cornea Švehlíková g. department of ophthalmology lf upjs v košiciach prednosta: prof. mudr....
TRANSCRIPT
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 !