Approach to corneal ulcer with colour coding of corneal lesions

2. Defination
 Keratitis: inflammation of the cornea characteried by
corneal oedema, cellular infiltration and ciliary
congestion.

3. Difference b/w keratitis and
corneal ulcer
 Keratitis is just the inflammation of cornea without an
epithelial defect. It means a cornea can harbor a bacterial or
viral infection (i.e bacterial and viral keratitis) without
having a loss of tissue (ulcer).
 Keratitis is of two types based upon topogrophy :
1) non ulcerative keratitis
2) ulcerative keratitis or corneal
ulcer.


4. A
CORNEAL ULCER / ulcerative
keratitis.
Corneal ulcer is discontinution /Breach in the
normal epithelial surface of cornea associated with
necrosis and sloughing of the sourrounding tissue.
So, a cornea may also have an ulcer without the
microbial infection. (ex : due to mechanical
trauma ).

10. Etiopathogenesis
 There are two main factors responsible in the production of
infective corneal ulcers:
1)Damage to the corneal epithelium.
2)infection of the eroded area by the microorganism.
 EXCEPTION; neisseria gonorrhoeae, neisseria meningitidis,
corynebacterium diphtheriae .
 these pathogens invade the intact corneal epithelium and
produces ulceration.
 Although clinical signs may be insufficient to confirm
infection, a break in the continuity of epithelium ass. With
underlying stromal infiltrate should be considered infectious
unless proved otherwise.

11. APPROACH & Work up of
corneal ulcer
1.) Examination 2.) Investigations
 Take short history and see
the sign n symptoms.
 Look for predisposing risk
factors
 Do the clinical examination
and find the pathognomic
signs.
 systemic investigations
 ocular investigations:
1) clinical investigations.
2) Microbiological
investigations : smear ex.
& culture exam.

12. HISTORY TAKING is very important
Asking short history from patient is always imp in making
some provisional diagnosis regarding a corneal ulcer.
 ask the patient if he has suffered any injury to the cornea?? (
really important to think for fungal ulcer if the history is from
any vegetative or agricultral material or from animal tail.
 Ask the patient if he has ever used or currently using contact
lenses or history of contact with muddy water ( imp. To think
for either acanthomeba or pseudomonas ulcer.)
 Ask the patient regarding medication history ( imp. If there is
history of steroid intake in the past or any traditional eyedrops
)

13.  Ask the patient if he is suffering from any systemic
disease to know the immune status of the patient. (
important if patient is having immunocompromised
status due to some disease like diabets and hiv)
 Ask the patient if his eyes have redness in the past also
and if it happens most of the times. ( it is important to
think for viral etioligy for recurrent infection from
HSV …..then we can check the corneal sensation and
stain the cornea to look for particualar dendritic
pattern of hsv keratitis).

14. sign & symptoms of corneal ulcer
includes
 PAIN : due to mechanical effects of lids + chemical effects of
toxins on exposed N. endings.
 WATERING : due to reflex hyperlacrimation.
 DISCHARGE : all most all cases of corneal ulcer presents with
complaint of discharge which is different in different conditions.
a) Watery in :- viral ulcer, reflex tearing, or small bacterial
ulcer.
b) Mucuopurelent in :- pseudomonas, gonococcus
c) Membranous discharge in :- keratitis caused by c.dipht.

15.  PHOTOPHOBIA : due to stimulation of N .endings.
 BLURRING OF VISION : results from corneal haze.
 REDNESS : an ass. Counjctivitis may cause severe redness due
to congestion of the circumcorneal vessels.
 DECREASE IN Va : most cases reports with history of sudden
decrease in vision which depends upon :-
a) location of lesion,
b) +of any ass. pupillary membrane,
c) +of ass. Hypopyon, cataract, glaucoma & endophthalmitis.

16.  onset of disease : is also very important .
Depends upon: virulence of org., status of ocular &
systemic immunity of the patient.
:- bacterial keratitis ( sudden and
rapid progression)
:-fungi & acanthoemba ( chronic &
gradual course).

17. look for predisposing risk factors
Ocular risk factors
Systemic risk factors
Occupational risk factors

18. Ocular risk factors
1.) TRAUMA:
causes breach in the intact corneal epithelium barrier which is the 1st line of
defence against keratitis.
 h/o: trauma by- vegetative material suggests fungal and acanthoemba
keratitis
 By animal bites –suspect of anaerobic inf.
2.) CONTACT LENS:
one of the commonest predisposing factor for association of keratitis ,
and depends upon;
 type of contact lens (soft > hard),
 duration of use ,
 method of lens care hyigene ( use of contaminated solutions- acanthoemba)’

19. 3.) LID AND ADNEXAL INFECTIONS:
 ulcerative keratitis caused by pneumococcus has
association With dacrocystits,
 inf. with actinomyces has association with canaliculitis.
 any lid abnormality like: trichisis, ectropion, entropion,
blepharitis, lagophthalmos, meibomitis ( all these have
predisposition for infectious keratitis.)
4.) OCULAR SURFACE DISEASE:
conditions like DES, chemical injury, allergic eye disease:-
decreases the integrity and adherence of corneal epithelium
, predisposes to infection.

20. 5) BULLOUS KERATOPATHY:
it is caused by endothelial decompensation disturbs the barrier
function of tearfilm & epithelium –corneal surface becomes
irregular and then erosions & epithelial defects occur.
6.)TOPICAL MEDICATIONS:
 prolong use of corticosteroids adversly affects the local
immunity and tear film and cause infectious keratitis.
It also decreases neutrophil migration in response to chemotactic
factors released during microbial keratitis.
 prolong use of NSAIDS, anasthetics, antibiotics, antiglaucoma
medications also predisposes to infectious keratitis by causing toxic
changes in epithelium.
 use of traditional eye medications in developimg countries like
india.

21.  SYSTEMIC RISK FACTORS:
 Diseases like : D.M, AIDS, S jogrens, steven jhonsns
decreases the immunity and thus predisposes for the
microbial keratitis.
 OCCUPATIONAL RISK FACTORS:
 fungal keratitis : most susceptible in persons
working in farming and agriculture.
 keratitis ass. With listeria monocytogens : known to
occur in cases of ANIMAL HANDELRS .

22. CLINICAL EXAMINATION
 First of all look at the general condition of the patient
give A close look at the facial features :
 look for any lesions or vesicles
 presence of any facial palsy
 abnormal blink rate
 excessive ocular exposure.
 Level of Va & size of lesion are imp. Indicators of severity of
a case of infective keratitis.
 Different organisms presents with different clinical picture
which helps in making diagnosis.

23. Sequence wise examination in a
patient of ulerative keratitis:
1.) record Va: UCVA
2.) external ocular examination & slit lamp exam.:
1 – eyelids : discussed above.
2 - lacrimal sac : discussed above.
3 – conjuctiva : examine both bulbar and palpebral
counjuctiva on S/L for any disease or lesion like vkc, akc,
presence of papillas. etc.
(look for any kind of discharge)
(congestion.)

24. 4- precorneal tearfilm: look for - debris (sign of active
keratitis)
- filaments (to rule out filamentry keratitis)
5- CORNEA –
a detail examination of ulcer & sourrounding areas should
be done and should be recorded in detail as follows:
(a) location of ulcer
(b) shape of ulcer
(c) margins
(d) size of ulcer
(e) epithelial defect
(f) infiltration
(e) sourrounding cornea

25. (a) location of ulcer:
whether central, paracentral, peripheral or total.
 Some organisms have a predilection for certain
specfic locations on cornea:
 shield ulcer - lower border in upper half of visual
axis.
 central ulcers - are usually ass. With –
staphylococcus species .
 peripheral corneal ulcers – may be caused by
M.tuberculosis & hsv.

26. (b) shape of ulcer:
 bacterial ulcer - punched out lesions usually.
 fungal ulcer - usually dry looking & with feathery
margins.
 HSV - dendritic pattern or may appear as amoeboid
pattern.
 acanthamoeba - RING shape lesion

27. (c) margins:
margins vary acc. to the stage of ulcer;
 infectious and sterile c.u - well defined margins
 active ulcer - indistinct margins
 mooren’s ulcer - overhanging margins.
(d) size:
 to be measured using s/l micrometer
 Measurement of the ulcer should be done at the intial level as
well as on follow up visits, till the resolution of ulcer( its an
imp. parameter for moniotoring the success of treatment.
 GRADING OF ULCER ACC .TO SIZE: <2mm - mild
2-5mm -moderate
>5mm - severe

28. (e) epithelial defect:
 size of the epithelial defect & size of the infiltration
should be measured separatly in two largest meridians.
 They must be measured separatly as their sizes may
not be similar.
 Epithelial defects should be stained with fluorescein
dye & the size should be measured using S/L
micrometer at all following steps.
 Characterstic staining patterns may be seen in diff.
types of infectious keratitis as discussed above

29. (f) infiltration:
 it’s an intrinsic component of supp. infectious
keratitis.
 May be single/multiple & maybe of varying sizes
depending on the organisms involve and duration of
infection.
If there are multiple infiltrates as seen in some fungal
corneal ulcer or in case of a poly microbial keratitis,
each one of them is measured separatly at all visits.

30. (g) sourrounding cornea:
may be clear or hazy due to edema depending upon the
virulence of organisms.
 Gram+ve cocci & candida - tends to cause localized
lesions with distinct border & minimum sourrounding
edema.
 Pseudomonas –produces ulcers in which sourrounding
cornea becomes edematous and hazy giving a GROUND
GLASS APPEARANCE.
(h) corneal vascularization:
may be superficial or deep in infectious keratitis &
suggests the commencement of healing of ulcer.
(i) corneal sensations: decreases in HSV keratitis.

31. ( j) corneal thinning/perforation: closely monitor the
ulcer for thinning, descemetocele formation & perforation.
Occurrence of perforation is an indication of medical therapy
and needs urgent surgical therapy.
6-ANTERIOR CHAMBER –
 look for mild cells & flare to severe hypopyon.
fixed immobile hypopyon :-
is a feature of fungal keratitis.

33. BACTERIAL KERATITIS
INTRO :
 bacteria are the most important cause of infectious
keratitis occuring either due to bact. Adherence over the
wounded corneal surface or by direct bacterial invasion
through intact epithelium in some special bacterias.
RISK FACTORS :
 discussed above (ocular, systemic, occupational factors)
contact lens wear and trauma are imp.

34. CLINICAL –FEATURES OF
BACTERIAL KERATITIS
SYMPTOMS
 Pain
 Photophobia
 Blurred vision
 Watering
SIGNS
 An epithelial defect with localised or diffuse
infiltration of epithelium or stroma is the most imp.
corneal sign.
 Swelling of the lids, blephrospasm of varying degree
may be present .
 Counjctival injection, chemosis & nonspecific
papillary response may be present.
 Stromal edema and folds in descmets memb.
 A.C cells and flare may be present in inlfammation
(HYPOPYON (sterile) if svere inlfam. +

35. TREATMENT
1) General conisderations : -
 hospital admission for patients who are not likely to comply
or are unable to self adminster treatment.
 discontinution of contact lens wear.
 a clear plastic eye shield should be worn between eye drop
instillation if significant thinning is present.
 decision to treat ; intensive treatment may not be required for
small infiltrates that are clinically sterile and may be treated by
mild topical antibiotics and steroids.
 It is very important to note that the causative organism cant
be reliably defined from ulcers appearance only, so empirical
broad spectrum treatment is usually initiated before microscopy
results are available.

36. 2) local therapy:
intially should consists of broad spectrum antibiotics that cover most of the
pathogens. Intial instillation is at hourly intervals day and night for 24-48
hrs then tappered acc.to clinical diagnosis.
 Antibiotic monotherapy- it has advantage over dual therapy of lower
surface toxicity as well as greater convenience.
 fluoroquinolones is the usual choice for empirical monotherapy
(ciprofloxacin, gatifloxacin, moxifloxacin)
 Ciprofloxacin instillation is ass. with white corneal precipitates.
 Moxifloxacin has superior ocular penetration.
 Antibiotic duotherapy: may be prferred as first line empirical treatment in
aggressive disease .
 a combination of two fortified antibiotics typically a
cephalosporin(cefazolin,cefuroxime or ceftazidime) and an aminoglycoside
(gentamycin)in order to cover both gram+ve and gram-ve bacteria.

37.  Subonjunctival antibiotics:
only indicated if there is poor compliance with topical antibiotics.
 . Steroids:
 steroids reduces inflammation, improve comfort and minimize corneal
scarring.
 however they may promote the replication of some organisms like
fungi, hsv and mycobacteria so are contraindicated if these are suspected
on clinical examination.
 the recent steroids for corneal ulcers (SCUT) found no eventual benefit
of steroids in most cases ,though severe cases tended to do better.
 epithelization may be retarded by steroids and they should be avoided
if there is significant thinning or delayed epithelial healing.
 regimens ; dexamethasone 0.1% every 2 hrs and prednisilone o.5%-
1% four times daily.

38.  Mydriatics:
use to reduce pain and to prevent the formation of posterior
synechiae .
3.) systemic therapy:
usually not given ,but may be appropriate for following
circumstances.
 N. meningitidis inf. (in which early systemic prophylaxis may be
life saving. Treatment is with i.m benzylpencillin or ceftriaxone)
 H.influenzae inf. to be treated with oral amoxicillin and
clavulanic acid
 severe corneal thinning with threatened perforation requires
both ciprofloxacin and tetracycline (doxycycline 100mg twice daily).

39. 4) treatment of impending perforation:
when ulcer progresses perforation seems imminent following
measures may help:-
 patient is advised to avoid strain from sneezing ,coughing etc.
 Pressure bandage should be applied to give some external
support.
 Lowering of i.o.p should be done
 Tissue adhesive glue such as cyanoacrylate is helpful
 Bandage contact lens is also helpful
 Counjctival flap can be used to cover the cornea to give support
to weak tissue.

40. 5.) treatment of perforated corneal ulcer:
 In small perforations - bandage contact lens and
tissue adhesive glue can be used to restore the integrity
of perforated cornea.
 In larger perforations - pentrating keratoplasty or
corneal patch graft is necessory.

41. FUNGAL KERATITIS
Intro:
 the incidence of suppurative corneal ulcers
caused by fungi has increased in the recent years due to
injudicious use of antibiotics and steroids.
 It is rare in temprate countries but is a major cause of
visual loss in tropical & developing countries.

42. Etiology :
 2 main types of fungi cause keratitis.
1) yeasts: (candida & cryptococcus are unicellular fungi
that reproduces by budding and are resposible for most
cases of fungal keratitis in temprate regions)
2) Filamentous fungi: (fusarium & aspergillus that
produces tubular projections k/a hyphae and are most
common pathogens in tropical climate.
 the fungi commonly reponsible for fungal corneal ulcer
are –aspergillus (most common worldwide), candida &
fusarium.

43. Modes of infection :
1.) injury by vegetative material.
2.) injury by animal tail.
3.) secodnry fungal ulcers – common in patients who are
immunosupressed systemically or localy such as dry
eye, herpetic keratitis , bullous keratopathy etc.

44. predisposing Risk factors :
already discussed above (ocular, systemic & occupational
risk factors)
 Excessive use of steroids in developing countries like
india as over the counter drug & trauma with agricultural
material is imp.

45. Clinical features of fungal keratitis
SYMPTOMS SIGNS
 Similar to central bacterial
corneal ulcer but in general
they are less marked than the
bacterial ulcer.
 Course is slow.
 Gradual onset of pain.
 Photophobia.
 grittiness
Signs are more than symptoms and a
typical fungal corneal ulcer has the
following features:-
 C.u is dry looking, grayish white with
elevated rolled out feathry margins.
 Sterlie yellow immune ring of
demarcation.
 Progressive infiltration often with
Multiple small satellite lesions may
be present near the ulcer.
 Big hyopyon even with small ulcer.

49. TREATMENT
1) general measures :
are same as that of bacterial keratitis although hospital
admission is usualy required.
2) debridment :
removal of epithelium over the lesion may enhance the
penetration of antifungal drugs. its also be helpful to
regularly remove mucus & necrotic tissue with a
spatula.

50. 3) topical antifungals:
 these are mainstay of treatment, and should only be
instituted where the corneal scrapings reveals the fungal
elements & culture reveals the presence of fungal
organisms at 36-48 hrs.
 We don’t recommend an empirical antifungal therapy
based upon the clinical evidence of fungal keratitis
alone. (unlike bacterial keratitits)

51.  Topical antifungals should initially be given hourly for 48
hrs then reduce as sign permits.
 Treatment should be continued for at least 12 weeks.
 For candida inf.: - natamycin 5% , amphotericin B 0.15%,
fluconazole 2%, clotrimazole 1% and voriconazole1or 1%.
 For Filamentous inf.:- natamycin 5% or econazole 1%
.alternatives amphotericn B 0.15% ,voriconazole 1 or 2%.
4) A broad spectrum antibiotic might also be considered to
prevent secondry bacterial infection.
5) cycloplegia: to reduce pain and prevent the formation of
posterior synechiae.

52. 6) systemic antibiotics : used in severe cases and for suspected
endophthalmitis. Voriconzole 400mg twice daily for 1 day
then 200mg twice daily.
7) tetracycline : may be given for its anticollagenease effect
8) For perforation : therapeutic keratoplasty is considered
when medical therapy is ineffective or following perforation.
9) anterior chamber washout : with intracameral antifungal
injection may be considered for unresponsive cases.
 There is no role of steroid use in fungal keratitis.

53. PROTOZOAL KERATITIS
keratitis can occur due to various protozoa out of
which acanthamoeba is most notorious. Other
protozoa which has increasingly been isolated from
corneal ulcer includes microsporidia.

54. Acanthamoeba keratitis
Intro:
 acanthamoeba has recently gained importance because of its
incidence, difficulty in diagnosis & unsatisfactory treatment.
 These are free living protozoa commonly found in soil, fresh
or brackish water, well water, sewage and upper resp.tract
 It exists in two forms trophozite form (active)
cystic form (dormant )
 In developed countries acanthamoeba keratitis is most
frequently ass. With contact lens wear especially if tap water is
used for rinsing.

55. Mode of infection:
occurs due to direct corneal contact with any material or water
contaminated with organism.
 Contact lens wearers : using home made saline is the
commonest situation recognised for acanth. Infection.
 Mild trauma : ass. With contaminated vegetable matter, salt
water diving ,wind blown contaminant and hot tub use.
 (trauma with organic matter and exposure to muddy water are
the major (90%) predisposing factor in developing countries like
india).
 Oppurtunistic inf. : acanth. Keratitis can also occur as
oppurtunistic inf. in patients with herpetic keratitis,bacterial
keratitis,bullous keratopathy & neuroparalytic keratitis.

56. Diagnosis:
 diagnosis is difficult to make & is usually made clinically
by exclusion with strong suspicion out of non responsive
patient being treated for bacterial fungal or herpetic
keratitis.
Clinical features:
symptoms:- 1) blurred vison & discomfort.
2) f.b sensation
3) pain is often severe &
chacterstically disproportionate to the degree of
inflammation and clinical signs.
4) watering & photophobia .

57. Signs
Early signs Late signs
 In early disease the epithelial surface
is irregular & grayish.
 Epithelial ridges.
 Epithelial pseudodendrites may
forms resembling herpetic lesions.
 Perineural infiltrates and radial
keratoneuritis reported in 50% of
cases are seen in early weeks and are
pathognomnic.
 Limbitis is reported in majority of
cases .
 Gradual enlargement &
coalescence of infiltrates to
form ring abscess is typical.
 Scleritis may develop and is
generally reactive.
 Slowly progressive stromal
opacification & vasculrization.

60. Differntial diagnosis
1) viral keratitis :
in early stages both epithelial pseudodendrites and early infiltrates are
often mistaken with viral keratitis, but these features can suggest a
diagnosis of acanth. Rather than HSV:-
 in acanth. keratitis the pain is more .
 Failure to respond to intial antiviral therapy.
 Risk factors such as contact lens or exposure to contaminated water.
2) fungal keratitis :
can also be misdiagnosed when ring infiltrates are ass. with hypopyon.
however severe pain & radial keratoneuritis are frequently absent in fungal
keratitis.
3) bacterial keratitis :
can be misdiagnosed in stage of stromal necrosis & ring abscess formation.

61. TREATMENT
 Treatment of acanthamoeba keratitis is based upon removal of
cysts from cornea. Although trophozites are susceptible to
many antimicrobial agents cysts are largely resistant.
 It is imp. to maintain a high level of suspicion for
acanthamoeba in any patient with a limited response to
antibacterial therapy.
1) debridement : is believed to be helpful to increase eye drop
penetration.

62. 2) topical amoebicides :
a) BIGUANIDES:-
polyhexamethylene biguanide(PHMB)0.02% & chlorhexidine o.o2% kill
trophozites and cysts both.
b) DIAMIDINES:-
hexamidine 0.1% or propamidine acts by inhibiting DNA synthesis.
c) voriconazole or other azole antifungal may be used.
d) multiple drug therapy : nths for-is needed for long time and (3-
4mnths for early epithelial lesion and 6-12 mnths for stromal lesions.

63. F) long term prophylatic therapy with PHMB twice a
day for 1 y.ear is recommended.
e) PENTRATING KERATOPLASTY : is frequently
required in non responsive cases & in perforated cases.

64. CORNEAL DIAGRAMS
 Following colour coding is used to document the finding
of anterior segment.
 BLACK COLOUR is used for :
a. Limbus
b. Scars
c. Degenerations
d. Foregin bodies
e. Sutures
f. Contact lens
g. BSK

66.  BLUE COLOUR is used for the documentation of:
a. Oedema
b. Small circles for epithelial edema
a. Wavy lines to document folds in the D.M

68.  BROWN COLOUR is used for :
a. Pigmentation iron or melanin
b. Pupil or iris
c. Iris nodules

69.  RED COLOUR is used for :
a. Blood vessels
b. Rose bengal staining
c. Haemorrages

71.  GREEN COLOUR is used for :
a. green small lines for filaments.
b. Green dots for SPK’S.
c. green shades for epithelial defects.

73.  YELLOW COLOUR is for :
a. Hypopyon
b. Infiltrates