Cornea Lecture1 PDF

Cornea Jose M De Jesus, OD, MD, MA Anatomy/Physiology Facts 11.5 mm v/12 mm h (average) 540um centrally, thicker towards periphery Avascular Nutrients/O2 - aqueous humor/tears – components Densely innervated – CN V1 sensory branches Sensory...

Cornea Jose M De Jesus, OD, MD, MA Anatomy/Physiology Facts 11.5 mm v/12 mm h (average) 540um centrally, thicker towards periphery Avascular Nutrients/O2 - aqueous humor/tears – components Densely innervated – CN V1 sensory branches Sensory Innervation Sensory Innervation Sensory Innervation  Corneal Layers Epithelium Epithelial stem cells Specialized cells located in the limbus Cells that play a crucial role in maintaining and regenerating the corneal epithelium Dysfunction may result in loss of transparency, corneal scarring, pain, and vision loss Palisade of Vogt Series of vertical, columnar cells that are arranged in a palisade-like formation Replenishment of corneal epithelial cells and for maintaining the integrity of the corneal surface  Bowman - acellular superficial layer of the stroma - collagen fibers - non-regenerating layer Stroma - Makes 90% corneal thickness - Regularly oriented collagen fibers to maintain transparency - Proteoglycan and modified fibroblasts (keratocytes) maintain separation of the fibers - Cannot be regenerated after damage - scar  Descemet - Fine latticework of collagen fibers - Anterior/posterior banded zone - Has regenerative potential Endothelium - Monolayer of polygonal cells - Sodium potasium pump - Adult density is about 2,500 to 3,000 cells/ mm² Specular Reflection Guttata Small, irregular excrescences or outgrowths found on the surface of the corneal endothelium Descemet folds Descemet breaks  New Corneal Layer Dr. Dua found new layer located between the corneal stroma and Descemet's membrane EM May help surgeons improve outcomes corneal grafts and transplants Also help in pathophysiology of corneal hydrops seen in keratoconus Superficial Epithelial Keratopathy  Superficial Punctate Keratopathy - pinpoint epithelial disruption of the corneal epithelium - not an inflammation - many times seen without fluorescein under the slit lamp - Fluorescein, Lissamine green, Rose bengal - Dry eye, infectious, medicamentose  Superficial Coarse Keratitis - Granular, opalescent, swollen epith cells sometimes presented with focal intraepithelial/subepithelial infiltrates - Can be visible w/o stain, but stain well w rose Bengal and fluorescein) - Causes: 1) Infections - ADV, chlamydia, molluscum contagiosum, early HSV and HZV 2) Medicamentosa Deep Epithelial Keratopathy Corneal Sub-epithelial Infiltrates (SEI) Infiltration – focal or diffuse composition of inflammatory cells and non-inflammatory protein causing increased permeability Signs - Tiny subepithelial foci of non-staining inflammatory opacities Causes - EKC - Marginal keratitis (bacterial conjunctivitis) - Rosacea (meibomianitis/meibomitis) - Thygeson’s - Hypoxia – contact lens wear - Preservatives contact lens solution  Treatment o Prednisolone Acetate 1% Oph. Susp. (Pred Forte) - Short term, 1 drop 4 times daily - Monitor IOP o Fluorometholone 0.1% Oph. Susp. (FML) - Soft steroid, long term, 1 drop 4 times daily o Loteprednol Etabonate 0.5%, 0.2% Oph. Susp.(Lotemax, Alrex) - Long term, monitor IOP with 0.5% concentration - 1 drop 4 times daily o Restasis 0.5% Oph. Emulsion (FDA approved for Tx of Immune-related DES) - Could be tried as off-label BID - MOA – blocks calcineurin Recurrent Corneal Erosions (RCE) Any damage to EBM or Bowmans will result in weak adhesions between epithelium and ant. Stroma - basal cells adhere epithelium to stroma – BM secretion - hemidesmosomes at BM attach to basal cells and to anterior stroma – also through anchoring fibrils - defective basement membrane = RCE - hemidesmosomes of the basal layer fail to adhere to the basement membrane (deficient attachment) - corneal epithelium remains loose - propensity to intercellular edema - loose epithelial layers are susceptible to separation and erosion Two Main Causes Past injury – deep corneal abrasion - Takes 8-12 weeks for attachments to re-form if BM is destroyed Chronic, persistent cause as : dystrophies (EBMD, lattice, Meesmann, Reis-Buckler, bullous ) Symptoms Recurrent pain attacks and photophobia upon awakening or during sleep when the eyelids are rubbed or opened May have hx of trauma or family hx of corneal dystrophy, cataract surgery, refractive surgery hx, DM, rosacea Signs Positive/negative fluorescein staining Localized roughening of epithelium May present without signs if the pt presents at the clinic in the afternoon If dystrophy – bilateral map dot fingerprint patterns Recurrent Corneal Erosions (RCE)  Recurrent Corneal Erosions (RCE) Work up History - recent trauma / corneal abrasion ( paper cuts, fingernails) - refractive surgery - corneal transplant, cataract surgery - disease history - corneal dystrophy SLE with fluorescein Treatment Acute - treat as an abrasion - may use a bandage contact lens (Ex: Focus night and day contact lens) - pressure patch (PP) ?? After epithelial defect is healed - artificial tears 4 to 8 day and/or hypertonic solution (5% sodium chloride solution) 4-8 times/day and ointment at hs for at least 3 mo.. - f/u q 3-4 weeks Treatment When corneal epithelium is loose and heaped, not healing (EMBD) - topical anesthesia - gentle debridement with moist cotton applicator, cellulose sponge, or tooth- forceps if lifted - topical NSAID - antibiotic ointment - bandage SCL - f/u daily - advise this may need to be repeated Study Study – upon injury leucocytes secrete metalloproteinases - degrade damaged BM and anchoring system In RCE there is abnormal high levels of metalloproteinases Bascom Palmer study - doxycycline 50mg bid for 2 months and topical prednisolone, tid for 2-3 weeks showed no recurrence in 21.9 months - conclusion - anti-inflammatory activity and metalloproteinase inhibition So recurrent/resistant cases to hypertonic tx - doxycycline 50mg PO bid for 2 months - lotemax qid for 1 month, then bid for I month - f/u 1month More Permanent Txs Anterior Stromal Puncture - 25-gauge needle - multiple punctures to the anterior stroma over problem area.5 to 1.0 mm apart - cycloplegia, AB ointment and PP 24-48 hrs - stimulate collagen and fibronectin - leaves a subepithelial scar – only away from the visual axis Anterior Stromal Puncture for the Treatment of Recurrent Corneal Erosion Syndrome: Patient Clinical Features and Outcomes Purpose To evaluate the clinical features and outcomes of patients with recurrent corneal erosion syndrome who underwent anterior stromal puncture. Study Design Retrospective, nonrandomized, consecutive case series. Methods Database search of patients from 2003-2013 who underwent anterior stromal puncture was conducted at a tertiary care hospital cornea clinic. Charts of 30 patients (35 eyes) were reviewed. Conclusion Anterior stromal puncture using a short (5/8 inch) 25 gauge bent needle is a simple, safe, and cost-effective procedure for symptomatic relief in patients with recurrent corneal erosion syndrome refractive to conservative measures. Repeat treatment may be performed prior to additional surgical intervention. More Permanent Txs (cont) Stromal puncture with Nd.Yag laser Excimer laser phototherapy keratectomy (PTK) - large, shallow ablation zone - removes enough of the superficial Bowman layer to permit formation of a new basement membrane with adhesion structures Corneal Neovascularization  Cornea is avascular! Ingrowth of neo-vessels from the limbal vascular plexus into the cornea – fragile, rupture, bleed Etiology - hypoxia - contact lens wear - chronic inflammatory disease 1) trauma – mechanical/chemical 2) anterior segment pathology a. IK b. Mooren’s ulcer formation c. Terrien’s marginal degeneration d. infectious/autoimmune 3) graft rejection  Superficial - MC with contact lens wear - limbal hyperemia and in-growth of vessels up to 4mm into the cornea Deep (PANNUS) - result of a chronic inflammatory condition or anterior segment pathology - leads to the development of an active inflammatory or fibrovascular - >4mm into the cornea  Symptoms: - may be asymptomatic / mild to severe decrease vision, photophobia; contact lens intolerance Management: - Supportive/ eliminating the underlying condition - Topical steroid - Diathermy/laser photocoagulation - Limbal grafting (e.g.chemical injuries) Corneal Opacities From corneal scarring Corneal lamellae to fibrous scar tissue Bowman Layer and below Types Nebula – mild opacification, like a fog, allows posterior details Macula - denser than nebula, like a spot or stain, post details less likely seen Leucoma - very dense, white totally opaque , obscuring view of iris and pupil Leucomas Adherent leucoma -When iris is adherent to leucomatous corneal opacity, following healing of perforation of corneal ulcer Corneoiridic scar (flat)- If iris is incarcerated in the scar tissue as a result of healing of sloughed corneal ulcer. Scar is flat Corneal Anterior staphyloma – if iris is incarcerated in the corneal tissue forming an ectatic scar Peripheral Leucoma : does not interfere with visual axis, may cause some astigmatism Central: interferes with visual axis Small central macular opacity leucoma Treatments Small Central Opacity - Tattooing an option for cosmesis if it doe not distort refraction of light, otherwise leave alone Treatments Large Central Opacity - Anterior/deep anterior Lamellar Keratoplasty - Penetrating Keratoplasty Non-Infectious Keratitis/ Keratopathy Filamentary Keratitis Pathophysiology Common Causes KCS (keratoconjunctivitis sicca) From disrupted epithelial integrity SLK (superior limbic keratoconjunctivitis) Dead epithelial cells combine with mucin VKC (vernal keratoconjunctivitis) to form threads (filaments) – one end is attached to a dry spot in cornea; the other end moves freely RCE (recurrent corneal erosions) EBMD (epithelial basement membrane disorder) Symptoms FB sensation Burning Lacrimation Photophobia Signs Free - floating filaments on corneal epithelium Signs of primary disease Filaments stain with rose bengal/NAFL Treatment Treat underlying condition Debridement – remove the filaments w/ a jeweler's forceps or Q-tip PF Lubricants – q2-4h and ung hs 5% NACL qid and ung hs Diclofenac sodium.1%(Voltaren) QID for 3-4 weeks F/U q1-2 weeks depending on case If moderate-severe or recurrent – 10% N-Acetylcysteine compound solution may be used qid for 3-4 weeks If severe and not responding to Txs above consider Bandage C/L Thygeson’s Keratitis General Aspects Bilateral, chronic, central, focal epithelial keratitis without conjunctival or stromal inflammation; “keeps no company” All ages, but > in 2-3 decade; female? Duration 6 months to 4 years active disease last 1-2 months, then go into remission for 4-6 months and then recurs after 2-4 years usually resolves Etiology Unknown, immunological autoimmune response Sub-clinical viral etiology suspected in the past has been disproven by recent studies Symptoms Photophobia FB sensation Lacrimation Tearing Mild decrease in vision Signs Active corneal lesion - coarse, ovaloid, slightly raised, white or gray dot that stains mildly with NAFL; normal epith. in between Inactive lesions - intraepith. and flat, do not stain Clear eye, corneal edema A/C non-reactive Treatment Mild - artificial tears q1-4 hr; ung hs Mod-sev. - mild steroid such as 0.1% FML, lotemax, alrex: tid-qid for 1-2 weeks and taper - restasis bid (off-label) Bandage CL if no improvement or as an alternate tx during recurrence F/U weekly and then q 3-12 months Exposure Keratopathy Causes Bell Palsy with secondary lagophthalmos Nocturnal lagophthalmos or incomplete closure Proptosis Ectropion Floppy eye lid Symptoms Signs FB sensation Signs of underlying etiology “dryness” more in AM after SPK in interpalpebral fissure cornea has been exposed all night Band Shaped SPK Work-up History Corneal sensitivity testing Exophthalmometry Evaluate Bell’s Palsy with or without Bell’s Phenomenon Treatment Address and treat underlying cause PF Lubricants q1-4 h; ung hs with lid taping F/U q 1-2 when no corneal ulcerations AB - infection or risk of infection Refer for Tarsorrhaphy if severe and not responding to treatment (e.g., ectropion) Neurotrophic Keratopathy General Aspects Degenerative disease of the corneal epithelium Cause characterized by impaired healing Herpes simplex Herpes zoster The hallmark is decreased Fifth nerve palsy (2nd most corneal sensitivity which leaves the cornea susceptible to common), others injury and decreases reflex tearing Topical anesthetics, NSAID’s Epithelial breakdown can lead to ulceration, infection, melting, and perforation secondary to poor healing Stages (The Mackie classification for neurotrophic keratopathy) I- Rose bengal staining of palpebral conjunctiva, low TBUT, tear mucus, SPK II- Localized loss of epithelial, ovoid shape, rolled borders, stromal edema, could have cells and flare III- Stromal lysis, perforation Management Stage I D/C topical drugs > Do not use Acular, Voltaren, et Lubricants PF q1h-q4h and ung hs Stage II If large ulcer – AB ung (tetracylcine), cycloplege w/ homatropine and bandage CL X 24 hrs Repeat procedure daily until healed Alternate tx for large ulcer – no BCL/patch, ab ung q2h and cycloplege w/ homatropine bid, F/U daily Doxycycline 100mg PO daily has been used to promote healing Treatment Stage III Thinning and lysis of stroma – cyanoacrylate glue w/ BCL, conjunctival flaps, amniotic membrane Larger defects may need penetrating keratoplasty