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Conjunctiva
Dr /Marwa Abdellah, MD
Lecturer of Ophthalmology
Sohag University
Anatomy
• The conjunctiva is a transparent mucous membrane that
lines the inner surface of the eyelids and the anterior
surface of the globe, terminating at the corneoscleral
limbus.
• It is richly vascular, supplied by the anterior ciliary and
palpebral arteries.
• there is a dense lymphatic network, with drainage to the
preauricular and submandibular nodes corresponding to
that of the eyelids.
• It has a key protective role, mediating both passive and
active immunity.
• Anatomically, it is divided into the following:
• The palpebral conjunctiva
• The forniceal conjunctiva
• The bulbar conjunctiva
Histology
• The epithelium is non-keratinizing and around
five cell layers deep.
• Basal cuboidal cells evolve into flattened
polyhedral cells, subsequently being shed from
the surface.
• Mucus-secreting goblet cells are located within
the epithelium, being most dense inferonasally
and in the fornices.
• The stroma (substantia propria) consists of richly vascularized
loose connective tissue.
• The accessory lacrimal glands of Krause and Wolfring are
located deep within the stroma.
• Secretions from the accessory lacrimal glands are essential
components of the tear film.
Clinical features of conjunctival
inflammation
•Discharge:
• Watery
• Mucoid
• Mucopurulent
• Moderately purulent
• Severe purulent
•Conjunctival reaction
•Hyperaemia
•Conjuctival
VS ciliary
injection??
• Haemorrhages
• Chemosis
• Membranes
• Pseudomembranes
• True membranes
• Subconjunctival cicatrization
• Follicles
• Signs. Multiple, discrete, slightly elevated lesions resembling translucent
grains of rice, most prominent in the fornices.
• Blood vessels run around or across rather than within the lesions.
• ○ Histology shows a subepithelial lymphoid germinal centre
• with central immature lymphocytes and mature cells
• peripherally
• ○ Causes
1. viral
2. chlamydial conjunctivitis,
3. Parinaud oculoglandular syndrome
4. Hypersensitivity to topical medications.
5. Small follicles are a normal finding in childhood (folliculosis),
•Papillae
• can develop only in the palpebral conjunctiva and in the
limbal bulbar conjunctiva where it is attached to the
deeper fibrous layer.
• Signs., a vascular core is present.
A. Micropapillae form a mosaic-like pattern of elevated red
dots as a result of the central vascular channel,
A. macropapillae (<1 mm
B. giant papillae (>1 mm)
• Histology shows folds of hyperplastic conjunctival
epithelium with a fibrovascular core and subepithelial stromal
infiltration with inflammatory cells
• Causes:
1. bacterial conjunctivitisallergic
2. conjunctivitis,
3. chronic blepharitis,
4. contact lens wear,
5. superior limbic keratoconjunctivitis
Lymphadenopathy
• Causes:
1. viral infectionchlamydial
2. severe bacterial conjunctivitis
3. Parinaud oculoglandular syndrome
conjuctivitis
1. Bacterial
• Simple bacterial conjunctivitis
• Gonococcal keratoconjunctivitis
2. Viral
• Adenoviral keratoconjunctivitis
• Molluscum contagiosum conjunctivitis
• Herpes simplex conjunctivitis
• Adult chlamydial keratoconjunctivitis
• Neonatal chlamydial conjunctivitis
• Trachoma
3. Chlamydial
CONJUNCTIVAL INFECTIONS
1. Bacterial
• Simple bacterial conjunctivitis
• Gonococcal keratoconjunctivitis
2. Viral
• Adenoviral keratoconjunctivitis
• Molluscum contagiosum conjunctivitis
• Herpes simplex conjunctivitis
• Adult chlamydial keratoconjunctivitis
• Neonatal chlamydial conjunctivitis
• Trachoma
3. Chlamydial
CONJUNCTIVAL INFECTIONS
Simple bacterial conjunctivitis
Crusted eyelids and conjunctival
injection
Subacute onset of mucopurulent
discharge
Treatment - broad-spectrum topical antibiotics
Signs
Gonococcal keratoconjunctivitis
Treatment
Acute, profuse, purulent discharge,
hyperaemia and chemosis
Corneal ulceration, perforation
and endophthalmitis if severe
• Topical gentamicin and bacitracin
• Intravenous cefoxitin or cefotaxime
Signs Complications
Adenoviral Keratoconjunctivitis
1. Pharyngoconjunctival fever
• Adenovirus types 3 , 7,11
• Typically affects children
2. Epidemic keratoconjunctivitis
• Upper respiratory tract infection
• Keratitis in 30% - usually mild
• Adenovirus types 8 19, 37
• Very contageous
• No systemic symptoms
• Keratitis in 80% of cases - may be severe
Signs of keratitis
Treatment
• Focal, epithelial keratitis • Focal, subepithelial keratitis
• May persist for months
- topical steroids if visual acuity
diminished by subepithelial keratitis
• Transient
Signs of viral conjunctivitis
Usually bilateral, acute watery
discharge and follicles
Subconjunctival haemorrhages and
pseudomembranes if severe
Treatment - symptomatic
Molluscum contagiosum conjunctivitis
Treatment
• Waxy, umbilicated eyelid nodule
• May be multiple
• Ispilateral, chronic, mucoid
discharge
• Follicular conjuntivitis
- destruction of eyelid lesion
Signs
Herpes simplex conjunctivitis
Treatment
Unilateral eyelid vesicles Acute follicular conjunctivitis
- topical antivirals to prevent keratitis
Signs
Adult chlamydial keratoconjunctivitis
Treatment
• Infection with Chlamydia trachomatis serotypes D to K
• Concomitant genital infection is common
Subacute, mucopurulent follicular
conjunctivitis
Variable peripheral keratitis
- topical tetracycline and oral tetracycline
or erythromycin
TRACHOMA
• Trachoma ( Egyptian ophthalmia) is a chronic
keratoconjunctivitis, primarily affecting the superficial
epithelium of conjunctiva and cornea simultaneously.
• It is characterised by a mixed follicular and papillary response
of conjunctival tissue.
• It is still one of the leading causes of preventable blindness in
the world.
• Etiology
• A. Causative organism. the Chlamydia trachomatis organism is
epitheliotropic and produces intracytoplasmic inclusion bodies
called Halberstaedter Prowazekebodies.
• Presently, 11 serotypes of chlamydia, (A, B, Ba, C, D, E, F, G, H,
J and K) have been identified using microimmunofluorescence
techniques.
• Serotypes A, B, Ba and C are associated with hyperendemic
(blinding) trachoma,
• while serotypes D-K are associated with
paratrachoma(oculogenital chlamydial disease).
• Symptoms
• -mild foreign body sensation
• occasional lacrimation, slight stickiness of the lids and scanty
mucoid discharge.
• -In the presence of secondary infection, typical
• symptoms of acute mucopurulent conjunctivitis
• develop.
• Signs
• A. Conjunctival signs
• 1-Congestionof upper tarsal and forniceal conjunctiva.
• 2-Conjunctival follicles. commonly seen on upper tarsal
conjunctiva and fornix.
• 3-Papillary hyperplasia. Papillae are reddish, flat topped raised
areas which give red and velvet appearance to the tarsal
conjunctiva
• B. Corneal signs
• 1-Superficial keratitis may be present in the upper part.
• 2-Herbert follicles refer to typical follicles present in the limbal
area. These are histologically similar to conjunctival follicles.
• 3-Pannus
• Infiltrationo f the cornea associated with vascularization is
seen in upper part. The vessels are superficial and lie between
epithelium and Bowman's membrane. Later on Bowman’s
membrane is also destroyed
• 4-Corneal ulcer
• may sometime develop at the advancing edge of pannus. Such
ulcers are usually shallow which may become chronic and
indolent.
• 5-Herbert pits are the oval or circular pitted scars, Left after
healing of Herbert follicles in the limbal area.
• 6-Corneal opacity may be present in the upper part. It
• may even extend down and involve the pupillary area
Grading of trachoma
• McCallan'sclassification
• Stage I(Incipient trachoma or stage of infiltration).
It is characterized by hyperaemiaof palpebral conjunctiva and
immature follicles.
• Stage II (Established trachoma or stage of florid infiltration).
It is characterized by appearance of mature follicles, papillae and
progressive corneal pannus.
• Stage III (Cicatrisingtrachoma or stage of scarring).
It includes obvious scarring of palpebral conjunctiva.
• Stage IV(Healed trachoma or stage of sequelae).
The disease is quite and cured but sequelae due to cicatrisation
give rise to symptoms.
WHO classification
• TF: Trachoma follicle
It is the stage of active trachoma with predominantly follicular
inflammation. To
diagnose this stage at least five or more follicles (each 0.5 mm or more
in
diameter).
• TI :Trachoma intense.
• inflammatory thickening of the upper tarsal conjunctiva obscures
more than half of the normal deep tarsal vessels.
• TS: Trachomatous scarring.
• the presence of scarring in the tarsal conjunctiva.
• TT: Trachomatous trichiasis.
• least one eyelash rubs the eyeball.
• CO: Corneal opacity.
• visible corneal opacity
Ophthalmia Neonatorum
• Ophthalmia neonatorum(neonatal conjunctivitis) is The name
given to bilateral inflammation of the Conjunctiva occurring in
an infant less than 30 days old. Itis serious because of the lack
of immunuty in the infant and the immaturity of the ocular
surface.
• Aetiology
• Sources of infection
• -Infected maternal passages
• -Contaminated towels and instruments.
• Causative agents
• 1-Gonococcalinfection is now an uncommon
• 2-Chlamydia trachomatis accounts for the majority
• of cases in developed countries.
• 3-Other pathogenesare Staphylococcus aureus,
• H. influenzaeand Streptococcus pneumoniae.
• 4-Herpes simplex ophthalmianeonatorumis a
• rare condition caused by herpes simplex-II virus.
• Clinical features
• Incubation period
• It varies depending on the type of the causative
• agent.
• Causative agent Incubation period Gonococcal 2-4 days
• .Other bacterial 4-5 days
• Neonatal inclusion conjunctivitis 5-14 days
• .Herpes simplex 5-7 days
• Symptoms and signs
• -Usually bilateral lid oedemawhich may be
• sever in gonococcal Infection.
• -Conjunctival discharge is purulent in gonococcal ophthalmia
neonatorumand mucoid or mucopurulent in other bacterial
cases and neonatal inclusion conjunctivitis.
• -Conjunctiva may show hyperaemia and chemosis.There might
be mild papillary reaction which may occasionally be
associated with pseudomembranes.
• -Corneal involvement is more sever with gonococcal infection
and Include corneal ulcer and perforation
• Investigations
• -Gram stain for diplococci and Giemsa stain for inclusion
bodies.
• -Cultures
• -Immunofluorescence test for chlamydia
• -PCR for chlamydia and neisseriaDNA
• Treatment
• Prophylaxis:
• Povidine-iodine 2.5% .
• Curative treatment:
• -Chlamydial infection is treated with oral
• eryrhromycinor azithromycin for 2 weeks and responds well to
topical tetracycline or erythromycin ointment.
• -Gonococcal infection requires ceftriaxone or
• cefotaxime.
• -Other bacterial ophthalmianeonatorumshould be
• treated by broad spectrum antibiotic drops and ointments for 2
weeks.
• -Herpes simplex conjunctivitis is usually a self-limiting disease.
However, topical antiviral drugs control the infection more
effectively and may prevent the recurrence
• .
• Types
• 1-Acute allergic conjunctivitis
• Seasonal allergic conjunctivitis (SAC)
• Perennial allergic conjunctivitis (PAC)
• 2-Vernal keratoconjunctivitis(VKC)
• 3-Atopic keratoconjunctivitis(AKC)
• 4-Giant papillary conjunctivitis (GPC)
• 5-Phlyctenularkeratoconjunctivitis
• 6-Contact dermoconjunctivitis(CDC)
Acute Allergic Conjunctivitis
• It is a mild, non-specific allergic conjunctivitis
• characterized by itching, hyperaemia and mild
• papillary response.
• Etiology
• 1-Seasonal allergic conjunctivitis. (Hay fever )
• is a response to seasonal allergens such as tree
• and grass pollens. It is commonest form
• occurring during spring and summer.
• 2 -Perennial allergic conjunctivitis
• is a response to perennial allergens such as
• house dust mite, animal dander and fungal
• allergens. It is less common and milder than
• Seasonal form occurring through out the year
• with exacerbations in the autumn.
Clinical picture
• Symptoms
• Include transient , acute attacks of redness,
• intense Itching, burning sensation and
• watering in the eyes associated with sneezing
• and nasal discharge.
• Signs
• Hyperaemia and chemosis.
• Mild papillary reaction.
• Lid oedema
Treatment
• 1-Elimination of allergens if possible.
• 2-mast cell stabilizers
• Sodium cromoglycate, nedocromil and
• lodoxamide
• 3-Antihistamine
• Levocabastine, emadastine and epinastine
• 4-combined Antihistamine and mast cell stabilizers
• Olopatadine, ketotifen and azelastine
• 5-Steroid eye drops
• 6-Systemic antihistaminic drugs
• 7-Desensitization
PHLYCTENULAR
CONJUNCTIVITIS
• this is a kerato-conjunctivitisproduced as an allergy to an
endogenous agent.
• ETIOLOGY
• Causative allergens
• It is type IV hypersensitivity reaction to endogenous microbial
• proteins. The endogenous toxin may be
• (1) Tuberculo-protein from TB focus.
• (2) Intestinal parasites.
• (3)Septic foci as tonsils and adenoids.
• (4) Secondary to staphylococcal blepharo-conjunctivitis
• Predisposing factors
• 1.Age. Peak age group is 3-15 years.
• 2. Sex. Incidence is higher in girls than boys.
• 3. malnourishment. Disease is more common in
• undernourished children.
• 4. Living conditions. Overcrowded and unhygienic.
• 5. Season.It occurs in all climates but incidence is high in
spring and summer seasons.
• .
Clinical picture
• Symptoms
• mild discomfort in the eye, irritation and reflex
• watering. However, usually there is associated
• mucopurulent conjunctivitis due to secondary
• bacterial infection
• Signs
• The characteristic lesion is the phlycten, which may affect any part
of the conjunctiva or the cornea but the most common sites are the
limbus and bulbar conjunctiva.
• 1-Around nodule 1-3 mm in size.
• 2-solitary nodule but at times there may be two nodules or multiple
phlyctens which may be
• arranged haphazardly or in the form of a ring around the limbus.
• 3-pinkish white nodule surrounded by
• Hyperaemia on the bulbar conjunctiva, usually
• near the limbus
• 4-The epithelium first intact but later ulcerates and secondary
staphylococcal infection takes place. Healing occurs rapidly without
any scar
• COMPLICATIONS
• A) Corneal phlycten
• may occur deep or superficial to B.M. It may
• ulcerate causing phlyctenularulcer or vascularized
• causing Phlyctenularpannus.
• B) Phlyctenular ulcers
• -Limbalulcer or multiple limbalulcers: The latter may fuse to
form a ring ulcer.
• -Fascicular ulcer: is a superficial ulcer, which creeps
• over the cornea towards the centre and is supplied by a leash
(bundle) of parallel vessels. When it heals, its track leaves
opacity maximum where it stops.
• C) Plyctenular pannus
• is vascularization + infiltration. It differs from trachomatous
pannus in the following:
• -Affects any part of the limbus.
• -Vessels are straight and lie deeper to B.M.
• -Thin and very vascular with marked irritation.
VERNAL KERATOCONJUNCTIVITIS
(VKC) OR SPRING CATARRH
• It is a recurrent, bilateral, self-limiting,
• allergic inflammation of the conjunctiva
• having a periodic seasonal incidence.
Etiology
• VKC is thought to be an atopicallergic disorder in
• many cases, in which IgE-mediated mechanisms play
• an important role. Such patients may give personal or
• family history of other atopic diseases such as hay
• fever, asthma, or eczema and their peripheral blood
• shows eosinophilia and increased serum IgE level
• Predisposing factors
• 1. Age and sex.
• Primarily affects boys and usually presents in the
• first decade of life (mean age 7 years).
• 2. Season.
• More common in summer; hence the name spring
• catarrh looks a misnomer.
• 3. Climate.
• More prevalent in tropics, rare in temperate zones
• and almost non-existent in cold climate.
Clinical picture
• Symptoms
• marked burning and itching sensation which is usually
intolerable
• Itching is more marked with palpebral form of disease.
• Other associated symptoms include: mild photophobia,
lacrimation, stringy (ropy)discharge and heaviness of lids.
• Signs
• 1)Palpebral Type (70%).
• The upper palpebral conjunctiva shows
• -Large flat-topped papillae.
• -Color is bluish white
• -Cobble stone in arrangement.
• -Fornix always free.
• If the upper lid is everted and the papillae are left
• exposed for 1-2 minutes a milky white film forms. This
• film is sticky and is rich in eosinophils.
• 2) Bulbar type(20%)
• Gelatinous masses (due to thickened epithelium and hyaline
degeneration) occur on the limbus, first lateral and medial and
later all-round.
• White spots are seen within these masses called Tranta spots
(Due to aggregation of eosinophils + epithelial debris +
calcium deposits).
• 3) Mixed type (10%)
Corneal manifestation Of Spring Catrah ??
• (1)Epithelial micro-erosions (punctate epitheliopathy) or
keretitissuperficilisvernalisof Tobgy.
• (2)Epithelial macro-erosions.
• (3) Plaques (coated areas of macro erosion with altered
exudate.
• (4) Sub-epithelial scarring usually in the form of ring scarring .
• (5) Pseudo-gernotoxonresembles arcus senilis.
• (6) Weakness of the cornea with higher incidence of
Keratoconus& Keratectasia
• (7) Shield ulcer
Treatment
General
• 1)Dark glasses, for photophobia
• 2)Cold compresses, for sensation of heat.
Local therapy
• 1-Topical steroids.
• 2-Mast cell stabilizers
• 3-Topical antihistaminics
• 4-Acetyl cysteine (0.5%)
• 5-Topical cyclosporine (1%) drops
• Systemic therapy
• 1.Oral antihistaminics
• Help sleep and reduce nocturnal eye rubbing
• 2. Immunosuppressive agents
• Like steroids, cyclosporine and azathioprine for a
• short duration have been recommended for
• advanced, very severe, nonresponsive
Treatment of large papillae
• 1-Supratarsal steroid injection
• 2-Cryoapplication
• 3-Surgical excision is recommended for extraordinarily large
papillae.
• Treatment of vernal keratopathy
• ■A large vernal plaque requires surgical excision by
• superficial keratectomy.
• ■Severe shield ulcer resistant to medical therapy may need
• surgical treatment in the form of debridement, superficial
• keratectomy, excimer laser therapeutic kerateotomy as well
as
• amniotic membrane graft to enhance reepithelialization
Giant papillary conjunctivitis
• Pathogenesis
• Repeated exposure to the environmental antigens
• that adhere to the mucus and protein which coat the surface
of contact lenses plus the trauma to the upper tarsal conj. by
the contact lens.
• Clinical picture
• -Ocular itching, mucous discharge
• -Macropapillae (from 0.3 -1 mm in diameter)
• -Giant papillae (greater than 1 mm in diameter
• Etiology:
• 1-Contact lens wears.
• 2-Artificial eye wears.
• 3-Patient with protruding ends of monofilament sutures
• Treatment:
• 1-Lens care thoroughly cleaned by non-preserved
• Preparations
• 2-Use of a different lens design.
• 3-Commonly sodium cromoglycate 4% four times/day even
with the contact lens in its place.
PINGUECULA
• Pinguecula is an extremely common degenerative condition of
the conjunctiva.
• It is characterized by formation of a yellowish white patch
on the bulbar conjunctiva near the limbus.
• Etiology
• Not known exactly.
• It has been considered as
• an age change,
• occurring more commonly in persons exposed to strong
sunlight , dust and wind.
• It is also considered a precursor of pterygium
• Pathology
• There is an elastotic degeneration of collagen fibers of the
substantia propria of conjunctiva, coupled with deposition of
• amorphous hyaline material in the substance of conjunctiva.
• Clinical features
• is a bilateral, usually stationary condition.
• presenting as
• yellowish white triangular patch near the limbus. Apex of the
triangle is away from the cornea.
• It affects the nasal side first and then the temporal
• side. When conjunctiva is congested, it stands out as an
avascular prominence.
• Treatment
• In routine no treatment is required for
• pinguecula .
• However,if so desired, it may be excised
PTERYGIUM
• Pterygium (Pterygion = a wing) is a wing shaped fold
• of conjunctiva encroaching upon the cornea from either side
within the interpalpebral fissure
• Etiology
1) Unknown, but it is a degenerative condition related to:
2) Chronic irritation , by dust, wind, fumes ... etc.
3) UV Rays : (sunrays) is the most important
4) ) Pinguecula : may be a precursor for the pterygium
• Incidence
• -
• Very common in Egypt.
• -
• Unilateral or bilateral.
• -
• Nasal side is commonest site. (??)
• Pathology
1) It is a fibrovascular
2) Pathology starts in the
3) Elastosis and hyaline degeneration are
4) Number of layers in Pterygium reaches up to 10 15 layers (while there
are only two layers in normal
5) Bowman's membrane and superficial layer of stroma are destroyed
6) Stocker's line: is a pigmented line of iron deposition in corneal
epithelium anterior to the advancing head of pterygium.
• Parts
• A fully developed pterygium consists of three
Parts
Head (apical part present on the
Neck limbal part)
Body (scleral part) extending between limbus and the canthus.
• Types
• ■Progressive pterygium
• Thick, fleshy and vascular with a few infiltrates in the
• cornea, in front of the head of the pterygium (called Cap of
pterygium).
• ■Regressive pterygium
• is thin, atrophic, attenuated with very little vascularity.
• There is no cap. Ultimately it becomes membranous
• But never disappears
• Symptoms
• 1) Usually
• 2) Disfigurment.
• 3) Chronic irritation : From intermittent
• episodes of congestion → hyperemia,photophopia,
lacrimation, FB sensation.
• 4) Visual impairment due to:
• a) Encroachment on papillary area.
• b) Irregular astigmatism.
• c) Symblepharon formation
• →limitation of ocular motility →diplopia
• Management
• 1) Follow up
• For a small asymptomatic pterygium.
• With patient reassurance.
• 2) Medical treatment
• Forsyptomatizing pterygium. Including : Ocular lubricants and
• weak steroids.
• 3) Surgical treatment
• Indications:
 Visual indications:
 Encroachment on the papillary area.
 Restriction of the lateral gaze
 diplopia.
 Optical indications: irregular astigmatism.
 Cosmetic indications.
• Recurrence
• of the pterygium after surgical
• excision is the main problem (30 50 %).
• However, it can be reduced by any of the following measures:
• Surgical excision with bare sclera, plus
• 1-Surgical excision with free conjunctival graft taken
• from the same eye or other eye is presently the preferred
• technique.
• 2-Surgical excision with amniotic membrane graft
• 3-Use of antimitotic drugs such as mitomycin C or thiotepa.
• 4-Postoperative beta irradiations
• 5-In recurrent recalcitrant pterygium, surgical
• excision should be coupled with lamellar keratectomy and lamellar
keratoplasty.
• 7Limbal stem cell transplantation
• Conjunctival and amniotic membrane graft
• 1 Acts as a mechanical barrier against development
• of new blood vessels from the conjunctiva to the
• cornea.
• 2 Allows rapid re epithelization of the bared sclera
• that acts as another barrier against recurrence.
• Importance
• 1 Best, safest & least incidence of recurrence (<
• 2Rapid Patient recovery & return to work within few
• days without irritation.
• MitomycinC
• Nature
• : antimetabolite alkylating
• Action:
• In pterygium:
• Prevent metaplasia of endothelial cells of
• the blood vessels into fibroblasts
• .
• Thioteba
• -
• Nature: antimetabolite alkylating agent.
• -
• Action: as Mitomycin C.
• -
• Application: Eye drops/ 3 hours post operative.
• Complications:
Conjunctiva

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Conjunctiva

  • 1. Conjunctiva Dr /Marwa Abdellah, MD Lecturer of Ophthalmology Sohag University
  • 2. Anatomy • The conjunctiva is a transparent mucous membrane that lines the inner surface of the eyelids and the anterior surface of the globe, terminating at the corneoscleral limbus. • It is richly vascular, supplied by the anterior ciliary and palpebral arteries. • there is a dense lymphatic network, with drainage to the preauricular and submandibular nodes corresponding to that of the eyelids. • It has a key protective role, mediating both passive and active immunity.
  • 3. • Anatomically, it is divided into the following: • The palpebral conjunctiva • The forniceal conjunctiva • The bulbar conjunctiva
  • 4.
  • 5. Histology • The epithelium is non-keratinizing and around five cell layers deep. • Basal cuboidal cells evolve into flattened polyhedral cells, subsequently being shed from the surface. • Mucus-secreting goblet cells are located within the epithelium, being most dense inferonasally and in the fornices.
  • 6. • The stroma (substantia propria) consists of richly vascularized loose connective tissue. • The accessory lacrimal glands of Krause and Wolfring are located deep within the stroma. • Secretions from the accessory lacrimal glands are essential components of the tear film.
  • 7. Clinical features of conjunctival inflammation •Discharge: • Watery • Mucoid • Mucopurulent • Moderately purulent • Severe purulent
  • 13. • Follicles • Signs. Multiple, discrete, slightly elevated lesions resembling translucent grains of rice, most prominent in the fornices. • Blood vessels run around or across rather than within the lesions. • ○ Histology shows a subepithelial lymphoid germinal centre • with central immature lymphocytes and mature cells • peripherally • ○ Causes 1. viral 2. chlamydial conjunctivitis, 3. Parinaud oculoglandular syndrome 4. Hypersensitivity to topical medications. 5. Small follicles are a normal finding in childhood (folliculosis),
  • 14.
  • 15. •Papillae • can develop only in the palpebral conjunctiva and in the limbal bulbar conjunctiva where it is attached to the deeper fibrous layer.
  • 16. • Signs., a vascular core is present. A. Micropapillae form a mosaic-like pattern of elevated red dots as a result of the central vascular channel, A. macropapillae (<1 mm B. giant papillae (>1 mm) • Histology shows folds of hyperplastic conjunctival epithelium with a fibrovascular core and subepithelial stromal infiltration with inflammatory cells
  • 17. • Causes: 1. bacterial conjunctivitisallergic 2. conjunctivitis, 3. chronic blepharitis, 4. contact lens wear, 5. superior limbic keratoconjunctivitis
  • 18. Lymphadenopathy • Causes: 1. viral infectionchlamydial 2. severe bacterial conjunctivitis 3. Parinaud oculoglandular syndrome
  • 20. 1. Bacterial • Simple bacterial conjunctivitis • Gonococcal keratoconjunctivitis 2. Viral • Adenoviral keratoconjunctivitis • Molluscum contagiosum conjunctivitis • Herpes simplex conjunctivitis • Adult chlamydial keratoconjunctivitis • Neonatal chlamydial conjunctivitis • Trachoma 3. Chlamydial CONJUNCTIVAL INFECTIONS
  • 21. 1. Bacterial • Simple bacterial conjunctivitis • Gonococcal keratoconjunctivitis 2. Viral • Adenoviral keratoconjunctivitis • Molluscum contagiosum conjunctivitis • Herpes simplex conjunctivitis • Adult chlamydial keratoconjunctivitis • Neonatal chlamydial conjunctivitis • Trachoma 3. Chlamydial CONJUNCTIVAL INFECTIONS
  • 22. Simple bacterial conjunctivitis Crusted eyelids and conjunctival injection Subacute onset of mucopurulent discharge Treatment - broad-spectrum topical antibiotics Signs
  • 23. Gonococcal keratoconjunctivitis Treatment Acute, profuse, purulent discharge, hyperaemia and chemosis Corneal ulceration, perforation and endophthalmitis if severe • Topical gentamicin and bacitracin • Intravenous cefoxitin or cefotaxime Signs Complications
  • 24. Adenoviral Keratoconjunctivitis 1. Pharyngoconjunctival fever • Adenovirus types 3 , 7,11 • Typically affects children 2. Epidemic keratoconjunctivitis • Upper respiratory tract infection • Keratitis in 30% - usually mild • Adenovirus types 8 19, 37 • Very contageous • No systemic symptoms • Keratitis in 80% of cases - may be severe
  • 25. Signs of keratitis Treatment • Focal, epithelial keratitis • Focal, subepithelial keratitis • May persist for months - topical steroids if visual acuity diminished by subepithelial keratitis • Transient
  • 26. Signs of viral conjunctivitis Usually bilateral, acute watery discharge and follicles Subconjunctival haemorrhages and pseudomembranes if severe Treatment - symptomatic
  • 27. Molluscum contagiosum conjunctivitis Treatment • Waxy, umbilicated eyelid nodule • May be multiple • Ispilateral, chronic, mucoid discharge • Follicular conjuntivitis - destruction of eyelid lesion Signs
  • 28. Herpes simplex conjunctivitis Treatment Unilateral eyelid vesicles Acute follicular conjunctivitis - topical antivirals to prevent keratitis Signs
  • 29. Adult chlamydial keratoconjunctivitis Treatment • Infection with Chlamydia trachomatis serotypes D to K • Concomitant genital infection is common Subacute, mucopurulent follicular conjunctivitis Variable peripheral keratitis - topical tetracycline and oral tetracycline or erythromycin
  • 30.
  • 31.
  • 32. TRACHOMA • Trachoma ( Egyptian ophthalmia) is a chronic keratoconjunctivitis, primarily affecting the superficial epithelium of conjunctiva and cornea simultaneously. • It is characterised by a mixed follicular and papillary response of conjunctival tissue. • It is still one of the leading causes of preventable blindness in the world.
  • 33. • Etiology • A. Causative organism. the Chlamydia trachomatis organism is epitheliotropic and produces intracytoplasmic inclusion bodies called Halberstaedter Prowazekebodies. • Presently, 11 serotypes of chlamydia, (A, B, Ba, C, D, E, F, G, H, J and K) have been identified using microimmunofluorescence techniques. • Serotypes A, B, Ba and C are associated with hyperendemic (blinding) trachoma, • while serotypes D-K are associated with paratrachoma(oculogenital chlamydial disease).
  • 34. • Symptoms • -mild foreign body sensation • occasional lacrimation, slight stickiness of the lids and scanty mucoid discharge. • -In the presence of secondary infection, typical • symptoms of acute mucopurulent conjunctivitis • develop.
  • 35. • Signs • A. Conjunctival signs • 1-Congestionof upper tarsal and forniceal conjunctiva. • 2-Conjunctival follicles. commonly seen on upper tarsal conjunctiva and fornix. • 3-Papillary hyperplasia. Papillae are reddish, flat topped raised areas which give red and velvet appearance to the tarsal conjunctiva
  • 36. • B. Corneal signs • 1-Superficial keratitis may be present in the upper part. • 2-Herbert follicles refer to typical follicles present in the limbal area. These are histologically similar to conjunctival follicles. • 3-Pannus • Infiltrationo f the cornea associated with vascularization is seen in upper part. The vessels are superficial and lie between epithelium and Bowman's membrane. Later on Bowman’s membrane is also destroyed
  • 37. • 4-Corneal ulcer • may sometime develop at the advancing edge of pannus. Such ulcers are usually shallow which may become chronic and indolent. • 5-Herbert pits are the oval or circular pitted scars, Left after healing of Herbert follicles in the limbal area. • 6-Corneal opacity may be present in the upper part. It • may even extend down and involve the pupillary area
  • 38. Grading of trachoma • McCallan'sclassification • Stage I(Incipient trachoma or stage of infiltration). It is characterized by hyperaemiaof palpebral conjunctiva and immature follicles. • Stage II (Established trachoma or stage of florid infiltration). It is characterized by appearance of mature follicles, papillae and progressive corneal pannus. • Stage III (Cicatrisingtrachoma or stage of scarring). It includes obvious scarring of palpebral conjunctiva. • Stage IV(Healed trachoma or stage of sequelae). The disease is quite and cured but sequelae due to cicatrisation give rise to symptoms.
  • 39. WHO classification • TF: Trachoma follicle It is the stage of active trachoma with predominantly follicular inflammation. To diagnose this stage at least five or more follicles (each 0.5 mm or more in diameter). • TI :Trachoma intense. • inflammatory thickening of the upper tarsal conjunctiva obscures more than half of the normal deep tarsal vessels. • TS: Trachomatous scarring. • the presence of scarring in the tarsal conjunctiva. • TT: Trachomatous trichiasis. • least one eyelash rubs the eyeball. • CO: Corneal opacity. • visible corneal opacity
  • 40. Ophthalmia Neonatorum • Ophthalmia neonatorum(neonatal conjunctivitis) is The name given to bilateral inflammation of the Conjunctiva occurring in an infant less than 30 days old. Itis serious because of the lack of immunuty in the infant and the immaturity of the ocular surface. • Aetiology • Sources of infection • -Infected maternal passages • -Contaminated towels and instruments.
  • 41. • Causative agents • 1-Gonococcalinfection is now an uncommon • 2-Chlamydia trachomatis accounts for the majority • of cases in developed countries. • 3-Other pathogenesare Staphylococcus aureus, • H. influenzaeand Streptococcus pneumoniae. • 4-Herpes simplex ophthalmianeonatorumis a • rare condition caused by herpes simplex-II virus.
  • 42. • Clinical features • Incubation period • It varies depending on the type of the causative • agent. • Causative agent Incubation period Gonococcal 2-4 days • .Other bacterial 4-5 days • Neonatal inclusion conjunctivitis 5-14 days • .Herpes simplex 5-7 days
  • 43. • Symptoms and signs • -Usually bilateral lid oedemawhich may be • sever in gonococcal Infection. • -Conjunctival discharge is purulent in gonococcal ophthalmia neonatorumand mucoid or mucopurulent in other bacterial cases and neonatal inclusion conjunctivitis. • -Conjunctiva may show hyperaemia and chemosis.There might be mild papillary reaction which may occasionally be associated with pseudomembranes.
  • 44. • -Corneal involvement is more sever with gonococcal infection and Include corneal ulcer and perforation
  • 45. • Investigations • -Gram stain for diplococci and Giemsa stain for inclusion bodies. • -Cultures • -Immunofluorescence test for chlamydia • -PCR for chlamydia and neisseriaDNA
  • 46. • Treatment • Prophylaxis: • Povidine-iodine 2.5% . • Curative treatment: • -Chlamydial infection is treated with oral • eryrhromycinor azithromycin for 2 weeks and responds well to topical tetracycline or erythromycin ointment. • -Gonococcal infection requires ceftriaxone or • cefotaxime. • -Other bacterial ophthalmianeonatorumshould be • treated by broad spectrum antibiotic drops and ointments for 2 weeks. • -Herpes simplex conjunctivitis is usually a self-limiting disease. However, topical antiviral drugs control the infection more effectively and may prevent the recurrence • .
  • 47.
  • 48. • Types • 1-Acute allergic conjunctivitis • Seasonal allergic conjunctivitis (SAC) • Perennial allergic conjunctivitis (PAC) • 2-Vernal keratoconjunctivitis(VKC) • 3-Atopic keratoconjunctivitis(AKC) • 4-Giant papillary conjunctivitis (GPC) • 5-Phlyctenularkeratoconjunctivitis • 6-Contact dermoconjunctivitis(CDC)
  • 49. Acute Allergic Conjunctivitis • It is a mild, non-specific allergic conjunctivitis • characterized by itching, hyperaemia and mild • papillary response. • Etiology • 1-Seasonal allergic conjunctivitis. (Hay fever ) • is a response to seasonal allergens such as tree • and grass pollens. It is commonest form • occurring during spring and summer. • 2 -Perennial allergic conjunctivitis • is a response to perennial allergens such as • house dust mite, animal dander and fungal • allergens. It is less common and milder than • Seasonal form occurring through out the year • with exacerbations in the autumn.
  • 50. Clinical picture • Symptoms • Include transient , acute attacks of redness, • intense Itching, burning sensation and • watering in the eyes associated with sneezing • and nasal discharge. • Signs • Hyperaemia and chemosis. • Mild papillary reaction. • Lid oedema
  • 51. Treatment • 1-Elimination of allergens if possible. • 2-mast cell stabilizers • Sodium cromoglycate, nedocromil and • lodoxamide • 3-Antihistamine • Levocabastine, emadastine and epinastine • 4-combined Antihistamine and mast cell stabilizers • Olopatadine, ketotifen and azelastine • 5-Steroid eye drops • 6-Systemic antihistaminic drugs • 7-Desensitization
  • 52. PHLYCTENULAR CONJUNCTIVITIS • this is a kerato-conjunctivitisproduced as an allergy to an endogenous agent. • ETIOLOGY • Causative allergens • It is type IV hypersensitivity reaction to endogenous microbial • proteins. The endogenous toxin may be • (1) Tuberculo-protein from TB focus. • (2) Intestinal parasites. • (3)Septic foci as tonsils and adenoids. • (4) Secondary to staphylococcal blepharo-conjunctivitis
  • 53. • Predisposing factors • 1.Age. Peak age group is 3-15 years. • 2. Sex. Incidence is higher in girls than boys. • 3. malnourishment. Disease is more common in • undernourished children. • 4. Living conditions. Overcrowded and unhygienic. • 5. Season.It occurs in all climates but incidence is high in spring and summer seasons. • .
  • 54. Clinical picture • Symptoms • mild discomfort in the eye, irritation and reflex • watering. However, usually there is associated • mucopurulent conjunctivitis due to secondary • bacterial infection
  • 55. • Signs • The characteristic lesion is the phlycten, which may affect any part of the conjunctiva or the cornea but the most common sites are the limbus and bulbar conjunctiva. • 1-Around nodule 1-3 mm in size. • 2-solitary nodule but at times there may be two nodules or multiple phlyctens which may be • arranged haphazardly or in the form of a ring around the limbus. • 3-pinkish white nodule surrounded by • Hyperaemia on the bulbar conjunctiva, usually • near the limbus • 4-The epithelium first intact but later ulcerates and secondary staphylococcal infection takes place. Healing occurs rapidly without any scar
  • 56. • COMPLICATIONS • A) Corneal phlycten • may occur deep or superficial to B.M. It may • ulcerate causing phlyctenularulcer or vascularized • causing Phlyctenularpannus. • B) Phlyctenular ulcers • -Limbalulcer or multiple limbalulcers: The latter may fuse to form a ring ulcer. • -Fascicular ulcer: is a superficial ulcer, which creeps • over the cornea towards the centre and is supplied by a leash (bundle) of parallel vessels. When it heals, its track leaves opacity maximum where it stops.
  • 57.
  • 58. • C) Plyctenular pannus • is vascularization + infiltration. It differs from trachomatous pannus in the following: • -Affects any part of the limbus. • -Vessels are straight and lie deeper to B.M. • -Thin and very vascular with marked irritation.
  • 59. VERNAL KERATOCONJUNCTIVITIS (VKC) OR SPRING CATARRH • It is a recurrent, bilateral, self-limiting, • allergic inflammation of the conjunctiva • having a periodic seasonal incidence. Etiology • VKC is thought to be an atopicallergic disorder in • many cases, in which IgE-mediated mechanisms play • an important role. Such patients may give personal or • family history of other atopic diseases such as hay • fever, asthma, or eczema and their peripheral blood • shows eosinophilia and increased serum IgE level
  • 60. • Predisposing factors • 1. Age and sex. • Primarily affects boys and usually presents in the • first decade of life (mean age 7 years). • 2. Season. • More common in summer; hence the name spring • catarrh looks a misnomer. • 3. Climate. • More prevalent in tropics, rare in temperate zones • and almost non-existent in cold climate.
  • 61. Clinical picture • Symptoms • marked burning and itching sensation which is usually intolerable • Itching is more marked with palpebral form of disease. • Other associated symptoms include: mild photophobia, lacrimation, stringy (ropy)discharge and heaviness of lids.
  • 62. • Signs • 1)Palpebral Type (70%). • The upper palpebral conjunctiva shows • -Large flat-topped papillae. • -Color is bluish white • -Cobble stone in arrangement. • -Fornix always free. • If the upper lid is everted and the papillae are left • exposed for 1-2 minutes a milky white film forms. This • film is sticky and is rich in eosinophils.
  • 63. • 2) Bulbar type(20%) • Gelatinous masses (due to thickened epithelium and hyaline degeneration) occur on the limbus, first lateral and medial and later all-round. • White spots are seen within these masses called Tranta spots (Due to aggregation of eosinophils + epithelial debris + calcium deposits). • 3) Mixed type (10%)
  • 64. Corneal manifestation Of Spring Catrah ?? • (1)Epithelial micro-erosions (punctate epitheliopathy) or keretitissuperficilisvernalisof Tobgy. • (2)Epithelial macro-erosions. • (3) Plaques (coated areas of macro erosion with altered exudate. • (4) Sub-epithelial scarring usually in the form of ring scarring . • (5) Pseudo-gernotoxonresembles arcus senilis. • (6) Weakness of the cornea with higher incidence of Keratoconus& Keratectasia • (7) Shield ulcer
  • 65.
  • 66. Treatment General • 1)Dark glasses, for photophobia • 2)Cold compresses, for sensation of heat. Local therapy • 1-Topical steroids. • 2-Mast cell stabilizers • 3-Topical antihistaminics • 4-Acetyl cysteine (0.5%) • 5-Topical cyclosporine (1%) drops
  • 67. • Systemic therapy • 1.Oral antihistaminics • Help sleep and reduce nocturnal eye rubbing • 2. Immunosuppressive agents • Like steroids, cyclosporine and azathioprine for a • short duration have been recommended for • advanced, very severe, nonresponsive
  • 68. Treatment of large papillae • 1-Supratarsal steroid injection • 2-Cryoapplication • 3-Surgical excision is recommended for extraordinarily large papillae. • Treatment of vernal keratopathy • ■A large vernal plaque requires surgical excision by • superficial keratectomy. • ■Severe shield ulcer resistant to medical therapy may need • surgical treatment in the form of debridement, superficial • keratectomy, excimer laser therapeutic kerateotomy as well as • amniotic membrane graft to enhance reepithelialization
  • 69. Giant papillary conjunctivitis • Pathogenesis • Repeated exposure to the environmental antigens • that adhere to the mucus and protein which coat the surface of contact lenses plus the trauma to the upper tarsal conj. by the contact lens. • Clinical picture • -Ocular itching, mucous discharge • -Macropapillae (from 0.3 -1 mm in diameter) • -Giant papillae (greater than 1 mm in diameter
  • 70. • Etiology: • 1-Contact lens wears. • 2-Artificial eye wears. • 3-Patient with protruding ends of monofilament sutures • Treatment: • 1-Lens care thoroughly cleaned by non-preserved • Preparations • 2-Use of a different lens design. • 3-Commonly sodium cromoglycate 4% four times/day even with the contact lens in its place.
  • 71.
  • 72. PINGUECULA • Pinguecula is an extremely common degenerative condition of the conjunctiva. • It is characterized by formation of a yellowish white patch on the bulbar conjunctiva near the limbus.
  • 73. • Etiology • Not known exactly. • It has been considered as • an age change, • occurring more commonly in persons exposed to strong sunlight , dust and wind. • It is also considered a precursor of pterygium
  • 74. • Pathology • There is an elastotic degeneration of collagen fibers of the substantia propria of conjunctiva, coupled with deposition of • amorphous hyaline material in the substance of conjunctiva. • Clinical features • is a bilateral, usually stationary condition. • presenting as • yellowish white triangular patch near the limbus. Apex of the triangle is away from the cornea. • It affects the nasal side first and then the temporal • side. When conjunctiva is congested, it stands out as an avascular prominence.
  • 75.
  • 76. • Treatment • In routine no treatment is required for • pinguecula . • However,if so desired, it may be excised
  • 77. PTERYGIUM • Pterygium (Pterygion = a wing) is a wing shaped fold • of conjunctiva encroaching upon the cornea from either side within the interpalpebral fissure • Etiology 1) Unknown, but it is a degenerative condition related to: 2) Chronic irritation , by dust, wind, fumes ... etc. 3) UV Rays : (sunrays) is the most important 4) ) Pinguecula : may be a precursor for the pterygium
  • 78. • Incidence • - • Very common in Egypt. • - • Unilateral or bilateral. • - • Nasal side is commonest site. (??) • Pathology 1) It is a fibrovascular 2) Pathology starts in the 3) Elastosis and hyaline degeneration are 4) Number of layers in Pterygium reaches up to 10 15 layers (while there are only two layers in normal 5) Bowman's membrane and superficial layer of stroma are destroyed 6) Stocker's line: is a pigmented line of iron deposition in corneal epithelium anterior to the advancing head of pterygium.
  • 79. • Parts • A fully developed pterygium consists of three Parts Head (apical part present on the Neck limbal part) Body (scleral part) extending between limbus and the canthus.
  • 80. • Types • ■Progressive pterygium • Thick, fleshy and vascular with a few infiltrates in the • cornea, in front of the head of the pterygium (called Cap of pterygium). • ■Regressive pterygium • is thin, atrophic, attenuated with very little vascularity. • There is no cap. Ultimately it becomes membranous • But never disappears
  • 81. • Symptoms • 1) Usually • 2) Disfigurment. • 3) Chronic irritation : From intermittent • episodes of congestion → hyperemia,photophopia, lacrimation, FB sensation. • 4) Visual impairment due to: • a) Encroachment on papillary area. • b) Irregular astigmatism. • c) Symblepharon formation • →limitation of ocular motility →diplopia
  • 82. • Management • 1) Follow up • For a small asymptomatic pterygium. • With patient reassurance. • 2) Medical treatment • Forsyptomatizing pterygium. Including : Ocular lubricants and • weak steroids. • 3) Surgical treatment • Indications:  Visual indications:  Encroachment on the papillary area.  Restriction of the lateral gaze  diplopia.  Optical indications: irregular astigmatism.  Cosmetic indications.
  • 83. • Recurrence • of the pterygium after surgical • excision is the main problem (30 50 %). • However, it can be reduced by any of the following measures: • Surgical excision with bare sclera, plus • 1-Surgical excision with free conjunctival graft taken • from the same eye or other eye is presently the preferred • technique. • 2-Surgical excision with amniotic membrane graft • 3-Use of antimitotic drugs such as mitomycin C or thiotepa. • 4-Postoperative beta irradiations • 5-In recurrent recalcitrant pterygium, surgical • excision should be coupled with lamellar keratectomy and lamellar keratoplasty. • 7Limbal stem cell transplantation
  • 84. • Conjunctival and amniotic membrane graft • 1 Acts as a mechanical barrier against development • of new blood vessels from the conjunctiva to the • cornea. • 2 Allows rapid re epithelization of the bared sclera • that acts as another barrier against recurrence. • Importance • 1 Best, safest & least incidence of recurrence (< • 2Rapid Patient recovery & return to work within few • days without irritation.
  • 85. • MitomycinC • Nature • : antimetabolite alkylating • Action: • In pterygium: • Prevent metaplasia of endothelial cells of • the blood vessels into fibroblasts • .
  • 86. • Thioteba • - • Nature: antimetabolite alkylating agent. • - • Action: as Mitomycin C. • - • Application: Eye drops/ 3 hours post operative. • Complications: