UNIVERSITY OF GONDAR,COLLEGE OF MEDICINE AND HEALTH SCIENCE

DEPARTMENT OF OPTOMETRY

Infectious and inflammatory corneal disease

BY: Mohammed S.

1
OUTLINE
 Introduction
 Bacterial keratitis

 Viral keratitis

 Fungal keratitis

 Protozoal keratitis

 Non-infectious inflammatory corneal disease

2
OBJECTIVES
 After
the end of this seminar session , all of us will:-
Diagnose different types of keratitis
Differentiate infectious from non infectious keratitis

Manage different types of keratitis

3
INTRODUCTION
 The cornea is a transparent, avascular tissue that measures 11-
12 mm horizontally and 10-ll mm vertically.
 Its refractive index (1.376)

 Anterior radius of curvature =7.8 mm.

 Posterior radius of curvature=6.5mm

 Contributes 74%, or 43.25 diopters (D), of the total dioptric
power

 Major source of astigmatism in the optical system.

4
CONT…
 Microscopically, the cornea consists of five layers
The epithelium

Bowman's layer (membrane)

The stroma

Descemet's membrane

The endothelium. 5
EPITHELIUM
Consists of five layers of cells .

Total thickness(50 to 60 µm.)

The superficial cells are flattened, nucleated, non

keratinized squamous cells, and the deepest cells
are columnar.

Metabolize glucose both aerobically and

anaerobically 6
BOWMAN'S LAYER
 Itis acellular lies immediately beneath the
basement membrane

 Consists of interwoven collage fibrils embedded

in intercellular substances.

 It measures about 8 to 12 µm in thickness.

7
STROMA
 Contributes 90 % of the corneal thickness

 Consists of many lamellae of collagen fibrils (type I)

that run parallel with the surface

 Among the lamellae ,are present

keratocytes,macrophages, histiocytes and a few
leucocytes.

8
CORNEAL ENDOTHELIUM
 Hexagonal non generable flattened cells(single layer)

 Theadult cell density(2500 cells/mm2). Decreases

with age (0.6% /year)
 At a cell density 500 cells/mm2 =corneal oedema

 Controls the normal hydration of the cornea

 Maintain the stroma in deturgesced state (78% water

content). 9
NERVE SUPPLY &NUTRIENTS
 Source:long ciliary nerves
 Devoid of a Schwann cell sheath

 Sensitivity(100 × of the conjunctiva)

 Nutrient: aqueous and limbal Vasculature

 Source of oxygen : air & limbal vasculature

 Central cornea =from air dissolved in tear

 Peripheral cornea=limbal vasculature

10
DEFENCE MECHANISMS
 The eyelid forms the physical barrier
 Eyelid blinking sweeps away debris

 The corneal and conjunctival epithelial cells act as a barrier to microbial invasion

 Tear turnover dilutes and removes microbes

 Tears also contain immunoactive substances such as

Lysozyme =degrades bacterial cell walls

Lactoferrin= inhibits bacterial metabolism

 Immunoglobulins=mediate antigen specific immunity

 Meibomian gland derived lipids=reduce evaporation
 Mucin=inhibits attachment of microbes
11
DETERMINANTS FOR CORNEAL
TRANSPARENCY
 Avascularity
 Devoid of nerve sheath

 Regular lattice arrangement of collagen fibrils

 Devoid of melanocytes of cells

 Relative state of dehydration(deturgesced)

12
CONT…
Therefore ,cornea should be evaluated in terms of
 Refractivity

 Reflectivity(lustrous)

 Shape(VKS)

 Thickness

 Curvature

 Clarity

 Vascularity

 Sensitivity (by cotton or Esthesiometry)

 Stain ability (fluorescein or rose bengal )

 Cellular size, density and distribution(specular

13
microscopy)
 Inflammation of the cornea (keratitis) is characterized by
KERATITIS

corneal oedema, cellular infiltration and ciliary congestion

 Based on etiology, it can be broadly classified into:

 Infectious keratitis
 Bacterial keratitis
 Viral keratitis

 Fungal keratitis

 Protozoal keratitis

 Chlamydial

 Spirochaetal

14
CONT…
 Non-infectious keratitis(immunological response)
 Associated with
 Local and systemic immune mediated disease
 Nutrition

 Diseases of skin
 Local & systemic infections

 Trauma
 Lacrimal

 Mechanical
 Idiopathic 15
TOPOGRAPHICAL (MORPHOLOGICAL) CLASSIFICATION

 Ulcerative keratitis (corneal ulcer)

 It can be further classified based on:
 Location: central & peripheral
 Purulence: purulent & non purulent)
 Association of hypopyon (with & without )
 Depth of ulcer (superficial,deep,with impending
perforation & perforated corneal ulcer)
 Slough formation(sloughing & non sloughing)

 Non –ulcerative keratitis

 Superficial
 Deep (suppurative and non-suppurative)

16
 GENERAL SIGNS OF CORNEAL INFLAMMATION

Superficial lesions Deep lesions

 Punctate epithelial erosions  Stromal infiltrates
 Punctate epithelial keratitis  Stromal edema

 Subepithelial infiltrates  Deep vascularization

 Filaments  Ulceration

 Epithelial edema  Lipid deposition

 Superficial neovascularization  Folds in Descemet membrane

 Descemetocele
 Pannus
 Breaks in Descemet membrane

 Aqueous leakage(Seidel test)

17
CONT…
Overall, such inflammatory signs end up with corneal opacity
Based on the involved layer and visualization of the posterior
segment, any opacity can be categorized as:

 Facet
 Nebular

 Macular

 Leucoma

 Adherent Leucoma cornea

 Kerectasia

 Anterior staphyloma

18
FACET
 A small superficial spot seen by focal illumination as a
distortion of corneal reflex

 Not visible with naked eye

 No scar tissue rather edematous epithelial cells

 No obscuration of posterior segment

19
NEBULAR
 Slight ,diffuse ,cloudlike opacity with indistinct borders
 Scar tissue is found in the superficial stroma

 Examined by sclerotic scatter illumination

20
MACULAR
 
 Moderately dense ,it involves the anterior of
corneal stroma

 It has circumscribed border

 Obscure visualization of posterior segment

21
LEUCOMA
 A white ,opaque scar involves >1/2 of the thickness of
the stroma

 Obscures the visualization of the posterior segment

 Involves large area of the cornea

22
ADHERENT LEUCOMA

 It results when healing occurs after perforation of cornea

with incarceration of iris

 Kerectasia:

 In this condition corneal curvature is increased at the

site of opacity (bulge due to weak scar).

23
ANTERIOR STAPHYLOMA
 An ectasia of psuedocornea (the scar formed from
organized exudates and fibrous tissue covered with
epithelium) which results after total sloughing of cornea,
with iris plastered behind it

24
25
PRINCIPLES OF TREATMENT
 Control of infection and inflammation
 Promotion of epithelial healing
 Reduction of exposure
 Lubrication with artificial tears
 Bandage soft contact lenses
 Surgical eyelid closure
 Amniotic membrane patch grafting
 Tissue adhesive
 Limbal stem cell transplantation

 Optical iridectomy (central macular or leucomatous corneal

opacities)
 Keratoplasty 26
INFECTIOUS KERATITIS

 Definition
 Etiology

 Risk factors

 Pathogenesis

 Classification

 Clinical presentation

 Complication

 Diagnosis

 Management

27
BACTERIAL KERATITIS
 Corneal disease caused by bacterial organisms

 Leading cause of monocular blindness in the developing

world.

 In this environment, corneal infections often follow trauma,

but they also contribute significantly to corneal blindness
associated with trachoma and xerophthalmia.

28
ETIOLOGY
 Sources of infection
 Exogenous(most common)
 From adjacent ocular tissue
 Endogenous(rare)

29
CAUSATIVE ORGANISMS

30
CONT…
 Common predisposing factors:
 Contact lens wear

 Trauma

 Contaminated ocular medication

 Ocular surface disease

 Local or systemic immunosuppression

 DM

 Malnutrition

31
CONT…
 Even if the majority of bacterial spp can cause keratitis in
compromised corneal epithelium, a few organisms can
penetrate an intact epithelium such as

 Corynebacteriumdiphtheriae
 Haemophilus aegyptius

 Neisseria
gonorrhoeae
 N. meningitidis

 Shigella
 Listeria species
32
PATHOGENESIS

 First (Adhesion and proliferation )

 Stage 1:progressive infiltration

 Stage 2: active ulceration

 Perforation
 Stage 3: regression
 Vascularization
 Phagocytosis

 Stage 4: cicatrization

33
CLASSIFICATION
 Broadly bacterial corneal ulcers may manifest as:

 Purulent corneal ulcer without hypopyon

 Hypopyon corneal ulcer (diffusion of bacterial toxins)

34
CLINICAL PRESENTATION

Symptoms
Rapid onset of pain

Redness

Photophobia

Tearing

Decreased vision 35
 C/F
 Chemosis

 Eyelidswelling
 Mucopurulent or purulent discharge

 Corneal ulcer
 Usually starts as an epithelial defect associated with
greyish-white circumscribed infiltrate

 Soon the epithelial defect and infiltrate enlarges &

Stromal oedema develops

36
CONT..
 Typical features of bacterial ulcer
 Yellowish-whiteoval or irregular in shape
 Swollen and over hanging margins

 Covered by necrotic material.(floor)

 Stromal oedema surrounding the ulcer area.

37
C/F
 Folds in Descemet membrane
 Anterior uveitis

 Hypopyon (often)

 Descemetocele formation and perforation due to severe

ulceration

 Endophthalmitis

 Scarring, vascularization and opacification

38
Bacterial keratitis. (A) Epithelial defect with infiltration; (B) enlargement 39
of the infiltrate; (C) hypopyon; (D) advanced disease; (E) perforation
associated with Pseudomonas infection
COMPLICATION
 Toxic Iridocyclitis

 Secondary glaucoma

 Descemetocele

 Perforation
 Prolapse of iris
 Subluxation or anterior dislocation of lens

 Anterior capsular cataract

 Corneal fistula

 Endophthalmitis

40
 Scaring
DIAGNOSIS
 Clinical
 Lab investigation
 Gram stain and Giemsa
 Culture

41
TREATMENT
 Depends on the severity of the ulcer

 Treatment for uncomplicated ulcer

 Empirical Duotherapy
 Fortified ceftriaxone or Cefuroxime 50mg/ml and Gentamicin
15mg/ml Q1H for 24–48 hours, and then is tapered according to
clinical progress

 Empirical Monotherapy (substitution)

 Fluoroquinolone( Ciprofloxacin (0.3%) eye drops, or Ofloxacin
(0.3%) eye drops, or Gatifloxacin (0.3%) eye drops)

42
43
44
CONT…
 Cycloplegics (cyclopentolate 1%, homatropine 2% or
atropine 1%) are used to prevent the formation of
posterior synechiae and to reduce pain

 Systemic antibiotics (if there is scleral involvement,

Severe corneal thinning and Potential for systemic
involvement)

 Ciprofloxacin for its antibacterial activity and

tetracycline (e.g. doxycycline 100 mg b.d.) for its
anticollagenase effect

45
CONT..
 Treatment of non-healing corneal ulcer
 Removal of any known cause of non-healing ulcer
 Mechanical debridement of ulcer
 Bandage soft contact lens

46
COMMON CAUSES OF NON-HEALING
ULCERS

Local cause: Systemic causes:

 Raised IOP  Diabetes mellitus

 Concretions  Severe anaemia

 Misdirected cilia  Malnutrition

 Impacted foreign body  Systemic steroids

 Dacryocystitis

 Inadequate therapy

 Wrong diagnosis

 Lagophthalmos
47
CONT...
 Treatment of corneal ulcer with impending
perforation & perforated cornea ulcer
 Avoid strain.

 Conjunctival flap

 Bandage soft contact lens

 Lowering of intraocular pressure

 Penetrating keratoplasty

48
VIRAL KERATITIS
 Etiology
 Herpes simplex
 Varicella –zosters
 Adenovirus

49
HERPES SIMPLEX KERATITIS
 Primary HSV-1 infection is asymptomatic or not recognized
more than 90 percent of the time .

 Most clinical ocular infections are manifestations of recurrent

disease; ocular involvement occurs in less than 5 percent of
primary infections .

 The majority of ophthalmic cases are unilateral, with

recurrences affecting the same eye.

50
FACTORS FOR REACTIVATION/RECURRENCE/
 Fever such as malaria, flu
 Exposure to ultraviolet rays

 General ill- health

 Emotional or physical stress

 Mild trauma

 Menstrual stress

 Following administration of topical or systemic steroids

and immunosuppressive agents

51
PATHOGENESIS
 Involves three processes:

 The active infection itself (Viral replication and Invasion of

nervous system)

 Inflammation caused by active infection

 Immune reaction to past infection

 Resulting structural changes in the cornea can lead to

additional forms of keratitis. 52
CLASSIFICATION
 Herpetic epithelial keratitis
 Punctate
 Dendritic
 Geographic
 Trophic keratitis (meta-herpetic)
 Stromal/Endothelial Keratitis
 Endotheliitis
 Localized endotheliitis /Disciform keratitis/
 Diffuse and linear endotheliitis

 Immune stromal keratitis /Interstitial keratitis/

 Necrotized keratitis
 Keratouveitis

53
C/F OF EPITHELIAL KERATITIS
 Symptoms :
Foreign-body sensation
Light sensitivity

Redness

Blurred vision

54
C/F OF EPITHELIAL KERATITIS
 PEK
 PEK coalesce into dendritic epithelial ulcers with
terminal bulbs(bulbous thickenings) at the end of each
branch.

 Swollen cornea epithelium at the edge of a herpetic

ulcer stains with rose Bengal and the bed of the ulcer
stains with fluorescein.

 Dendritic ulcer coalesce further and enlarge into a more

expansive geographic epithelial ulcer.

55
CONT…
 Ciliary flush and mild conjunctival injection.
 Mild stromal edema

 Subepithelial cellular infiltration

 Focal or diffuse reduction in corneal sensation

56
METAHERPETIC (TROPHIC) ULCER
 Not associated with live virus and results from inability of
the epithelium to heal.

 Usually caused by drug toxicity

 The border of the ulcer is grayish, elevated, and consist of

multiple layers of epithelium.

 Reverse staining in contrast to geographic ulcers,

57
Fluorescein staining of herpetic dendritic keratitis 58
Herpetic geographic epithelial keratitis

59
HERPETIC DISCIFORM KERATITIS

Characterized
 by:
Focal
 disc shaped epithelial& stromal edema in a round or oval
distribution without necrosis

KP &
 raised IOP associated with Iridocyclitis
Folds in descement membrane in severe cases


Reduced vision & corneal sensation



Ring
 of stromal infiltrates due to antigen –antibody complexes
(wessely ring)
Sometimes epithelial lesions may be associated with disciform keratitis
.

60
.
 61
Disciform herpes simplex keratitis. (A) Central
epithelial and stromal oedema; (B) underlying keratic
precipitates
; (C) Wessely ring precipitates

62
IMMUNE STROMAL KERATITIS/IK/

 This manifests as focal, multifocal, or diffuse stromal opacities

or an immune ring.

 Often accompanied by stromal edema and a mild anterior

chamber reaction.

 The epithelium and endothelium are relatively spared.

 Unlike syphilitic IK, HSV neovascularization is usually

sectoral and leads to a stromal scar.

63
Ring ulcer 64
NECROTIZING KERATITIS
 Characterized by:
 Ulcer involving epithelial and stromal layer

 Stromal infiltrates

 The edges of the epithelial ulcer do not stain with rose Bengal dye.

 Corneal stromal vascularization

 Keratic precipitates

 Anterior chamber reaction

 Hypopyon or hyphema

 Corneal perforation 65
66
KERATOUVEITIS
 Usually granulomatous with large “mutton-fat” keratic
precipitates on the endothelium .

 Usually immune-mediated

 It can lead to significant morbidity from synechiae,

cataracts, and glaucoma.

 Unilateral uveitis associated with high intraocular pressure is

almost always caused by HSV.

67
Keratouveitis. 68
 COMPLICATIONS

 Metaherpetic ulcer
 Neuroparalytic ulcer

 Secondary infection.

 Glaucoma

 Cataract

 Iris atrophy secondary to keratouveitis.

69
 TREATMENT
Herpetic
 epithelial keratitis

Approximately
 50% of cases, resolves spontaneously

Treatment
 is necessary for ulcers larger than 4 mm, marginal ulcers, and
ulcers with underlying stromal inflammation

Acyclovir
 3% ointment 5× /day for 7-10 days
Topical trifluridine 1% soln 8×/ daily


Topical
 ganciclovir 0.15% gel (Zirgan) one drop 5× daily and then 3× daily
for one week.

Oral
 acyclovir, 400 mg 5× daily, is equivalent to topical treatment and avoids
corneal epithelial toxicity
70
CONT…
 Topical corticosteroids are contraindicated in the
presence of active herpetic epithelial keratitis

 However for patient who are using systemic

corticosteroids for other indications should be treated
aggressively with systemic antiviral therapy.

71
CONT…
Stromal keratitis
 1% prednisolone drops every 2 hours and then tapered every
1-2 weeks

 Prophylactic oral antiviral drug (Acyclovir 400 mg PO bid

or valacyclovir 500 mg PO once a day)

 When disciform keratitis is present with an infected epithelial

ulcer, antiviral drugs should be started 5-7 days before the
steroids.

72
KERATOPLASTY

 Penetrating keratoplasty (PK) is indicated in selected patients

with visually significant stromal scarring and astigmatism not
correctable by spectacle or contact lens
 Prophylactic antiviral and steroids are mandatory before and
after the surgery

73
HERPES ZOSTER OPHTHALMICUS

 It is an acute infection of Gasserian ganglion of the fifth

cranial nerve by VZV.

 It constitutes approximately 10 percent of all cases of

herpes zoster

 Mode of infection:
 The infection is contracted in childhood, which
manifests as chickenpox and the child develops
immunity
74
CORNEAL LESIONS 2ND HZO
 Zoster keratitis occurs in 40 percent of all patients
 Fine or coarse punctate epithelial keratitis.

 Microdendritic epithelial ulcers

 Nummular keratitis

 Disciform keratitis occurs in about 50 percent of cases

 Neuroparalytic ulceration may occur as a sequelae

 Exposurekeratitis 75
 Mucous plaque keratitis develops in 5% of cases
Types of zoster keratitis : A, Punctate epithelial
keratitis; B, Microdendritic epithelial ulcer; C,
Nummular keratitis; D, Disciform keratitis
76
LOCAL THERAPY FOR OCULAR LESIONS

 For zoster keratitis, iridocyctitis and scleritis

 Topical steroid eye drops 4 times a day.
 Cycloplegics OD.
 Topical acyclovir 3% ointment 5×/day for about 2 wks.

 Topical antibiotics to prevent secondary infections

 For secondary glaucoma
 0.5% timolol or 0.5% betaxolol drops BD.
 Acetazolamide 250 mg QID.

 For neuroparalytic corneal ulcer

 lateral tarsorrhaphy

 For persistent epithelial defects use :

 i. Lubricating artificial tear drops, and
 ii. Bandage soft contact lens.
77
 Keratoplasty
SYSTEMIC THERAPY FOR HERPES
ZOSTER
 Oral antiviral drugs
 Acyclovir in a dose of 800 mg 5 times a day for 10 days, or
 Valacyclovir in a dose of 500mg TDS

 Analgesics
 Systemic steroids

 Cimetidine in a dose of 300 mg QID for 2-3 weeks starting

within 48-72 hours of onset

 Amitriptyline10–25 mg at night increasing gradually to 75

mg daily if appropriate
78
 HOW TO DIFFERENTIATE HSK FROM
HZK?

HSK HZK

 Macro dendritic ulcer  Stellate ulcer(micro)

 Have bulbs  No bulbs

 Central ulcer  Peripheral ulcer

 Mild pain  Severe pain

 No hx of semifacial lesions  Hx of semifacial lesions

 Highly compromised corneal  Less compromised

sensation

79
FUNGAL KERATITIS
 Fungi are a group of microorganisms that have rigid
walls and a distinct nucleus with multiple chromosomes
containing both DNA and RNA.

 Fungal keratitis is rare in temperate countries but is a

major cause of visual loss in tropical and developing
countries.

 Fungal keratitis is less common than bacterial keratitis

80
CONT…
 The two main types of fungi causing keratitis are:

 Yeasts (e.g. genus Candida), ovoid unicellular organisms

that reproduce by budding, are responsible for most
cases of fungal keratitis in temperate climates.

 Filamentous fungi (e.g. genera Fusarium and

Aspergillus), multicellular organisms that produce
tubular projections known as hyphae.

 They are the most common pathogens in tropical

climates.
81
PREDISPOSING FACTORS
 Trauma to the cornea with plant or vegetable material or animal
tail

 Trauma related to contact lens wear

 Topical antibiotics & corticosteroids

 Corneal surgery(eg, PK, radial keratotomy)

 Chronic keratitis (eg, herpes simplex [HSV), herpes zoster, or

82
vernal/ allergic conjunctivitis).
CLINICAL PRESENTATION
 Initially ,fungal keratitis is less symptomatic than bacterial
keratitis

 May have little or no conjunctival injection upon (white eye).

83
CONT…
 Symptoms
 Gradual onset of pain

 Grittiness

 Photophobia

 Blurred vision

 Watery or mucopurulent discharge

84
SIGNS
 Corneal ulcer is dry-looking, greyish white, with elevated rolled
out margins

 Delicate feathery finger-like extensions into the surrounding

stroma under the intact epithelium.

 A sterile immune ring (yellow line of demarcation)

 Multiple, small satellite lesions may be present around the ulcer.

 An endothelial plaque and/or hypopyon

 Perforation & vascularization is rare 85

Fungal keratitis. (A) Candida keratitis; (B) filamentous keratitis with
satellite lesions and a small hypopyon 86
DIAGNOSIS
 Clinical
 lab IX

 Blood, Sabouraud's, and brain-heart infusion media

are preferred media for fungal culture.

87
DDX

 Bacterial keratitis
 Herpetic keratitis

 Acanthamoebal keratitis.

88
TREATMENT
Removal of the epithelium(debridment)

Topical treatment
Amphotericin B 0.15% eye drops
Econazole 1% eye drops
Natamycin 5% eye drops Q1H for 48hrs & then taper

& continued for at least 12 wks

Fluconazole 2% eye drops
clotrimazole 1% eye drops

A broad-spectrum antibiotic
Cycloplegia to prevent synechiae and alleviate pain

Systemic antifungals & antibiotics

89
 Therapeutic keratoplasty
SYSTEMIC ANTIFUNGAL AND ANTIBIOTICS
 May be given in severe cases, when lesions are near the
limbus, or for suspected endophthalmitis

 Voriconazole 400 mg b.d. for one day then 200 mg b.d.

 Itraconazole 200 mg daily, reduced to 100 mg daily, or

fluconazole 200 mg b.d.

 Doxycycline 100 mg b.d. may be given for its anticollagenase

effect

90
ACANTHAMOEBAL KERATITIS
 Acanthamoebae sp. are free-living protozoa found in air-soil and
fresh or brackish waters.

 They exist in both active trophozites and dormant (cystic) forms.

 The cystic form is resilient and able to survive for prolonged

periods under hostile environmental conditions

 Under appropriate environmental conditions, the cysts turn into

trophozites

 Trophozites produce variety of enzymes that aid tissue penetration

and destruction. 91
RISK FACTORS
 Contact lens wear
 using home-made saline (from contaminated tap
water )

 Mild trauma associated with

 contaminated vegetable matter
 salt water diving
 wind blown contaminant
 organic matter
 Exposure to muddy water

92
CLINICAL PRESENTATION
 Symptoms
 very severe pain (out of proportion to the degree of
inflammation)

 Watering

 Photophobia

 blepharospasm

 blurred vision

93
SIGNS
 Limbitis , small patchy anterior stroma and perineural infiltrates
(radial keratoneuritis)(1-4 weeks)

 Epithelium may be intact or manifest punctate or pseudo-dendritic

keratitis.

 Central or paracentral ring abscess due to enlargement and

coalescence of the infiltrates

 Small white satellite lesions may develop peripheral to the ring.

 Slowly progressive , stromal opacification, scleritis and ultimately

descemetocele formation
94
Acanthamoeba keratitis. (A) Cysts in a corneal biopsy; (B) epithelial
pseudodendrites; (C) focal anterior stromal infiltrates; (D) radial
95
perineuritis; (E) ring abscess; (F) melting
DIAGNOSIS
 Clinical
 Laboratory diagnosis
Potassium hydroxide(KOH) mount
Calcofluor white stain
Lactophenol cotton blue stained film
Culture on non-nutrient agar

96
TREATMENT
 Duration of medical treatment(6 months to 1 year)

 Polyhexamethylene biguanide (0.01%–0.02% solution)

 0.1% propamidine isethionate (Brolene) drops

 Chlorhexidine 0.02% eye drops

 Topical and oral imidazoles such as fluconazole, itraconazole

 Oral NSAID( flurbiprofen 100 mg q.i.d.)to control pain

 Penetrating keratoplasty (non-responsive cases.)

97
98
 How to differentiate fungal keratitis from bacterial keratitis?
 How to differentiate HSK from HZK?

 How to differentiate fungal keratitis from Acanthamoeba

keratitis?
 How to treat disciform keratitis having epithelial defect?

 Pathophysiology of disciform keratitis

 How to differentiate Mooren's ulcer from PUK?

 How to differentiate marginal infiltrate from PUK?

 Advantage of Cycloplegics

 Sloughing vs non sloughing

 Rx of HSK

99