Conjunctiva

1. CONJUNCTIVA
 Anatomy
 Microbiology
 Infections

2. PALPEBRALCONJUNCTIVA
 Marginal
Lid margin -sulcus sub tarsalis ( 2mm)
 Tarsal conjunctiva
Vascular, Adherent to tarsal plate
 Orbital part
Tarsal plate limbus

3. BULBARCONJUNCTIVA
 Thin ,Tpt, loose
 Separated from Sclera by episcl tissue
 Limbal conj -- 3mm wide-- strongly adherent
 Rectus Muscle tendon insertions

4. FORNIX
 Joins bulbar and palpebral conj
 Superior
 Inferior
 Lateral
 Medial

5. HISTOLOGY
 Epithelium 2-5 layers
 Adenoid Layer is Lymphoid layer
Fine connective tissue
After3-4 months
 Fibrous layer
Collagenous & elastic fibres
Bv & nerves

6. CONJGLANDS
 Mucin secreting
Goblet cells– epithelium
Crypts of Henle—Tarsal conj
Glands of Manz—Limbal conj
 Acc Lacrimal glands
Glands of Krause – Fornices– 42/8
Glands ofWolfring – Along tarsal border

7. PLICASEMINULARIS
 Crescentic fold– medial canthus
 Represents nictitating membrane

8. CARUNCLE
 Ovoid body medial to plica
 5x3 mm
 Piece of modified skin
 st sq epithelium
 Sweat & seb glands, hair follicle

9. BLOODSUPPLY
 Palpebral conj & fornixis
-Peripheral art arcade
-Marginal art arcade
 Bulbar conj
-Posterior conj arcade
-Anterior conj arteries

10. LYMPHATICDRAINAGE
 Lat side- Preauricular
 Medial side – Submandibular

11. NERVESUPPLY
 Circum corneal – long ciliary
 Rest – Lacrimal
Infratrochlear
supratrochlear
Frontal
Supraorbital

12. Inflammationsofconjunctiva
 Conj hyperemia ass. with discharge which
may be
Watery
Mucoid
Mucopurulent
Purulent

13. Typesofconjunctivitis
 Infective
Bacterial
Chlamydial
Viral
Ophthalmia neonatorum
Granulomatous
 Allergic
Simple allergic
VKC
Atopic
Giant papillary
Phlectanular
 Cicatricial
 Toxic

14. Infectiveconjunctivitis
Natural protective mechanism
 Low temp
 Physical protection –lids
 Flushing – tears
 Antibacterial action – tear lysozymes
 Humoral protection- tear immunoglobulins

15. Bacterialconjunctivitis

16. Predisposingfactors
 Poor hygiene
 Flies
 Hot dry climate
 Poor sanitation
 Dirty habits

17. Etiology
 Staph Aureus
 Staph epidermis
 Strep Pneumoniae
 Strep Pyogens
 H Influenzae
 Moraxella
 N Gonorrhoeae/ Meningitidis
 C Diphtheriae

18. Modeofinfection
 Exogenous
Direct - Close contact, water borne
Vector – Flies
Fomites – Hands, towels
 Local spread - Lac sac, lids, nose
 Endogenous - Blood

19. pathology
 Vascular response – cong, increased
permeability of conj bv
 Cellular response – exudation of polymorphs
& inflm cells
 Conj tissue response – Conj oedema,
degeneration of epith cells, Proliferation of
basal layers & goblet cells
 Conj discharge –Tears, mucin, epi cells,
bacteria & diapedesis of RBC

20. Acutebact.conjunctivitis
 Conj hyperemia with mucopurulent discharge
 Mucopurulent conj
 Staph Aureus, Strepto, Pneumo
 Ass. with measles

21. symptoms
 FB sensation
 Mild photophobia
 Muco purulent discharge
 Lid sticking
 Halos

22. signs
 Mucopus in fornix & canthus
 Congestion – palp conj, fornix
 Chemosis
 Matted cilia
 Oedema of eyelids
 Papillae
peaks in 3-4 days
lasts for 1-2 wksS

23. complications
 SPK
 Keratitis
 Blepharitis

24. rx
 Topical antibiotics - Broad spectrum
Drops 2-4 hrly
Oint at night
 Wash/ irrigate conj sac
 Dark goggles
 NSAID
 No bandage
 No Steroids

25. Chronicconjunctivitis

26. predisposingfactors
 Chronic exposure – dust, smoke, chemicals
 Local irritants – cilia, concretions
 Eye strain
 Excess alcohol / smoking
 StaphAureus, K Pneumoniae

27. Symptoms
 Burning / Grittiness esp in evenings
 Redness
 Feeling of dryness / heat in eyes
 Mild discharge
 Watering
 Tiredness & sleepiness in eyes

28. signs
 Congestion
 Papillary hypertrophy
 Sticky conj
 Congested lid margins

29. rx
 Eliminate predisposing factors
 Topical antibiotics
 Astringent eye drops

30. Chlamydia
 Bet. bacteria & viruses.
 Share some properties of both.
 Like viruses -obligate intracellular & filterable
 Like bacteria contain both DNA and RNA,
divide by binary fission & are sensitive to
antibiotics.
 PLT gp (Psittacosis, LGV,Trachomatis)

31. Lifecycleofchlamydia
 Infective particle invades cytoplasm of
epithelial cells
 Swells up forms ‘initial body’.
 Rapidly divide into ‘elementary bodies’
 Liberated when cells burst.
 ‘Elementary bodies’ infect other cells
 Whole cycle repeated.

32. trachoma
 Greek word - Rough
 Egyptian ophthalmia
 Chronic keratoconjunctivitis, affecting sup.
Epith. of conj & cornea simultaneously
 Mixed follicular & papillary response of
conjunctival tissue
 Leading causes of preventable blindness

33. etiology

34. Causativeorganism
 Chlamydia trachomatis
 Produces intra cytoplasmic incl bodies
 H.P bodies (Halberstaedter Prowazeke)
 11 serotypes

35. Predisposingfactors
 Age- Infancy & early childhood.
 Sex- Females
 Race- Common in Jews. less in negroes.
 Climate- Dry dusty weather
 Socio economic status-Poor classes
Unhygienic living condition, overcrowding,
unsanitary conditions, flys, paucity of water, lack
of separate towels handkerchiefs, lack of
education
 Evironmental factors- Exposure to smoke,
irritants, sunlight etc.

36. Sourceofinjection
 Conjunctival discharge of the affected
person.

37. Modesofinfection
 Direct spread- water-borne modes.
 Vector transmission-Files
 Material transfer-
Contaminated fingers of doctors nurses
contaminated tonometers
Towels, hankys, bedding
“surma” rods.

38. Prevalence
 Worldwide disease
 Highly prevalent in North Africa, Middle East
& South-East Asia.

39. Clinical profile
 Incubation period- 5-21 days
 Onset - insidious
 Clinical Course- Depends on presence or absence of
secondary infection
Pure trachoma - mild symptomless.
Secondary infection - typical symptoms of acute
conjunctivitis
 Natural History-
1st decade - slow progression,
2nd decade - inactive
3rd decade - sequale
4th to 5th decade - Blindness

40. symptoms
 In absence of sec infection-
Mild f b sensation
Occ lacrimation
Slight stickness of lids
Scanty mucoid discharge
 In presence of sec infection-
Symptoms of acute MP conjunctivitis.

41. Signs

42. Conjunctival signs
 Congestion- Upper tarsal & forniceal conj
 Conjunctival follicles- Boiled sago grains- upper
tarsal conj & fornix. If bulbar conj follicle -
pathognomic
Follicle- Scattered aggregation of
lymphocytes & other cells in adenoid layer.
Central part - mononuclear histiocytes, lympho
& large multinucleated cells (Leber cells)
Cortical part - lymphocytes showing active
proliferation. Bvs in most peripheral part
Later stage - signs of necrosis.

43.  Papillary hyperplasia- Papillae - reddish, flat
topped raised areas - give red velvety
appearance to t tarsal conjunctiva.
Central core of numerous dilated bvs
surrounded by lymphocytes
 Conjunctival scarring- Linear scar -sulcus
sub-tarsalis (Arlt’s line)
 Concretions- Hard looking whitish deposits
(accumulation of dead epithelial cells &
inspissated mucus)

44. Corneal signs
 Superficial keratitis
 Herbert follicles-Typical follicles - limbal area.
 Pannus- Infiltration of cornea ass with
vascularization in upper part
progressive/ regressive pannus.
 Corneal ulcer
 Herbert pits – scars after follicles heal
 Corneal opacity

45. Gradingoftrachoma

46. Mccallan’s classification
 Stage-1 ( Incipient trachoma or stage of
infiltration).
 Stage-2 (Established trachoma or stage of
florid infiltration).
 Stage-3 (Cicatrising trachoma or stage of
scarring).
 Stage-4 (healed trachoma or stage of
sequelae).

47. Who classification
 TF:Trachomatous inflammation-follicular.
 TI:Trachomatous inflammation intense.
 TS:Trachomatous scarring.
 TT:Trachomatous trichiasis.
 CO: Corneal opacity.

48. Sequelae of trachoma
 Lids-Trichiasis, entropion, tylosis, ptosis,
madarosis, ankyloblepharon
 Conjunctiva- Concertions, pseudo cyst,
xerosis, symblepharon
 Cornea- Corneal opacity, ectasia, xerosis,
total corneal pannus
 Others – Ch dacryocystitis Ch dacryoadenitis
 Complication- Corneal Ulcer

49. diagnosis
 Clinical diagnosis
 Laboratory diagnosis-
-Conj cytology- Giemsa stain predominantly
polymorphonuclear reaction. Plasma & leber
cells
- Detection of incl bodies
- Enzyme-linked immunosorbent assay (ELISA)
- Isolation of chlamydia – Mc Coy cell culture
- Sero typing ofTRIC agents - microimmuno-
fluorescence

50. Management

51. Rxofactive trachoma
 Topical therapy
Tetracycline (1%) or erythromycin (1%) eye
ointment qid for 6 weeks
Sulfacetamide (20%) eye drops tds = 1 %
tetracycline oint at bed time for 6 weeks.
Continuous Rx follwed by intermittent Rx in
endemic areas

52.  Systemic therapy
Tetracycline or erythromycin 250mg orally,
qid for 3-4 weeks or
Doxycline 100mg orally bd for 3-4 weeks
Azithromycin 1 gm stat or 250mg od x 4 days
 Combined topical & systemic therapy
(i)Tetracycline (1%) or erythromycin eye
ointment qid for 6 weeks
(ii)Tetracycline or erythromycin 250 mg orally
qid for 2 weeks

53. Rx of trachoma sequelae
 Concertions- Removal
 Trichiasis- Epilation, electrolysis
 Entropion- Surgery
 Xerosis- Artificial tears.

54. Prophylaxis for trachoma
 Hygienic measures.
 Early Rx of conjunctivitis.
 Blanket antibiotic therapy-WHO
1 % tetracycline eye ointment bd for 5
days in a month for 6 months.

55. Ophthalmianeonatorum
 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

56. etiology

57. Sourceandmodeofinfection
 Before birth- Infected liquor amnii in mother
with ruptured membrances.
 During birth- Most common mode of infected
birth canal especially.
 After birth- First bath of newborn from soiled
clothes or fingers infected lochia.

58. Causativeagents
 Chemical conjunctivitis- Silver nitrate or
antibiotics used
 Gonococal infection- Used to be responsabile for
50% of blindness in children. Eliminated it in
developed countries. Many developing countries
it still continues to be a problem.
 Other bacterial infections- Staphylococcus
aureus, Streptococcus haemolyticus, and
Streptococcus pneumoniae,
 Neonatal inclusion conjunctivitis caused
 Herps simplex

59. Clinicalfeatures

60. Incubationperiod
 Causative agents Incubation period
 Chemical 4-6 hours
 Gonococcal 2-4 days
 Other bacterial 4-5 days
 Neonatal inclusion
Conjunctivitis 5-14 days
 Herpes simplex 5-17 days

61. Symptomsandsigns
 Pain and tenderness
 Conjunctival discharge
 Lids
 Conjunctiva- Hyperaemia and chemosis.
 Corneal involvement,- Superficial punctate
keratitis

62. Complications
 Corneal ulceration, may perforate resulting in
corneal spacification or staphyloma
formation.

63. Treatment

64. Prophylaxis
 Antenatal meaures-Treatment of genital
infection
 Natal measures
Deliveries- conducted under hygienic
conditions
The newborn baby’s closed lids should be
thoroughly cleaned and dried.
 Postnatal measures include:
1% teteacyline ointment or 0.5%
erythromycin onitment

65. Curativetreatment
 Chemical ophthalmia neonatorum is a self-
limiting
 Gonococcal ophthalmia meomatorum
Topical therapy
Saline lavage
Bacitracin eye ointment 4 time/day
Systemic therapy
Ceftriaxone 75-100mg/kg/day IV or IM, QID
Ciprofloxacin 10-20 mg/kg/day

66.  Other bacterial ophthalmia neonatorum-
Board spectrum antbiotic drops and
ointments for 2 weeks
 Neonatal inclusion conjunctivitis
Responds well topical tetracyline 1% or
erythromycin 0.5% eye ointment QID for 3
weeks
 Herpes simplex conjunctivitis
Topical antiviral

67. ALLERGIC CONJUNCTIVITIS

68. VERNAL KERATOCONJUNCTIVITIS
(SPRING CATARRH)

69. VKC
 Recurrent bilateral seasonal
conjunctivitis
 Intense itching, photophobia, white
ropy discharge
 Papillary hypertrophy on palpebral
conj
 Gelatinous thickening at limbus
 Self limiting & burns out in 10 -15 yrs

70. AETIOLOGY
 Hypersensitivity reaction to
exogenous allergen
 Atopic allergic disorder
 IgE mediated mechanism
 Family h/o asthma, hay fever,
eczema

71. PREDISPOSING FACTORS
 Age : 4-20 yrs
 Sex : Boys > girls
 Season : summer (warm weather
conjunctivitis). Spring catarrh – misnomer
 Climate :Tropics
 Exacerbations with change of weather

72. PATHOLOGY
 Conj epithelium : Hyperplasia
 Adenoid layer : Cellular infiltration
 Fibrous layer : proliferation & hyaline
changes
 Conj b v : Proliferation ,increase
permeability, vasodilation

73. SYMPTOMS
 Marked itching
 Photophobia
 Lacrimation
 White ropy discharge
 Heaviness of lids

74. SIGNS
• Palpebral form
Upper tarsal conjunctiva
cobblestone appearance
Hypertropy of Papillae – cauliflower like
Ropy discharge
• Bulbar form
Horner-Trantas dots
Limbal gelatinous thickening
Dusky red congestion of bulbar conjunctiva
over palpebral area
• Mixed form

75. VERNAL KERATOPATHY
 Punctate epithelial keratitis
 Shield ulceration
 Corneal plaques
 Sub-epithelial scarring
 Pseudogerontoxon

76. LOCAL
TREATMENT
• Topical steroid drops-Beware of steroid
toxicity & self medication
• Mast cell stabilizers
Sodium cromoglycate --(2-4%) – 6 hrly
Olopatadine --(1%) 12 hrly
Ketorolac --(0.5%) 12 hrly)
• Topical antihistamine drops
• Acetyle cystine drops
• Cyclosporine eye drops
• Sub tarsal injTriamcinolone in severe cases

77. GENERAL MEASURES
 Dark glasses
 Cold compress
 Change of place

78. SYSTEMIC THERAPY
 Antihistaminics
 Steroids

79. OTHER MEASURES
 Cryotherapy
 Surgical excision
 Desensitisation

80. ETIOPATHOGENESIS
 Nodular lesion
 World wide more in developing countries
 Type IV delayed cell mediated
hypersensitivity
 Tuberculous proteins and Staphylococcal
proteins
 Worm infestation and other endogenous
bacterial proteins causing adenoids and
tonsillitis

81. PREDISPOSING FACTORS
 Age : 3-15 yrs
 Sex :Girls > boys
 Nutrition
 Socioeconomic status
 Season

82. PATHOLOGY
 Stage of nodule formation
 Stage of ulceration
 Stage of granulation
 Stage of healing

83. SYMPTOMS
 Mild discomfort
 Irritation
 Watering
 Associated MP conjunctivitis

84. SIGNS
 Nodules or blebs, pinkish in color over
bulbar conjunctiva, near the limbus
 Usually solitary
 Later epith necrosis-> tiny ulcers of
conj
 Corneal involvement ->fascicular
ulcer

85. D/D
 Episcleritis
 Inflamed pinguecula
 FB granuloma
 Suture cyst

86. TREATMENT
 Improve general health
 Treat concurrent infections
 Dietary supplementation inclVitamins
 Hot compresses
 Dark glasses
 Steroids & Antibiotics drops
 Cycloplegics and antibiotics in corneal
involvement

87. PTERYGIUM
 Latin =Wing
 Wing shaped encroachment of conj
on the cornea in palp fissure
 SE Asia, Australia, Middle East, South
Africa,Texas

88. ETIOLOGY
• Exact cause not known
• Sunlight and UV rays
• Dry heat and dust
• Wind
• Current theory growth disorder due
to a/m factors & damage to limbal
stem cells

89. PATHOLOGY
 Elastoid deg of s/c tissue
 Destruction of epithelium, BM, and
sup stroma
 Fibrovascular proliferation

90. CLINICAL FEATURES
• Age : Older age
• Sex : males> females
• Location : Nasal >Temporal
• Symptoms
F B sensation
Cosmetic
Defective vision
Redness

91. SIGNS
• Growth on cornea
• 4 parts
Head = Blunt apex
Cap = Infiltrates in front of apex
Neck = Constricted part over limbus
Body = Part over sclera
Stocker’s line = Iron deposits in front
of apex

92. COMPLICATIONS
• Inflm
• Inf
• Cystic deg
• Neoplastic changes
Progressive vs Regressive

93. TREATMENT
 Indications
 Surgical Excision-Bare sclera
technique
 Excision with auto graft
 Amniotic membrane graft
 Role of beta rays and mitomycin C