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Ophthalmology
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Diseases of the Cornea

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Atul K Shankar

31

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ESSAY

Write in detail about the etiopathogenesis, clinical features,

diagnosis and treatment of Mycotic Corneal Ulcers.
ETIOPATHOGENESIS OF MYCOTIC CORNEAL ULCERS:

- Fungi
o classified as
 Filamentous fungi
 Aspergillus
 Fusarium
 Alternaria
 Cephalosporum
 Curvularia
 Penicillium
 Yeasts
 Candida
 Cryptococcus
 Dimorphic Fungi
 Histoplasma
 Coccidioides
 Blastomyces
- Modes of infections are
o Injury by vegetative material
 common sufferers are field workers especially during
harvesting seasons
o Injury by animal tail
o Secondary fungal ulcers in immunosuppressed systemically
or locally such as patients suffering from dry eye, herpetic
keratitis, bullous keratopathy or post-operative cases of
keratoplasty
- Role of Antibiotics and Steroids
o Antibiotics disturb the symbiosis between bacteria and fundi
o Steroids make the fungi facultative pathogens
o excessive use of these drugs predisposes the patients to fungal
infections

CLINICAL FEATURES:

- Symptoms
o similar to central bacterial corneal ulcers
o less marked than the equal sized bacterial ulcer
o overall course is slow and torpid
 - Signs
o Corneal ulcer is greyish white, dry looking with elevated rolled
out brownish
o Pigmented ulcer (brownish) is caused by some species of fungi
(dematiaceous fungi)
o Delicate feathery finger-like extensions
 present into the surrounding stroma under the intact
epithelium
o Sterile immune ring (yellow line of demarcation) may be present
where fungal antigen and host antibodies meet
o Multiple, small satellite lesions may be present around the ulcer
o Hypopon is present even if the ulcer is very small
o Endothelial plaque is located under the stromal lesions
 may be present in the absence of hypopon
o Perforation in mycotic ulcer is rare but can occur
o Corneal vascularisation is conspicuously absent in pure mycotic
ulcers

DIAGNOSIS

- Clinical Diagnosis
o Typical clinical manifestations with history of injury by vegetative
material are high suspicious of a mycotic corneal ulcer
o Chronic ulcer worsening should arouse suspicious of mycotic
involvement
o Confocal microscopic examination of cornea is reported to identify
actual fungi

- Laboratory investigations are required to identify the causative fungi

o Corneal scrapings is performed under topical anaesthesia,
and the following test should be performed:
 Examination of wet KOH mount preparation may reveal
filamentous fungi as branched, septate hyphae or non-
filamentous yeast like fungi
 Gram’s and Giemsa stained films may reveal fungal
hyphae and inflammatory cells
 Culture on Sabouraud’s Agar Medium should also be
performed for fungi
 Polymerase chain reaction is recommended for rapid
results
 Anterior chamber paracentesis may be carried out in
cases with intraocular extension
 Corneal biopsy is indicated in cases where repeated
cultures from scrapings are negative
TREATMENT OF MYCOTIC CORNEAL ULCERS:

- Definitive treatment
o Topical Anti-Fungal Eye Drops
 For filamentous fungi
 Natamycin 5%
 Amphotericin B (0.1-0.3%)
 Fluconazole 0.2%
 For yeasts
 Amphotericin B
 Nystatin
o Intracameral and Intracorneal administration of Voriconazole
o Systemic antifungal drugs are required for severe cases of deeper
fungal keratitis
 Fluconazole
 Ketoconazole
 Voriconazole
- Adjunctive Therapy
o Non-specific treatment and general measures are similar to that of
bacterial corneal ulcers
 Cyclopegic drugs
 Systemic analgesics and anti-inflammatory drugs
 Vitamins
- Therapeutic Penetrating Keratoplasty
o required for non-responsive cases
 Discuss in detail about the etiology, clinical features,
complications and treatment of Bacterial Corneal Ulcers
Etiology of Bacterial Corneal Ulcers

1) Corneal Epithelial Damage

o pre-requisite for most of the infecting organisms
o may occur in the following conditions
 Corneal abrasions
 Epithelial drying
 Necrosis of epithelium
 Epithelial damage due to tropic changes
o the pathogens that can produce ulceration are
 Neisseria gonorrhoeae
 Corynebacterium diphtheriae
 Neisseria meningitidis
 Haemophilus aegyptius
 Listeria species
2) Sources of Infection
o bacterial corneal infections arises from exogenous sources
 Conjunctivitis sac
 Lacrimal Sav
 Infectious foreign bodies
 Infected vegetative material
 Waterborne/Airborne infections
3) Causative Organisms
o Gram positive Cocci
 S. aureus
 S. epidermidis
 S. pneumoniae
o Gram negative cocci
 N. gonorrhoeae
 N. meningitidis
o Gram positive Bacilli
 C. diphtheria
 C. xerosis
 Bacillus cereus
 Listeria
 Clostridium
o Gram Negative Bacilli
 Pseudomonas
 Enterbacteriaceae (Klebsiella, Proteus, E.coli)
 Moraxella
 H.influenzae
o G-positive filamentous bacteria – Nocardia, Actinomyces
o Mycobacteria – NTB, M.tuberculosis
Pathology of Bacterial Corneal Ulcer

1) Stage of Progressive Infiltration

o characterised by infiltration of Polymorphonuclear and/or
lymphocytes into the epithelium from the peripheral circulation
supplemented by similar cells from the underlying stroma
o necrosis of the involved tissue may occur
2) Stage of Active Ulceration
o results from necrosis and sloughing of the epithelium,
Bowman’s membrane and involved stroma
o walls of the active ulcer projects into swelling of the lamellae by
the imbibition of fluid and the packing of masses of
leucocytes between them
o zone of infiltration extends to a considerable distance around and
under the ulcer
o sides and floor of the ulcer may show grey infiltration and
sloughing
3) Stage of Regression
o induced by natural host defence mechanisms and the
treatment
o line of demarcation develops around the ulcer
 consists of leucocytes that neutralize and phagocytose
the offending organisms and necrotic cellular debris
o digestion of necrotic material may result in initial enlargement of
the ulcer
o may be accompanied by superficial vascularisation that
increases the humoral and cellular immume reponse
o ulcer now begins to heal and epithelium grows over the edges
4) Stage of Cicatrization
o healing continues by progressive epithelisation
 forms a permanent covering
o fibrous tissue is laid down partly by the corneal fibroblasts and
partly by the endothelial cells of the new vessels
o stroma thickens and fills in under the epithelium,
 pushes the epithelial surface anteriorly
o degree of scarring from healing varies
 if ulcer is very superficial and involves epithelium only,
it heals without leaving any opacity behind
 when ulcer involves Bowman’s membrane, the resultant
scar is called a Nebula
 Macula and Leucoma result after healing of ulcers involving
up to 1/3 and more than that of corneal stroma
respectively
Clinical Features of Bacterial Corneal Ulcers

- Symptoms
o Pain and foreign body sensation
o Watering from the eye due to hyperlacrimation
o Photophobia
o Blurred vision
o Redness of eyes
- Signs
o Swelling of eyelids
o Blepharospasm
o Chemosed conjunctiva
o Conjunctival hyperaemia
o Ciliary congestion
o Anterior chambers may or may not show pus
o Iris is slightly muddy in colour
o Pupil is small due to associated toxin-induced iritis
o Intraocular pressure may sometimes be raised

Complications of Bacterial Corneal Ulcer

- Toxic iridocyclitis
o due to absorption of toxins in the anterior chamber
- Secondary Glaucoma
o occurs due to fibrinous exudates blocking the angle of
anterior chamber
- Descemetocoele
o ulcer herniates as a transparent vesicle
o sign of impending perforation
o usually associated with severe pain
- Perforation of corneal ulcer
o sudden strain due to cough, sneeze or spasm of orbicularis
muscle may convert the impending perforation into actual
perforation
o following perforation, pain is immediately decreased and
patient feels hot liquid (aqueous) coming out of eyes
o sequelae includes
 Prolapse of iris
 Subluxation or anterior dislocation of lens
 Anterior capsular cataract
 Corneal fistula
 Purulent uveitis
 Endophthalmitis
 Panophthalmitis
 Intraocular haemorrhage
- Corneal Scarring
Management of Bacterial Corneal Ulcer

- Clinical Evaluation
o Thorough history taking
o General physical examination
o Ocular Examination
 Diffuse light examination for gross lesions
 Regurgitation test and syringing to rule out lacrimal sac
infection
 Biomicroscopic examination
- Laboratory Investigations
o Routine laboratory investigations
o Microbiological investigations
 identifies the causative organism
- Treatment
o Definitive treatment
 Topical Antibiotics
 Fortified cefazoline
 Fortified tobramycin or fortified Vancomycin
 Systemic antibiotics
 cephalosporine and aminoglycoside is given in
fulminating cases with perforation or when sclera is
also involved
o Adjunctive/concurrent therapy
 Cycloplegic drugs
 1% Atropine eye drops
 2% Homatropine eye drops
 Systemic Analgesics and Anti-inflammtory Drugs
 Paracetamol
 Ibuprofen
 Vitamins A, B-complex and C
o Physical and General Measures
 Hot fomentation
 local application of heat gives comfort, reduces pain
and decreases oedema
 Dark goggles are used to prevent photophobia
 Rest, good diet and fresh air may have a soothing
effect
 Describe the etiopathogenesis, clinical features and
management of Hypopon Corneal Ulcers.
Etiopathogenesis of Hypopon Corneal Ulcers

- Causative Organism
o Pneumococcus
o Staphylococci
o Streptococci
o Gonococci
o Moraxella
o Pseudomonas
- Source of Infection
o source of infection for pneumococcal infection is usually the
chronic dacrocycstitis
o purulent keratitis with hypopon is almost always exogenous, due
to pyogenic organisms
- Factors pre-disposing to development of hypopon
o 2 main factors which predispose to development of hypopon with
corneal ulcer are virulence o the infecting organism and the
resistance of the tissues
o hypopon ulcers are much more common in old debilitated or
alcoholic subjects
- Mechanism of development of hypopon
o Corneal ulcer is often associated with some iritis owing to diffusion
of bacterial toxins
o when iritis is severe, outpouring of leucocytes from the vessels
the cells gravitate to the bottom of the anterior chamber to
form a hypopon

Clinical Features of Hypopon Corneal Ulcers

- Symptoms
o Pain and foreign body sensation
o Watering from the eye due to hyperlacrimation
o Photophobia
o Blurred vision
o Redness of eyes
- Signs
o Swelling of eyelids
o Blepharospasm
o Chemosed and hyperaemic conjunctiva
o Ciliary congestion
o Anterior chambers may or may not show pus
o Iris is slightly muddy in colour
o Pupil is small due to associated toxin-induced iritis
o Intraocular pressure may sometimes be raised
CHARACTERISTIC FEATURES OF ULCUS SERPENS

- Greyish-white or yellowish disc-shaped ulcer

- occurs near the centre of cornea
- ulcer has a tendency to creep over the cornea in a serpiginous
fashion
- violent iridocyclitis is associated with definite hypopon
- Hypopon increases in size very rapidly and often results in
secondary glaucoma
- Ulcer spreads rapidly and has tendency for early perforation

Management of Hypopon Corneal Ulcers

- Clinical Evaluation
o Thorough history taking
o General physical examination
o Ocular Examination
 Diffuse light examination for gross lesions
 Regurgitation test and syringing to rule out lacrimal sac
infection
 Biomicroscopic examination
- Laboratory Investigations
o Routine laboratory investigations
o Microbiological investigations
 identifies the causative organism
- Treatment
o Definitive treatment
 Topical Antibiotics
 Fortified cefazoline
 Fortified tobramycin or fortified Vancomycin
 Systemic antibiotics
 cephalosporine and aminoglycoside is given in
fulminating cases with perforation or when sclera is
also involved
o Adjunctive/concurrent therapy
 Cycloplegic drugs
 1% Atropine eye drops
 2% Homatropine eye drops
 Systemic Analgesics and Anti-inflammtory Drugs
 Paracetamol
 Ibuprofen
 Vitamins A, B-complex and C
o Physical and General Measures
 Hot fomentation
 Dark goggles
SHORT NOTES

Keratoconus
- progressive, non-inflammatory bilateral ecstatic condition of
cornea in its axial part
- it usually starts at puberty and progresses slowly

Etiopathogenesis:

- the etiology is still not clear

- various theories proposed includes
o Developmental condition
o Degenerative condition
o Hereditary dystrophy
o Endocrine anomaly

Clinical Features

- Symptoms
o defective vision, primarily due to progressive myopia and
irregular astigmatism
o vision becomes progressively more blurred and distorted with
associated glare, halos around lights, light sensitivity and
ocular irritation
o Vision loss occurs primarily from irregular astigmatism and
myopia, and secondarily from corneal scarring
- Signs
o Distorted window reflex
o Placido disc examination shows irregularity of the circles
o Slit-lamp examination shows thinning and ectasia of central
cornea, opacity at the apex, Fleischer’s ring at the base of
cone, and folds in Descemet’s and Bowman’s Membrane
o Positive Munson’s sign

Complications of Keratoconus

- Acute hydrops, due to rupture of Descemet’s membrane

o characterized by sudden development of corneal oedema
associated with marked defective vision, pain, photophobia
and Lacrimation

Treatment of Keratoconus

- Spectacle correction
- Contact lenses
- Intacs
- Corneal collagen cross-linking with riboflavin
- Keratoplasty
 Interstitial Keratitis
- denotes an inflammation of the corneal stroma without primary
involvement of the epithelium or endothelium
- it is a non-suppurative inflammation
- characterized by cellular infiltration of the corneal stroma

Etiology:

- inflammation may either be the direct result of infectious process or

secondary to an immunologic response to a specific foreign antigen
- this immunologic response may take the form of
o antigen-antibody complex deposition
o Complement mediated disease
o Delayed type hypersensitivity reaction
- Causes of interstitial keratitis
o Viral
 HSV, Herpes Zoster, EBV, Mumps, Measles
o Bacterial
 TB, Syphilis, Lyme disease, LGV, Leprosy
o Others
 Sarcoidosis, Onchocerciasis, Cogan syndrome,
Rheumatoid arthritis, Malaria

Clinical Features:

- Initial Progressive Stage

o begins with oedema of the endothelium and deeper stroma,
secondary to anterior uveitis
o there is associated pain, Lacrimation, photophobia,
Blepharospasm, and circumcorneal injection
- Florid Stage
o eye remains acutely inflamed
o deep vascularisation of cornea, consisting of radial bundle of
brush-like vessels develops
o they look a dull reddish pink, which is called salmon patch
appearance
o there is moderate degree of superficial vascularisation
- Stage of Regression
o resolves with the progressive appearance of vascular invasion
o clearing of cornea is slow and begins from periphery and
advances centrally
o leaves behind some opacities and ghost vessels

Treatment

- Local Treatment – topical corticosteroids, atropine, dark goggles

- Systemic treatment – penicillin, systemic steroids
 Keratoplasty and its indications
- also known as Corneal grafting, or corneal transplantation
- an operation in which the patient’s diseased cornea is replaced by
the healthy clear cornea

TYPES

- Autokeratoplasty
o Rotational keratoplasty
 patients own cornea is trephine and rotated to transfer the
papillary area, having a small corneal opacity to the
periphery
o Contralateral keratoplasty
 indicated when cornea of one eye is opaque and the other
eye is blind due to posterior segment disease
 cornea of 2 eyes are exchanged with each other
- Allografting or Allo-keratoplasty
o Penetrating keratoplasty
o Lamellar Keratoplasty
 Anterior Lamellar Keratoplasty
 Superficial Anterior Lamellar Keratoplasty
 Deep Anterior Lamellar Keratoplasty
 Posterior Lamellar Keratoplasty
o Small Patch Graft
 for small defects

INDICATIONS AFTER PENETRATING KERATOPLASTY

- Optical – to improve vision

o Corneal opacity, Bullous keratopathy, Corneal dystrophies,
advanced Keratoconus
- Therapeutic – to replace inflamed cornea not responding to conventional
therapy
- Tectonic Graft – to restore integrity of eyeball
o corneal perforation
o marked corneal thinning
- Cosmetic – to improve the appearance of the eye

INDICATIONS OF ENDOTHELIAL KERATOPLASTY

- Fuchs Endothelial Dystrophy

- Pseudophakic corneal oedema
- Posterior polymorphous dystrophy
- Aphakic corneal oedema
- Iridocorneal endothelium syndrome
- Failed corneal graft
 Herpes Zoster Ophthalmicus
- acute infection of Gasserian ganglion of the 5 th cranial nerve by
the Varicella-Zoster Virus
- constitutes approximately 10% of all cases of Herpes zoster
- occurs more commonly in immunocompromised individuals

ETIOLOGY

- Varicella Zoster Virus

o DNA virus that produces acidophilic intranuclear inclusion
bodies
o neurotropic in nature

PATHOGENESIS

- infection is contracted in childhood which manifests as chicken pox and

child develops immunity
- virus remains dormant in the sensory ganglion of trigeminal nerve
- in elderly people, virus reactivates, replicates and travels down one
of the branches of the ophthalmic division of the trigeminal nerve
o produces cutaneous and ocular lesions

CLINICAL FEATURES

- Acute Phase Lesions

o General features
 onset is sudden with fever, malaise, and severe neuralgic
pain
o Cutaneous lesions
 skins of eye lids become red and oedematous, followed
by vesicle formation
 vesicles convert to pustules which burst to become
crusting ulcers
o Ocular Lesions
 Conjunctivitis
 Zoster Keratitis
 Episcleritis and scleritis
 Iridocyclitis
 Acute retinal necrosis
 Secondary glaucoma
 Anterior Segment necrosis and phthisis bulbi
- Chronic Phase Lesions
o Post Herpetic Neuralgia
o Lid Lesions – Ptosis, trichiasis, entropion, notching
o Conjunctival Lesions – chronic mucous secreting conjunctivitis
o Corneal Lesions – neuroparalytic ulceration, exposure keratitis
o Scleritis and uveitis
TREATMENT

- Systemic Therapy
o Oral Antiviral Drugs
 Acyclovir
 Valaciclovir
o Analgesics
 Mephanemic acid and
Paracetamol/Pentazocin/Pethidine(severe cases)
o Systemic Steroids
o Cimetidine
o Amitriptyline

- Local Therapy for Skin Lesions

o Antibiotic-Corticosteroid Skin Ointment

- Local Therapy for Ocular Lesions

o For Zoster Keratitis, Iridocyclitis and Scleritis
 Topical Steroid Eye drops
 Cyclopegics – cyclopentolate
 Topical Acyclovir Eye Ointment
o To prevent secondary infections
 Topical Antibiotics
o For secondary glaucoma
 0.5% Timolol or 0.5% Betaxolol
 Acetazolamide
o For mucous plaques
 Topical Mucolytics – Acetyl Cysteine
o For Persistent Epithelial Defects
 Lubricating artificial tear drops
 Bandage soft contact lens

- Surgical Treatment
o Indicated for Neuroparalytic corneal ulcers only
 Lateral Tarsorrhaphy
 Amniotic membrane transplantation, or conjunctival
flap
 Tissue Adhesive for corneal perforation
 Keratoplasty
 Dendritic Ulcer
- typical and most common lesion of recurrent epithelial keratitis
- ulcer is of an irregular, zigzag linear branching shape
- branches are generally knobbed at the ends
- floor of the ulcer stains with fluorescein and the virus laden cells at
the margin take up rose Bengal
- there is associated marked diminution of corneal sensations
- Treatment:
o Definitive Treatment
 Antiviral drugs
 Acycloguanosine (Acyclovir)
 Ganciclovir
 Trifluorothymidine
 Adenine arabinoside (Vidarabine)
 Mechanical Debridement
 involved area is removed along with a rim of
surrounding healthy epithelium with the help of
sterile cotton applicator under magnification
 reserved for cases with non-compliance and those
allergic to antivirals
 Systemic Antiviral Drugs
 Acyclovir 400mg
 Famciclovir 250mg
 Valaciclovir 500mg

Mooren’s Ulcer
- severe inflammatory peripheral ulcerative keratitis
- Etiology
o not known
o most probably an autoimmune disease
- Clinical Features
o Benign
 unilateral, affects the elderly, relatively slow progression
o Virulent
 affects young African patients, rapid progression, high
incidence of sclera involvement
o Symptoms
 severe pain, photophobia, Lacrimation, defective vision
- Treatment
o Topical Corticosteroids
o Immunosuppressive therapy with systemic steroids
o Soft contact lenses
o Lamellar or full thickness corneal grafts
 Herpes Simplex Keratitis
- very common form of viral corneal ulcers
- constitutes herpetic keratoconjunctivitis and iritis

Etiology

- Causative Organism – Herpes Simplex Virus

- Mode of Infection
o HSV-1 infection
 acquired by kissing or coming in close contact with patient
suffering from herpes labialis
o HSV-2 infection
 transmitted to eyes or neonates through infected genitalia
of the mother

Clinical Features of Primary Herpes Simplex Keratitis

- Systemic Features
o mild fever, malaise and non-suppurative lymphadenopathy
- Skin lesions
o vesicular lesions on the skin of face, lips, lids, periorbital region
and lid margin
- Ocular lesions
o Acute Follicular Conjunctivitis with regional lymphadenitis
o Keratitis

Treatment

- Primary infection is usually self-limiting but virus travels up to the

trigeminal ganglion and establishes the latent infection
- treatment is recommended to limit corneal involvement
o topical Trifluridine or Vidarabine, or Oral Acyclovir
o Cycloplegic (atropine) is added for comfort of ciliary spasm
 Corneal Opacities
- loss of normal transparency of cornea
- used particularly for the lossof transparency due to scarring

Causes:

- Congenital Opacities (Mnemonic STUMPED)

o Sclerocornea
o Tear in Descemet’s membrane
o Ulcer
o Mucopolysaccharidosis, Mucolipidosis
o Posterior corneal defect, Peter’s anomaly, Posterior Keratoconus
o Endothelial dystrophy
o Dermoid
- Healed Corneal Wounds
- Healed corneal ulcers

Clinical Features

- loss of vision – when dense opacity covers the pupillary area

- blurred vision – due to astigmatic effect

Types

- Nebular corneal opacity

- Macular corneal opacity
- Leucomatous corneal opacity
- Adherent leucoma
- Corneal Facet
- Kerectasia
- Anterior staphyloma

Treatment

- Optical Iridectomy
o performed in cases of central macular or leucomatous
corneal opacities
- Phototherapeutic keratectomy
o with excimer laser is useful in superficial corneal opacities
- Keratoplasty in uncomplicated cases
- Cosmetic Coloured Contact lens
o for good cosmetic appearance in an eye with ugly scar