INFLAMMATION OF CONJUNCTIVA

[CONJUNCTIVITIS]

OPTOM FASLU MUHAMMED

 CONJUNCTIVITIS : Conjunctival Hyperemia
+
DISCHARGE
( Watery, Mucoid, Mucopurulent, Purulent)

CLINICAL SIGNS

• CONGESTION • PAPILLAE
• CHEMOSIS • FOLLICLES
• SUBCONJUNCTIVAL • PSEUDOMEMBRANE
HEMORRHAGES • PANNUS
• DISCHARGE • PRE AURICULAR
• MEMBRANE LYMPH NODES
CONGESTION
CHEMOSIS
SUBCONJUNCTIVAL HEMORRHAGES
DISCHARGE
MEMBRANE
PAPILLAE
FOLLICLES
PSEUDOMEMBRANE
PANNUS
 CLASSIFICATION

ETIOLOGICAL CLINICAL

• ACUTE CATARRHAL/MUCOPURULENT
• INFECTIVE • ACUTE PURULENT
• ALLERGIC • SEROUS
• CHRONIC SINGLE
• IRRITATIVE • ANGULAR
• KERATOCONJUNCTIVITIS • MEMBRANOUS
• PSEUDOMEMBRANOUS
• WITH SKIN & MUCOUS MEMB • PAPILLARY
DISORDERS • FOLLICULAR
• OPTHALMIA NEONATORUM
•UNKNOWN ETIOLOGY • GRANULAMATOUS
• TRAUMATIC • ULCERATIVE
• CICATRISING
 NATURAL PROTECTIVE
MECHANISMS IN THE CONJUCTIVA
 LOW TEMPERATURE - EXPOSURE TO AIR
 PHYSICAL PROTECTION BY LIDS
 FLUSHING ACTION OF TEARS
 ANTIBACTERIAL ACTIVITY OF LYSOZYMES
 HUMORAL PROTECTION BY THE TEAR
IMMUNOGLOBULINS
 INFECTIVE CONJUNCTIVITIS
 INFLAMMATION OF THE CONJUNCTIVA CAUSED
BY MICRO-ORGANISMS IS THE COMMONEST
VARIETY.

TYPES
BACTERIAL SPIROCHAETAL
CHLAMYDIAL PROTOZOAL
VIRAL PARASITIC
FUNGAL OTHERS
RICKETTISIAE
 BACTERIAL CONJUNCTIVITIS

EPIDEMIC
SPORADIC
(MONSOON)

NORMAL (NON-PATHOGENIC ORGANISMS THAT INVADE

COMMENSALS INTACT CORNEA

• Staph. aureus
• Staph. Epidermidis • Neisseria Gonorrhoea
• Diphtheroids • Corynebacterium
• Corynebacterium xerosis Diphtheriae
• Propioniobacterium acnes
 ETIOLOGY

 PREDISPOSING FACTORS

 CAUSATIVE ORGANISMS

 MODE OF INFECTION
 ETIOLOGY
• Predisposing factors for bacterial
conjunctivitis, especially epidemic forms, are
flies, poor hygienic conditions, hot dry
climate, poor sanitation and dirty habits.
These factors help the infection to establish,
as the disease is highly contagious
• Mode of infection. Conjunctiva may get
infected from three sources, viz, exogenous,
local surro1. Exogenous infections may spread:
(i) directly through close contact, as air-borne
infections or as water-borne infections
 (ii) through vector transmission (e.g., flies); (iii)
through material transfer EG infected fingers
of doctors, nurses, common towels,
handkerchiefs, and infected tonometers.
• 2. Local spread from neighbouring structures
like infected lacrimal sac, lids, and naso
pharynx. Also a change in the character of
relatively innocuous organisms present in the
conjunctival sac itself may cause infections.
• 3. Endogenous infections may occur very
rarely through blood e.g., gonococcal and
meningococcal infections
 CAUSATIVE ORGANISMS
STAPH AUREUS BACRTERIAL CONJUNCTIVITIS
BLEPHARO CONJUNCTIVITIS
STAPH EPIDERMIDIS BLEPHARO CONJUNCTIVITIS
(INNOCUOUS FLORA)
STREPTOCOCCUS PNEUMONIAE PETECHIAL SUBCONJUNCTIVIAL
(PNEUMOCOCCUS) HEMORRHAGES
STREPTOCOCCUS PYOGENES PSEUDOMEMBRANOUS
(HEMOLYTICUS) CONJUNCTIVITIS
VIRULENT
HEMOPHILUS INFLUENZA MUCUPURULENT CONJUNCTIVITIS (RED
(aegypticus koch –weeks bacillus EYE)
MORAXELLA LACUNATE Angular conjunctivitis
(Morax- Axenfeld bacillus) Angular BLEPHARO CONJUNCTIVITIS
PSEUDOMANAS PYOCYANEA Invades Cornea
(Virulent)
NEISSIERIA GONORRHOEA ACUTE PURULENT CONJUNCTIVITIS
OPHTHALMIA NEONATORUM
NEISSIERIA MENINGIDIS MUCUPURULENT CONJUNCTIVITIS
CORYNEBACTERIUM DIPHTHERIAE MEMBRANOUS CONJUNCTIVITIS
 PATHOLOGY
Severity depends on
- degree of inflammation
- causative organisms

1. VASCULAR RESPONSE
2. CELLULAR RESPONSE
3. CONJUNCTIVAL TISSUE RESPONSE
4. CONJUCTIVAL DISCHARGE
 VASCULAR RESPONSE
• CONGESTION
• ↑ PERMEABILITY OF
CONJUNCTIVAL VESSELS
• CAPILLARY PROLIFERATION

P
A
CONJUNCTIVAL DISCHAGE
T CELLULAR RESPONSE
MILD SEVERE
TEARS DIAPEDISIS OF H Exudation of PMNs &
MUCUS RBC’S O Inflammatory cells into
INF. CELLS L substantia propria &
DESQ. EPI. CELLS + ↓
FIBRIN BLOOD O conjunctivial SAC.
BACTERIA STAINED G
Y

CONJUNCTIVAL TISSUE RESPONSE

• EDEMA
• EPITHELIUM
• SUPERFICIAL CELLS : Degenerate
become loose desquamate.
• Basal Cells : Proliferate
• ↑ Goblet Cells
 CLINICAL TYPES OF BACTERIAL
CONJUNCTIVITIS:
• ACUTE MUCOPURULENT CONJUNCTIVITIS IS
the most common type of acute bacterial
conjunctivitis. characterised by marked
conjunctival hyperaemia and mucopurulent
discharge .
• Common causative bacteria are:
Staphylococcus aureus, Koch-Weeks bacillus,
Pneumococcus andStreptococcus.
Mucopurulent conjunctivitis accompanies
exanthemata such as measlesand scarlet fever.
 Clinical picture
Symptoms
• Discomfort & f b sensation d/t engorgemt of
vessels.
• Mild photophobia,
• Mucopurulent discharge from the eyes.
• Sticking together of lid margins during sleep.
• Slight blurring of vision due to mucous flakes
infront of cornea.
• Sometimes coloured halos due to prismatic
effect of mucus present on cornea.
Signs
• Conjunctival congestion, more marked in
palpebral conjunctiva, fornices and peripheral
bulbar conjunctiva, ‘fiery red eye’. The
congestn is less marked in circumcorneal
zone.
• Chemosis i.e., swelling of conjunctiva.
• Petechial haemorrhages are seen when the
causative organism is pneumococcus.
• Flakes of mucopus are seen in the fornices,
canthi and lid margins.
• Cilia are usually matted together with yellow
crust
• Clinical course. Mucopurulent conjunctivitis
reaches its height in three to four days. If
untreated, in mild cases the infection may be
overcome and the condition is cured in 10-15
days; or it may pass to less intense form, the
‘chronic catarrhal conjunctivitis’.
• Complications. Occasionally
• complicated by marginal corneal ulcer,
superficial keratitis, blepharitis or
dacryocystitis.
• Differential diagnosis
• 1. From other causes of acute red eye .
• 2. From other types of conjunctivitis. It is made
out from the typical clinical picture of disease
and is confirmed by conjunctival cytology and
bacteriological examination of secretions and
scrapings .
 Treatment
• 1. Topical antibiotics. Ideally, the antibiotic
should be selected after culture and sensitivity
tests. However, in routine, most of the
patients respond well to broad specturm
antibiotics. . newer antibiotic drops such as
ciprofloxacin (0.3%), ofloxacin (0.3%) or
gatifloxacin (0.3%) may be used.
• Dark goggles may be used to prevent
photophobia.
• No bandage should be applied in patients
with mucopurulent conjunctivitis
• Anti-inflammatory and analgesic drugs (e.g.
ibuprofen and paracetamol) may be given in
sensitive patients.
 ACUTE PURULENT CONJUNCTIVITIS

• Acute purulent conjunctivitis also known as

acute blenorrhea or hyperacute conjunctivitis
is characterised by a violent inflammatory
response. It occurs in two forms:
(1) Adult purulent conjunctivitis
(2) Ophthalmia neonatorum in newborn
• Etiology
• affects adults, predominantly males.
• Commonest causative organism is
Gonococcus; but rarely it may be
Staphylococcus aureus or Pneumococcus.
Gonococcal infection directly spreads from
genitals to eye.
 Clinical picture
• three stages:
1. Stage of infiltraton. It lasts for 4-5 days and is
• characterised by painful and tender eyeball.
• Bright red velvety chemosed conjunctiva.
• Lids are tense and swollen.
• Discharge is watery or sanguinous.
• Pre-auricular lymph nodes are enlarged.
• 2. Stage of blenorrhoea. It starts at about fifth
day, lasts for several days and is characterised
by:
• Frankly purulent, copious, thick discharge
trickling down the cheeks .
• Other symptoms are increased but tension in
the lids is decreased
• 3. Stage of slow healing. in this stage, pain is
decreased & swelling of the lids subsides.
• Conjunctiva remains red, thickened & velvety.
• Discharge diminishes slowly & in the end
resolution is complete.

• Associations. Gonococcal conjunctivitis is

usually associated with urethritis and arthritis.
 Complications
• 1. Corneal involvement frequent as the gono
can invade an intact k epithelium. It may
occur in the form of diffuse haze and oedema,
central necrosis, corneal ulceration or even
perforation.
• 2. Iridocyclitis may also occur.
• 3. Systemic complications, though rare,
include gonorrhoea arthritis, endocarditis and
septicaemia.
 INVESTIGATIONS
• Only in severe cases
• Conj scraping: gram’s stain
• Culture in chocalate agar or thayer martin
media
• PCR for resistant infns.
 Treatment
1. Systemic therapy : more critical than topical
for N.gonorrhoeae and N. meningitidis.
• penicillin & tetracyline are no longer
adequate as first-line treatment.
• Norflox, Cefoxitim 1.0 gm or cefotaxime 500
mg. IV qi dor ceftriaxone 1.0 gm IM qid, all
for 5 days; or Spectinomycin 2.0 gm IM for 3
days.
All of the above regimes be followed
by a 1 week course of either doxycycline 100
mg bid or erythromycin 250-500 mg orally
qid.
2. Topical antibiotic therapy includes ofloxacin,
ciprofloxacin or tobramycin eye drops or
bacitracin or erythromycin eye ointment every
2 hours for the
first 2-3 days and then 5 times daily for 7 days.
3. Irrigation of the eyes frequently with sterile
saline : washing away infected debris.
4. Other general measures are similar to acute
mucopurulent conjunctivitis.
5. Topical atropine 1 per cent eye drops should
be instilled OD or BD if cornea is involved.
6. Patient and the sexual partner should be
referred for evaluation of other STD.
AC. MEMBRANOUS CONJUNCTIVITIS
• an acute inflammation of the conjunctiva,
charac by formation of a true membrane on the
conjunctiva.
• Now VERY RARE, because of markedly
decreased incidence of diphtheria.
• Etiology : The disease is typically caused by
Corynebacterium diphtheriae and occasionally
by virulent type of Streptococcus haemolyticus
Pathology
• Corynebacterium diphtheriae produces a
violent inflammation of the conjunctiva,
associated with deposn of fibrinous exudate
on the surface as well as in the substance of
the conjunctiva resulting in formation of a
membrane. Usually in the palpebral
conjunctiva.
• There is associated coagulative necrosis,
resulting in sloughing of membrane.
Ultimately healing takes place by granulation
tissue.
 Clinical features
• usually affects children between 2-8 years of
age who are not immunised against diphth.
may have a mild or very severe course. The
child is toxic and febrile.
• three stages:
1. Stage of infiltration is characterised by:
• Scanty conjunctival discharge and severe pain
in the eye.
• Lids are swollen and hard.
• Conjunctiva is red, swollen and covered with a
thick grey-yellow membrane which is tough &
firmly adherent to the conj, which on
removing bleeds and leaves behind a raw
area. Pre-auricular lymph nodes are enlarged.
• 2. Stage of suppuration. In this stage, pain
decreases and the lids become soft. The
membrane is sloughed off leaving a raw
surface. There is copious outpouring of
purulent discharge.
3. Stage of cicatrisation. In this stage, the raw
surface covered with granulation tissue is
epithelised. Healing occurs by cicatrisation,
which may cause trichiasis and conjunctival
xerosis
• Complications1. Corneal ulceration is a
frequent complication in acute stage. The
bacteria may even involve the intact corneal
epithelium.
• 2. Delayed complications due to cicatrization
include symblepharon, trichiasis, entropion
and conjunctival xerosis.
• Diagnosis
• Diagnosis is made from typical clinical features
and confirmed by bacteriological examination.
 Treatment
A. Topical therapy
• 1. Penicillin eye drops (1:10000 units per ml)
should be instilled every half hourly.
• 2. Antidiphtheric serum (ADS) should be
instilled every one hour.
• 3. Atropine sulfate 1 percent ointment should
be added if cornea is ulcerated.
• 4. Broad spectrum antibiotic ointment should
be applied at bed time.
• B. Systemic therapy
• 1. Crystalline penicillin 5 lac units should be
injected intramuscularly BD for 10 days.
• 2. (ADS) (50 thousand units) im stat.
• C. Prevention of symblepharon
Once the membrane is sloughed off, sym
blepharon which be prevented by applying
contact shell or sweeping the fornices with a
glass rod smeared with ointment.
• Prophylaxis
• 1. Isolation of patient
• 2. Proper immunization against diphtheria
 PSEUDOMEMBRANOUS CONJ
• It is a type of acute conjunctivitis, charac by
formation of a pseudomembrane (which can
be easily peeled off leaving behind intact
conjunctival epithelium) on the conjunctiva.
• Etiology
• 1. Bacterial infection. Commonly Coryne
bacterium diphtheriae of low virulence,
staphylococci, streptococci, H. influenzae and
N. gonorrhoea..
• 2. Viral infections such as herpes simplex and
adenoviral epidemic keratoconjunctivitis may
be associated with pseudomembrane formn.
• 3. Chemical irritants such as acids, ammonia,
lime, silver nitrate and copper sulfate are also
known to cause formation of such membrane
• Pathology inflammation of conjunctiva
associated with pouring of fibrinous exudate
on its surface which coagulates and leads to
formation of a pseudomembrane.
• Clinical picture
• Pseudomembranous conjunctivitis is charac by
Acute m p conjunctivitis, like features assoc
with Pseudomembrane formation which is
thin yellowish-white membrane seen in the
fornices and on the palpebral conjunctiva .
• Pseudomembrane can be peeled off easily and
does not bleed.
• Treatment
similar to m p conjunctivitis
 CHRONIC CATARRHAL
CONJUNCTIVITIS
• also known as ‘simple chronic conjunctivitis’ is
charac by mild catarrhal inflamm of the conj.
• Etiology A. Predisposing factors
1. Chr exposure to dust, smoke, & chem irritants.
2. Local cause of irritation such as trichiasis,
concretions, f b & seborrhoeic scales.
3. Eye strain d/t ref errors, phorias or conv insuff.
4. Abuse of alcohol, insomnia and metabolic
disorders
• B. Causative organisms
• Staphylococcus aureus : commonest cause .
• Gram negative rods such as Proteus mirabilis,
Klebsiella pneumoniae, Escherichia coli and
Moraxella lacunata are other rare causes
• C. Source and mode of infection.
• 1. As continuation of acute mp conjunctivitis
when untreated or partially treated.
• 2. As chr infection fm chr dacryocystitis , chr
rhinitis or chronic upper respiratory catarrh.
• 3. As mild exogen infectn which results fm dir
contact, air-borne or material transfer of infn
 Clinical picture
• Symptoms of simple chronic conjunctivitis inc:
• Burning and grittiness in the eyes, especially
in the evening.
• Mild chronic redness in the eyes.
• Feeling of heat & dryness on the lid margins.
• Difficulty in keeping the eyes open.
• Mild mucoid discharge esp in the canthi.
• Off and on lacrimation.
• Feeling of sleepiness and tiredness in the eyes
Signs. Grossly the eyes look normal but careful
examination may reveal following signs:
• Congestion of posterior conjunctival vessels.
• Mild papillary hypertrophy of the palpebral
conjunctiva.
• Surface of the conjunctiva looks sticky.
• Lid margins may be congested.
 Treatment
1. Predisposing factors when associated should
be treated and eliminated.
2. Topical antibiotics such as chloramphenicol or
gentamycin should be instilled 3-4 times a day
for about 2 weeks to eliminate the mild
chronic infection.
3. Astringent eye drops such as zinc-boric acid
drops provide symptomatic relief.
 ANGULAR CONJUNCTIVITIS
• a type of chr conjunctivitis charac by mild
inflammation confined to the conj & lid
margins near the angles associated with
maceration of the surrounding skin.
• Etiology
1. Predisp factors same as for 'simp chr conj.
• 2. Causative organisms. Moraxella Axenfeld is
commonest causative organism. so the
disease is also called 'diplobacillary conjunc'.
Rarely, staph may also cause angular conj.
• 3. Source of infection is usually nasal cavity.
• 4. Mode of infection. transmitted fm nasal
cavity to the eyes by contam fingers or hanky.
• Pathology The MA bacillus prod a proteolytic
enzyme which acts by macerating the
epithelium. This enzyme collects at the angles
by the action of tears & thus macerates the
epithelium of the conjunctiva, lid margin &
the skin the surr angles of eye. The
maceration is foll by vascular and cellular
responses in the form of mild grade chronic
inflammation. Skin may show eczematous
changes.
 Clinical picture
• Symptoms
• Irritation, smarting sensation and feeling of
discomfort in the eyes.
• History of collection of dirty-white foamy
discharge at the angles.
• Redness in the angles of eyes.
• Signs include:
• Hyperaemia of bulbar conjunctiva near the
canthi.
• Hyperaemia of lid margins near the angles.
• Excoriation of the skin around the angles.
• Presence of foamy mucopurulent discharge at
the angles.
• Complications : blepharitis and shallow
marginal catarrhal corneal ulceration
• Treatment
A. Prophylaxis includes treatment of associated
nasal infection and good personal hygiene.
B. Curative treatment consists of :
• 1. Oxytetracycline (1%) eye ointment 2-3 times
a day for 9-14 days will eradicate the infection.
• 2. Zinc lotion instilled in day time and zinc
oxide ointment at bed time inhibits the
proteolytic ferment and thus helps in reducing
the maceration.
 CHLAMYDIAL CONJUNCTIVITIS
• Chlamydia :Like viruses are obligate intra
cellular and filterable, whereas like bacteria
contain both DNA and RNA, divide by binary
fission & r sensitive to antibiotics. PLT group
• Life cycle of the chlamydia. The infective
particle invades the cytoplasm of epithelial
cells, where it swells up and forms the 'initial
body'. They rapidly divide into 'elementary
bodies‘ embedded in glycogen matrix which
are liberated when the cells burst. Then the
'elementary bodies' infect other cells where
the whole cycle is repeated
• Jones' classification. three classes :
Class 1 : Blinding trachoma. refers to hyper
endemic trachoma caused by serotypes A, B,
Ba and C of Chlamydia trachomatis associated
with secondary bacterial infection.transmitted
from eye to eye by transfer of ocular discharge
• Class 2 : Non-blinding trachoma. Chlamydia
trachomatis serotypes A, B, Ba, and C; but is
usually not associated with secondary
bacterial infections. It occurs in mesoendemic
or hypoendemic areas with better socio
economic conditions. is a mild form of disease
with ltd transmission d/t improved hygiene.
Class 3: Paratrachoma. oculogenital chlamydial
disease caused by serotypes D to K of
chlamydia trachomatis.
• It spreads from genitals to eye and mostly
seen in urban population. It manifests as
either adult inclusion conjunctivitis or
ophthalmia neonatorum
 TRACHOMA
• Trachoma (previously known as Egyptian
ophthalmia) is a chronic keratoconjunctivitis,
affecting the superficial epithelium of conj and
cornea simultaneously.
• It is charac by a mixed follicular and papillary
response.
• leading causes of preventable blindness .
• 'trachoma' :Greek word for 'rough' which
describes the surface appearance of the
conjunctiva in chronic trachoma
 Etiology
• A. Causative organism. Bedsonian organism,
the Chlamydia trachomatis belonging to the
(PLT) group. The organism is epitheliotropic
and produces intracytoplasmic inclusion
bodies called H.P. bodies (Halberstaedter
Prowazeke bodies). Presently, 11 serotypes of
chlamydia, (A, B, Ba, C, D, E, F, G, H, J and K)
have been identified using microimmuno
fluorescence techniques.
• Serotypes A, B, Ba and C are associated with
hyperendemic (blinding) trachoma, while D-K
are associated with paratrachoma .
B. Predisposing factors.
• 1. Age. infancy & early childhood.
• 2. Sex. in females ( in number & in severity)
• 3. Race. very common in Jews and less
common among Negroes.
• 4. Climate. dry and dusty weather.
• 5. Socioeconomic status. in poor classes
owing to unhygienic , overcrowded,unsanitary
conditions, fly population, paucity of water,
lack of sep towels & handkys, & lack of
education abt spread of contagious diseases.
• 6. Env fact like dust, smoke, irritants , sunlight
• C. Source of infection. In endemic zones the
main source of infection is conj discharge of
affected person. Therefore, superimposed
bacterial infections help in transmission by
increasing the conjunctival secretions.
• D. Modes of infection.:
1. Direct spread of infection through contact by
air-borne or water-borne modes.
2. Vector transmission is common thru flies.
3. Material transfer occurs thru contaminated
fingers of doctors, nurses & contam tono
meters. Other sources are use of common
towel, handkerchief, bedding and surma-rods.
 Clinical profile of trachoma
• Incubation period of trachoma varies from 5-
21 days. Onset is insidious (subacute),rarely it
may present in acute form.
• Clinical course of trachoma is determined by
the presence or absence of secondary
infection. In absence of infn , pure trachoma
is mild and symptomless. But, mostly the
picture is complicated by secondary infection.
In early stages it is clinically indistinguishable
from bacterial conjunctivitis & term
'trachomadubium' is used for this stage.
• Natural history. In an endemic area natural
history of trachoma is characterized by the
development of acute disease in the first
decade of life which continues with slow
progression, until the disease becomes
inactive in the second decade of life.
• The sequelae occur at least after 20 years of
the disease.
• Thus, the peak incidence of blinding sequelae
is seen in the fourth and fifth decade of life
 Symptoms
• In the absence of secondary infection,
symptoms are minimal and include mild
foreign body sensation in the eyes, 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
 SIGNS
• A. Conjunctival signs
1. Congestion of upper tarsal & forniceaL conJ.
2. Conjunctival follicles. commonly seen on
upper tarsal conjunctiva and fornix; but may
also be present in the lower fornix, plica
semilunaris and caruncle. Sometimes, (follicles
may be seen on the bulbar conjunctiva
(pathognomic of trachoma).
• Structure of follicle. Follicles are aggregation of
lymphocytes & other cells in the adenoid
layer. Central part of each follicle is made up
of mononuclear histiocytes, few lymphocytes
and large multinucleated cells called Leber
cells. The cortical part is made up of a zone of
lymphocytes showing active proliferation.
Blood vessels are present in the most
peripheral part. In later stages signs of
necrosis are also seen. Presence of Leber cells
and signs of necrosis differentiate trachoma
follicles from follicles of other forms of
follicular conjunctivitis.
TI FOLLICULAR
• 3. Papillary hyperplasia. Papillae are reddish,
flat topped raised areas which give red and
velvety appearance to the tarsal conjunctiva .
• Each papilla consists of central core of
numerous dilated blood vessels surrounded by
lymphocytes and covered by hypertrophic
epithelium.
TI INTENSE
• Conjunctival scarring which may be irregular,
star-shaped or linear. Linear scar present in
the sulcus subtarsalis is called Arlt's line.
• 5. Concretions may be formed due to
accumulation of dead epithelial cells and
inspissated mucus in the depressions called
glands of Henle.
 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 i.e., infiltration of 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. Pannus may be progressive or
regressive.
• In progressive pannus, infiltration of cornea is
ahead of vascularization.
• In regressive pannus (pannus siccus) vessels
extend a short distance beyond the area of
infiltration.
• 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, the
limbal area .
• 6. Corneal opacity may be present in the upper
part. It may even extend down and involve the
pupillary area. It is the end result of
trachomatous corneal lesions.
1 Active trachoma is most common in pre-
school children and is charac BY Mixed
follicular/papillary conjunctivitis + muco
purulent discharge. In children under 2 years
the papillary component may predominate.
Superior epithelial keratitis and pannus
formation .
2 Cicatricial trachoma is most prevalent in
middle age.
 Grading of trachoma
• McCallan's classification 1908
• Stage I (Incipient trachoma or stage of
infiltration). characterized by hyperaemia of
palpebral conjunctiva and immature follicles.
• Stage II (Established trachoma or stage of
florid infiltration). characterized by
appearance of mature follicles, papillae and
progressive corneal pannus
• Stage III (Cicatrising trachoma or stage of
scarring). obvious scarring of palpebral conj.
• Stage IV (healed trachoma or stage of
sequelae). disease is cured but sequelae due
to cicatrisation give rise to symptoms.
• WHO classification 1987 (FISTO):
• 1. TF: Trach inflam-follicular. : stage of active
trachoma with follicular inflammation. at
least 5 or more follicles ( 0.5 mm or more in
dia) must be present on the utc. Further, the
deep tarsal vessels should be visible through
the follicles and papillae.
• 2. TI : Trachomatous inflammation intense.
This stage has pronounced inflammatory
thickening of the upper tarsal conjunctiva
obscures more than half of the normal deep
tarsal vessels.
• 3. TS: Trachomatous scarring. This stage is
diagnosed by the presence of scarring in the
tarsal conjunctiva. These scars are easily
visible as white, bands or sheets (fibrosis) in
the tarsal conjunctiva
• 4. TT Trachomatous trichiasis.: labelled when
at least 1 eyelash rubs the eyeball. recent
removal of inturned eyelashes also graded as
• 5. CO: Corneal opacity. This stage is labelled
when easily visible corneal opacity is present
over the pupil. This sign refers to corneal
scarring that is so dense that at least part of
pupil margin is blurred when seen through the
opacity.
• The definition is intended to detect corneal
opacities that cause significant visual
impairment (less than 6/18).
 Sequelae of trachoma
1. Sequelae in the lids may be trichiasis
entropion, tylosis (thickening of lid margin),
ptosis, madarosis and ankyloblepharon.
2. Conjunctival sequelae include concretions,
pseudocyst, xerosis and symblepharon.
3. Corneal sequelae may be corneal opacity,
ectasia, corneal xerosis and total corneal
pannus (blinding sequelae).
4. Other sequelae may be chronic dacryocystitis,
and chronic dacryoadenitis
• Complications
• The only complication of trachoma is corneal
ulcer which may occur due to rubbing by
concretions, or trichiasis with superimposed
bacterial infection.
 Diagnosis

• A. The clinical diagnosis is made from its

typical signs; at least 2 sets of signs should be
present :
1. Conjunctival follicles and papillae
2. Pannus progressive or regressive
3. Epithelial keratitis near superior limbus
4. Signs of cicatrisation or its sequelae
• Clinical grading of each case :as per WHO
classfication into TF, TI, TS, TT or CO.
• B. Laboratory diagnosis. Advanced
laboratory tests includes :
• 1. Conjunctival cytology. Giemsa stained
smears : a pred polymorphonuclear reaction
+plasma cells and Leber cells is suggestive.
• 2. Detection of inclusion bodies in conjunctival
smear by Giemsa stain, iodine stain or
immunofluorescent staining esp in active
trachoma
3. ELISA for chlamydial antigens.
4. Polymerase chain reaction (PCR) is also useful.
5. Isolation of chlamydia is : yolk-sac inoculatn
method and tissue culture technique.
• Standard single-passage McCoy cell culture
requires at least 3 days.
• 6. Serotyping of TRIC agents : by detecting
specific antibodies using micro-IF method.
Direct monoclonal fluorescent antibody
microscopy of conjunctival smear is rapid and
inexpensive.
 Differential diagnosis
• 1. Trachoma with follicular hypertrophy from
acute adenoviral follicular conjunctivitis
(epidemic keratoconjunctivitis) asfollows :
• Distribution of follicles in trachoma on UTC
and fornix, while in EKC : LPC and fornix .
• Associated signs such as papillae and pannus
are characteristic of trachoma.
• In clinically indistinguishable cases, laboratory
diagnosis of trachoma helps in differentiation.
• 2. Trachoma with papillary hypertrophy
differentiated from palpebral form of VKC:
• Papillae large in size and cobble-stone
arrangement in spring catarrh.
• pH of tears is usually alkaline in spring catarrh
while in trachoma it is acidic,
• Discharge is ropy in spring catarrh.
• In trachoma, there may be associated follicles
and pannus.
• In clinically indistinguishable cases,
conjunctival cytology and other laboratory
tests for trachoma usually help in diagnosis.
 Management
• The SAFE strategy for trachoma management
supported by the WHO and other agencies
encompasses Surgery for trichiasis, Antibiotics
for active disease, Facial hygiene, and
Environmental improvement.
• 1 Antibiotics should be administered to
those affected and to all family members. A
single antibiotic course is not always effective
in eliminating infection in an individual, and
communities may need to receive annual
treatment to suppress infection.
• A single dose of azithromycin (20 mg/kg up
to 1g) is the treatment of choice.
• Erythromycin 500 mg b.d. for 14 days is an
alternative for women of childbearing age.
• Topical 1% tetracycline ointment is less
effective than oral treatment; it should be
given for 6 weeks.
2 Facial cleanliness
3 Environmental improvement such as access
to adequate water and sanitation, as well as
control of flies, is important.
4 Surgery is aimed at relieving entropion and
trichiasis and maintaining complete lid closure
with bilamellar tarsal rotation
 Management
• A. Treatment of active trachoma
• Antibiotics : locally or systemically, but topical
treatment ispreferred because: cheaper, no
systemic side-effECTS & effective against
associated bacterial conjunctivitis
• 1. Topical therapy regimes.:consists of 1
percent tetracycline or 1 percent erythromycin
eye ointment 4 times a day for 6 weeks or 20
percent sulfacetamide eye drops three times a
day along with 1 percent tetracycline eye
ointment at bed time for 6 weeks.
.
2. Systemic therapy
3. Combined topical and systemic: preferred
when the ocular infection is severe (TI) or in
associated genital infection.
(i) 1 per cent tetracycline or erythromycin eye
ointment QID for 6 weeks; and (ii)
tetracycline or erythromycin 250 mg orally 4
times a day for 2 weeks
• B. Treatment of trachoma sequelae
1. Concretions : removed with a hypodermic
needle.
2. Trichiasis treated by epilation, electrolysis or
cryolysis .
3. Entropion should be corrected surgically
• 4. Xerosis should be treated by artificial tears.
• C. Prophylaxis :reinfections and recurrences
are likely to occur.
• 1. Hygienic measures.health education on
trachoma . The use of common towel,
handkerchief, surma rods etc. should be
discouraged. A good environmental sanitation
will reduce the flies. A good water supply
would improve washing habits.
• 2. Early treatment of conjunctivitis. Every case
of conjunctivitis should be treated as early as
possible to reduce transmission of disease.
• 3. Blanket antibiotic therapy (intermittent
treatment). WHO : in endemic areas to
minimise the intensity and severity of disease.
The regime : apply 1 percent tetracycline eye
ointment twice daily for 5 days in a month for
6 months.
 ADULT INCLUSN CONJUNCTIVITIS
• a type of acute follicular conjunctivitis with
mucopurulent discharge.
• sexually active young adults.
• Etiology serotypes D to K of Chlamydia
trachomatis. The primary source of infection is
urethritis in males and cervicitis in females.
• The transmission of infection : to eyes either
through contaminated fingers/ contaminated
water of swimming pools ( swimming pool
conjunctivitis).
 Urogenital infection
1 In males chlamydia is the m c cause of non-
gonococcal urethritis (NGU), also termed non-
specific urethritis (NSU). Chlamydial urethritis
is frequently asymptomatic in men. C.
trachomatis may also cause epididymitis, and
can act as a trigger for Reiter's disease.
2 In females chlamydial urethritis typically
causes dysuria and discharge. It may progress
to pelvic inflammatory disease (PID), carrying
a risk of infertility; 5–10% of women with PID
develop perihepatitis (Fitz-Hugh–Curtis
 Clinical features
Incubation period : 4-12 days.
Symptoms : Ocular discomfort, foreign body
sensation, Mild photophobia, and Muco
purulent discharge from the eyes.
Signs of inclusion conjunctivitis are:
• Conj hyperaemia, more marked in fornices.
• Acute follicular hypertrophy in LPC
• Superficial keratitis in upper half of cornea.
• superior micropannus may also occur.
• Pre-auricular lymphadenopathy
• Clinical course. benign course and often
evolves into the chr follicular conjunctivitis,
may develop mild conjunctival scarring and
superior corneal pannus.
• Differential diagnosis must be made from
other causes of acute follicular conjunctivitis.
 TREATMENT
1 Referral to a genitourinary specialist is
mandatory, for exclusion of other STI,
contact tracing and pregnancy testing.
2 Systemic therapy
• Azithromycin 1 g repeated after 1 week is
drug of choice, a 2ND or a 3RD dose is
required in 30% of cases.
• Doxycycline 100 mg b.d. for 10 days
(tetracyclines are relatively contraindicated in
pregnancy/breastfeeding and in children
under 12 years of age).
• Erythromycin, amoxicillin and ciprofloxacin
are alternatives.
3 Topical antibiotics : erythromycin or tetra
cycline ointment : rapid relief of symptoms
4 Reduction of transmission risk abstinence
of sexual contact until completion of
treatment (1 week after azithromycin),
together with other precautions as for any
infectious conjunctivitis.
• Symptoms take weeks to settle, follicles &
corneal infiltrates can take months to resolve
due to a prolonged hypersensitivity response
to chlamydial antigen
 Neonatal conjunctivitis
• Neonatal conjunctivitis (ophthalmi
neonatorum) Is conjunctival inflammation
developing within the first month of life.
• m c infection in neonates, up to 10%.
• identified as a specific entity distinct fM conj
in older infants because it is the result of
infecTn transm. fm mother to Child during
delivery.
• any discharge or even watering from the eyes
in 1st week of life should arouse suspicion as
tears are not formed till then.
 Causes
• C. trachomatis, N. gonorrhoeae and occ HSV
(typically HSV-2), which may be associated
with severe ocular or systemic complications.
• Staph causes mild conjunctivitis; others inc
Streptococci, H influenzae & various Gram-
negative organisms.
• Topical prep used in prophylaxis against
infection , themselves cause conjunc irritation.
• Despite poor neonatal tear production, a
persistently mildly watery eye with recur bact
conj may be secondary to congenital NLDO.
• Source and mode of infection in three ways:
before birth, during birth or after birth.
• 1. Before birth infection is very rare through
infected liquor amnii in mothers with ruptured
membrances.
• 2. During birth. most common mode of
infection from the infected birth canal esp in
face presentation or forceps delivery.
• 3. After birth. Infection may occur during first
bath of newborn or from soiled clothes or
fingers with infected lochia.
 Diagnosis
1 Timing of onset • Chem irritation: few
days.
• Gonococcal: first week.
• Staphy & other bact: end of the first wk.
• Herpes simplex: 1–2 weeks.
• Chlamydia: 1–3 weeks.
2 History • Instillation of a prophylactic
chemical preparation.
• Parental symptoms of sexually
transmitted infections.
• Recent conjunctivitis in close contacts.
• Systemic illness such as pneumonitis,
rhinitis and otitis in chlamydial infection, skin
vesicles and features of encephalitis in herpes
simplex.
• Prior persistent watering without
inflammation may indicate an uncanalized
nasolacrimal duct
• Incubation period
• It varies depending on the type of the
causative agent as shown below:
• Causative agent Incubation period
• 1. Chemical 4-6 hours
• 2. Gonococcal 2-4 days
• 3. Other bacterial 4-5 days
• 4. Neonatal inclusion conjunctivitis 5-14 days
• 5. Herpes simplex 5-7 days
• Signs • The type of discharge varies
according to the underlying cause.
• Reflux of mucopurulent material on
pressure over the lacrimal sac is suggestive of
delayed canalization of the lacrimal duct.
• Severe eyelid oedema occurs in
gonococcal infection .
• Eyelid and periocular vesicles may occur
in HSV infection.
• Keratitis in gonococcal or HSV infection.
 Investigations
• Conjunctival scrapings for Gram and Giemsa
staining . Multinucleated giant cells may be
present on Gram stain in HSV infection.
• Conjunctival swabs for bacterial culture ON
chocolate agar or Thayer–Martin for N.
gonorrhoeae).
• Separate conjunctival scrapings PCR, ESP for
chlamydia.
• Conjunctival scrapings or fluid from skin
vesicles can be sent for viral culture for HSV.
 Treatment
• 1 Prophylaxis Antenatal measures : care of
mother and treatment of genital infections
when suspected.
• 2. Natal measures.
• Deliveries should be conducted under
hygienic conditions taking aseptic measures.
• The newborn baby's closed lids should be
thoroughly cleansed and dried.
• 3. Postnatal measures includeno standard
protocol.
• A single instillation of povidone-iodine 2.5%
solution is eff against common pathogen
• Erythromycin 0.5% or tetracycline 1% ointmt
• Silver nitrate 1% solution agglutinates
gonococci . administered in conjunction with a
single intramuscular dose of benzylpenicillin
when maternal infection is present.
2 Chemical conjunctivitis does not require
treatment apart from artificial tears.
3 Mild conjunctivitis is very common in
neonates and may require a broad-spectrum
topical antibiotic such as chloramphenicol or
fusidic acid.
4 Moderate to severe cases should be
investigated as above.
• If bacteria evident on Gram stain, a broad-
spectrum topical antibiotic STARTED.
• Chlamydial infection is treated with oral
erythromycin for two weeks. Erythromycin or
tetracycline ointment can be used in addition
5 Severe conjunctivitis, or systemic illness
requires hospital admission.
• Gonococcal conjunctivitis :systemic third-
generation cephalosporin. Co-treatment for
chlamydia is prudent.
• Herpes simplex infection should always be
regarded as a systemic condition and is
treated with high-dose intravenous aciclovir
under paediatric specialist care. Early
diagnosis and treatment of encephalitis may
be life-saving or prevent serious neurological
disability. Topical aciclovir may be considered
in addition.
• 6 Specialist advice from a microbiologist or
paediatrician should be sought as appropriate
in patients with severe involvement,
particularly with systemic features. A
genitourinary specialist referral for the mother
and her sexual contacts is important when a
sexually-transmitted infection is diagnosed;
the neonate should also be screened for other
sexually-transmitted infection
Viral conj:Adenoviral conjunctivitis
• Pathogenesis : an adenovirus (a non-
enveloped double-stranded DNA virus).
• Infection : sporadic or in epidemics in
workplaces (including hospitals), schools and
swimming pools.
• spread facilitated by ability of virus to survive
on dry surfaces for weeks, viral shedding
occurs for many days before clinical features
• Transmission by contact with respiratory or
ocular secretions, including via fomites,
 Presentation
• 1 Non-specific acute follicular conjunctivitis
most common . Ocular involvement is milder
than in other forms of adenoviral infection
although accompanying systemic symptoms
such as a sore throat or cold are frequent.
2 Pharyngoconjunctival fever (PCF) is
caused by adenovirus serovars 3, 4 and 7. It is
spread by droplets within families with upper
respiratory tract infection. Keratitis develops
in about 30% of cases but is seldom severe.
• 3 Epidemic keratoconjunctivitis (EKC) is
caused by adenovirus serovars 8, 19 and 37. It
is the most severe type and is associated with
keratitis in about 80% of cases.
4 Chronic/relapsing adenoviral
conjunctivitis, characterized by chronic non-
specific follicular/papillary lesions, is rare but
can persist for year
 Signs
1 lid oedema & tender pre-auricular lnopathy.
2 Prominent conjunctival hyperaemia and
follicles .
3 Severe inflammation may be associated with
conjunctival haemorrhages (usually petechial
in adenoviral infection), chemosis, membranes
(rare) and pseudomembranes
4 Pseudomembranes or membranes with mild
conjunctival scarring after resolution
5 Keratitis is characterized by
• Epithelial microcysts during early stage.
• Punctate epithelial keratitis develops with
in 7–10 days of the onset of symptoms and
resolves within 2 weeks.
• Focal white subepithelial/anterior stromal
infiltrates may develop beneath the fading
epithelial lesions, probably as an immune
response to the virus , and may persist or
recur over months or years
6 Mild anterior uveitis is uncommon.
 Differential diagnosis
1 Acute haemorrhagic conjunctivitis in
tropical areas and usually caused by entero
and coxsackievirus. a rapid onset & resolves
in 1–2 weeks; conj haemorrhages r seen
2 Herpes simplex virus (HSV) a follicular
conjunctivitis, , which is usually unilateral and
often associated with skin vesicle
3 Systemic viral infections ( varicella, measles
and mumps) follicular conjunctivitis.V-z v : a
conj as part of ophthalmic shingles. An HIV
conjunctivitis is also recognized.
 Management
• Spontaneous resolutn in 2–weeks.
1 Investigations unnecessary; unless diag is in
doubt or the condition unresolved.
• Giemsa stain : mononuclear cells in adeno
conj & multinucleated giant cells in herpes.
• PCR are sensitive and specific for viral DNA.
• Viral culture with isolation is the reference
standard but expensive , slow (days–weeks),
and requires specific transport media.
• immunochromatography : detects adeno Ag
in tears; sensitivity & specificity are excellent.
2 Reduction of transmission risk hand
hygiene, avoidi eye rubbing & towel sharing.
disinfection of instruments & clinical surfaces
after examinatn of an infected patient (e.g.
sodium hypochlorite, povidone-iodine).
3 Topical steroids pred 0.5% q.i.d. in severe
memb or pseudomemb adenoviral conj.
Symptomatic keratitis : weak topical steroids;
use with caution : do not speed resolution
only suppress inflamm ; lesions recur after
premature stopping. Steroids enhance viral
replication & extend period of patients
infectivitys. IOP should be monitored.
• Other measures • Discontinuation of
contact lens wear until resolution.
• Artificial tears q.i.d. symptomatic relief.
• Cold (or warm) compresses for
symptomatic relief.
• Removal of symptomatic
pseudomembranes or membranes.
• Topical antibiotics if secondary bacterial
infection is suspected.
• Povidone-iodine is very effective against
free (although less so against intracellular)
adenovirus, and has been proposed as a
means of decreasing infectivity.
 Molluscum contagiosum
conjunctivitis
• Pathogenesis :Molluscum contagiosum is a
skin infection caused by a human specific
double-stranded DNA poxvirus which typically
affects otherwise healthy children, with a peak
incidence between the ages of 2 and 4 years.
Transmission is by contact, with subsequent
autoinoculation. The eyelash line should be
examined carefully in patients with chronic
conjunctivitis so as not to overlook a
molluscum lesion
 Diagnosis
1 Presentation is with chronic unilateral ocular
irritation and mild discharge.
2 Signs • A pale, waxy, umbilicated nodule
on the lid margin associated with follicular
conjunctivitis and mild mucoid discharge .
• Bulbar nodules and multiple cutaneous
lesions that may be confluent may occur in
immunocompromised patients.
• Untreated long-standing cases may
develop a fine epithelial keratitis and
sometimes pannus.
 Treatment
• Although the lesions are self-limiting in the
immunocompetent, removal is often
necessary to address secondary conjunctivitis
or for cosmetic reasons. Expression is
facilitated by making a small nick in the skin at
the margin of the lesion with the tip of a
needle.
 ALLERGIC CONJUNCTIVITIS
• immediate (humoral) or delayed (cellular).
• conj x 10 sensitive than skin to allergens .
• Types
1. Simple allergic conjunctivitis
• Hay fever conjunctivitis
• Seasonal allergic conjunctivitis (SAC)
• Perennial allergic conjunctivitis (PAC)
2. (VKC) 3. Atopic keratoconjunctivitis (AKC)
4. Giant papillary conjunctivitis (GPC)
5. Phlyctenular keratoconjunctivitis (PKC)
6. Contact dermoconjunctivitis (CDC)
SIMPLE ALLERGIC CONJUNCTIVITIS
• a mild, non-specific allergic conjunctivitis
charac by itching, hyperaemia & mild papillary
response. Basically, it is an acute or subacute
urticarial reaction.
• Etiology It is seen in following forms:
• 1. Hay fever conjunctivitis. It is commonly
associated with hay fever (allergic rhinitis).
The common allergens are pollens, grass and
animal dandruff..
• 2. Seasonal allergic conjunctivitis (SAC). SAC is
A response to seasonal allergens such as grass
pollens. It is of very common occurrence.
• 3. Perennial allergic conjunctivitis (PAC) is a
response to perennial allergens such as house
dust and mite. It is not so common
• Pathology
• 1. Vascular response is charac by sudden and
extreme vasodilation and increased
permeability of vessels leading to exudation.
• 2. Cellular response is in the form of
conjunctival infiltration and exudation in the
discharge of eosinophils, plasma cells and
mast cells producing histamine and histamine-
like substances.
• 3. Conjunctival response is in the form of
boggy swelling of conjunctiva followed by
increased connective tissue formation and
mild papillary hyperplasia.
• Clinical picture
• Symptoms include intense itching and
burning sensation in the eyes associated with
watery discharge and mild photophobia.
• Signs. (a) Hyperaemia and chemosis which
give a swollen juicy appearance to the
conjunctiva. (b) Conjunctiva may also show
mild papillary reaction. (c) Oedema of lids.
• Diagnosis
• Diagnosis is made from : (1) typical symptoms
and signs; (2) normal conjunctival flora; and
(3) presence of abundant eosinophils in the
discharge.
 TREATMENT
1. Artificial tears for mild symptoms
2 Mast cell stabilizers (sodium cromoglicate,
nedocromil sodium, lodoxamide) are suitable
(except lodoxamide) for long-term use
3 Antihistamines (emedastine, epinastine,
levocabastine, bepotastine) for symptomatic
exacerbations and are as effective as mast
cell stabilizers
4 Combined preparation of an antihistamine
and a vasoconstrictor
5 Dual action antihistamine and mast cell
stabilizers (azelastine, ketotifen, olopatadine)
are often very effective for exacerbations.
6 Topical steroids are effective but rarely
necessary.
7 Oral antihistamines for severe symptoms.
Some, such as diphenhydramine, cause
significant drowsiness and may be useful in
aiding sleep; others such as loratadine have
less sedative action
 VERNAL KERATOCONJUNCTIVITIS
OR SPRING CATARRH
• recurrent, bilateral, interstitial, self-limiting,
allergic inflammation having periodic
seasonal incidence.
• Etiology a hypersensitivity reaction to exoge
allergen, such as grass pollens. VKC is an
atopic allergic disorder , IgE-mediated mechs
play important role. personal or family
history of atopic diseases such as hay fever,
asthma, or eczema ; peripheral blood shows
eosinophilia and inceased serum IgE levels.
• Predisposing factors
• 1. Age and sex. 4-20 years; more common in
boys than girls.
• 2. Season. More common in summer; as
'Warm weather conjunctivitis'.
• 3. Climate. More prevalent in tropics, less in
temperate zones and almost non-existent in
cold climate.
• Pathology
• 1. Conjunctival epith : hyperplasia & sends
downward projections into subepith tissue.
• 2. Adenoid layer shows marked cellular
infiltration by eosinophils, plasma cells,
lymphocytes and histiocytes.
• 3. Fibrous layer shows proliferation which
later on undergoes hyaline changes.
• 4. Conjunctival vessels show proliferation,
increased permeability & vasodilation. All
these lead to formation of mulT pap in the
UTC
• Symptoms. Spring catarrh is characterised by
marked burning and itching sensation which is
usually intolerable and accentuated when
patient comes in a warm humid atmosphere.
• Itching is more marked with palpebral form of
disease.
• Other associated symptoms include: mild
photophobia, lacrimation, stringy (ropy)
discharge and heaviness of lids.
• Signs : three clinical forms:
1. Palpebral form. UsuallY UTC of b e is involved.
• The typical lesion is charac by the presence of
hard, flat topped, papillae arrged 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.
2. Bulbar form. It is characterised by:
(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).
• 3. Mixed form. It shows combined features of
both palpebral and bulbar forms .
• Vernal keratopathy. Corneal involvement in
VKC may be primary or secondary to extensn
of limbal lesions. Vernal keratopathy includes
following 5 types of lesions:
• 1. Punctate epithelial keratitis involving upper
cornea is usually associated with palpebral
form of disease. The lesions always stain with
rose bengal and with fluorescein dye.
• 2. Ulcerative vernal keratitis (shield ulceratioN
a shallow transverse ulcer in upper part of
cornea. results due to epitheliaL macro
erosions.may be complicated by bacterial
keratitis.
• 3. Vernal corneal plaques result due to coating
of bare areas of epithelial macroerosions with
a layer of altered exudates .
• 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
• A. Local therapy
• 1. Topical steroids. These are effective in all
forms of spring catarrh. However they
frequently cause steroid induced glaucoma.
monitoring of intraocular pressure. Frequent
instillation (4 hourly) to start with (2 days)
should be followed by maintenance therapy
for 3-4 times a day for 2 weeks.
• fluorometholone , betamethasone or
dexamethasone.
 Treatment
• General measures
• 1 Allergen avoidance, if possible. An
allergy specialist opinion can be requested if
appropriate; allergen patch testing is
sometimes useful, but often gives non-specific
findings.
2 Cool compresses may be helpful.
3 Lid hygiene should be used for
associated staphylococcal blepharitis.
Moisturizing cream such as E45 can be applied
to dry fissured skin.
Local treatment
1 Mast cell stabilizers reduce frequency of
acute exacerbations & need for steroids, al
though seldom effective in isolation. Sev days
of treatment are needed & in some cases
long-term therapy may be needed. In some
patients adding a NSAID (ketorolac, diclofe
nac) may give added benefit.
2 Antihistamines are suitable for acute
exacerbations but generally not for long-term
use. A trial of several different agents may be
worthwhile.
3 Combined preparations of an antihistamine
and a vasoconstrictor usually offer only
limited relief while dual action antihistamine
/mast cell stabilizers are often effective.
4 Steroids are used for (a) severe exacerbation
of conjunctivitis and (b) sig keratopathy in
which reducing conjunctival activity leads to
corneal improvement.
• Steroids (fluorometholone 0.1%, rimexolone
1%, prednisolone 0.5% or loteprednol
etabonate 0.2% or 0.5%) are prescribed in
short but intensive courses, aiming for prompt
tapering.
• Stronger prep like prednisolone 1% can be
used but carry a higher risk of steroid-induced
glaucoma.
• Supratarsal steroid injection considered in
severe palpebral disease, for non-compliance
or patients resistant to conventional therapy.
injection is given into the conjunctival surface
of the anaesthetized everted upper eyelid;
0.1 mL of betamethasone sodium phosphate
4 mg/mL (Betnesol), dexamethasone 4 mg/mL
or triamcinolone 40 mg/mL is given.
• 5 Immune modulators a Ciclosporin
0.05% b.d. indicated if steroids are ineffective,
inadequate or poorly tolerated, or as a
steroid-sparing agent in patients with severe
disease. The drug may cause ocular irritation
and blurred vision when used for several
weeks and relapses occur if stopped suddenly.
b Tacrolimus 0.03% ointment can be
effective in AKC for severe eyelid disease.
Instillation into the fornices has been effective
in modulating conjunctival inflammation in
refractory cases.
• 6 Other measures a Antibiotics are used
in conjunction with steroids in severe
keratopathy to prevent or treat bacterial
infection.
b Acetylcysteine is a mucolytic agent that
is useful in VKC for dissolving mucus filaments
and deposits, and addressing early plaque
formation
 Systemic treatment
1 Antihistamines help itching, promote sleep
and reduce nocturnal eye rubbing. Because
other inflammatory mediators are involved
besides histamines, effectiveness is not
assured.
2 Antibiotics (doxycycline 50–100 mg daily
for 6 weeks or azithromycin 500 mg once daily
for 3 days) to reduce blepharitis-aggravated
inflammation, usually in AKC.
• 3 Immunosuppressive agents (e.g.
steroids, ciclosporin, tacrolimus, azathioprine)
may be effective at relatively low doses in AKC
unresponsive to other measures. Short
courses of high-dose steroids may be
necessary to achieve rapid control in severe
disease. Monoclonal antibodies against T cells
have shown some promise in refractory cases.
4 Aspirin may be useful in VKC, although
the risk of Reye's syndrome means it should
be avoided in children and adolescents (the
group predominantly affected by VKC)
• Surgery
1 Bandage contact lens wear : aid the
healing of persistent epithelial defects.
2 Superficial keratectomy reqd to remove
plaques or debride shield ulcers and allow
epithelialization. Med treatmt be maintained
until the cornea has reepithelialized in order
to prevent recurrences. Excimer laser PTK is an
alternative.
• 3 Surface maintenance-restoration surgery
amniotic membrane overlay grafting or LK, or
eyelid procedures such as botulinum toxin-
induced ptosis or lateral tarsorrhaphy, may be
required for severe persistent epithelial
defects or ulceration. Gluing may be
appropriate for focal (‘punched-out’) corneal
perforations
 Atopic keratoconjunctivitis (AKC)
• an adult equivalent of vernal KC and assoc
with atopic dermatitis. Most of the patients
are young atopic adults, with male
predominance.
Symptoms include:
• Itching, soreness, dry sensation.
• Mucoid discharge.
• Photophobia or blurred vision.
Signs :Lid margins chron inflamed with rounded
posterior borders.
• Skin changes consist of erythema, dryness,
scaliness and thickening, sometimes with
fissuring, and scratches (‘excoriation’) due to
intense itching.
• Assoc staphy blepharitis and madarosis
• Keratinization of the lid margiIN
• Hertoghe sign is characterized by absence of
the lateral portion of the eyebrows
• Tightening of the facial skin may cause lower
lid ectropion and epiphora.
• Conj involvement is pref inferior palpebral, in
VKC superiorly.
• Discharge is more watery than in VKC.
• Papillae initially smaller than VKC ; larger
lesions develop later
• Diffuse conjunctival infiltration and scarring
may give a whitish, featureless appearance
• Cicatricial changes lead to mod sym
blepharon, forniceal shortening, keratinization
of the caruncle
• Limbal involvement , including Horner–Trantas
dots, Tarsal conjunctiva has milky app. There
are very fine papillae, hyperaemia and
scarring with shrinkage.
• Keratopathy a Punctate epithelial erosions
over inferior third of the cornea are common
b Persistent epithelial defects, with
associated focal thinning, can occasionally
progress to perforation.
c Plaque formation may occur.
d Peripheral vascularization and stromal
scarring are more common than in VKC.
e Other manifestations
• Predisposition to secondary bacterial and
fungal infection, and to aggressive herpes
simplex keratitis
• Keratoconus is common (about 15%) and
secondary to chronic ocular rubbing.
• 5 Cataract • Presenile shield-like anterior
or posterior subcapsular cataracts are
common , exacer by long-term steroid RX
• Because of the high lid margin carriage of
S. aureus, cataract surgery carries an
increased risk of endophthalmitis.

6 Retinal detachment is more common

than in the general population corneal
vascularization, thinning and plaques.
Clinical course. Like the dermatitis with which it
is associated, AKC has a protracted course
with exacerbations and remissions. Like vernal
keratoconjunctivitis it tends to become
inactive when the patient reaches the fifth
decade.
Treatment is often frustrating.
• Treat facial eczema and lid margin disease.
• Same as VKC
 Giant (mechanically-induced)
papillary conjunctivitis
• Pathogenesis :Mechanically-induced papillary
conjunctivitis, the severe form of which is
known as giant papillary conjunctivitis (GPC),
can occur secondary to a variety of
mechanical stimuli of the tarsal conjunctiva. It
is most frequently seen with contact lens (CL)
wear, when it is termed contact lens-
associated papillary conjunctivitis (CLPC).
• The risk is increased by the build-up of
proteinaceous deposits and cellular debris on
the contact lens surface . Ocular prostheses,
exposed sutures and scleral buckles, corneal
surface irregularity and filtering blebs can all
be responsible. A related phenomenon is the
so-called ‘mucus fishing syndrome’, when, in a
variety of underlying anterior segment
disorders, patients develop or exacerbate a
chronic papillary reaction due to repetitive
manual removal of mucus
 Diagnosis
1 Symptoms foreign body sensation, redness,
itching, increased mucus production, blurring
and loss of CL tolerance. Symptoms may be
worse after lens removal. Patients should be
questioned about CL cleaning and
maintenance.
2 Signs • Variable mucous discharge.
• Protein deposits on the CL.
• Excessive CL mobility .
• Superior tarsal hyperaemia and initially
fine-medium size papillae (>0.3 mm).
• Focal apical ulceration and whitish scarring
may develop on larger papillae in advanced
cases.
• Keratopathy is rare because of the
relatively subdued secretion of inflammatory
cytokines.
• Ptosis may occur mainly as a result of
irritative spasm and tissue laxity secondary to
chronic inflammation.
 Treatment
1 Remove the stimulus • CL wear should
be discontinued for several weeks .
• For mild–moderate disease, this may be
adequate for resolution, sometimes in
conjunction with reduced wearing time.
• In severe disease a longer interval without
lens wear may be needed.
• Removal of other underlying causes such as
exposed sutures or scleral buckle.
• Assessmt of the status & fit of oc prosthesiS
• Refashioning filtering blebs or GDD.
• 2 Ensure effective cleaning of CL or
prosthesis • Changing the type of CL
solution, ESP preservative-containing prep.
• Switching to mthly then daily disposable
CL if the condition persists after renewing
non-disposable lenses.
• Rigid lenses carry a lesser risk of CLPC
(5%) because they are easier to clean .
• Cessation of CL wear and substituting
spectacles or refractive surgery for severe or
refractory disease.
• Regular (at least weekly) use of contact lens
protein removal tablets.
• Prostheses should be cleaned & polished
• Topical • Mast cell stabilizers should be non-
preserved in patients wearing soft contact
lenses, or can be instilled when the lenses are
not in the eye, with a delay of perhaps half an
hour after drop instillation prior to lens
insertion. can be continued long-term .
.
• Antihistamines, non-steroidal anti-
inflammatory agents and combined
antihistamines/mast cell stabilizers may each
be of benefit.
• Topical steroids can be used for the acute
phase of resistant cases, particularly those
where effective removal of the stimulus is
difficult, as in bleb-related disease
 PHLYCTENULAR
KERATOCONJUNCTIVITIS
• Phlyctenular keratoconjunctivitis is a
characteristic nodular affection occurring as
an allergic response of the conjunctival and
corneal epithelium to some endogenous
allergens to which they have become
sensitized. Phlyctenular conjunctivitis is of
worldwide distribution. However, its incidence
is higher in developing countries.
• Etiology It is believed to be a delayed
hypersensitivity (Type IV-cell mediated)
response to endogenous microbial proteins.
I. Causative allergens
1. Tuberculous proteins were considered,
previously, as the most common cause.
• 2. Staphylococcus proteins are now thought to
account for most of the cases.
• 3. Other allergens may be proteins of
Moraxella Axenfeld bacillius and certain
parasites (worm infestation).
• II. Predisposing factors
• 1. Age. Peak age group is 3-15 years.
• 2. Sex. Incidence is higher in girls than boys.
• 3. Undernourishment. Disease is more
common in undernourished children.
• 4. Living conditions. Overcrowded &
unhygienic.
• 5. Season. It occurs in all climates but
incidence is high in spring and summer
seasons.
 Pathology
• 1. Stage of nodule formation. In this stage
there occurs exudation and infiltration of
leucocytes into the deeper layers of
conjunctiva leading to a nodule formation.
The central cells are polymorphonuclear and
peripheral cells are lymphocytes.
• The neighbouring blood vessels dilate and
their endothelium proliferates.
• 2. Stage of ulceration. Later on necrosis occurs
at the apex of the nodule and an ulcer is
formed. Leucocytic infiltration increases with
plasma cells and mast cells.
• 3. Stage of granulation. Eventually floor of the
ulcer becomes covered by granulation tissue.
• 4. Stage of healing. Healing occurs usually
with minimal scarring
 Clinical picture
• Symptoms in simple phlyctenular
conjunctivitis are few, like mild discomfort in
the eye, irritation and reflex, watering.
However there is associated mucopurulent
conjunctivitis due to secondary bacterial
infection.
• Signs. The phlyctenular conjunctivitis can
present in three forms: simple, necrotizing
and miliary.
• 1. Simple phylctenular conjunctivitis. It is the
most commonly seen variety. It is
characterised by the presence of a typical
pinkish white nodule surrounded by
hyperaemia on the bulbar conjunctiva, usually
near the limbus. Most of the times there is
solitary nodule but at times there may be two
nodules . In a few days the nodule ulcerates at
apex which later on gets epithelised. Rest of
the conjunctiva is normal.
• 2. Necrotizing phlyctenular conjunctivitis is
characterised by the presence of a very large
phlycten with necrosis and ulceration leading
to a severe pustular conjunctivitis.
• 3. Miliary phlyctenular conjunctivitis is
characterised by the presence of multiple
phlyctens which may be arranged haphazardly
or in the form of a ring around the limbus and
may even form a ring ulcer.
 Phlyctenular keratitis
• . Corneal involvement may occur secondarily
from extension of conjunctival phlycten; or
rarely as a primary disease. It may present in
two forms: the 'ulcerative phlyctenular
keratitis' or 'diffuse infiltrative keratitis
A. Ulcerative phlyctenular keratitis may occur
in the following three forms:
• 1. Sacrofulous ulcer is a shallow marginal ulcer
formed due to breakdown of small limbal
phlycten
• . It differs from the catarrhal ulcer in that
there is no clear space between the ulcer and
the limbus and its long axis is frequently
perpendicular to limbus. Such an ulcer usually
clears up without leaving any opacity.
• 2. Fascicular ulcer has a prominent parallel
leash of blood vessels . This ulcer usually
remains superficial but leaves behind a
bandshaped superficial opacity after healing.
• 3. Miliary ulcer. In this form multiple small
ulcers are scattered over a portion of or whole
of the cornea.
• B. Diffuse infiltrative phlyctenular keratitis
may 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.
• Clinical course is usually self-limiting and
phlycten disappears in 8-10 days leaving no
trace. However, recurrences are very common.
 Differential diagnosis
• Phlyctenular conjunctivitis needs to be
differentiated from the episcleritis, scleritis,
and conjunctival foreign body granuloma.
• Presence of one or more whitish raised
nodules on the bulbar conjunctiva near the
limbus, with hyperaemia usually of the
surrounding conjunctiva, in a child living in
bad hygienic conditions (most of the times)
are the diagnostic features of the phlyctenular
conjunctivitis.
 Management
1. Local therapy.
i. Topical steroids .
ii. Antibiotic drops and ointment to take care of
the associated secondary infection.
iii. Atropine (1%) when cornea is involved.
2. Specific therapy. eradicate causative conditns
i. Tuberculous infection should be excluded.
ii. Septic focus tonsillitis, adenoiditis, or caries
teeth,
iii. Parasitic infestation should be ruled out.
CONTACT DERMOCONJUNCTIVITIS
• an allergic disorder, involving conjunctiva and
skin of lids along with surrounding face.
• Etiology
• It is a delayed hypersensitivity (type IV)
response to prolonged contact with chemicals
and drugs.
• common topical ophthalmic medications
which cdc are
• atropine, penicillin, neomycin, soframycin and
gentamycin..
• Clinical picture
• 1. Cutaneous involvement is in the form of
weeping eczematous reaction, involving all
areas with which medication comes in
contact.
• 2. Conjunctival response is in the form of
hyperaemia with a generalised papillary
response affecting the lower fornix and lower
palpebral conjunctiva more than the upper
• Diagnosis is made from: Typical clinical
picture. Conjunctival cytology shows a
lymphocytic response with masses of
eosinophils. Skin test to the causative allergen
is positive in most of the cases.
• Treatment consists of:
1. Discontinuation of the causative medication,
2. Topical steroid eye drops to relieve symptoms
3. Application of steroid ointment on the
involved skin.
 Conj in blistering mucocutaneous
diseases
• Mucous membrane pemphigoid
• S–J syndrome-TEN(Lyell syndrome)
• Atopic (and less commonly vernal) KC
• Conjunctival chemical and thermal burns
• Severe bacterial or viral conjunctivitis
• Trachom • Drug-induced
• OtherS: epidermolysis bullosa, pemph vulg,
linear IgA disease, dermatitis herpetiformis,
lichen planus, porphyria cutanea tarda, xerode
pigmentosum, scleroderma, xerophthalmia
 Mucous membrane pemphigoid
• (MMP)/ cicatricial pemphigoid (CP): a chr
autoimmune mucocutaneous blistering
diseases charac by linear antibody and
complement deposition at epithelial BM
• involve the skin & mucous membranes of the
mouth, nasopharynx, upper airways, genitalia,
and gastrointestinal tract.
• Particular clinical forms :bullous pemphigoid
(BP) shows a predilection for skin, also affects
the mouth and other tissues. (OCP) involves
the conjunctiva and causes (cicatrization).
• The disease typically presents in old age and
affects females more than males 2 : 1 ratio
• Ocular features
• 1 Presentation is with the insidious onset
of non-specific conjunctivitis which is bilateral,
but frequently asymmetrical. Because of its
rarity, the diagnosis is often overlooked or
there may be misdiagnosis, with specific
treatment being delayed.
2 Conjunctiva • Papillary conjunctivitis,
diffuse hyperaemia and oedema, and necrosis
• Fine lines of subconjunctival fibrosis and
shortening of the inferior fornices .
• Flattening of the plica and keratinization
of the caruncle .
• Symblepharon (plural symblephara) is an
adhesion between the bulbar and palpebral
conjunctiva .
• Dry eye is caused by a combination of
destruction of goblet cells and accessory
lacrimal glands as well as occlusion of the
main lacrimal ductules. .
• The chronically progressive course of the
disease may be punctuated by exacerbations.
• Disease progression should be regularly
monitored by measuring the depth of the
fornices and noting the position of adhesion
• 3 Cornea • Epithelial defects associated
with drying and exposure
• Infiltration and peripheral vascularization
• Keratinization and ‘conjunctivalization’ of
the corneal surface following damage to the
limbus & conseq epithelial stem cell failure
• End-stage disease is characterized by
total symblepharon and corneal opacification (
• 4 Eyelids • Aberrant (dysplastic) lashes,
chronic blepharitis and keratinization of the lid
margin.
• Ankyloblepharon, in which there are
adhesions at the outer canthus between the
upper and lower lids.s
• Systemic features
• 1 Mucosal involvement is characterized by
subepidermal blisters, frequently oral . The
blisters rupture within a day or two leaving
erosions & ulcers that heal without significant
scarring. Ulcers in other sites typically heal
with scarring which result in stricture formatn.
Stricture of the oesophagus can result in
regurgitation and aspiration of food. Laryngeal
or tracheal stenosis may be life-threatening.
2 Skin lesions less common (25%) present
as tense blisters and erosions. involve head
and neck , the groins and extremities
 Systemic treatment
• 1 Dapsone first-line treatment in patients
with mild–moderate disease, at1 mg/kg daily
increasing to 100 mg or 200 mg, if tolerated;
approximately 70% of patients respond. The
drug is contraindicated in G6PD deficiency.
2 Antimetabolites such as azathioprine,
methotrexate or mycophenolate mofetil are
alternatives for mild–moderate disease if
dapsone is contraindicated, ineffective or
poorly tolerated, and are suitable for long-
term therapy.
• 3 Steroids (oral prednisolone 1–1.5 mg/kg)
are effective for rapid disease control, but
adverse effects virtually preclude the long-
term use of higher doses.
4 Other measures • Intravenous
immunoglobulin therapy has shown promising
results in some patients unresponsive to other
agents.
• Ciclosporin has been used with apparent
benefit although data to support its effect are
limited.
• Local treatment
• 1 Topical • Artificial tears
• Steroids as adjunctive treatment.
• Retinoic acid may reduce keratinization.
• Antibiotics when indicated.
• Lid hygiene and low-dose oral
tetracycline for blepharitis.
2 Subconjunctival mitomycin-C and/or
steroid injection may be used if systemic
immunosuppression is not possible.
3 Contact lenses may be used with caution
to protect the cornea from aberrant lashes
and from dehydration.
• Reconstructive surgery under systemic steroid
cover, considered when active disease is
controlled.
• • Aberrant eye lashes can be treated by
laser ablation or cryotherapy; the latter may
be combined with lid splitting
• Severe dry eyes may be helped by
punctal occlusion if no punc scarring.
• Promotion of healing of persistent or
recu corneal epithelial defects by lat tarsorr
haphy or botulinum toxin-induced ptosis.
• • Entropion managed by a procedure (e.g.
retractor plication) that does not involve
conjunctival incision.
• Conjunctival keratinization may be
addressed by mucous membrane autografting
(e.g. oral) or amniotic membrane
transplantation; these techniques can also be
used for forniceal restoration.
• Limbal stem cell transfer may be
attempted for corneal epithelialization failure.
• Keratoplasty carries a high risk of failure
due to surface morbidity; lamellar grafts may
be effective for perforations.
• Keratoprostheses in end-stage disease.
 Stevens–Johnson syndrom TEN
(Lyell syndrome)
• Definition :Previously, the terms ‘Stevens–
Johnson syndrome (SJS)’ and ‘erythema
multiforme major’ used synonymously.
However, i now erythema multiforme is a
distinct disease, milder and recurrent,
dissimilar c f and a tendency for diff ppitating
factors (erythema multiforme predominantly
infections, Stevens–Johnson predominantly
drugs).
• ‘Toxic epidermal necrolysis’ (TEN – Lyell
syndrome) is a severe variant of SJS.
Classically, SJS/TEN patients tend to be young
adults, though other age groups, including
children and the elderly, may be affected. An
SJS-type presentation is more common in
males than females, with the reverse probably
true for TEN
• Pathogenesis
• a cell-mediated delayed hypersensitivity
immune reaction , either directly to drugs or
to epithelial cell antigens modified by drug
exposure. drugs incriminated includE
antibiotics (esp sulfonamides and trimetho
prim), analgesics, cough and cold remedies,
cocaine, NSAIDS, anticonvulsants allopurinol.
• Micro-org incl Mycoplasma pneumoniae and
herpes simplex virus (HSV). Because symp
take 3 wks to develop after exp, in 50%
ppting cause cant be identified with certainty.
• 1 Presentation is with flu-like symptoms
which last up to 14 days before the app of
mucocutaneous lesions.
2 Acute signs • Haemorrhagic crusting
of lid margins that may become confluent.
• Papillary conjunctivitis, which can range
from mild, transient & self-limiting to severe.
• Conjunctival membranes & pseudo
membranes, severe hyperaemia, hrhages,
blisters and patchy infarction.
• Keratopathy : a spectrum fm punctate
erosions to larger epithelial defects, secondary
bacterial keratitis and occasi perforation.
• Late signs • Keratinization of the
conjunctiva and lid margi, sometimes with
abrasive plaque formation.
• Posterior lid margin disease with opening
of meibomian gland orifices onto the lid
surface .
• Forniceal shortening and symblepharon
formation.
• Eyelid complications include cicatricial
entropion and ectropion, trichiasis,
metaplastic lashes and ankyloblepharon.
• Keratopathy including scarring,
vascularization and keratinization as a result of
the primary inflammation and/or infection, as
well as cicatricial entropion and aberrant
lashes.
• Watery eyes due to fibrosis of the
lacrimal puncta. Dry eyes may also occur as a
result of fibrosis of lacrimal gland ductules and
conjunctival metaplasia with loss of goblet
cells.
• Systemic features
• 1 Mucosal involvement is characterized by
blistering and haemorrhagic crusting of the
lips . The blisters may also involve the tongue,
oropharynx, nasal mucosa and occasionally
the genitalia.
2 Skin • Small purpuric, vesicular or
necrotic lesions involving the extremities, face
and trunk . These are usually transient but
may be widespread. Healing usually occurs
within 1–4 weeks, leaving a pigmented scar.
• Widespread sloughing of the epidermis is
uncommon.
• 3 ‘Target’ lesions showing the classic three
zones are now viewed as characteristic of
erythema multiforme rather than SJS/TEN, but
the mucosal lesions appear similar in both
conditions
• Systemic treatment
• 1 Removal of the precipitant if possible,
such as discontinuation of drugs and
treatment of suspected infection.
2 General supportive measures such as
maintenance of adequate hydration,
electrolyte balance and nutrition (especially
protein replacement) are critical.
Management in a specialist burns unit should
reduce the chance of infection when the
extent of skin involvement is substantial.
• 3 Systemic steroids remain controversial.
There are reports of increased mortality in
older papers, but later research has raised the
possibility that early high-dose intravenous
treatment may improve outcomes.
4 Other immunosuppressants including
ciclosporin, azathioprine, cyclophosphamide
and intravenous immunoglobulin may be
considered in selected cases, but are
controversial and controlled trials are lacking.
5 Systemic antibiotics may be given as
prophylaxis against skin or other systemic
infection, avoiding those known to be at
higher risk of precipitating SJS/TEN
• Ocular treatment
• 1 Acute disease • Topical lubricants.
• Topical steroids may be used but their
efficacy has not been demonstrated
conclusively.
• Lysis of developing symblephara with a
sterile glass rod or damp cotton bud.
• A scleral ring, consisting of a large haptic
lens with the central zone removed, may help
to prevent symblepharon formation .
• Pseudomembrane/membrane peeling
can be considered
• Treatment of bacterial keratitis.
• 2 Chronic disease management addressing
complications. • Adequate lubrication,
including punctal occlusion if necessary.
• Topical transretinoic acid 0.01% or
0.025% may reverse keratinization.
• Treatment of aberrant lashes.
• Bandage contact lenses (typically gas
permeable scleral lenses ) to maintain surface
moisture, protect the cornea from aberrant
lashes, and address irregular astigmatism.
• Mucous membrane grafting (e.g. buccal
mucosa autograft) for forniceal
reconstruction.
• 3 Corneal rehabilitation may involve the
following: • Superficial keratectomy for
keratinization.
• In eyes with reasonable stem cell
function, lamellar corneal grafting may be
used for superficial scarring and is generally
preferred to penetrating keratoplasty.
• Amniotic membrane grafting.
• Limbal stem cell transplantation
(cadaveric or living relative).
• Keratoprosthesis implantation in end-
stage disease.
Superior limbic keratoconjunctivitis
• uncommon chr disease of the superior limbus
and the superior bulbar and tarsal conjunc.
• affects both eyes of middle-aged women,
approx 50% of whom have abnormal thyroid
function (usually hyperthyroidism); approx 3%
of patients with thyroid eye disease have SLK.
• symptoms are more severe than signs. course
over years although remission spontaneous.
• similarities to mech-induced papillary conj,
contact lens wear and following upper lid
surgery or trauma.
 Diagnosis
1 Presentation : non-specific symptoms often
intermittent: FB sensation, burning, mild
photophobia, mucoid disch & freq blinking.
2 Conjunctiva Papillary hypertrophy of the
superior tarsus, often a diffuse velvety app.
• Hyperaemia of a radial band of the sup
bulbar conjunctiva & limbal pap hypertrophy .
• Light downward pressure on the upper
lid results in a fold of redundant conjunctiva
crossing the upper limbus .
• Petechial haemorrhages may be present.
• 3 Cornea • Superior punctate corneal
epithelial erosions are common and are often
separated from the limbus by a zone of
normal epithelium.
• Superior filamentary keratitis develops in
about one-third of cases.
• Mild superior pannus resembling arcus
senilis may develop in long-standing disease.
4 Keratoconjunctivitis sicca is present in
only about 50% of cases.
5 Thyroid function testing should be
performed if the patient is not already known
to have thyroid dysfunction.
 Treatment
1 Topical a Lubricants to reduce friction b/n
the tarsal & bulbar conjunctiva
b Acetylcysteine 5% or 10% q.i.d. to break
down filaments and provide lubrication.
c Mast cell stabilizers antiinflammatory ;
steroids : best used in short intensive courses
with rapid tapering, esp severe cases.
d Ciclosporin 0.05% b.d. as prim or adjunctive
therapy, esp in keratoconjunctivitis sicca
e Retinoic acid to retard keratinization
f Auto serum 20% drops; up to 10 times/ day
2 Soft contact lenses between the lid and the
superior conjunctiva, are effective in some
cases. , a unilat lens may provide bilatl relief.
3 Supratarsal steroid injection. 0.1 mL of
triamcinolone 40 mg/mL antiinflammatory.
4 Temporary superior and/or inferior
punctal occlusion using a plug.
5 Resection of sup limbal conj, in a zone
2 mm from the sup limbus or of area staining
with rose bengal, in resistant disease. Lax conj
removed, with regrowth firmly anchored.
6 Conjunctival ablation by Ag NO3 0.5% or
thermocautery to the affected area.
7 Treatment of assoc thyroid dysfunction.
 Ligneous conjunctivitis
• a very rare disorder charac by recurrent, often
bilat fibrin-rich pseudomembranous lesions of
wood-like consistency that develop on the
tarsal conj.
• It is a systemic condition which may involve
the periodontal tissue, the upper and lower
respiratory tract, kidneys, middle ear and
female genitalia. It can be sight-threatening,
and death can occasionally occur from
pulmonary involvement.
 Diagnosis
1 Presentation is with nonspecific conjunc,
usually in childhood (median age 5 years),
although onset may be at any age. .
2 Signs • Red-white lobular conjunctival
masses .
• The lesions may be covered by a yellow-
white thick mucoid discharge .
• Corneal scarring, vascularization,
infection or melting in advanced disease.
 Treatment
Treatment: unsatisfactory & spont resolutn
rare. discontinue any antifibrinolytic
drugs. 1 Surgical removal with diathermy
of the base of the lesion. Pre-op topical
plasminogen may soften pseudomembranes
and facilitate removal.
2 Topical • Foll membrane removal,
hrly heparin and steroids are given until the
wound has re-epithelialized, with tapering
over weeks until signs of inflamm disappear.
• Recurrence may be retarded by long-
term ciclosporin and steroid instillation.
• 3 Other modalities • Intravenous or
topical plasminogen.
• Amniotic membrane transplantation to
the conjunctiva following lesion removal.
 GRANULOMATOUS
CONJUNCTIVITIS
• specific chronic inflammations of the
conjunctiva, characterised by proliferative
lesions which r localized to one eye and
associated with regional lymphadenitis
• Tuberculosis of conjunctiva
• Sarcoidosis of conjunctiva
• Syphilitic conjunctivitis
• Leprotic conjunctivitis
• Conjunctivitis in tularaemia
• Ophthalmia nodosa
• Parinaud's oculoglandular syndrome : group
of conditions characterised by:
1. Unilateral granulomatous conjunctivitis
(nodular elevations surrounded by follicles),
2. Preauricular lymphadenopathy, and
3. Fever.
• Its common causes are tularaemia, cat-
scratch disease, tuberculosis, syphilis and
lymphogranuloma venereum
• Ophthalmia nodosa (Caterpillar hair
conjunctivitis) a granulomatous inflammation
of the conjunctiva characterized by formation
of a nodule on the bulbar conjunctiva in
response to irritation caused by the retained
hair of caterpillar.
• The disease is, therefore common in summers.
may be often mistaken for a tubercular
nodule.
• Histopathological examination reveals hair
surrounded by giant cells and lymphocytes.
• Treatment consists of excision biopsy of the
nodule.
 Factitious conjunctivitis
• Self-injury often intentional: inadvertently in
mucous fishing syndrome & contact lens
removal .
• Damage may be the result of either
mechanical abrasion or perforation, or of the
instillation of irritant but readily accessible
household substances, such as soap.
• Occasionally over-instillation of prescribed
ocular medication is responsible.
 Diagnosis
• Inferior conjunct injection & staining with
rose bengal , with a quiet sup bulbar conjunc.
• Linear K abrasions, persistent epithelial
defects & occasionally focal K perforation.
• Secondary infection with Candida spp.
• Sterile ring infiltrate and hypopyon.
• Corneal scarring.
• The patient may have sought multiple
medical opinions over an extended perioD
• symptoms disproportionate to signs.
Management
• Exclude other diagnoses.
• Close observation may be required
• Confrontation often leads to failure to return
for review.
• A psychiatric opinion may be appropriate.
 Degenerations : Pingueculum
• A pingueculum : common, innocuous, bilat
and asymptomatic ‘elastotic’ degeneration of
collagen fibres of conjunctival stroma.
• The cause is : actinic damage, similar to the
aetiology of pterygium .
• 1 Signs. A yellow-white mound or aggregn of
smaller mounds on bulbar conjunc adjacent
to the limbus. more frequently located at the
nasal than the temporal limbus , although is
frequently present at both. Calcification is
occasionally visible.
• 2 Treatment is usually unnecessary because
growth is very slow or absent. Occasionally,
however, a pingueculum may become acutely
inflamed (pingueculitis) and require a short
course of a weak steroid such as
fluorometholone. Excision is occasionally
performed for cosmetic reasons or if a large
lesion is causing significant irritation
 Pterygium
• A pterygium is a triangular fibrovascular
subepithelial ingrowth of degen bulbar conj
tissue over the limbus onto the cornea.
• It typically develops in patients who living in
hot climates and, as with pinguecula, may
represent a response to ultraviolet exposure
and possibly to other factors such as chronic
surface dryness.
• A pterygium is histo similar to a pingueculum
and shows elastotic degenerative changes in
vascularized subepithelial stromal collagen
 Types
• . Depending upon the progression it may be
progressive or regressive pterygium.
• Progressive pterygium is 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.
 Clinical features
• Symptoms • asymptomatic.
• Irritation & grittiness caused by dellen effect
advancing edge d/t interference with tear film.
• Pts using contact lenses develop symptoms
of irritation at an earlier stage due to edge lift.
• Interference with vision by obscuring the
visual axis or inducing astigmatism.
• Intermittent inflam similar to pingueculitis
• Cosmesis may be a significant problem
• If pseudopterygium is suspected, there may
be a history of a causative episode
• Signs. A pterygium is made of 3 parts: a ‘cap’
(an avascular halo-like zone at the advancing
edge), a head, and a body. a Type 1
extends less than 2 mm onto the cornea . A
deposit of iron (Stocker line) may be seen in
the corneal epithelium anterior to the
advancing head of the pterygium.
b Type 2 involves up to 4 mm of the cornea &
may be primary or recurrent following surgery
c Type 3 encroaches onto more than 4 mm of
the cornea and involves the visual axis
CAP

BODY

HEAD
• d Pseudopterygium is caused by a band of
conjunctiva adhering to an area of
compromised cornea at its apex. It forms as a
response to an acute inflammatory episode
such as a chemical burn , corneal ulcer
(especially if marginal), trauma and cicatrizing
conjunctivitis
 Treatment
• 1 Medical treatment of symptomatic patients
involves tear substitutes, & topical steroids for
inflammation. The patient may be advised to
wear sunglasses to reduce ultraviolet
exposure decrease the growth stimulus.
• 2 Surgical technique. Simple excision (‘bare
sclera’ technique) is associated with a high
rate of recurrence (around 80%) that may be
more aggressive than the initial lesion. .
• Simple conjunctival flap
• Conjunctival autografting, currently the most
popular approach. The donor conjunctival
patch is usually harvested from the superior
paralimbal region – the site usually heals well.
• Adjunctive treatment with mitomycin C or
beta-irradiation; may rarely be complicated by
late scleral necrosis.
• Amniotic membrane patch grafting (
reserved for aggressive lesns or recurrences).
• Occasionally peripheral lamellar keratoplasty
is required for deep lesions
 Concretions
• v common & usually assoc with aging,though
they can also form in patients with chronic
conjun inflam such as trachoma
• 1 Signs • Multiple tiny cysts containing
yellowish-white deposits of epithelial debris
including keratin, usually located
subepithelially in the inferior tarsal and
forniceal conjunctiva .
• Can become calcified and, particularly if
large, may erode the overlying epithelium and
cause irritation.
• 2 Treatment of symptomatic concretions
involves removal at the slit-lamp with a needle
under topical anaesthesia.
Tumours
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