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CORNEAL ULCER
 CORNEAL ULCER: Discontinuation in normal epithelial
surface of cornea associated with necrosis of surrounding
corneal tissue.
ETIOLOGICAL CLASSIFICATION
 INFECTIVE KERATITIS
• Bacterial keratitis
• Viral keratitis
• Fungal keratitis
• Chlamydial keratitis
• Protozoal keratitis
• Spirochaetal keratitis
 ALLERGIC KERATITIS
• Phlyctenular keratitis
• Vernal keratitis
• Atopic keratitis
 TROPHIC KERATITIS
• Exposure keratitis
• Neuropathic keratopathy
• Keratomalacia
• Atheromatous ulcer
 TRAUMATIC KERATITIS
 IDIOPATHIC KERATITIS
• Moorens ulcer
• Superior limbic keratoconjunctivitis
• Superficial punctate keratitis of thygeson
TOPOGRAPHICAL CLASSIFICATION
A. ULCERATIVE KERATITIS
1. Depending on location
• Central corneal ulcer
• Peripheral corneal ulcer
2. Depending on purulence
• Purulent corneal ulcer
• Non purulent corneal ulcer
3. Depending upon depth of ulcer
• Superficial corneal ulcer
• Deep corneal ulcer
• Corneal ulcer with impending perforation
• Perforated corneal ulcer
4. Depending upon association of hypopyon
• Simple corneal ulcer
• Hypopyon corneal ulcer
5. Depending upon on slough formation
• Non sloughing corneal ulcer
• Sloughing corneal ulcer
B. NON- ULCERATIVE KERATITIS
1. Superficial keratitis
• Diffuse superficial keratitis
• Superficial punctate keratitis
2. Deep keratitis
a. Non suppurative keratitis
• Interstitial keratitis
• Disciform keratitis
• Keratitis profunda
• Sclerosing keratitis
b. Suppurative deep keratitis
• Central corneal abscess
• Posterior corneal abscess
BACTERIAL CORNEAL ULCER
occurs when
 Local ocular defence mechanism is jeopardised
 Hosts immunity is compromised
 Causative organism is virulent
 If there is some local predisposing factor
 ETIOLOGY: 2 main factors
1. Damage to corneal epithelium
2. Infection of eroded area
3. three pathogens can invade
4. the intact corneal epithelium and produce ulceration:
Neisseria gonorrhoeae, Corynebacterium
diphtheriae and Neisseria meningitidis
 CORNEAL EPITHELIAL DAMAGE :
• Corneal abrasion  small foreign body,
• misdirected cilia, concretions and trivial trauma
• in contact lens wearers
• Epithelial drying  xerosis and exposure keratitis
• Necrosis of epithelium  keratomalacia
• Desquamation of epithelial cells  corneal oedema as in bullous keratopathy.
• Epithelial damage due to trophic changes  neuroparalytic keratitis
 2. Source of infection :
i. Exogenous infection : 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
 The uveal tract to the endothelium of cornea.
 Endogenous infection: . Owing to avascular nature of the cornea,
endogenous infections are of rare occurrence
 Causative organisms. : Staphylococcus aureus,
Pseudomonas pyocyanea,
Streptococcus pneumoniae,
E. coli,
Proteus,
Klebsiella,
N. gonorrhoea,
N. meningitidis and C. diphtheriae.
.
Pathogenesis and pathology of corneal
ulcer :
[A] Pathology of localised corneal ulcer
1. Stage of progressive infiltration
 It is characterised by the infiltration of polymorphonuclear and/or lymphocytes into the
epithelium from the peripheral circulation supplemented by similar cells from the
underlying stroma
 Subsequently necrosis of the involved tissue may occur, depending upon the virulence of
offending agent and the strength of host defence mechanism.
2. Stage of active ulceration
 Active ulceration results from necrosis and sloughing of the epithelium, Bowman's
membrane and the involved stroma. The walls of the active ulcer project owing to
Ulceration may further progress by lateral extension resulting in diffuse superficial
ulceration or
 it may progress by deeper penetration of the infection
leading to Descemetocele formation
corneal perforation.
 When the offending organism is highly virulent and/or host defence mechanism
is jeopardised there occurs deeper penetration
3. Stage of regression
 Regression is induced by the natural host defence mechanisms
and the treatment which augments the normal host response.
 A line of demarcation develops around the ulcer, which consists of leucocytes
that neutralize and eventually phagocytose the offending organisms and necrotic
cellular debris.
 The digestion of necrotic material may result in initial enlargement of the ulcer.
This process may be accompanied by superficial vascularization that increases the
humoral and cellular immune response.
 The ulcer now begins to heal and epithelium starts growing over the edges
4. Stage of cicatrization .
 In this stage healing continues by progressive epithelization which forms a
permanent covering.
 Beneath the epithelium, fibrous tissue is laid down partly by the corneal
fibroblasts and partly by the endothelial cells of the new vessels.
 The stroma thus thickens and fills in under the epithelium, pushing the epithelial
surface anteriorly.
 The degree of scarring from healing varies.
 If the ulcer is very superficial and involves the epithelium only, it heals without
leaving any opacity behind.
 'nebula - Bowman's membrane and few superficial stromal lamellae
 Macula and leucoma - one-third and more than that of corneal stroma,
respectively
[C] Pathology of sloughing corneal ulcer and formation of anterior staphyloma
 When the infecting agent is highly virulent and/or body resistance is very low,
cornea sloughs
total prolapse of iris .
The iris becomes inflamed and exudates block the pupil and cover the iris surface; false
cornea is formed.
exudates organize pseudocornea is formed.
anterior staphyloma
 Clinical picture
 Symptoms :
1.Pain and foreign body sensation
2. Watering
3. Photophobia.
4. Blurred vision results from corneal haze.
5. Redness of eyes
.
 Signs
1. Lids are swollen.
2. Marked .
3. Conjunctiva is chemosed and
shows conjunctival hyperaemia and
ciliary congestion
4. Corneal ulcer
 starts as an epithelial defect
associated with greyish-white
circumscribed
 infiltrate (seen in early stage).
 Epithelial defect and infiltrate
enlarges and stromal oedema
 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.
 Characteristic features
staphylococal aureus and streptococcal pneumoniae
 an oval, yellowish white densely opaque ulcer which is surrounded by
relatively clear cornea.
Pseudomonas species
 an irregular sharp ulcer with thick greenish mucopurulent exudate,
diffuse liquefactive necrosis and semiopaque (ground glass) surrounding
cornea. spread very rapidly and may even perforate within 48 to 72 hours.
 Enterobacteriae (E. coli, Proteus sp., and Klebsiella sp.)
 a shallow ulcer with greyish white pleomorphic suppuration
and diffuse stromal opalescence. The endotoxins produced
by these Gram –ve bacilli may produce ring-shaped corneal
infilterate
 5. Anterior chamber (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)
 corneal ulcer with hypopyon
 Etiopathogenesis
 Causative organisms. Many pyogenic
organisms
 (staphylococci, streptococci, gonococci,
Moraxella) may produce hypopyon,
but by far the most dangerous are
pseudomonas pyocyanea and
pneumococcus.
HYPOPYON CORNEAL ULCER
 'hypopyon corneal ulcer’ is the term used for the
characteristic ulcer caused by pneumococcus and the term
'corneal ulcer with hypopyon' for the ulcers associated with
hypopyon due to other causes.
 The characteristic hypopyon corneal ulcer caused by
pneumococcus is called ulcus serpens.
 Source of infection for pneumococcal infection is usually the
chronic dacryocystitis.
 Factors predisposing to development of hypopyon.
 virulence of the infecting organism and the resistance of the
tissues.
 Hence, hypopyon ulcers are much more common in old
debilitated or alcoholic subjects.
 Mechanism of development of hypopyon.
 some iritis owing to diffusion of bacterial toxins.
 When the iritis is severe the outpouring of leucocytes from the vessels is so
 great that these cells gravitate to the bottom of the anterior chamber to form a hypopyon.
outpouring of polymorphonuclear cells is due to the toxins and not due to actual invasion by
bacteria.
 Once the ulcerative process is controlled, the hypopyon is absorbed.
 Clinical features
 Symptoms are the same as described above for bacterial corneal ulcer.
 remarkably little pain
 Signs. In general the signs are same as described above for the bacterial
ulcer.
 Typical features of ulcus serpens are :
 Ulcus serpens is a greyish white or yellowish disc shaped ulcer occuring
near the centre of cornea
 The ulcer has a tendency to creep over the cornea in a serpiginous
fashion. One edge of the ulcer, along which the ulcer spreads, shows
more infiltration.
 The other side of the ulcer may be undergoing simultaneous cicatrization
and the
 edges may be covered with fresh epithelium.
 Violent iridocyclitis is commonly associated with a definite hypopyon.
 Hypopyon increases in size very rapidly and often results in secondary
glaucoma.
 Ulcer spreads rapidly and has a great tendency for early perforation.
Management
 Management of hypopyon corneal ulcer is same as for other bacterial corneal ulcer.
Secondary glaucoma should be anticipated and treated with 0.5% timolol maleate, B.I.D. eye
drops
 and oral acetazolamide.
Source of infection, i.e., chronic dacryocystitis if detected, should be treated by
dacryocystectomy
 Complications of corneal ulcer
1. Toxic iridocyclitis.
2. Secondary glaucoma.
3. Descemetocele. .
4. Perforation of corneal ulcer.
 Sequelae of corneal perforation include :
 i. Prolapse of iris. It occurs immediately following perforation in a bid to plug it.
 ii. Subluxation or anterior dislocation of lens may occur due to sudden stretching and
rupture
 of zonules.
 iii. Anterior capsular cataract. It is formed when the lens comes in contact with the
ulcer following a perforation in the pupillary area.
 iv. Corneal fistula. It is formed when the perforation in the pupillary area is not
plugged by iris and is lined by epithelium
Purulent uveitis, endophthalmitis or even panophthalmitis
vi. Intraocular haemorrhage
5. Corneal scarring
Management of a case of corneal ulcer
[A] Clinical evaluation
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.
3. Ocular examination should include:
i. Diffuse light examination for gross
ii. Regurgitation test and syringing to rule out lacrimal sac infection.
iii. Biomicroscopic examination after staining of corneal ulcer with 2 per
cent freshly prepared aqueous solution of fluorescein dye or sterilised
fluorescein impregnated filter paper strip to note site, size, shape, depth,
margin, floor and vascularization of corneal ulcer. presence of keratic
precipitates
 Laboratory investigations
 Routine laboratory investigations such as Hb, TLC, DLC,
ESR, blood sugar, complete urine and stool examination
should be carried out in each case.
 Microbiological investigations.
 Confirm the diagnosis and guide the treatment to be instituted.
 Gram and Giemsa stained smears for possible identification of infecting
organisms.
 10 per cent KOH wet preparation for identification of fungal hyphae.
.
 Calcofluor white (CFW) stain preparation is viewed under
fluorescence microscope for fungal filaments, the walls of
which appear bright apple green.
 Culture on blood agar medium for aerobic organisms
 Culture on Sabouraud's dextrose agar medium for fungi.
 [C] Treatment
 I. Treatment of uncomplicated corneal ulcer
1. Specific treatment for the cause.
2. Non-specific supportive therapy.
3. Physical and general measures.
1. The specific treatment
(a) Topical antibiotics.
 should be with combination therapy to cover both gram-negative and
gram-positive organisms.
 start fortified gentamycin (14 mg/ml) or fortified tobramycin
(14mg/ml) eyedrops along with fortified cephazoline (50mg/ ml), every
½ to one hour for first few days and then reduced to 2 hourly.
 Ciprofloxacin (0.3%) eye drops, or
 Ofloxacin (0.3%) eye drops, or
 Gatifloxacin (0.3%) eye drops.
(b) Systemic antibiotics are usually not required.
 cephalosporine and an aminoglycoside or oral ciprofloxacin
(750 mg twice daily)
 may be given in fulminating cases with perforation and
when sclera is also involved
 2. Non-specific treatment
(a) Cycloplegic drugs. 1 percent atropine eye ointment or drops should be used
• to reduce pain from ciliary spasm and
• to prevent the formation of posterior synechiae from secondary
 iridocyclitis.
• also increases the blood supply to anterior uvea by relieving pressur on the
anterior ciliary arteries and so brings more antibodies in the aqueous
humour. It also
• reduces exudation by decreasing hyperaemia and vascular permeability.
 Other cycloplegic 2 per cent homatropine.
 (b) Systemic analgesics and anti-inflammator drugs such as
paracetamol and ibuprofen relieve the pain and decrease
oedema.
 (c) Vitamins (A, B-complex and C) help in early healing of ulcer.
 3. Physical and general measures
 (a) Hot fomentation. Local application of heat (preferably dry)
gives comfort, reduces pain and causes vasodilatation.
 (b) Dark goggles may be used to prevent photophobia.
 (c) Rest, good diet and fresh air may have a soothing effect.
 II. Treatment of non-healing corneal ulcer
1.Removal of any known cause of non-healing ulcer.
2. Mechanical debridement of ulcer
3. Cauterisation of the ulcer may also be considered
4. Bandage soft contact lens may also help in healing.
5. Peritomy,
 III. Treatment of impending perforation
1. No strain. advised to avoid sneezing, coughing and straining during stool etc.
2. Pressure bandage should be applied
3. Lowering of intraocular pressure by
 use of acetazolamide 250 mg QID orally,
 intravenous mannitol (20%) drip stat,
 oral glycerol twice a day,
 0.5% timolol eyedrops twice a day, and
 even paracentesis
4. Tissue adhesive glue such as cynoacrylate is helpful in preventing
perforation.
5. Conjunctival flap(GUNDERSEN FLAP). The cornea may be
covered completely or partly by a conjunctival flap to give
support to the weak tissue.
6. Bandage soft contact lens may also be used.
7. Penetrating therapeutic keratoplasty(tectonic graft)
 IV. Treatment of perforated corneal ulcer
 Best is to prevent perforation.
 However, if perforation has occurred,
 immediate measures should be taken to restore the integrity of perforated cornea.
• use of tissue adhesive glues,
• covering with conjunctival flap(GUNDERSEN FLAP),
• use of bandage soft contact lens
• therapeutic keratoplasty
MYCOTIC KERATITIS/FUNGAL
CORNEAL ULCER
 ETIOLOGY
1. PREDISPOSING FACTORS
• Injury by vegetative material like leaf, branch of tree, thorn, wood etc
• Injury by animal tail
• Systemic immunosuppression
• Local immunosuppression
2. Causative fungi
a. Filamentous fungi: aspergillus, fusarium, Alternaria, curvularia, penicillium,
mucor, Rhizopus.
b. Yeasts: candida, cryptococcus
c. Dimorphic fungi: histoplasma, coccidioides, Blastomyces
Most common organisms responsible for mycotic corneal ulcer are
• Aspergillus fumigatus
• Candida
• fusarium
 Symptoms
• Less marked
• Pain
• Watering
• Photophobia
• Blurred vision
• Redness of eyes
 Signs
More prominent than symptoms
• Corneal ulcer is greyish white, dry looking with feathery finger like extensions
• Sterile immune ring aka wessely ring – yellow line of demarcation where fungal
antigen and host antibodies meet may be present
• Multiple , small satellite lesions may be present
• Hypopyon – large, thick, immobile with upper convex border is formed
• Hypopyon is not sterile
 Endothelial plaque – composed of fibrin and leucocytes may be located under
stromal lesion
 Perforation of ulcer is rare
 Diagnosis
 Direct microscopy
• KOH – wet mount preparation
• Gram stain
• Giemsa stain
• Lactophenol cotton blue
• Calcoflor white
 Culture on sabouraud’s agar medium
 PCR
 Anterior chamber paracentesis
 Corneal biopsy
 Definitive treatment includes anti-fungal ulcer
 Topical antifungal eyedrops
• Filamentous fungi – 5% natamycin eye drops
0.1 to 0.3% amphotericin B eye drops
0.2% fluconazole
miconazole (10mg/ml)
voriconazole(10%) instilled hrly then tapered slowly over 6-8
weeks
• For yeast – amphotericin B eye drops(DOC)
Natamycin 3.5% eye ointment five times a day is effective
• Intracameral and intracorneal/ intrastromal administration of voriconazole in
cases with intraocular extension or anterior chamber involvement.
• Systemic antifungal drugs – deep fungal keratitis
BACTERIAL ULCER FUNGAL ULCER
symptoms more symptoms Less symptoms
ulcer Yellowish white,well defined margins Greyish white, dry looking with
feathery finger like extensions
Base of ulcer clean necrotic
Satellite lesions absent present
hypopyon Sterile, mobile, upper concave border Big, thick, immobile with upper
convex border, non-sterile
Wessely ring absent present
Risk factors Contact lens wearers , trauma Injury with vegetative material
BACTERIAL ULCER FUNGAL ULCER
investigations gram stain, blood agar KOH mount, SDA
treatment Based on culture and sensitivity
Fortified antibiotics
5% natamycin
Oral anti- fungal drugs
Perforation of cornea common rare
ULCER.pptx

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ULCER.pptx

  • 2.  CORNEAL ULCER: Discontinuation in normal epithelial surface of cornea associated with necrosis of surrounding corneal tissue.
  • 3. ETIOLOGICAL CLASSIFICATION  INFECTIVE KERATITIS • Bacterial keratitis • Viral keratitis • Fungal keratitis • Chlamydial keratitis • Protozoal keratitis • Spirochaetal keratitis
  • 4.  ALLERGIC KERATITIS • Phlyctenular keratitis • Vernal keratitis • Atopic keratitis  TROPHIC KERATITIS • Exposure keratitis • Neuropathic keratopathy • Keratomalacia • Atheromatous ulcer
  • 5.  TRAUMATIC KERATITIS  IDIOPATHIC KERATITIS • Moorens ulcer • Superior limbic keratoconjunctivitis • Superficial punctate keratitis of thygeson
  • 6. TOPOGRAPHICAL CLASSIFICATION A. ULCERATIVE KERATITIS 1. Depending on location • Central corneal ulcer • Peripheral corneal ulcer 2. Depending on purulence • Purulent corneal ulcer • Non purulent corneal ulcer
  • 7. 3. Depending upon depth of ulcer • Superficial corneal ulcer • Deep corneal ulcer • Corneal ulcer with impending perforation • Perforated corneal ulcer 4. Depending upon association of hypopyon • Simple corneal ulcer • Hypopyon corneal ulcer
  • 8. 5. Depending upon on slough formation • Non sloughing corneal ulcer • Sloughing corneal ulcer
  • 9. B. NON- ULCERATIVE KERATITIS 1. Superficial keratitis • Diffuse superficial keratitis • Superficial punctate keratitis 2. Deep keratitis a. Non suppurative keratitis • Interstitial keratitis • Disciform keratitis
  • 10. • Keratitis profunda • Sclerosing keratitis b. Suppurative deep keratitis • Central corneal abscess • Posterior corneal abscess
  • 11. BACTERIAL CORNEAL ULCER occurs when  Local ocular defence mechanism is jeopardised  Hosts immunity is compromised  Causative organism is virulent  If there is some local predisposing factor
  • 12.  ETIOLOGY: 2 main factors 1. Damage to corneal epithelium 2. Infection of eroded area 3. three pathogens can invade 4. the intact corneal epithelium and produce ulceration: Neisseria gonorrhoeae, Corynebacterium diphtheriae and Neisseria meningitidis
  • 13.  CORNEAL EPITHELIAL DAMAGE : • Corneal abrasion  small foreign body, • misdirected cilia, concretions and trivial trauma • in contact lens wearers • Epithelial drying  xerosis and exposure keratitis • Necrosis of epithelium  keratomalacia • Desquamation of epithelial cells  corneal oedema as in bullous keratopathy. • Epithelial damage due to trophic changes  neuroparalytic keratitis
  • 14.  2. Source of infection : i. Exogenous infection : 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  The uveal tract to the endothelium of cornea.
  • 15.  Endogenous infection: . Owing to avascular nature of the cornea, endogenous infections are of rare occurrence  Causative organisms. : Staphylococcus aureus, Pseudomonas pyocyanea, Streptococcus pneumoniae, E. coli, Proteus, Klebsiella, N. gonorrhoea, N. meningitidis and C. diphtheriae. .
  • 16. Pathogenesis and pathology of corneal ulcer : [A] Pathology of localised corneal ulcer 1. Stage of progressive infiltration  It is characterised by the infiltration of polymorphonuclear and/or lymphocytes into the epithelium from the peripheral circulation supplemented by similar cells from the underlying stroma  Subsequently necrosis of the involved tissue may occur, depending upon the virulence of offending agent and the strength of host defence mechanism.
  • 17. 2. Stage of active ulceration  Active ulceration results from necrosis and sloughing of the epithelium, Bowman's membrane and the involved stroma. The walls of the active ulcer project owing to Ulceration may further progress by lateral extension resulting in diffuse superficial ulceration or  it may progress by deeper penetration of the infection leading to Descemetocele formation corneal perforation.
  • 18.  When the offending organism is highly virulent and/or host defence mechanism is jeopardised there occurs deeper penetration
  • 19. 3. Stage of regression  Regression is induced by the natural host defence mechanisms and the treatment which augments the normal host response.  A line of demarcation develops around the ulcer, which consists of leucocytes that neutralize and eventually phagocytose the offending organisms and necrotic cellular debris.
  • 20.  The digestion of necrotic material may result in initial enlargement of the ulcer. This process may be accompanied by superficial vascularization that increases the humoral and cellular immune response.  The ulcer now begins to heal and epithelium starts growing over the edges
  • 21. 4. Stage of cicatrization .  In this stage healing continues by progressive epithelization which forms a permanent covering.  Beneath the epithelium, fibrous tissue is laid down partly by the corneal fibroblasts and partly by the endothelial cells of the new vessels.  The stroma thus thickens and fills in under the epithelium, pushing the epithelial surface anteriorly.
  • 22.  The degree of scarring from healing varies.  If the ulcer is very superficial and involves the epithelium only, it heals without leaving any opacity behind.  'nebula - Bowman's membrane and few superficial stromal lamellae  Macula and leucoma - one-third and more than that of corneal stroma, respectively
  • 23.
  • 24.
  • 25.
  • 26. [C] Pathology of sloughing corneal ulcer and formation of anterior staphyloma  When the infecting agent is highly virulent and/or body resistance is very low, cornea sloughs total prolapse of iris . The iris becomes inflamed and exudates block the pupil and cover the iris surface; false cornea is formed. exudates organize pseudocornea is formed. anterior staphyloma
  • 27.  Clinical picture  Symptoms : 1.Pain and foreign body sensation 2. Watering 3. Photophobia. 4. Blurred vision results from corneal haze. 5. Redness of eyes .
  • 28.  Signs 1. Lids are swollen. 2. Marked . 3. Conjunctiva is chemosed and shows conjunctival hyperaemia and ciliary congestion
  • 29. 4. Corneal ulcer  starts as an epithelial defect associated with greyish-white circumscribed  infiltrate (seen in early stage).  Epithelial defect and infiltrate enlarges and stromal oedema
  • 30.  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.
  • 31.  Characteristic features staphylococal aureus and streptococcal pneumoniae  an oval, yellowish white densely opaque ulcer which is surrounded by relatively clear cornea. Pseudomonas species  an irregular sharp ulcer with thick greenish mucopurulent exudate, diffuse liquefactive necrosis and semiopaque (ground glass) surrounding cornea. spread very rapidly and may even perforate within 48 to 72 hours.
  • 32.  Enterobacteriae (E. coli, Proteus sp., and Klebsiella sp.)  a shallow ulcer with greyish white pleomorphic suppuration and diffuse stromal opalescence. The endotoxins produced by these Gram –ve bacilli may produce ring-shaped corneal infilterate
  • 33.  5. Anterior chamber (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)
  • 34.  corneal ulcer with hypopyon  Etiopathogenesis  Causative organisms. Many pyogenic organisms  (staphylococci, streptococci, gonococci, Moraxella) may produce hypopyon, but by far the most dangerous are pseudomonas pyocyanea and pneumococcus.
  • 35. HYPOPYON CORNEAL ULCER  'hypopyon corneal ulcer’ is the term used for the characteristic ulcer caused by pneumococcus and the term 'corneal ulcer with hypopyon' for the ulcers associated with hypopyon due to other causes.  The characteristic hypopyon corneal ulcer caused by pneumococcus is called ulcus serpens.
  • 36.  Source of infection for pneumococcal infection is usually the chronic dacryocystitis.  Factors predisposing to development of hypopyon.  virulence of the infecting organism and the resistance of the tissues.  Hence, hypopyon ulcers are much more common in old debilitated or alcoholic subjects.
  • 37.  Mechanism of development of hypopyon.  some iritis owing to diffusion of bacterial toxins.  When the iritis is severe the outpouring of leucocytes from the vessels is so  great that these cells gravitate to the bottom of the anterior chamber to form a hypopyon. outpouring of polymorphonuclear cells is due to the toxins and not due to actual invasion by bacteria.  Once the ulcerative process is controlled, the hypopyon is absorbed.
  • 38.  Clinical features  Symptoms are the same as described above for bacterial corneal ulcer.  remarkably little pain  Signs. In general the signs are same as described above for the bacterial ulcer.  Typical features of ulcus serpens are :  Ulcus serpens is a greyish white or yellowish disc shaped ulcer occuring near the centre of cornea
  • 39.  The ulcer has a tendency to creep over the cornea in a serpiginous fashion. One edge of the ulcer, along which the ulcer spreads, shows more infiltration.  The other side of the ulcer may be undergoing simultaneous cicatrization and the  edges may be covered with fresh epithelium.
  • 40.  Violent iridocyclitis is commonly associated with a definite hypopyon.  Hypopyon increases in size very rapidly and often results in secondary glaucoma.  Ulcer spreads rapidly and has a great tendency for early perforation.
  • 41. Management  Management of hypopyon corneal ulcer is same as for other bacterial corneal ulcer. Secondary glaucoma should be anticipated and treated with 0.5% timolol maleate, B.I.D. eye drops  and oral acetazolamide. Source of infection, i.e., chronic dacryocystitis if detected, should be treated by dacryocystectomy
  • 42.  Complications of corneal ulcer 1. Toxic iridocyclitis. 2. Secondary glaucoma. 3. Descemetocele. . 4. Perforation of corneal ulcer.
  • 43.
  • 44.  Sequelae of corneal perforation include :  i. Prolapse of iris. It occurs immediately following perforation in a bid to plug it.  ii. Subluxation or anterior dislocation of lens may occur due to sudden stretching and rupture  of zonules.  iii. Anterior capsular cataract. It is formed when the lens comes in contact with the ulcer following a perforation in the pupillary area.  iv. Corneal fistula. It is formed when the perforation in the pupillary area is not plugged by iris and is lined by epithelium
  • 45. Purulent uveitis, endophthalmitis or even panophthalmitis vi. Intraocular haemorrhage 5. Corneal scarring Management of a case of corneal ulcer [A] Clinical evaluation 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.
  • 46. 3. Ocular examination should include: i. Diffuse light examination for gross ii. Regurgitation test and syringing to rule out lacrimal sac infection. iii. Biomicroscopic examination after staining of corneal ulcer with 2 per cent freshly prepared aqueous solution of fluorescein dye or sterilised fluorescein impregnated filter paper strip to note site, size, shape, depth, margin, floor and vascularization of corneal ulcer. presence of keratic precipitates
  • 47.  Laboratory investigations  Routine laboratory investigations such as Hb, TLC, DLC, ESR, blood sugar, complete urine and stool examination should be carried out in each case.
  • 48.  Microbiological investigations.  Confirm the diagnosis and guide the treatment to be instituted.  Gram and Giemsa stained smears for possible identification of infecting organisms.  10 per cent KOH wet preparation for identification of fungal hyphae. .
  • 49.  Calcofluor white (CFW) stain preparation is viewed under fluorescence microscope for fungal filaments, the walls of which appear bright apple green.  Culture on blood agar medium for aerobic organisms  Culture on Sabouraud's dextrose agar medium for fungi.
  • 50.  [C] Treatment  I. Treatment of uncomplicated corneal ulcer 1. Specific treatment for the cause. 2. Non-specific supportive therapy. 3. Physical and general measures.
  • 51. 1. The specific treatment (a) Topical antibiotics.  should be with combination therapy to cover both gram-negative and gram-positive organisms.  start fortified gentamycin (14 mg/ml) or fortified tobramycin (14mg/ml) eyedrops along with fortified cephazoline (50mg/ ml), every ½ to one hour for first few days and then reduced to 2 hourly.  Ciprofloxacin (0.3%) eye drops, or  Ofloxacin (0.3%) eye drops, or  Gatifloxacin (0.3%) eye drops.
  • 52. (b) Systemic antibiotics are usually not required.  cephalosporine and an aminoglycoside or oral ciprofloxacin (750 mg twice daily)  may be given in fulminating cases with perforation and when sclera is also involved
  • 53.  2. Non-specific treatment (a) Cycloplegic drugs. 1 percent atropine eye ointment or drops should be used • to reduce pain from ciliary spasm and • to prevent the formation of posterior synechiae from secondary  iridocyclitis. • also increases the blood supply to anterior uvea by relieving pressur on the anterior ciliary arteries and so brings more antibodies in the aqueous humour. It also • reduces exudation by decreasing hyperaemia and vascular permeability.  Other cycloplegic 2 per cent homatropine.
  • 54.  (b) Systemic analgesics and anti-inflammator drugs such as paracetamol and ibuprofen relieve the pain and decrease oedema.  (c) Vitamins (A, B-complex and C) help in early healing of ulcer.
  • 55.  3. Physical and general measures  (a) Hot fomentation. Local application of heat (preferably dry) gives comfort, reduces pain and causes vasodilatation.  (b) Dark goggles may be used to prevent photophobia.  (c) Rest, good diet and fresh air may have a soothing effect.
  • 56.  II. Treatment of non-healing corneal ulcer 1.Removal of any known cause of non-healing ulcer. 2. Mechanical debridement of ulcer 3. Cauterisation of the ulcer may also be considered 4. Bandage soft contact lens may also help in healing. 5. Peritomy,
  • 57.  III. Treatment of impending perforation 1. No strain. advised to avoid sneezing, coughing and straining during stool etc. 2. Pressure bandage should be applied 3. Lowering of intraocular pressure by  use of acetazolamide 250 mg QID orally,  intravenous mannitol (20%) drip stat,  oral glycerol twice a day,  0.5% timolol eyedrops twice a day, and  even paracentesis
  • 58. 4. Tissue adhesive glue such as cynoacrylate is helpful in preventing perforation. 5. Conjunctival flap(GUNDERSEN FLAP). The cornea may be covered completely or partly by a conjunctival flap to give support to the weak tissue. 6. Bandage soft contact lens may also be used. 7. Penetrating therapeutic keratoplasty(tectonic graft)
  • 59.  IV. Treatment of perforated corneal ulcer  Best is to prevent perforation.  However, if perforation has occurred,  immediate measures should be taken to restore the integrity of perforated cornea. • use of tissue adhesive glues, • covering with conjunctival flap(GUNDERSEN FLAP), • use of bandage soft contact lens • therapeutic keratoplasty
  • 60. MYCOTIC KERATITIS/FUNGAL CORNEAL ULCER  ETIOLOGY 1. PREDISPOSING FACTORS • Injury by vegetative material like leaf, branch of tree, thorn, wood etc • Injury by animal tail • Systemic immunosuppression • Local immunosuppression
  • 61. 2. Causative fungi a. Filamentous fungi: aspergillus, fusarium, Alternaria, curvularia, penicillium, mucor, Rhizopus. b. Yeasts: candida, cryptococcus c. Dimorphic fungi: histoplasma, coccidioides, Blastomyces Most common organisms responsible for mycotic corneal ulcer are • Aspergillus fumigatus • Candida • fusarium
  • 62.  Symptoms • Less marked • Pain • Watering • Photophobia • Blurred vision • Redness of eyes
  • 63.  Signs More prominent than symptoms • Corneal ulcer is greyish white, dry looking with feathery finger like extensions • Sterile immune ring aka wessely ring – yellow line of demarcation where fungal antigen and host antibodies meet may be present • Multiple , small satellite lesions may be present • Hypopyon – large, thick, immobile with upper convex border is formed • Hypopyon is not sterile
  • 64.  Endothelial plaque – composed of fibrin and leucocytes may be located under stromal lesion  Perforation of ulcer is rare
  • 65.  Diagnosis  Direct microscopy • KOH – wet mount preparation • Gram stain • Giemsa stain • Lactophenol cotton blue • Calcoflor white
  • 66.  Culture on sabouraud’s agar medium  PCR  Anterior chamber paracentesis  Corneal biopsy
  • 67.  Definitive treatment includes anti-fungal ulcer  Topical antifungal eyedrops • Filamentous fungi – 5% natamycin eye drops 0.1 to 0.3% amphotericin B eye drops 0.2% fluconazole miconazole (10mg/ml) voriconazole(10%) instilled hrly then tapered slowly over 6-8 weeks
  • 68. • For yeast – amphotericin B eye drops(DOC) Natamycin 3.5% eye ointment five times a day is effective • Intracameral and intracorneal/ intrastromal administration of voriconazole in cases with intraocular extension or anterior chamber involvement. • Systemic antifungal drugs – deep fungal keratitis
  • 69. BACTERIAL ULCER FUNGAL ULCER symptoms more symptoms Less symptoms ulcer Yellowish white,well defined margins Greyish white, dry looking with feathery finger like extensions Base of ulcer clean necrotic Satellite lesions absent present hypopyon Sterile, mobile, upper concave border Big, thick, immobile with upper convex border, non-sterile Wessely ring absent present Risk factors Contact lens wearers , trauma Injury with vegetative material
  • 70. BACTERIAL ULCER FUNGAL ULCER investigations gram stain, blood agar KOH mount, SDA treatment Based on culture and sensitivity Fortified antibiotics 5% natamycin Oral anti- fungal drugs Perforation of cornea common rare