COMMON DISORDERS OF CORNEA

AND SCLERA

DR. FAIZUR RAHMAN

ASSOCIATE PROFESSOR
PESHAWAR MEDICAL COLLEGE

KERATITIS/CORNEAL ULCERS
Anatomical classification:
Superficial
Epithelial
Suppurative
Purulant keratitis
Hypopion ulcer

KERATITIS/CORNEAL ULCERS
Non-suppurative
Marginal ulcer
Moorens 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 ULCERScont.
Etiological classification:
Microbial
Bacterial
Viral
Fungal
Protozoal

KERATITIS/CORNEAL ULCERScont.
Non-infective
Keratitis associated with systemic disorders
Collagen vascular disorders
Rheumatoid arthritis
Systemic lupus erythamatosis
Wegners granulomatosis

KERATITIS/CORNEAL ULCERScont.
Neurotrophic
Cogans syndrome
Others
Hypersensitivity
Marginal ulcer
Phlyctenular ulcer
Autoimmune
Moorens ulcer
Other autoimmune diseases

KERATITIS/CORNEAL ULCERScont.
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 2030% 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, Listeriamonocytogenes, 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: 525 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 trimethoprimsulfamethoxazole 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

May enlarge to become geographic
Stains with fluorescein

Treatment
Aciclovir 3% ointment x 5 daily
Trifluorothymidine 1% drops 2-hourly
Debridement if non-compliant

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 KPs 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

Acute epithelial keratitis

Nummular 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
May become chronic

Treatment - topical steroids, if appropriate

Marginal keratitis

Hypersensitivity reaction to Staph. exotoxins

May be associated with Staph. blepharitis
Unilateral, transient but recurrent
Progression

Subepithelial infiltrate Circumferential spread Bridging vascularization

followed by resolution
separated by clear zone

Treatment - short course of topical steroids

Marginal keratitis

Hypersensitivity reaction to Staph. exotoxins

May be associated with Staph. blepharitis
Unilateral, transient but recurrent
Progression

Subepithelial infiltrate Circumferential spread Bridging vascularization

followed by resolution
separated by clear zone

Treatment - short course of topical steroids

Contact Lenses
Optical
Soft
Flexible
Hard
Therapeutic
Cosmetic

Indications
Optical
Refractive errors
Irregular astigmatismkeratoconus
Superficial corneal irregularitis
Therapeutic
Corneal diseases
Protection to cornea
Splintage

Indicationscont..
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
Decreases myopia by flattening cornea
Deep incisions from edge of optical zone to limbus

Main indications

Main complications

Stable myopia of up to 8D Accidental perforation

Otherwise normal cornea Intrastromal epithelial cysts

Technique of penetrating keratoplasty

Excision of donor tissue

a, b - Excision of host tissue

c - Fixation of donor tissue

Laser in-situ keratomileusis (LASIK)

Indications - similar to PRK but corrects higher degrees of myop

Technique

Complications

Thin flap of cornea fashioned

Wrinkles in flap

Bed treated with excimer laser

Cellular interface proliferation

Flap repositioned

Non-contact laser thermal keratoplasty

Indications
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

Normal

Episcleritis

Radial superficial episcleral

Maximal congestion
vessels
of episcleral vessels
Deep vascular plexus
adjacent to sclera

Scleritis

Maximal congestion of
deep vascular plexus
Slight congestion of
episcleral vessels

Simple episcleritis
Common, benign, self-limiting but frequently recurrent
Typically affects young adults
Seldom associated with a systemic disorder

Simple sectorial episcleritis

Simple diffuse episcleritis

Treatment
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

Deep scleral part of slit-beam

Localized nodule which can be moved over sclera
not displaced

Causes and Systemic Associations of Sclerit

1. Rheumatoid arthritis
2. Connective tissue disorders
Wegener granulomatosis
Polyteritis nodosa
Systemic lupus erythematosus

3. Miscellaneous
Relapsing polychondritis
Herpes zoster ophthalmicus
Surgically induced

Diffuse anterior non-necrotizing scleritis

Relatively benign - does not progress to necrosis
Widespread scleral and episcleral injection

Treatment
Oral NSAIDs
Oral steroids if unresponsive

Nodular anterior non-necrotizing scleritis

More serious than diffuse scleritis

On cursory examination resembles

nodular episcleritis

Scleral nodule cannot be moved over

underlying tissue

Treatment - similar to diffuse non-necrotizing scleritis

Anterior necrotizing scleritis with inflammat

Painful and most severe type

Complications - uveitis, keratitis, cataract and glaucoma
Progression

Avascular patches

Scleral necrosis and

visibility of uvea

Spread and coalescence

of necrosis

Treatment
Oral steroids
Immunosuppressive agents (cyclophosphamide, azathioprine, cyclosporin)
Combined intravenous steroids and cyclophosphamide if unresponsive

Anterior necrotizing scleritis with inflammation

(scleromalacia perforans)
Associated with rheumatoid arthritis
Asymptomatic and untreatable

Progressive scleral thinning with exposure of underlying uvea

Posterior scleritis
About 20% of all cases of scleritis
About 30% of patients have systemic disease
Treatment similar to necrotizing scleritis with inflammation

Signs

Proptosis and
ophthalmoplegia

Disc swelling

Ring choroidal
detachment

Choroidal folds

Exudative retinal
detachment

Subretinal exudation

Imaging in posterior scleritis

Ultrasound

Axial CT
a

a - Thickening of posterior sclera

b -Fluid in Tenon space (T
sign)

Posterior scleral thickening

Thank you