conjunctiva

1. VKC
PHLYCENULAR KERATOCONJUCTIVITIS
XEROPHTHALMIA
OPHTHALMIA NEONATORUM
Conjunctiva-II

2. VERNAL KERATOCONJUNCTIVITIS
(VKC) OR
SPRING CATARRH
 It is a recurrent, bilateral, interstitial, self-limiting,
allergic inflammation of the conjunctiva having a
periodic seasonal incidence.
 An atopic allergic disorder in many cases, in
which IgE-mediated mechanisms play an
important role.

3. Predisposing factors
1. Age and sex. 4-20 years; more common in boys.
2. Season. More common in summer; hence the
name spring catarrh looks a misnomer.
Recently it is being labelled as 'Warm weather
conjunctivitis'.
3. Climate. More prevalent in tropics, less in
temperate zones and almost non-existent in cold
climate.

4. Clinical picture
 Symptoms. Spring catarrh is characterised by
marked burning and itching sensation, mild to
severe photophobia, lacrimation, stringy (ropy)
discharge and heaviness of lids.
 Signs of vernal keratoconjunctivitis can be
described in following three clinical forms:
 1. Palpebral form.
 2. Bulbar form.
 3. Mixed form.

5.  1. Palpebral form. Usually upper tarsal
conjunctivaof both eyes is involved.
 The typical lesion is characterized by the
presence of hard, flat topped, papillae
arranged in a 'cobble-stone' or 'pavement
stone', fashion.
 In severe cases, papillae may hypertrophy to
produce cauliflower like excrescences of 'giant
papillae'. Conjunctival changes are associated
with white ropy discharge.

6.  2. Bulbar form.
(i) dusky red triangular
congestion of bulbar
conjunctiva in palpebral area;
(ii) gelatinous thickened
accumulation of tissue around
the limbus; and
(iii) presence of discrete whitish
raised dots along the limbus
(Tranta's spots)

7.  Vernal keratopathy. Corneal involvement in
VKC may be primary or secondary due to
extension of limbal lesions.
 1. Punctate epithelial keratitis involving upper
cornea is usually associated with palpebral
form of disease.
 2.Ulcerative vernal keratitis (shield ulceration)
presents as a shallow transverse ulcer in
upper part of cornea.
 3. Vernal corneal plaques

8.  4. Subepithelial scarring occurs in the form of a ring scar.
 5. Pseudogerontoxon is characterised by a classical
‘cupid’s bow’ outline.
 Clinical course of disease is often self-limiting and
usually burns out spontaneously after 5-10 years.
 Differential diagnosis. Palpebral form of VKC needs
to be differentiated from trachoma with pre-dominant
papillary hypertrophy

9. Treatment
 A. Local therapy
1. Topical steroids.
2. Mast cell stabilizers such as sodium
cromoglycate (2%) drops.
3. Topical antihistaminics.
4. Topical cyclosporine drops.
B. Systemic antihistamincs

10.  C. General measures include :
 Dark goggles to prevent photophobia.
 Cold compresses and ice packs have soothing effects.
 Change of place from hot to cold area is recommended
for recalcitrant cases.

11.  D. Treatment of vernal keratopathy
 Punctate epithelial keratitis requires no extra
treatment except that instillation of steroids should be
increased.
 Severe shield ulcer resistant to medical therapy may
need surgical treatment in the form of debridment,
superficial keratectomy, excimer laser therapeutic
kerateotomy as well as amniotic membrane
transplantation to enhance re-epithelialization.

12. PHLYCTENULAR
KERATOCONJUCTIVIT
S
 Nodular affection (phlycten) occurring as an allergic
response of the conjunctival and corneal epithelium to
some endogenous allergens to which they have
become sensitized.

13. ETIOLOGY
 Delayed hypersensitivity (Type IV-cell mediated)
I. Causative allergens
- Tuberculous,Staphylococcus proteins
- Proteins of Moraxella,Axenfeld bacillus,parasites (worm infestation).
II. Predisposing factors
-Age-3-15years
-Sex- f>m
-Undernourishment
-Living conditions-Overcrowded and unhygienic
-Season-All climates(spring and summer seasons)

14. PATHOLOGY
 Stage of nodule formation
-Exudation and infiltration of leucocytes
-Neighbouring blood vessels dilate and their endothelium proliferates.
 Stage ofulceration
-Necrosis at the apex of the nodule and an ulcer is formed.
 Stage of granulation.
-Floor of the ulcer becomes covered by granulation tissue.
 Stage of healing.
-Healing with minimal scarring

15. SYMPTOMS
 Very few
 Mild discomfort
 Irritation
 Reflex watering
 Associated mucopurulent conjunctivitis due to secondary bacterial
infection.

16. SIGNS
 Simple phlyctenular conjunctivitisIt
-Pinkish white nodules surrounded by hyperaemia,near the limbus
ulcerates
epithelised. Rest of the conjunctiva is normal.
 Necrotizing phlyctenular conjunctivitis
-Large phlycten with necrosis and ulceration severe pustular
conjunctivitis.
 Miliary phlyctenular conjunctivitis
- Multiple phlyctens
- Arranged haphazardly or in the form of a ring around the limbus
ring ulcer

17. PHLYCTENULAR
KERATITIS
ULCERATIVE DIFFUSE
SACROFULO
US
FASICULAR MILIARY

18. Ulcerative phlyctenular
keratitis
 Sacrofulous ulcer- Shallow
marginal ulcer formed due to
breakdown of small limbal
phlycten.Clears out without leaving
any opacity.
 Fascicular ulcer -prominent
parallel leash of blood vessels with
superficial ulcer but leaves behind
a band- shaped superficial opacity
after healing.
 Miliary ulcer- Multiple small ulcers
are scattered over a portion or

19. Diffuse infiltrative phlyctenular
keratitis
 Appear in the form of central infiltration of cornea
 with characteristic rich vascularization from the periphery, all around the
limbus.
 It may be superficial or deep.

20. TREATMENT
Local therapy
1. Topical steroids (dexamethasone / betamethasone)
2. Topical antibiotic
3. Atropine {1%) eye ointment when cornea involved
Specific therapy
1. Diagnosis & management of TB
2. Septic foci like caries,tonsillitis to be treated
3. Parasitic infestations to be ruled out and treated
General measures
1. High protein diet
2. Vitamin A,C,D supplementation

21. XEROPHTHALMIA
 Leading cause of preventable blindness (among infants &
children)
INCLUDES
STRUCTURAL
CHANGES
(affecting
conjunctiva,cornea&retin
a)
BIOPHYSICAL
DISORDERS
of retinal rods & cones

22. Etiology
 Vitamin A deficiency
1.)Dietary deficiency of vitamin A-less intake,severe dieting
2.)Defective metabolism
-malabsorption
-malnutrition
-chronic alcoholism
• Accompanied by protein-energy malnutrition (PEM) and infections.

23. WHO classification (1982)

24. Clinical features
1.) XN (Night Blindness)-nyctalopia
-Earliest symptom in children
-Eye discomfort,loss of vision
-detailed history to elicit
-offers as a screening tool to identify xerophthalmia

25. 2.) Xl A (Conjuctival Xerosis)
-one or more patches of dry, lustreless, non wettable conjunctiva
-loss of goblet cells,squamous metaplasia and keratinization
-emerging like sand banks at receding tide
-in interpalpebral area of the temporal quadrants and often the nasal
quadrants
-Later, entire bulbar conjunctiva may be affected
-Xerosis ,conjuctival thickening, wrinkling and pigmentation.

26. 3.) XIB (Bitot's spots)
-Raised, silvery white, foamy, triangular patch of keratinised epithelium
-Situated on the buIbar conjunctiva in the interpalpebral area
-B/L and temporal, and less frequently nasal.

27. 4.) X2 (Corneal Xerosis)
-Punctate keratopathy (earliest change)- in the lower nasal quadrant
-Xerosis and keratinization
-Haziness
-Lustreless cornea,granular pebbly dryness

28. 5.) X3A and X3B (Corneal ulceration/ keratomalacia)
-Stromal defects due to colliquative/liquefactive necrosis
-Peripheral small ulcers (1-3 mm),circular,steep margins,sharp
demarcation
-Large ulcers involving entire cornea
-can result in perforation
-X3A <1/3 of corneal surface-heals with appropriate theraphy
-X3B >1/3 of corneal surface-may result in blindness

29. 6.) XS (Corneal scars)
-Stromal defects –corneal scars of different densities and sizes
-pupillary area may/may not be involved

30. 7.) XF (XEROPHTHALMIC FUNDUS)
-Seed like, raised, whitish or yellowish lesions scattered uniformly
over the fundus at the level of optic disc

31. TREATMENT
1.) Local Ocular Therapy
-for conjunctival xerosis-Artificial tears (0.7% hydroxypropyl methyl
cellulose or 0.3% hypromellose) 3-4 hourly.
-for keratomalacia, treatment as of bacterial corneal ulcer
2.)Vitamin A Theraphy
-all stages of active xerophthalmia (XN-X3B)
-oral form recommended
-im inj (severe diarrhoea,repeated vomiting)

32. Vitamin A theraphy

33. 3.) Treatment of underlying cause and associated conditions
-PEM
-Nutritional disorders
-Diarrhoea & dehydration
-Infections
-Alcoholism

34. PROPHYLAXIS
1.)Short-term approach (Vit A supplementation)

35. 2.) Medium-term approach
-Food fortification
3.) Long-term approach
-health promotion and education
All 3 approaches combined gives the best result

36. OPHTHALMIA NEONATORUM
 Neonatal conjunctivitis
 Bilateral inflammation of the conjunctiva
occurring in an infant, less than 30 days old.
 Any discharge or even watering from the eyes
in the first week of life should arouse
suspicion of ophthalmia neonatorum, as tears
are not formed till then.

37. Source and mode of infection
1.) Before birth infection -through infected liquor
amnii in mothers with ruptured membranes.
2.) During birth-M/C mode
-from the infected birth canal
3.) After birth -during first bath of newborn or
from soiled clothes or fingers with infected
lochia.

39.  Causative agents with incubation period
1.) Chemical neonatal conjunctivitis. (in older days silver nitrate was the
common cause) or antibiotics used for prophylaxis. (6 HOURS)
2.)Gonococcal infection (4 DAYS)
3.)Staphylococcus aureus, Haemophilus species, Streptococcus
haemolyticus, and Streptococcus pneumoniae. (5 DAYS)
4.)Neonatal inclusion conjunctivitis caused by serotypes D to K of
Chlamydia trachomatis is at present the commonest cause of ophthalrnia
neonatorum in developed countries. (21 DAYS)
5.)Herpes simplex ophthalmia neonatorum - caused by herpes simplex-II
virus from the infected birth canal. (15 DAYS)

40.  Symptoms and signs
 Pain and tenderness
 Conjunctival discharge-
-Purulent-gonococcal
-Mucoid or mucopurulent -other bacterial cases
 Swollen lids
 Eyelids and periocular vesicles in HSV infection.
 Conjunctiva – hyperaemia,chemosis,papillary response.
 Corneal involvement- superficial punctate keratitis in herpes simplex
ophthalmia neonatorum.

41. Prophylaxis
I.Antenatal measures
• Thorough care of mother
• Treatment of genital infections when suspected
2.Natal measures-
 Deliveries should be conducted under hygienic conditions taking all aseptic
measures.
 Neonates closed lids should be thoroughly cleansed and dried.
3. Postnatal measures-
• Povidon-iodine 2.5% solution
• 1% tetracycline ointment or 0.5% erythromycin ointment
• Single Injection ceftriaxone 50mg/kg IM or IV (not to exceed 125mg)-to infants
born to mothers with untreated gonococcal infection

42. Treatment
l. Chemical ophthalmia neonatorum - self-limiting condition
2. Gonococcal ophthalmia neonatorum-
• Topical therapy :
 Saline lavage hourly
 Bacitracin eye ointment-4 times/day
 If cornea is involved - Atropine sulphate ointment
 Systemic therapy:
 Ceftriaxone75-100mg/kg/day iv or im ,qid
 Cefotaxime 100- 150 mg/ kg/ day IV or IM, 12 hourly
 Ciprofloxacin I0-20 mg/kg/day or norfloxacin 10mg/kg/day
 Crystalline benzyl penicillin G 50,000 units-full term
20,000 units-premature/LBW given im twice
for 3 days

43. 3. Other bacterial ophthalmia neonatorum –
Broad-spectrum antibiotic drops and ointments such as neomycin-bacitracin or
tobramycin for 2 weeks
4. Neonatal inclusion conjuctivitis –
-Topical tetracycline l % or erythromycin 0.5% eye ointment qid for 3 weeks
-Azithromycin 20 mg/ kg either as a single dose or once daily for 3 days
-Both parents should be treated
5. Herpes simplex conjunctivitis - self-limiting disease.
-Acyclovir e/o 5 times a day
-iv Acyclovir 45 mg/kg/day for 14-21 days

44. THANK YOU!