The document outlines the processes and functions of eye donation and eye banks, including the collection, storage, and distribution of corneas for transplantation and research. It also details various corneal conditions such as corneal edema, ulcers, opacities, and degenerations, along with their clinical features and treatment options, primarily focusing on keratoplasty. Additionally, it discusses corneal dystrophies and their classifications, emphasizing the importance of eye donation and the role of eye banks in improving vision for those in need.
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The document outlines the processes and functions of eye donation and eye banks, including the collection, storage, and distribution of corneas for transplantation and research. It also details various corneal conditions such as corneal edema, ulcers, opacities, and degenerations, along with their clinical features and treatment options, primarily focusing on keratoplasty. Additionally, it discusses corneal dystrophies and their classifications, emphasizing the importance of eye donation and the role of eye banks in improving vision for those in need.
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EYE DONATION & CONDITIONS
WHERE KERATOPLASTY IS DONE
- HARRISH SA 029 EYE DONATION Collection, storage and distribution of cornea for the purpose of corneal grafting, research and supply of the eye tissue for other ophthalmic purposes. Functions of an eye bank Promotion of eye donation Registration Collection Receiving and processing Preservation Distribution Research activities EYE COLLECTION CENTRE Peripheral satellites of an eye bank for better functioning. One collection centre for urban population of 200000. About 4–5 collection centres are attached with each eye bank. Functions of eye collection centre are: • Local publicity for eye donation. • Registration of voluntary donors. • Arrangement for collection of eyes after death. • Initial processing, packing and transportation of collected eyes to the attached eye bank. Personnel needed for eye collection centre are: 1. Ophthalmic technician trained in eye bank. 2. Local honorary workers/voluntary agencies like Lions Club, Rotary Club, etc. to boost the eye donation campaign. 3. Services of honorary ophthalmic surgeon or medical officer trained in enucleation available on call. • Almost anyone at any age can pledge to donate eyes after death; all that is needed is a clear healthy cornea. • The eyes have to be removed within six hours of death. • Eye donation gives sight to two blind persons as one eye is transplanted to one blind person. • The eyes can be pledged to an eye bank and can be actually donated to any nearest eye bank at the time of death. • The donated eyes are never bought or sold. Eye donation is never refused. • The eyes cannot be removed from a living human being in spite of his/her consent and wish. CORNEAL EDEMA The water content of normal cornea is 78%. It is kept constant by a balance of factors which draw water in the cornea and the factors which draw water out of cornea. Disturbance of any of the above factors leads to corneal oedema, wherein its hydration becomes above 78%, central thickness increases and transparency reduces. Causes of corneal oedema 1. Raised intraocular pressure 2. Endothelial damage 3. Epithelial damage Clinical features Stromal haze with reduced vision. Loss of vision, pain, discomfort and photophobia. Treatment Conservative Management Penetrating keratoplasty is required for long- standing cases of corneal oedema, non-responsive to conservative therapy. CORNEAL ULCER Corneal ulcer may be defined as discontinuation in normal epithelial surface of cornea associated with necrosis of the surrounding corneal tissue. Treatment of impending perforation: Penetrating therapeutic keratoplasty can be done. Treatment of perforated corneal ulcer: Depending upon the size of perforation and availability, measures like use of tissue adhesive glues, covering with conjunctival flap, use of bandage soft contact lens or therapeutic keratoplasty should be undertaken. Best option is an urgent tectonic keratoplasty. CORNEAL OPACITY Loss of normal transparency of cornea due to scarring. Causes 1. Congenital opacities may occur as developmental anomalies or following birth trauma. 2. Healed corneal wounds. 3. Healed corneal ulcers. Clinical features Corneal opacity may produce loss of vision Blurred vision Treatment Penetrating keratoplasty is done in the case of leucomatous opacity CALCIFIC DEGENERATION (BAND SHAPE KERATOPATHY) Band shape keratopathy (BSK) is essentially a degenerative change associated with deposition of calcium salts in Bowman’s membrane, most superficial part of stroma and in deeper layers of epithelium. Etiology Ocular diseases Metabolic Age related Clinical features It typically presents as a band-shaped opacity in the interpalpebral zone with a clear interval between the ends of the band and the limbus. Treatment Chelation PTK Keratoplasty is done where vision is fully obscured SALZMANN’S NODULAR DEGENERATION
Etiology: This condition occurs in eyes
with recurrent attacks of phlyctenular keratitis, rosacea keratitis and trachoma. Pathogenesis. In Salzmann’s nodular degeneration, raised hyaline plaques are deposited between epithelium and Bowman’s membrane.Associated with destruction of membrane. Clinical features: Clinically, one to ten bluish white elevations (nodules), arranged in a circular fashion. Vision loss Discomfort SPHEROID DEGENERATION a.k.a Climatic droplet keratopathy/Labrador keratopathy/ Bietti’s nodular dystrophy/corneal elastosis Etiology: It typically occurs in men who work outdoors, especially in hostile climates. Clinical features: In this condition, amber-coloured spheroidal granules (small droplets) accumulate at the level of Bowman’s membrane and anterior stroma in the interpalpebral zone. Treatment in advanced cases is by corneal transplantation. TERRIEN’S MARGINAL DEGENERATION
Terrien’s marginal degeneration is non-
ulcerative thinning of the marginal cornea. Clinical features: Mostly involves superior peripheral cornea. Initial lesion is asymptomatic corneal opacification separated from limbus by a clear zone. The lesion progresses very slowly over many years with thinning and superficial vascularization. Dense yellowish white deposits. Irritation and defective vision. Treatment is non-specific. In severe thinning, a patch of corneal graft may be required. HYALINE DEGENERATION Hyaline degeneration of cornea is characterised by deposition of hyaline spherules in the superficial stroma and can be primary or secondary. 1. Primary hyaline degeneration is bilateral and noted in association with granular dystrophy. 2. Secondary hyaline degeneration is unilateral and associated with various types of corneal diseases including old keratitis, long-standing glaucoma, trachomatous pannus. It may be complicated by recurrent corneal erosions. Treatment of the condition when it causes visual disturbance is keratoplasty. PSEUDOPHAKIC BULLOUS KERATOPATHY Pseudophakic bullous keratopathy is usually a continuation of postoperative corneal oedema produced by surgical or chemical insult to a healthy or compromised corneal endothelium. PBK is becoming a common indication of penetrating keratoplasty (PK). KERATOCONUS Keratoconus (conical cornea ) is a non- inflammatory bilateral (85%) ectatic condition of cornea in its axial part. Etiopathogenesis. It is still not clear. Clinical features: Patient presents with a defective vision due to progressive myopia and irregular astigmatism, which does not improve fully despite full correction with glasses. Treatment Spectacle correction Contact lenses Corneal collagen crosslinking with riboflavin(CXL or C3R) and UV-A rays may slow the progression of disease. Keratoplasty may be required in later CORNEAL DYSTROPHIES Cells have some inborn defects due to which pathological changes may occur with passage of time leading to development of corneal haze in otherwise normal eyes that are free from inflammation or vascularisation III. Stromal dystrophies
IC3D CLASSIFICATION 1. TGFb1 corneal dystrophies
a. Lattice corneal dystrophy I. Epithelial and subepithelial dystrophies 1. Epithelial basement membrane dystrophy b. Granular corneal dystrophy (EBMD). 2. Macular corneal dystrophy (MCD). 3. Schnyder corneal dystrophy (SCD). 2. Epithelial recurrent erosion dystrophy (ERED). 3. Subepithelial mucinous corneal dystrophy 4. Congenital stromal corneal dystrophy (CSCD). (SMCD). 5. Fleck corneal dystrophy (FCD). 6. Posterior amorphous corneal dystrophy 4. Mutation in keratin genes: Meesmann corneal (PACD). dystrophy (MECD). 7. Central cloudy dystrophy of Francois (CCDF). 5. Lisch epithelial corneal dystrophy (LECD). 8. Pre-Descemet corneal dystrophy (PDCD). 6. Gelatinous drop-like corneal dystrophy IV. Descemet membrane and endothelial dystrophi (GDLD). 1. Fuchs endothelial corneal dystrophy (FECD). II. Bowman layer dystrophies 2. Posterior polymorphous corneal dystrophy (PPC 1. Reis-Bucklers corneal dystrophy (RBCD) 3. Congenitalhereditaryendothelialdystrophy1 (CH Granular corneal dystrophy type 3. 1). 2. Thie-Behnke corneal dystrophy (TBCD). 4. Congenitalhereditaryendothelialdystrophy2 (CH 2). 3. Grayson-Wilbrandtcornealdystrophy(GWCD). 5. X-linked endothelial corneal dystrophy (XECD). Treatment is based on the thickness of the cornea involved. Keratoplasty is done either lamellar or penetrating. THANK YOU
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