Dr. Tushar Kumar discusses the profiling, examination, diagnostic testing, and management of various types of corneal ulcers. Key points include: 1. A thorough history and physical exam is important to categorize ulcers as infectious, non-infectious, and determine etiology. Signs and symptoms provide clues to common infectious causes. 2. Examination includes visual acuity, slit lamp evaluation of the eyelids, conjunctiva, cornea and anterior chamber. Features of the ulcer like size, depth and borders are noted. 3. Diagnostic testing depends on severity and response to initial treatment, and may include cultures, smears, biopsy or imaging to identify organism or guide management

1. Dr Tushar Kumar

2. PROFILING THE ULCER

3. CATEGORISING
INFECTIOUS
NON
INFECTIOUS

4. HISTORY TAKING
 Talk to patient to find out the Etiology of the ulcer.
 Enquire about Pain.
Superficial > Deep
Excruciating: Acanthameoba (Radial Keratoneuritis)
Absent: Fungal
Sudden relief: Perforation
 Redness

5.  Photophobia (d/t Anterior ciliary Nerve)
 Discharge
Watery (Viral)
Mucopurulent /Purulent (Bacterial)
Greenish Yellow (Pseudomonas)
Membranous discharge (Corynebacterium diphtheriae)
 Diminision of Vision
 Topical medication

6.  Contact Lens use
 Any relavent systemic illness
 Any relavent ocular disease
 Medication allergies

7. EXAMINATION

8. PHYSICAL EXAMINATION
External
Examination
Visual
Acuity
Ocular
Examination

9. GENERAL EXAMINATION
 Potential source of Infection
 General appearance of the patient, including skin
conditions
 Facial examination

10. VISUAL ACUITY
 Document the BASELINE visual acuity

11. OCULAR EXAMINATION
 Globe position
 Eyelids and eyelid closure (Blepharospasm)
 Conjunctiva
 Nasolacrimal apparatus
 Corneal sensation testing (Reduced)
 Neurotropic
 Chronic Surface Disease
 Herpetic Infection
 Chronic contact lens use

12. SLIT LAMP EXAMINATION
Eyelid margins
 Inflammation
 Ulceration
 Meibomian gland dysfunction/anterior blepharitis
 Eyelash abnormalities, including trichiasis/distichiasis
 Lagophthalmos
 Lacrimal punctal anomalies
 Ectropion/entropion

13. Conjunctiva
 Discharge
 Inflammation
 Morphologic alterations
 Ischemia
 Foreign body
 Filtering bleb
 Loss of tissue or of the epithelium

14. Sclera
 Inflammation (e.g., infectious versus immune)
 Ulceration
 Thinning
 Nodule
 Ischemia

15. Limbus
Limbal Stem Cell Deficiency
Congestion

16. Cornea
 Epithelium, including defects and punctate keratopathy,
edema, epithelial movement patterns
 Stroma, including ulceration, thinning, perforation,
infiltrate and edema
 Endothelium (endothelial plaque)
 Foreign body, including sutures

17.  Satellite lesions
 Signs of corneal dystrophies
 Previous corneal inflammation (thinning, scarring, or
neovascularization)
 Signs of previous corneal or refractive surgery

18.  Vascularisation
 Fluorescein or rose bengal/lissamine green staining of the
cornea is usually performed.

21. AC
 Cells and flare
 Hypopyon
 Fixed: Fungal
 Mobile: Bacterial
 Pink: Serratia
 Depth
Anterior Vitreous
Posterior Segment Examination
Fellow eye

22. Examination of Corneal Ulcer
 Site
 Size
 Shape
 Margins
 Depth
 Vascularization
 Infiltration
 Thinning/ Perforation
 Hypopyon (Size, mobility, Color)
 Satellite lesion
 Corneal Diagram

28. DIAGNOSTIC TESTS
CULTURES AND SMEARS
Indications
 Corneal infiltrate is central, large, and/or is associated with significant
stromal involvement or melting
 Infection is chronic or unresponsive to broad-spectrum antibiotic therapy
 History of corneal surgeries
 Atypical clinical features are present that are suggestive of fungal,
amoebic, or mycobacterial keratitis
 Infiltrates are in multiple locations on the cornea

31. CORNEAL BIOPSY & DEEP STROMAL CULTURE
Indications
Response to treatment is poor
Repeated cultures have been negative and the clinical picture continues
to suggest an infective etiology
Infiltrate is located in the mid or deep stroma with overlying
uninvolved tissue
Organisms were identified by culture in 42% of corneal biopsies and
identified on histopathological examination in 40% of cases.
Younger JR, Johnson RD, Holland GN, Page JP, Nepomuceno RL, Glasgow BJ, Aldave AJ, Yu F, Litak J, Mondino BJ, Service UC.
Microbiologic and histopathologic assessment of corneal biopsies in the evaluation of microbial keratitis. American journal of
ophthalmology. 2012 Sep 1;154(3):512-9.

32. CORNEAL IMAGING
 Scanning laser confocal microscopy is used to image the various
levels of the cornea from the epithelium through stroma to the
endothelium in vivo.
 Optical coherence tomography may also be helpful in
determining depth of involvement
RANDOM BLOOD SUGAR

33. INFECTIOUS KERATITIS

34. TREATMENT
BACTERIAL ULCER
Antibacterials:
Topical Moxifloxacin 0.5% & Gatifloxacin 0.5%: Gram +
Subconjunctival
Scleral Involvement
Perforation
Compliance
Systemic Therapy

35. Contd…
 Central or severe keratitis (e.g., deep stromal
involvement or an infiltrate larger than 2 mm with
extensive suppuration), a loading dose every 5–15
minutes followed by frequent applications hourly is
recommended.
 Fortified topical antibiotics(cefta+ …..) should be
considered for large or visually significant corneal
infiltrates, especially if a hypopyon is present. Also for
eyes non responsive to initital therapy.

36. Corticosteroids:
Advantages:
Suppression of inflammation, which may reduce subsequent
corneal scarring and associated visual loss
Disadvantages:
Recrudescence of infection
Local immunosuppression
Inhibition of collagen synthesis predisposing to corneal
melting
Increased intraocular pressure

37. Contd…
 SCUT treatment study found no benefit of concurrent topical
corticosteroid therapy using prednisolone phosphate 1% in
conjunction with broad-spectrum topical antibiotic.*
 Benefit for using corticosteroids in Pseudomonas keratitis and in
more severe cases of bacterial keratitis.**
 Treatment of Nocardia keratitis with corticosteroids resulted in
poor visual outcomes.**
Srinivasan M, Mascarenhas J, Rajaraman R, Ravindran M, Lalitha P, Glidden DV, Ray KJ, Hong KC, Oldenburg CE, Lee SM, Zegans
ME. Corticosteroids for bacterial keratitis: the Steroids for Corneal Ulcers Trial (SCUT). Archives of ophthalmology. 2012 Feb
1;130(2):143-50.
Lalitha P, Srinivasan M, Rajaraman R, Ravindran M, Mascarenhas J, Priya JL, Sy A, Oldenburg CE, Ray KJ, Zegans ME, McLeod SD.
Nocardia keratitis: clinical course and effect of corticosteroids. American journal of ophthalmology. 2012 Dec 1;154(6):934-9.
*:
**:

38.  Conservative approach would avoid prescribing
corticosteroid treatment for presumed bacterial ulcers
until
 Organism has been identified
 Epithelial defect is healing
 Ulcer is consolidating
 Cycloplegics: Decrease synechiae formation and pain,
and are indicated when substantial anterior chamber
inflammation is present.
 Antiglaucoma drugs( If IOP )

39. FUNGAL ULCER
Topical E/D Natamycin 5% (Fusarium) 1hrly upto 48 hrs
Topical E/D Voriconazole 1-2% / E/D Amphotericin B 0.15%(Candida)
(Treatment to be continued for 3 months)
 Oral Antifungals
 Indications:
 Near Limbus
 Suspected Endophthalmitis
 Tab Voriconazole 400mg 1 bd x 1 day f/b 200mg 1 bd
 Tab Itraconazole 200 mg 1 od
 Oral Tetracyclin(Doxycycline 100 mg bd): Anticollagenase
 Antigalucoma drugs( If IOP ) )
 Intracameral antifungal injection (enlarging endothelial exudation
with stable corneal infiltration)

40. VIRAL ULCERS
 Topical E/O Aciclovir 3% 5 times a day
Topical E/O Ganciclovir 0.15% 5 times a day
 Debridement (Resistant cases)
Epithelium removed 2mm from the ulcer edge
 Oral therapy
Aciclovir 200-400 mg 5 times a day
Valacyclovir 500 md bd 7-10 days
Indications
Immunosuppressed
Children
Ocular surface disease

41. Contd…
 Interferon therapy
Monotherapy not beneficial
Combination with debridement or nucleoside antiviral speeds healing
 Cycloplegics ( E/D Homide 2%) od/bd
 Topical antibiotics variably recommended
 IOP control ( Prostaglandin analogues are
CONTRAINDICATED)

42. PARASITIC ULCERS (ACANTHAMOEBA)
Treatment in based on eradication of cysts.
1st Line (Cysticidal):
E/D Chlorhexidine (0.02%) & polyhexamethylene biguanide (0.02%)
(Hourly initially for few days f/b qid for 4-6 wks)
Clinical resistant patients: E/D Chorhexidine 0.04-0.06%

43. NON INFECTIOUS KERATITIS

44.  Corneal inflammation with no known infectious
etiology

45. THYGESON’S SUPERFICIAL
PUNCTATE KERATITIS
 Chronic Bilateral punctate inflammation
 Long duration with remission, exacerbations
 Healing without scarring
 No response to topical antibiotics
 Striking response to topical steroids

46.  Corneal Scrapping
 Atypical and degenerated epithelial cells
 Mild mono and polymorphonuclear cell infiltration
 Confocal Microscopy
 Accumulation and aggregation of Langerhans cells in
basal cell layer of corneal epithelium
 Management
 Topical low dose corticosteroids (Loteprednol 0.5%)
(Long duration slow taper)

47.  Topical Cyclosporin 2%
 Therapeutic soft contact lens
 Lubricants for symptomic relief
 Phototherapeutic keratectomy

49. SUPERIOR LIMBIC
KERATOCONJUNSTIVITIS OF
THEODORE
 Classic sign:
 B/L local hyperemia of superior bulbar conjunctiva
which appears keratinized, thickened and redundant
 Papillary reaction with hyperemia: Opposing
palpebral conjunctiva
 Fine fluoresceine staining +

50.  25-50% associated with keratoconjunctivitis sicca
 Superior fimamentary keratitis +/-
 Associated with thyroid eye disease
 Management:
 Unpreserved topical lubricants
 Bandage contact lens
 Topical hypertonic saline solution
 N-acetylcysteine
 Surgical resection/recession of abnormal conjunctiva +
tenon

53. MOOREN’S ULCER
 PAIN predominant feature
 2 Clinical types
 Limited type:
 Older patients
 U/L
 Good response to therapy
 Second type:
 Younger patients (3rd decade)
 B/L
 Poor response to therapy

54.  Progressive, cresentric, peripheral corneal ulcer
 Extensive, undermined, overhanging edges
 Yellow-white infiltrate + on leading margin
 Limbitis + but Scleritis –
 LUCID interval –
 Vascularisation + upto the leading edge but NOT
beyond

56. Management
 Start on hourly corticosteroids
 Low frequency antibiotic drops
 Topical Cyclosporin (2%) but delayed onset of action
 Anticollagenases ( Acetlycyteine 10-20%, Tab
Doxycycline 100 mg bd)
 Topical unpreserved lubricants
 Systemic immunosuppression (Oral Steroids)
 Conjunctival resection (4mm back from limbus &
2mm beyond circumference of margin)
 Lamellar keratectomy

57. TERRIEN MARGINAL DEGENERATION
 75% patients are MALES
 Usually Bilateral
 Asymptomatic but gradual DOV (d/t astigmatism)
 NO epithelial defect
 LUCID interval +

58.  Starts SUPERIORLY
 Slowly progressive peripheral thinning
 Outer slope shelves gradually central part rises sharply
 Band of lipid + central corneal edge
 Pseudopterygium +/-

60.  Management:
 Safety spectacles (if corneal thinning)
 Soft lenses with RGP lens (Piggybacking)
 Crescentic/ Annular excision of gutter with lamellar/
fullthickness transplantation

61. NEUROTROPHIC KERATOPATHY
 Loss of TRIGEMINAL innervation
 Causes:
 Trigeminal ganglion surgical abalation (neuralgia)
 Stroke
 Tumour
 Peripheral neuropathy (DM)
 Past HSV/HZO infection

62.  Cranial Nerve examination is MANDATORY
 Stages:
 Stage 1: Interpalpebral epithelial irregularity + staining,
mild opacification, oedema, tiny focal defects
 Stage 2: Larger persistent epithelial defect with rolled
and thickened edges, PUNCH OUT configuration,
stromal edema
 Stage 3: Stromal melting

64.  Management:
 Discontinuation of toxic medications
 Topical unpreserved lubricants
 Anticollagenases( Acetylcysteine drops, Topical/Oral
Tetracyclines)
 Taping of the lids at night
 Botulinum induced ptosis

65.  Therapeutic silicon contact lenses
 Amniotic membrane patching with temporary
tarsorrhaphy

66. PERIPHERAL ULCERATIVE KERATITIS
Peripheral Corneal Ulceration
Unilateral/ Bilateral
Progresses circumferentially, posteriorly and may perforate
Associated +/- Collagen vascular disorders
Rheumatoid Arthritis is the most commonly associated CVD

67.  Associations:
 Episcleritis
 Scleritis (Necrotising type) indicative of vasculitis
 Iridocyclitis

68.  Epithelial loss, stromal infiltrates, corneal melting
(keratolysis)
 Lucid interval +/-
 Increased peripheral corneal thickness (upto 700µ)
 Vascular arcade from anterior ciliary artery upto
0.5mm of clear cornea

72. Management:
Mild U/L cases:
Topical steroids (RA associated)
Conjunctival resection
Severe cases:
Systemic steroids (0.5-1 mg/kg/day): Acute management
Pulsed methylprednisolone 0.5-1 g x 3 days: If ulcer progresses

75.  Conjunctival
resection
 Cyanoacrylate
adhesives in
impending
perforation
 Amniotic
membrane
grafts