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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.

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Švehlíková G.

Department ofOphthalmology LF UPJS v Košiciach

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

anatomy of the cornea
  • Epitelium
  • Stroma
  • Endotelium

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

Corneal Topography Map



Normal cornea


Pachymetry - corneal thickness

specular microscope

Normal endothelial cells

Pathologic endothelium

  • rare, hereditary,
  • horizontalcorneal diameter is 10 mm or less
  • otherwisenormalstructure
  • otherocularabnorm. – glaucoma, cataract, iris abnorm...
  • 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
Arcuslipoides - senilis
  • yellow-whitecircularopacity in theperipheralcornea
  • consistoflipidsdeposited in thecornealstroma
  • highprevalence – arcussenilis
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 dystrophies1
  • Classification
  • 1. anteriorD. – 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 polymorphousD
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 obtainedby specular microscopyshows destruction ofthe endothelialcells (right side ofimage). In comparison,the leftside andthe middle (magnifiedview) ofthe image showan intact endotheliumwith aclearly visible honeycombstructure


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
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
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
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

  • 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
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
  • 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 transplantation1
Corneal transplantation
  • different types:
  • Penetrating Keratoplasty
  • Lamellar Keratoplasty
  • Decemet’s Stripping with Endothelial Keratoplasty (DSEK)
corneal transplantation2

Penetrating Keratoplasty

Lamellar Keratoplasty

Decemet’sStrippingwithEndothelialKeratoplasty (DSEK)

  • to improve vision
  • to reduce pain
  • or to maintain the structural integrity of the eye


- 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
PenetratingKeratoplasty ( PK)
  • full thickness corneal transplantation, PK is the commonest type of corneal graft
  • the sutures are normally removed 1 to 2 years after surgery

Interrupted sutures

Single runningsuture

Suturing techniques


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 keratoplasty1

Advantages 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
Decemet’sStrippingwithEndothelialKeratoplasty (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
  • 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


  • technical difficulty

Only patients with endothelial cell problems are candidates for DSEK

  • 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 infections





epidemic keratoconjunctivitis


Epidemic – highly infectious

Inicial acute conjunctivitis, after 3 weeks – subepitelial opacities – spontaneously disappear

herpes simplex infection
Herpes simplexinfection
  • DNA virus
  • infectionextremnlycommon, 90% ofthepopulation are seropositivefor HSV antibidies
  • most infection are subclinical
  • twotypes :

HSV-1 ( face, lips, eyes)

HSV-2 (genital)

  • HS virus
hsv1 latent infection
HSV1 LatentInfection
  • primaryinf. – subclinical or mildsymptoms
  • recurentinf. – thevirustravelsuptheaxonofsensory nerve to its ganglion, whereit lies in a latent state
  • in somepatientsthevirusreactivates, replicates and travelsdowntheaxon to itstargettissue, causingrecurrentlesion
primary ocular infection
  • Typicaly in children


  • benign, self-limited
  • skin lesioninvolvethelids and periorbitalarea
  • conjunctivitis – akute, waterydischarge, preauricularadenopathy.
  • Th : topicalantiviralointment 5x/day


  • uncommon, fineepitelialpunctate
  • in somepatientsprogress
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 keratitis1

round ulcer with deep stromal infiltration


broad-spectrum ATB

  • 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-livingprotozoans

- found in air, soil and water

  • exist in bothactive

( trophozoide ) and dormant ( cystic ) forms

  • cysticforms – able to surviveforprolongedperiods
  • contactlenswearer

- keratitismayoccurfollowing a minorcornealerosion

acanthamoeba keratitis1
  • Presentation
  • Early signs : 1-4 weeks limbitis, small anterior stromal infiltrates
  • infiltrates gradually enlarge, form central or paracentral ring
  • Th- diamidin and imidazole derivatives