corneal ulcers

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Corneal Disorders
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Overview

• Cornea- Anatomy and physiology
• Corneal Ulcer
• Other corneal disorders

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Cornea-Applied anatomy

• Dimensions
• The horizontal diameter is 11.7
• vertical diameter of 11 mm.
• The posterior surface of cornea is circular with
  an average diameter of 11.5 mm.
• Thickness of cornea in the centre is about
  0.52mm while at the periphery it is 0.7 mm.
  Radius of curvature.
• The central 5 mm area of the

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• Cornea forms the powerful refracting surface of
  the eye.
• The anterior and posterior radii of curvature of
  this central part of cornea are 7.8 mm and 6.5
  mm, respectively.
• Refractive power of the cornea is about 45
  dioptres, which is roughly three-fourth of the
  total refractive power of the eye (60 dioptres).

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• Histology
• Histologically, the cornea consists of five
  distinct layers. From anterior to posterior these
  are
• epithelium,
• Bowmans membrane,
• substantia propria (corneal stroma),
• Descemets membrane and
• endothelium

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Applied physiology

• The two primary physiological functions of the
  cornea are
• (i) to act as a major refracting medium
• (ii) to protect the intraocular contents.
• Cornea fulfills these duties by maintaining its
  transparency and replacement of its tissues.

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Corneal transparency

• The transparency is the result of
• Peculiar arrangement of corneal lamellae
  (lattice theory of Maurice),
• Avascularity, and
• Relative state of dehydration, which is
  maintained by barrier effects of epithelium and
  endothelium and the active bicarbonate pump of
  the endothelium.
• Consistent refractive index of all layers

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• Source of nutrients
• 1. Solutes (glucose and others) enter the cornea
  by either simple diffusion or active transport
  through aqueous humour and by diffusion from the
  perilimbal capillaries.
• 2. Oxygen is derived directly from air through
  the tear film. This is an active process
  undertaken by the epithelium.

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Corneal ulcer

• Corneal ulcer is the discontinuation in the
  corneal epithelia.

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Classsification

• Corneal ulcer can be classified variously.
• 1. Depending on location
• (a) Central corneal ulcer
• (b) Peripheral corneal ulcer
• 2. Depending on purulence
• (a) Purulent corneal ulcer or suppurative corneal
  ulcer (most bacterial and fungal).
• (b) Non-purulent corneal ulcers (most of viral,
  chlamydial and allergic corneal ulcers).

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• 3. Depending upon association of hypopyon
• (a) Simple corneal ulcer (without hypopyon)
• (b) Hypopyon corneal ulcer
• 4. Depending upon depth of ulcer
• (a) Superficial corneal ulcer
• (b) Deep corneal ulcer
• (c) Corneal ulcer with impending perforation
• (d) Perforated corneal ulcer
• 5. Depending upon slough formation
• (a) Non-sloughing corneal ulcer
• (b) Sloughing corneal ulcer

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BACTERIAL CORNEAL ULCER

• Being the most anterior part of eyeball, the
  cornea is exposed to atmosphere and hence prone
  to get infected easily.
• At the same time cornea is protected from the
  day-to-day minor infections by the normal defence
  mechanisms present in tears in the form of
  lysozyme, betalysin, and other protective
  proteins.

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• Therefore, infective corneal ulcer may develop
  when either
• the local ocular defence mechanism is
  jeopardised, or
• there is some local ocular predisposing disease,
  or
• host's immunity is compromised, or
• the causative organism is very virulent

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Etiology

• There are two main factors in the production of
  purulent corneal ulcer
• Damage to corneal epithelium and
• Infection of the eroded area.
• However, following three pathogens can invade the
  intact corneal epithelium and produce ulceration
• Neisseria gonorrhoeae,
• Corynebacterium diphtheriae
• Neisseria meningitidis

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Corneal epithelial damage

• It is a prerequisite for most of the infecting
  organisms to produce corneal ulceration. It may
  occur in following conditions
• i. Corneal abrasion due to small foreign body,
  misdirected cilia or trauma
• ii. Epithelial drying as in xerosis and exposure
  keratitis.
• iii. Necrosis of epithelium as in keratomalacia.
• iv. Desquamation of epithelial cells as a result
  of corneal oedema as in bullous keratopathy.
• v. Epithelial damage due to trophic changes as in
  neuroparalytic keratitis.

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• Source of infection include
• Exogenous infection.
• Most of the times corneal infection arises from
  exogenous source like conjunctival sac, lacrimal
  sac (dacryocystitis), infected foreign bodies,
  infected vegetative material and water-borne or
  air-borne infections.
• ii. From the ocular tissue.
• Owing to direct anatomical continuity, diseases
  of the conjunctiva readily spread to corneal
  epithelium, those of sclera to stroma, and of the
  uveal tract to the endothelium of cornea

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• iii. Endogenous infection.
• Rare due to avascular nature of the cornea.

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• Causative organisms.
• Common bacteria associated with corneal
  ulceration are
• Staphylococcus aureus,Pseudomonas pyocyanea,
  Streptococcus pneumoniae, E. coli, Proteus,
  Klebsiella, N. gonorrhoea, N. meningitidis and C.
  diphtheriae.

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Clinical picture

• In bacterial infections the outcome depends upon
• the virulence of organism,
• its toxins and enzymes,
• and the response of host tissue.
• In general, following symptoms and signs may be
  present

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• Symptoms
• 1. Pain and foreign body sensation occurs due to
  mechanical effects of lids and chemical effects
  of toxins on the exposed nerve endings.
• 2. Watering from the eye occurs due to reflex
  hyperlacrimation.
• 3. Photophobia, i.e., intolerance to light
  results from stimulation of nerve endings.
• 4. Blurred vision results from corneal haze.
• 5. Redness of eyes occurs due to congestion of
  circumcorneal vessels.

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• Signs
• 1. Lids are swollen.
• 2. Marked blepharospasm may be there.
• 3. Conjunctiva is chemosed and shows conjunctival
  hyperaemia and ciliary congestion.
• 4. Corneal ulcer usually starts as an epithelial
  defect associated with greyish-white
  circumscribed infiltrate (seen in early stage).
  Soon the epithelial defect and infiltrate
  enlarges and stromal oedema develops

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• A well established bacterial ulcer is
  characterized by
• Yellowish-white area of ulcer which may be oval
• or irregular in shape.
• Margins of the ulcer are swollen and over
  hanging.
• Floor of the ulcer is covered by necrotic
  material.
• Stromal oedema is present surrounding the ulcer
  area.

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• 5. Anterior chamber may or may not show pus
  (hypopyon).
• 6. Iris may be slightly muddy in colour.
• 7. Pupil may be small due to associated toxin
  induced iritis.
• 8. Intraocular pressure may some times be raised
  (inflammatory glaucoma).

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Management of corneal ulcer

• Principals of mgnt
• Enhance wound healing
• Prevent perforation
• Address the underlying condition
• Clinical evaluation
• Each case with corneal ulcer should be subjected
  to
• 1. Thorough history taking to elicit mode of
  onset, duration of disease and severity of
  symptoms
• 2. General physical examination, especially for
  built, nourishment, anaemia and any
  immunocompromising disease

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• 3. Ocular examination should include
• i. Diffuse light examination for gross lesions of
  the lids, conjunctiva and cornea includingtesting
  for sensations.
• ii. Regurgitation test and syringing to rule out
  lacrimal sac infection.
• iii. Biomicroscopic examination after staining of
  corneal ulcer with fluorescein dye or sterilized
  fluorescein impregnated filter paper

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• Laboratory investigations
• (a) Routine laboratory investigations such as
  FBP, ESR, blood sugar,
• (b) Microbiological investigations. These studies
  are essential to identify causative organism,
  confirm the diagnosis and guide the treatment to
  be instituted.

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Treatment

• 1. Specific treatment for the cause -Topical and
  systemic antibiotic
• 2. Non-specific supportive therapy- Cycloplegic,
  analgesics, vitamins
• 3. Physical and general measures

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COMPLICATION
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Complication

• Corneal perforation
• Uveitis
• Anterior and posterior synerchia
• desmatocele
• Endophtalmitis
• Corneal opacity

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Hypopion
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Desmatocele
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CORNEAL DEGENERATIONS

• Corneal degenerations refers to the conditions in
  which the normal cells undergo some degenerative
  changes under the influence of age or some
  pathological condition.
• They may be classified depending upon location as
  axial or peripheral or depending on the etiology
  as Age-Related degenerations and Pathological
  degenerations.

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I. AGE-RELATED DEGENERATIONS

• Arcus senilis
• Arcus senilis refers to an annular lipid
  infiltration of corneal periphery. This is an
  age-related change occurring bilaterally in 60
  percent of patients between 40 and 60 years of
  age and in nearly all patients over the age of
  80.
• Sometimes, similar changes occur in young persons
  (arcus juvenilis) which may or may not be
  associated with hyperlipidemia

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II. PATHOLOGICAL DEGENERATIONS

• Fatty degeneration (Lipoid keratopathy)
• Fatty degeneration of cornea is characterised by
  whitish or yellowish deposits. The fat deposits
  mostly consist of cholesterol and fatty acids.
• Lipid keratopathy can be primary or secondary
• Primary lipid keratopathy is a rare condition
  which occurs in a cornea free of vascularization.
  Serum lipid levels are normal in such patients.
• Secondary lipid keratopathy occurs in
  vascularised corneas secondary to diseases such
  as corneal infections, interstitial keratitis,
  ocular trauma, glaucoma, and chronic iridocyclitis

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Band Keratopathy

• Precipitation of Calcium salts on corneal surface
• Causes
• Eye drops ie pilocaprine
• Hypercalcemia developing in patients with renal
  failure, sarcoidosis and hyperparathyroidism

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Risk factor

• Systemic
• Hyperparathyroidism
• Excessive Vit D
• Renal failure
• Local ocular
• Chronic uveitis, End-stage glaucoma
• Juvenile idiopathic arthritis

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ECTATIC CONDITIONS OF CORNEA

• KERATOCONUS
• Keratoconus (conical cornea) is a noninflammatory
  bilateral (85) ectatic condition of cornea in
  its axial part.
• It usually starts at puberty and progresses
  slowly
• Its cause is still not clear.
• It is labeled as developmental condition,degenerat
  ive condition, hereditary dystrophy and endocrine
  anomaly.
• Essential pathological changes are thinning and
  ectasia which occur as a result of defective
  synthesis of mucopolysaccharide and collagen
  tissue.

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Treatment

• Falling vision may not be corrected by glasses
  due to irregular astigmatism
• Contact lenses usually improve the vision in
  early cases
• In later stages penetrating Keratoplasty may be
  required

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KERATOGLOBUS

• It is a familial and hereditary bilateral
  congenital disorder characterised by thinning and
  hemispherical protrusion of the entire cornea.
• It is non-progressive and inherited as an
  autosomal recessive trait.

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CORNEAL DYSTROPHIES

• Cornea dystrophies are group of genetic, often
  progressive, eye disorders in which abnormal
  material often accumulates in the cornea.
• Asymptomatic.
• May cause significant visual impairment.
• Most forms of corneal dystrophy affect both eyes
  and most forms are inherited as autosomal
  dominant

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• ..END.