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COMMON DISORDERS OF CORNEA AND SCLERA
DR. FAIZUR RAHMANASSOCIATE PROFESSOR
PESHAWAR MEDICAL COLLEGE
KERATITIS/CORNEAL ULCERS
• Anatomical classification:
Superficial
Epithelial
Suppurative
Purulant keratitis
Hypopion ulcer
KERATITIS/CORNEAL ULCERS
Non-suppurative
Marginal ulcer
Mooren’s ulcer
Keratomalacia
Exposure keratitis
Neuroparalytic keratitis.
Anterior stromal
KERATITIS/CORNEAL ULCERS
Deep
Stromal
Interstitial keratitis (Syphilis)
Disciform keratitis (Virus)
Other microbial keratitis
Endothelial
KERATITIS/CORNEAL ULCERS—cont.
• Etiological classification:
Microbial
Bacterial
Viral
Fungal
Protozoal
KERATITIS/CORNEAL ULCERS—cont.
• Non-infective
Keratitis associated with systemic disorders
Collagen vascular disorders
Rheumatoid arthritis
Systemic lupus erythamatosis
Wegner’s granulomatosis
KERATITIS/CORNEAL ULCERS—cont.
• Neurotrophic
• Cogan’s syndrome
• Others
Hypersensitivity
Marginal ulcer
Phlyctenular ulcer
Autoimmune
Moorens ulcer
Other autoimmune diseases
KERATITIS/CORNEAL ULCERS—cont.
Neuroparalytic
Exposure of cornea
Tear film abnormalities
Chemical burns
Eyelid abnormalities
Lagophthalmos
Vit. A deficiency
Atheromatous ulcer
BACTERIAL CORNEAL ULCER
• ORGANISMS THAT CAN INVATE INTACT CORNEAL EPITHELIUM
1. Neiseria gonorrhoea and Neisseria
meningetides
2. Corynbacterium diphtheriae
3. Haemophylis influenzea
• OTHERS
CORNEAL ULCER
• It is a break in corneal epithelium with
underlying stromal necrosis.
• Corneal ulcerations accounts for 20—30% of all
blindness in developing world.
• Infective corneal disease is the leading cause of
this problem in South Asia.
Pathogenesis
Two main agents:
• Microbial infections.
• Immunologic conditions.
• Microbial pathogens causes corneal damage
directly or release of toxins and enzymes.
• Activation of Immune mechanism:
Antigens initiate the response with B and T lymphocytes.
• That will proceed inflammatory reaction.
Stages of corneal ulceration
• Progressive stage.
Regressive stage.
Healing stage.
BACTERIAL CORNEAL ULCER
• Cornea is equipped with two layers of mucous substances: Glycocalyx, Mucous layer.
• Inhabited bacteria of lid margins: Staphylococcus sp, Bacillus and Corynbacterium sp.
• Staphylococcus aureus --- Alpha, beta, gamma, delta, exfoliative, leukocidin and enterotoxin.
• Alpha toxin acts on cell membrane.
• Beta toxin --- RBC, Leucocytes, macrophages.
• Streptococcus pneumaniae produces a hemolytic agent.
• Pseudomonas produces a unique toxin known as exotoxin A.
Etiologic factors
• Gram +ve Cocci: Staphylococci, Streptococci.
• Gram +ve Bacilli : Corynbacterium, Listeria-
monocytogenes, Actinomyces sp.
• Gram-ve Cocci: Neisseria gonorrhea.
• Gram-ve Bacilli: Pseudomonas sp, Proteus sp,
Brucella, E. Coli.
• Mycobacteria: M. Tuberculosis, M. Leprae.
Clinical Features
• Pain, conjuntival inj, photophobia and decrease vision.
• Dense focal infiltrate, Stromal oedema, Striae near the infiltrate margins.
• Limbal, Corneoscleral and conjunctival hyperemic area with mucopurulent exudate.
• Products of infection on the surface of the ulcer, AC cells, flare, fibrous exudates and hypopyon.
• Rarely organisms are capable of passing through Descemet Membrane.
FUNGAL CORNEAL ULCER
• It represents 1-30 % of corneal infections in reported clinical cases.
• Frank fungal ulcers i-e epithelium, bowman and stoma are ulcerated.
• Stromal invasions: it often extends beyond the apparent clinical ulcer.
• Present in deep stroma.
• Elaborates proteases and toxins.
• Candida species produce proteolytic enzymes and lipase.
Etiologic factors
• Truama to cornea with plant or vegetable.
• Most common fungi--- Septate, Filamentous
fungi.
• Rarely ---- Non-septate fungi.
• Filamentous fungi: Fusarium sp, Aspergillus
sp.
• Yeast and Yeast like fungi: Candida sp,
Cryprtococcus sp.
Clinical features
• Filamentous fungal keratitis : It occurs in previously
healthy individuals with no pre-existing eye disease.
• It frequently manifest as gray-white, dry appearing
infiltrate that has delicate filamentous or feathery
edge.
• Multifocal or satellite infiltrates.
• Endothelial plaque and hypopyon.
• Dematiaceous fungi can cause brown or black
discolorations of ulcer surface.
ACANTHAMOEBA CORNEAL ULCER
• Free living protozoa.
• Habitat resistant to: Freezing, dessication, levels of
clorination in municipal water supplies, swimming
pools and hot tubs.
• Pathogenesis: With or without minor trauma
followed by organism inoculation.
• Pre-existing conjunctival flora do not support the
growth of numerous Acanthamoeba.
Etiology & risk factors
• Direct contact.
• Water contamination, Trauma.
• Insect, paint thinner, glass dust, wind blown
contamination, hot tub use, salt water diving etc.
• Contact lens wear.
• Extended and daily wear hydrogel contact lens, gas
permeable and hard contact lens.
• Cultures obtained from soft contact lenses, saline
solution, distal water and solution in soft contact
lenses.
Clinical Features
• Symptoms: Severe ocular pain, photophobia, blurred vision.
• Early signs: Limbitis, small patchy anterior stromal infiltrates, perineal infiltrates, radial keratoneuritis (decrease corneal sensations), mild punctuate keratitis. Central or paracentral ring abscess. Hypopyon Small white satellite lesions.
• Late signs: Stromal opacification, scleritis, descematocele.
INTERSTITIAL KERATITIS
• IK is an inflammation of the corneal stroma
with no primary involvement of the
epithelium or endothelium.
• Causes:
Congenital syphilis, Cogan syndrome.
• LUETIC INTERSITITIAL KERATITIS:
• Presentation: 5—25 yrs.
• Pain, blurring of vision.
• Signs: Salmon patch with corneal clouding.
• Untreated ------ Nonperfused ---- Ghost vessels---- Re- inflamed
--- Refill---- Stromal bleed.
• Healing stage: Stromal thinning.
• Inactive stage: Deep stromal scar, Ghost vessels.
• COGAN SYNDROME:
• Presentation: Middle age with acute tinitis,
vertigo, deafness.
• Keratitis: Anterior stromal infiltrate.
Diagnosis of ulcer
• Collection and processing of corneal scrapings:
- Direct visualization, slit lamp or operating microscope.
- Loose debris cleaned with sterile cotton swab.
- Edge of blade should not touch the lid margin or conj.
• Multiple scrapings are taken.
• Linear shaped or C- shaped inoculations are made at multiple sites in agar.
• For preparation of KOH mount corneal scraping is Ist transferred to slide.
• 1-2 drops of 10% KOH containing 0.1% glycerol.
Treatment- Bacterial
• Initial treatment: Broad spectrum topical
antibiotics.
• Dual therapy: Aminoglycoside & cephalosporin.
• Mono therapy: Fluoroquinolone.
• Oral antibiotics:
• Atropine.
• Steroid therapy: ?
• Systemic analgesics:
Treatment - Bacterial
• Choosing the appropriate antibacterial
treatment.
• Gram Positive Cocci: 1st generation
Cephalosporins such as Cephazolin & 3rd
generation Cephalosporins.
• Gram Negative Cocci: Benzyl Penicillin,
Chloramphenicol or Ampicillin for Heamophilus.
Treatment - Bacterial
• Gram Positive Rods: Penicillin G, Topical trimethoprim-
sulfamethoxazole for nocardia.
• Gram Negative Rods: Gentamycin & Tobramycin.
• Acid Fast Bacilli:
Amikacin Sulphate.
• No Organism Identified:
Topical fortified Gentamycin & Cephazoline.
Treatment - Bacterial
Causes of failure:
• Wrong diagnosis.
• Incorrect treatment.
• Drug toxicity.
Treatment- Fungal
• Polyenes:
Natamycin 5%: Filamentous fungi. Amphotericin B: Filamentous fungi.
• Imidazole:
Miconazole 1%: Candida, Aspergillus.
Systemic: Itraconazole, Ketoconazole.
• Pyramidine:
Flucytosine 1%: Candida.
Treatment- Acanthamoeba
• Topical:
Propamidine Isothionate 0.1% (Brolene), Dibromopropamidine Isothionate 0.15%, Miconazole 1%.
• Systemic:
Ketoconazole.
Surgical management of corneal ulceration
• When pharmacological approaches are not
effective: Conjunctival Flap or keratoplasty.
• Extensive scarring & stromal destruction:
Total conjunctival flap.
• Peripheral area: Partial conjunctival flap.
• Keratoplasty when the inflammation settles.
Herpes Simplex Keratitis
• HSV is a DNA virus.
• HSV-I infection above waist.
• HSV-II infection below waist.
• Primary infection in childhood - droplet transmission.
• Recurrent disease – sensory nerve ganglion.
Herpes simplex epithelial keratitis
• Dendritic ulcer with terminal bulbs
• Stains with fluorescein
• May enlarge to become geographic
• Aciclovir 3% ointment x 5 daily
• Trifluorothymidine 1% drops 2-hourly
• Debridement if non-compliant
Treatment
Herpes simplex stromal necrotic keratitis
• Active viral invasion and tissue necrosis.
• Impairment of vision, discomfort and pain.
• Cheesy and necrotic stroma or opacification.
• Associated anterior uveitis with KP’s and active stromal infiltration.
• Scarring, vascularization, lipid keratopathy and perforation.
• Antiviral, antibiotics combined with steroids?
Herpes Zoster Ophthalmicus
• Varicella zoster virus - DNA.
• Chicken pox, shingles.
• Sensory root ganglion.
Ocular damage:
• Direct viral invasion – epithelial keratitis and conjunctivitis.
• Secondary inflammation, occlusive vasculitis and alteration in autoimmune – stromal keratitis, uveitis, scleritis and episcleritis.
• Hypoaesthesia – neurotrophic keratitis.
Risk of ocular involvement
• Herpes zoster ophthalmicus – 15%.
• Hutchinson sign: External nasal N – Nasociliary N – Ophthalmic division of V nerve.
• Age.
• AIDS.
Herpes zoster keratitis
• Develops in about 50% within 2 days of rash
• Small, fine, dendritic or stellate epithelial lesions
• Tapered ends without bulbs
• Resolves within a few days
• Develops in about 30% within 10 days of rash
• Multiple, fine, granular deposits just beneath Bowman membrane
• Halo of stromal haze
Nummular keratitisAcute epithelial keratitis
• May become chronic
Treatment - topical steroids, if appropriate
Marginal keratitis
Subepithelial infiltrate separated by clear zone
Circumferential spread Bridging vascularization followed by resolution
• Hypersensitivity reaction to Staph. exotoxins
• May be associated with Staph. blepharitis
• Unilateral, transient but recurrent
Progression
Treatment - short course of topical steroids
Marginal keratitis
Subepithelial infiltrate separated by clear zone
Circumferential spread Bridging vascularization followed by resolution
• Hypersensitivity reaction to Staph. exotoxins
• May be associated with Staph. blepharitis
• Unilateral, transient but recurrent
Progression
Treatment - short course of topical steroids
Contact Lenses
• Optical
Soft
Flexible
Hard
• Therapeutic
• Cosmetic
Indications
• Optical
Refractive errors
Irregular astigmatism—keratoconus
Superficial corneal irregularitis
• Therapeutic
Corneal diseases
Protection to cornea
Splintage
Indications—cont..
• Cosmetic – Anridia
– Corneal opacity
– Showbiz
• Diagnostic
Fundoscopy
Gonioscopy
ERG
Coplications.
• Allergic conjunctivitis
• Giant papillary conjunctivitis
• Superior limbic KC
• Corneal epithelial edema
• Corneal vascularization
• Sterile corneal infilterates
• Infections
• Warping
Keratoplasty.
• Full thickness
• Partial thickness
Superficial lamellar
Deep lamellar
Corneal refractive surgery
• Radial keratotomy
• PRK
• LASIK
• LASEK
• Laser thermal keratoplasty
• Keratoprosthesis
Radial keratotomy
Main indications
• Stable myopia of up to 8D
• Otherwise normal cornea
• Accidental perforation
• Intrastromal epithelial cysts
Main complications
• Decreases myopia by flattening cornea
• Deep incisions from edge of optical zone to limbus
Technique of penetrating keratoplasty
Excision of donor tissuea, b - Excision of host tissue
c - Fixation of donor tissue
Laser in-situ keratomileusis (LASIK)Indications - similar to PRK but corrects higher degrees of myopia
• Thin flap of cornea fashioned
• Bed treated with excimer laser
• Flap repositioned
Complications
• Wrinkles in flap
• Cellular interface proliferation
Technique
Non-contact laser thermal keratoplastyIndications• Patients over 40 years with hypermetropia up to 2D• Following overcorrection of myopia
• Corneal curvature is steepened by application of laser heat to stroma
• Holmium laser spots applied to mid-cornea
EPISCLERITIS AND SCLERITIS
1. Episcleritis
• Simple• Nodular
2. Anterior scleritis
• Non-necrotizing diffuse
• Non-necrotizing nodular
• Necrotizing with inflammation
• Necrotizing without inflammation
( scleromalacia perforans )
3. Posterior scleritis
Applied anatomy of vascular coats
Scleritis
• Maximal congestion of deep vascular plexus
• Slight congestion of episcleral vessels
• Maximal congestion of episcleral vessels
EpiscleritisNormal
• Radial superficial episcleralvessels
• Deep vascular plexus adjacent to sclera
Simple episcleritis
• Common, benign, self-limiting but frequently recurrent
• Typically affects young adults
Treatment
• Seldom associated with a systemic disorder
Simple sectorial episcleritis Simple diffuse episcleritis
• Topical steroids
• Systemic flurbiprofen ( 00 mg tid if unresponsive
Nodular episcleritis• Less common than simple episcleritis
• May take longer to resolve
• Treatment - similar to simple episcleritis
Localized nodule which can be moved over scleraDeep scleral part of slit-beam not displaced
Causes and Systemic Associations of Scleritis
1. Rheumatoid arthritis
• Wegener granulomatosis
• Polyteritis nodosa
• Systemic lupus erythematosus
2. Connective tissue disorders
3. Miscellaneous
• Relapsing polychondritis• Herpes zoster ophthalmicus• Surgically induced
Diffuse anterior non-necrotizing scleritis
• Widespread scleral and episcleral injection
• Relatively benign - does not progress to necrosis
• Oral steroids if unresponsive
Treatment
• Oral NSAIDs
Nodular anterior non-necrotizing scleritis
Scleral nodule cannot be moved over underlying tissue
More serious than diffuse scleritis
On cursory examination resembles nodular episcleritis
Treatment - similar to diffuse non-necrotizing scleritis
Anterior necrotizing scleritis with inflammation
Progression
• Painful and most severe type
• Complications - uveitis, keratitis, cataract and glaucoma
Treatment • Oral steroids
• Immunosuppressive agents (cyclophosphamide, azathioprine, cyclosporin)
• Combined intravenous steroids and cyclophosphamide if unresponsive
Scleral necrosis and visibility of uvea
Spread and coalescence of necrosis
Avascular patches
• Asymptomatic and untreatable
• Associated with rheumatoid arthritis
Progressive scleral thinning with exposure of underlying uvea
Anterior necrotizing scleritis with inflammation(scleromalacia perforans)
Posterior scleritis
Signs
• About 20% of all cases of scleritis• About 30% of patients have systemic disease• Treatment similar to necrotizing scleritis with inflammation
Choroidal folds Subretinal exudation
Proptosis and ophthalmoplegia
Disc swelling Exudative retinal detachment
Ring choroidal detachment
Imaging in posterior scleritis
Ultrasound
a - Thickening of posterior sclera
b -Fluid in Tenon space (‘T’ sign)
Axial CT
Posterior scleral thickening
a
b
a
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