ENFERMEDADES DE LA CRNEA Diseases of the cornea-

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C ontents C o rn e a B a s ic s : A n a to m y a n d E v a lu a t io n ...................... 1 Norm al anatom y o f the c o r n e a .......................................................... 2 Norm al histology o f the corn ea..........................................................2 Special stains fo r epithelial lesion s.................................................19 C o n g e n ita l C o m e a l C o n d it io n s .........................................2 9 M icrophthalm os................................................................................ 30 N anophllialm as................................................................................. 30 M egalocornea.....................................................................................33 B uphthalm os......................................................................................33 K tratoglobtis......................................................................................34 Posterior keratocon n s.......................................................................37 Peter's an om aly................................................................................. 37 Posterior em bryotoxon.....................................................................37 Cornea p la n a ......................................................................................37 Sclerocorn ea....................................................................................... -13 Keratectasin........................................................................................ 45 C o rn e a l E d e m a a n d B u llo u s K e r a t o p a t h y .................4 7 Corneal ed em a................................................................................... 4S Bullous keratop ath y ......................................................................... 5$ K e ra titis : S u p p u r a tiv e / In fe r tio u s ....................................69 Definition o f kera titis....................................................................... 70 K e r a titis : O th e r T y p e s — N o n in fe c tio u s and P e r ip h e r a l................................................................................... 1 2 9 L/igophthabnic (exposure) keratitis.............................................130

N eurotrophic keratitis (N T K )...................................................... 130 Nummular k era titis ....................................................................... 133 M arginal keratitis (catarrhal u lcer)............................................133 M arginal ulcers w ith system ic collagen diseases or peripheral ulcerative keratitis (P U K ).................................... 133 Phlyctenular k era titis ................................................................... 138 Interstitial keratitis ( I K ) ...............................................................140 Punctate epithelial erosions (P E E )............................................. 142 Punctate epithelial keratitis (Đ Đ• Đš ).............................................145 Superficial punctate keratitis ( o f Thygesons)...........................145 Superior limbic keratoconjunctivitis (S L K )............................. 145 Atheromatous u lc er .......................................................................149 Striate keratopathy (keratitis)...................................................... 151 Filamentary keratopathy (keratitis)............................................ 151 Shield ulcer in veriuil keratoconjunctivitis.............................. 154 Keratitis m e d ic a m e n t s ...............................................................154 Sclerosing kera titis ...................................................................... 154 6. C o rn e a l D e g e n e r a t io n s ......................................................1 6 1 Corneal degeneration.....................................................................162 Arcus senilis (gerontoxcn)...........................................................162 Peripheral fu rrow degen eration ..................................................162 Terrien's marginal degen eration ................................................ 164 Pellucid marginal degeneration (PMD) ................................... 168 M ooren's u lcer................................................................................ 171 Hand-shaped keratopathy (P S K )..................................................275 Salzmanil's nodular d egen eration ..............................................178 Spheroidal degeneration (Climatic droplet keratop athy).....178 Lipid degeneration (keratopathy)................................................ 178 White limbat girdle o f V og t...........................................................1S2

Contents / xi 7 . C o m e a l D y s tr o p h ie s ............................................................1 8 7 Corneal dystrophy: fe a t u r e s ....................................................... 188 Anterior dystrophies (epithelium and Bowman's m em bran e)................................................................. 1SS Stromal dystrophies...................................................................... 295 Posterior dystrophies................................................................... 21S K eratoconns....................................................................................236 8. M is c e lla n e o u s C o rn ea l C o n d it io n s ............................ 2 4 7 Corneal abrasio n ........................................................................... 24S Keratoconjunctivitis sicca (K C S ).............................................. 24$ Vortex keratopathy....................................................................... 257 Descemet's d etachm en t...............................................................260 Descemet's te a r ..............................................................................262 Descemet’s fo ld s and tw in kles....................................................265 Krukenberg's s p in d le .................................................................. 269 Corneal d ellcn ................................................................................ 269 C ra o d ile sh a g r en ......................................................................... 273 Prominent corneal n erv es...........................................................273 Xerophthalmia (conical signs in Avilaininosis-A)............... 276' Tunnel a b s c e s s ..............................................................................27S Recurrent corneal erosion (R C E ).............................................. 282 Blood staining o f the c o rn ea ........................................................ 283 Corneal tu m ors..............................................................................286 9. C o m e a l G ra ft-re la te d P r o b l e m s .................................. 2 9 1 Important corneal problems/complications in P K ..................298 Recurrence o f previous diseases in g r a ft..................................305 10. R e fr a c tiv e S u rg e ry -re la te d C o m e a l P r o b le m s ... 3 3 3 Late rupture o f RK w ou n d ......................................................... 334

Post-PRK corneal h a z e ................................................................. 334 Wrinkling o f the L A S IK flay .......................................................340 Epithelial in g row th .......................................................................340 LASIK fla p displacem en t.............................................................344 Post-LASIK ectasia....................................................................... 344 Post-LASIK dry e y e .....................................................................344 Corneal nicer and/or interface in fection ...................................348 Recurrence o f original disease after P T K ................................ 348 Lute fla p displacement or lost f l a p ..............................................350 11. C o n ta c t L e n s -re la te d C o rn e a l P r o b le m s ..................3 5 1 Superficial punctate keratitis......................................................352 Contact lens-immune response keratitis..................................352 Acute hypoxia o f corn ea............................................................... 352 Tight lens sy n d rom e.....................................................................356 Corneal n eovasailarisation ......................................................... 356 Contact lens (Toxic) keratopathy............................................... 35S Infectious corneal infiltrates/ulcer............................................358 Giant fwpillary conjunctivitis.....................................................358 12. D e s e a s e s o f th e S c l e r a ...................................................... 3 6 5 In d ex ............................................................................................... 397

Chapter

Cornea Basics: Anatomy and Evaluation

NORMAL ANATOMY O F THE CORNEA GROSS ANATOMY (FIGS 1.1A AND B) • • • • •

Elliptical from fro n t 12 mm horizontally and 11 5 mm vertically Posteriorly, it is circular with a diam eter o f 11.5 mm Centrally, it is 0.5 mm thick and thicker at periphery Cornea is optically clear with hom ogeneous appearance Cornea is avascular and richly supplied by thin non-myelinated nerves derived from fifth nerve • It is the main refractive element o f the eye, constitutes about 43-45 diopter. NORMAL HISTOLOGY OF THE CORNEA CORNEA CONSISTS OF 5 LAYERS (FIG. 1.2) (FROM ANTERIOR TO POSTERIOR) 1. Stratified squam ous epithelium : 5-6 cells deep (continuous with conjunctival epithelium) The epithelial stem cells are m ainly located at the superior and inferior area in the limbal palisades of Vogt. They are im portant for the maintenance o f healthy corneal epithelium. They also act as a junction barrier which prevents conjunctival tissue to grow into comen. 2. B o w m a n 's m e m b ra n e: W hen in ju re d , lea v es beh in d a superficial com eal scar. 3. Strom a: 90% o f total corneal thickness and continuous with sclera. 4. D escem et's m em brane: Elastic, regenerates after any injury. 5. Endothelium (sing le layer flatten ed cells): N ever regene­ rates in hum an beings after any injur)' or loss It plays the most vital role in m aintaining com eal transparency.

Fig. 1.1A: Normal cornea

Fig. 1.1 B: Normal cornea in slit section

Fig. 1.2: Layers of cornea CORNEAL EVALUATION S y m p tom s T he main sym ptom s o f com eal diseases are: Pain: The cornea is richly supplied by sensory nerve endings. In corneal abrasions or bullous keratopathy, the direct stimulation o f bare nerve endings causes severe pain D ecreased visual acuity It is caused by loss o f central corneal transparency Colored halos: They are due to diffraction of light by epithelial and sub epithelial edema Photophobia: Sensitivity to light Lacriniotion: II is due to reflex stim ulation o f the corneal nerve Signs The precise localization of corneal defects is best done by slit* lamp b iom icroscopy.

M ajor signs are in thir. E pithelium : P un ctate ero sio n s, ed em a, filam ents, su perficial punctate keratitis, and staining with fluorescein and rose Bengal Stroma: Infiltrates, edem a, vascularization, deposits,and scarring (opacities). D escem et's m em b ra n e: B re a k s , fo ld s, lo ca liz e d th ick en in g (excrescences), etc. Deposition o f pigm ents: C om eal pigm ent deposition is associated with a variety o f disorders. (S e e Figs 1.15 to 1.23). Conical thickness (by pochymetry): Either by the optical or ultrasonic pach ym eter • It indicates the functional integrity o f the com eal endothelium • U ltrasonic pachym elry is useful b efore LASIK and other kerato-refractive operations. • Central corneal thickness (CCT) m easurem ent is also required fo r c o rre c tio n o f in tra o c u la r p r e s s u re b y a p p la n a tio n tonom eter. CORNEAL EXAMINATIONS Pen-torch Light and Binocular Loupe: To assess the gross abnorm ality • In young children who cannot sit for slit lamp exam ination • For com atose patients, in lying down position • For field study or quick screening. SLIT LAMP EXAMINATION OF THE CORNEA The slit lamp consists o f an illum ination system and a binocular observation system , which when correctly aligned will result in a coincidental focus o f the slit and m icroscope (Fig. 1.3).

Fig. 1.3: Slit lamp biomicroscope It offers a variety o f illum inating and observing methods: 1 Diffuse illumination 2. Direct (focal) illumination: a. Broad beam (parallelepiped) b Narrow beam (optic section). 3. Indirect illumination 4 Retrcillum inalion: a Direct b. Indirect 5 Specular reflection 6. Sclerotic scatter 7. O scillator)' illumination.

М а те р и а л заштийен ауторским правима

Direct Diffuse Illumination (Figs 1.4A to C) It is a good method of observing the eye and adnexa in general. Diffusers arc generally ground glass plates that cover the light source. The slit should be opened wide and the magnification should be set as low as possible to enable a large field o f view Direct Focal Illumination This is the most com m on method o f viewing all tissues o f the anterior eye; the focused slit is viewed directly by Ihe observer through Ihe microscope The magnification can be increased quite markedly (10x to 4 0 * or m ore) to view any areas o f interest in greater detail Generally, a very w ide beam is used for surface study, whilst a verv narrow one is used for sections. *

A

М а те р и а л заштиТюн ауторским правима

Ń Figs 1.4A to C: Direct diffuse illumination

a. Narrow Beam {O ptical Section) (Figs 1.5A and B) O nce an abnorm ality has been found, il is easier to determ ine the precise depth using an op tical section. G enerally the angle between the illum inating and observation systems should b eset around *15 to 60 degrees. A good com eal section will allow at least 4 layers to be seen— tears (outer), epithelium (and Bowman's membrane), strom a seen as the central gray granular area and the fainter back line which is the endothelium (and D escem et's m em brane). b. Broad Beam (Parallel-piped) (Figs 1.6A and B) A useful com bination o f the two is the parallel-piped section of the cornea, which uses a 2m m slit width enabling com eal surface as well as strom a to b e studied This allow s us to ascertain the d ep th o f any interesting featu re, e g foreign bod y, corneal abrasion Direct illumination on the front surface o f the crystalline lens reveals the 'o ra n g e peel' e ffe ct and on the iris allow s observation o f iris pattern. Indirect Illumination (Figs 1.7A and B) Structures are often easier to see under indirect illumination as glare is reduced, e. g. opacities, com eal nerves and limbal vessels W hen using the slit lam p, direct and indirect illumination are viewed sim ultaneously,structures viewed in the illuminated Field are seen under direct illum ination, but as this does not fill the w hole of the field o f view, anything which reflects or scatters light from outside the illuminated area is being viewed by indirect illumination To view certain features by indirect illumination, first locate il by d ire c t illu m in a tio n an d k e e p in g th e v ie w in g sy stem unchanged, sw ing the lamp to one side.

Bahan dengan hak cipta

小 胁 Figs 1.6A and B: Direct focal (broad beam illumination)

Bahan dengan hak cipta

Retrollumination The light is reflected o ff the deeper structures, such as the iris or retina, w hile the m icroscope is focused lo study the cornea in the reflected light. Features that are opaque to light appear dark against a light background (e g scars, pigm ents, and vessels containing blood). F o r d ir e c t r etr o illm n in a tio n (Figs 1.8A and B): The observed feature on the cornea is viewed in the direct pathw ay o f reflected light The angle betw een the microscope and the illuminating arm is about 60о. F o r in d irect r e tr o illu m in a tio n (Figs 1.9A and B): T he angle betw een Ihe m icroscope and slit-lamp arms is greatly reduced or increased so that the feature on the cornea is viewed against a dark background. Specular Rofloclion (Figs 1.10A and B) This type o f viewing is achieved by positioning the beam o f light and m icroscope such that the angle o f incidence is equal to the angle o f reflection. The light can be reflected from either the anterior (i.e. tears and epithelium ) or posterior (i.e. endothelium) corneal surface. Mote that the reflected light should pass through only one eyepiece, and therefore this method is monocular. M eth o d fo r v ie w in g th e p o s t e r io r su rface: The angle betw een the light and m icroscope arm s should be about 50°-6t>° A 2 mm w ide parallelepiped and magnification o f 20-25 x is used Find the image of the illuminating bulb, then move the light beam until the image o f thebu lbisjust behind the posterior surface

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o f the parallelepiped (Incidence= reflection when the dazzle from the precorneal fluid is seen). Focus on the back o f the parallelepiped A mosaic o f hexagonal endothelial cells w ill appear. The posterior endothelium and ke ratio precipitates may thus be studied. This method o f illumination is particularly useful to exam ine the endothelium layer o f the cornea (e.g. blebs, polym egathism ), although very high m agnification is necessary, nt least 40x is required and to see individual cells, at least SOx (Fig. 1.10C) Sclerotic Scatter (Figs 1.11 A and B) This method uses the principle o f total internal reflection A narrow vertical slit (1-1.5 mm in w idth) is directed in line with the temporal (or nasal) limbus. A halo o f light will be observed around

A

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в Figs 1.11 A and B: Sclerotic scatter

the limbus as light is internally reflected within the cornea, but scattered by the sclera. Any corneal opacities, edem a or foreign bodies will be made visible by the scattering light, appearing as bright patches against the dark background o f the iris and pupil It is important that the room illum ination is as dark as possible Oscillatory Illumination A b eam o f lig h t is rocked b ack and fo rth b y m o v in g the illum inating arm or rotating the prism o r m irror Occasional aqueous floaters and glass foreign body in the anterior cham ber are easier to observ e SPEC IA L STA IN S: FOR EPITHELIAL LESIO N S F lu o r e s c e in s t a in in g (F ig . 1.12): T o stain v a rio u s corn eal p ath o lo g ies in the ep ith eliu m lev el, e g corn eal ab rasio n , erosions, filam ents, epithelial defects, dendrite in 1ISV keratitis, SPKs, for Seidel's test, Tear film break up time (TFBUT), etc. R o s e B en g a l sta in in g (Fig. 1.13): Is useful for devitalized tissue, e g. dendrite in 1 ISV keratitis, PEE in dry eye and other lesions, conjunctival stain in dry eyes. It causes mild to moderate irritations o f the eyes L is s a m in e g reen stain in g (Fig. 1.14): It is sam e as rose Bengal, except it does not cause much irritation. CORNEAL SENSATION P roced u re: Corneal sensation is tested with a w isp o f cotton Patient is explained the procedure and asked to look straight. The wisp o f cotton is brought from the side so as to avoid optical blinking. The norm al fellow eye is tested in a sim ilar m anner

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Fig. 1.14: Lissamine green staining of cornea

In ter p r e ta tio n : Norma) blink reflex indicates norm al corneal s e n s a tio n C o ch e t-B o n n e t A e sth e s io m c te r q u a n tita tiv e ly measures corneal sensation. C a u s e s o f d e c r e a s e /lo s s o f t o m e a ! s e n s a t io n : N eurotrophic k era titis; v iral k era titis, corn eal su rg ery (iim bal in cision s, p e n e tr a tin g k e r a to p la s ty , la m e lla r k e r a to p la s ty , ra d ia l keratotom y, excim er laser surgery), 5th nerve lesions, topical m edications, diabetes, etc

PIGMENTS DEPOSITION IN THE CORNEA Iro n Keratoconus Fleischer's ring (Fig. 1.15)

Epithelium

Old opacity Hiidson-Stnhl line ( Fig. 1.16)

Epithelium

Pterygium Sloikcr's li)ic (Fig. 1.17)

Epithelium

Filtering bleb Ferry's line (Fig. 1.18)

Epithelium

Siderosis (Fig. 1.19)

Strom a

Blood staining (Fig. 1.20)

Strom a

C opper W ilson's disease Kiu/ser Fleischer (K F) ring (Figs 1.21Đ› and B)

D escem et's level

M elan in Pigment dispersion (Fig. 1.22) Krukenberg's spindle

Endothelium

D ye Tattooing o f com eal opacity (Fig. 1.23)

Subepithelial

Fig. 1.15: Fleischer s ring

Fig. 1.16: Hudson-Stahl line

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Chapter

Congenital Corneal Conditions

MICROPHTHALMOS Unilateral o r bilateral congenital abnormality in which the axial length is reduced (Figs 2.1 and 2.2). Visual acuity is usually poor and depends upon the associated anom alies Microphthalmos may b e with or without colobom a (Figs 2.3 and 2.4) T reatm en t: Not available, precautions to be taken during any intraocular surgery. NANOPHTHALMOS Uncom m on, congenital, bilateral condition, with small globe in nil dim ensions (nano means 'dw arf') Anatomically, the eye is grossly normal Deep set eyeball with very high hypermetropia (Figs 2.5A and B), axial length is less than 20 mm. Fundus shows a crowded disk with vascular tortuosity and m acular hypoplasia

Fig. 2.1: Microcornea with microphthalmos— RE

Fig 2,2: Severe bilateral microphthalmos

Fig. 2.3: Microcornea with coloboma— BE

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Fig. 2.5B: Nanophthalmos high hypermetropia

T reatm en t: I ligh plus power spectacles correction, contact lens, and during cataract surgery in later life, precaution is to be taken to prevent com p lications, like ch oroid al effu sion , expulsive hem orrhage, etc. MEGALOCORNEA • • • • •

Rare, congenital and bilateral conditions. Corneal diam eter is more than 13 mm (Fig. 2.6). Very deep anterior chamber. I ligh myopia and astigm atism , but with good visual acuity. Normal intraocular pressure

T reatm en t: No active treatment is required BUPHTHALMOS Unilateral or bilateral condition in which the eyeball is large due to Stretching as a result o f inc reased intraocular pressure within first three year* o f life

Fig. 2.6: Megalocornea

Largo co rn ea w ith v a ria b le sca rrin g (F ig s 2.7A and B), horizontal tear of the D escem et's m em brane (I laab’s striae); very deep anterior harnber, disk cupping in long standing cases T reatm en t: First reduce the IOP by different glaucom a surgical p ro ced u res a p p licab le for co n g en ital glau com a. A lter that penetrating keratoplasty may be considered in selected cases KERATO GLO BUS Congenital bilateral very rare condition Mid-peripheral thinning resulting in protru sion or bulging o f w hole cornea, with an appearance o f globular shape (Figs 2.8Л and B) Very deep anterior cham ber. A cute hydrops may occur in extrem e cases. T reatm en t: Contact lens and later penetrating keratoplasty under extrem e precaution and with special technique

Fig. 2.7A: Buphthaimos— right eye

Fig. 2.7B ' Buphthaimos— bilateral

Figs 2.8A and B: Keratoglobus

P O STER IO R KERATOCONUS • Rare, unilateral or bilateral condition no progression • The posterior cornea is having excavation and the anterior cornea does not protrude (Figs 2.9A and B) • Common association w ith Peter's anomaly. T reatm en t: Central lesion needs penetrating keratoplasty.

P E T E R 'S ANOMALY Central corneal opac ity, due to defect in embryogenesis In milder form, il only causes posterior keratoconus. Bui in mosl cases, it is associated with an terio r polar cataract, iris adhesion, angle abnorm alities, or secondary' glaucom a (Figs 2.10 A and B) 'Treatment is difficult and depends on clinical situation and visual potential o f that eye. PO STERIO R EMBRYOTOXON An unusual prominence o f Schwalbe's line which is the peripheral termination o f D escem et's membrane. It appears as ring opacity in the deeper layer o f the cornea (Figs 2.11A and B) T reatm en t nol required. O nly periodical intraocular pressure m onitoring is required CORNEA PLANA • Rare, congenital, bilateral conditions • Severe decrease in corneal curvature • I ligh hyperm etropia, shallow anterior cham ber (Figs 2.12Л and B), but som etim es may b e associated w ith high myopia.

в Figs 2.9A and B: Posterior keratoconus

в Figs 2.1 OA and B: Peter’s anomaly

в Figs 2.11 A and B: Posterior embryotoxon

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• May be associated with microcornea and partial sclerocom ea (Figs 2.12C and D) T reatm en t: Only refractive correction. SCLERO CO RN EA • Rare, congenital, usually bilateral condition, opacification and vascularization o f peripheral or entire comen. • Cornea appears sm aller if the scelerization is only peripheral (Figs 2.13A and B) • In p a rtia l v a r ie ty , Ih e p a tie n t h a v e b e tte r p ro g n o sis (Fig. 2.13C) • May be associated with microphthalmos, blue sclera or cornea plana. T r e a t m e n t : D ifficu lt. M ay b e co n sid e re d fo r p e n e tra tin g keratoplasty in extrem e rases.

Fig. 2.1 ЗА: Sclerocomea— bilateral

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Fig. 2.14: Keratectasia

KERATECTASIA • Rare, usually unilateral condition, probably due to intrauterine k eratitis or m aternal vitam in A d e ficie n cy fo llow ed byperforation • Severe com eal ectasia beyond the eyelid w ith opacification and vascularization (Fig. 2.14) T reatm en t; N ot available Only for cosmetic purpose, evisceration and followed by prosthesis

Chapter

Corneal Edema and Bullous Keratopathy

CORNEAL EDEMA il is associated w ith increased in corn eal th ickness d u e lo accum ulation o f fluid with variable degree o f loss in com eal transparency. Edema may be focal (Figs 3.1A and B) or generalized (Figs 3.2A and B), may be w ith epithelial defect (Fig. 3.3) Som etim es, it is so severe, that anterior cham ber structures are not visible (Figs 3.4Л and B) Im p o rta n t causes:

Inflammatory: C om eal ulcer, erosions, acute iridocyclitis (due to end oth elial d am age) (Fig. 3 .5), herpetic disciform keratitis (Figs 3.6Л and B) D egenerative: As in iridocorneal endothelial (ICE) syndrom e (Figs 3.7A to C) Increased IO P: A cu te edem a in a n g le -d o su re glau com a and epidem ic dropsy glaucoma. C h ro n ic ed em a in lo n g -sta n d in g cases— as in a b so lu te glaucom a and buphthalmos (Fig. 3.8) T rau m a tic: M ech a n ica l trau m a and p o stsu rg ica l - d u e to endothelial dam age, espec ially, when vitreous remains adherent to it (Fig. 3.9) Som etim es, lens fragm ents in anterior cham ber or haptic o f IOL touching the endothelium m ay be responsible (Figs 3.10A and B), even with PCIOL (Figs 3.11A and B) Dystrophic condition o f the cornea: For exam ple, Fuc h s’ endothelial dystrophy, hydrops in keratoconus. Hypoxia o f the cornea: As in contact lens w earer due to epithelial edem a, as a result o f prolonged deprivation o f atm ospheric oxygen.

Fig. 3.1 A: Corneal edema local

Fig. 3.1 B: Corneal edema focal— slit section

Fig. 3.2A: Corneal edema generalized

Fig. 3.2B: Comeal edema generalized— slit section

Fig. 3.3: Corneal edema with epithelial defect

Fig. 3.4A: Severe corneal edema

Fig. 3.4B: Sever© corneal edema— slit section

Fig. 3.5: Comeal edema in iridocyclitis

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Fig. 3.6A: Corneal edema in disciform keratitis

Fig. 3.6B: Corneal edema in disciform keratitis— slit section

Fig. 3.7A: Corneal edema in hydrops

Fig. 3.7B: Corneal edema in ICE syndrome

Fig. 3.7C: Corneal edema in ICE syndrome— slit section

Fig. 3.8: Corneal edema in absolute glaucoma

Fig. 3.9: Corneal edema—vitreocorneal touch

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Fig. 3.10A: Corneal edema— ACIOL

Fig. 3.10B: Corneal edema— ACIOL— slit section

Fig. 3.11A: Corneal edema in PCIOL

Fig. 3.11B: Corneal edema in PCIOL— slit section

Toxic or chciitic/il injury: As after acid or alkali b u m ; contact with toxic su bstan ces, plant ju ice (alkaloid s)— as in contact with cnlolropis latex (Figs 3.12 A and B), etc. BU LLO U S KERATOPATHY (FIG S 3 .1 3 TO 3 In long-standing cases, Ihe epithelium tends to be raised into large vesicles or bullae, leading to bullous keratopathy. It may b e phakic, aphakic or pseudophakic type Vitreocom eal touch and AC IOL is an im portant factor in aphakic or pseud op hakic bu llous keratop athy P hakoem u lsification in co m p ro m ised co rn e a and in su p ra h a rd c a ta r a c ts is a lso responsible T reatm en t: U se o f hot air (by hair-drycr), frequent instillation of concentrated sodium chloride (5%) solution o r ointment; bandage

Fig. 3.12A : Corneal edema calotropis latex

Fig. 3.12B: Corneal edema calotropis latex— slit section

Fig. 3.13A: Cornea! edema— epithelial bedewing

m Fig. 3.13B: Corneal edema in epithelial bedewing— slit section

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Fig. 3.14A: Corneal edema— microbullae

Fig. 3.14B: Corneal edema— bullae

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Fig. 3.16B: Bullous keratopathy— phakic slit section

Fig. 3.17A: Bullous keratopathy— pseudophakic PCIOL

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U Fig. 3.18B: Pseudophakic bullous keratopathy ACIOL

Fig. 3.19: DSEK in ACIOL of F.g. 3.18

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so ft co n tact lenses, esp ecially in case o f ruptured bullae or m ultiple anterior strom al puncture with BC1., epithelium is stripped off, and is lo be replaced with a thin conjunctival flap; D escem et's strippingendolhelial keratoplasty (DSEK) (Figs 3.17 and 3.18) or FK to im prove visual status

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Chapter _й.

Keratitis: Suppurative/Infectious

DEFINITION O F KERATITIS Keratitis is the inflammation o f the cornea. A com eal ulcer o r suppurative keratitis is defined as a loss o f corneal epithelium with underlying strom al infiltration and suppuration associated with sig n s o f inflam m ation with or without hypopyon SUPPURATIVE KERATITIS

E xog en o u s in fectio n is m ost co m m o n and a lm o st alw ays associated with som e kind o f trauma. Som etim es associated with underlying other ocular factors, e g corn eal erosio n , bullous keratopathy, herpetic keratitis, lagophthalmos, dry eyes, chronic dacryocystitis, etc O ther factors like, use o f topical steroids, diabetes, immuno足 com prom ise states are also important. It may be bacterial, fungal, or due to acanthamoeba. BACTERIAL KERATITIS'ULCER Most frequent causative agents are Staph, aureus, Pseudomonas and Strept. pneum oniae Signs vary with the severity and the type o f causative agents. Lid edem a, marked ciliary congestion, Epithelial breakdown followed by strom al suppuration. U lcer u su ally s ta rts as a g ra y ish -w h ite circu m scrib e d infiltration; Edem a o f the surrounding tissue, M argins are over足 hanging and the floor is covered by necrotic material (Figs 4.1 to 4.4) Overall look o f the ulcer is wot. Hypopyon m ay bo present in variable amount with flat border Secondary anterior uveitis and glaucom a in som e cases.

Fig. 4.1: Corneal infiltration

Fig. 4.2: Linear cut with corneal infiltration

Fig. 4.3: Bacterial corneal ulcer— wet look

Fig. 4.4: Severe corneal ulcer with stromal melting

S p ecia l featu res o f sp ec ific bacterial keratitis S ta p h y lo c o c c a l k e r a titis (Figs 4.5A  id B): Well-defined grayishw hite or cream y strom al infiltrate which may progress to form dense strom al abscess. T he surrounding cornea is relatively clear. P iicu m o co cc a l k e r a t it is (Fig. 4.6): Spread superficially with a serpiginous leading edge and associated w ith severe anterior uveitis w ith hypopyon form ation The surrounding cornea is relatively clear. P se u d o m o n a s k e r a t it is (Fig. 4.7): Rapidly spreading, melting su ppu rative lesion associated with hypopyon and greenish m uco-purulenl discharge. 'G round g lass' appearance o f the surrounding cornea E n te r o b a c te r ia c e o e (E. c o li, P roteu s o r K le b s ie lla ) (Figs 4.8A and B): Shallow ulcer with pleom orphic grayish-white necrotic areas. Som etim es, they produce ring shaped corneal infiltrates. C o rn ea l a b s c e s s (Figs 4.9A and B): Localized suppuration in the deeperstrom a under intact comeal epithelium Usually associated with staphylococcal infection T reatm en t: Scraping and sm ear preparation to identify the micro­ organism quickly and then prom pt initiation of therapy with frequent (hourly) topical broad-speetrum antibiotics. O ther th erap y in c lu d e s-a tro p in e , trea tin g se co n d a ry g lau co m a Therapeutic PK is required in extrem e cases (Figs 4.10A and B). FUNGAL KERATITIS OR KERATOMYCOSIS Causative agent m ay be filam entous fungi o r Candida. Typically preceded by o cu lar traum a w ith agricu ltu ral and vegetable matters.

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в Figs 4.8A and B: Bacterial ulcer— Enterobacteriaceae

F igs 4.9A and B: Corneal abscess

Fig. 4.10B: After therapeutic PK

Relatively painless, dry looking, elevated yellow ish-w hite lesion w ith indistinct margin. D elicate, leathery, finger-like projections into Ihe adjacent stroma. M assive dense hypopyon is seen which is im m obile with convex upper border (Figs 4.11 to 4.14). Slow ly progressive stromal destruction m ay lead to com eal perforation with its sequeale. F ila m en ta ry fu n g a l k e r a t it is (Figs 4.15 and 4.16): Typical feathery appearance with finger-like projection and satellite lesion. C an d id a k e r a titis (Figs 4.17 and 4.1S): Gray-white infiltrate (often as collar-button abscess) sim ilar to bacterial ulcer D em a tia c eo u s fu n g a l k e r a t it is (Figs 4.19 to 4.21): Often produces pigments on the surface o f the uleer. T reatm en t: Topical anti fungal agents— natam ycin (5%), am pho­ tericin В (0 .1 5 % ), o r v o rico n a z o le e y e d ro p - 1-2 hourly. Intracam eral am photericin В is helpful in deep keratitis with plaque (Figs 4.22A and B) and may require therapeutic PK in nonresponsive cases. ACANTHAMOEBA KERATITIS Very rare unilateral keratitis that typically affects the soft contact lens wearer. Pseudodendrite (Fig. 4.23A), Radial keratoneurids (Fig. 4.23B), progressive chronic strom al keratitis with recurrent breakdown o f c o m e a l e p ith eliu m (F ig s 4.24A and B). P a ra ce n tra l or paracentral ring-shaped ulcer or infiltrates (Figs 4.25Л and B) is the hallm ark o f advanced infection. T r e a t m e n t : РИ М 15, p ro p a m id in e is e th io n a te , n e o m y cin , chlorohexidine eye drops in frequent doses, etc. Therapeutic PK is required in resistant cases.

Fig. 4.11: Fungal corneal infiltrates

Fig. 4.13: Fungal keratitis—dry look and elevated

Fig. 4.14: Fungal com eal ulcer— convex hypopyon

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Fig. 4.16: Fungal ulcer with satellite lesions— filamentary

Fig. 4.17: Fungal corneal ulcer— Candida

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Fig. 4.20: Dematiaceous fungal keratitis

Fig. 4.21: Pigment producing dematiaceous fungi

Fig. 4.22A: Fungal keratitis— Candida

Fig. 4.22B: Fungal keratitis— Candida— after intracameral amphotericin В injection

Fig. 4.23A: Acanthamoeba keratibs pseudodendnte

Fig. 4.23B: Acanthamoeba keratitisradial keratoneuritis

в Figs 4.24A and B: Acanthamoeba keratitis— stromal melting

Fig. 4.25A: Acanthamoeba keratitis— ring-shaped ulcer

Fig. 4.25B: Acanthamoeba keratitis— ring infiltrates

PERFORATED CORNEAL ULCER C om eal perforation may occur in any type o f corneal ulcer in advanced cases. Prior to that the patient m ay present with D escem etocele, i.e. herniation o f the elastic D escem et's membrane as a transparent vesicle (Figs 4.26A and B) T he other types o f presentation are C orn eal fis t u la : S e id e l's test is im p o rta n t to d e te rm in e it (Figs 4.27A and B). Cifstoids cicatrix: Seidel's lest may also be positive (Figs 4.2SA and B) Iris prolapse: If the perforation is large peripheral or paracentral (Figs 4.29Đ› and B). Psciidocornea formatio>i (Figs4.30A and B) Ectatic cicatrix (Fig. 4.31): Thinned, scarred cornea bulges even under norm al IOP. Anterior staphylom a: Partial or total (Figs 4.32A and B) Phthisis bull)! (Fig. 4.33) tndophihaln iitisain i Panophthalm itis(Figs 4. 34 and 4.35) SEQUEL OF CORNEAL ULCER N eb u la (F ig . 4 .3 6 ), M acu la (F ig s 4.37A and B ), L eu com a (Figs 4.3SA and B), A dherent leucom a (Figs 4.39A and B), Anterior staphylom a. Phthisis bulbi Vascularization (Figs 4.40A and B) may occur in any form of opacity.

Fig. 4.26A: Descemetocele

Fig. 4.26B: Descemetocele— slit section

Fig. 4.27A: Corneal fistula

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Fig. 4.27B: Corneal fistula— Seidel’s test positive

Fig. 4.28A: Cystoid cicatrix

Fig. 4.28B: Cystoid cicatrix— Seidel's test positive

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Fig. 4.30A: Pseudocornea formation

Fig. 4 .30B: Pseudocornea formation— slit section

Fig. 4.31: Healing ulcer— ectatic cicatrix

Fig. 4.32A: Anterior staphyloma— partial

Fig. 4.33: Corneal ulcer— phthisis bulbi

Fig. 4.34: Corneal ulcer— endophthalmitis

Fig. 4.35: Corneal ulcer— panophthalmitis

Fig. 4.36: Cornea! opacity— nebula— faint opacity

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в Figs 4.37A and B: Corneal opacity— macula— partial thickness involvement

Fig. 4.36A: Corneal opacity— leucoma

Fig. 4.38B: Corneal opacity— leucoma— full thickness involvement

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в Figs 4.39A and B: Corneal opacity— adherent leucoma

Fig. 4.40A: Leucoma with severe vascularization

Fig. 4.40B: Vascularized corneal opacity

HERPES SIMPLEX VIRUS (HSV) KERATITIS • In fectio n w ilh herp es sim plex virus (H SV ) is extrem ely com m on • The m ajority o f the patients present with recurrent lesion PRIMARY HSV INFECTION • • • •

Usually subclinical or may present with mild ocular problem Typically, il occurs between 6 months to 5 years of age The main lesion is acute follicular conjunctivitis Fine epithelial keratitis may be present, which som etim es, progresses to dendritic figure (Fig. 4.41A) • Vesicular eruptions and edem a o f the lids (Fig. 4.41B) • It seldom causes serious ocular problem Trent m a il: Acyclovir eye ointm ent - 5 times daily for 2-3 weeks

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RECURRENT HSV KERATITIS T he virus travels dow n along the sensory division o f the fifth cranial nerve to affect the target tissues. Associated with som e predisposing factors. DENDRITIC HSV KERATITIS Initially starts as superficial punctuate erosions which coalesce (Fig. 4.42Đ›). They send nut lateral branches with knobbed ends, to form 'dendritic' or 'tree-like' figure and this is pathognom onic (Fig. 4.42B). Bed o f the ulcer stains with fluorescein (Fig. 4.42C) and the sw ollen diseased cells nt Ihe margin take up Rost' Bengal slain (Fig. 4.42P ). T reatm en t: Debridement, topical acyclovir ointm ent 5 times daily fo r 2-3 w eek s, m ild cyclop leg ic, o ral a cy clo v ir to p reven t recurrence. GEOGRAPHICAL (AMOEBOID) KERATITIS Larger epithelial lesion - m ay bo o f 'geographical' or 'am oeboid' configuration (Fig. 4.43A). M ay occur as a continued enlargement o f dendritic keratitis (dendro-geographic) (Figs 4.43B and C) M ore likely to occur following inadvertent use o f topical steroids. T reatm en t: Sim ilar to dendritic keratitis. STROMAL NECROTIC KERATITIS May be associated with epithelial breakdow n and anterior uveitis (Figs 4.44A and B) Cheesy and necrotic appearance o f the stroma (Figs 4.45A and B) Vascularization, scarring and even perforation may 0 occur

Fig. 4.42A: Early dendritic keratitis

Fig. 4.42B: Dendritic keratitis

Fig. 4.42C: Dendritic Keratitis— multiple lesions

Fig. 4.42D: Dendritic keratitis— rose Bengal staining

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Fig. 4.43A: Geographical keratitis

Fig. 4.43B: Dendro— geographical ulcer

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T rea tm en t: O ral acyclovir, topical antiviral, cycloplegic and judicious use o f topical steroids METAHERPETIC KERATITIS (TROPHIC ULCER)

Due to persistent dcfoets in the basement m embrane, m argin is gray, thickened and rolled out due to heaped-up epithelium (Figs 4.46A a n d B). Not an active viral disease. T reatm en t: Artificial tears and bandage contact lens (BCL) AMT may require in som e cases. DISCIFORM KERATITIS

Deep keratitis with disk-liko edem a— im m unogenic reaction to HSV Focal central strom al edem a with fine KPs (Figs 4.47A and B).

Material com direitos autorais

в F igs 4.45A and B: HSV stromal necrotic keratitis

*> в F igs 4.46A and B: Metaherpetic keratitis

F ig s 4.47A and B: Disciform keratitis

Presence o f Descemet's; folds and increased central com eal thickness in severe cases (Figs 4.48A and B). W essely's immune ring surrounding the edema in long standing cases (Figs 4.49A and B). Treatm ent: Topical steroids (full strength or diluted) with acyclovir eye ointm ent in equal frequency for 2-4 weeks in tapering doses and cycloplegic. HERPES ZOSTER O PHTHALM ICUS (HZO)

• Caused by vericella-zoster virus affecting the elderly people • M ore com m on in im muno-com prom ised hosts • V esicu lar eruptions around the ey e, forehead and scalp (Fig. 4.50) • Severe pain along theophthalm ic division o f fifth cranial nerve • I lulchm son's rule/sign W hen the tip o f the nose is involved, the eye will also be involved, since both arc supplied by the nasociliary nerve (Fig. 4.51) • The ocular lesions mav be acute, chronic or recurrent. в A cute O c u la r L e sio n s

Lids: Redness, edem a and vesicular eruptions Cornea: Punctate epithelial keratitis M icrodendntes: Sm all, fine, multiple dendritic or stellate lesions (Fig. 4.52). Nummular keratitis: M ultiple granular lesions surrounded by a halo o f stromal haze (Fig. 4.53) • Sensation m ay be diminished • Disciform keratitis

Fig. 4.48A: HSV disciform keratitis— severe case

Fig. 4.48B: HSV disciform keratitis— slit section

Fig. 4.49A: Disciform keratitis— Wessely s immune ring

Fig. 4.49B: VVessely's immune nng

Fig. 4.50: Herpes-zoster ophthalmicus—fresh lesions

Fig. 4.51: Herpes-zoster ophthalm icus— Hutchinson's rule

Fig. 4.52: HZV— microdendrites

Iris: Acute iridocyclitis w ith hyphem a and patches of iris atrophy (Fig. 4.54) Neurophthalmological. Optic neuritis and cranial nerve palsies affecting the 3rd (m ost com m on), 4th and 6th nerves (Fig. 4.55) C h ro n ic O cu la r Lesion

• • • •

Ptosis duo to scarring o f the lid Trichiasis, entropion and lid notching S ile r it is, numm ular keratitis, ocular surface instability Recurrent lesion: M ucous plaque keratitis, neuro trophic keratitis (Fig. 4.56) or secondary glaucoma.

T reatm en t: In acute cases, oral acyclovir (SOU mg 5 limes daily for 7 days), and topical steroids in presence o f keratitis or iridocyclitis; system ic corticosteroids in neuro-ophthalm ologic problems

Fig. 4.53: Nummular keratitis

Fig. 4.54: HZO— uveitis with hyphema

Fig. 4.55: HZO— lateral rectus palsy

ATYPICAL MYCOBACTERIAL KERATITIS Atypical or nontuberculous mycobactcria (NTM ) are known to cause infectious keratitis, m ost o f them caused by two species M. fortuitum and M .chelonae. Commonly, it occurs after either accidental or surgical trauma and more recently alter LASIK and photorefractive keratectomy (Fig- 4.57). Keratitis is usually characterized by indolent course (relatively slow rate o f progress), and resistance to m edical Ireatmenl Clinical signs, which often develop w ithin 2 to S w eeks after LASIK reveals the formation o f a sharply demarcated gray-w hite branching, round or needle-like opacities in the corneal interface Ring infiltrates are com m on (Fig. 4.58) and may cause confusion with herpetic, fungal or АсапИммоеЬа keratitis Intact overlying epithelium is som etim es observed.

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Fig. 4.58: Atypical mycobacterial keratitis

T rea tm en t: Intensive therapy with topical fourth generation fluoroquinolones (moxifloxacin or gatifloxacin) Topical Amikacin 1 5% may also be effective. Oral Clarithrom ycin - 500 m g 2 times for 2 weeks simultaneously. Topical antibiotics are to be continued for months. A superficial keratectom y or flap amputation may be needed in post LAS1K cases NOCARDIA KERATITIS N o card ia a s te ro id s , a G ra m -p o s itiv e , a e ro b ic filam en to u s bacterium ,affect the immunocompromised individuals,following m inor trauma II m ay be m isdiagnosed clinically, as the picture may resem ble mycotic keratitis (Fig. 4.59) or keratitis caused by atypical mycobacteria.

Fig. 4.59: Nocardia keratitis with hypopyon M ultiple anterior stromal pin-head like infiltrations, typically a rra n g e d in the form o f a rin g , ca lle d " w r e a th " p attern (Fig. 4.60) Patchy infiltrates which are predominantly anterior stro m a l w ith a sso cia te d in v o lv e m e n t o f e p ith e liu m and subepilhelial tissues, are pathognom onic o f Nocardia keratitis T reatm en t: Fortified amikacin (2 0*2.5%) eye drop is the treatment o f choice. G entam ycin and 4th generation fluoroquinolones (m oxifloxacin and gatilloxacin) are also effective. MICROSPORIDIAL KERATITIS M icrosporidia are eukaryotic, spore forming obligate intracellular parasites. Only tw o species— N osem a and Enccphalitozoon, arcknown to cause ocular infections, mainly keratitis.

Fig. 4.60: Nocardia keratitis— typical wreath pattern Com m on features w ere follicular papillary conjunctivitis and superficial coarse punctate epithelial lesions in 3 patterns—diffuse, peripheral, and paracentral - evolving into num m ular keratitis before resolution (Fig. 4.61). The other type o f presentation is - com eal stromal keratitis w hich begins insidiously and m im ics a progressive herpetic disciform keratitis with corneal edem a (Figs 4.62A and B) There m ay be associated diffuse endotheliitis and limbitis. Diagnosis can be made on corneal biopsy Treatm ent: Topical propamidine iscthionale(0.1%) six times daily, N cosporin eye ointm ent— twice daily; oral albendazole 400 mg three times daily for a week, and then 400 mg daily for 4-6 weeks Identifying m icrosporidia to species specific level could have important im plications in the clinical management

Fig. 4.61: Microsporidial keratitis— nummular appearance

Fig. 4.62A: Microsporidial keratitis— nummular and disciform appearance

Fig. 4.62B: Microsporidial keratitis disciform appearance

INFECTIOUS CRYSTALLINE KERATITIS It is a rare indolent infection usually associated with long-term use o f topical steroids as in PK II is usually caused by Streptococcus viridin n s, though o th e r o rgan ism m ay also b e resp on sible (Fig. 4.63A). It ap p ea rs as slo w ly p ro g ressiv e g ra y -w h ite bran ch in g o p acities in Ihe an terio r or mid strom a T here is m inim um in fla m m a tio n and o v e r ly in g e p ith e liu m is in ta c t T o be d ifferen tia ted from n o n -in fectio u s cry sta llin e k eratop ath y (Fig. 4.63B). T reatm en t: Intensive topical antibiotics (fluoroquinolones) for several weeks Sudden w ithdraw al o f steroids drops without topical antibiotic may aggravate this condition or even frank suppuration

h Fig. 4.63A: Infectious crystalline keratitis

Fig. 4.63B: Noninfectious crystalline keratitis

Chapter

K eratitis: O th er T yp esN oninfectious and Peripheral

LAGOPHTHALMIC (E X P O SU R E ) KERATITIS Ow ing to dryness arid desiccation, the low er third o f epithelium is ca st o ff and the raw a rea is invaded by m icro o rg an ism s (Figs 5.1A and B). It is seen typically in facial palsy, leprosy, proptosis, thyroid exophthalm os, com atose patient, etc I lealed keratitis is having characteristic scar in the inferior cornea (Fig. 5.1C) T rea tm en t: Lid taping, tarsorrhaphy, lid-load operation and treatment o f the cause NEUROTROPHIC KERATITIS (NTK) Occurs in anesthetic cornea which alters the m etabolism o f the epithelium. M ostly seen in IISV and 11ZV keratitis. Punc tate epithelial erosion involving the intrapalpebral area. Edema and exfoliation followed by epithelial ulceration (Figs 5.2A and B)

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в Figs 5.1A and B: Lagophthalmic keratitis

T reatm en t: O intm ent and patching, in severe cases nmniotic membrane transplantation (AM T) or tarsorrhapy. NUMMULAR KERATITIS Unilateral or bilateral subepithelial lesions mainly seen in varicella zoster virus infection Large, multiple, round or oval granular subepithelial deposits just beneath the Bow m an's layer and surrounded by a halo of strom al haze (Figs 5.3A and B). T reatm en t: Topical dilute steroid drops in tapering doses and tear lubricants. MARGINAL KERATITIS (CATARRHAL ULCER) Caused by hypersensitivity reaction to staphylococcal exotoxin Subepithelial infiltrates at the periphery, m ostly at 4-8 o'clock position, or at 10-2 o'clock position (Figs 5.4A and B) T reatm en t: Topical corticosteroids, steroid-antibiotic ointm ent and sim ultaneous treatm ent o f blep h aritis w ith a course o f system ic tetracyc line or doxycycline. MARGINAL U L C ER S WITH SY STEM IC COLLAGEN D IS E A SE S OR PERIPH ERAL ULCERATIVE KERATITIS (PUK)__________________________________ • Seen in rheumatoid arthritis, polyarteritis nodosa, SLE, or in W egener's granulomatosis. • Ulceration and thinning (Figs5.5A to C), peripheral keratolysis, sclerosing keratitis, 'contact lens cornea' (Figs 5.5D and E),elc. T r e a tm e n t: Sy stem ic and topical stero id s, tear su bstitu tes, im m unosuppressive agents (e g oral azathioprim ), peritom y, glue and BCL, or peripheral tectonic (patch) graft

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Fig. 5.5A: PUK— thinning and recurrent melts к i

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Fig. 5.5C: PUK— peripheral melts

Fig. 5.5D: PUK— rheumatoid melts

Fig. 5.5E: Total peripheral keratolysis with

contact lens cornea PHLYCTENULAR KERATITIS • Predom inantly affects the children. • Corneal phlycten is a gray nodule, slightly raised above the surface, and a phlyctenular ulcer is yellow in color (Fig. 5.6) It m ay resolve spontaneously or may extend towards the center o f cornea • Fascicular u lc e r Phlyctenular ulcer slowly migrates from the limbus towards the center o f the cornea in a serpiginous way. Il carries leash o f blood vessels which lie in a shallow gutter formed bv Ihe ulcer • Form ation o f corneal opacity w hich is densest at it apex (Fig. 5.7) • M ultiple phlyctens m ay be associated to form phlyctenular pannus and coalesce to form a ring ulcer

Fig. 5.6: Phlyctenular keratitis— multiple lesions

Fig. 5.7: Phlyctenular keratitis— fascicular ulcer

T r e a tm e n t: T op ical co rtico stero id s, cy clop leg ic and topical antibiotic. INTERSTITIAL KERATITIS (IK) • In fla m m a tio n o f th e co rn e a l stro m a w ith o u t p rim ary involvem ent o f epithelium or endothelium Rare bilateral condition,seen in syphilis, tuberculosis or Cogan's syndrom e • V ascularized, m idstrom al, nonsuppurative inflam m ation, giving a ground-glass appearance (Figs 5.8A and B) There m ay be intrastrom al bleeding (Fig. 5 .8 0 . In inactive stage, there is variable strom al scarring with ghost vessels (Fig. 5.9) • H utchinson's triad: IK, deafness and I lutchinson's teeth— a part o f congenital syphilis. T reatm en t: System ic penicillin, topical steroids, cycloplegic and AT drugs in selective cases.

Fig. 5.8A: Interstitial keratitis

Fig. 5.8B: Interstitial keratitis— salmon patch

Fig. 5.8C: Interstitial keratitis— intrastromal hemorrhage

Fig. 5.9: Interstitial keratitis— ghost vessels PUNCTATE EPITHELIAL ER O SIO N S (P EE) • Very com m on nonspecific corneal epithelial lesions seen in variety of corneal d b ia se s • T he cau ses a re k eratocon jun ctivitis sicca, m eibom ianitis, co n ta ct len s w e a rers, fo reig n body in su b tarsal su lcu s, caterpillar hair, keratitis m edicam entosa, photokeratitis, etc • Tiny, grayish-w hite, slig h tly depressed d ots scattered in different fashion on the cornea (Figs 5.10A to D) • They represent the area o f epithelial discontinuity and stain with fluorescein but not with rose-Bengal. T reatm en t: Tear substitutes and others are directed towards the cause

Fig. 5.1 OA: Punctate epithelial erosion (PEE)—CL wear

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Fig. 5.10B: Punctate epithelial erosion— dry eye

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PUNCTATE EPITHELIAL KERATITIS (РЕК) • Punctate epithelial lesions scattered all over the cornea • Usually seen after acute follicular conjunctivitis o f viral origin or after IIZV infection • The epithelial opacities appear as raised gray dots, scattered all over the cornea (Figs 5.11A and B) • Som etim es, they extend into the Bow m an's m em brane and superficial stroma. • T he lesions stain poorly w ith fluorescein, but turn bright red with rose-Bengal T reatm en t: Tear substitutes and dilute topical steroids SU PERFICIA L PUNCTATE KERATITIS (O F TH YG ESO N S) • Uncom m on, usually bilateral, idiopathic condition. • Round, oval or stellate conglom erations o f grayish-w hite distinct dots which are intraopithclial. May be associated with mild subepithelial haze (Figs 5.12A and B). • The conjunctiva is not involved. T reatm en t: Tears substitutes in frequent doses. SU PERIO R LIMBIC KERATOCONJUNCTIVITIS (SLK ) • More in female and with thyroid dysfunction • Bilateral chronic inflammation o f the superior tarsal and bulbar conjunctiva. • Papillary hypertrophy o f the superior tarsal conjunctiva. • Edem a and thickening of the conjunctiva at the superior limbus (Figs 5.13A and B) • Superiorcom eashow spunctaleepilhelialerosionand filaments which stains with fluorescein and rose-Bengal (Fig. 5.14)

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в F igs 5.11 A and B: Punctate epithelial keratitis—adenoviral

в Figs 5.12A and B: Superficial punctate keratitis (Thygesons)

в Figs 5.1 ЗА and B: Superior limbic keratoconjunctivitis

T reatm en t: Artificial tears, bandage contact lens, block resection o f superior bulbar conjunctiva o r Ihermocauterizalion. Topical cyclosporine (0 05% ) m ay be helpful in som e cases

Fig. 5.14: Superior limbic keratoconjunctivitisrose-Bengal staining

ATHEROMATOUS ULCER • Develops over an old leucoma with degenerative changes • T he ulcer progresses rapidly with little tendency to heal (Figs 5.15A and B) • Easily gets infected and perforation m ay occur T reatm en t: Ointment and patching, BCL and tears substitutes

Fig. 5.15A: Atheromatous ulcer

4

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Л Fig. 5.15B: Atheromatous ulcer— slit section

STRIA TE KERATOPATHY (KERATITIS) Unilateral oom eal edema with D esrem et's folds occurs usuallv ✓ after a cataract surgery 11 appears as delicate gray lines in deeper cornea (Fig. 5.16). U sually, they d isap p ear sp o n tan eo u sly Sometim es, they persist and end up with corneal decompensation T reatm en t: Like those o f corneal edema

FILAMENTARY KERATOPATHY (KERATITIS) Mostly seen in severe dry eye Form alion o f epithelial threads (filaments) on the cornea which adhere to the cornea by one end, w hile the other end moves freely (Figs 5.17A and B) It is stained beautifully by fluorescein dye It m ay also b e seen in other conditions (Figs 5.17C and D)

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Figs 5.17A and B: Filamentary keratitis in dry eye

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Fig. 5.17C: Filamentary keratitis—mtcrosporidiosis

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Fig. 5.17D: Filamentary keratitis— tarsal foreign body

T reatm en t: Rem oval of filam ents by scraping then BCL and frequent artificial tears SHIELD ULCER IN VERNAL KERATOCONJUNCTIVITIS • It occurs occasionally in patients with severe vernal catarrh • Superior oval elevated lesion with grayish opacification o f the bed. • Better to b e designated as plaque (Figs 5.18Л .utd B). • O ther signs o f vernal conjunctivitis, like large tarsal papillae, limbal lesions (Figs 5. ISC and D) T reatm en t: Scraping or dissection o f the plaque followed by BCL o r a m n io tic m em b ran e g ra ft and su p ra ta rsa l injei tion o f triamcinolone acetonide KERATITIS MEDICAMENTOSA It is caused by the preservatives present in eye drop or drug itself Initial presentation is superficial punctate keratitis, scattered all over the cornea (Figs 5.19A to D) Later, patient may present with dry eye with other signs. T reatm en t: W ithdrawal o f specific drug and preservative-free artificial tears SC LERO SIN G KERATITIS • Rare condition m ay occur in isolation or with scleritis. • Gradual peripheral strom al thickening and opacification (Figs 5.20A to C) • Vascularization and lipid deposition may also occur. T reatm en t:Systemic/topical steroids and systemic investigations.

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Fig. 5.18C: Shield ulcer— VKC tarsal papillae

Fig. 5.18D: VKC— shield ulcer large

Fig. 5.19 A: Keratitis medicamentosa

Fig. 5.19B: Keratitis medicamentosa— fluorescein staining

Fig. 5.19D: Keratitis medicamentosa— ciprofloxacin deposits

Ń Figs 5.20A to C: Sclerosing keratitis

Chapter

Corneal D egenerations

CORNEAL DEGENERATION 1. 2 3 4 5 6.

Usuailv unilateral and asymmetrical. Located peripherally Accompanied by vascularization. No inheritance pattern Onset in m iddle life or later S e c o n d a ry to s o m e c o m p r o m is in g fa c to r , e .g . a g in g , inflam m ation, chem icals, trauma or system ic diseases.

A RCUS SENILIS (GE • Bilateral lipid degeneration o f the peripheral cornea, affects most elderly persons. • Starts in the superior and inferior perilim bal cornea • Then progresses circum ferentially to form a w hite band 1 mm wide (Fig. 6.1) • Peripheral sharp edge is separated from the lim bus by a clear /one o f cornea which may becom e thin to form senile furrow. • W hen it occurs below the age o f 40 years, it is called arcus juveniles (anterior em bryotoxon), w hich may be associated with system ic hyperlipidem ia (Fig. 6.2) • P s e u d o g e ro n to x o n m o st fr e q u e n tly se en in v e rn a l conjunctivitis and takes cupid’s Bow configuration T reatm en t: No treatment is required PERIPH ERAL FURROW DEGENERATION • Bilateral, innocuous, peripheral lesions in elderly patients • Mild thinning peripheral to the an us senilis (Fig. 6.3) • Epithelium is alw ays intact T reat w en t: No treatment is required

Fig. 6.1: Arcus senilis

Fig. 6.2: Arcus juvenilis

Fig 6.3: Peripheral furrow degeneration

T E R R IE N 'S MARGINAL DEGENERATION Lesion starts as fine yellow-white punctate strom al opacities at the upper part o f the cornea Sharp edge tow ards the center becom es demarcated by yellow -w hite lipid deposits (Figs 6.4A .uid B). Eventually, it becom es very thin to form a peripheral gutter (Figs 6.4C and D) O verlying epithelium is intact and vascularization i* prominent. T here may be pseudopterygium formation (Fig. 6.4E). Rarely it may occur in inferior part of the cornea (Fig. 6.4F) T reatm en t: RGP contact lens, deep lam ellar sectorial keratoplasty in severe cases or peripheral tectonic PK in perforation

Fig 6.4A: Terrien's marginal degeneration

\ Fig. 6.4B: Terrien's marginal degeneration— slit section

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Fig. 6.4E: Terrien's marginal degeneration— pseudopterygium

Fig. 6.4F Terrien's degeneration— inferior Descemetocele with pseudopterygium

PELLUCID MARGINAL DEGENERATION (PMD) Thinning involves only the inferior cornea between 4 to 7 o'clock position, with ectasia just above the area o f thinning, giving rise to the a p p e a ra n ce o f k orato con u s (F ig s 6.5A and B) No vascularization (as in M ooren's or Terrien's), or no lipid deposition as in T e rrie n 's. R a re ly , an a ty p ica l su p e rio r form is seen (Fig. 6 . 5 0 H ydrops m ay o ccu r as keratoconus (Figs 6.5D and E) Rarely there may b e associated keratoconus (sec Figs 7.13M and N). T rea tm en t: C orrection o f astigm atism by RG P contact lens, tectonic patch graft if required C3R may also be tried in early case to prevent progression.

в Figs 6.5A and B: Pellucid marginal degeneration (PMD)

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Fig. 6.5C: Atypical PMD—superior

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MOOREN’S ULCER Chronic peripheral ulcer o f unknown etiology due lo ischemic necrosis from vasculitis o f perilimbnl vessels (Figs 6.6A and B) Peripheral ulcer with overhanging edge. Later involves the e n tire circu m fe re n ce and also sp read s tow ard s the cen ter (F ig . 6.6C ) M ay be se co n d a rily in fected w ith h y p op y on formation (Fig. 6.6D) Perforation may occur by minor trauma with iris prolapse (Fig. 6.6E). T r e a tm e n t: P erito m y , g lu e w ith BCI. (F ig . 6 .6 F ), system ic im m uno-suppressants, lam ellar banana-shaped tectonic graft (Fig. 6.6G ), etc

Fig, 6.6A: Mooren's ulcer

Fig. 6.6B Mooren's ulcer— overhanging edge in slit section

Fig. 6.6C: Mooren’s ulcer— extensive, spreading centrally

Fig. 6.6D: Moorcn s ulccr—secondary infection and hypopyon

Fig. 6.6E: Mooren's ulcer— perforation

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BAND-SHAPED KERATOPATHY (BSK ) Calcific horizontal band, largely at the palpebral fissure, separated from limbus by a clear zone Begins at p erip hery-3 and 9-o'clock position, and then affects the central area (Fig. 6.7A). M ay be prim ary (Fig. 6.7B), or secondarily associated with idiopathic juvenile rheum atoid arthritis w ith chronic uveitis (Fig. 6.7C), following VR surgery (Fig. 6.7D), etc. May be associated with other types of corneal degeneration (Fig. 6.7E). T reatm en t: Scraping o f the epithelium , treatment with chelating agent like, di-sodium EDTA, and lam ellar keratoplasty in severe cases PTK is also helpful in selective cases

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Fig. 6.7D: Band-shaped keratopathy— following VR surgery

Fig. 6.7E: Band-shaped keratopathy— lipid degeneration

SALZM ANNS NODULAR DEGENERATION Uncom m on,and mostly unilateral. Elevated subepithelial bluishgrey nodules in a scarred cornea and surrounding cornea are clear (Figs 6.8A and B) T reatm en t: N ot necessary, photorefractive keratoplasty (PTK) or lam ellar keratoplasty in case of central lesion. S P H E R O ID A L D E G E N E R A T IO N (C LIM A T IC D R O P L E T K E R A T O P A T H Y )

Rare, bilateral, small am ber colored granules in the superficial stroma and conjunctiva,m ainly in the interpalpebral area. Lesions (hen spread centrally and coalesce lo becom e denser It may be primary (Figs 6.9A and B) or secondary toother com eal diseases, like in BSK, old corneal opacity, lattice dystrophy,etc. (Figs 6.9C to E) T reatm en t: Lamellar or penetrating keratoplasty, especially in second ary cases. LIPID DEGENERATION (KERATOPATHY) Tw o types Prim ary and secondary. P rim a ry : It is v ery ra re and o c c u rs sp o n ta n e o u sly . It is characterized by yellowish-white deposit w ithin corneal stroma without any vascularization (Fig. 6.10A). Secondary: It is m uch more com m on and is associated with previous corneal d isease or injury A lw ays associated w ith vascularization (Figs 6.10B and C) and som etim es hem orrhage (Fig. 6.10D ). M ost com m only seen after herpetic (both 1ISV and IIZ O ) keratitis.

Đ’ Figs 6.8A and B: Salzmann nodular degeneration

Fig. 6.9A: Spheroidal degeneration

Fig. 6 9B: Spheroidal degeneration— slit section

Fig. 6.9C: Spheroidal degeneration—old corneal opacity

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Fig. 6.9D: Spheroidal degeneration in BSK

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T rea tm en t: M edical control o f prim ary disease. Argon laser photocoagulation or needle cautery o f blood vessels m ay be successful to reduce lipid deposition. Subconjunctival injection of Avastin may help to reduce the deposition. PK may be required in advanced cases. WHITE LIMBAL GIRDLE OF VOGT • Very com m on, bilateral, innocuous age-related condition • Chalky w hile, crescentic linear opacities along the nasal and / or temporal lim bus, found al the interpalpebral area (Figs 6.11A and B). • No treatment is required.

Fig 6 1OA: Lipid keratopathy— primary

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с Figs 6.1 OB and С Lipid keratopathy— secondary

Fig. 6.10D: Lipid keratopathy— intracorneal hemorrhage

Fig. 6.11 A: Umbal girdle of Vogt

Fig. 6.1 IB . White limbal girdle of Vogt

Chapter

Corneal D ystrophies

CORNEAL DYSTRO PH Y: FEA TU R ES 1 2 3 4. 5. 6.

Usually bilateral and symm etrical Located centrally N o vascularization I lereditary (usually autosom al dominant) Earlv J in onset Unrelated to any system ic or local disease, or condition.

ANTERIOR D YSTRO PH IES (EPITHELIUM AND BOWMAN'S MEMBRANE) • Probably, the m ore com m on d ystrop h ies, but frequently misdiagnosed due to variable presentation. • M ost o f the patients remain asym ptom atic, but the others develop recurrent com eal erosions. • All are autosom al dominant inheritance. COMMON VARIETIES

\ Iay-dot~ fin g erp rin t d y s tro p h y (C ogan 's m icro cy stic) • Variety o f m icrocysts, dots, fingerprint or map-like epithelial lesions (Figs 7.1 A and B). • May occur singly or in combination and best appreciated in oblique illumination o r sclerotic scalier • Patient may present w ith signs o f bilateral recurrent com eal erosions (Fig. 7 . 1 0 T reatm en t is often required for recurrent corneal erosions by tear substitutes and BCL

Bahan dengan hak cipta

Fig 7.1C: Map-dot-fingerprint dystrophy— with erosion

M cesm an n d y stro p h y • Very rare and innocuous condition • Tiny epithelial cysts all over the cornea and more numerous in interpalpebral areas (Figs 7.2Л and B) • They are best visible by retroillumination or by sclerotic scatter (Fig. 7.2C), otherw ise they appear gray (Fig. 7.2D). • No treatment is necessary. R eis-B u ck ler's d y stro p h y • R ela tiv ely co m m on , b ila tera l co n d itio n w ith au tosom al dom inant inheritance. • Reduced visual acuity in second or third decade • R ing-shaped su b cp ith clia l o p acities giv ing 'h o n ey co m b ' appearance (Figs 7.3A and B) • The entire cornea is affected with more involvem ent o f the central area (Figs 7.3C and D)

Bahan dengan hak cipta

Bahan dengan hak cipta

Fig. 7.3A : Reis-Buckler’s dystrophy— early

Fig. 7.38: Rets-Buckler’s dystrophy-—early slit section

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T reatm en t: Tear lubricants, lamellar o r deep anterior lamellar keratoplasty (DALK) in selective cases. STROMAL D YSTRO PH IES G R A N U LA R DYSTROPHIES

• Relatively com m on, autosom al dom inant, bilateral disease • Starts around puberty and progresses slowly • T he lesions appear as discrete, crum b-like w hile granules within the anterior strom a o f the central cornea (Figs 7.4A to D); som e lesions may be linear (Figs 7.4E and F) • W ith time the lesions becom e larger and more num erous and extend into deeper strom a (Figs 7.4G to I) • The stroma in betw een the opacities and the peripheral cornea remains clear. • In m ost o f the cases, visual acuity usually remains good

Fig. 7.4A: Granular dystrophy— discrete lesion— early lesion

Fig. 7.4B: Granular dystrophy— discrete lesions

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Material com direitos autorais

T r e a tm e n t: D eep a n terio r lam ellar keratop lasty (D A LK ) or p e n e tra tin g k era to p la sty in s e v e re ca se s P h o to re fra ctiv e keratectomy may be tried, but there is high chance of recurrence (Figs 7.4J and K). MACULAR OYSTROPHY Rare, bilateral d isease w ith autosom al recessive inheritance (Figs 7.5A and B) Three ty p es: • T y p e I: P re se n ts in ch ild h o o d w ith re cu rre n t ero sio n (Figs 7 .5 0 and D) • T y p e II: P resen ts in se co n d d e ca d e w ith m ild ero sio n (Figs 7.5H and F) • T y p e III: Presents in infancy with severe erosive attacks (Figs 7.5G and H) SIGNIFICANT IMPAIRMENT OF VISION AT AN EARLY STAGE

• Central, focal, gray-w hite poorly defined opacities in cloudy strom a. • T he lesions involve the entire thickness o f strom a and it also extends up to the limbus • In s o m e c a s e s , th e r e m ay b e a s s o c ia te d D e s c e m e t'e excrescences (cornea guttata) or frank endothelial dysfunctions (Figs 7.51 to L) T reatm en t: Penetrating keratoplasty (Figs 7.5M and N); DAI К may be possible in selected cases.

Material com direitos autorais

D Figs 7.5C and D: Macular dystrophy— Type I with erosion

Material com direitos autorais

н Figs 7.5G and H: Macular dystrophy— Type III severe

Fig. 7.5M

Macular dystrophy— before PK

LATTICE DYSTROPHY

Uncom m on, bilateral condition with mixed inheritance Л /so three types:

• T y p e I: A utosom al dom inant; fine bran ch in g spid er-like refraclile lines which interlace and overlap at different levels within the strom a (Figs 7.6A and B) • T y p e II: A u tosom al d om in ant associated with system ic am yloidosis, thicker lattice lines and less num erous (Figs 7.6C and D) • T yp e III: Autosomal recessive; Lattice lines coarser than type I and may extend up to the lim bus (Fig. 7.6E). With lime, n diffuse corneal haze develops Again like macular dystrophy, fine D escem et's excrescences are seen in many cases (Fig. 7.6F). Visual acuity may b e significantly impaired by 30-40 years o f age.

A

D Figs 7.6C and D ' Lattice dystrophy— Type II

Fig. 7.6E: Lattice dystrophy— Type III

Fig

7.6F: Lattice dystrophy— Descem et's excrescences

R e cu rre n t e ro sio n s (F ig s 7 .6 G an d II) an d se co n d a ry spheroidal degeneration (Fig. 7.61) are the com m on problems. T reatm ent: Penetrating keratoplasty or DAl.K. Recurrence o f Iho disease in the graft is common A V E LLIN O (G R A N U LA R -LA TTIC E ) DYSTROPHY

• Very rare, autosom al dominant • Geographically, more found in A vellino, 1taly. • Anterior stromal dystrophy is granular and posterior stromal lesions suggestive o f lattice dystrophy (Figs 7.7A to D) • H isloehem ieally positive both for hyaline (granular) and amyloid (lattice). T reatm en t: Penetrating keratoplasty or DALK.

CENTRAL (SCHNYDEH) CRYSTALLINE DYSTROPHY

• Very rare w ith autosom al dom inant inheritance • Needle-shaped crystalline lesions involving thecentral stroma • Associated with diffuse central strom al haze T reatm en t: Not required CONGENITAL HEREDITARY STRO M AL DYSTROPHY

• Very rare, bilateral, with autosomal dom inant inheritance and usual manifestation during infancy. • C o rn eal clo u d in g w ith o u t ed em a (w ith norm al corn eal thickness) (Figs 7.SA and B) • Usually associated with nystagm us and squint • 11 is to be differentiated from C l 1HD and congenital glaucom a

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D

E Figs 7.9D and E: Posterior polymorphous dystrophy— band like

Fig 7.9F Posterior polymorphous dystrophy— geographical type

CORNEA GUTTATA • A com m on aging process resulting in focal accum ulation of ex crescen ces on the p o sterio r su rfa ce o f the D escem et's m em brane. • They disrupt the norm al endothelial mosaic. • W ith confluent lesions, they appear as dark spots or beaten metal appearance (Figs 7.10A and B) • They m ay be seen in early stage o f Fuchs' dystrophy. T reatm en t: Close observation w ith serial specular m icroscopy to see the progress (Figs 7.10C and D ) Special precaution to be taken to protect endothelium during cataract surgery.

FUCHS ENDOTHELIAL DYSTROPHY

• R ela tiv ely co m m on , b ila tera l co n d itio n with au tosom al dom inant inheritance. • Slow ly progressive, and m ore com m on in elderly female • C e n tra l co rn e a l g u tta ta w ith o u t a n y sy m p to m w h ich gradually spreads towards periphery (Fig. 7.11 A) • Stroma becomes edematous with endothelial decompensation (Figs 7.11B to E) • Epithelial edem a gradually develops w ith im pairm ent o f vision. • U ltim a te ly , b u llo u s k era to p a th y d e v elo p s w ith sev ere sym ptom s (Figs 7.11F and G) • G radually, scarring occurs w ith vascularization (Fig. 7 .1 1H to J). Treatm ent: I lypertonic saline. Bandage contact lens and ultimately DSEK (Figs 7.11K and L) or rarely PK in scarred cornea.

Fig. 7 .11A Fuchs' dystrophy— guttata changes in specular reflection

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Fig. 7.11F: Fuchs dystrophy— epithelial edema with bulkHJS changes

Fig 7 11G Fuchs' dystrophy— epithelial edema with severe bullous changes

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L Figs 7.11 К and L: Fuchs' dystrophy— DSEK same patient of Figures 7 11H end I CONGENITAL HEREDITARY ENDOTHELIAL DYSTROPHY

T iro ty p es: Cl IED1 and C l IED2. Both arc bilateral and rare • CHED1 is autosomal dom inant and less severe (Figs 7.12A and B), whereas. • C IIE D 2 is autosom al recessive and more severe with total absence o f endothelium (Figs 7.12C and D). • They present as bilateral com eal edem a any lim e during first decade o f life. In m ilder form , cornea is grou nd -glass in appearance (Fig. 7.12E and F) • Bui in severe form , co rn ea is totally op aq u e (Fig. 7.12G and II) • In fa n tile form should b e d ifferen tiated from congen ital glaucom a (Fig. 7.121 and J)

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О Figs 7.12C and D Congenital hereditary endothelial dystrophy— CHED2

Fig. 7.12G: Congenital hereditary endothelial dystrophy

Fig. 7.12H: Congenital hereditary endothelial dystrophy— severe edema

T reatm en t: Penetrating keratoplasty at the earliest. DSEK can also be performed with favorable results KERATOCONUS • Bilateral conical protrusion o f the central part o f the cornea with thinning (Fig 7.13A and B) • Starts around puberty and slow ly progressive. • May b e associated w ith vernal conjunctivitis, ectopia len liso r D ow n's syndrome. • Irreg u lar retin o sco p ic reflex and high irregu lar m yopic astigmatism. • Abnorm al oil-droplet red reflex. • Thinning o f thecentral cornea with protrusion just below and nasal to the center (Fig. 7.13C) • Munson's sign: Bulging o f low er lids in dow n gaze (Fig. 7.13D) • Vogt’s lines (strine): Vertical folds at the level o f deep stroma and Desceinet's membrane (Fig. 7.13E) • Fleischer's ring: Epithelial iron line a t the base o f the cone (Figs 7.13E and F), best seen under cobalt blue filter • Rizzuti's sign: Corneal refraction as an 'arrow -head' on the nasal limbus when light is thrown from the temporal limbus (Fig. 7.13G) • Prom inent com eal nerves (Fig. 7.13H) • Acute hydrops: Sudden com eal edem a due to acute seepage o f Ihe aqueous into the com eal strom a and epithelium resulting from rupture o f D escem et's m em brane (Figs 7.131 and J) • V ariable degree o f apical com eal scarring (Figs 7.13K and L) • R a re ly it m ay b e a s s o c ia te d wi t h pe l l u c i d ma r g i n a l degeneration (Figs 7.I3M and N)

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J Figs 7.131 and J : Keratoconus— acute hydrops

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N Figs 7.13M and N: Keratoconus with pellucid marginal degeneration

Fig. 7 .1 3 0 : DALK in keratoconus— preoperative

Fig. 7.13P: DALK in keratoconus— postoperative

Fig. 7.13Q: DALK in keratoconus— postoperative

T r e a tm e n t: S p ecta cles, corn eal co llag en cro ss-lin k in g with riboflavin (C3R), RGP contact lenses, Rose Đš contact lens, deep anterior lam ellar keratoplasty (D A LK ) (Figs 7 .1 3 0 to Q ) or penetrating keratoplasty.

Chapter

M iscellaneous C orneal C onditions

CORNEAL ABRASION Common unilateral condition usually associated with trauma Epithelial defect can be easily diagnosed by diffuse illumination and after fluorescein staining (Figs 8.1A to C> T reatm en t: Antibiotic ointment and patching for 24 hours, usually sufficient for epithelial healing It is important to exam ine the patient on the next day KERATOCONJUNCTIVITIS SICCA (KCS) • Very com m on bilateral condition, m ainly occurs in postm eno­ pausal wom en which may occur in isolation or in association with som e system ic diseases, like rheumatoid arthritis. • M ucus debris or plaque (Fig. 8.2Л). • Decreased tear meniscus height (Fig. 8.2B)

Fig. 8 1A : Corneal abrasion— small

Fig. 8.1 В : Comeal abrasion after fluorescein staining

Fig 8.1C: Corneal abrasion— large area

Fig. 8.2A

Keratoconjunctivitis sicca (KCS>— mucus debris

Fig. 8.2B: KCS— reduced tear meniscus height

• Reduced tear film break-up-tim e (<10 seconds is clinically significant) • Staining o f inlerpalpebral area with rose Bengal in triangular fashion (Fig. 8.2C), later on staining «if the cornea (Figs 8.2D and E). Lissam ine green can be used to stain instead o f Rose Bengal and it is less irritating (Fig. 8.2F) • Lustureless cornea (Fig. 8.2G) • Superficial punctate keratitis stained w ith Rose Bengal or fluorescein (Figs 8.211 and I) • Filamentary keratopathy stained with fluorescein (Fig. 8.2J) • D ellen and co rn eal th in n in g lead in g lo d e sce m e lo cele formation (Figs 8.2K and L) • Vascularization (Fig. 8.2M ) and keratinization (Fig. 8.2N) in severe cases

Fig. 8 2D: KCS— rose 8engal staining— more

Fig 8 2E KCS— rose Bengal staining— extensive

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Fig. 8.2H: KCS— fluorescein stain— SPK

Fig. 8.21: KCS— fluorescein staining— extensive

Fig 8.2J: KCS— filaments

Fig. 8.2K: Dry eye—-Dellen formation

Fig. 8.2N: Dry eye— keralinization

T reatm en t: Preservative-free tear substitute 4 times to 1 hourly, topical eyclosporine (0 05%) tw ice daily for at least 6 months; soft steroids like loteprcdnol in tapering doses, punctal occlusion, autologous serum drops (20% ), partial tarsorrhaphy, etc VORTEX KERATOPATHY • Bilateral condition, more com m only caused by a variety o f oral medicine and also in Fabry's disease • T h e d ru g s a re h y d r o x y c h lo r o q u in e , a m io d a ro n e , indom ethacin, tam oxifen, chlorprom azine, etc (Figs 8.3A and B) • A p pear as m inute grayish or golden epith elial deposits arranged in a vortex fashion • They start at a point below the pupil and sw irling outw ards without involving the lim bus (Figs 8.3C and D)

Fig 8.ЗА

Vortex keratopathy— chlorprom azine-induced

Fig. 8.3B: Vortex keratopathy— chlorpromazineinduced sclerotic scatter

Fig. 8.4B: Descemet’s detachment— partial with localized PBK

Fig. 8.4C: Descemet's detachment— curled

Fig. 8.5C: Haab's striae—congenital glaucoma

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Fig. 8.6A: Descemet’s fold following phakoemulsification

в Fig. 8.6B: Descemet's fold— surgical trauma— small lens fragment in AC

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E Figs 8.6E and F Descem ets fold following toxic keratopathy (calotropis latex)

Fig. 8.6F: Descemet’s folds— disciform keratitis

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Figs 8.8A and B: Corneal dellen— small

CROCODILE SHAGREN U n com m o n , b ila tera l, in n ocu o u s co n d itio n G ray ish -w h ite polygonal opacities separated by clear spaces. A nterior crocodile shagren— involve anterior two-third o f strom a and usually more peripheral (Fig. 8.9A). 11 is more frequent than p osterior typ e w hich is usually central in location (Figs 8.9B and C). T reatm en t: Not required PROMINENT CORNEAL N ERVES T h ey a re asso ciated w ith a variety o f o cu la r and sy stem ic conditions The causes are. neurofibrom atosis, leprosy, primary am yloidosis, keratoconus, acanthamoeba keratitis, failed graft, etc (Figs 8.10A to C) No treatment is required

Fig. 8.9A Crocodile Shagren— anterior more penpheral

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Fig. 8 .IOC: Keratoconus— prominent corneal nerve

XEROPHTHALMIA (CORNEAL SIGN S IN AVITAMINOSIS-A) Corneal xerosis (X2): Ila z y lusterless, dry cornea, mainly in the inferior pari (Fig. 8.11 A) K eratotm lacia (ХЗА, 3B ): R ou nd, oval, punched out defects, surrounded by xerotic cornea, perforation may occur within 24 hours with pseudocornea and anterior staphylom a formation (Fig. 8.11B) • X3A when <1 /3 cornea is involved • X3B when >1/3 cornea is involved X erop h th n lm ic scar (X s): H ealed se q u e la e o f p rio r co rn ea involvement typically inferior in location (Fig. 8.11C) It includes nebula, macula, leucom a, adherent leucom a, etc

Fig. 8 11C: Xerophthalmic scar— Xs

T reatm en t: It is a medical em ergency; massive dose o f vitam in A (orally nr parenterally), treating m alnutrition and underlying systemic- illness; prophylactic vitamin A therapy up to the a g e of 6 years. TUNNEL A B S C E S S Associated with infiltrations within the tunnel after phaco- or manual SICS (Figs 8.12A and B) Variable degree o f anterior ch am ber reactions and eventu ally it m ay progress to frank endophthalm itis (Fig. 8.12C) Som etim es, it may perforate with iris prolapse (Fig. 8.12D). T reatm en t: Exploration and scraping the m aterials ior culture and sensitivity,and tunnel wash with vancomycin and amikacin, or am pholericin-B depending upon the infection Prognosis is usually poor In difficult cases, a tectonic sclera-corneal patch graft often saves the eye ball (Figs 8.12E and F)

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It isacondition in which there is disturbance al the level o f corneal epithelial basement m em brane, resulting in defective adhesions and recurrent breakdow ns o f the epithelium. It m ay o ccu r a fte r m inor traum a (fin g er n a il in ju ry ) or spontaneously (as in diabetes or dystrophy). Painful blurring of vision, foreign body sensation, photophobia, and epithelial defects stained with fluorescein (Figs S.13A and B) T reatm en t: Topical artificial tears, bandage contact lens (BCL), debridem ent o f epithelium and basem ent m em brane followed by BCL, anterior strom al m icropuncture, excim er laser PTK in difficult cases

Fig. 8.13A: Recurrent comeal erosion

Fig. 8.13B: Recurrent cornea! erosion— fluorescein stain

BLOOD STAINING OF THE CORNEA Occurs after a traumatic hyphema with raised intraocular pressure and if treatment is delayed, whole cornea is stained with greenishbrown appearance (Figs 8.14Đ› and B). W ith treatment, cornea slowly clears up from the periphery towards the center with vascularization, and usually takes around two years or more (Figs 8.14C and D). T reatm en t: M ay require PK in som e cases Prognosis is always poor

Fig. 8.14C: Blood staining ol the cornea— la te same patient after 6 months as Figure 8.14A

Fig. 8.14D: Blood staining of the cornea— la te same patient after 6 months as Figure 8.14B

Fig. 8.15F: Conjunctival melanoma encroaching onto the cornea

w Fig. 8.15G: LK— before operation (big limbal dermoid)

Chapter

Corneal G raft-related Problem s

A corneal transplantation may b e lull thickness (penetrating keratoplasty or PK) (Figs 9.1 A and B) or partial thickness (lamellar keratoplasty or I.K) In spile o f ils gold-standard, full thickness keratoplasty has more com plications than Ihe others A lam ellar k eralo p lasty m ay b e a n terio r lam ellar, deep anterior lam ellar keratoplasty (DALK) (Figs 9.1C and D ) or posterior lam ellar keratoplasty (PLK). D escem et's stripping (autom ated) endothelial keratoplasty or DSEK/DSAEK, (most popular type o f PLK) is now the choice of surgery in endothelial dysfunctions (Fig. 9.1E) A therapeutic PK is performed in an em ergency basis lo save Ihe integrity o f the globe The typical exam ple is non-healing com eal ulcer, com eal ulcer with threatened perforation, etc (Figs 9 .IF and G)

Fig. 9.1 A: Penetrating keratoplasty before

Fig. 9.1 Đ’ : Penetrating keratoplasty after

Figs 9.1 D: Deep anterior lamellar keratoplasty in koratoconus

Fig. 9.1 E: Descemet stripping endothelial keratoplasty (DSEK)

Material com direitos autorais

Fig. 9.1J: Boston keratoprosthesis

Tectonic graft is required to support cornea as in corneal thinning, peripheral ulcerative keratitis or Descemetocele (Figs 9.1H and I) K eratoprosthesis is the* artificial com eal im plants, used in extrem e cases w here the chance o f graft survival is very poor after conven tional keratop lasty (Fig. 9.1J). T here are many ty p es o f k e ra to p ro sth e sis, like B o sto n 's K e ra to p ro sth esis (KPRO); O steo-odonto-keratoprosthesis (ОСЖР) or Pintucci's keratoprosthesis. Each type has its own indications and limitations ЛИ types o f corneal transplantation surgery including KPRO, have problems which can b e easily solved But, in neglected cases, they m ay have serious consequences. I lore, the follow-ups are much more im portant than the surgery itself.

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Fig. 9.3C: Persistent epithelial defect— Fluorescein staining

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Fig. 9.4A: Loose sutures post-PK

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Fig. 9.4D: Loose suture with vascularization in DALK

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T reatm en t: All the offending sutures are to be removed under sterile precautions In non-infective cases, the steroid drops frequency is to be increased for a short time and antibiotics drops 4 times for few days In infective eases, remove the suture by pulling through the shortest possible route Sm ear preparation to detect bacteria or fungus; and culture o f the sutures and treat it intensively with topical fluoroquinolones/fortified antibiotics or antifungal as given in microbial keratitis. EARLY GRAFT INFECTION It may b e due to bacteria or fungi, and seen w ithin 1-3 weeks of tr a n s p la n ta tio n It is s o m e tim e s a s s o c ia te d w ith fra n k endophthalm itis (Figs 9.5A and B). P rim arily occurs due to contaminated donor tissue The picture is sim ilar to that o f bacterial or fungal keratitis. It is m ost com m on in therapeutic graft. Early interface infection m ay occur after DALK (Figs 9.5C and D) or DSEK procedures (Figs 9.5E and F). T rea tm en t: A ggressive antim icrobial therapy. D onor-button culture reports are helpful to determ ine the type o f infection and initiation o f therapy Urgent regrafting is required in many cases with a fresh donor button. RECU RREN C E O F PREVIOUS D IS E A SE S IN GRAFT T h e im p ortan t d ise a se s a rc: L a ttice d y stro p h y , G ran u lar dystrophy or Rcis-Bucklers' dystrophy (Fig. 9.6A); IISV keratitis (Figs 9.6B and C), etc. T reatm en t: May be required in som e cases. HSV keratitis is to be treated m edically as per protocol. Tab Acyclovir (400 mg) twice daily j for 6 months to 1 jyear may j reduce recurrence rate.

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* Ń F ig s 9.6B and C: Recurrence of previous diseases in graft HSV INDUCED HIGH AND IRREGULAR ASTIGMATISM

In spite o f crystal clear graft, som e patients may not gain good vision due to high and irregular astigm atism It is due to suturing problem (F ig s 9.7A and B) R efraction (abnorm al shad ow ), keratom etry and corneal topography can detect this condition T r e a tm e n t: Selectiv e su tu re rem oval, RGP contact lens can im prove the vision. Post-PK LASIK is required in som e cases to reduce the astigmatism LATE PK-W OUND DEHISCENCE

Keratoplasty wound never heals. Late dehiscence of wound may occur after a minor trauma in the eve or som etim es even after a ÂĽ forcible slap on cheek several years after the surgery (Figs 9.8A to C) In full-lhickness graft, the stroma never attaches completely with Ihe host A ttachm ents only occur at the epithelium by proliferation and endothelial layer by sliding.

Fig. 9.7A: Induced high and irregular astigmatism

Fig. 9.8A: Late wound dehiscence in PK alter 1 year

Fig. 9.8C: Late wound dehiscence in PK even alter 8 years

Treatm ent: Emergency re-suturing o f the wound as tar as possible Then consider for regrafting. LATE GRAFT INFECTION It m ay occur lately due to surface or suture-related problem The keratitis m ay be cl ue to bacterial (Fig. 9.9Đ›) or fungal (Fig. 9.9B). In fungal infection, Candida is the m ost com m on organism (Figs 9.9C to E). T reatm en t: Intensive antim icrobial therapy after scraping and sm ear preparation. Culture reports are im portant to change the antimicrobial agent In severe cases, a regrafting procedure is required w ith a fresh donor cornea. Prognosis is always poor

Fig. 9.9E: Late graft infection in DALK double hypopyon

ALLOGRAFT REJECTION Com eal allograft rejection o fan y layer can occur following PK and less frequently in LK procedures. Endothelial rejection is most com m on and m ost serious as it mav lead tosevereendolhelial cell j loss followed by decompensation. Epithelial and stromal rejections are less frequent and less serious. They are often asymptomatic and diagnosed on routine follow-up examination E p ith elia l rejectio n : Circum ciliary congestion accompanied by irregu lar elevated line o f abnorm al ep ith eliu m , often called epithelial rejection line S t r o m a l r e j e c t io n : L o calized stro m a l n e o v a scu la riz a tio n , subepilhelial infiltrates, surrounding stromal edem a, multiple w hite spots in anterior strom a (Krachm er's spots) in the donor cornea (Figs 9.I0A and B)

в Figs 9.10 A and B: Graft rejection— stromal

T reatm en t: Increased frequency o f topical steroids and topical cydoplegic are sufficient to control both strom al and epithelial rejections. ENDOTHELIAL REJECTION Photophobia and w atering is present, but no discharge Ciliary congestion, anterior cham ber reaction, new kora tic precipitates (K P s) (F ig s 9 .1 1 Л a n d B ), o fte n th ese K P s d e p o s it in a c h a ra c te ris tic lin e a r p a tte rn o n the c o rn e a l e n d o th e liu m , called Khodadoust's line (endothelial rejection line) (Figs 9.11 С and D) There are associated areas o f inflam mation at the graft m argin A ssociated strom al edem a is an indication o f graft failure. Endothelial rejection also occurs in DSEK (Figs 9.1 IE and F)

Fig. 9.11D: Endothelial rejection— Khodadousl's line in slit section

Fig. 9.11E: Endothelial graft rejection in DSEK

Fig. 9.12A: Graft rejection in PK

Fig. 9.12B: Endothelial graft rejection in PK after medical treatment

Fig. 9.13E: Failed opaque graft with severe vascularization Critical endothelial cell count is around 400-500 cells/sq mm, below which cornea starts decompensating In lo n g -sta n d in g ca se s, the g ra ft beco m es o p aq u e and vascularization (Figs 9.13C and D) may occur in variable degree T reatm en t: Regrafting with a healthy donor cornea In many cases, DSEK is also possible with better results For vascularized repeat tailed gralt (Fig. 9.13E), it is better not to regraft. But, lor o n e eyed cases, Boston keratoprosthesis may be an answer. DONOR DISLOCATION IN DSEK It is a unique com plication o f DSEK/DSAEK, w here the donor button is dislocated w ithin the anterior cham ber It typically happens within 1-7 days following DSEK. Both the host cornea and donor com eal button appears edematous (Figs 9.14A and B) It is more com m on with ACIOL, aphakia or Post PK cases

T reatm en t: Urgent re-bubbling with air is necessary to reattach

the donor button against recipient corneal strom a (Figs 9.14C and D) If it fails, consider for Re-DSEK or PK DOUBLE ANTERIOR CHAMBER IN DALK This is also a unique com plication o f deep anterior lam ellar keratoplasty or DALK where there is non-attachm ent o f recipient D escem et's m em brane with donor cornea. This usually occurs within 1-3days following DALK Clinically, theanterior chamber appears double, first one is in between donor posterior surface and recipient D escem et's m em brane, and the second one is between recipient endothelium and iris-lens diaphragm (Fig. 9.15) T reatm en t: Air bubble tamponade or C3FS gas and try to keep that for few days IOP is to be checked during the follow-up period

LATE INTERFACE SCARRING IN LK This may happen as a late com plication in ALK (Fig. 9.16A) and DSEK (Figs 9.16B and C), but very rarely in DALK This is due to scarring at the grail-h o st interface; and it may reduce som e am ount of vision. Interface ha/e is seen under slit-lnmp in focal oblique (parallelepiped) illumination. T reatm en t: If the vision is within acceptable lim it,no intervention is required. O therw ise a PK is the treatm ent o f choice

Fig. 9.16A: Late interface scarring in ALK

LATE SECONDARY GLAUCOM A

L aic secondary glaucom a m ay o ccu r in any lype o f corneal grafting II is prim arily due to steroid-induced glaucom a as a result o f poor follow -up O ther cau ses include— Peripheral anterior synechia, suture induced, vitreous in anterior cham ber, ICE syndrom e, etc. Patients often presents late w ith decreased vision, graft edem a and with epithelial bedew ing (Figs 9.17Л and B). T reatm en t: Careful m onitoring o f IOP is a must for all cases o f keratoplasty— PK, DALK or DSEK Timely shift to soft steroids is important Antiglaucoma medication is used routinely. In severe cases, trabeculectom y with M M C is required or in recalcitrant cases glaucom a drainage valve operation m ay be done.

Fig. 9.17B: Late secondary glaucoma— epithelial bedewing

Chapter

Refractive Surgery-related C orneal Problem s

LATE RU PTURE O F RK WOUND Old radial keratotom y wound may ruplure easily even w ilh minor trauma M ultiple linear rupture ÂŤif the cornea along the radial cuts and it gives multiple wedge-shaped corneal parls attached to the lim bus It may be associated with iris prolapse (Figs 10.1A and B) Sometimes, it may be associated wilh sighl-lhreatening corneal abscess and endophthalm itis (Fig. 1 0 .1 0 T reatm en t: Urgent repair with 10-0 nylon (Figs 10.1D and F.). Bui it is alw ays very difficult P O ST -P R K CORNEAL HAZE Corneal scarring (haze) may be seen in som e cases after 2 weeks to several months (Figs 10.2A and B).

в Figs 10.1A and B: RK rupture with ins prolapse

Fig. 10.1C: RK rupture with endophthalmitis

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It is associated with irregular astigm atism . Late post-PRK subepithelial scarring is also a problem (Figs 10.2C and D). Raised IOP may b e a com em Late central com eal haze is also a problem with old-fashioned extensive RK (Figs 10.2E and F) T reatm en t: Increase frequency o f steroid drops Severe haze may require PTK with or without m itom ycin С W R IN K LIN G O F TH E L A S IK F LA P

It may b e seen in early weeks. M ultiple Пар folds are seen in a concentric manner (Figs 10.3A and B). Visual acuity may reduce. T reatm en t: Imm ediately lift the flap and refloat within 24 hours Som etim es suturing may be required. DIFFUSE LAM ELLAR KERATITIS (DLK)

It is also known as "sands of Sahara" because o f its appearance. It may develop within 3-7 days following LASIK and appears as multiple fine granular inflammatory infiltrates in the flap interface Best visible by sclerotic scatter method (Figs 10.4A and B) T reatm en t: Intensive treatment w ith frequent topical steroids with topical antibiotic cover. In severe cases, the interface may be irrigated w ith BSS al ter lilting the flap. E P IT H E L IA L IN G R O W TH

Epithelial ingrowth may occur after an epithelial defect (Figs 10.5A and B). Vision may b e affected in case o f central lesion T reatm en t: Observation, especially if the lesion is peripheral and not affecting the vision. Surgical debridem ent is required if it is dense and central involving the visual axis.

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Fig. 10.8B: Post-LASIK dry eye— rose Bengal staining

C O R N E A L U LC ER A N D /O R IN T E R F A C E IN FE C TIO N

Usually bacterial, may be bilateral in som e cases. T he picture is sim ilar as bacterial keratitis (Fig. 10.9). The com m on m icro­ organisms responsible arc— atypical Mycobacteria, Nocardia, etc T r e a t m e n t : U rgent liftin g o f the flap and irrig a tio n w ith vancom ycin and am ikacin In severe cases the flap m ay be a m p u ted fo llo w e d b y in te n s iv e a n tib io tic s d ro p a fte r m icrobiological evaluation. Fourth generation fluoroquinolones are more potent for atypical M ycobacteria R E C U R R E N C E OF O R IG IN A L D IS E A S E A F T E R PTK

For superficial lesions, like BSK, granular dystrophy, Avellino dystrophy, PTK is indicated by som e surgeons But, in som e cases, the original disease may recur (Figs 10.I0A and B).

в Figs 10.10A and B: Recurrence ol granular dystrophy after PTK

T r e a tm e n t: D eep a n terio r lam ellar keratop lasty (D A LK ) is indicated in such cases. LA T E F LA P D IS P LA C E M E N T O R L O S T F L A P

LASIK Пар never heals There may b e detachm ent or loss o f LASIK flap with minor trauma or rubbing o f the eyes several years after LASIK procedure. This situation may sim ilarly occur during V R procedures it' it is required Inter on. T reatm en t: Urgent anterior lam ellar therapeutic keratoplasty

Chapter

C ontact Lens-related Corneal Problem s

Any contact lens w earer w ith p h o top h obia, p ain , redness, discharge or watering should immediately discontinue the use o f lens and have a through eye exam ination as early as possible T he im p o r ta n t p r o b le m s are: S U P E R F IC IA L P U N C T A T E K E R A T IT IS

• Most com m on complication • Fluorescein staining pattern may be an im portant clue for its detection (Figs l l . l A and B) T reatm en t: Frequent tears substitute, temporary withdrawal o f CL or reduce lens w earing time, may require change of CL. C O N T A C T LE N S -IM M U N E R E SP O N SE K E R A T IT IS

CLARE or contact lens-related m ule red eve mnv b e associated with m arginal infiltrates on the cornea May b e the result o f sensitivity reaction to bacterial toxins and sim ilar to marginal keratitis associated with blepharitis (Figs 11.2A and B) T reatm en t: D iscontinue CL wear, antibiotics and steroids eye drops and lens hygiene. A C U T E H Y P O X IA O F C O R N E A

E p ith e lia l m iero ey sts fo rm a tio n w ith n e cro sis and sm all endothelial blebs (Figs 11.ЗА and B). M icroerosions can be demonstrated by fluorescein staining. CL overw ear may be the cause T reatm en t: Reduce w earing lim e drastically, higher DK-value CL and frequent tear substitutes.

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T IG H T LE N S SY N D R O M E

Usually develops within I -2 days o f use o f CL usually with a soft lens No lens movement with blinking and CL appears 'suckedon' to the cornea Staining o f the conjunctival epithelium as a ring around cornea (Fig. 11.4); m ay be associated w ith central com eal edem a, SPKs and anterior cham ber reaction T r e a tm e n t D iscontinue CL wear; cycloplegic, Refit the patient with flatter lens

Fig. 11.4: Tight lens syndrome C O R N E A L N E O V A S C U L A R IZ A T IO N

Superficial corneal vascularisntion more than 1 mm inside limbus (Figs 11.5A and B) Chronic hypoxia is the main cause due to overuse or may be seen in extended wear lenses.

T reatm en t: Discontinue w earing CL temporarily; soft steroids, like loteprednol 0.5% 4 limes daily; Refit with higher oxygen perm eable CL C O N T A C T LE N S (T O X IC ) K E R A T O P A T H Y

Also ÂŤailed pseudo-superior limbic keratoconjunctivitis; Redness and fluorescein staining o f superior bulbar conjunctiva at the limb us; SPKs and sub-epithelial ha/e (Figs 11.6A and B) May represent chronic toxicity o f preservatives in contact lens solution (especially with thiomersal) resulting in apparent limbal stem cell failure T reatm en t: Preservative-free tears substitute; loteprednol 0 5% 4 lim es daily; concom itant antibiotics drop, Thiom ersol-free contact lens solution for cleaning, shift to daily disposable CL IN FE C TIO U S C O R N E A L IN F ILT R A T E S /U LC E R

Caused by bacterial (Pseudom onas being the m ost com m on). Fungal, Acanthamebal o r by Nocardia (Figs 11.7A to E) (see also Chapter 4). T reatm en t: Immediate scraping, smears and culture. Contact lens and solution should also be cultured separately. Slarl intensive antim icrobial agents e v e r y 30 minutes for two hours and then hourly, atropine/hom atropine eye drop 2-3 times For further management— see Chapter 4. G IA N T P A P IL L A R Y C O N JU N C T IV IT IS

Sev ere itching; m ucoid discharge and large/giant (>1 mm) superior tarsal conjunctival papillae (Figs 11.8A and B); lens

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Fig. 11.7C: Contact lens-induced keratitis— Fungal

Fig. 11.7D: Contact-lens induced keratitis— A cantham oeba

Chapter

Diseases o f the Sclera

Diseases o f the sclera are relatively rare. The reasons are: i. Relative avascularity o f Ihe sclera il Lack o f reaction o f its dense fibrous tissue to any insult For the sam e reasons, when they d o occur, the diseases tend to be chronic and sluggish. BLUE SCLERA

Sclera appears m ore on blue side than w hite, m ainly d u e to increased visibility of the underlying uveal pigm ent through thin sclera. C au ses: 1. Normally in babies 2. Osteogenesis im perfecta (blue sclera, fragilitas ossium and deafness) 3 buphthaimos (Fig. 12.IA ) 4 I ligh myopia 5 Follow ing healed diffuse scleritis (Fig. 12.1 B) 6. Ciliary/equatorial staphylom a (Fig. 12.1C) 7. Oculoderm al inelanocvtosis (Fig. 12.ID ) S. EhlerS'Danios syndrom e (Figs 12.1E and F) 9. M arian's svndrom e Ń„ FO CAL DISCO LO RATIO N OF THE SCLERA

Localized discoloration (blue or brow n-black) o f the sclera seen in a variety o f condition. C au ses: I lealed focal scleritis (Fig. 12.2A), Long standing metallic foreign body, alkaptonuria (pigm entation al the insertion o f the horizontal recti) (Fig. 12.2B) or in extrem e old ag e (Fig. 12.2C)

Fig. 12.1A: Blue sclera buphthalmos

Fig. 12.1 B: Blue sclera following healed scleritis

Fig. 12.1C: Focal blue discoloration equatorial staphyloma

F Figs 12.1 E and F: Blue sd era Ehlers-Danlos syndrome

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Differences bchiven Episcleritis and S deritis Episclcritis

Sclcritis

Definition

A superficial disease of episcleral tissue, a mild condition

A deep severe destructive disease of sclera; not a mild condition.

Symptoms

Redness is the main presentation.

Severe boring pain is the main presentation.

Signs

Less tender. Eto^ht red in color, Only superficial edema. No KPs, no feature of uveitis.

More tender nodule. Purplish in color. Sclera appears thickened. Presence of KPs, feature of uveitis.

Drug test with 10% Phenylephrine

Quick blanching of blood vessels.

No such blanching of blood vessels.

Prognosis

Favourable, No Complications

Poor, complications like visual toss, sclera thinning, staphyloma and sometimes perforation may occur.

EPISCLERITIS

It is the benign inflam m ation o f the episcleral tissu e (deop subconjunctival connective tissue), not so serious. It may bo: S im p le: Sectorial redness involving the m iddle episcleral vessels (Figs 12.3A and B); or som etim es, it may be sim ultaneously bilateral (Figs 12.3C and D)

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Material com direitos autorais

N od u lar: Purple solitary nodule with surrounding injection which can be moved over the sclera (Figs 12.3E and F) T reatm en t: Normally, the condition is transient with spontaneous remission within a few days. Oral anti-inflam matory agents, like ibuprofen, indom ethacin or diclofenac; mild corticosteroids eye drops in reducing doses; Non-steroidal anti-inflam m atory drops (NASIDs), e g flurbiprofen or diclofenac, ketorolac, nepafenac drop, etc. when steroids are contraindicated Cold artificial tears - 4 times daily may give relief from congestion and pain. ANTERIOR SCLERITIS

Inflammation o f sclera associated with collagen disorders in 50% o f the ca se s, e g. rheum atoid arth ritis, p olyarteritis nodosa, sy stem ic lupus e ry th em ato su s, W eg en er's g ran u lom ato sis, relapsing polychondritis, e tc Mny be diffuse, nodular or necrotizing D iffu se a n te rio r s c le r itis : Involves either a segm ent or the entire anterior sclera Diffuse redness and distortion ofp attern o f deep episcleral vascular plexus (Figs 12.4A to C). The entire anterior sclera may be involved with intense deep seated vascularization, called braw ny scleritis (Fig. 12.4D ), which may be associated with anterior uveitis N o d u la r s c ler itis (n on -n ecro tizin g ): Extremely lender, usually, solitary or m ultiple, firm im m obile nodule separated from the overlying congested episcleral tissue (Figs 12.5A and B). Multiple nodules (Fig. 1 2 .5 0 m ay extend around the lim bus causing annular scleritis. A n te r io r n e cro tiz in g s c le r itis w it h in fla m m a tio n : Avascular patches with scleral necrosis and melting. Marked thinning o f the sclera with increased visibility o f underlying uvea (Figs 12.6A and B); associated anterior uveitis (Fig. 12.6C).

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Outward extension onto the orbit may give rise to proptosis and extraocular musrles involvement. T r e a tm e n t: In v estig atio n s for sy stem ic collag en d iso rd ers System ic and topical corticosteroids, NSAIDs, system ic immuno足 suppressant in severe Kind unresponsive cases, atropine eye drop; S u b -co n ju n ctiv a l injection is co n train d icated for fear o f perforation o f the globe SURGICALLY INDUCED NECROSIS OF SCLERA (SINS) Rare, postoperative im mune mediated necrosis o f the sclera It may be triggered by excessive cautery or use o f antimetabolites during surgery C om m only seen fo llo w in g ca ta ra ct su rg ery (F ig s 12.9A and B), following pterygium surgery (Figs 12.9C to G) or after Vitreo-retina (VR) surgery (Figs 12.911 and I).

Fig. 12.9A: Surgically induced necrosis of sclera (SINS) post-cataract surgery

Fig. 12.9G: SINS following pterygium surgery. Same patients after 2 years

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Index A

Acanthamoeba keratitis 21L £& pseudodendrite iiZ radial kcratoncuritis £Z ring infiltrates №L shaped ulcer £2. Acutc hydrops 236. 211 hypoxia of cornea 332*. 1*5.1 ocular lesions 1U. Adherent leucoma 1U2 Allograft rejection 31fr Amoeboid keratitis 105 Anterior crocodile shagren 273 dystrophies 1#8 necrotizing sderitis with inflammation 2Zh+ Ш л 381 sderitis 371, 37(> multinodular 3SQ staphyloma HiL li£u 2Z Apical scarring 242 Arcus juvenilis 1Ы senilis 162163 Atheromatous ulcer H i I5ii Atypical mycobacteria keratitis 1?1 122 Avellino dystrophy 214. 216

В

Bacterial corneal ulccr Z2 keratitis/ulcer Ztl ulcer Ih j S i staphylococcal Z1 Band-shaped keratopathy 173121 Bilateral congenital glaucoma 235 Blood staining of cornea 2Ю. 284 Blue sclera 2f& buphthalmos 2£tZ Ehlar-Danlos syndrome 369 following healed sderitis 3liZ oculodermal melanocytosis 36H Blunt trauma 269 Boston keratoprosthesis 297 Bowman's membrane 2 Broad beam illumination 11 slit section 192 Broken suture graft infection with hypopyon with infiltration Ж* Bullous keratopathy 2 * phakic 62 slit section ill

pseudophaltic PCIOL slit section ill buphthaimos £ L 25.

early keratitis 364) induced keratitis acanthamoeba 361 keratitis fungal 3nl keratitis nocardia 362 С keratitis pseudomonas 360 Candida keratitis Zi> SPK 351 Catarrhal ulccr H i keratopathy 25.{2 Caterpillar hair 144 Cornea ILL Central guttata 221. 222 comeal in siderosis 25 dermoid 286 plana iZ* 1L. 12 edema 226,222. plana with sderocomea 12 thickness 5 Corneal crystalline dystrophy 214 abrasion 248f 249 Chronic ocular lesion litL after fluorescein staining 2i2 Ciprofloxacin deposits 158 abscess ZX ZZ Cobalt blue filler 239 degeneration 162 Coloboma 31 Dellcn 269, 2Z1* 272 Colored halos 1 dystrophy 1 8 8 Congenital edema lb glaucoma 26-1 ACIOL slit section 5Z hereditary bullae 61 endothelial dystrophy calotropis latex slit section 230 -:? 35 2l strom al dystrophy 2 1 4 r epithelial bedewing slit HZ section 6Ц. Conical protrusion with thinning epithelial bullae Ctl 237 focal slit section il> Conjunctival melanoma 2jiiL generalized slit section 5LL Contact lens in disciform keratitis slit immune response keratitis section 51 352. 251 in hydrops 51 induced in ice syndrome slit section dry eye 364 55

in iridocyclitis 52 in PCIOL slit section microbullae (d. vitrcocomcal touch 5ii with epithelial defect £1 evaluation 1 examinations 5. fistula Ж 22 infiltration ZL neovascularization 35Ll 357 opacity 99-102 sensation 12 thickness 5 topography 311 tumors 286 ulccr 2iL 34£L xerosis 276. 277 Crocodile shagren 273. 274 Cystoids cicatrix SiiL ill

keratitis 106. 107 multiple lesions 1Q7 I)endro-geographical keratitis Ш . ulcer Ш Descemet's dctachmcnt 260 excrescences 212 folds 2ы>, 2<*Я. 269 and wrinkles 265 membrane £ 5. stripping endothelial keratoplasty 2У4 tear 262, 263, 265 Descemetocele IL Diffuse anterior scleritis 376 r 378 illumination C l lamellar keratitis 340 scleritis brawny 378 Direct D diffuse illumination I* DALK in keratoconus 211 r 211 focal illumination 7 Decreased visual acuity i. rctroilhunmation 1A Deep Disciform keratitis 104. 113, 116. anterior lamellar keratoplasty 26 к 222 DLK after LASIK 242. fungal corneal ulcer Donor dislocation in DSEK 325. Definition of keratitis 2ll ^21 Dematiaceous fungal keratitis Double anterior chamber in 21L&LZ5. DALK 22k 328 I )endritic Dry eye 255*257 IISV keratitis 105 Dystrophic condition of cornea IS

E

Early dendritic keratitis 106 graft infection 305, 306 interface infection in DALK 307 1JSEK Ш Ectatic cicatrix 21L *26. Endophthalmitis thL 23iL Endothelial graft rejection in I)SEK 220.321 PK 322 rejection 318r 319 En torobacteriarea e 21 Episcleritis 322 Epithelial ingrowth 340 rejection 316 Epithelium 2* 22 Extension of conjunctival squamous cell carcinoma 288 F Fascicular ulcer 138. 139 ferry's line 2 21 Filamentary fungal keratitis Z2 keratitis 151 keratilis in dry eye 152 keratopathy 151 Filtering bleb 22

Fleischer's ring 22* 23* Fluorescein staining l i . 157. 301 o f cornea 211 Focal blue discoloration equatorial staphyloma 36K Focal discoloration alkaptonuria 370 healed sderitis 370 of sclera old age 371 Fuchsf dystrophy 224-226. 2 2 i 229 endothelial dystrophy 221 Fungal corneal infiltrates Ш ulcer Sl^ S3, £1 keratitis 23* »MKS2» ulcer .22 with satellite lesions S I G Geographical keratitis 108 Gerontoxon 1 ^ 2 Giant рарШагу conjunctivitis

358^363 Granular dystrophy ГА5-17У lattice dystrophy 214 H I lealing ulcer Li£*

I ferpes simplex virus keratitis 103 zoster ophthalmicus 114, 117 HSV disdfarm keratitis 115 epithelial and stromal keratitis 110 stromal nocrotic keratitis 111 I ludson-Stahl line 22*22 Hutchinson's rule 117 triad 140 I (ypoxia of cornea is.

Keratoconus 236-243, 276 Kenttoglobus 2=L 26 Keratoma Iacia 276 Keratopathy 17S Khodadoust's line 318 Khodadust line 319 Krukenberg's spindle 22, 2Z269, 270 L

Lacrimation 4 Lagophthalmic keratitis 130, 131 LASIK 1 complication 343 Infectious flap displacement 215. corneal infiltrates/ulcer 358 Late crystalline keratitis 126, 127 donor failure 321, 323 Inflammation of sdera 371 Пар displacement 350 Interface infection 2АЙ graft infection 313 Interstitial keratitis 140-142 in DALK double Intracorneal hypopyon 315, 316 hemorrhage i n . 1 8 1 in PK 314, 315 endothelial syndrome Щ interface scarring in Iron 22 DSEK 330 LK 329 secondary glaucoma 331, К 212 Lateral rectus palsy 1211 Kayser-Fleischer ring 22, 2L Keratectasia 45 Lattice dystrophy 209-213 Keratitis 151 Layers of cornea 4 medicamentosa 154, 157. 158 Leucoma 100, 101 Keratoconjunctivitis sicca 248, with severe vascularization 250 1112

Lids 114 Limbal girdle of Vogt 1*5. Lipid degeneration 17tS keratopathy 183, 184 Ltoaminc green staining 19. 11Loss of comeal sensation 21 Lusturclcss cornea 251 M

Macula 100 Macular dystrophy 2 0 1 r 2 0 2 r

205-21)8* Map dot fingerprint dystrophy ldlL 190 Marginal keratitis 133, 135. Meesmann dystrop h у 190-192 Megalocomea 3i Melanin 22 Metaherpetic keratitis 109. 112 Microcornea 30-32 Microdendrites 118 Microphthalmos Щ. 22 Microsporidial keratitis 123. 125 disciform appcarancc 126 Microsporidiosis 153 Moorcnr5 nlccr 172-174 perforation 296 tectonic patch graft 296 Multiple limbal dermoid on cornea 287 Munson's sign 238

N

Nanophthalmos 3lL 32 high hypermetropia Nebula 99 Necrotizing scleritis without inflammation 382 Neurotrophic keratitis 120r 122124, 130, 132 Nodular episcleritis 375 sdcritis 3Zk 379 Normal anatomy of cornea 2 cornea 3 in slit section 3 histology of cornea 2 Nummular keratitis 114, 119. 133, Ш P

Pain 4 Panophthalmitis 90, 98 Pellucid marginal degeneration U.S. 169. 243 Penetrating keratoplasty 292, 293 Perforated comeal ulcer 90, 94 Peripheral furrow degeneration U»2. 164 Persistent epithelial defect 300, 301 Peter's anomaly 22L22 Phlyctenular keratitis 13s. 139

Photophobia 4 Phthisis bulbi 90 Pigmentary glaucoma ZL. 270 Pigments deposition in corned 22. Pneumococcal keratitis 22 Posterior dystrophies 21S embryotoxon 2L 4(1 keratoconus 2Z.2& polymorphous dystrophy 218-221 sderitis 2Z2*382, 384 Post-LASIK dry eye 344, 347, iUL ectasia 344, 346, 347 infectious keratitis 349 Post-PR К corneal haze 334 stromal haze 337 Primary donor failure 298, 299 HSV infection JILL l i l l Prominent corneal nerves 240, 273, 275 Pseudocornea formation 90, 95 Pseudomonas keratitis 22 Pseudophakic bullous keratopathy ACIOL b L £& P te ry g iu m 2 1 surgery 386-388 Punctate epithelial erosion l42f 143 keratitis 145. 146

R Recurrence of granular dystrophy after PTK 200.'350 original disease after PTK previous diseases in graft HSV Ш Ш Recurrent corneal erosion 282, 283 HSV keratitis 105 Reduccd tear mcniscus height 250 Keis-Buckler's dystrophy 190, 122- 121 Ri/zuti's sign 240 Rose Bengal staining l i t 107, 251, 2 2 l of cornea 211 S Salmon patch 11L Salzmann’s nodular degeneration 178. 179 Sand of sahara 342 Scleral abscess caterpillar hair 391 thorn prick 392 tubercular 221 cyst 394, 395 patch graft 390 Sclerocomea 12* 11 Sderocomeal cyst 395

intracomeal pseudohypopyon 396 pseudohypopyon 396 Scleromalat*ia perforans 3.44 Sclerosing keratitis 154, 159. 160 Sclerotic scatter lix. l i * l t i i 1 £ I Seidel's test positive 92, 93 Sequel of comcal ulcer 90 Severe bilateral microphthalmos 1L corneal edema 51 ulcer with stromal melting

Superficial punctate keratitis 145 147 352 Superior limbic keratoconjunctivitis m . lliL 149 Suppurative keratitis Zil Surgically induced necrosis of sclera 385 Svstemic collagen diseases or 133 T

Tarsal foreign body 153 Tattooing of corneal opacity 22 Shield ulcer 155, 156 'Yemen's small 155 degeneration HiZ Siderosis 22 marginal degeneration 164Simple episcleritis H I 1£Z Single layer flattened cells 2 Therapeutic keratoplasty 295 Slit lamp Tight lens syndrome 356 biomicroscopc 6 Total peripheral keratolysis 138 examination of cornea 5 Trophic ulcer 1U9 Slit section 191 Tunnel abscess 27,4 Specular reflection I X 17 after phakoemulsificadon Spheroidal degeneration 178. 221 1*0 1K1 treated with tectonic graft Staphylococcal keratitis 21 281 Stocker's line 22* 21 with endophthalmitis 280 Stratified squamous epithelium 2 with gross hypopyon 281 Striate keratopathy 151 with iris prolapse 280 Stroma 2- 5 Stromal dystrophies 195 U necrotic keratitis l i £ Uveitis with hyphema Uil rejection 316

22

v Vascularized corneal opacity IQ3 failed graft 324 Vogt's striae 239 Vortex keratopathy 237-259

White limbal girdle of Vogt 182, m Wilson's disease 21 Wrinkled LASIK flap 341 Wrinkling of LASIK Пар Ж X

W

Wcsslcy's immune ring 116

Xerophthalmia 276 Xerophthalmk scar 276r 278

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