orneal ulcer, also called keratitis, is an inflammatory or, more seriously, infective condition of the cornea involving disruption of its epithelial layer with involvement of the corneal stroma. It is a common condition in humans particularly in the tropics and in farming. In developing countries, children afflicted by vitamin A deficiency are at high risk for corneal ulcer and may become blind i
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