Lecture 6, Cornea (Part I) - New PDF

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Mansoura University

Dr. Mohamed ElEssawy

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ophthalmology cornea anatomy physiology

Summary

This document is a lecture on the cornea, covering its definition, histology, function, and causes of opacity. It discusses factors of corneal transparency, causes of corneal vascularization, and corneal sensitivity reflexes. It also includes information on the treatment of corneal ulcers and different types of keratitis

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 CORNEA: the transparent anterior 1/6 of the outer coat of the eye. DEFINITION  LIMBUS: the junction between cornea & sclera.  Non keratinized stratified squamous epithelium covered by tear film ① EPITHELIUM (regenerate rapidly) ② BOWMAN'S...

 CORNEA: the transparent anterior 1/6 of the outer coat of the eye. DEFINITION  LIMBUS: the junction between cornea & sclera.  Non keratinized stratified squamous epithelium covered by tear film ① EPITHELIUM (regenerate rapidly) ② BOWMAN'S  condensed superficial layer of stroma (Doesn't regenerate) MEMBRANE  (90% of corneal thickness) uniformly spaced collagen fibers (Scar rather ③ STROMA than regenerate). ④ DUA (PRE-  Recent (surgical rather than anatomical) DESCEMET’S) ⑤ DESCEMET'S  Basement membrane of the endothelium. MEMBRANE ⑥ ENDOTHELIUM  Single layer of polygonal cells that doesn’t regenerate upon damage.  Normal count at birth >3000/mm2  Decrease with age 0.6% per year  To maintain a normal corneal pump mechanism and guard against corneal edema, the density of endothelial cells should be kept above 500 cells/cm2  Endothelial cell density, shape, and size can be measured using specular microscopy ENOTHELIUM ① Epithelium: Continue with conjunctival epithelium ② Bowman's membrane: continue as conjunctival stroma ③ CT stroma: Transform into sclera. ④ Descemet’s membrane: Ends at Schwalb’s line. ⑤ Endothelium: continue with endothelial lining of trabecular meshwork. CHANGES AT LIMBUS  Refraction: main refractive media of the eye (Power: 42 D)  The power is dependent on :  Corneal curvature: anterior surface of the cornea is 7.8 mm, posterior surface is about 6.5 mm  Refractive index: 1.33  The corneal power can be measured using:  keratometer which gives the power and axis of the steep and the flat meridian  The corneal topography can measure the corneal power at each point CORNEAL FUNCTION  At the center: 500-550 micron (0.5-0.55 mm)  At the Periphery: 500-900 micron (0.5-0.9 mm)  The corneal thickness can be measured using:  Ultrasound pachymetry.  Corneal tomography(pentacam) can determine: ① Corneal power map ② Corneal thickness map ③ Elevation maps  Anterior segment OCT CORNEAL THICKNESS  The cornea is avascular and its nutrition is obtained by: CORNEAL  Perilimbal blood vessels: Limbal capillaries from anterior ciliary vessels. NUTRITION  Aqueous humor: It supplies glucose and other nutrients  Tear film: supplies oxygen derived directly from atmospheric air. ① Corneal infection. ② Chemical injuries. ③ Autoimmune condition. CAUSES OF ④ Corneal hypersensitivity. CORNEAL ⑤ Corneal pannus. VASCULARIZATION ⑥ Post-corneal transplantation. ⑦ Post-traumatic. ⑧ Extended use of contact lenses.  Long ciliary nerves to  Nasociliary to  phthalmic to  Trigeminal nerve  Corneal sensitivity Reflex:  Stimulus: Corneal touch  Afferent: Nasociliary  Center: Trigeminal nucleus  Efferent: facial nerve  Response: Blinking  Tested by: Cochet Bonnet aesthesiometer CORNEAL SENSATIONS  Causes of decreased or lost corneal sensations: ① Infections e.g. Herpes, Syphilis, Leprosy. ② Trauma. ③ Post-operative ④ Post-irradiation ⑤ Compression by tumors e.g. orbital apex syndrome, superior orbital fissure syndrome FACTORS OF MAINTAIN CORNEAL CAUSES OF CORNEAL OPACITY: TRANSPARENCY: ① Avascular ① Corneal inflammation (keratitis). ② Non-myelinated nerves ② Corneal degeneration. CORNEAL ③ Uniformity of collagen ③ Corneal dystrophies. TRANSPARENCY bundles ④ Corneal ectasia. ④ Non-keratinized epithelium ⑤ Corneal edema. ⑤ Integrity of the endothelium. ⑥ Corneal pigmentation. ⑦ Pannus.  Corneal facet: defective healing with thinning and minimal opacity  Nebula: faint opacity from which iris structure can be seen  Macula: from which iris details are not seen but we can distinguish between iris and pupil.  Leucoma: dense opacity from which the iris structure can’t be seen.  Keratectasia: Loss of more stroma, healing with corneal thinning and dense scarring. TYPES OF CORNEAL OPACITY PERIPHERAL CENTRAL  Cosmetic  Superficial  Colored contact lens  PTK (Phototherapeutic keratectomy)  Tattooing  DALK (Deep Ant. Lamellar keratoplasty)  Astigmatism  Deep  Glasses  PKP (Penetrating Keratoplasty)  Contact lens INFECTIVE NON INFECTIVE ① Bacterial (Hypopion) ① Marginal Catarrhal Ulcer ② Fungal (Mycotic) ② Exposure keratitis ③ Viral (Herpetic) ③ Traumatic ④ Protozoal (Acanthamoeba). ④ Neuropathic keratopathy ⑤ Keratomalacia ⑥ Atheromatous ulcer  Presence of pus in anterior chamber that may be present in bacterial, fungal, or mixed corneal ulcers.  Referred as bacterial corneal ulcer since bacteria is most common cause. DEFINITION  Pus in hypopion corneal ulcer is usually sterile contains exudates, living, and dead inflammatory cells but not organisms. Therefore, it can resolve spontaneously after treatment of infection and does not need drainage..  Typical ulcers (70-80% of cases): are caused by pneumococci.  Atypical ulcers (20-30% of cases): are caused by staphylococci, pseudomonas, Moraxella, any other bacteria, or even fungal infection.  The main predisposing factor is: chronic dacryocystitis  Organisms that can invade intact corneal epithelium: ETIOLOGY  Gonococci  Diphtheria  Hemophilus  The most common organism associated with contact lens is  Pseudompnas ① Corneal abrasion/trauma (most ⑤ Decreased resistance important). ⑥ Epithelial Corneal edema. ② Dryness (xerosis). ⑦ Trichiasis and entropion. RISK FACTORS ③ Exposure (lagophthalmos). ⑧ Long-term use of steroids. ④ Loss of Sensations (hypothesia or ⑨ Use of contact lenses. anesthesia). ⑩ Poor hygiene. ① Pain due to exposure of nerve endings and ciliary muscle spasm. ② Lacrimation due to irritation. ③ Photophobia due to spasm of constrictor pupillae muscle. SYMPTOMS ④ Blepharospasm (spasm of orbicularis oculi). ⑤ Haloes around light. ⑥ Blurring and diminution of vision ① Lid edema, ciliary injection (circumcorneal ciliary flush). ② Corneal ulceration, loss of luster, and opacification. ③ Anterior chamber reaction (cells and flare) that may precipitate forming hypopyon. ④ Pupillary constriction (miosis). ⑤ +ve Fluorescein staining SIGNS  The aqueous gushes out resulting in hypotony and collapse of AC.  Sudden ↓↓ IOP  Pain ↓ ↓  Iris and lens touch the cornea.  Improved nutrition to cornea. CORNEAL PERFORATION: BEFORE PERFORATION AFTER PERFORATION ① Corneal opacity ① Central Small ② Corneal vascularization ② Central Large ③ Toxic iridocyclitis ③ Peripheral small ④ Secondary glaucoma ④ Peripheral Large ⑤ Descematocele/ keratocele OTHER COMPLICATIONS See next page CENTRAL SMALL CENTRAL LARGE  Peripheral ant. Synechia (PAS)  Total iris prolapse  Ant. polar cataract  Lens dislocation/expulsion  Corneal fistula  Corneal Staphyloma  2ry glaucoma  2ry glaucoma  IO infection  IO Hemorrhage/infection PERIPHERAL SMALL PERIPHERAL LARGE  Anterior synechia  Anterior synechia  Leucoma adherent  Partial iris prolapse  IO infection  Leucoma adherent  Lens subluxation IO infection  Corneal scrap >> culture & sensitivity  Start Immediately with broad spectrum AB  Mydriatic (Prevent synechia) cycloplegic (↓ ↓ ciliary spam induced pain)  Eye protection  Vitamins (A & C), Lubricants.  No role for systemic antibiotics.  Do not use!!!  Topical steroids  Topical anaethesia  Eye patch ① Filamentous (Asprigillus/Fusarium): Trauma by vegetable/contact lens ORGANISMS ② Yeast (Candida): Immunocompromised SYMPTOMS SIGNS  Lacrimation  Feathery borders CLINICAL PICTURE  Phtophobia, haloes  Satellite lesion  Blurring of vision  Stromal infiltration  Little pain  Hypopion  Scrapping: gram, giemsa stain, culture (Sabaroud dextrose agar)  Topical Antifungal (6-8 weeks) e.g Natamycin, Voriconazole MANAGEMENT:  Topical Antibiotics, Cycloplegics, Lubricants  Systemic Antifungal may be needed  Keratoplasty  Occurs as kerato- conjunctivitis associated with lymphadenopathy.  Usually self-limited, thereafter, the virus becomes latent in trigeminal ganglion.  Reactivation on immune stress.  Shape (Denderitic/Geographic)  Recurrent EPITHELIAL  Hypothesia KERATITIS  No vascularization DOUBLE  Edges with → rose Bengal STAINING  Floor with → fluorescein HSV STROMAL KERATITIS  Topical antiherpetic (Acyclovir oint/Gancyclovir drops): For epithelial cases.  Systemic antiherpetic (Acyclovir tablets): for stromal cases TREATMENT  Lubricants  Prophylactic antibiotics  Topical steroids: for stromal cases. PRIMARY RECURRENCE  HZ ① Dermatitis?? imp ② Keratitis: epithelial/stromal TYPES ChickenPox ③ Scleritis, episcleritis ④ Iridocyclitis ⑤ Chorio retinitis ⑥ Optic neuritis ① Systemic Antiherpetic (Acyclovit tab 800 mg 1*5) ② Topical Acyclovir cream TREATMENT ③ Analgesics, Anti-inflammatory ④ Topical antibiotics ⑤ Steroids  History of contact lens use / swimming pool  Sever pain exceeding the signs of the ulcer  Dendritic like peripheral perineural infiltrates → Ring ulcer CLINICAL PICTURE  Treatment may extend to 6-12 m.  Include: ① Topical Anti-amoeba TREATMENT ② Topical Antibiotics ③ Cycloplegics ④ Lubricants ⑤ Therapeutic Keratoplasty

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