Transcript The cornea
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 Pachymetry - corneal thickness keratoconus 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, ReisBucklers 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 - yellowbrown 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 Crosslinking 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 KERATOPLASTY 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) 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 INFECTIONS Viruses Bacteria Fungi Protozoa 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 preexisting 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 !