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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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