In all patients with glaucoma% the necessity #or treatment and its e##ecti"eness are assessed by regular determination o# intraocular pressure &tonometry'% inspection o# optic dis!s% and measurement o# "isual #ields. (he management o# glaucoma is best underta!en by an ophthalmologist% but detection o# asymptomatic cases is dependent on the cooperation and assistance o# all medical personnel% particularly optometrists. .phthalmoscopy to detect optic dis! cupping and tonometry to measure intraocular pressure should be part o# the routine ophthalmologic e9amination o# all patients o"er ,5 years o# age. (hey are especially important in patients with a #amily history o# glaucoma and in high/ris! groups such as blac!s% who should undergo regular screening e"ery 1 years #rom age ,5 and annually #rom age 5A. Physiology o# *queous 7umor Intraocular pressure is determined by the rate o# aqueous production and the resistance to out#low o# aqueous #rom the eye. Composition o# *queous (he aqueous is a clear liquid that #ills the anterior and posterior chambers o# the eye. Its "olume is about 15A L% and its rate o# production% which is sub$ect to diurnal

"ariation% is about 1.5 L8min. (he osmotic pressure is slightly higher than that o# plasma. (he composition o# aqueous is similar to that o# plasma e9cept #or much higher concentrations o# ascorbate% pyru"ate% and lactate and lower concentrations o# protein% urea% and glucose. =ormation F =low o# *queous *queous is produced by the ciliary body. *n ultra#iltrate o# p lasma produced in the stroma o# the ciliary processes is modi#ied by the barrier #unction and secretory processes o# the

ciliary epithelium. +ntering the posterior chamber% the aqueous passes through the pupil into the anterior chamber &=igure 11)1' and then to the trabecular meshwor! in the anterior chamber angle. -uring this period% there is some di##erential e9change o# components with the blood in the iris. =igure 11)1.

*nterior segment structures. *rrows indicate direction o# #low o# aqueous. Intraocular in#lammation or trauma causes an increase in the protein concentration. (his is called plasmoid aqueous and closely resembles blood serum. .ut#low o# *queous (he trabecular meshwor! is composed o# beams o# collagen and elastic tissue co"ered by trabecular cells that #orm a #ilter with a decreasing pore si e as the canal o# 4chlemm is approached. Contraction o# the ciliary muscle through its insertion into the trabecular meshwor! increases pore si e in the meshwor! and hence the rate o# aqueous drainage. Passage o# aqueous into 4chlemm:s canal depends on cyclic #ormation o# transcellular channels in the endothelial lining. +##erent channels #rom 4chlemm:s canal &about ,A collector channels and 11 aqueous "eins' conduct the #luid directly into the "enous system. 4ome aqueous passes between the bundles o# the ciliary muscle into the suprachoroidal space and then into the "enous system o# the ciliary body% choroid% and sclera &u"eoscleral #low' &=igure 11)1'. (he ma$or resistance to aqueous out#low #rom the anterior chamber is the $u9tacanalicular tissue ad$acent to the endothelial lining o# 4chlemm:s canal% rather than the "enous system. Cut the pressure in the episcleral "enous networ! determines the minimum le"el o# intraocular pressure that can be achie"ed by medical therapy. Pathophysiology o# Glaucoma (he ma$or mechanism o# "isual loss in glaucoma is retinal ganglion cell apoptosis% leading to thinning o# the inner nuclear and ner"e #iber layers o# the retina and a9onal loss in the optic ner"e. (he optic dis! becomes atrophic% with enlargement o# the optic cup &see below'. (he pathophysiology o# intraocular pressure ele"ationGwhether due to open/angle or to angle/closure mechanismsGwill be discussed as each disease entity is considered &see below'. (he e##ects o# raised intraocular pressure are in#luenced by the time course and magnitude o# the rise in intraocular pressure. In acute angle/closure glaucoma% the intraocular pressure reaches 6A)?A mm 7g% resulting in acute ischemic damage to the iris

with associated corneal edema and optic ner"e damage. In primary open/angle glaucoma% the intraocular pressure does not usually rise abo"e ,A mm 7g and retinal ganglion cell damage de"elops o"er a prolonged period% o#ten many years. In normal/tension glaucoma% retinal ganglion cells may be susceptible to damage #rom intraocular pressures in the normal range% or the ma$or mechanism o# damage may be optic ner"e head ischemia. Clinical *ssessment in Glaucoma (onometry (onometry is measurement o# intraocular pressure. (he most widely used instrument is the Goldmann applanation tonometer% which is attached to the slitlamp and measures the #orce required to #latten a #i9ed area o# the cornea. Corneal thic!ness in#luences the accuracy o# measurement. Intraocular pressure is o"erestimated in eyes with thic! corneas and underestimated in eyes with thin corneas. (his di##iculty may be o"ercome by the Pascal dynamic contour tonometer. .ther applanation tonometers are the Per!ins tonometer and the (ono/Pen% both o# which are portable% and the pneumatotonometer% which can be used with a so#t contact lens in place when the cornea has an irregular sur#ace. (he 4chiot tonometer is portable and measures the corneal indentation produced by a !nown weight. &=or #urther discussion o# tonometry% see Chapter 1H #or tonometer disin#ection techniques% see Chapter 11.' (he normal range o# intraocular pressure is 1A)11 mm 7g &=igure 11)1'. (he distribution is Gaussian% but with the cur"e s!ewed to the right. In the elderly% a"erage intraocular pressure is higher% gi"ing an upper limit o# 12 mm 7g. In primary open/angle glaucoma% ,1)5AB o# a##ected indi"iduals will ha"e a normal intraocular pressure when #irst measured. Con"ersely% isolated raised intraocular pressure does not necessarily mean that the patient has primary open/angle glaucoma% since other e"idence in the #orm o# a glaucomatous optic dis! or "isual #ield changes is necessary #or diagnosis. I# the intraocular pressure is consistently ele"ated in the presence o# normal optic dis!s and "isual #ields &ocular hypertension'% the patient may be obser"ed periodically as a glaucoma suspect. =igure 11)1.

-istribution o# intraocular pressure in indi"iduals o"er the age o# 2A years. Gonioscopy &4ee *lso Chapter 1' (he anterior chamber angle is #ormed by the $unction o# the peripheral cornea and the iris% between which lies the trabecular meshwor! &=igure 11),'. (he con#iguration o# this angle Gie% whether it is wide &open'% narrow% or closedGhas an important bearing on the out#low o# aqueous. (he anterior chamber angle width can be estimated by oblique

illumination with a penlight &=igure 11)2' or by slitlamp obser"ation o# the depth o# the peripheral anterior chamber% but it is best determined by gonioscopy% which allows direct "isuali ation o# the angle structures &=igure 11),'. I# it is possible to "isuali e the #ull e9tent o# the trabecular meshwor!% the scleral spur% and the iris processes% the angle is open. Ceing able to see only 4chwalbe:s line or a small portion o# the trabecular meshwor! means that the angle is narrow. Ceing unable to see 4chwalbe:s line means that the angle is closed. =igure 11),.

Composite illustration showing anatomic *le+t, and gonioscopic *right, "iew o# normal anterior chamber angle. &Courtesy o# ; 4ha##er.' =igure 11)2.

+stimation o# depth o# anterior chamber by oblique illumination &diagram'. &Courtesy o# ; 4ha##er.' Large myopic eyes ha"e wide angles% and small hyperopic eyes ha"e narrow angles. +nlargement o# the lens with age narrows the angle and accounts #or some cases o# angle/ closure glaucoma. .ptic -is! *ssessment (he normal optic dis! has a central depressionGthe physiologic cupGwhose si e depends on the bul! o# the #ibers that #orm the optic ner"e relati"e to the si e o# the scleral opening through which they must pass. In hyperopic eyes% the scleral opening is small% and thus the optic cup is smallH the re"erse is true in myopic eyes. Glaucomatous optic atrophy produces speci#ic dis! changes characteri ed chie#ly by loss o# dis! substanceGdetectable as enlargement o# the optic dis! cupGassociated with dis! pallor in the area o# cupping. .ther #orms o# optic atrophy cause widespread pallor without increased dis! cupping. In glaucoma% there may be concentric enlargement o# the optic cup or pre#erential superior and in#erior cupping with #ocal notching o# the rim o# the optic dis! &=igure 11)5'. (he optic cup also increases in depth as the lamina cribrosa is displaced bac!ward. *s cupping

de"elops% the retinal "essels on the dis! are displaced nasally &=igure 11)6'. (he end result o# glaucomatous cupping is the so/called Ibean potI cup in which no neural rim tissue is apparent &=igure 11)<'. =igure 11)5.

+arly glaucoma showing in#erior #ocal notching o# the neuroretinal rim *arrow,. =igure 11)6.

(ypical glaucomatous cupping. 0ote the nasal displacement o# the "essels and hollowed/ out appearance o# the optic dis! e9cept #or a thin border. =igure 11)<.

Glaucomatous &Ibean/potI' cupping o# the optic dis!. (he Icup)dis! ratioI is a use#ul way o# recording the si e o# the optic dis! in glaucoma patients. It is the ratio o# cup si e to dis! diameter% eg% a small cup is A.1 and a large cup A.@. In the presence o# "isual #ield loss or ele"ated intraocular pressure% a cup)dis! ratio greater than A.5 or signi#icant asymmetry between the two eyes is highly suggesti"e o# glaucomatous atrophy. Clinical assessment o# the optic dis! can be per#ormed by direct ophthalmoscopy or by e9amination with the <?/diopter lens or special corneal contact lenses that gi"e a three/ dimensional "iew. .ther clinical e"idence o# neuronal damage in glaucoma is atrophy o# the retinal ner"e #iber layer% which precedes the de"elopment o# optic dis! changes. It is detectable by ophthalmoscopy or #undal photography% both aided by using red/#ree light% optical coherence tomography% scanning laser polarimetry% or scanning laser tomography. Jisual =ield +9amination

;egular "isual #ield e9amination is essential to the diagnosis and #ollow/up o# glaucoma. Glaucomatous #ield loss is not in itsel# speci#ic% since it consists o# ner"e #iber bundle de#ects that may be seen in other #orms o# optic ner"e diseaseH but the pattern o# #ield loss% the nature o# its progression% and the correlation with changes in the optic dis! are characteristic o# the disease. Glaucomatous #ield loss in"ol"es mainly the central ,A degrees o# #ield &=igure 11)?'. (he earliest change is baring o# the blind spot. Contiguous e9tension into C$errum:s area o# the "isual #ieldGat 15 degrees #rom #i9ationGproduces a C$errum scotoma and then an arcuate scotoma. =ocal areas o# more pronounced loss within C$errum:s area are !nown as 4eidel scotomas. -ouble arcuate scotomasGabo"e and below the hori ontal meridianG are o#ten accompanied by a nasal step &o# ;oenne' because o# di##erences in si e o# the two arcuate de#ects. Peripheral #ield loss tends to start in the nasal periphery as a constriction o# the isopters. 4ubsequently% there may be connection to an arcuate de#ect% producing peripheral brea!through. (he temporal peripheral #ield and the central 5)1A degrees are a##ected late in the disease. Central "isual acuity is not a reliable inde9 o# progress o# the disease. In end/stage disease% there may be normal central acuity but only 5 degrees o# "isual #ield in each eye. In ad"anced glaucoma% the patient may ha"e 1A81A "isual acuity and be legally blind. =igure 11)?.

Jisual #ield changes in glaucoma. &;eproduced% with permission% #rom 7arrington -.: The Visual Fields: A Textbook and Atlas of Clinical Perimetry, 5th ed. >osby% 1@?1.' Jarious ways o# testing the "isual #ields in glaucoma include the automated perimeter &#or e9ample% 7umphrey% .ctopus% or 7enson'% the Goldmann perimeter% the =riedman #ield analy er% and the tangent screen. &=or testing techniques% see Chapter 1.' Con"entional automated perimetry% most commonly using the 7umphrey perimeter% employs a white stimulus on a white bac!ground &white/on/white perimetry'. Jisual #ield de#ects are not detected until there is about 2AB retinal ganglion loss. ;e#inements to detect earlier "isual #ield changes include blue/on/yellow perimetry% also !nown as short/wa"elength automated perimetry &4W*P'% #requency/doubling perimetry &=-P'% and high/pass resolution perimetry. (reatment o# ;aised Intraocular Pressure >edical (reatment

4uppression o# *queous Production (opical )eta-a!renergic )loc-ing agents may be used alone or in combination with other drugs. (imolol maleate A.15B and A.5B% beta9olol A.15B and A.5B% le"obunolol A.15B and A.5B% metipranolol A.,B% and carteolol 1B solutions twice daily and timolol maleate A.1B% A.15B% and A.5B gel once daily in the morning are the currently a"ailable preparations. (he ma$or contraindications to their use are chronic obstructi"e airway diseaseGparticularly asthmaGand cardiac conduction de#ects. Ceta9olol% with its relati"ely greater selecti"ity #or 1 receptors% less o#ten produces respiratory side e##ects% but it is also less e##ecti"e at reducing intraocular pressure. -epression% con#usion% and #atigue may occur with the topical beta/bloc!ing agents. (he #requency o# systemic e##ects and the a"ailability o# other agents has reduced the popularity o# the beta/ adrenergic bloc!ing agents. Apracloni!ine &A.5B solution three times daily and 1B solution be#ore and a#ter laser treatment' is an 1/adrenergic agonist that decreases aqueous humor #ormation without e##ect on out#low. It is particularly use#ul #or pre"enting rise o# intraocular pressure a#ter anterior segment laser treatment and can be used on a short/term basis in re#ractory cases. It is not suitable #or long/term use because o# tachyphyla9is &loss o# therapeutic e##ect o"er time' and a high incidence o# allergic reactions. .pinephrine and !ipi e+rin ha"e some e##ect on aqueous production but are rarely used these days &see below'. &rimoni!ine &A.1B solution twice daily' is an /adrenergic agonist that primarily inhibits aqueous production and secondarily increases aqueous out#low. It may be used as a #irst/line or ad$uncti"e agent% but allergic reactions are common. (or/olami!e hy!rochlori!e 1B solution and )rin/olami!e 1B &two or three times daily' are topical carbonic anhydrase inhibitors that are especially e##ecti"e when employed ad$uncti"ely% although not as e##ecti"e as systemic carbonic anhydrase inhibitors. (he main side/e##ects are a transient bitter taste and allergic blepharocon$uncti"itis. -or olamide is also a"ailable combined with timolol in the same solution. 4ystemic car)onic anhy!rase inhi)itorsGaceta olamide is the most widely used% but dichlorphenamide and metha olamide are alternati"esGare used in chronic glaucoma when topical therapy is insu##icient and in acute glaucoma when "ery high intraocular pressure needs to be controlled quic!ly. (hey are capable o# suppressing aqueous production by 2A)6AB. *ceta olamide can be administered orally in a dosage o# 115)15A mg up to #our times daily or as -iamo9 4equels 5AA mg once or twice daily% or it can be gi"en intra"enously &5AA mg'. (he carbonic anhydrase inhibitors are associated with ma$or systemic side e##ects that limit their use#ulness #or long/term therapy.

7yperosmotic agents in#luence aqueous production as well as dehydrate the "itreous body &see below'. =acilitation o# *queous .ut#low (he prostaglan!in analogsGbimatoprost A.AA,B% latanoprost A.AA5B% and tra"oprost A.AA2B solutions% each once daily at night% and unoprostone A.15B solution twice dailyG increase u"eoscleral out#low o# aqueous. (hey are highly e##ecti"e #irst/line or ad$uncti"e agents. In many countries but not the 3nited 4tates% latanoprost is a"ailable combined with timolol in the same solution #or use once daily in the morning. *ll the prostaglandin analogs may produce con$uncti"al hyperemia% hyperpigmentation o# periorbital s!in% eyelash growth% and permanent dar!ening o# the iris &particularly in green/brown and yellow/brown irides'. (hese drugs ha"e also been rarely associated with reacti"ation o# u"eitis and herpes !eratitis and can cause macular edema in predisposed indi"iduals. $arasympathomimetic agents increase aqueous out#low by action on the trabecular meshwor! through contraction o# the ciliary muscle. $ilocarpine is not commonly used since the ad"ent o# prostaglandin analogs but can be use#ul in some patients. It is gi"en as A.5)6B solution instilled up to #our times a day or as 2B gel instilled at bedtime. Carbachol A.<5),B is an alternati"e cholinergic agent. Parasympathomimetic agents produce miosis with dimness o# "ision% particularly in patients with cataract% and accommodati"e spasm that may be disabling to younger patients. ;etinal detachment is a serious but rare occurrence. .pinephrine0 A.15)1B instilled once or twice daily% increases aqueous out#low with some decrease in aqueous production. (here are se"eral e9ternal ocular side e##ects% including re#le9 con$uncti"al "asodilation% adrenochrome deposits% #ollicular con$uncti"itis% and allergic reactions. (ipi e+rin is a prodrug o# epinephrine that is metaboli ed intraocularly to its acti"e state. 0either epinephrine nor dipi"e#rin should be used in eyes with narrow anterior chamber angles. Coth agents ha"e an ad"erse e##ect on the outcome o# subsequent glaucoma drainage surgery. ;eduction o# Jitreous Jolume Hyperosmotic agents render the blood hypertonic% thus drawing water out o# the "itreous and causing it to shrin!. (his is in addition to decreasing aqueous production. ;eduction in "itreous "olume is help#ul in the treatment o# acute angle/closure glaucoma and in malignant glaucoma when anterior displacement o# the crystalline lens &caused by "olume changes in the "itreous or choroid' produces angle closure &secondary angle/closure glaucoma'. .ral glycerin *glycerol,0 1 mL8!g o# body weight in a cold 5AB solution mi9ed with lemon $uice% is the most commonly used agent% but it should be used with care in diabetics. *lternati"es are oral isosorbide and intra"enous urea or mannitol &see Chapter , #or

dosages'. >iotics% >ydriatics% and Cycloplegics Constriction o# the pupil is #undamental to the management o# primary angle/closure glaucoma and the angle crowding o# plateau iris. Pupillary dilation is important in the treatment o# angle closure secondary to iris bombE due to posterior synechiae. When angle closure is secondary to anterior lens displacement% cycloplegics &cyclopentolate and atropine' are used to rela9 the ciliary muscle and thus tighten the onular apparatus in an attempt to draw the lens bac!ward. 4urgical F Laser (reatment Peripheral Iridotomy% Iridectomy% and Iridoplasty Pupillary bloc! in angle/closure glaucoma is most satis#actorily o"ercome by #orming a direct communication between the anterior and posterior chambers that remo"es the pressure di##erence between them. Laser peripheral iridotomy is best done with the neodymium:K*G laser% although the argon laser may be necessary in dar! irides. 4urgical peripheral iridectomy is per#ormed i# K*G laser iridotomy is ine##ecti"e. K*G laser iridotomy is pre"enti"e when used in patients with narrow angles be#ore closure attac!s occur. In some cases o# acute angle closure when it is not possible to control the intraocular pressure medically or K*G laser iridotomy cannot be per#ormed% argon laser peripheral iridoplasty &*LPI' can be underta!en. * ring o# laser burns on the peripheral iris contracts the iris stroma% mechanically pulling open the anterior chamber angle. (here is a ,AB ris! o# peripheral anterior synechiae and chronically ele"ated intraocular pressure% but this may re#lect the re#ractory nature o# the cases treated. Laser (rabeculoplasty *pplication o# laser &usually argon' burns "ia a goniolens to the trabecular meshwor! #acilitates aqueous out#low by "irtue o# its e##ects on the trabecular meshwor! and 4chlemm:s canal or cellular e"ents that enhance the #unction o# the meshwor!. (he technique is applicable to many #orms o# open/angle glaucoma% and the results are "ariable depending on the underlying cause. (he pressure reduction usually allows decrease o# medical therapy and postponement o# glaucoma surgery. (reatments can be repeated &see Chapter 12'. Laser trabeculoplasty may be used in the initial treatment o# primary open/ angle glaucoma. In most cases% the intraocular pressure gradually returns to the pretreatment le"el 1)5 years later. (he outcome o# subsequent glaucoma drainage surgery may be ad"ersely a##ected.

Glaucoma -rainage 4urgery (he increased e##ecti"eness o# medical and laser treatment has reduced the need #or glaucoma drainage surgery% but surgery is able to produce a more mar!ed reduction in intraocular pressure. Tra)ec%lectomy is the procedure most commonly used to bypass the normal drainage channels% allowing direct access #rom the anterior chamber to the subcon$uncti"al and orbital tissues &=igure 11)@'. (he ma$or complication is #ibrosis in the episcleral tissues% leading to closure o# the new drainage pathway. (his is most li!ely to occur in young patients% in blac!s% in patients with glaucoma secondary to u"eitis% and in those who ha"e pre"iously undergone glaucoma drainage surgery or other surgery in"ol"ing the episcleral tissues. Perioperati"e or postoperati"e ad$uncti"e treatment with antimetabolites such as 5/ #luorouracil and mitomycin C reduces the ris! o# bleb #ailure and is associated with good intraocular pressure control but may lead to bleb/related complications li!e persistent ocular discom#ort% bleb in#ection% or maculopathy #rom persistent ocular hypotony. (rabeculectomy mar!edly accelerates cataract #ormation. =igure 11)@.

(rabeculectomy showing an upper nasal IblebI and peripheral iridectomy. Implantation o# a silicone tube to #orm a permanent conduit #or aqueous #low out o# the eye is an alternati"e procedure #or eyes that are unli!ely to respond to trabeculectomy. (his includes eyes with secondary glaucomaGparticularly neo"ascular glaucomaGand glaucoma #ollowing corneal gra#t surgery. 1iscocanalostomy an! !eep sclerectomy with collagen implant a"oid #ull/thic!ness incisions into the eye. (he intraocular pressure reduction is not as good as that achie"ed with trabeculectomy% but there is less potential #or complications. (hey are technically di##icult to per#orm. Goniotomy and trabeculotomy are use#ul techniques in treating primary congenital glaucoma% in which there appears to be an obstruction to aqueous drainage in the internal portion o# the trabecular meshwor!. Cyclodestructi"e Procedures =ailure o# medical and surgical treatment in ad"anced glaucoma may lead to consideration o# laser or surgical destruction o# the ciliary body to control intraocular pressure. Cryotherapy% diathermy% thermal mode neodymium:K*G laser% or diode laser can all be

used to destroy the ciliary body. (reatment is usually applied e9ternally through the sclera% but endoscopic laser application systems are a"ailable. Primary Glaucoma Primary .pen/*ngle Glaucoma Primary open/angle glaucoma is the most common #orm in blac!s and whites. In the 3nited 4tates% 1.1@)1B o# persons o"er age 2A% rising to 2.<B o# persons o"er age <5% are estimated to ha"e primary open/angle glaucoma. (he disease is #our times more common and si9 times more li!ely to cause blindness in blac!s. (here is a strong #amilial tendency in primary open/angle glaucoma% and close relati"es o# a##ected indi"iduals should undergo regular screening. (he chie# pathologic #eature o# primary open/angle glaucoma is a degenerati"e process in the trabecular meshwor!% including deposition o# e9tracellular material within the meshwor! and beneath the endothelial lining o# 4chlemm:s canal. (his di##ers #rom the normal aging process. (he consequence is a reduction in aqueous drainage leading to a rise in intraocular pressure. Du"enile/onset open/angle glaucoma &a #amilial primary open/angle glaucoma with early onset'% about 5B o# #amilial cases o# primary open/angle glaucoma% and about ,B o# non#amilial cases o# primary open/angle glaucoma are associated with mutations in the myocilin gene on chromosome 1. ;aised intraocular pressure precedes optic dis! and "isual #ield changes by months to years. *lthough there is a clear association between the le"el o# intraocular pressure and the se"erity and rate o# progression o# "isual loss% there is great "ariability between indi"iduals in the e##ect on the optic ner"e o# a gi"en pressure ele"ation. 4ome eyes tolerate ele"ated intraocular pressure without de"eloping dis! or #ield changes &ocular hypertensionH see below'H others de"elop glaucomatous changes with consistently InormalI intraocular pressure &low/tension glaucomaH see below'. 0e"ertheless% higher le"els o# intraocular pressure are associated with greater #ield loss at presentation. When there is glaucomatous #ield loss on #irst e9amination% the ris! o# #urther progression is much greater. 4ince intraocular pressure is the only treatable ris! #actor% it remains the #ocus o# therapy. (here is strong e"idence that control o# intraocular pressure slows dis! damage and #ield loss. =or each 1/mm 7g reduction o# intraocular pressure% there is an appro9imately 1AB decreased ris! o# progression o# glaucoma. I# there are e9tensi"e dis! changes or #ield loss% it is ad"isable to reduce the intraocular pressure as much as possible% pre#erably to less than 15 mm 7g. * patient with only a suspicion o# dis! or #ield changes may need less "igorous treatment. In all cases% the incon"eniences and possible complications o# treatment must be considered. >any glaucoma patients are old and #rail and may not tolerate "igorous treatment. In order to gain a perspecti"e on the need #or treatment% an initial period o# obser"ation without treatment may be necessary to determine the rate o# progression o# dis! and #ield changes.

(here is no $usti#ication #or sub$ecting an elderly patient to e9tremes o# treatment when the li!elihood o# their de"eloping signi#icant "isual loss during their li#etime is small. -iagnosis (he diagnosis o# primary open/angle glaucoma is established when glaucomatous optic dis! or #ield changes are associated with ele"ated intraocular pressures% a normal/ appearing open anterior chamber angle% and no other reason #or intraocular pressure ele"ation. *t least one/third o# patients with primary open/angle glaucoma ha"e a normal intraocular pressure when #irst e9amined% so repeated tonometry may be necessary be#ore the diagnosis can be established. 4creening #or Glaucoma (he ma$or problem in detection o# primary open/angle glaucoma is the absence o# symptoms until relati"ely late in the disease. When patients #irst notice #ield loss% substantial optic ner"e damage has already occurred. I# treatment is to be success#ul% it must be started early in the disease% and this depends on an acti"e screening program. 3n#ortunately% glaucoma screening programs are hampered by the unreliability o# a single intraocular pressure measurement in the detection o# primary open/angle glaucoma and the comple9ities o# relying on optic dis! or "isual #ield changes. *t present it is necessary to rely #or early diagnosis predominantly on regular ophthalmologic assessment o# #irst/ degree relati"es o# a##ected indi"iduals. Course F Prognosis Without treatment% open/angle glaucoma may progress insidiously to complete blindness. I# antiglaucoma drops control the intraocular pressure in an eye that has not su##ered e9tensi"e glaucomatous damage% the prognosis is good &although "isual #ield loss may progress despite normali ed intraocular pressure'. When the process is detected early% most glaucoma patients can be success#ully managed medically. (rabeculectomy is a good option in patients who progress despite medical treatment &=igure 11)@'. 0ormal/(ension Glaucoma &Low/(ension Glaucoma' 4ome patients with glaucomatous optic dis! or "isual #ield changes ha"e an intraocular pressure consistently below 11 mm 7g. (hese patients ha"e normal/tension or low/tension glaucoma. (he pathogenesis may in"ol"e an abnormal sensiti"ity to intraocular pressure because o# "ascular or mechanical abnormalities at the optic ner"e head% or this may be a purely "ascular disease. (here may be an inherited predisposition% normal/tension glaucoma being particularly common in Dapan. * #ew #amilies with normal tension glaucoma ha"e an abnormality in the optineurin gene on chromosome 1A. 4ome studies ha"e shown an association with "asospasm. -is! hemorrhages are more #requently seen in normal/tension than in primary open/angle glaucoma and o#ten herald progression o# #ield

loss. Ce#ore the diagnosis o# low/pressure glaucoma can be established% a number o# entities must be e9cluded: 1. Prior episode o# raised intraocular pressure% such as caused by anterior u"eitis% trauma% or topical steroid therapy. 1. Large diurnal "ariation in intraocular pressure with signi#icant ele"ations% usually early in the morning. ,. Postural changes in intraocular pressure with a mar!ed ele"ation when lying #lat. 2. Intermittent ele"ations o# intraocular pressure% such as in subacute angle closure. 5. 3nderestimation o# intraocular pressure due to reduced corneal thic!ness. 6. .ther causes o# optic dis! and #ield changes% including congenital dis! abnormalities% inherited optic neuropathy% and acquired optic atrophy due to tumors or "ascular disease. *mong patients diagnosed with normal/tension glaucoma% appro9imately 6AB ha"e progressi"e "isual #ield loss% suggesting the possibility o# acute ischemic e"ents in the pathogenesis o# those without progression. ;eduction o# intraocular pressure is bene#icial in patients with progressi"e "isual #ield loss% but this may not be achie"ed with medical therapy. Glaucoma drainage surgery with an antimetabolite may be required. (he possibility o# a "ascular basis #or normal/tension glaucoma has led to the use o# systemic calcium channel bloc!ers% but de#inite bene#it #rom this inter"ention has yet to be demonstrated. .cular 7ypertension .cular hypertension is ele"ated intraocular pressure without dis! or #ield abnormalities and is more common than primary open/angle glaucoma. (he rate at which such indi"iduals de"elop glaucoma is appro9imately 1)1B per year. (he ris! increases with increasing intraocular pressure% increasing age% greater optic dis! cupping% a positi"e #amily history #or glaucoma% and perhaps myopia% diabetes mellitus% and cardio"ascular disease. (he de"elopment o# dis! hemorrhages in a patient with ocular hypertension also indicates an increased ris! #or de"elopment o# glaucoma. Patients with ocular hypertension are considered glaucoma suspects and should undergo regular monitoring &once or twice a year' o# intraocular pressures% optic dis!s% and "isual #ields. It is li!ely that many ocular hypertensi"es who do not de"elop glaucoma ha"e relati"ely thic! corneas% producing an o"erestimation o# intraocular pressure. >easurement o# central corneal thic!ness may thus be use#ul to determine which patients do not require such care#ul monitoring. Con"ersely% many indi"iduals with ocular hypertension may ha"e glaucoma% but the retinal ganglion cell damage is not detectable with currently a"ailable techniques. -e"elopments in perimetry and retinal ner"e #iber layer imaging are

addressing this issue. Primary *ngle/Closure Glaucoma Primary angle closure occurs in anatomically predisposed eyes without other pathology. +le"ation o# intraocular pressure is a consequence o# obstruction o# aqueous out#low by occlusion o# the trabecular meshwor! by the peripheral iris. (he condition may mani#est as an ophthalmic emergency or may remain asymptomatic until "isual loss occurs. (he diagnosis is made by e9amination o# the anterior segment and care#ul gonioscopy. Primary angle/closure glaucoma is the term that should be used only when primary angle closure has resulted in optic ner"e damage and "isual #ield loss. ;is! #actors include increasing age% #emale gender% #amily history o# glaucoma% and 4outh/+ast *sian% Chinese% or Inuit ethnic bac!ground. *cute *ngle Closure *cute angle closure &Iacute glaucomaI' occurs when su##icient iris bombE de"elops to cause occlusion o# the anterior chamber angle by the peripheral iris. (his bloc!s aqueous out#low% and the intraocular pressure rises rapidly% causing se"ere pain% redness% and blurring o# "ision. *ngle closure de"elops in hyperopic eyes with pree9isting anatomic narrowing o# the anterior chamber angle% usually when it is e9acerbated by enlargement o# the crystalline lens associated with aging. (he acute attac! is o#ten precipitated by pupillary dilation. (his occurs spontaneously in the e"enings% when the le"el o# illumination is reduced. It may be due to medications with anticholinergic or sympathomimetic acti"ity &eg% atropine #or preoperati"e medication% antidepressants% nebuli ed bronchodilators% nasal decongestants% or tocolytics'. It may occur rarely with pupillary dilation #or ophthalmoscopy. I# pupillary dilation is necessary in a patient with a shallow anterior chamber &easily detected by oblique illumination with a penlight L=igure 11)2M'% it is best to rely on short/acting mydriatics% a"oid constricting the pupil with pilocarpine% and ad"ise the patient to see! attention immediately in the e"ent o# ocular pain or redness or increasingly blurred "ision. Clinical =indings *cute angle closure is characteri ed by sudden onset o# "isual loss accompanied by e9cruciating pain% halos% and nausea and "omiting. Patients are occasionally thought to ha"e acute gastrointestinal disease. .ther #indings include mar!edly increased intraocular pressure% a shallow anterior chamber% a steamy cornea% a #i9ed% moderately dilated pupil% and ciliary in$ection. It is important to per#orm gonioscopy on the #ellow eye to con#irm the anatomic predisposition to primary acute angle closure. -i##erential -iagnosis

&4ee -i##erential -iagnosis o# Common Causes o# In#lamed +ye' *cute iritis causes more photophobia than acute glaucoma. Intraocular pressure is usually not ele"atedH the pupil is constricted or irregular in shape and the cornea is usually not edematous. >ar!ed #lare and cells are present in the anterior chamber% and there is deep ciliary in$ection. *cute con$uncti"itis is usually bilateral% and there is little or no pain and no "isual loss. (here is discharge #rom the eye and an intensely in#lamed con$uncti"a but no ciliary in$ection. (he pupillary responses and intraocular pressure are normal% and the cornea is clear. Complications F 4equelae I# treatment is delayed% the peripheral iris may adhere to the trabecular meshwor! &anterior synechiae'% producing irre"ersible occlusion o# the anterior chamber angle requiring surgery. .ptic ner"e damage is common. (reatment Acute angle closure is an ophthalmic emergency! (reatment is initially directed at reducing the intraocular pressure. Intra"enous and oral aceta olamideGalong with topical agents% such as beta/bloc!ers and apraclonidine% and% i# necessary% hyperosmotic agentsGwill usually reduce the intraocular pressure. Pilocarpine 1B should be instilled one/hal# hour a#ter commencement o# treatment% by which time reduction o# iris ischemia and lowering o# intraocular pressure allow the sphincter pupillae to respond to the drug. (opical steroids may also be used to reduce secondary intraocular in#lammation. .nce the intraocular pressure is under control% laser peripheral iridotomy should be underta!en to #orm a permanent connection between the anterior and posterior chambers% thus pre"enting recurrence o# iris bombE. (his is most o#ten done with the neodymium:K*G laser &see abo"e'. 4urgical peripheral iridectomy is the con"entional treatment i# laser treatment is unsuccess#ul% but *LPI may be per#ormed. (he #ellow eye should always undergo prophylactic laser iridotomy. 4ubacute *ngle Closure (he same etiologic #actors operate in subacute as in acute angle closure e9cept that episodes o# ele"ated intraocular pressure are o# short duration and are recurrent. (he episodes o# angle closure resol"e spontaneously% but there is accumulated damage to the anterior chamber angle% with #ormation o# peripheral anterior synechiae. 4ubacute angle closure will occasionally progress to acute closure. (here are recurrent short episodes o# unilateral pain% redness% and blurring o# "ision

associated with halos around lights. *ttac!s o#ten occur in the e"enings and resol"e o"ernight. +9amination between attac!s may show only a narrow anterior chamber angle with peripheral anterior synechiae. (he diagnosis can be con#irmed by gonioscopy. (reatment consists o# laser peripheral iridotomy. Chronic *ngle/Closure Glaucoma Patients with the anatomic predisposition to anterior/chamber angle closure may ne"er de"elop episodes o# acute rise in intraocular pressure but #orm increasingly e9tensi"e peripheral anterior synechiae accompanied by a gradual rise in intraocular pressure. (hese patients present in the same way as those with primary open/angle glaucoma% o#ten with e9tensi"e "isual #ield loss in both eyes. .ccasionally% they ha"e attac!s o# subacute angle closure. .n e9amination% there is ele"ated intraocular pressure% narrow anterior chamber angles with "ariable amounts o# peripheral anterior synechiae% and optic dis! and "isual #ield changes. Laser peripheral iridotomy should always be underta!en as the #irst step in the management o# these patients. Intraocular pressure is then controlled medically i# possible% but the e9tent o# peripheral anterior synechia #ormation and sluggish out#low through the remaining trabecular meshwor! ma!e pressure control "ery di##icult% so that drainage surgery is o#ten required. Cataract e9traction with intraocular lens implantation can be e##ecti"e in controlling the intraocular pressure% pro"ided no more than two quadrants o# synechial angle closure are present. +pinephrine and strong miotics must not be used unless peripheral iridotomy or iridectomy has been per#ormed because they will accentuate angle closure. Plateau Iris Plateau iris is an uncommon condition in which the central anterior chamber depth is normal but the anterior chamber angle is "ery narrow because o# an anterior position o# the ciliary processes. 4uch an eye has little pupillary bloc!% but dilation will cause bunching up o# the peripheral iris% occluding the angle &angle crowding'% e"en i# peripheral iridotomy or iridectomy has been per#ormed. *##ected indi"iduals present with acute angle closure at a young age% with recurrences a#ter peripheral laser iridotomy or surgical iridectomy. Long/ term miotic therapy or laser iridoplasty is required. Congenital Glaucoma Congenital glaucoma is rare. It can be subdi"ided into &1' primary congenital glaucoma% in which the de"elopmental abnormalities are restricted to the anterior chamber angleH &1' the anterior segment de"elopmental anomaliesG*9en#eld/;ieger syndrome and Peters anomaly% in which iris and corneal de"elopment are also abnormalH and &,' a "ariety o# other conditionsGincluding aniridia% 4turge/Weber syndrome% neuro#ibromatosis/1% Lowe

syndrome% and congenital rubellaGin which the de"elopmental anomalies o# the angle are associated with other ocular or e9traocular abnormalities. Clinical =indings Congenital glaucoma is mani#est at birth in 5AB% diagnosed in the #irst 6 months in <AB% and diagnosed by the end o# the #irst year in ?AB. (he earliest and most common symptom is epiphora. Photophobia and decreased corneal luster may be present. Increased intraocular pressure is the cardinal sign. Glaucomatous cupping o# the optic dis! is a relati"ely earlyGand the most importantGchange. Later #indings include increased corneal diameter &abo"e 11.5 mm is considered signi#icant'% epithelial edema% tears o# -escemet:s membrane% and increased depth o# the anterior chamber &associated with general enlargement o# the anterior segment o# the eye'% as well as edema and opacity o# the corneal stroma &=igure 11)1A'. =igure 11)1A.

Congenital glaucoma &buphthalmos'. -i##erential -iagnosis >egalocornea% corneal clouding due to congenital dystrophy or mucopolysaccharidoses% and traumatic rupture o# -escemet:s membrane should be ruled out. >easurement o# intraocular pressure% gonioscopy% and e"aluation o# the optic dis! are important in ma!ing the di##erential diagnosis. *ssessment generally requires e9amination under general anesthesia. Course F Prognosis In untreated cases% blindness occurs early. (he eye undergoes mar!ed stretching and may e"en rupture with minor trauma. (ypical glaucomatous cupping occurs relati"ely soon% emphasi ing the need #or early treatment. (reatment is always surgical% and either a goniotomy or trabeculectomy can be underta!en. *nterior 4egment -e"elopmental *nomalies (hese rare diseases constitute a spectrum o# malde"elopment o# the anterior segment% in"ol"ing the angle% iris% cornea% and occasionally the lens. 3sually there is some hypoplasia o# the anterior stroma o# the iris% with bridging #ilaments connecting the iris stroma to the cornea. I# these bridging #ilaments occur peripherally and connect to a prominent% a9ially displaced 4chwalbe:s line &posterior embryoto9on'% the disease is

!nown as A2en+el! syn!rome. I# there are broader iridocorneal adhesions associated with the disruption o# the iris% with polycoria and% in addition% s!eletal and dental anomalies% the disorder is called 3ieger syn!rome &an e9ample o# iridotrabecular dysgenesis'. I# adhesions are between the central iris and the central posterior sur#ace o# the cornea% the disease is !nown as $eters anomaly &an e9ample o# iridocorneal trabeculodysgenesis'. (hese diseases are usually dominantly inherited% although sporadic cases ha"e been reported. >utations on chromosomes 2% 6% and 1,% probably in"ol"ing homeobo9 genes% ha"e been identi#ied in pedigrees with *9en#eld/;ieger syndrome. Glaucoma occurs in appro9imately 5AB o# such eyes and o#ten does not present until late childhood or early adulthood. Goniotomy has a much lower success rate in these cases% and trabeculotomy or trabeculectomy may be recommended. >any such patients require long/term medical glaucoma therapy% and the prognosis is guarded #or long/term retention o# good "isual #unction. *niridia (he distinguishing #eature o# aniridia% as the name implies% is the "estigial iris. In many cases% little more than the root o# the iris or a thin iris margin is present. .ther de#ormities o# the eye may be present% such as congenital cataracts% corneal dystrophy% and #o"eal hypoplasia. Jision is usually poor. Glaucoma #requently de"elops be#ore adolescence and is usually re#ractory to medical or surgical management. (his rare syndrome is genetically determined. Coth autosomal dominant and autosomal recessi"e inheritance ha"e been reported. I# medical therapy is ine##ecti"e% glaucoma drainage surgery should be underta!en. 4econdary Glaucoma Increased intraocular pressure occurring as one mani#estation o# some other eye disease is called secondary glaucoma. (hese diseases are di##icult to classi#y satis#actorily. (reatment in"ol"es controlling intraocular pressure by medical and surgical means but also dealing with the underlying disease i# possible. Pigmentary Glaucoma Pigment dispersion syndrome is characteri ed by abnormal deposition o# pigment in the anterior chamberGnotably in the trabecular meshwor! that presumably impedes out#low o# aqueous and on the posterior corneal sur#ace &Nru!enberg:s spindle'Gand iris transillumination de#ects. 3ltrasound studies show a posterior bowing o# the iris with contact between the iris and onules or ciliary processes% suggesting that pigment granules are rubbed o## #rom the bac! sur#ace o# the iris as a result o# #riction% resulting in the iris transillumination de#ects. (he syndrome occurs most o#ten in myopic males between the

ages o# 15 and 2A who ha"e a deep anterior chamber with a wide anterior chamber angle. (he pigmentary changes may be present without glaucoma% but such persons must be considered Iglaucoma suspects.I 3p to 1AB de"elop glaucoma within 5 years o# presentation and 15B within 15 years &pigmentary glaucoma'. * number o# pedigrees o# autosomal dominant inheritance o# pigmentary glaucoma ha"e been reported% and a gene #or pigment dispersion syndrome has been mapped to chromosome <. Coth miotic therapy and laser peripheral iridotomy ha"e been shown to re"erse the abnormal iris con#iguration% but whether they ha"e long/term bene#it on glaucoma de"elopment and progression is not yet clear. &Cecause the patients are usually young myopes% miotic therapy is poorly tolerated unless administered as pilocarpine once daily% pre#erably at bedtime.' Coth pigment dispersion syndrome and pigmentary glaucoma are notable #or a propensity to episodes o# mar!edly ele"ated intraocular pressureGcharacteristically a#ter e9ercise or pupillary dilationGand pigmentary glaucoma may progress rapidly. *n additional problem is the young age at which pigmentary glaucoma usually de"elops% increasing the chance that glaucoma drainage surgery will be necessary and that antimetabolite therapy will be required. Laser trabeculoplasty is #requently used in this condition but is unli!ely to ob"iate the need #or drainage surgery. Pseudoe9#oliation Glaucoma In pseudoe9#oliation syndrome% #ine white deposits o# a #ibrillary material are seen on the anterior lens sur#ace &in contrast to the true e9#oliation o# the lens capsule caused by e9posure to in#rared radiation% ie% Iglassblower:s cataractI'% ciliary processes% onule% posterior iris sur#ace% loose in the anterior chamber% and in the trabecular meshwor! &along with increased pigmentation'. (hese deposits can also be detected histologically in the con$uncti"a% suggesting a more widespread abnormality. (he disease usually occurs in patients o"er age 65 and is reported to be particularly common in 4candina"ia% although this may re#lect ascertainment bias. (he cumulati"e ris! o# de"eloping glaucoma is 5B at 5 years and 15B at 1A years. (reatment is as #or primary open/angle glaucoma. +yes with pseudoe9#oliation syndrome ha"e a greater incidence o# complications during cataract surgery. Glaucoma 4econdary to Changes in the Lens Lens -islocation (he crystalline lens may be dislocated as a result o# trauma or spontaneously% as in >ar#an:s syndrome. *nterior dislocation may cause obstruction o# the pupillary aperture% leading to iris bombE and angle closure. Posterior dislocation into the "itreous is also associated with glaucoma% although the mechanism is obscure. It may be due to angle

damage at the time o# traumatic dislocation. In anterior dislocation% the de#initi"e treatment is lens e9traction once the intraocular pressure has been controlled medically. In posterior dislocation% the lens is usually le#t alone and the glaucoma treated as primary open/angle glaucoma. Intumescence o# the Lens (he lens may ta!e up considerable #luid during cataractous change% increasing mar!edly in si e. It may then encroach upon the anterior chamber% producing both pupillary bloc! and angle crowding and resulting in acute angle closure. (reatment consists o# lens e9traction once the intraocular pressure has been controlled medically. Phacolytic Glaucoma 4ome ad"anced cataracts may de"elop lea!iness o# the anterior lens capsule% which allows passage o# lique#ied lens proteins into the anterior chamber. (here is an in#lammatory reaction in the anterior chamber% and the trabecular meshwor! becomes edematous and obstructed with lens proteins% leading to an acute rise in intraocular pressure. Lens e9traction is the de#initi"e treatment once the intraocular pressure has been controlled medically and intensi"e topical steroid therapy has reduced the intraocular in#lammation. Glaucoma 4econdary to Changes in the 3"eal (ract 3"eitis (he intraocular pressure is usually below normal in u"eitis because the in#lamed ciliary body is #unctioning poorly. 7owe"er% ele"ation o# intraocular pressure may also occur through a number o# di##erent mechanisms. (he trabecular meshwor! may become bloc!ed by in#lammatory cells #rom the anterior chamber% with secondary edema% or may occasionally be in"ol"ed in an in#lammatory process speci#ically directed at the trabecular cells &trabeculitis'. .ne o# the most common causes o# raised intraocular pressure in indi"iduals with u"eitis is the use o# topical steroids. Chronic or recurrent u"eitis produces permanent impairment o# trabecular #unction% peripheral anterior synechiae% and occasionally angle neo"asculari ation% all o# which increase the chance o# secondary glaucoma. 4eclusio pupillae due to ,6A/degree posterior synechiae produces iris bombE and acute angle/closure glaucoma. (he u"eitis syndromes that tend to be associated with secondary glaucoma are =uchs heterochromic cyclitis% 7L*/C1<)associated acute anterior u"eitis% and u"eitis due to herpes oster and herpes simple9. (reatment is directed chie#ly at controlling the u"eitis with concomitant medical glaucoma therapy as necessary% a"oiding miotics because o# the increased chance o# posterior synechia #ormation. Latanoprost may also need to be withheld because o# reports o# e9acerbation and reacti"ation o# u"eitis. Long/term therapy% including surgery% is o#ten

required because o# irre"ersible damage to the trabecular meshwor!. *cute angle closure due to seclusion o# the pupil may be re"ersed by intensi"e mydriasis but o#ten requires laser peripheral iridotomy or surgical iridectomy. *ny u"eitis with a tendency to posterior synechia #ormation must be treated with mydriatics whene"er the u"eitis is acti"e to reduce the ris! o# pupillary seclusion. (umor 3"eal tract melanomas may cause glaucoma by anterior displacement o# the ciliary body% causing secondary angle closure% direct in"ol"ement o# the anterior chamber angle% bloc!age o# the #iltration angle by pigment dispersion% and angle neo"asculari ation. +nucleation is usually necessary. Ciliary Cody 4welling =orward rotation o# the ciliary body% resulting in anterior displacement o# the lens/iris diaphragm and secondary angle/closure glaucoma% may also occur a#ter "itreoretinal surgery or retinal cryotherapy% in posterior u"eitis% and with topiramate therapy. Iridocorneal +ndothelial &IC+' 4yndrome &+ssential Iris *trophy% Chandler:s 4yndrome% Iris 0e"us 4yndrome' (his rare idiopathic condition o# young adults is usually unilateral and mani#ested by corneal decompensation% glaucoma% and iris abnormalities &corectopia and polycoria'. Glaucoma 4econdary to (rauma Contusion in$uries o# the globe may be associated with an early rise in intraocular pressure due to bleeding into the anterior chamber &hyphema'. =ree blood bloc!s the trabecular meshwor!% which is also rendered edematous by the in$ury. (reatment is initially medical% but surgery may be required i# the pressure remains ele"ated% which is particularly li!ely i# there is a second episode o# bleeding. Late e##ects o# contusion in$uries on intraocular pressure are due to direct angle damage. (he inter"al between the in$ury and the de"elopment o# glaucoma may obscure the association. Clinically% the anterior chamber is seen to be deeper than in the #ellow eye% and gonioscopy shows recession o# the angle. >edical therapy is usually e##ecti"e% but drainage surgery may be required. Laceration or contusional rupture o# the anterior segment is associated with loss o# the anterior chamber. I# the chamber is not re#ormed soon a#ter the in$uryGeither spontaneously% by iris incarceration into the wound% or surgicallyGperipheral anterior

synechiae will #orm and result in irre"ersible angle closure. Glaucoma =ollowing .cular 4urgery Ciliary Cloc! Glaucoma &>alignant Glaucoma' 4urgery upon an eye with mar!edly increased intraocular pressure and a closed or narrow angle can lead to ciliary bloc! glaucoma. Postoperati"ely% the intraocular pressure is higher than e9pected and the lens is pushed #orward as a result o# the collection o# aqueous in and behind the "itreous body. Patients initially become aware o# blurred distance "ision but impro"ed near "ision. (his is #ollowed by pain and in#lammation. (reatment consists o# cycloplegics% mydriatics% aqueous suppressants% and hyperosmotic agents. 7yperosmotic agents are used to shrin! the "itreous body and let the lens mo"e bac!wards. Posterior sclerotomy% "itrectomy% and e"en lens e9traction may be needed. Peripheral *nterior 4ynechiae Dust as with trauma to the anterior segment &see abo"e'% surgery that results in a #lat anterior chamber will lead to #ormation o# peripheral anterior synechiae. +arly surgical re#ormation o# the chamber is required i# it does not occur spontaneously. 0eo"ascular Glaucoma 0eo"asculari ation o# the iris &rubeosis iridis' and anterior chamber angle is most o#ten secondary to widespread retinal ischemia such as occurs in ad"anced diabetic retinopathy and ischemic central retinal "ein occlusion. Glaucoma results initially #rom obstruction o# the angle by the #ibro"ascular membrane% but subsequent contraction o# the membrane leads to angle closure. (reatment o# established neo"ascular glaucoma is di##icult and o#ten unsatis#actory. Coth the stimulus to neo"asculari ation and the raised intraocular pressure need to be treated. (opical atropine 1B and intensi"e topical steroids should be gi"en to reduce in#lammation and impro"e com#ort. In many cases% "ision is lost and cyclodestructi"e procedures are necessary to control the intraocular pressure. Glaucoma 4econdary to ;aised +piscleral Jenous Pressure ;aised episcleral "enous pressure may contribute to glaucoma in 4turge/Weber syndrome% in which a de"elopmental anomaly o# the angle is also o#ten present% and carotid/ca"ernous #istula% which may also cause angle neo"asculari ation due to widespread ocular ischemia. >edical treatment cannot reduce the intraocular pressure below the le"el o# the abnormally

ele"ated episcleral "enous pressure% and surgery is associated with a high ris! o# complications. 4teroid/Induced Glaucoma (opical% periocular% and intraocular corticosteroids may produce a type o# glaucoma that simulates primary open/angle glaucoma% particularly in indi"iduals with a #amily history o# the disease% and will e9aggerate the intraocular pressure ele"ation in those with established primary open/angle glaucoma. Withdrawal o# the medication usually eliminates these e##ects% but permanent damage can occur i# the situation goes unrecogni ed too long. I# topical steroid therapy is absolutely necessary% medical glaucoma therapy will usually control the intraocular pressure. 4ystemic steroid therapy is less li!ely to cause a rise in intraocular pressure. It is imperati"e that patients recei"ing topical or systemic steroid therapy undergo periodic tonometry and ophthalmoscopy% particularly i# there is a #amily history o# glaucoma. ;e#erences *GI4 &*d"anced Glaucoma Inter"ention 4tudy' In"estigators: <. (he relationship between control o# intraocular pressure and "isual #ield deterioration. *m D .phthalmol 1AAAH1,A:21@. LP>I-: 11A12215M *nderson -; et al: 0atural history o# normal/tension glaucoma. .phthalmology 1AA1H1A?:12<. LP>I-: 1115?<@2M *nderson ;4: (he psychophysics o# glaucoma in impro"ing the structure8#unction relationship. Prog ;et +ye ;es 1AA6H15:<@. LP>I-: 16A?1,11M *ung ( et al: Con#iguration o# the drainage angle% intraocular pressure and optic disc cupping in sub$ects with chronic angle/closure glaucoma. .phthalmology 1AA5H111:1?. LP>I-: 1561@?16M Cusbee CG: 3pdate on treatment strategies #or bleb/associated endophthalmitis. Curr .pin .phthalmol 1AA5H16:1<A. LP>I-: 15?<A5<2M Casson ;D et al: Combined surgery in the treatment o# patients with cataract and primary open/angle glaucoma. D Cataract ;e#ract 4urg 1AA1H1<:1?52. LP>I-: 11<A@161M Chen PP et al: Clindness in patients with treated open/angle glaucoma. .phthalmology 1AA,H11A:<16. LP>I-: 116?@?@2M Collaborati"e 0ormal/(ension Glaucoma 4tudy Group: Comparison o# glaucomatous progression between untreated patients with normal/tension glaucoma and patients with therapeutically reduced intraocular pressures. *m D .phthalmol 1@@?H116:2?<. LP>I-: @<?AA@,M -rance 4 et al: ;is! #actors #or progression o# "isual #ield abnormalities in normal/tension

glaucoma. *m D .phthalmol 1AA1H1,1:6@@. LP>I-: 11,?2562M +dmunds C et al: =actors associated with success in #irst/time trabeculectomy #or patients at low ris! o# #ailure with chronic open/angle glaucoma. .phthalmology 1AA2H111:@<. LP>I-: 12<11<1@M Collaborati"e 0ormal/(ension Glaucoma 4tudy Group: (he e##ecti"eness o# intraocular pressure reduction in the treatment o# normal/tension glaucoma. *m D .phthalmol 1@@?H116:2@?. LP>I-: @<?AA@2M =ingert D7 et al: >yocilin glaucoma. 4ur" .phthalmol 1AA1H2<:52<. LP>I-: 115A2<,@M =oster PD et al: (he de#inition and classi#ication o# glaucoma in pre"alence sur"eys. Cr D .phthalmol 1AA1H?6:1,?. LP>I-: 11?15,52M =riedman -4 et al: 4urgical strategies #or coe9isting glaucoma and cataract: *n e"idence/ based update. .phthalmology 1AA1H1@A:1@A1. LP>I-: 11,5@611M Gordon >. et al: (he .cular 7ypertension (reatment 4tudy: Caseline #actors that predict the onset o# primary open/angle glaucoma. *rch .phthalmol 1AA1H11A:<12. LP>I-: 11A2@5<5M Green#ield -4 et al: (he cupped disc. Who needs neuroimagingO .phthalmology 1@@?H1A5:1?66. LP>I-: @<?<,56M 7ei$l * et al: ;eduction o# intraocular pressure and glaucoma progression: ;esults #rom the +arly >ani#est Glaucoma (rial. *rch .phthalmol 1AA1H11A:116?. LP>I-: 11,65@A2M 7erndon LW: Central corneal thic!ness as a ris! #actor #or ad"anced glaucoma damage. *rch .phthalmol 1AA2H111:1<. LP>I-: 12<1?1?@M 7ong C7 et al: Glaucoma draining de"ices: * systemic literature re"iew and current contro"ersies. 4ur" .phthalmol 1AA5H5A:2?. LP>I-: 15611A<<M 7ughes + et al: 12/hour monitoring o# intraocular pressure in glaucoma management: * retrospecti"e re"iew. D Glaucoma 1AA,H11:1,1. LP>I-: 11<?1?21M Dampel 7- et al: Perioperati"e complications o# trabeculectomy in the Collaborati"e Initial Glaucoma (reatment 4tudy &CIG(4'. *m D .phthalmol 1AA5H12A:16. LP>I-: 15@,@,?@M Dohnson -7: Progress in glaucoma: +arly detection% new treatments% less blindness. .phthalmology 1AA,H11A:6,2. LP>I-: 11<@@1<,M Donas DC et al: Intraocular pressure ele"ation a#ter intra"itreal triamcinolone acetonide in$ection. .phthalmology 1AA5H111:5@,. LP>I-: 15?A?12@M Nass >* et al: (he .cular 7ypertension (reatment 4tudy: * randomi ed trial determines

that topical ocular hypotensi"e medication delays or pre"ents the onset o# primary open angle glaucoma. *rch .phthalmol 1AA1H11A:<A1. LP>I-: 11A2@5<2M Nersey DP% Croadway -C: Corticosteroid/induced glaucoma: * re"iew o# the literature. +ye 1AA6H1A:2A<. LP>I-: 15?<<A@,M Nonstas *GP et al: =actors associated with long/term progression or stability in e9#oliation glaucoma. *rch .phthalmol 1AA2H111:1@. LP>I-: 12<1?1@1M Lama PD et al: *nti#ibrotics and wound healing in glaucoma surgery. 4ur" .phthalmol 1AA,H2?:,12. LP>I-: 11<25AA5M Les!e >C et al: =actors #or glaucoma progression and the e##ect o# treatment: (he early mani#est glaucoma trial. *rch .phthalmol 1AA,H111:2?. LP>I-: 1151,??2M Lichter P; et al: Interim clinical outcomes in the Collaborati"e Initial Glaucoma (reatment 4tudy comparing initial treatment randomi ed to medications or surgery. .phthalmology 1AA1H1A?:1@2,. LP>I-: 11<1,A61M >artus P et al: Predicti"e #actors #or progressi"e optic ner"e damage in "arious types o# chronic open/angle glaucoma. *m D .phthalmol 1AA5H1,@:@@@. LP>I-: 15@5,21@M >endicino >+ et al: Long/term surgical and "isual outcomes in primary congenital glaucoma: ,6A degrees trabeculotomy "ersus goniotomy. D **P.4 1AAAH2:1A5. LP>I-: 1A@511@5M 0ouri/>ahda"i N et al: Predicti"e #actors #or glaucomatous "isual #ield progression in the *d"anced Glaucoma Inter"ention 4tudy. .phthalmology 1AA2H111:161<. LP>I-: 15,5A,12M .ltho## C> et al: 0oncompliance with ocular hypertensi"e treatment in patients with glaucoma or ocular hypertension: *n e"idence based re"iew. .phthalmology 1AA5H111:@5,. LP>I-: 15??5<@5M Parrish ;N et al: * comparison o# latanoprost% bimatoprost% and tra"oprost in patients with ele"ated intraocular pressure. * 11/wee!% randomi ed% mas!ed/e"aluator multicentre study. *m D .phthalmol 1AA,H1,5:6??. LP>I-: 11<1@A<?M Pereira >L et al: ;ate and pattern o# "isual #ield decline in primary open/angle glaucoma. .phthalmology 1AA1H1A@:11,1. LP>I-: 11266162M Pus!a P> et al: 3nilateral e9#oliation syndrome: Con"ersation to bilateral e9#oliation and to glaucoma. * prospecti"e 1A/year #ollow/up study. D Glaucoma 1AA1H11:51<. LP>I-: 112?,A@?M Puigley 7*: 0ew paradigms in the mechanisms and management o# glaucoma. +ye

1AA5H1@:1121. LP>I-: 1552,1<@M ;acette L et al: Primary open/angle glaucoma in blac!s: * re"iew. 4ur" .phthalmol 1AA,H2?:1@5. LP>I-: 161?661<M ;itch ; et al: Long/term success o# argon laser peripheral iridoplasty in the management o# plateau iris syndrome. .phthalmology 1AA2H111:1A2. LP>I-: 12<11<1AM 4aw 4 et al: Inter"entions #or angle/closure glaucoma: *n e"idence/based update. .phthalmology 1AA,H11A:1?6@. LP>I-: 12511<56M 4himmyo > et al: Intraocular pressure% Goldmann applanation tension% corneal thic!ness% and corneal cur"ature in Caucasians% *sians% 7ispanics and *#rican *mericans. *m D .phthalmol 1AA,H1,6:5@,. LP>I-: 151?,?,@M 4iddiqui K et al: What is the ris! o# de"eloping pigmentary glaucoma #rom pigment dispersion syndrome. *m D .phthalmol 1AA,H1,5:<@2. LP>I-: 11<??11?M 4i"a!/Callcott D* et al: +"idence/based recommendations #or the diagnosis and treatment o# neo"ascular glaucoma. .phthalmology 1AA1H1A?:1<6<. LP>I-: 115?1A2<M 4paeth GL et al: (he use o# antimetabolites with trabeculectomy: * critical appraisal. D Glaucoma 1AA1H1A:l25. LP>I-: 112211<2M 4pry PG- et al: Identi#ication o# progressi"e glaucomatous "isual #ield loss. 4ur" .phthalmol 1AA1H2<:15?. LP>I-: 11@1??@6M "an der Jal! ; et al: Intraocular pressure/lowering e##ects o# all commonly used glaucoma drugs: * meta/analysis o# randomi ed clinical trials. .phthalmology 1AA5H111:11<<. LP>I-: 15@11<2<M Weinreb ;0 et al: Primary open/angle glaucoma. Lancet 1AA2H,6,:1<11. LP>I-: 1515?6,2M Weinreb ;0 et al: ;is! assessment in the management o# patients with ocular hypertension. *m D .phthalmol 1AA2H1,?:25?. LP>I-: 15,621,AM Wil!ins > et al: Intra/operati"e mitomycin C #or glaucoma surgery. Cochrane -atabase 4yst ;e" 1AA1H1:C-AA1?@<. LP>I-: 111<@<<,M Wormald ; et al: Post/operati"e 5/#luorouracil #or glaucoma surgery. Cochrane -atabase 4yst ;e" 1AA1H,:C-AA11,1. LP>I-: 116?6@<<M Wu-unn - et al: * prospecti"e randomi ed trial comparing intraoperati"e 5/#luorouracil "s mitomycin C in primary trabeculectomy. *m D .phthalmol 1AA1H1,2:511. LP>I-: 11,?,?A?M

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