CORNEA

Švehlíková G.

Department of Ophthalmology LF UPJS v Košiciach

Prednosta: prof. MUDr. Juhás T., DrSc.

ANATOMY OF THE CORNEA

Epitelium Stroma Endotelium

CLINICAL EVALUATION

SLIT-LAMP BIOMICROSCOPY

Fluorescein staining of the cornea

CORNEA Keratometry - measuring the curvature of the anterior surface of the cornea, particularly for assessing the extent and axis of astigmatism

Corneal Topography Map

CORNEA

keratoscopy

Normal cornea keratoconus

Pachymetry - corneal thickness

SPECULAR MICROSCOPE

Normal endothelial cells Pathologic endothelium

DEVELOPMENTAL ANOMALIES

MICROCORNEA

rare, hereditary, horizontal corneal

diameter is 10 mm or less

otherwise normal structure

other ocular abnorm. – glaucoma, cataract, iris abnorm...

MEGALOCORNEA

rare, bilat. corneal diameter is

13 mm or more structure is normal high myopia,

astigmatism

DEGENERATIVE CHANGES OF THE CORNEA

Occur with age or secondary to exogenous noxious agents

Often more pronounced in one eye

ARCUS LIPOIDES - SENILIS

yellow-white circular opacity in the peripheral cornea

consist of lipids deposited in the corneal stroma

high prevalence – arcus senilis

BAND KERATOPATHY deposition of calcium salts in

the subepitelial space causes - chronic iridocyclitis,

phtisis bulbi, metabolic – increased serum calcium , chronic renal failure

Treatment:

- repeated application of calcium binding agent EDTA (ethylenediaminetetraacetic acid)

- Excimer laser phototherapeutic keratectomy has been effectively performed to treat more extensive cases

SPHEROID DEGENERATION

yellow subepitelial and stromal deposits

visual impairment, severe fotofobia, pain

frequent exposure to sunlight

SALZMANN´S NODULAR DERENERATION

multiple bluish-white superficial nodules

occurs secondary to chronic keratitis and trauma

CORNEAL DYSTROPHIES

Progresive, usualy bilateral, genetically determined disorders

Age of presentation – 1. – 4. decade

CORNEAL DYSTROPHIES

Classification

1. anterior D. – Cogan microcystic D, Reis- Bucklers D, Meesman D, Schnyder D

2. stromal D. – latice D, granular D, macular D

3. posterior D. – Fuchs endotelial, posterior polymorphous D

COGAN MICROCYSTIC DYSTROPHY

map-dot-fingerprint D

four types of lesion are seen either in isolation or in combination : dots, microcysts, map-like, fingerprint-like

often asymptomatic 10% recurent

cornela erosions

MEESMANN DYSTROPHY

AD rare, multiple

intraepithelial cysts across the entire cornea

symptoms – foreign body sensation, photophobia

usually no th

LATTICE DYSTROPHY

AD subepitelial and

intrastromal branching lattice figures

accumulation of amyloid material

complication – recurent epitelial breaks

GRANULAR DYSTROPHY

AD multiple grey-white,

snowflake-like, sharply demarcated opacites

beginning in the epithelium, later in the entire stroma

histology – hyaline deposits

MACULAR DYSTROPHY

systemic disorder of keratan sulfate metabolism

AR progresive, greyish

opacification

FUCHS ENDOTELIAL DYSTROPHY slowly progresive disease Signs: Asymmetrical, bilateral,

presents in the fifth or sixth decade

bilateral primary cornea guttata and a reduced endothelial cell density

advanced stage: endothelial cell pump

decompensation results in corneal edema

bullous keratopathy histology shows a thickened

Descemet’s membrane and endothelial cell loss.

Image obtained by specular microscopy shows destruction of the endothelial cells (right side of image). In comparison, the left side and the middle (magnified view) of the image show an intact endothelium with a clearly visible honeycomb structure

KERATOCONUS degenerative, non-inflammatory

disorder of the cornea number of patients affected

varies between 1 in 3,000 and 1 in 10,000 depending on geographic location

asymetrical progresive thinning manifestation between the age of

10-20

the causes of keratoconus are poorly understood

- increased activity of proteinase enzymes and a reduced activity in the proteinase enzyme inhibitors. This imbalance can destroy the structural proteins and supporting substrates within the cornea, resulting in thinning and loss of the normal mechanical strength.

Early signs irregular astigmatism slit-lamp examination: - Vogt lines - very fine,

vertical lines in the cornea

- Fleishers ring - yellow-brown ring of iron pigment seen at the base of the cone beneath the epithelium

corneal topography is the most sensitive method for detecting very early keratoconus by identifying subtle, inferior corneal steepening

Late signs progressive corneal thinning, with poor vision from marked irregular astigmatism

the apex of the cone is the thinnest area and is usually displaced inferiorly just below the centre

corneal protrusion causing bulging of the lower lid on looking down (Munson sign).

Acute Hydrops in advanced cases,

spontaneous ruptures of the Descemet's membrane can occur, causing a tear near the apex of the cone

the rupture allows aqueous to pass into the cornea resulting in significant corneal oedema and opacification

although the break usually heals within 6-10 weeks and the corneal oedema clears, a variable amount of corneal scarring may develop

corneas that do not recover transparency may require a corneal transplant

Treatment

depends of the degree of ectasia

early and mild cases can be treated with astigmatic spectacle correction and soft toric contact lenses

as the disease progresses - rigid contact lenses

10-25% of patients with keratoconus progress – surgical intervention

Surgical options include:

1. Corneal Collagen Cross-linking with Riboflavin

2. Corneal transplantation

3. Intra-corneal ring segment insert

Corneal Collagen Cross-linking with Riboflavin

new treatment modality, stabilize the process the aims of the treatment are to

increase the mechanical stability of the cornea by inducing cross linkage between the corneal collagen fibres

under topical anaesthesia as riboflavin does not penetrate

the corneal epithelium this is removed and riboflavin (vitamin B2) is applied as a photosensitiser

the tissue is then exposed to UVA (370nm) light for about 30 minutes

this allows the generation of additional connections, so-called cross-linkings, between the individual collagen fibres of the cornea.

Corneal transplantation

Corneal transplantation (grafting) replaces the central 7-8 millimeters of the cornea with a donor cornea that has been prepared by an eye bank 

Corneal transplantation

different types:

Penetrating Keratoplasty Lamellar Keratoplasty Decemet’s Stripping with Endothelial

Keratoplasty (DSEK)

Corneal transplantation

Penetrating Keratoplasty

Lamellar Keratoplasty

Decemet’s Stripping with Endothelial Keratoplasty (DSEK)

Indications

- to improve vision - to reduce pain - or to maintain the structural integrity of the

eye

Disorders:- Bullous keratopathy (pseudophakic or

aphakic, Fuchs' endothelial dystrophy)- Keratoconus- Keratitis or postkeratitis (caused by viral,

bacterial, fungal, or Acanthamoeba infection or perforation)

- Corneal stromal dystrophies

PENETRATING KERATOPLASTY ( PK)

full thickness corneal transplantation, PK is the commonest type of corneal graft

the sutures are normally removed 1 to 2 years after surgery

PK

PK

PK

Suturing techniques

Interrupted sutures

Single running suture

Double running suture

Stp. PK

LAMELLAR KERATOPLASTY

in DLK a central disc of tissue including the front 95% of the cornea is replaced with a transplant tissue

importantly, the endothelial cell layer is left in place

performed as an alternative to PK in keratoconus, because this cell layer remains healthy in keratoconus

LAMELLAR KERATOPLASTYAdvantages for DLK include: fewer problems with rejection - the endothelial cell layer is the main target of immunological

attack in corneal transplant rejection reactions, and damage to this layer during graft rejection can cause the graft to fail

- leaving the original endothelial layer in place with a DLK avoids most rejection problems

Disadvantages for DLK include reduced visual clarity - some visual clarity is lost as a result

of light scatter at the interface between the transplant and the host tissue in all partial thickness corneal grafting techniques

technical difficulty

DECEMET’S STRIPPING WITH ENDOTHELIAL KERATOPLASTY (DSEK)

partial-thickness corneal transplant that replaces only the endothelial layer

instead of replacing the entire cornea the surgeon strips-away a delicate membrane along the backside of the cornea

thin piece of donor tissue containing the endothelial cell layer is inserted onto the back surface of the patient’s cornea

can be performed with topical anesthesia and small incisions

no stitching is required

DSEK

is appropriate for patients in which the endothelial cell layer is dysfunctional in cases of Fuchs’ dystrophy or post cataract surgery endothelial dysfunction (pseudophakic bullous keratopathy)

Advantages of DSEK as compaired to standard corneal transplantation may include:

Better shape – problems with astigmatism are uncommon, visual recovery is faster

No suture problems - two of the commonest reasons for graft failure in PK are rejection and infection. Both problems may be precipitated by suture loosening or breakage. Because there are no sutures on the corneal surface after DSEK, these problems are avoided

Disadvantages technical difficulty

DSEK

Only patients with endothelial cell problems are candidates for DSEK

Complications:

Graft rejection Infection (intraocular and corneal) Wound leak Glaucoma Graft failure High refractive error (especially astigmatism,

myopia, or both) Recurrence of disease (with herpes simplex

or hereditary corneal stromal dystrophy).

CORNEAL INFECTIONSVirusesBacteriaFungiProtozoa

EPIDEMIC KERATOCONJUNCTIVITIS

Adenovirus Epidemic – highly

infectious Inicial acute

conjunctivitis, after 3 weeks – subepitelial opacities – spontaneously disappear

HERPES SIMPLEX INFECTION

DNA virus infection extremnly

common, 90% of the population are seropositive for HSV antibidies

most infection are subclinical

two types : HSV-1 ( face, lips,

eyes)HSV-2 (genital)

HS virus

HSV1 LATENT INFECTION

primary inf. – subclinical or mild symptoms

recurent inf. – the virus travels up the axon of sensory nerve to its ganglion, where it lies in a latent state

in some patients the virus reactivates, replicates and travels down the axon to its target tissue, causing recurrent lesion

PRIMARY OCULAR INFECTION Typicaly in children

Blepharoconjunctivitis- benign, self-limited- skin lesion involve the lids

and periorbital area- conjunctivitis – akute, watery

discharge, preauricular adenopathy.

- Th : topical antiviral ointment 5x/day

Keratitis - uncommon, fine epitelial

punctate- in some patients progress

DENDRITIC KERETITIS

the epithelial infection of the cornea

corneal sensitivity is reduced

recurens

STROMAL NECROTIC KERATITIS

is caused by active viral invasion and destruction

rare may follow epitelial

disease or may be associated with an intact epithelium

Th – difficult antiviral agents,

lubricant ointments

DISCIFORM KERATITIS

aetiology is controversial

either by a reactivated viral inf. or hypersensitivity reakcion to antigen

signs – central zone of epith. oedema, stromal thickening, surrounding ring of precipitates

Th. top. steroids comb. with antiviral th.

BACTERIAL KERATITIS- Pathogens able to produce

corneal infection of an intact epithelium are –

- Neisseria gonorhoe, Corynebacterium diphtheriae, Listeria sp., Haemophilus sp.

- Other bacteria only after loss of corneal epithelial integrity

- Predisposing factors – - contact lens wear,

trauma, corneal exposure, dry eye, topical steroids, systemic immunosupresive agents

BACTERIAL KERATITIS

round ulcer with deep stromal infiltration

hypopyon broad-spectrum ATB

CAUSES

Staph. aureus, Strep. pneumoniae

Pseudomonas Enterobacteriaceae

FUNGAL KERATITIS

clinical appearance varies with the infectious agent and stage of the disease

1. filamentous fungal keratitis

2. candida keratitis

FILAMENTOUS FUNGAL KERATITIS

Aspergillus or Fusarium sp.

ocular trauma, organic material – wood

greyish – white ulcer with indistrict margins

CANDIDA KERATITIS

usualy develops in association with pre-existing chronic corneal disease or in an immunocompromised pacient

yellow-white ulcer with dense suppuration

ACANTHAMOEBA KERATITIS free-living protozoans- found in air, soil and

water- exist in both active ( trophozoide ) and

dormant ( cystic ) forms- cystic forms – able to

survive for prolonged periods

contact lens wearer - keratitis may occur

following a minor corneal erosion

ACANTHAMOEBA KERATITIS

Presentation- Early signs : 1-4

weeks limbitis, small anterior stromal infiltrates

- infiltrates gradually enlarge, form central or paracentral ring

Th- diamidin and imidazole derivatives

QUESTIONS AND DISCUSSION

THANK YOU FOR YOUR ATTENTION !