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The Latest in Corneal Degenerations and Dystrophies Corneal

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The Latest in Corneal Degenerations and Dystrophies Corneal 5/20/2014 Epithelial (Anterior) Basement Membrane CORNEAL DEGENERATION Dystrophy (EBMD or ABMD) • Non-familial, late onset • Easy to overlook: The Latest In Corneal • Asymmetric, unilateral, central or peripheral – typically bilateral though often asymmetric, Degenerations and Dystrophies • Changes to the tissue caused by inflammation, – females>males, age, or systemic disease. – often first diagnosed b/w ages of 40-70 Blair B Lonsberry, MS, OD, MEd., FAAO Characterized by a deposition of material, a Diplomate, American Board of Optometry • Clinic Director and Professor thinning of tissue, or vascularization Pacific University College of Optometry Portland, OR [email protected] Epithelial (Anterior) Basement Membrane Epithelial (Anterior) Basement Membrane Dystrophy (EBMD or ABMD) Dystrophy (EBMD or ABMD) • Most common • Primary features of this “dystrophy” are: findings are: – abnormal corneal epithelial regeneration and – chalky patches, maturation, – intraepithelial – abnormal basement membrane microcysts, and • Often considered the most common dystrophy, – fine lines (or any but may actually be an age-related degeneration. combination) in the central 2/3rd of CORNEAL DYSTROPHIES – large number of patients with this condition, cornea – increasing prevalence with increasing age, and – its late onset support a degeneration vs. dystrophy. 2 2 8 Epithelial (Anterior) Basement Membrane Epithelial (Anterior) Basement Membrane Corneal Dystrophies Dystrophy (EBMD or ABMD) Dystrophy (EBMD or ABMD) • Group of corneal diseases that are: • Not all patients are symptomatic (range 10- • Often referred to as: – maps, – genetically determined and 69%) • Most common symptom is mild FB sensation – dots or – have been traditionally classified with respect to – fingerprints the corneal layer affected which is worse in dry weather, wind and air conditioning • Emerging molecular science: • Blurred vision from irregular astigmatism or is redefining traditional thought on the – rapid TBUT dystrophies and • Pain is usually secondary to a RCE (recurrent – offering potential avenues for therapeutic intervention. corneal erosion) in apprx 10% 9 1 5/20/2014 Recurrent Corneal Erosion: EBMD-Negative Staining Treatment Amniotic Membrane Transplant • If severe enough to cause vision loss or • Amniotic membrane is a biologic tissue with: repeated episodes: – antiangiogenic, – antiscarring, • oral doxycycline with/without topical corticosteroid – antimicrobial, and – Doxy 50 mg bid and FML tid for 4-8 weeks – anti-inflammatory properties that promotes healing of the ocular – both meds inhibit key metalloproteinases important in surface disease pathogenesis • Amniotic membrane grafts have been used for a variety of ocular – Azasite (topical azithromycin) conditions including: – Corneal burns • debridement, – Neurotrophic ulcers • stromal puncture, or – Stem cell damage • PTK – Persistent epithelial defects • Latest development: amniotic membrane transplant e.g. Prokera Epithelial (Anterior) Basement Membrane Dystrophy (EBMD or ABMD): Treatment Stromal Puncture Amniotic Membrane Transplant • Typically directed towards • Traditionally, amniotic membrane grafts had to be preventing RCE sutured • If RCE ’s develop: – With the advent of tissue adhesives, amniotic transplants – awake with painful eye can now be sutureless that improves as day • ProKera was approved by the FDA in 2003 as a Class II wears on medical device which has a polycarbonate ring which – chalky patches/dots in holds a cryopreserved amniotic membrane lower 2/3rd of cornea • ProKera is indicated in the treatment of corneal erosions, neurotrophic corneas, recalcitrant corneal inflammation, acute ocular surface burns, acute Stevens Johnson syndrome, and descemetoceles. RCE: Treatment CORNEAL DEBRIDEMENT RCE and LASIK • Soften epithelium • Initial treatment • 1-2 gtt topical anesthetic • Patients who have a history of EBMD may not includes: • q 15-30 seconds for 2-3 be ideal candidates for LASIK and should be minutes – use of hyperosmotic • Use cotton swab, spatula, spud carefully screened for prior to surgery. ointment at • or jewelers forceps • Remove flaps by pulling edges bedtime, toward center – bandage contact • Don ’t pull directly up or out lens and • Remove flaps down to tight, • firm edges. – lubrication. • Tx abrasion (>50-100%) – Recurrence Rate 18% 12 18 2 5/20/2014 Granular Dystrophy: Macular (Groenouw Type II) Lattice (Type I) (Groenouw Type I) • Grayish opacities in • RCE are common with • The central cornea is the superficial stroma associated pain. progressively opacified resulting is scarring and • With age: • Decreased vision results deterioration of vision – extension into deeper from subepithelial while the periphery stromal layers scarring or dense stromal remains clear. – intervening stroma deposits. • RCE ’s often present. becomes hazy • Surgical treatment • May require surgical – progressive loss of includes penetrating intervention with vision, keratoplasty or DALK diminished vision. – photophobia and (Deep Anterior Lamellar – PK ocular discomfort. Keratoplasty). – DALK 22 25 Central Crystalline Dystrophy of Macular Corneal Dystrophy PTK Treatment for GRANULAR Schnyder • Surgical treatment • Opacities consist of: usually required by – small, needle-shaped 2nd or 3rd decade of refractile crystals life. that are either white or polychromatic – PK – may extend into – DALK not indicated deeper stroma but as may have damage epithelium remains to Descemets normal. SCLAFANI 26 Granular Dystrophy: Central Crystalline Dystrophy of Lattice (Type I) (Groenouw Type I) Schnyder • Discrete white • Characteristic clinical granular opacities in central anterior appearance includes: • Vision is typically mildly affected though there corneal stroma. – linear, maybe associated systemic complications • With age: – refractile, – systemic cholesterol should be evaluated – increasing number, density, size and depth – branching deposits of opacities within the anterior – intervening stroma stroma. and peripheral cornea remain clear 3 5/20/2014 Penetrating Keratoplasty Deep Anterior Lamellar Keratoplasty (DALK) • Advantages over PK: – No “open sky” during surgery so lesser chance of expulsive hemorrhage – Much decreased rejection potential because patient keeps their own endothelium • Stromal rejection is rare and easily treated – Low to no rejection risk so steroids are tapered more quickly (usually twice as fast) – Heals faster as steroids tapered sooner allowing sutures to be SURGICAL TREATMENTS: PK AND removed earlier and more rapid visual stabilization (apprx 6 DALK months) – More tectonic stability as patient keeps own endo PK Surgery: Full Thickness Surgery Deep Anterior Lamellar Keratoplasty (DALK) Normal Changes to the Endothelium • Removal of all tissue EXCEPT Descemet ’s and • Descemet ’s layer thickens from 3-17u Donor tissue Recipient tissue sutured into endothelium • There is a decrease in the # of endothelial removed recipient – Most common rejection seen in PK is endothelial cells Central trephine cut rejection observed in apprx 20% of low-risk cases – from 3500 cells/mm2 to 1200 made ’ – Repeated PK s increase chance that the graft will – this single layer spreads out: lacks mitosis be rejected • High density mitochondria : 90% pump – DALK can avoid risk of endothelial rejection with similar optical results as PK • Lenses produce reversible polymegathism Full thickness block Sutures create an Smooth Surface with only of tissue removed just irregular surface endothelial disease to get to the endothelium with astigmatism and blurring SCLAFANI Deep Anterior Lamellar Keratoplasty (DALK) Abnormal Changes to the Endothelium • Indicated for patients with • Endothelial cells become more irregular – Keratoconus • Cells secrete collagen – Corneal scars towards Descemet’s – Corneal stromal dystrophies causing multilamination – Basically any pathology that spares the = guttata endothelium • This breaks down the • Contraindicated barrier function and results in stromal and – Bullous keratopathy epithelial edema – Fuch’s SCLAFANI 4 5/20/2014 Fuch ’s Dystrophy Fuch ’s Dystrophy: Guttata Fuch ’s Dystrophy • Endothelium: • Patient symptoms vary with degree of guttata – acts as both a barrier and pump function and compromised pump function – responsible for maintaining corneal transparency • Moderate guttata by reducing corneal hydration – may affect visual function • Fuch ’s: – may result in light scatter (haloes) – typically noticed upon waking – occurs bilaterally, • With increased disruption to the pump: – AD inheritance, – vision decreases – females 3x more likely to develop condition – potential development of bullous keratopathy Fuch ’s Dystrophy: Guttata • Corneal guttata Healthy endo: Cornea Thin and clear Endo dropout: Cornea swells, mild vision loss – excessive accumulation of abnormal endo secretions is associated with the disease process – usually first noticed in the central cornea in the patients 30 ’s and 40 ’s – corneal physiology is affected adversely by interference with pump action – guttata appear as small refractile “drops ” on the Severe swelling, blisters on surface, Va drops, pain Chronic swelling, surface scarring corneal endo Normal Endothelial Mosaic Stages of Fuch ’’’s Dystrophy Fuch ’s Dystrophy: Guttata Fuch ’s: Bullous Keratopathy • closer inspection with specular reflection reveals an “orange peel-like ” dimpling of the endo • with the decreased pump function, the overlying stroma becomes edematous • long standing corneal edema may result in corneal
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