brief discussion about cornea :)

1. CORNEA

2. INTRODUCTION:
 CORNEA:
“It is a round, convex, transparent structure,
forming anterior one-sixth of the outer fibrous
envelope of an eye”.

3. ANATOMY & PHYSIOLOGY:
 DIMENSIONS:
 ANTERIOR SURFACE:
Eliptical, about 11.7mm
horizontally & 10.6mm
vertically.
 POSTERIOR SURFACE:
Circular, about 11.7mm in
diameter.

4.  SHAPE:
Centrally, 1/3 of the cornea i.e. 4mm is spherical
while in the periphery the cornea becomes flatter.
 THICKNESS:
 The cornea is thinnest at its centre ranges from
0.5mm to 0.54mm.
 The thickness increases gradually from centre to
periohery, where it is 0.65mm to 1mm.

5.  RADIUS OF CURVATURE:
 Anterior convex surface is 7.8mm(range 6.7 to
9.4mm).
 Posterior concave surface is 6.2 to 6.8mm.
 Refractive index is 1.376.
 REFRACTIVE POWER:
 Anterior convex surface has = +48D.
 Posterior concave surface has=+-5D.
 Average power of cornea is= +43D.

6.  COMPOSITION OF HUMAN CORNEA:
Water: 78%
Collagen: 15%
of which: Type-l: 50-55%
Type-lll: 1%
Type-lV: 8-10%
Type-Vl: 25-30%
Other protein: 5%
Keratin sulphate: 0.7%
Condriotin/dermatan sulphate: 0.3%
Hyaluraonic acid: +
Salts: 1%

7.  EMBRYONIC ORIGIN OF CORNEA:
The formation of cornea is induced by the lens
and the optic cup at tha 7th weeks of intrauterine life.
 Corneal Epithelium --- Surface ectoderm
 Bowman’s membrane --- Mesenchyme
 Stroma --- Mesenchyme & Neural crest
 Descemet’s membrane --- Synthesized by
endothelium.
 Endothelium --- Neural crest.

8.  STRUCTURE:
Behind the precorneal tear film there are 05
layers of cornea:
1. Epithelium
2. Bowman’s layer
3. Stroma
4. Descemet’s membrane
5. Endothelium

9.  EPITHELIUM:
 Its thickness is about 50um.
 It is Stratified, Squamous &
non-keratinised.
 Continuous with conjunctival
epithelium at limbus but
having no goblet cells.
 Consists of 5 or 6 layers of
nucleated cells resting on a
basal lamina, namely:
a.Basal cells
b.Wing cells.
c.Surface cells.

10.  BOWMAN’s MEMBRANE:
 It is 8-14um thick.
 It is cellular layer of condensed collagen fibrils.
 It ends abrubtly at the periphery of the cornea,
 It has no power of regeneration after the damage.

11.  STROMA: (Lamina propria)
 It comprises about 90% thickness of the cornea.
 Collagen lamella are made up of collagen fibrils, the
lamella are uniform in size & regularly spaced.
 Ground substance is proteoglycan.
 Keratocytes are collagen-producing fibroblasts.

12.  DESCEMET’S MEMBRANE:
 10 to 12 um thick.
 It is the basement membrane of the endothelium.
 Terminates at periphery as prominent line called Schwalb’s
line.
 ENDOTHELIUM:
 Single layer of hexagonal
cells.
 Plays a vital role in
maintaining dehydration
of cornea.
 Damage causes corneal
edema.

13.  BLOOD SUPPLY:
It is avascular, but corneoscleral limbus is supplied by
the perilimbal plexuses.
 NERVE SUPPLY:
Long cilliary nerves, branches of ophthalmic division of
trigeminal nerve.
 FUNCTIONS:
 Acts as powerful refracting? focusing the rays on retina.
 Average refreactive power of the cornea is +43 diopters.

14. BACTERIAL KERATITIS:
 PATHOGENESIS:
 Usually develops only when ocular defenses have been
compromised.
 However, some bacteria , including Neisseria gonorrhoea,
Neisseria meningitidis, Corynebacterium diphtheria &
Hemophilus influenza are able to penetrate a healthy corneal
epithelium. Usuallyin association with severe conjunctivitis.
 Common pathogens include:
o Pseudomonas aeruginosa
o Staphylococcus aureus
o Streptococci.

15.  RISKS FACTORS:
 Contact lens wear.
 Trauma, including referactive surgery (LASIK). In
developing countries agricultural injury is the major
risk factor.
 Ocular surface disease, herpetic keratitis,
bullous keratopathy, dry eye, chronic blepharitis,
corneal anaesthesia etc.
 Other factors, include local or systemic
immunosuppression, diabetes & vit A deficiency.

16.  CLINICAL FEATURES:
o PRESENTATION:
 Pain
 Photophobia
 Blurred vision
 Mucopurulent or purulent discharge.
o SIGNS:
 An epithelial defect with infiltrate involving larger area.
 Stromal edema
 Chemosis & eyelid swelling (in moderate to severe cases).
 Severe ulceration may lead to descematocele formation &
perforation (pseudomonas infection).
 Endophthalmitis (rare in absence of perforation).
 Subsequent scarring may be severe.
o REDUCED CORNEAL SENSATION

17. EARLY ULCER LARGER ULCER
ADVANED DIS WD HYPOPYON
PERFORATION ASSO WD
PSEUDOMONAS INF.

18.  DIFFERENTIAL DIAGNOSIS:
Include:
 Keratitis due to other microorganisms(fungi,
acanthamoeba,stromal herpes simplex etc).
 Marginal keratitis
 Sterile inflammatory corneal infiltrates asso wd
contact lens wear
 Periptheral ulcerative keratitis
 Toxic keratitis.

19.  INVESTIGATIONS:
 Corneal sampling (this may not require for a small infiltrate,
particularly one without an epithelial defect & away from visual axis.
Corneal srapping Culture media
S.Aureus grown on blood agar forming
golden colonies with a shiny surface
N.Gonorrhoeae grown on chocolate agar.

20.  Conjunctival swabs, (may be worthwhile in addition
to corneal scraping, particularly in severe cases).
 Contact lens cases, (as well as bottles of solution and
lenses themselves, should be obtained when possible and sent to
the laboratory for culture).
 Gram staining,
 Differentiates bacterial species into ‘Gram-positive’ and
Gram-negative’ based on the ability of the dye (crystal
violet) to penetrate the cell wall.
 Bacteria that take up crystal violet are Gram-positive
and those that allow the dye to wash off are Gram-negative.
“Culture & sensitivity reports should be obtained as soon
as possile . The type of bacteria alone will generally
provide an indication of the antibiotic category to be
used”

21.  TREATMENT:
o GENERAL CONSIDERATIONS:
 Hospital admission (for pts who aren’t likely tp comply or are
unable to self administer Rx. Also for aggressive diz).
 Discontinuation of contact lens wear is mandatory.
 A clear plastic eye shield (if significant thinning/perforation
is present).
 Decision to treat:
o Intensive Rx may not be requiredfor small infiltrates & that may be
treated by lower-frequency topical antibiotic &/or steriod & by
temporary cessation of contact lens wear.
o Empirical broad-spectrum Rx is usually initiated before microscopy
results are available.

22.  LOCAL THERAPY:
Topical therapy can achieve high tissue concentration
& initially should consist of broad spectrum
antibiotics that cover most pathogens.
 ANTIBIOTIC MONOTHERAY:
 Has the major advantage over duotherapy of lower surface
toxicity as well as greater convenience.
 Fluoroquinolones is the usual choice for empirical
monotherapy.
 Ciprofloxacin instillation is associated
 with the white corneal precipitates
that may delay epithelial healing.

23.  ANTIBIOTIC DUOTHERAPY:
 May be preferred as first-line empirical Rx in
aggressive diz or if microscopy suggests st.cocci
or specific microorganism that may be more
effectively treated bt tailored regimen.
 It usually involves a combination of 02 fortified
antib otics, typically Cephalosporin and an
aminoglycoside.

24.  SUBCOJUNCTIVAL ANTIBIOTICS:
 Are usually only indicated if there is poor
compliance with topical Rx.
 MYDRIATICS:
 Are used to prevent the formation of post,
synechiae & to reduce pain.
 STERIODS:

25.  SYSTEMIC ANTIBIOTICS:
but may be appropriate in are usually not given,the
conditions like:
 Potential for systemic involvement,e.g. when N.meningitidis,
H.influenza, N.gonorrhoeae are involved.
 Severe corneal thinning with threatened or actual
perforation.
 Scleral involvement.
 PERFORATION:
 Small perforation: bandage contact lens, tissue glue is often
A/Q for slightly larger ones.
 Larger perforation: penetrating keratoplasty or corneal patch
graft

26. FUNGAL KERATITIS:
 PATHOGENESIS:
 Fungi are microorganisms with rigid cell-wall
having both DNA & RNA.
 Two main types of fungi causes keratitis:
 FILAMENTOUS FUNGI (Aspergillus,
Fusarium) are multicellular organisms that
produce hyphae.They are the most common
pathogens in topical climates.
 YEASTS (Genus Candida), are unicellular
organisms that produce by budding & occasionally
form hyphae & are the most common pathogens in
temperate climates.

27.  RISKS FACTORS:
 Ocular trauma: Agricultural material
 Long term use of topical corticosteriods
 Chronic ocular surface disease
 Contact lens wear
 Systemic immunosuppression & DM

28.  CANDIDAL & FILAMENTOUS KERATITIS:
 CLINICAL FEATURES:
(Its C/F very much similar to bacterial corneal infections
so Dx is frequently delayed unless there is a high index
of suspicion).
 SYMPTOMS:
• Gradual onset of pain
• Grittiness
• Photophobia
• Blurred vision
• Watery & mucopurulent discharge.

29.  CANDIDAL KERATITIS:
• Yellow-white densely suppurative infiltrate is typical.
 FILAMENTOUS KERATITIS:
• Grey or yellow-white stromal infiltrate with indistinct fluffy
margins.
• Progressive infiltration, often with satelite lesions.
• Feathery branch-like extensions or a ring-shaped infiltrate
may develop.
• Rapid progression with necrosis & thinning can occur.
• Penetration of an intact Descemet membrane may occur
& lead to endophthalmitis without evident perforation.

30.  AN EPITHELIAL DEFECT is not
invariable & is sometimes small when present.
 OTHER FEATURES,
• Anterior uveitis
• Hypopyon
• Endothelial plaque
• Raised IOP
• Scleritis & sterile or infective endophthalmitis

31. Severe candidal keratitis
Filamentous keratitis with fluffy
edges—there is a large epithelial
defect & fold in Descemet
membrane.

32. Satelite lesions Satelite lesions
Ring infiltrate with satelite lesions and
a hypopyon.

33.  DIFFERENTIAL DIAGNOSIS:
 Bacterial, herpetic & acanthamoeal keratitis.
 INVESTIGATIONS:
Samples of lab investigations should be acquired before
commencing anti-fungal therapy.
 Staining (Giemsa,KOH,methamine silver stain)
 Culture (on sabouraud’s agar, dextrose agar & blood
agar).
 PCR analysis
 Corneal Bx
 Anterior chamber tap

34.  TREATMENT:
 TOPICAL ANTIFUNGAL THERAPY:
• Natamycin 5% suspension is effective for most of filamentous
keratitis.
• Fluconazole 2% suspension.
• Amphotericin B 0.15% solu effective for filamentous as well as
yeast keratitis.
 SUBCONJUNCTIVAL FLUCONAZOLE: May be
used in severe cases with hypopyon.
 SYSTEMIC ANTIFUNGAL: Are used for severe
cases. Ketoconazole 200-400mg/day.
 MECHANICAL DEBRIDEMENT: Enhances the
penetration of anti-fungal drugs.
 THERAPEUTIC KERATOPLASTY: Indicated
when deep lesion are unresponsive to topical antifungal
therapy.

35. ACANTHAMOEBA
KERATITIS:
It is potentially blinding condition which needs
immediate Rx.
 ETIOLOGY:
 Acanthamoeba spp.
 Free living protozoa found in fresh or brackish
water & soil.
 Exists as an active trophozoite form or dormant
cystic form resistent to killing by freezing,
desiccation & routine chlorination of water.

36.  RISKS FACTORS:
 Contact lens wearer
 Ocular trauma
 CLINICAL FEATURES:
 SYMPTOMS:
• Blurred vision
• Severe pain & photophobia which may be out of
proportion to clinical findings.

37.  SIGNS:
 Epithelial keratization that may appear as:
• Diffuse punctate epitheliopathy
• Epithelial pseudodendrites
 Limbitis, with diffused or focal ant stromal infiltrates.
 Ring infiltrate ( ring abcess) is formed with the
progression of peripheral infiltrates.
 The perineural infiltrates ( radial keratoneuritis) & the
enlargement of corneal nerves are pathognomonic sign.
 Corneal melting may occur at any stage.

39.  DIAGNOSIS:
 Smear & culture of organism, obtained by corneal
scrapping.
 Calcofluor white
 Laminar corneal Bx , when organism penetrates deeper
to the tissue.
 TREATMENT:
Early epithelial stage: short course i.e.3-4 months.Whereas
stromal infiltrate: long course Rx for 6-12 months.
 Debridement in early infective epithelial stage.
 Topical amoebicides are given as a dual therapy.
 Therapeutic keratoplasty is required in progressive &
unresponsive cases.

40. HERPES SIMPLEX KERATITIS
 INTRODUCTION:
 DNA virus.
 Major cause of unilateral corneal scarring worldwide.
 Divided into 02 types:
 HSV-type l:
 Predominantly, causes infection above waist i.e. face, lips
& eyes.
 Usually acquired by droplet infection or close contact.
 HSV-type ll:
 Typically causes infection below waist (genital herpes).
 Acquired venerally.
 Transmitted to the eyes through infected genital
secretions.

41.  HSV OCULAR LESIONS:
PRIMARY OCULAR INFECTION i.e. no
previous exposure to the virus.
 Skin: Periocular vesicles.
RECURRENT KERATITIS: (Reactivation of virus
in the presence of immunity).
 Active epithelial keratitis.
• Dendritic ulcer
• Geographic ulcer
 Stromal keratitis
• Necrotic stromal keratitis
• Disciform keratitis
 Kerato-uveitus

42.  PATHOGENESIS OF HSV:
 PRIMARY HSV INFECTION:
 Through droplet infection or direct inoculation.
 Primary infection is sub-clinical or may cause mild fever
& malaise.
 After primary infection, virus travels up axons of sensory
nerves to its ganglions.
 HSV type-l to Trigeminal ganglion.
 HSV type-ll to Spinal ganglion.
 RECURRENT HSV KERATITIS:
 Virus in ganglion is reactivated, replicates & travels down
axons of sensory nerve to target tissue causing recurrent
infection.
 Stimuli associated with recurrence are: poor general
health, exposure to UV rays, fever, psychiatric
disturbance, use of steriods.

43. ACUTE EPITHELIAL KERATITIS:
(Dendritic Ulcer/ Geographical Ulcer/
Amoeboid Ulcer)
“It is an acute or chronic corneal ulceration where an ulcer has a
shape of linear branching tree i.e. dendritic or geographical
configuration.”
 ETIOLOGY:
It is caused by Herpes simplex virus, both type-1 & type-2.
 CLINICAL FEATURES:
 SYMPTOMS:
• Foreign body sensation
• Lacrimation
• Photophobia
• Pain-mild to moderate
• Reduction of vision

44.  SIGNS:
• Ciliary conjestion
• Corneal sensitivity is markedly diminished.
• Corneal staining with 2% Fluorescein or Rose Bengal
shows dendritic or geographical (amoeboid)shaped ulcer.
• Fluorescein(bed of ulcer) while Rose Bengal(margin of
ulcer laden with virus).
Stellate lesion Bed of dendritic ulcer stained with
fluoresin

45. Margin of dendritic ulcer stained with
Rose bengal.
Geographic ulcer

46.  DIAGNOSIS:
 Morphological appearance of the corneal ulcer
 Diminised corneal sensitivity
 DIFFERENTIAL DIAGNOSIS:
 Herpes zoster keratitis
 Acanthamoeba keratitis
 Healing corneal abrasion
 Epithelial rejection in a corneal graft
 TREATMENT:
 Topical antivirals
 Debridement ( for resistent cases).
 Oral antiviral therapy
 Interferon monotherapy
 Topical antibiotic cover
 IOP control

47. STROMAL NECROTIC
KERATITIS:
It is caused by an active viral invasion & destruction.
It may be associated with an intact epithelium or
may follow an epithelial disease”.
 CLINICAL FEATURES:
 Corneal stroma appears cheesy & necrotic,
resembling bacterial & fungal infection.
 May be associated with ant uveitis.
 All other C/F of active epithelial keratitis may be
present.

48.  TREATMENT:
 Topical antiviral
 Topical antibiotics
 In case of delayed epithelial
healing, add lubricants with
pressure patching or
bandage contact lens.

49. DISCIFORM KERATITIS:
“It is viral endothelitis. It is a disc-shaped, localized greyish
area of stromal edema with localized keratic precipitates”.
 ETIOLOGY:
 Reactivated viral infection of keratocytes & endothelium of
cornea.
 It may also be exaggerated hypersensitivity reaction to
viral antigen.

50.  CLINICAL FEATURES:
 Central zone of epithelial edema.
 Stroma thickening is due to edema.
 Folds in Descemet’s membrane
may be present.
 Mild to moderate anterior uveitis.
 Keratic precipitates beneath the
 involved cornea.
 Corneal sensitivity is reduced.
 TREATMENT:
 Topical antiviral.
 Topical prophylactic antibiotics.
 Topical weak steriods.
 Cycloplegic.

51. HERPES ZOSTER OPHTHALMICUS:
“Herpes zoster ophthalmicus is an ocular & periocular
disease due to the involvement of ophthalmic division of
trigeminal nerve by HERPES ZOSTER virus.”
 ETIOLOGY:
 Human herpes virus:3(HHV-3) is the causative agent.
 Causes two different clinical conditions:
• Varicella – chicken pox
• Zoster : Shingles
: Zoster ophthalmicus

52.  PATHOGENESIS:
HZO, a potentially devastating form of acute HZ, results
from the reactivation of VZV in the trigeminal (5th CN)
nerve.
 MECHANISM OF DAMAGE:
 Cellular infiltration
 Ischemic vasculitis
 Inflammatory granulomatous reaction

53.  CLINICAL FEATURES:
o SKIN LESIONS:
 Pain: severe unilateral disabling neuralgia in the distribution
of the nerve.
 Rashes: i.e vesicles.Vesicular erruption appears after few
days of pain that rupture to form crusting ulcers, which heal
in several weeks leaving pitted scars.
 Edema & tenderness : Initially rash is accompanied
periorbital edema & tenderness.
 Post herpetic neuralgia: Pain disappears in almost 2 weeks
bt small % of cases ,post herpetic neuralgia, resistent to Rx
& persistd for many years.

54. Hutchinson sign-involving side o nose
Severe rash
Boggy edema-affecting both upper eyelids

55.  OCULAR LESIONS:
 Cornea shows following features:
• Acute epithelial keratitis
• Microdendritic ulcers
• Filamentary keratitis
• Nummular keratitis
• Disciform keratitis
 Conjunctivitis is acute follicular type,always associated
with vesicles on the eyelid margin.
 Episcleritis occurs in 1/3 of cases at the onset of rashes.
 Secondary glaucoma , 20% of cases due to trabeculitis.
 Anterior uveitis associated with keratic precipitates.

56.  NEUROLOGICAL COMPLICATIONS:
 Cranial nerve palsies affects the 3rd nerve most commonly.
 Optic neuritis may occur in about 1:400 cases.
 TREATMENT;
o Systemic Therapy:
 Acyclovir 800mg tabs 5 times daily for 3-7 days within 72 hours
of the onset is the Rx of choice.
 Analgesics
 Antiobiotics
 Systemic steriods
o Topical Therapy:
 Antiviral
 Steriods’
 Antibiotics
 Cycloplegic
 Antiglaucoma drugs

57. MOOREN’S ULCER:
“It is the chronic painful peripheral corneal ulcer”.
 ETIOLOGY:
Autoimmune diz causing vasculitis of limbal vessels
resulting ischemic necrosis that produces enzymes such as
collagenase & proteoglyconase which play role in causation
of ulceration.
 TYPES:
 Limited form:
often unilateral, relatively benign occurring in older pts.
 Progressive form:
often bilateral,relatively progressive ocurring in young pts.

58.  CLINICAL FEATURES:
o Symptoms:
 Pain‘
 Photophobia
 Red eye
 Decreased vision
o Signs:
 Begins as excavating ulceration at periphery of the cornea
near the limbus.
 It has typically raised borders and an overhang ridge at
advancing edge.
 Spreads circumferentially & centripetally.
 Perforation is rare.

59.  TREATMENT:
o Medical:
 Topical steriods
 Systemic immunosuppressive therapy
 Topical cycloplegic
 Antibiotics
o Surgical:
 Conjunctival resection
 Keratoplasty

60. INTERSTITIAL KERATITIS:
“It is inflammation of the corneal stroma without primary
involvement of epithelium or endothelium of cornea”.
 ETIOLOGY:
 Congenital syphilis
 T.B
 Herpes virus
 Cogan’s disease
 Leprosy
 Onchocersiasis

61.  CLINICAL FEATURES:
 V.A is reduced.
 Stromal corneal opacity
 Ghost vessels are seen within the stroma
 KPs on endothelium of cornea
 Corneal sensitivity may be reduced.

62.  INVESTIGATIONS:
 CBC & ESR
 Chest XRAY
 Mantoux test
 VDRL tests
 FTA-ABS
 TREATMENT:
It depends upon the cause:
 Systemic penicilin inj: (Leprosy).
 Acyclovir E oint: (Herpes virus).
 Topical corticosteriods
 Cycloplegics

63. KERATOPATHY
“It is a non-inflammatory disease of the cornea,
resulting due to the disturbance in metabolic
activity of corneal epithelium”.
It includes:
 Neurotrophic keratopathy
 Exposure keratopathy

64. NEUROTROPHIC KERATOPATHY
“It is a degenerative disease of the corneal epithelium,
resulting from impaired corneal innervation”.
 ETIOLOGY:
Impaired corneal sensation occurs due to damage to the 5th
CN, which is caused by:
 Surgical trauma
 Tumor (e.g Acoustic neuroma)
 Systemic diseases (DM, Leprosy etc).
 Ocular disease (HZO)
 Ocular surgery

65.  PATHOGENESIS:
 Loss of trigeminal innervation to cornea: corneal hypoesthesia
or anaesthesia & disturbance of corneal reflex.
 As a conseqence, metabolic activity is disturbed,resulting into
epithelial keratopathy, corneal ulceration & perforation.
 CLINICAL FEATURES:
 Painless red eye ( characteristic feature).
 Dec V.A
 Dec lacrimation
 Marked ciliary conjestion
 Dec or absence of corneal sensation
 Corneal appearance is dull due to corneal edema
 Epithelial defects
 Progressive sterile ulcers
 Corneal stromal melting
 Sec infection leading perforation & loss of eye may occur.

66. Early central epithelial changes Persistent epithelial defects wd rolled edges
Sec inf wd marked thinning
Punched-out epithelial defects with
underlying stromal edema & early melting

67.  TREATMENT:
 Artificial tears during daytime & eye oint at bed time.
 Topical nerve growth factor drops.
 Autologous serum drops are also useful.
 Protection of ocular surface.

68. EXPOSURE KERATOPATHY
“It is condition that results from disease process that limits
the eyelid closure”.
 MECHANISM:
 Due to incomplete closure of eyelids, there is desiccation
of corneal epthelium, resulting into punctate epithelial
erosion, which may develop into ulcer.
 ETIOLOGY:
 Neurogenic disease: 7th nerve palsy (Bell’s palsy).
 Orbital disease: Thyroid eye diz & proptosis.
 Eye abnormalities: Ectropion.
 Blepharoplasty

69.  CLINICAL FEATURES:
 Punctate epithelial keratopathy, usually involve inferior
third of cornea.
 Large epithelial defects & ulcers
 Sec infection & perforation
 Irritable red eyes may be worse in the morning.
Inferior epithelial defect Stromal melting Sec bacterial infection

70.  TREATMENT:
 Ensure A/Q lubrication
 Ensure A/Q eyelid closure.
 Topical antibiotics
 Correction of any associated condition e.g Ectropion.

71. KERATOCONUS
“It is a non-inflammatory bilateral (85%) ectatic condition of the
central part of the cornea”.
 ETIOLOGY:
 It is a corneal dystrophy.
 Prevalance: 400/100,000.
o PRIMARY:
• Idiopathic
• Autosomal dominant in 10% cases.
o SECONDARY:
• Ocular disease
• Congenital ocular anomalies
• Allergic conjunctivitis in 70% of cases
• Systemic disorders
• Chromosomal disorders
• Cutaneous disorders
• Connective tissue disorders
• Osteogenesis imperfecta

72.  PATHOGENESIS:
 There is defective synthesis of MPS & collagen tissue,
which results into fragmentation of basement membrane of
epithelium, Bowman’s membrane & degeneration of stromal
collagen fibres.
 This causes thinning & forward bulging of cornea, resulting
into axial myopia & stigmatism.

73.  CLINICAL FEATURES:
 Onset: is usually at the time of puberty.
 Incidence: 1:10000 to 1:25000.
 Both eyes are affected
 SYMPTOMS:
 Painless progressive deterioration of vision for near & far.
 Photophobia
 Monocular diplopia
 SIGNS:
 V.A is reduced due to myopia & astigmatism.
 Distant direct ophthalmoscopy: shows ‘oil droplet reflex’.
 Munson’s sign: bulging of lower eyelid, when the pt looks down.
 Keraotoscopy Placido disc: shows irregular rings.
 Retinoscopy: shows scissors reflex.
 Slit lamp exam: thinning & forward bulging of central cornea,
vogt’s lines,corneal nerves become prominent & visible,
fleischer’s ring, corneal scarring in advanced cases.

74. Oil droplet red reflex
Vogt straie in deep stroma
Fleisher ring Typical cone

75.  INVESTIGATIONS:
 Corneal topography most sensitive method for detecting a
very early keratoconus.It shows a refractive error in graphic
pattern.
 Keratometry shows myopia & irregular astigmatism.
 COMPLICATION:
 Acute corneal hydrops sudden onset of painless visual loss
due to rupture of Descemet’s membrane & entry of fluid into
the stroma.
 Scarring of central cornea.

76.  TREATMENT:
 Spectacles: to correct refractive error in early cases.
 Rigid contact lenses: to correct higher degree of
astigmatism.
 Intacs (intra corneal ring segment): useful in early cases.
 Collagen cross linking (CXL): To stop progression
 Deep ant lamellar keratoplasty: effective in pts intolerant to
contact lenses.
 Keratoplasty: when significant corneal scarring
 Acute hydrops: Rx with hypertonic saline & patching or
bandage contact lens.

77. FILAMENTARY KERATITIS
“It is superficial punctate keratitis associated with the
formation of corneal filaments”.
 CAUSES:
 Dry eye is the most common cause.
 Superior limbic keratoconjunctivitis
 Recurrent erosion syndrome
 Neurotrophic keratitis
 Eye patching for prolonged period
 Essential blepharospasm

78.  CLINICAL FEATURES:
o SYMPTOMS:
 Mild to moderate pain, discomfort, F.B sensation,
lacrimation & photophobia.
o SIGNS:
 Corneal filaments stain well with rose bengal .
 Superficial punctate keratitis of varying may be present.

79.  TREATMENT:
 Mechanical removing of filaments and 24 hours, followed
by lubricants.
 Hypertonic 5% saline to encourage loose epithelium.
 Mucolytic agents such as 5% or 10%
 Bandage contact lenses may be used in cases.
 Rx of underlying causes to prevent recurrence.

80. CORNEAL DEGENERATIONS
Corneal degenerations are acquired opacifying disorders.
 TYPES:
 ARCUS SENILIS:
 MC peripheral corneal opacity,due
to infiltration of lipids.
 It is very common in old age.
 LIPID KERATOPATHY:
 Primary is rare, appears as white stromal
deposits of cholesterol fats & phospholipids.
 It is non-vascularized.
 Secondary is more common & is
associated with vascularization.

81.  BAND KERATOPATHY:
Common condition, characterized by
deposition of Ca salts in Bowman’s
layer, epithelial basement membrane
& ant stroma.
 SPHEROIDAL DEGENERATION:
(Climatic dropletkeratopathies).
Amber coloured granules are deposited
in the superficial stroma.
 SALZMAN NODULAR
DEGENERATION:
 Occurs sec to chr keratitis, especially,
trachoma.
 Grey white nodular opacities are
deposited in the superficial stroma.

82. CORNEAL DYSTROPHIES
“Corneal dystrophies are a group of genetic, often
progressive, eye disorders in which abnormal material
often accumulates in the transparent outer layer of
cornea. These may asymptomatic in some individuals; in
others cause significant vision impairment”.
 CLASSIFICATION:
On the basis biomicroscopic & histopathological
features,they are classified into:
 Anterior dystrophies
 Stromal dystrophies
 Posterior dystrophies

83.  ANTERIOR DYSTROPHIES:
 Epithelial basement membrane dystrophy
 Reis-Buckler’s dystrophy
 Recurrent corneal erosion syndrome.
 STROMAL DYSTROPHIES:
 Granular dystrophy
 Lattice dystrophy
 Macular dystrophy
 POSTERIOR DYSTROPHIES:
 Fuch’s endothelial dystrophy
 Hereditary endothelial dystrophy

84. KERATOPLASTY
(Corneal grafting/Corneal transplantation)
“It is the operation, in which the pt’s diseased cornea is
replaced by donor’s healthy cornea”.
 TYPES:
 Penetrating keratoplasty (full thickness graft).
 Lamellar keratoplasty (partial thickness graft).
• Superficial lamellar keratoplasty
• Deep anterior lamellar keratoplasty
• Descemtet’s stripling endothelial keratoplasty

85. CONTACT LENSES
“A contact lens is a thin lens placed directly on the surface of
the eye.”
These are considered medical devices & can be worn:
 To correct vision or
 For cosmetic or
 Therapeutic reasons

86.  THERAPEUTIC USES:
 Optical indications are aimed at improving V.A when this
cannot be achieved by spectacles.
 Promotion of epithelial healing
 Pain relief(e.g bullous keratopathy,filamentary keratopathy
etc).
 Preservation of corneal integrity
 Miscellaneous indications
 COMPLICATIONS:
 Mechanical & hypoxic keratitis
 Immune response (hypersentivity) keratitis
 Toxic keratitis
 Suppurative keratitis

87. CONGENITAL ANOMALIES OF THE
CORNEA & GLOBE:
 Microcornea
 Microphthalmos
 Anophthalmos
 Nanophthalmos
 Megalocornea
 Sclerocornea
 Cornea plana
 Keratectasia
 Posterior keratoconus