Glaucoma Glaucoma Surgery: Section 2

Section 2
Glaucoma AND Glaucoma Surgery
TOPIC 1
LIM B U S, C ILIAR Y B O DY AND T R AB E C U L AR M E SH W O R K

Overal yi d: l el Cl ni exam : V i i cal va: Essay: MCQ :
Q Opening Question: W
here i the Li bus? s m
The limbus is the structure between the cornea and the sclera. I can be dened in 3 ways . t Lim b u s 1. Anatom i l m bus: cal i A nterior limit of limbus f ormed by a line j oining end of Bowman and end of D escemet s s (Schwalbe line) s Posterior limit is a curved line marking transition between regularly arranged corneal collagen bres to haphazardly arranged scleral collagen bres 2. Pathol cal l m bus: ogi i A nterior limit same as in one Posterior limit f ormed by line perpendicular to surf ace of conj unctival epithelium about 1. mm behind end of Bowman membrane 5 s 3. Surgi l m bus: cal i A nnular band 2 mm wide with posterior limit overlying scleral spur D ivided into: A nterior blue zone (between Bowman and s Schwalbe line) s Posterior white zone (between Schwalbe s line and scleral spur)
Exam ti ps: Som e of the m ost com m onl asked anatom y or physi ogy questi y ol ons i the n exam i ons. nati
W hat i the Anatom y of the Ci i Body? s l ary The ciliary body is a triangular structure located at the j unction between the anterior and posterior segment. A natomically it is part of the uveal tract.
Section 2: G laucoma and G laucoma Surgery
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C iliary B o d y 1. Functi of the ci i epi i on l ary thel um Secretion of aqueous humor by ciliary nonpigmented epithelium (N PE) A ccommodation C ontrol of aqueous outow Part of BLOOD -A Q U EOU S Barrier: Formed by tight j unctions between N PE (as well as nonf enestrated iris capillaries) M aintain clarity of aqueous humor required f optical f or unction Secretion of hyaluronic acid into vitreous 2. Gross anatom y C iliary body, iris and choroid comprise vascular uveal coat C iliary body: 6 mm wide ring in inner lining of globe Extending f rom ora serrata posteriorly to scleral spur anteriorly Tri angul in cross section: ar A nterior surf ace (uveal portion of trabecular meshwork) Outer surf ace (next to sclera, potential suprachoroidal space between ciliary body and sclera) I nner surf ace (next to vitreous cavity) Smooth pars plana (posterior 2/ 3) Ridged pars plicata (anterior 1/ 3) Pars plicata 70 ciliary processes 3. Bl ood suppl y A rterial supply: Seven anteri ci i or l ary arteri and tw o l es ong posteri ci i arteri or l ary es A nastomosis of the two f orms the maj or arterial circle of iris Located at base of the iris within ciliary process stroma V enous drainage C iliary processes venules drain into pars plana veins, which drain into vortex system 4. Nerve suppl y M ain innervation f rom branches of l ong posteri ci i and short ci i nerves or l ary l ary Parasympathetic bers f rom Edinger estphal -W nucleus to sphincter pupillae as f ollows: Edinger estphal nucleus -W IIC N I Branch to I muscle O C iliary ganglion Short ciliary nerves Sphincter pupillae Sympathetic bers f rom superior cervical ganglion to ciliary body as f ollows: Superior cervical ganglion C iliary ganglion Short ciliary nerves M uscle and blood vessels of ciliary body Sensory bers f rom ciliary body to C N S as f ollows: C iliary body Long posterior ciliary nerves N asociliary nerve Ophthalmic division of V C N Brainstem

5. Mi croscopi anatom y c H istologically divided into three parts: C iliary epithelium (double layer) C iliary stroma C iliary muscle Longitudinal, radial and circumf erential Inner nonpi ented epi i (NPE) gm thel um D irect contact with aqueous humor C olumnar cells with numerous organelles Extension of sensory retina with basal membrane, an extension of inner limiting membrane Outer pi ented epi i (PE) gm thel um Between N PE and stroma C uboidal cells, with numerous melanosomes, f ewer organelles compared to N PE Extension of RPE with basal membrane, an extension of Bruch membrane s N PE and PE lie apex to apex D if erent types of intercellular j f unction j N PE oin and PE: Tight j unctions between N PE (with nonf enestrated iris vessels) f orm BLOODAQ UEOUS Barri er D esmosomes f ound between internal surf aces of N PE cells G ap j unctions f ound between N PE and PE
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The Ophthalmology Examinations Review
Exam ti ps: Com pare and contrast the tw o epi i l thel al ayers (nonpi ented vs pi ented gm gm epi i ). Note that w hi e the pi ented epi i i an extensi of thel um l gm thel um s on the RPE (as expected), i i NOT part of the BLOOD-AQ UEOUS Barri ts er (unexpected, as the RPE form s the bl ood reti barri nal er).
W hat i the Anatom y of the Trabecul Meshw ork? s ar The trabecular meshwork is located at the angle of the anterior chamber beneath the limbus. , I main f ts unction is drainage of aqueous.
Trab ecu lar M esh w o rk 1. Gross anatom y Triangular in shape: Base located at scleral spur A nterior tip located at Schwalbe line s (= termination of D escemet s) 2. Mi croscopi anatom y c Three zones (f rom innermost to outermost): Uveal meshwork: From root of iris to Schwalbe line s 70 m in diameter (least resistance to ow) Corneoscl eral meshwork: From scleral spur to Schwalbe line s 35 m in diameter (moderate resistance) Juxtacanal cul i ar: Lines the endothelium of Schlemm canal s 7 m in diameter (highest resistance to ow)

Exam ti ps: The pore di eter i the j am n uxtacanal cul m eshw ork i 10 ti es sm al er than i ar s m l the uveal m eshw ork, w hi e the corneoscl l eral m eshw ork i 2 ti es sm al er. s m l
W hat are the Bl ood Ocul Barri ar ers? W hen are They Breached? There are two blood ocular barriers . They are breached in certain circumstances .
B lo o d O cu lar B arriers 1. Cl cati assi on Blood-aqueous barrier (BA B): N onf enestrated iris capillaries Tight j unctions between ciliary nonpigmented epithelium (N PE) Blood retinal barrier (BRB): N onf enestrated retinal capillaries Tight j unctions between RPE C iliary processes and choroidal capillaries are f enestrated and do not contribute to barrier 2. Breach of the barri ers Physiological: D ef ect in BRB exists at level of optic disc: W ater -soluble substances may enter ON head by dif usion f f rom extravascular space in choroid Endocrine modications: Rapid, reversible increments in permeability via secretion of hormones (histamine, serotonin, bradykinin, etc. ) Pathological: D ef ect in BRB in vascular diseases: D iabetic retinopathy and hypertensive retinopathy BRV O, C RV O D ef ect in BA B and BRB af cataract or other ter intraocular surgery D ef ect in BA B and BRB in ocular tumors D ef ect in BA B and BRB in ocular inammatory or inf ectious diseases
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TOPIC 2
AQ U E O U S H U M O R AND INT R AO C U L AR P R E SSU R E

hat i the Aqueous H um or? s
The aqueous humor is the uid in the anterior (A C ) and posterior chamber (PC ). I has the f t ollowing properties . A nd its f unctions include, rst, the maintenance of . The aqueous humor is f ormed in the PC by . A q u eo u s H u m o r 1. Properti es C lear uid C omposition: N o cells and less than 1% of proteins compared to plasma Same sodium and chloride, slightly lower potassium and 30% lower bicarbonate than plasma Thi rty ti es higher ascorbate than plasma m Ref ractive index (RI = 1. ) 33 Theref ore, diverges light (!) because RI of cornea: 1. 37 V olume in A C and PC = 0. m l 30 0. 25 ml in A C 0. 05 ml in PC Rate of secretion = 3 ul i (theref takes /m n ore 100 min to completely ref orm A C and PC !) 2. Three functi ons M aintains volume and I OP N utrition f avascular ocular tissue: or Posterior cornea, trabecular meshwork, lens and anterior vitreous Optical role 3. Form ati and out ow on Three form ati mechanisms f on rom ciliary body process (nonpigmented epithelium): A ctive transport (most important) U ltraltration D if usion f Three out ow mechanisms: Trabecular meshwork/ pressure dependent ow 90% of outow Related to I OP via G oldman equation (see below) U veoscleral/ pressure independent ow: 10% of ow A queous enters ciliary body into the suprachoroidal space and vortex veins Rate of aqueous ow quite constant and independent of I OP Other routes I ris veins Retinal veins V ia the cornea
Exam ti ps: Noti the i portance of num ber 3 i aqueous hum or physi ogy! ce m n ol Another possi e questi i W hat are the di bl on s, fferences betw een aqueous and pl a? asm
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W hat i the Gol an Equati s dm on? The G oldman equation states that the I is determined by three interrelated f OP actors.
T h e G o ld m an E q u atio n : 1. Gol an equati states that the fol ow i dm on l ng factors determ i IOP ne I = F/ + Pr OP C Rate of aqueous secretion (F, in l/ min) Level of episcleral venous pressure (Pr in , mmH g) Resistance encountered in outow channel (R in ul/ min/ mmH g): Resistance to ow related to f acility of outow R = 1/ , where R is resistance and C is f C acility of outow
H ow does IOP V ary? The I can have long term variation and short term uctuations, and are af ected by drugs. OP f
IO P V ariatio n 1. Long term vari ons ati A ge: I ncrease with age Blood pressure: I ncrease with BP but not linearly Body weight: I ncrease with increase in body mass C limate: I ncrease in winter 2. Short term uctuati ons C V P changes C hange in body position and valsalva maneuver D iurnal variation: I ncrease in morning N ormal variation = 4 mmH g (> 10 mmH g in glaucoma) C orrelates with increase in endogenous cortisol and catecholamines A ccentuated in POA G Eye movement C linically important in restrictive ophthalmopathy (e. thyroid eye disease, g. pseudotumor) Exercise: D ecrease in I OP C orrelated to metabolic acidosis and changes in extracellular uid volume and osmolality 3. Pharm acol cal effects ogi M iotics G enerally decreases I OP Ef ects: f C ontraction of iris sphincter C ontraction of ciliary muscle pulls scleral spur leading to change in trabecular , meshwork and increase in outow D irect parasympathomimetics (pilocarpine, carbachol) and indirect (phospholine iodide) M ydriatics: G enerally increases I OP Ef ects f A llows peripheral portion of anterior iris stroma to move f orward towards inner aspect of uveoscleral meshwork, leading to decrease in trabecular outow f acility Others: Beta adrenergic blockers (e. timolol) g. reduces production of aqueous and I OP C arbonic anhydrase inhibitors (e. diamox) g. af ects membrane transport of bicarbonate f and water across ciliary epithelium, thereby reducing production of aqueous and I OP H yperosmotic agents (e. mannitol, glycerol) g. elevates blood osmolality with resulting uid shif out of the vitreous t Steroids (page 72)
Exam ti ps: The vari ons can be easi y rem em bered as A, B, C, D, E and F (pharm acoati l l cal ogi )!
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W hat i Tonom etry? s Tonometry is the measurement of the I OP. There are three types of tonometry .
To n o m etry 1. Appl anati tonom etry on D etermines f orce necessary to atten a xed area of cornea Based on the I mbert-Fick principle: Force required to atten an area of a perf ect sphere is proportional to pressure inside sphere G oldman tonometer: D ouble prism in tonometer tip to f acilitate visualization Tonometer tip has diameter of 3. 06 mm Surf ace tension of tear meniscus = corneoscleral rigidity (cancels each other) End point occurs when inner border of two semicircular halves of tear meniscus touch one another I OP measured in mmH g A ir puf tonometer: f N on-contact Pressurized air current directed against a xed area of cornea N ot reliable in extremes 2. Indentati tonom etry on D etermines extent of indentation of cornea by xed w ei ght Schiotz tonometer Plunger with known weight indents cornea W eights of 5. 5, 7. or 10 g 5
M ethod: Patient in supine position Topical anesthetic Tip of plunger allowed to rest on surf ace of eye f orcing an indentation D epth of indentation registered on scale in mm I OP in mmH g read of f f rom conversion chart
3. Com bi ned appl anati oni ndentati tonom etry on M ackay-M arg tonometer: C ontains a spring-mounted plunger and surf ace f ootplate Plunger has 1. mm area that protrudes 5 10 m through center of f ootplate I nitially plunger indents cornea (indentation) End point occurs when plunger indents enough to be ushed with f ootplate (applanation) Other examples (e. tonopen) g. 4. Tonom etry that reduces the i uence of the n corneal bi echani properti om cal es D ynamic control tonometry (D C T) Ocular response analyzer tonometry (ORA )
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TOPIC 3
O P T IC DISC C H ANGE S IN GL AU C O M A
Overal yi d: l el Cl ni exam : i cal Vi va: Essay: MCQ :
hat are the Opti Di Changes i Gl c sc n aucom a?
Optic disc changes in glaucoma can be divided into specic and less specic signs. Specic signs include an increase in cup disc ratio (C D R) . O p tic D isc C h an ges In G lau co m a 1. Speci c si gns Optic disc cupping: Large optic cup (vertical C D R 0. or more) 7 A symmetry of optic cup (dif erence of C D R f 0. or more) 2 Progressive enlargement of optic cup D oes not obey the I T rule SN Focal signs: N otching of rim Regional pallor

Splinter (D rance) hemorrhage N erve ber layer thinning
2. Less speci c si gns: Lamellar dot sign N asalization of vessels Peripapillary crescent (Beta zone) Barring of circumlinear vessels
Exam ti ps: There are four cup si gns, four focal si gns and four l speci c si ess gns.
W hat are the Cl ues that a Large Opti Cup i Physi ogi ? c s ol cal
P h ysio lo gical C u p p in g 1. Opti di c sc: N o progression in cupping Symmetrical cupping Follows I T rule SN Optic disc may be large Nof ocal changes or vessel abnormalities 2. Associ ated w i consi th stentl norm al IOP and V F y
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W hat are the New Im agi Techni ng ques Avai abl for Gl l e aucom a Eval on? uati The imaging techniques can be classied into anterior segment and posterior segment techniques .
Im agin g Tech n iq u es in G lau co m a 1. Anteri segm ent or U ltrasound biomicroscopy: Evaluate angle ofA C and ciliary body Requires contact of ultrasound probe with ocular surf ace I ndications: A ngle closure glaucoma M alignant glaucoma Plateau iris syndrome A nterior segment optical coherence tomography (A S-OC T): Evaluates angle ofA C , but penetration insuf cient f imaging the ciliary body or A dvantages: N on-contact modality no distortion of A C angle M ore obj ective than gonioscopy Faster and easier to obtain images compared to ultrasound biomicroscopy D isadvantages: Scleral spur not easily identied in at least 20% ofA S-OC T images U nable to image ciliary body Q uality of vertical images inf erior to horizontal images 2. Posteri segm ent or Stereoscopic optic disc photography (stereodisc photography): D ocument optic disc changes A dvantages: C heap and simple M ore obj ective than clinical evaluation G laucomascope: C omputer raster stereography where a series of equidistant parallel lines are proj ected onto optic disc at an oblique angle. D eection of lines gives an indication of depth of optic cup A dvantage: M ore quantitative than stereodisc photos N eeds minimal pupil size of 4 mm and clear media C onf ocal scanning laser ophthalmoscopy: H eidelberg Retinal Tomograph (H RT): Sequential images of coronal sections of optic disc are obtained via laser H RT sof tware automatically denes a ref erence plane: C up: Structures below ref erence plane Rim: Structures above ref erence plane Optic nerve head analysis (H RT-I I I) Stereometric parameters: Linear cup/ disc ratio C up shape measure Rim area Rim volume H eight variation contour M ean RN FL thickness D isc size M oorelds Regression A nalysis (M RA ) G laucoma Probability Score (G PS) Progression analysis A dvantages: H igher resolution M iotic pupils and media clarity not important A utomated denition of disc margin (H RT-I I I) Superior to OC T in detecting progression D isadvantages: Physiologic variability of optic nerve head conguration high Poor accuracy in: Tilted discs V ery large or small discs Peripapillary atrophy Optical coherence tomography: I mage f ormation based on optical backscatter similar to ultrasound B scan of , optic disc A dvantages: H ighest resolution N oncontact, noninvasive M iotic pupils and media clarity not important D isadvantages: Time domain OC T inf erior to H RT in detecting glaucoma progression G laucoma sof tware f spectral domain or OC T still in initial phases and expensive RN FL reduced in other conditions e. myopia g.
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TOPIC 4
T H E V ISU AL FIE LDS

hat i the V i s sual Fi d? W hat i an Isopter? And W hat i a Scotom a? el s s
The visual eld (V F) is one of the f unctional components of vision. I is dened as the area that is perceived si ul t m taneousl by a xati eye. y ng V isu al Field B asics 1. Deni on: ti A rea that is perceived simultaneously by a xating eye N ot 2- but 3-dimensional I sland of vision in a sea of darkness (Traquair s denition) 2. Li i m ts: 60 nasally, 50 superiorly, 90110 temporally, 70 inf eriorly Blind spot 15 temporal to xation 3. Isopter Li i V F connecting points with same vi ne n sual threshol d Encloses an area within which a target of a given size and intensity is visible 4. Scotom a and V F defect Scotoma A bsolute or relative decrease in retinal sensitivity w i n V F, bounded by areas of thi normal retinal sensitivity V F def ect A bsolute or relative decrease in retinal sensitivity extendi f ng rom edge ofV F 5. Lum i nance and vi sual threshol d Luminance: I ntensity of light A postilb (asb) is an absol ute unit of luminance N ormal human range: 2 to 9, 000 asb H umphrey V F can measure f rom 0. to 08 10, 000 asb D ecibel (dB) is a rel ve unit of luminance ati I nverse log scale 10, 000 asb = 0 dB; 1 asb = 40 dB V isual threshold: Luminance of stimulus which is perceived 50% of time The brighter the stimulus needed to be perceived, the lower the visual threshold Therefore, bri sti ul = hi asb = ght m us gh l dB = l vi ow ow sual threshol d
Exam ti ps: See al the vi so sual el exam i on i neuro-ophthal ol d nati n m ogy (page 309).
W hat i Peri etry? W hat are the Types and Advantages of Each? s m Perimetry is the quanti cati of the V F. on I can be divided into . t
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P erim etry B asics 1. Cl cati assi on C ampimetry (at surf ace): Tangent screen: M anual and kinetic Test central 30 Subj ect seated 1 or 2 meters f rom black screen Target is presented by examiner Perimetry (curved surf ace): Li ster: M anual and kinetic Extend beyond 30 (peripheral elds) Gol dm an bowl perimeter: M anual and kinetic or static H emispherical bowl with radius of 33 cm (subj at 33 cm) ect Stimuli has dif erent intensities (14) and f sizes (I ) V
Extend beyond 30 (peripheral elds) H um phrey vi sual el anal d yzer (H V F): A utomated and static Test central 30
2. Advantages of autom ated (over m anual ): M ore quantitative N o examiner bias C onstant monitoring of xation A utomated re-testing of abnormal points C omputer sof tware f analysis or 3. Advantages of stati (over ki c): c neti M ore obj ective and quantitative M ore sensitive to shallow scotomas Random presentation of stimuli (less anticipation of subj ect) Faster
Exam ti ps: Com pari son betw een Gol an and H V F i a com m on questi dm s on.
W hat are the Uses ofV i sual Fi d i Ophthal ol el n m ogy? V F is used f diagnosis and f or ollow-up of ophthalmic conditions.
U ses o f V isu al Field 1. Di agnosi of s G laucoma Optic nerve diseases (optic neuritis, anterior ischemic optic neuropathy, toxic neuropathy) U nexplained visual loss M alingering patients 2. Fol ow -up of l G laucoma Tumors (pituitary adenoma)
Tel m e about the H um phrey V i l sual Fi d Anal el yzer. H umphrey visual eld analyzer is an autom ated stati perimetry. c M aps the V F by quantif ying the vi sual threshol of the retinal at predetermined locations. d
H u m p h rey V isu al Field A n alyzer 1. Basi c A utomated static perimetry Stimuli (size = G oldman size I I with duration of I 0. s) 2 Background illumination = 31. asb 5 2. Test strategi es Full threshold strategy: U ses the 42 bracketing algorithm at each retinal point 58

Stimuli intensity increases in 4 dB steps until threshold is crossed (patients see stimuli) Threshold is recrossed with stimuli intensity decreasing in 2 dB steps Test pattern: 242 test pattern: Test central 24 of xation and on either side of meridian (242) as opposed to tests on meridians as well (241) 301 or 302 (Test central 30 of xation)
Related threshold strategies: Full threshold with prior data: Faster uses prior V F data, presents each , point at 2 dB higher than patient s previous threshold values and tests each point in 2 dB decrement Fast threshold: Even f aster presents entire eld at 2 dB , higher than patient previous threshold s
values and then tests only abnormal points Suprathreshold test strategy: Fast screening test Presents stimuli at 6 dB higher than expected threshold Each point is recorded as normal vs abnormal
H ow do You Read the H um phrey V i sual Fi d? el This is a H V F f the lef and right eyes respectively. or t D one on J anuary 2nd, 1999, using the 242 threshold test pattern . First, the reliability indices are .
E valu atin g th e H V F 1. Rel abi i i ces i l ty ndi Fixation loss: Positive response to blind spot stimulation M oving eyes around N ormal: Less than 20% False positive: Positive response but no stimuli H appy clicker N ormal: Less than 33% False negative: N egative response with brighter than threshold stimuli Falling asleep N ormal: Less than 33% Other clues: Short-term uctuation signicantly raised C lover leaf pattern on grayscale (inattentiveness with time) I ncreased eye (upstroke) or lid (downstroke) movement on eye tracker line 2. Gl obal i ces ndi M ean deviation (M D ): A verage deviation of each point f rom age-corrected normal (e. 5 dB M D means g. that on average, each point has a 5 dB lower threshold than normal) M inus is bad Pattern standard deviation (PSD ): Standard deviation of each point f rom age-corrected normal M easures the variability/ irregularity of eld (e. a high PSD indicates irregular eld) g. Plus is bad Short-term uctuation (SF): Retests 10 pre-selected points and calculates dif erences between original test and retest f thresholds M easures consistency One of earliest signs of glaucoma (patient sometimes sees it and sometimes does not) M ay also be indicator of reliability C orrected pattern standard deviation (C PSD ): PSD corrected f SF or M easures localized variability/ irregularity (a high C PSD indicates localized irregularity) G laucoma hemield test (G H T): 5 clusters of points in upper and lower half of V F are compared Early indicator of glaucoma 3. Fi gures Raw numeric values and grayscale: Threshold at each point (e. 25 dB at that g. point means visual threshold is 25 dB) Total deviation: A ge-corrected normal minus raw threshold value (e. 2 dB at that point means visual g. threshold is 2 dB less than what is normal at that point) Similar to M D Pattern deviation: Total deviation adj usted upwards or downwards to pick up localized def ects M easures localized def ects Similar to C SPD
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In terp retatio n MD N ormal A bnormal N ormal A bnormal CSPD N ormal N ormal A bnormal A bnormal Total devi on ati pl ot C lean M any abnormal points M any abnormal points M any abnormal points Pattern devi on ati pl ot C lean C lean Similar abnormal points Di agnosi s N ormal G eneralized loss of sensitivity (e. cataract) g. Localized def ect (e. glaucoma) g.
Less abnormal points Both generalized and but not clean localized def ects
Exam ti ps: You m ay be gi ven a H V F pri ntout to read.You need to be system ati and not c j p at the obvi V F defect seen. um ous Rem em ber Mean devi on = Mi ati nus i bad. Pattern standard devi on = Pl s ati us i bad. s
W hat are the V i sual Fi d Defects i Gl el n aucom a? The V F def ects can be divided into early and late.
G lau co m a V isu al Field D efects 1. Earl y: Paracentral nasal def ect N asal step/ temporal wedge Scotoma in Bj errum area (1020 of xation) s Siedal scotoma (def extending f s ect rom blind spot) 2. Late: A rcuate def double arcuate ect/ Temporal island with central vision C entral vision only (tunnel vision)
W hat are the New er V F Techni ques? K nows when to quit when standardized amount of inf ormation is obtained U ses all inf ormation f rom every point
N ew er P erim etry Tech n iq u es 1. SITA (Sw edi Interacti Threshol ng Al sh ve di gori ) thm A ims to increase speed without losing accuracy SI Standard: TA Full version comparable to standard threshold algorithm in sensitivity and accuracy tw i ce but as f ast SI Fast: TA Similar to suprathreshold algorithm in sensitivity and accuracy but twice as f ast H ow SI works: TA Smart questions and smart pacing A ll f actors considered as test occurs, producing estimate of threshold at each point U ses normal age-corrected threshold values as starting point Real time calculation and re-calculation of threshold values as test proceeds 60

2. SW AP (Short W avel ength Autom ated Peri etry) m Blue on yellow perimetry Bl ue-yel ow gangl on cells rst lost in l i glaucoma SW A P detects abnormal V F 25 years bef ore white on white V F abnormal The presence of cataracts may af ect the f accuracy of SW A P 3. Frequency doubl ng peri etry i m Low spatial f requency sinusoidal grating undergoing high temporal f requency icker Tests m agnocel ul pathway, which appears to l ar be rst lost in glaucoma Possible screening tool f f or uture
TOPIC 5
GO NIO SC O P Y
hat i Goni s oscopy?
G onioscopy is an evaluation of the A C angle. I overcomes total internal reection . t There are two types of lens used to evaluate the angle. G o n io sco p y 1. Pri pl nci e Light f rom A C angle exceeds critical angle at cornea-air interf ace, undergoes total internal reection and cannot be seen G oniolens has similar ref ractive index as cornea and alters cornea-air interf ace to allow light to pass f rom A C through cornea into lens C ritical angle of new interf ace between lens and air is not exceeded and theref images f ore rom angle can be visualized I ndirect goniolens provide mirror image of angle, while direct lens provide actual view of angle 2. Indi rect goni ens ol G oldman goniolens: D iameter of 12 mm Stabilizes globe and theref ore good f argon or laser trabeculoplasty N eeds coupling uid 2-mirror lens angled at 62 3-mirror lens: Largest mirror at 73 (visualize posterior pole to equator) Second largest at 67 (visualize equator to retinal periphery) Smallest (semicircular) at 59 (visualize angles) Z eiss goniolens: D iameter of 9 mm and atter than cornea C an be used f or i ndentati onal gonioscopy Lack stability and theref ore not good f or argon laser trabeculoplasty 4-mirror angled at 64 C an see entire extent of angle N o coupling uid needed Better visualization Posner 4-mirror and Sussman 4-mirror lens (modied Z eiss with handle)
3. Di rect goni ens ol D iagnostic: Koeppe (prototype diagnostic goniolens): Stable Entire extent of angle can be viewed Surgical: Barkan (prototype surgical goniolens), M edical W orkshop,Thorpe and others
Exam ti ps: Candi dates sel dom answ er the pri pl of goni nci e oscopy w el . l The com pari son betw een Gol an and Z ei i another favori questi dm ss s te on.
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H ow do You Perform a Goni oscopi Exam i on? c nati G onioscopy is an evaluation of the A C angle. A systematic evaluation of the structures of the angle is done as f ollows .
G o n io sco p ic E xam in atio n 1. Grade the angl (see bel ) e ow Standard gonioscopy I ndentational gonioscopy D if erentiate appositional closure f f rom synechial closure 2. Assess the structures A nterior displacement of Schwalbe line s Posterior embryotoxon Trabeculum pigmentation: P seudoexf oliation and pigment dispersion syndrome I ritis G laucoma (post angle closure glaucoma) M elanomosis of angles (oculodermal melanosis) E ndocrine (diabetes and A ddison s syndrome) N evus (C ogan Reese syndrome) T rauma Peripheral anterior synechiae Blood in Sclemms canal (raised episcleral venous pressure): C arotid cavernous stula Sturge-W eber syndrome Superior vena cava obstruction Ocular hypotony Post gonioscopy
Exam ti ps: The di fferenti di al agnoses for trabecul pi entati can be rem em bered by ar gm on the m nem oni PIGMENT! c
Notes C ompared to iris processes, peripheral anterior synechiae are denser more , irregular and extend beyond scleral spur
H ow i the Angl Cl ni l Graded? s e i cal y The angle is graded according to classication systems such as .
G rad in g o f A n gle Shaffer system (0 4) G rade 4 (40) C iliary body seen G rade 3 (30) Scleral spur seen G rade 2 (20) Trabeculum seen G rade 1 (10) Schwalbe line seen s G rade 0 (closed angle) I ridocorneal contact 62
Schei s system e (IIV ) G rade I G rade I I G rade I I I G rade I V
Spaeth system A ngular approach (degrees) C urvature of peripheral iris Regular (normal) Steep (risk of closure) Q ueer (aphakia, pigmentary glaucoma, subluxed lens) I insertion ris A = A bove Schwalbe line s B = Below Schwalbe line s C = A t scleral spur D = A nterior part of ciliary body E = C iliary body
H ow do You Cl ni l Assess the AC Depth? i cal y W e can clinically assess separately the central or peripheral A C at the slit lamp.
C lin ical A C D ep th A ssessm en t 1. Peri pheral (V an H eri s m ethod): ck N arrow slit beam f rom 60 Beam aligned vertically and directed j inside ust limbus D istance between corneal endothelium and iris compared with corneal thickness A C considered shallow when this distance is < 1/ corneal thickness 4 2. Central (Redm an-Sm i m ethod): th N arrow slit beam f rom 60 Beam is aligned horizontally and f ocused between the corneal endothelium and lens A dj width of slit: ust A lign the nasal end of corneal slit with temporal end of lens slit This length is measured in mm A C depth = length of slit (mm) 1. + 0. 1 5
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TOPIC 6
C O NGE NIT AL GL AU C O M AS
hat are the Causes of Congeni Gl tal aucom as?
C ongenital glaucoma can be classied into two groups: Primary or secondary. Secondary causes include . C lassi catio n o f C o n gen ital G lau co m a 1. Pri ary: m C ongenital (birth), inf antile (12), j uvenile (216) 2. Secondary: Systemic disorders: C hromosomal disorders M etabolic disorders (Lowe syndrome, s Z ellweger syndrome) s
Phakomatoses (Sturge-W eber syndrome) Ocular developmental disorders: A nterior segment dysgenesis, aniridia C ongenital ectropion uvea, nanophthalmos Ocular diseases: Retinoblastoma, ROP, persistent hyperplastic primary vitreous, trauma, uveitis
Exam ti ps: The cl cati i exactl the sam e as for congeni cataracts (page 11)! assi on s y tal
W hat are the Causes of Cl oudy Cornea at Bi rth? C loudy corneas can be caused by many dif erent disorders. f They can be classied based on the size of the eye.
C lo u d y C o rn ea at B irth 1. Large eye: C ongenital glaucoma M esenchymal dysgenesis 2. Sm al eye: l M icrophthalmos Severe prenatal inf ection M esenchymal dysgenesis 3. Norm al si eye: ze D if use opacity: f C ongenital hereditary endothelial dystrophy C ongenital hereditary stromal dystrophy Sclerocornea M ucopolysaccharidosis M ucolipidosis I nterstitial keratitis C ongenital glaucoma
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Regional opacity Linear: Forceps inj ury C ongenital glaucoma (H aab striae) s
Round: I ective keratitis nf Peter anomaly s Localized mesenchymal dysgenesis
Exam ti ps: Di fferenti di al agnosi of cl s oudy cornea at bi rth: S Scl erocornea T Traum a U Ul cer M Metabol c di i sease P Peter anom al s y E Endothel al dystrophy i D Descem et m em brane breaks s
H ow do You Manage Congeni Gl tal aucom as? The management of congenital glaucoma is dif cult. A nd involves a m ul di pl nary team approach. ti sci i The important i ssues include . A complete history and physical examination, usually under anesthesia, is needed.
M an agem en t o f C o n gen ital G lau co m a 1. Issues i m anagem ent n A ssessing eti ogy and i ol nheri tance of congenital glaucoma M anaging system i problems of secondary c congenital glaucoma D eciding on type of surgery (corneal diameter as a guide): < 13 mm: G oniotomy/ trabeculotomy > 14 mm: Trabeculotomy/ trabeculectomy/ valve implant > 16 mm: C yclodestructive procedures (usually very poor prognosis) M anaging associated ocular problems and am bl yopi a: Ref ractive errors C orneal opacity C ataract Squint 2. Physi exam i on cal nati Symptoms: Tearing Photophobia Blepharospasm Red eye Poor vision Signs: A xial myopia B uphthalmos C loudy cornea D escemet breaks (H aab striae) s s D iameter of cornea enlarged D isc cupping E xamination under anesthesia Examination under anesthesia: Ketamine anesthetic (other agents like isourane, halothane give f alsely low I OP) I OP (tonopen or Perkins) Opthalmoscopy (disc) G onioscopy (Koeppe) Ref raction (retinoscopy) C orneal diameter (horizontal and vertical)

Exam ti ps: Li m anagem ent of congeni cataracts (page 11), thi i a fai y di cul ke tal s s rl f t questi to handl on e. Provi preci openi statem ents to capture spectrum of rel de se ng ated probl s. em
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Notes The clinical signs can be remembered as A BC D E
W hat i Goni s otom y and Trabecul otom y? G oniotomy and trabeculotomy are surgical operations f congenital glaucoma. or
Treatm en t O p tio n s fo r C o n gen ital G lau co m a 1. Goni otom y Establish communication between A C and Schlemm canal s I ndications: U sually in children < 3 years C ommon conditions: Primary congenital glaucoma, Sturge-W eber syndrome, Lowe s s syndrome Requires cl cornea ear Procedure: I ncision made at supercial layer of meshwork, m i dpoi of trabecular band nt (midpoint of Schwalbe line and scleral spur) s Each sweep f 120 or I should drop posteriorly ris Repeat f rom opposite side Results: G ood initial results (85% success) H owever 40% need re-operation , Repeated up to three times 2. Trabecul otom y Establish communication between A C and Schlemm canal by removal of a portion of s trabecular meshwork (goniotomy ab externo) I ndications: U sually in children > 3 years C ommon conditions: J uvenile glaucoma, A xenf s anomaly, Peter anomaly eld s Poor corneal vi bi i si l ty Procedure: Scleral ap f ashioned, usually inf erotemporal region (preserve superotemporal conj unctiva f trabeculectomy later) or Radial incision made over Schlemm canal s until it is inserted C heck location of Schlemm canal by s threading 5/ nylon into canal 0 Trabeculotome inserted into canal and rotated into A C , tearing meshwork W ithdraw trabeculotome and introduce it in the opposite direction Results: Similar results as goniotomy but conj unctiva violated
3. Trabecul al s odi ysi Similar to goniotomy U sually f children with secondary glaucoma or f rom inammation (Juveni e chroni arthri s) l c ti D if ers f f rom goniotomy in that knif cuts are e made at Schw al s l ne be i M eshwork is pushed inf eriorly using at side of blade and is disinserted f rom scleral spur 4. Trabecul ectom y N eeds mitomycin C / uorouracil application 5 Problems with trabeculectomy in children Thick Tenon s Thin sclera D if culty in identif ying limbus H igher rates of scarring and trabeculectomy f ailure Risk of endophthalmitis C hronic post-op hypotony f requent 5. Gl aucom a drai nage i pl m ants M itomycin C or 5-uorouracil application usually indicated in congenital glaucoma Some advocate the use of glaucoma drainage implants as a primary surgical intervention in congenital glaucoma, due to the problems with trabeculectomy in children Of more than one implant needed ten I ndication: Ref ractory primary congenital glaucoma C omplications (similar to those in adults): H ypotony Tube exposure Endophthalmitis C orneal decompensation Persistent I ritis
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6. Cycl odestructi on I ndications: Painf blind eye ul G laucoma ref ractory to other f orms of treatment Patient not t f surgery or C omplications: C hronic hypotony/ phthisis V ision loss C ataracts 7. Medi therapy cal Problems N ot very ef ective f
C ompliance: Toxi ty, especi l system i toxi ty ci al y c ci A lpha2 agonists: Bradycardia, hypotension, apnea (cross blood-brain barrier in children) Prostaglandin analogues and miotics: Of inef ective in congenital glaucoma ten f Beta blockers: A sthma, bradycardia Side ef ects are usually very dif erent f f f rom those of adults (e. f g. ailure to thrive, bed wetting, abnormal school behavior)
W hat are Mesoderm al Dysgeneses? M esodermal dysgeneses are a group of congenital disorders. W hich involves the cornea, iris and A C angle. A nd f requently associated with congenital glaucoma.
M eso d erm al D ysgen eses an d A n irid ia Ri eger anom al s y and syndrom e AD
Axenfel s anom al d y I nheritance AD
Peter anom al s y AD
Ani di ri a AD A R (M ental retardation) Sporadic (W ilm s tumor)
I ris
Posterior embryo- Posterior embryo- Posterior embryo- A niridia toxon toxon toxon I hypoplasia, ris I hypoplasia, ris I strands ris corectopia, corectopia, polycoria, polycoria, ectropion uvea ectropion uvea C orneal opacity Keratolenticular adhesions C orneal plana, sclerocornea C ataract C orneal opacity Keratolenticular adhesions C orneal plana, sclerocornea C ataract Foveal hypoplasia N ystagmus C horoidal coloboma
C ornea
Others
G laucoma Systemic
G laucoma rare N one
G laucoma in 50% G laucoma in 50% G laucoma in 50% D ental and f acial N one malf ormations in Rei s syndrom e ger W ilm tumor in s A R trait
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Clinical approach to mesodermal dysgenesis The most obvious abnormality is the presence of posterior embryotoxon. There are also diffuse areas of iris atrophy, corectopia, ectropion uvea. Look for Corneal opacity (Peters syndrome) Lenticular opacities anterior polar cataracts (Peters syndrome) Keratolenticular adhesions (Peters syndrome) Abnormality in fellow eye (bilateral condition) Maxillary hypoplasia, teeth (hypodontia, microdontia) This young patient has mesodermal dysgenesis. Ill like to Check IOP Perform gonioscopy Assess optic disc Look at visual elds Assess family members for similar condition
Clinical approach to aniridia The most obvious abnormality is the absence of iris . Look for Corneal opacity, microcornea, sclerocornea Limbal dermoid Lenticular opacities Keratolenticular adhesions Check fellow eye (bilateral condition) N ystagmus This young patient has aniridia. Ill like to Check IOP Perform gonioscopy Check fundus (foveal and disc hypoplasia, choroidal coloboma) Assess family members for similar condition If sporadic, refer to renal physician to exclude W ilm tumor s
Exam ti ps: Another nam e i i docorneal dysgenesi Do not confuse thi w i the s ri s. s th i docorneal endothel al syndrom es (ICE). ri i Ani di i NOT part of the spectrum , but i uded i the tabl for com pari ri a s ncl n e son. Rem em ber that W i m tum or i associ l s s ated w i sporadi type of ani di th c ri a.
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TOPIC 7
O P E N ANGLE GL AU C O M AS
hat i Gl s aucom a?
G laucoma is a specic type of optic neuropathy. W ith characteristic optic disc changes and V F abnormalities. The maj risk f or actor is an increase in I OP. G laucoma can be classied into open and closed angle and also as primary and secondary . G lau co m a 1. Deni on ti Optic neuropathy with characteristic optic disc changes and V F abnormalities I is one of the risk f OP actors 2. Cl cati assi on Open angle glaucoma (OA G ): Primary (POA G ) Secondary: Paratrabecular (membrane) Trabecular (pigment dispersion, pseudoexf oliation syndrome, neovascular glaucoma) Post-trabecular (raised episcleral venous pressure) A ngle closure glaucoma (A C G ): Primary (PA C G ) Secondary: Posterior pushing f orces (posterior synechiae, phacomorphic glaucoma) A nterior pulling f orces (peripheral anterior synechiae, neovascular glaucoma)
W hat i the Pathogenesi of Pri ary Open Angl Gl s s m e aucom a? A bnormal blood coagulability N octurnal hypotension, signicant blood loss 4. Neurodegenerati factors ve Primary ON damage leads to release of glutamate,which interacts with cell receptors that leads to an increase in intracellular calcium levels This triggers cell death via apoptosis and leads to f urther release of glutamate and a vicious cycle occurs
1. Geneti cs M YOC : M yocilin (G LC 1A ), associated with j uvenile open angle glaucoma and ~ 4% of adults with POA G OPTN : Optineurin (G LC 1E) Other loci: G LC 1B, G LC 1C etc. 2. Pressure-dependent (m echani ) factors cal I ncreased I compression and backward OP bowing of lamina cribrosa obstruction of axoplasmic transport ganglion cell death 3. Ischem i factors (especi l si cant for NTG) c al y gni V ascular perf usion compromise (D M , H PT, migraine, Raynaud phenomenon) s
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W hat i Steroi Response? s d Steroid response is the change in I with steroid administration. OP
Stero id R esp o n se 1. Deni on ti Based on 6-week course of topical betamethasone, there are three groups of persons: H igh responders (> 30 mmH g): 5% of population 90% of POA G 25% of POA G relatives M oderate responder (2230 mmH g): 35% of population Low responder (21 mmH g or less): 60% of population 2. Ri i IOP dependent on: sk n Strength of steroids Strong steroids (dexamethasone, betamethasone and prednisolone, etc. more ) likely to produce I rise than weak steroids OP (uorometholone etc. ) Route of administration: Systemic steroids less likely to produce I OP rise D uration, f requency and dose 3. Mechani sm D ecrease phagocytosis I nterf with transport in trabeculum ere D ecrease in prostaglandin activity
W hat are the Factors W hi In uence the Managem ent of Open Angl Gl ch e aucom a? The f actors which will inuence the management of a patient with open angle glaucoma include .
Facto rs th at D eterm in e th e M an agem en t o f O p en A n gle G lau co m a 1. Severi and progressi of di ty on sease: I level (most important f OP actor) Optic nerve head changes V isual eld changes Ocular risk f actors (C RV O, Fuch endothelial s dystrophy, retinitis pigmentosa) 2. Pati factors: ent A ge Race (blacks higher rate of progression) Family history of blindness f rom glaucoma Only eye or f ellow eye blind f rom glaucoma C oncomitant risk f actors (D M , H PT, myopia, other vascular diseases) C ompliance to f ollow-up and medication use Socioeconomic status (costs of drugs vs surgery) R eso u rces A vailab le to th e P atien t Surgery f POA G in places which has no or resources f long term f or ollow-up
Exam ti ps: Si i ar to factors affecti m anagem ent of cataract and gl m l ng aucom a (page 29). A very useful approach to m any di fferent gl aucom a questi ons. For exam pl e, the exam i ner m ay ask, H ow do you m anage a 70-year-ol m an w i d th uncontrol ed POAG i one eye and i bl nd i the other eye from advanced l n s i n POAG?
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W hat i the Rel onshi betw een IOP and Gl s ati p aucom a? W hat are Ocul H ypertensi and Norm al ar on Tensi Gl on aucom a (NTG)? Ocular hypertension is dened as I > 95th percentile of the normal distribution in that population OP (see below). N TG is dened as (see below).
Sp ectru m o f P O A G , O cu lar H yp erten sio n an d N TG IOP Increased N ormal Opti di c sc Abnormal Abnormal VF Abnormal Abnormal Di agnosi s G laucoma (POA G ) N TG Exclude POA G with diurnal I variation OP Exclude optic neuropathy D ecide on treatment approach D etermine risk of POA G D ecide on treatment approach Exclude either POA G or N TG Exclude either POA G or N TG Cl ni approach i cal
Increased N ormal N ormal N ormal
N ormal N ormal Abnormal N ormal
N ormal Abnormal N ormal N ormal
Ocular hypertension G laucoma suspect G laucoma suspect N ormal
W hat i Ocul H ypertensi (OH T)? H ow do You Manage OH T? s ar on Ocular hypertension is dened as an I > 95th percentile of the normal distribution in that population. OP The ON and V F are normal. But the I is consistently > 21 mmH g. OP The management has to be individualized. I would discuss the management options with the patient: H e can either be observed or glaucoma treatment can be commenced. I would be more inclined to start treatment if these risk f actors f developing POA G are present: . or
O cu lar H yp erten sio n 1. Natural hi story V F loss about 2% per year Treatment decreases V F loss to 1% per year H owever mean years f , rom initial V F loss to death (12 years in whites, 16 years in blacks) Theref elderly patient with OH T rarely ore becomes blind even without treatment! 2. Ri factors for devel ng POAG (Ocul sk opi ar H ypertensi Treatm ent Study) on A ge of patient (older) Larger vertical C D R H igher I OP Thinner C C T (< 555 m) greater PSD on H V F Family history of glaucoma (though not signicant in OH TS) M yopia, migraine, hypertension were not f ound to be risk f actors D M was protective against development ofPOA G 3. Managem ent Establish baseline and f ollow-up opti di c sc appearance (stereodisc photos, H RT) Establish baseline and f ollow-up V F (to detect progression and to improve patient reliability) D etermine central corneal thickness (C C T) Patient pref s erence is an important f actor in the management
W hat i Norm alTensi Gl s on aucom a (NTG)? H ow do You Manage NTG? N ormal tension glaucoma is a common f orm of POA G . I which the ON and V F changes are characteristic of POA G . n But the I is consistently < 21 mmH g. OP The management of N TG is dif cult and controversial. I includes establishing the diagnosis and f t ollow-up f progression of disease. or
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The ndings ofthe C ollabor ative N ormal Tension G laucoma Study (C N TG S) suggest that N TG is of ten non-progressive.W hen V FD or optic nerve damage is progressive,medical and surgical treatment is indicated. Some patients progress despite treatment, suggesting that f actors other than I may play a more OP important role in optic nerve damage.
N o rm al Ten sio n G lau co m a 1. Cl ni exam i on and di i cal nati agnosti approach c Ai m Exclude other types of glaucoma: POA G with diurnal variation? (daily changes) I ntermittent A C G ? Old secondary glaucoma? Exclude optic neuropathy: C ompressive optic neuropathy (consider neurological consultation and C T scan) C ongenital disc anomalies A nterior ischemic optic neuropathy Radiation and toxic optic neuropathy Hi story Risk f actors f N TG : or Severe vascular compromise (shock, maj or accidents, maj surgery) or V ascular diseases (D M , H PT, migraine, smoking, Raynaud disease) s Family history of POA G I ntermittent ocular pain (intermittent A C G ) Radiotherapy,TB treatment (optic neuropathy) Establish baseline and f ollow-up opti di c sc appearance (stereodisc photos, H RT) Establish baseline and f ollow-up V F (to detect progression and to improve patient reliability) D etermine C C T to exclude articially low I OP readings I there are reliable and progressive optic disc f and V F changes, consider phasi ng: I raised I f OP f ound, treat as POA G I normal I f OP with wide diurnal uctuation f ound, treat as f N TG or I normal I f OP with no uctuation, exclude optic nerve disease, and consider neurol cal consul on and CT scan ogi tati I neurological consultation and C T scan are f normal, treat as f N TG or 2. Treatm ent N o proven treatment M aintain I as low as possible (latanoprost OP and other new drugs): C N TG S f ound that decreasing I by 30% OP reduced rate ofV F progression f rom 35% to 12% Treat associated vascular risk f actors (D M , H PT) Systemic vasodilator and C alcium channel blockers (nif edipine, namodipine, lisinopril) N europrotective agents (betoptic, brominidine, akatinol/ memantine) Trabeculectomy H as been shown in some studies to preserve V F in N TG
Notes Ref to the C ollaborative N ormal Tension G laucoma Study (Am J er Ophthalmol 1998; 126:487 497) M ulti-center randomized controlled trial to determine whether a substantial drop in I would halt/ OP slow the progression of N TG W hat optic discs changes are more common in N TG compared with POA G ? G reater rim thinning Peripapillary crescent more common Splinter hemorrhage more common Optic disc pallor more than cupping Optic disc pits more common W hat V F changes are more common in N TG compared to POA G ? V F loss closer to xation Steeper slopes
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W hat are the Other Im portant Gl aucom a Studi es? Earl Mani y fest Gl aucom a Tri al Advanced Gl aucom a Interventi Study on To assess the long-term outcome of intervention sequences (TAT vs ATT) in eyes that have f ailed initial medical treatment f or glaucoma Col aborati Ini al l ve ti Gl aucom a Treatm ent Study To compare long-term ef ect f of treating newly diagnosed POA G with standard medical treatment (meds A LT trab) vs ltration surgery (trab A LT meds)
A im
To compare the ef ects of f immediate treatment (Betaxolol and A LT) vs no/ late treatment on the progression of newly detected POA G To determine the extent of I reduction attained OP by treatment and explore f actors that can inuence glaucoma progression M ulticenter randomized , controlled trial N ewly diagnosed and untreated POA G G laucoma progression (visual eld and optic disc) 25% reduction in I OP reduced progression f rom 49% to 30% at 4 years
D esign I nclusion Endpoint Results
M ulticenter randomized , controlled trial POA G uncontrolled by medication V isual acuity, visual eld Black patients tended to preserve vision with ATT while whites did better with TAT Eyes with I < 18 OP mmH g did not progress on the visual elds over 6 years
M ulticenter randomized , controlled trial N ewly diagnosed and untreated POA G V isual acuity, visual eld, I OP, quality of lif e Both groups had substantial and sustained reduction in I (surgical group had I OP OP about 23 mmH g lower) N o substantial dif erence f in V F or quality of lif e between the 2 groups
W hat i the Rel s evance of Central CornealThi ckness to Gl aucom a? The Ocular H ypertension Treatment Study (OH TS) showed C C T to be a powerf predictor of the ul development of glaucoma. Eyes with C C T < 555 m had a threef greater risk of developing glaucoma than those who had old C C T > 588 m.
1. Im portance of CCT: Thicker corneas cause f alsely higher I OP readings, and thinner corneas cause f alsely lower I readings OP Thin C C T may be an independent risk f actor f or the development of glaucoma (evidence lacking) 2. Measurem ent of CCT: U ltrasound pachymetry: C ontact required, accuracy dependent on technician expertise s
Scanning slit topography (Orbscan): N on-contact, higher readings compared to pachymetry Specular microscopy: Provides pachymetric measurements and specular microscopy simultaneously 3. Tonom etry that reduces the i uence of the n corneal bi echani properti om cal es: D ynamic control tonometry (D C T) Ocular response analyzer tonometry (ORA )
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TOPIC 8
ANGLE C LO SU R E GL AU C O M A
hat i Pri ary Angl Cl s m e osure Gl aucom a? H ow do You Get Angl Cl e osure?
Primary A ngle C losure G laucoma (PA C G ) is a specic type of glaucoma. A queous outow is blocked as a result of closure of the angles. The risk f actors can be divided into patient and ocular f actors. P rim ary A n gle C lo su re 1. Pathogenesi ri factors s sk Patient f actors: A ge (increases with age) Sex (f emales) Race (more common in orientals, Eskimos) Ocular f actors: A natomical: Shallow A C N arrow angle 2. Stages Stages Primary A ngle C losure Suspect Cl ni presentati i cal on Treatm ent opti ons Relative anterior location of iris-lens diaphragm Risks increases with increasing lens thickness, small corneal diameters and short axial lengths (hypermetropia) Physiological Relative pupil block: M id-dilated pupil (semi-dark lighting) A utonomic neuropathy (loss of pupil hippus)
C onsider no treatment vs I ridotrabecular contact of 180 benet of Laser PI degrees or more N ormal I OP, no peripheral anterior synechiae (PA S) I ridotrabecular contact of 180 degrees or more Raised I or PA S present OP I ridotrabecular contact of 180 degrees or more G laucomatous optic neuropathy and visual eld loss A cute presentation Laser PI f both eyes or M edical treatment or surgery if I still raised OP Laser PI f both eyes or M edical treatment or surgery if I still raised OP A cute management Laser PI Surgery might be required
Primary A ngle C losure
Primary A ngle C losure G laucoma
A cute PA C
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Exam ti ps: The pathogenesi of PACG i usual y not w el answ ered.There m ust be a cl s s l l ear and system ati pl c an.
W hat are the Mechani s of Angl Cl sm e osure? Pupil block is the most common mechanism of angle closure. H owever mechanisms other than pupil block are now increasingly recognized . ,
M ech an ism s o f A n gle C lo su re 1. Pupi bl l ock (m ost com m on) 2. Abnorm al ti anteri to i s i es or ri PA S I E syndrome: A bnormal endothelial cells C Rubeotic glaucoma: N eovascular membranes 3. Abnorm al ti of i s and ci i body i es ri l ary Plateau iris I and ciliary body cysts ris Thick peripheral iris, peripheral iris roll 4. Abnorm al ti of l i es ens Thick intumescent lens: Phacomorphic glaucoma Subluxed lens 5. Abnorm al ti posteri to l i es or ens M alignant glaucoma
Notes C auses of raised I post PI f angle closure: OP or Plateau iris PA S Steroid response N on-patent PI M alignant glaucoma Subluxed lens
W hat i the Pl s ateau Iri Syndrom e? s Plateau I syndrome is a f ris orm of angle closure glaucoma. There is no pupil block but the ciliary body is anteriorly positioned and the iris is inserted anteriorly. W ith characteristic clinical f eatures.
P lateau Iris Syn d ro m e 1. Cl ni features: i cal Younger patient Less hypermetropic (may be m yopi c) A C normal depth, at iris plane G onioscopy I inserted anteriorly (A or B under Spaeth ris classication, page 63)

Angl crow di (keyword) e ng I ndentation gonioscopy does not open angles (double hump sign)
2. Treatm ent: Laser PI should still be perf ormed (plateau iris syndrome is diagnosed only af PI ter ) Laser iridoplasty
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Clinical approach to angle closure glaucoma On examination, the AC is shallow . Look for Pigmented deposits on the endothelium of cornea, which is otherwise clear Shallow AC, especially peripheral AC Iris: W idespread iris atrophy (spiral atrophy) Patent laser PI at superonasal quadrant Old laser iridoplasty scars Posterior synechiae on pupil margin Pupil may be dilated and xed (sphincter ischemia) G laukom ecken (grayish opacities) Trabeculectomy blebs This patient has a previous attack of angle closure glaucoma. Ill like to Check IOP Perform a gonioscopy Assess optic disc Look at VF
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TOPIC 9
SE C O NDAR Y GL AU C O M AS
hat are the Causes of Neovascul Gl ar aucom a?
N eovascular glaucoma is a secondary glaucoma. C an be either open angle or closed angle. The most common etiologies are diabetic retinopathy, C RV O and ocular ischemia. M anagement is extremely dif cult and prognosis is usually very poor . Treat underlying condition and the glaucoma. E tio lo g y o f N eo vascu lar G lau co m a: R etinopathy and Retinal vein occlusion (prolif erative diabetic retinopathy, C RV O) R etinal detachment U veitis B RV O E ales disease O cular ischemic syndrome T rauma I ntraocular tumors (choroidal melanoma) C arotid cavernous stula
Clinical approach to neovascular glaucoma On examination of the anterior segment, the most obvious abnormality is at the iris. N ew vessels are seen at the pupil border at 3 o clock . Look for Ciliary inj ection Cornea clarity AC activity (microscopic hyphema) and AC depth Trabeculectomy/ ltering shunt Iris: Peripheral anterior synechiae at limbus Posterior synechiae on pupil margin Pupillary distortion and ectropion uveae Pupil may be xed and dilated Lens clarity (cataract) This patient has Rubeosis iridis. Ill like to Check IOP Perform gonioscopy (new vessels and peripheral anterior synechiae at the angle) (Continued )
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(Continued ) D o a fundus examination to look for proliferative D M retinopathy, CRVO, RD , retinal tumors Assess optic disc Examine other eye Ask for VA and whether patient has any pain (management purpose)
Exam ti ps: A very good anteri segm ent exam i on case. or nati Rem em ber the eti ogy by the m nem oni "RUBEOTIC. ol c, "
H ow w oul You Manage thi Pati d s ent? M anagement of this condition is di cul and prognosi is usually very poor f t s . I ll need to manage both the underl ng di yi sease and the neovascular gl aucom a in both eyes. This will depend on the patient vi s sual potenti and whether there is signicant pai . al n I the case of good visual potential, I ll . n
M an agem en t o f N eo vascu lar G lau co m a 1. Scenari 1: Good vi o sual potenti al Treat underlying condition (PRP f D M or retinopathy and C RV O) C ontrol I with medications OP C onsider early surgical ltering operation if I OP not controlled Shunts M odied trabeculectomy with M M C C yclodestructive procedure as a last resort 2. Scenari 2: Poor vi o sual potenti al N ot in pain Treat underlying condition Symptomatic relief (steroids, timolol, atropine) I pain with high I n OP C ontrol I OP with medication C yclodestructive procedure early
Tel m e About Pi ent Di l gm spersi Syndrom e and Pseudoexfol ati on i on. Pigment dispersion syndrome is a type of secondary open angle glaucoma. Pseudoexf oliation syndrome is a type of secondary open angle glaucoma.
P igm en t D isp ersio n Syn d ro m e an d P seu d o exfo liatio n Syn d ro m e Pi ent di gm spersi syndrom e on D emographics 3050 years (a decade younger) M en Related to m yopi a W hite race Pseudoexfol ati syndrom e i on 60 years M en and women Related to aorti aneurysm s c (abnormal basement membrane) Scandinavian countries Systemic disease of abnormal basem ent m em brane (skin, viscera, eyes) Secretion of amyloid-like material (oxytalon) in A C D eposit in zonules and trabeculum Trabecular block (Continued) 82
Pathogenic mechanisms
Posteri bow i of iris or ng C onstant rubbing of posterior pigment iris and zonules Rel ease of pi ents gm Trabecular block
(Continued) Pi ent di gm spersi syndrom e on C linical f eatures K rukenberg spindle s D eep A C , with iris bowing posteriorly (reverse pupi bl l ock) I atrophy in peri ris phery of iris Pigment deposit on lens (Z entmayer line) s Pseudoexfol ati syndrom e i on Pseudoexfol ati m ateri , i ve al dandruf -like appearance f throughout A C Pupil dif cult to dilate I atrophy at edge of pupil margin ris D eposit on lens is characteristic (target-like appearance, called hoarf rost ring) Lens subluxation (weak zonules) Sam paol l ne (pigmented line esis i anterior to Schwalbe line) s Pseudoexf oliative material G laucoma risk: 1% per year (5% in 5 years, 15% in 15 years) Bilateral disease: 30% Fair prognosis M edical treatment not very ef ective f A rgon laser trabeculoplasty m ore effecti in the short term ve Trabeculectomy same as POA G C ataract surgery is particularly dif cult: W eakened zonules Small pupil Raised I (risk of OP suprachoroidal hemorrhage)
G onioscopy
H eavily pigmented over enti re angle Q ueer iris conguration G laucoma risk: 10% at 5 years, 15% at 15 years Bilateral disease: 90% G ood prognosis M edical treatment same as POA G A rgon laser trabeculoplasty m ore effecti ve Pilocarpine and laser PI may work sometimes (reverse pupil block) Trabeculectomy same as POA G
Treatment
Tel m e about Uvei c Gl l ti aucom a. U veitic glaucoma is a type of secondary glaucoma. M anagement can be dif cult and involves controlling both the inammation and the raised I OP.
U veitic G lau co m a 1. Mechani s of rai sm sed IOP A ngle closure with pupil block (seclusion pupillae) A ngle closure without pupil block (PA S) Open angle glaucoma Steroid responders Specic hypertensive uveitis syndromes: Fuch heterochromic uveitis s Posner -Schlossman syndrome 2. Managem ent C ontrolling inammation: Steroids: Topical, periocular intravitreal or , systemic N SA I S: Topical, systemic D I mmunomodulators Lowering I OP M edication: -blockers, agonists and carbonic 2 anhydrase inhibitors are rst-line agents Relatively contr aindicated: M iotics, prostaglandin analogues (though can be used cautiously in stable,well-controlled uveitis) H yperosmotic agents (e. g. mannitol): Rapid reduction of I in acute settings OP Surgery: W hen I OP is not well-controlled with medication

83
Ensure inammation is well-controlled bef surgery: C onsider preoperative ore steroids H igher risk of complications: H ypotony, inammation, malignant glaucoma, choroidal ef usion f Trabeculectomy: W ith antimetabolites (5FU , M M C )
G laucoma drainage devices: I ncreasingly used f uveitic glaucoma or Laser: Longer duration of steroids post-laser PI W hen pupil block present : TC P: U se with caution because high rates of hypotony post-TC P N o role f or A LT
Tel m e about Lens-Induced Gl l aucom as Lens-induced glaucomas are a group of common secondary glaucomas. They are classied into .
Len s-In d u ced G lau co m as 1. Cl cati assi on Phacomorphic: Secondary A C G I ntumescent lens causing pupil block Phacolytic: Secondary OA G H ypermature cataracts, leakage of lens proteins through an i ntact capsule Phaco-antigenic: Secondary OA G A utoimmune granulomatous reaction to exposed lens proteins f rom a ruptured capsule Lens particle glaucoma: Secondary OA G Following cataract extraction, capsulotomy or trauma. Lens particles obstruct trabecular meshwork Lens subluxation and dislocation
2. Managem ent Phacomorphic: M anage acute attack like f acute PA C G or A void miotics I I f OP is not controlled, carry out urgent cataract surgery Phacolytic and phaco-antigenic glaucoma M edical control of I OP Semi-elective cataract surgery
Notes Possi e questi bl ons: H ow would you manage this patient if he had a symptomatic cataract? H ow would you remove this patient cataract? s
Notes W hat are the potential problems of operating on an eye with phacomorphic glaucoma? I amed eye (bleeding) n C orneal edema (increased risk of PC R) H igh I OP (increased risk of suprachoroidal hemorrhage) W hite mature cataract (increased dif culty in perf orming capsulorrhexis)
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Clinical approach to trabeculectomy patients This patient has had a trabeculectomy operation. The bleb is at 10 o clock and is avascular, not in amed . Look for signs of Post acute angle closure glaucoma: Pigments on endothelium Shallow AC Spiral iris atrophy G lauckom ecken Laser PI Pigment dispersion syndrome: Krukenberg spindle s D eep AC Peripheral iris atrophy Posterior bowing of the iris Pigmentary deposits on lens Pseudoexfoliation syndrome: Pigments on endothelium D eep AC G ray white dandrufflike deposits at the pupil border Iris atrophy at pupil border H oarfrost ring Subluxed lens Ill like to Check IOP Perform gonioscopy (pigmentation, Sampaolesi line and pseudoexfoliation s material) Assess optic disc Perform VF
W hat are the Effects of Intraocul H em orrhage? ar
In trao cu lar H em o rrh age 1. H yphem a A cute glaucoma (trabecular blockage) C hronic glaucoma (trabecular damage) C orneal blood staining (hemosiderin) 2. H em osi derosi bul s bi 3. Ghost cel gl l aucom a 4. V i treous hem orrhage Synchysis scintillans Tractional retinal detachment 5. Expul ve suprachoroi hem orrhage si dal
Exam ti ps: Rem em ber that si affects rebl ze eedi rate, both of w hi affect IOP l ng ch evel s, and al three i l ncrease ri of corneal bl sk ood stai ng! ni Therefore, surgi i cal nterventi i targeted speci l at these com pl cati on s al y i ons.
85
H ow do You Manage a Pati w i H yphem a? ent th H yphema is commonly caused by blunt ocular inj ury, but may also occur under other circumstances. The main management issues are .
H yp h em a 1. Eti ogy ol Trauma (blunt, penetrating) Spontaneous: V ascular abnormalities (rubeosis and its causes, page 81) Tumors C lotting disorders (sickle cell, anticoagulant treatment, blood dyscrasias) 2. Cl ni cl cati i cal assi on M icroscopic G rade I (< 1/ A C volume) 3 G rade I (1/ I 31/ A C volume) 2 G rade I I ( > 1/ A C volume) I 2 G rade I (total) V 3. Probl s and com pl cati em i ons Rebleeding: D ependent on si of hyphema ze G rade I hyphema (25% will rebleed) G rade I I hyphema (75% will rebleed) I I ncreased I OP D ependent on si and rebl ze eedi ng C orneal blood staining D ependent on si ze, IOP and rebl eedi ng 4. Indi ons for surgi treatm ent cati cal Ocular f actors (A nn Ophthalmol 1975; 7: 659662): C orneal blood staining Total hyphemas with I > 50 mmH g f OP or 5 days (to prevent optic nerve damage) H yphemas that are initially total and do not resolve below 50% at 6 days with I OP 25 mmH g (to prevent corneal blood staining) H yphemas that remain unresolved f 9 days or (to prevent PA S) Patient f actors: Risk of glaucoma damage (elderly, glaucoma patient, vascular diseases) Sickle cell anemia Risk of corneal blood staining and amblyopia (children)
5. Managem ent C onservative: Bed rest, head elevation Topical steroids and cycloplegic agents Others: Topical glaucoma medication A minocaproic acid Tranexamic acid A void aspirin Types of surgical treatment: A C paracentesis and washout C lot expression and limbal delivery A utomated hyphectomy
Tel m e about Angl Recessi Gl l e on aucom a. A ngle recession glaucoma is a complication of blunt ocular trauma. The main management issues are .
A n gle R ecessio n G lau co m a 1. Deni on: ti A ngle recession: Rupture of anteri surface of or ciliary body, extending between longitudinal and oblique/ circular bers C yclodialysis: D isinsertion of l ongi tudi nal bers of ciliary body f rom scleral spur I ridodialysis: Rupture of i s di ri aphragm at iris base f rom ciliary body 2. Ri of gl sk aucom a: M ore than 50% of patients with gross traumatic hyphema have angle recession but only 10% develop glaucoma Risk of glaucoma depends on extent of recession (risk signicant if > 180) M echanism: Trabecular damage (not the recession itself )
Exam ti ps: K now the di fference betw een angl recessi i dodi ysi and cycl al s. e on, ri al s odi ysi
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Tel m e about Aphaki Gl l c aucom a. A phakic glaucoma is a dif cult glaucoma to manage.
A p h akic G lau co m a 1. Mechani s sm I rido-vitreal/ pupillo-vitreal block (secondary ACG ) V itreal-trabeculectomy contact (secondary OC A G ) V itreal-peripheral iridectomy block 2. Preventi on Two or more peripheral iridectomies during surgery Extensive anterior vitrectomy during surgery 3. Treatm ent M iose pupils with pilocarpine D ecrease production (diamox, mannitol) H igh risk trabeculectomy
Clinical approach to iridocorneal endothelial ( ICE)syndromes On examination of the anterior segment of this middle aged lady. There are diffuse areas of iris atrophy seen. Look for Corectopia, ectropion uvea, peripheral anterior synechiae Iris nevus (CoganReese syndrome) s Corneal edema (Chandler syndrome) s Lenticular opacities Trabeculectomy blebs Symptoms in fellow eye (should be normal) This patient has iridocorneal endothelial syndrome. Ill like to Check IOP Perform gonioscopy Assess optic disc Look at VF
Exam ti ps: Rem em ber ICE as consi ng of Iri nevus, Chandl s syndrom e (w i Corneal sti s er th i nvol vem ent) and Essenti i s atrophy! al ri
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TOPIC 10
M E DIC AL T R E AT M E NT O F GL AU C O M A
Id eal D ru g 1. Effecti (i l eri IOP) ve n ow ng
hat i the Ideal Drug for Gl s aucom a?
The ideal drug carries certain characteristics . 3. Mi m al si effects ni de 4. Conveni dosage regi ents ent m 5. Rel vel i ati y nexpensi ve
2. Acti on m ul pl fronts (decrease producti ve ti e on, i ncrease out ow , neuroprotecti ve)
Exam ti ps: Thi i a good approach to m ost W hat i the i s s s deal steroi for uvei s? or d ti W hat i the i s deal anti oti for endophthal i s? bi c m ti
W hat are the Current Drugs Avai abl for Treatm ent of Gl l e aucom a? C urrent drugs available can be divided into their ef ectiveness in lowering I f OP .
Effecti veness i l eri IOP n ow ng C lass I (30% reduction in I OP)
Exam pl es Beta blockers Latanoprost A lpha 2 agonist (brimonidine) U noprostone Pilocarpine D orzolamide A lpha agonist (apraclonidine) Beta 1 blockers (betoptic) Propine Other older alpha agonists
C lass I (20% ) I
C lass I I (10% ) I
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Exam ti ps: One of the m ost i portant pharm acol cal questi m ogi ons i the exam i ons. n nati Cl fy accordi to IOP effect, m ode of acti (di cul or tradi onal assi ng on f t) ti vs new drugs.
W hat are the Tradi onal Drugs for Treatm ent of Gl ti aucom a?
Trad itio n al D ru gs Drug Beta blockers (timolol, betaxolol, carteolol, metipranolol) Pharm acodynam i cs Decrease aqueous producti on Twice daily dosage (T1/ = 12 hours 2 C oncentration: 0. 25 and/ to 0. or 5% Effecti veness/Advantages Si effects de
M ild local side ef ects f Cl I prototype ass (decrease corneal 30% drop in I in OP sensation, allergic 8090% of patients (e. g. reaction, cicatricial 24 to 16 mmH g) conj unctivitis) G ood compliance Severe systemic side A dditive ef ects with f ef ects (pulmonary f pilocarpine but not with bronchospasm, bradysympathetic agents cardia, hypoglycemia) C heap C ommon systemic side ef ects (lethargy, f decreased libido, depression) Cl II prototype ass 20% drop in I OP A dditive ef ects with f beta blockers and sympathetic agents C heap M iosis (impairment of night vision) M yopia and headache (spasm of accommodation f rom circular muscle contraction) Retinal detachment (longitudinal muscle contraction) U veitis (increased permeability f or blood-aqueous barrier) A ngle closure glaucoma Allergic conj unctivitis (20% in one year 50% , in 5 years) Angle closure glaucoma Adrenachrome deposition Aphakic cystoid macular edema Risk f actor f or trabeculectomy f ailure (Continued)
M iotics (pilocarpine)
Increase aqueous drai nage (miosis with opening of angle and contraction of longitudinal bers of ciliary body) W orks only if sphincter pupillae is not ischemic Four times daily dosage C oncentration: 116%
Sympathetic agents (adrenaline and propine)
Decrease aqueous producti (alpha 2 on ef ect) f Increase aqueous drai nage (beta 2 ef ect) f Twice daily dosage C oncentration: 0. , 5% 1% , 2% (adrenaline) C oncentration: 0. 1% (propine)
Cl III prototype ass 10% drop in I OP A dditive with pilocarpine but not with beta blockers C heap
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(Continued) Drug Pharm acodynam i cs Effecti veness/Advantages Ef ect independent of f I levels OP U sef f short term ul or treatment Si effects de Tingling of ngers and toes Renal (metabolic acidosis, hypokalemia and renal stones) G astrointestinal symptoms Stevens-J ohnson syndrome M alaise, f atigue, weight loss Bone marrow suppression (aplastic anemia) C ontraindications: Sulphur allergy K idney or liver disease Sickle cell anemia Renal stones G 6PD Pregnancy or lactation C ardiovascular overload (use with caution when cardiovascular or renal disease present) U rinary retention N ausea H eadache Backache A lteration of mental state, conf usion
C arbonic anhydrase Decrease aqueous inhibitors (acetazolaproducti (inhibit on mide) carbonic anhydrase) Oral/ V I C oncentration: 250 mg/ 500 mg
H yperosmotic agents (glycerol, mannitol, isosorbide)
D ehydrates vitreous Oral/ V I C oncentration: G lycerol and isosorbide 1g/ kg M annitol 20% 1g/ kg
Rapid onset: Peak action within 30 minutes f or mannitol
Exam ti ps: The si effects of adrenal ne can be rem em bered by A. de i
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92
W hat are the New Drugs for Treatm ent of Gl aucom a?
N ew D ru gs
Drug Latanoprost (X alatan) Travoprost (Travatan) Bimatoprost (Lumigan)
Pharm acodynam i cs PG F2 alpha agonist Increase uveoscl eral out ow Once nightly dosage (T1/ = 12 hours) 2 C oncentration: 0. 005%
Effecti veness/Advantages Better or as ef ective as f timolol (depending on which study) Cl I drug. 30% drop in I in 8090% ass OP of patients (e. 24 to g. 16 mmH g) I ef ect at night OP f G ood compliance A dditive ef ects with other f medications Ef ective f 2 years with no drif f or t
Si effects de Little systemic SE (T1/ in plasma = 7 s): 2 occasional headache/ RTI symptoms U C onj unctival inj ection (10% will complain of redness, 30% obj ective inj ection) I ammation (contraindicated in uveitis) n H ypertrichosis (increase in length, number and thickness) I pigmentation (melanin deposition,no melanoris cytic hyperplasia,theref no risk ofmelanoma) ore C ystoid macular edema (pseudophakics/ aphakics) Expensive
Brimonidine (A lphagan) A praclonidine (I opidine)
A lpha 2 agonist three ef ects: f 1. D ecreases aqueous production 2. I ncrease uveoscleral outow 3. N europrotective Twice daily dosage C oncentration: 0. 2% Rapid onset (30 min)
A llergic blepharoconj unctivitis (10% ) Cl I drug ass C orneal irritation (10% ) A lpha 2 selectivity aqueous production suppression (without vasoactivity ef ects of D ry mouth (10% ) f alpha 1) Less side ef ects compared with older f non-specic alpha agonists (apraclonidine) 1. Tachyphylaxis (30% ) 2. C hemosis and stinging (30% ) A dditive ef ects with other medications f (Continued)
(Continued) Drug D orzolamide (Trusopt) Brinzolamide (A zopt)

Pharm acodynam i cs Topical carbonic anhydrase inhibitor Only 1/ as ef ective as oral 3 f Three times daily dosage C oncentration: 0. 2%
Effecti veness/Advantages Cl II drug ass Less side ef ects compared with oral f
Si effects de I ection and stinging (30% ) nj Less ef ective than timolol f Corneal opaci cati in compromised corneas on (inhibits endothelial pump f unction) Less systemic SE compared to acetazolamide Similar to latanoprost
U noprostone (Rescula)
ass PG F2 alpha metabolite agonist: Cl I drug A s ef ective as timolol f 1. I ncrease conventional M ay also increase optic nerve head outow perf usion 2. I ncrease uveoscleral outow Twice daily dosage C oncentration: 0. 12%
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C o m b in atio n E yed ro p s: 1. Cosopt:Ti ol + dorzol i m ol am de 2. X al acom :Ti ol + l m ol atanoprost 3. Ti Pi o:Ti ol + pi ocarpi m l m ol l ne
4. Com bi gan:Ti ol + al m ol phagan 5. Duotrav:Ti ol + travoprost m ol
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TOPIC 11
L ASE R T H E R AP Y FO R GL AU C O M A
hat are the Uses of Lasers i Gl n aucom a?
Lasers can be used f di or agnosti and therapeuti purposes. c c Therapeutic use can be divided anatomically into . D iagn o stic 1. Confocal scanni l ng aser ophthal oscope (opti m c nerve head eval on) uati T h erap eu tic Anatom i cal si te I ris Procedure nam e Peripheral iridotomy (PI ) Type of l aser N d:YA G or sequential A rgon-YA G Indi ons cati PA C G N arrow, occludable angles Secondary A C G (phacomorphic, uveitic) Notes Settings: A rgon (1. W ,0. s,50 m) 1 05 f ollowed by N d:YA G (23 mJ ) Lens: A braham syndrome or s W ise syndrome s Laser 1 ring around iris (stretches angles and dilates pupil to relieve pupil block) 2. Laser reti doppl ow m etry (opti nerve head nal er c perfusi on)
Laser iridoplasty
A rgon
M edically unresponsive PA C G A ngle crowding Plateau iris Laser PI block Prior to A LT in POA G with narrow angles A s in laser iridoplasty
Laser pupilloplasty
A rgon
Laser 3 rings around pupils (dilates pupil to relieve pupil block) (Continued)
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(Continued) Anatom i cal si te A ngles Procedure nam e Laser trabeculoplasty (A LT) Type of l aser A rgon
Indi ons cati Temporizing procedure that tends to f in the long ail term. Less ef ective than f medications and surgery in V F preservation M edically unresponsive POA G Pigment dispersion and pseudoexf oliation Elderly patient not t f or surgery D oes not cause structural/ coagulative damage to TM unlike A LT
Notes Settings: A rgon (0. W , 0. s, 2 1 50 m) Extent: 180 or 360o N umber ofshots: 40 1/ of patients do not 3 respond at all A verage decrease in I ~ 30% (replaces OP one eyedrop) Settings: 400 m, 0. 61. mJ 3 ns 2 , Extent and number of shots: 4555 spots over 180o Laser new vessels at iris W hy not cryotherapy? A dvantages of laser lower , risk of : Phthisis bulbi Sympathetic ophthalmia C hemosis and pain
Selective laser trabeculoplasty (SLT)
Laser trabeculocoagulation C iliary body C iliary body ablation 1. Transscleral cyclophotocoagulation (TC P) 2. Transpupillary cyclophotocoagulation 3. Endoscopic cyclophotocoagulation Laser sclerostomy
A rgon D iode (1. 82 W ) C ontinuous wave YA G (89 W )
N eovascular glaucoma Ref ractory glaucomas N eovascular U veitic Traumatic Failed trabeculectomy C ongenital
Sclera
H olium YA G
POA G
M akes 300 m hole in sclera Little collateral damage because using picoseconds pulses H igh incidence of f ailure Settings: A rgon (0. W , 0. s, 2 1 50 m) Lens: H oskins Settings: YA G (22. mJ 1 pulse 5 , per burst) Lens: C apsulotomy lens
Laser suture lysis
A rgon
Post trabeculectomy (U sef 13 weeks af ul ter trabeculectomy to improve ltration) M alignant glaucoma
V itreous
YA G capsulotomy f malignant or glaucoma
YA G
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Exam ti ps: One of the m ore com m onl asked l y asers and procedures questi ons i n exam i ons. Devel notes based on your ow n techni nati op que.
H ow do You Perform Cycl odestructi Usi Laser? on ng I would use a di ode l aser to perf orm a transscleral cyclophotocoagulation (TC P).
D io d e TC P 1. Procedure: Retrobulbar anesthesia C ontact ber -optic probe Settings: 1. to 2 W 8 12 s 3040 shots Extent: 360 13 mm f rom limbus, sparing 3 and 9 o clock areas H ear pop sound (microablation of ciliary body epithelium) 2. Post-procedure: A nalgesics Steroids C heck I 3 weeks later OP 3. Com pl cati i ons: Pain H ypotony, phthisis bulbi I ammation, iritis n Scleral thinning D ecrease in V A H yphema M alignant glaucoma
W hen do You Perform a Laser Peri pheral Iri dotom y (PI)? The laser peripheral iridotomy is indicated f therapeutic and prophylactic purposes. or
In d icatio n s fo r a Laser P erip h eral Irid o to m y 1. Therapeuti c: PA C G (acute A C G , intermittent A C G , chronic ACG ) POA G with narrow angles Secondary A C G (irido-I block, irido vitreal OL block, subluxed lens with pupil block) 2. Prophyl c: acti Fellow eye of patient with PA C G N arrow occludable angles
H ow do You Perform a Laser PI? I would perf orm a N d:YA G laser PI as f ollows . or I would perf orm a sequential A rgon YA G laser PI as f ollows .
P ro ced u re fo r Laser P erip h eral Irid o to m y 1. Prepare the pati ent: M iosed pupil with 2% pilocarpine I nstil 1% apraclonidine 1 hour bef procedure ore Topical anesthetic and position patient at laser machine 2. Argon bl green l ue aser setti ngs: 1. W , 0. s, 1 05 50 m 3. Abraham i dotom y l s ri ens 4. Locati of PI: on U pper nasal iris (to avoid diplopia and macular burn) 1/ distance f 3 rom limbus to pupil I crypt if possible ris A pply 2030 burns until iris is penetrated 5. Si gns of penetrati on: Plomb of iris pigments D eepening ofA C
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Retroilluminate to see patent PI G onioscopy to see opened angles 6. Nd: YAG l aser setti 2. m J, 35 shots: ng: 5 PI size should ideally be 300500 m
7. Post-procedure: I nstil 1% apraclonidine C heck I 1 hour later OP Topical steroids f 1 day or
Notes W hat are the unique f eatures ofA braham iridotomy lens? s C ontact lens with +66D lenticule Stabilizes globe during procedure H igh magnication I ncreases cone angle and energy at site by 4: Theref ore, the spot area is ef ectively reduced 4 and radius reduced f 2 (square root of 4) (i. 50 m spot size is reduced to 25 m) e. I addition, the energy around the cornea and iris reduced by 4 n
W hat are the Com pl cati i ons of a Laser PI?
C o m p licatio n s 1. Conti guous dam age: C ornea C ataract 2. Iri s: I bleeding ris I ritis I ncreased I OP 3. Mal gnant gl i aucom a 4. Monocul di opi ar pl a
Exam ti ps: Rem em ber MIC.
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TOPIC 12
SU R GIC AL T R E AT M E NT FO R GL AU C O M A
hat are the Indi ons for Trabecul cati ectom y i Gl n aucom a?
There are no absolute indications f trabeculectomy . or I general . n C ommon scenarios include . In d icatio n s 1. Treatm ent shoul be i vi d ndi dual zed w i no xed i th rul e 2. General pri pl W hen IOP i rai nci e: s sed to a l evel w here there i evi s dence of progressi V F or ON ve changes w hi w i l threaten qual ty of vi ch l i sual functi despi adequate m edi treatm ent on, te cal 3. Com m on scenari i ude: os ncl
U ncontrolled POA G with maximal medical treatment: Fai ure of medical treatment (I l OP not controlled with progressive V F or ON damage) Si de effects of medical treatment
Noncom pl ance with medical treatment i A dditional considerations: Young patient with good quality of vision One-eyed patient (other eye blind f rom glaucoma) Family history of blindness f rom glaucoma G laucoma risk f actors (H PT, D M ) U ncontrolled PA C G af laser PI and ter medical treatment Secondary OA G or A C G

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H ow does Medi Therapy Com pare w i Surgi Therapy i Gl cal th cal n aucom a? I is dif cult to compare medical with surgical treatment, with new research showing both having t advantages and disadvantages.W e can compare the two in f our maj areas . or
Medi treatm ent cal Ef ectiveness f 40% respond readily and consistently to low dose medicine 50% eventually require complex medical regimen, adj uvant A LT and ltration surgery
Surgi treatm ent cal 510% poor response to medical treatment in rst instance and require surgery I mproved surgical technique has led to 8090% success rates Better control ofI (delay OP V F/ ON progression) I ncrease morbidity associated with delaying surgery until evidence of V F/ ON damage A ctual cost may be less in the long term
C ost
C heaper initially,but accumulates over years I the U nited States, cost of n bilateral surgery = cost of 8 years of topical medication Poor compliance with multiple medications Less control of I with OP continuing ON damage M inor side ef ects is troublesome f M aj side ef ects can occur: or f A plastic anemia (with diamox) Respiratory and cardiac side ef ects (beta blockers) f I ncrease risk of bleb f ailure (with chronic topical eyedrop use)
Saf Problems ety/
Even af surgery, may ter require adj uvant medical treatment N o long term proof that good I control alone OP will stop ON damage (I only one risk f OP actor) U sually no minor side ef ects f M aj side ef ects (comor f mon): A nesthetic and surgical morbidity Risk ofendophthalmitis and malignant glaucoma Shallow A C ,hypotony, progression ofcatar acts Better quality of lif e
Q uality of lif e
Poorer quality of lif (with use of e multiple eyedrops)
Exam ti ps: As expected, thi topi w i l be a constant debate w i new research ndi s c l th ngs every m onth. Sti to a conservati approach but keep an open m i about ck ve nd new i deas.
100
H ow do You Perform a Trabecul ectom y? I would perf orm a trabeculectomy as f ollows.
Trab ecu lecto m y 1. Preparati on: Retrobulbar anesthesia I erior corneal traction suture with 7/ silk nf 0 2. Conj uncti ap: val Superonasally or superotemporally Fornix or limbal based ap (stick to one approach, see below) D issect Tenons with W escott scissors Remove all episcleral tissue 3. Scl eral ap: Outline ap with diathermy Size 4 3 mm C ut with beaver blade 1/ to 2/ scleral 2 3 thickness D issection with crescent blade until surgical limbus is seen (page 47) W here is the surgical limbus? 4. Paracentesi perform ed at di s stant l ocati on 5. Scl erostom y: Enter A C through scleral ap with a beaver blade Excise 2 1 mm block of sclera with Kelly s punch orV anna scissor 6. Peri pheral i dectom y: ri Prevent blockage of sclerectomy site by iris 7. Cl osure: Scleral ap sutured with 8/ vicryl or 10/ nylon 0 0 Ref orm A C and check aqueous egress C onj unctiva sutured with 8/ vicryl 0
Exam ti ps: As i cataract surgery, be conci but accurate w i the steps, as i you had n se th f done the procedure a hundred ti es. Say,I w i l perform a superotem poral m l l m bal i -based conj uncti ap i val nstead of conj uncti ap. val
Notes W hy perf orm a paracentesis? D ecompress A C prior to sclerectomy Ref orm A C later C heck aqueous egress later
W hat are the Advantages and Di sadvantages of Forni x-Based vs Li bal m -Based Fl aps?
Fo rn ix-b ased vs Lim b al-b ased C o n ju n ctival Flap Forni x-based A dvantages Faster to create and close G ood exposure Easier to identif limbal landmarks y Less dissection (less bleeding and risk of button hole) A voids posterior conj unctival scarring (limits posterior ltration of aqueous) Li bal m -based Easier to excise Tenon s Less risk of wound leak and at A C N o limbal irregularity (dellen) A llows adj unctive use of antimetabolites with less corneal toxicity
D isadvantages
I ncrease risk of at A C H arder to excise Tenon s I control not as good as with OP limbal-based ap
Slower and more surgical experience needed Poorer exposure Risk of button hole higher 101
W hat are the Com pl cati i ons of a Trabecul ectom y? The complications can be divided into intraoperative, early postoperative and late postoperative.
C o m p licatio n s 1. Intraoperati (not com m on, usual y due to poor ve l surgi techni cal ques): Suprachoroidal hemorrhage (most important complication, as in cataract surgery) Button hole in conj unctival ap Subconj unctival hemorrhage f rom bridle suture H yphema 2. Earl postoperati y ve: Fl AC and m al gnant gl at i aucom a (see bel ) ow Endophthalmitis
H yphema Suprachoroidal hemorrhage W ipe-out syndrome C ystoid macular edema
3. Late postoperati ve: Fi trati fai ure (see bel ) l on l ow Endophthalmitis, blebitis C ataract progression V F loss progression Ref ractive errors H ypotony
H ow do You Manage a Shal ow AC after a Trabecul l ectom y? M anagement involves an assessment of the severi of shal ow i and the eti ogy. ty l ng ol This depends on the IOP and presence/ absence of a bl eb.
Sh allo w A C 1. Grades of shal ow AC: l G rade I I : rido-corneal touch (can af ord to be f conservative) 2. Eti ogy ol IOP H igh Bl eb N o bleb Siedal sign +ve s Di fferenti di al agnoses M alignant glaucoma Suprachoroidal H b Pupil block glaucoma W ound leak Managem ent See below Fundus examination (dark brown mass) D ilate pupil (A C may deepen) Enlarge surgical PI with laser G rade I : Pupillo-corneal touch I G rade I I Lenticulo-corneal touch (need to I: intervene surgically)
Low
N o bleb + ve Siedal sign + ve s
C onservative: U sually will resolve within 24 hours D ecrease steroids and increase antibiotics (gentamicin) to induce scarring D ilate pupil with mydriatic (atropine) D ecrease aqueous production (timolol and diamox) Pressure pad/ bolster Simmon shell/ s oversized (ex) contact lens Surgical: Resuture
G ood bleb Siedal sign ve s
Excessive ltration
C onservative: D ecrease steroids, increase antibiotics, dilate pupil and decrease aqueous production Pressure pad/ bolster I ect gas (air or SF6) or viscoelastic into A C nj I ection of autologous blood into bleb nj C ompression mattress suture Surgical: Resuture
102
H ow do You Manage a Mal gnant Gl i aucom a? M alignant glaucoma is a serious complication of glaucoma surgery. M anagement involves an assessment of the severi (grades ofA C shallowing). ty A nd can be conservati or surgi . ve cal
M align an t G lau co m a 1. Conservati ve: Topical mydriatics (atropine) Lower I (diamox and osmotic agents) OP Enlarge PI N d:YA G laser to disrupt anterior vitreous f ace (see laser therapy, page 96) 2. Surgi : cal Chandl s procedure (see vitreous tap, page 39): er 19G needle inserted into vitreal cavity, about 12 mm f rom tip to drain 11. ml of aqueous 5 and separate solid vitreous f rom trapped aqueous V itrectomy
H ow do You Manage a Fi trati Fai ure? l on l M anagement involves an evaluation of the causes of f ailure. A nd can be conservative or surgical.
Filtratio n Failu re 1. Eti ogy ol Early: Blockage by ocular components (lens, iris, D escemet membrane, vitreous, scleral s remnants) Blockage by surgical intervention (blood, viscoelastic) Late: Subconj unctival brosis 2. Conservati ve I ncrease topical steroids M edical control of I OP Scleral depression at posterior lip of scleral ap D igital massage Laser suture lysis: D one usually at 13 weeks af ter surgery (see laser therapy, page 96) N eedling of bleb: D one usually at 6 weeks af ter surgery Topical anesthetics under sterile conditions A pproach f rom unoperated conj unctiva with 27G needle M ay be combined with 5 FU inj ection 3. Surgi cal Revision of trabeculectomy/ new trabeculectomy with antimetabolites
Notes Risk f actors f subconj or unctival brosis = indications f antimetabolite or used
W hat are the Indi ons for Usi Anti etabol tes i Trabecul cati ng m i n ectom y? A ntimetabolites are used in trabeculectomy when a hi ri of fai ure with the conventional operation gh sk l is anticipated. This is related to either pati or ocul f ent ar actors.
In d icatio n s fo r A n tim etab o lites 1. Pati factors: ent Young (< 40 years) Black race Previous chronic medical therapy (especially with A drenaline) Previous f ailed trabeculectomy Previous conj unctival surgery (e. pterygium g. surgery) 2. Ocul factors: ar Secondary glaucomas (neovascular and uveitic glaucoma)
103
Traumatic glaucomas A phakic/ pseudophakic glaucomas I ridocorneal endothelial syndromes (I E) C
C ongenital/ pediatric glaucomas C onj unctival scarring
Notes W hat additional measures must be taken in trabeculectomies with antimetabolites? Prevent antimetabolites f rom entering eye: Limbal-based aps W atertight wound (interrupted non-absorbable conj unctival sutures) C aref dissection to prevent button hole f ul ormation
Tel m e about Anti etabol tes Used i Gl l m i n aucom a Surgery. 5 Fl uorouraci (5 FU) l Mi yci C (MMC) tom n N atural antibiotic compound/ kyl ng al ati agent C ross-links with D N A strands by f ormation of covalent bonds A f ects cells in al phases f l K ills broblast permanently and stop brosis
Pharmacology
Fluorinated pyri i ne analogue m di Binds intracellular thymidylate synthetase (inhibits thymidine and D N A synthesis) A f ects only cells in m i c phase of f toti cell cycle I the eye, inhibits broblast n prolif eration and delays brosis
D osage Results C omplications
I ntraoperative dose: 2550 mg/ ml I ntraoperative dose: 0. 20. mg/ 4 ml Postoper ative drops: 5 mg/ f 1 week ml or I mproves success rate of ltration operation C orneal epithelial toxicity H yphema W ound leak I ection nf N o randomized trial results Better than 5 FU ? Prolonged hypotony A vascular bleb Endothelial,ciliary body and retinal damage H yphema W ound leak I ection nf
Exam ti ps: Refer to three-year fol ow -up of the Fl l uorouraci Fi teri Surgery Study (Am l l ng JO phthalmol 1993; 115: 8292).
W hat i the Fl s uorouraci Fi teri Surgery Study? l l ng The Fluorouracil Filtering Surgery Study is a multicenter prospective randomized clinical trial which evaluates the ef ectiveness of adj f uvant subconj unctival 5 FU f ollowing trabeculectomy.
1. Incl on cri a usi teri 213 patients considered to be at a higher risk of surgical f ailure on the basis of having previous 104
cataract extraction or previous f ailed ltering surgery in a phakic eye
2. Treatm ent Trabeculectomy with adj uvant postop subconj unctival 5 FU inj ections vs trabeculectomy alone 3. Outcom e Treatment f ailure dened as: Reoperation to decrease I OP, or An I OP > 21 mmH g with or without adj uvant I OP-lowering medications
4. Resul ts Treatment f ailure at 3 years: 51% with 5 FU vs 74% without 5 FU C omplications associated with 5 FU : C orneal epithelial erosions Early wound leaks 5. Concl on usi 5 FU indicated af trabeculectomy only in ter patients at high risk of f ailure
Tel m e about Fi teri Shunts. l l ng Filtering shunts are communications between A C and sub Tenon space. s They are indicated when a hi ri of fai ure with the conventional operation is anticipated. gh sk l This is related to either pati or ocul f ent ar actors. The shunts can be divided into . The complications include .
Filterin g Sh u n ts 1. Indi ons cati Patient f actors: Previous f ailed trabeculectomy Previous maj anterior segment surgery or Ocular f actors: Secondary glaucomas (neovascular and uveitic glaucoma) Traumatic glaucomas A phakic/ pseudophakic glaucomas I ridocorneal endothelial syndromes (I E) C Pediatric glaucomas 2. Type of shunts V ary with shape and size V alves (K rupin-D enver A hmed) vs no valves , (M olteno, Baerveldt) M aterial: PM M A , silicon, polypropylene 3. Com pl cati i ons I ntraoperative: H yphema Lens damage and cataract G lobe perf oration M uscle disinsertion and laceration Postoperative: Functional (excessive drainage, blockage of tube by blood and uveal tissue) M echanical (corneal endothelial decompensation, cataract) D iplopia due to extraocular muscle limitation Bleb encapsulation over f ootplate poor drainage Late endophthalmitis 4. Efcacy com pared to trabecul ectom y Tube vs Trabeculectomy Study (Am J Ophthalmol 2009; 148:670684) Tube shunt surgery had a higher success rate compared to trabeculectomy with M M C during rst 3 years of f ollow-up Both procedures associated with similar I OP reduction and use of supplemental medical therapy at 3 years Postoperative complications higher f ollowing trabeculectomy with M M C relative to tube shunt surgery, but most complications were transient and self -limited
Exam ti ps: The i cati ndi ons are nearl IDENTICAL to that of anti etabol te use. y m i
105

Glaucoma Glaucoma Surgery: Section 2

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Glaucoma Glaucoma Surgery: Section 2

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Section 2

Glaucoma AND Glaucoma Surgery

LIM B U S, C ILIAR Y B O DY AND T R AB E C U L AR M E SH W O R K

here i the Li bus? s m

Section 2: G laucoma and G laucoma Surgery

The Ophthalmology Examinations Review

Section 2: G laucoma and G laucoma Surgery

AQ U E O U S H U M O R AND INT R AO C U L AR P R E SSU R E

hat i the Aqueous H um or? s

Section 2: G laucoma and G laucoma Surgery

The Ophthalmology Examinations Review

Section 2: G laucoma and G laucoma Surgery

hat are the Opti Di Changes i Gl c sc n aucom a?

Splinter (D rance) hemorrhage N erve ber layer thinning

Section 2: G laucoma and G laucoma Surgery

The Ophthalmology Examinations Review

T H E V ISU AL FIE LDS

hat i the V i s sual Fi d? W hat i an Isopter? And W hat i a Scotom a? el s s

Section 2: G laucoma and G laucoma Surgery

Section 2: G laucoma and G laucoma Surgery

hat i Goni s oscopy?

Section 2: G laucoma and G laucoma Surgery

Schei s system e (IIV ) G rade I G rade I I G rade I I I G rade I V

Section 2: G laucoma and G laucoma Surgery

hat are the Causes of Congeni Gl tal aucom as?

Round: I ective keratitis nf Peter anomaly s Localized mesenchymal dysgenesis

The Ophthalmology Examinations Review

Notes The clinical signs can be remembered as A BC D E

Section 2: G laucoma and G laucoma Surgery

M eso d erm al D ysgen eses an d A n irid ia Ri eger anom al s y and syndrom e AD

Axenfel s anom al d y I nheritance AD

Ani di ri a AD A R (M ental retardation) Sporadic (W ilm s tumor)

G laucoma rare N one

The Ophthalmology Examinations Review

Section 2: G laucoma and G laucoma Surgery

Section 2: G laucoma and G laucoma Surgery

The Ophthalmology Examinations Review

Increased N ormal N ormal N ormal

N ormal N ormal Abnormal N ormal

N ormal Abnormal N ormal N ormal

Ocular hypertension G laucoma suspect G laucoma suspect N ormal

The Ophthalmology Examinations Review

D esign I nclusion Endpoint Results

Section 2: G laucoma and G laucoma Surgery

Primary A ngle C losure

Primary A ngle C losure G laucoma

Section 2: G laucoma and G laucoma Surgery

The Ophthalmology Examinations Review

Section 2: G laucoma and G laucoma Surgery

hat are the Causes of Neovascul Gl ar aucom a?

Section 2: G laucoma and G laucoma Surgery

Section 2: G laucoma and G laucoma Surgery

The Ophthalmology Examinations Review

W hat are the Effects of Intraocul H em orrhage? ar

Section 2: G laucoma and G laucoma Surgery

The Ophthalmology Examinations Review

Section 2: G laucoma and G laucoma Surgery

hat i the Ideal Drug for Gl s aucom a?

2. Acti on m ul pl fronts (decrease producti ve ti e on, i ncrease out ow , neuroprotecti ve)

Effecti veness i l eri IOP n ow ng C lass I (30% reduction in I OP)

Section 2: G laucoma and G laucoma Surgery

Sympathetic agents (adrenaline and propine)